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Fluids &
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Fluids &
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STAFF The clinical procedures described and recommended in

this publication are based on research and consultation
Executive Publisher with medical and nursing authorities. To the best of our
Judith A. Schilling McCann, RN, MSN knowledge, these procedures reflect currently accepted
Editorial Director clinical practice; nevertheless, they can’t be considered
William J. Kelly absolute and universal recommendations. For individual
application, treatment recommendations must be con-
Clinical Director sidered in light of the patient’s clinical condition and,
Joan M. Robinson, RN, MSN before administration of new or infrequently used drugs,
in light of the latest package-insert information. The
Senior Art Director authors and the publisher disclaim responsibility for any
Arlene Putterman adverse effects resulting directly or indirectly from the
Editorial Project Manager suggested procedures, from any undetected errors, or
Catherine E. Harold from the reader’s misunderstanding of the text.

Clinical Project Managers © 2006 by Lippincott Williams & Wilkins. All rights re-
Tamara M. Kear, RN, MSN, CNN; served. This book is protected by copyright. No part of it
Beverly Ann Tscheschlog, RN, BS may be reproduced, stored in a retrieval system, or
transmitted, in any form or by any means — electronic,
Editor mechanical, photocopy, recording, or otherwise —
Nancy Priff without prior written permission of the publisher, except
Clinical Editors for brief quotations embodied in clinical articles and
Karen Hamel, RN, BSN; Kate McGovern, RN, MSN reviews and test and evaluation materials provided by
publisher to instructors whose schools have adopted its
Copy Editor accompanying textbook. Printed in the United States of
Jenifer F. Walker America. For information, write Lippincott Williams &
Wilkins, 323 Norristown Road, Suite 200, Ambler, PA
Designers 19002-2756.
Will Boehm (book design),
E. Jane Spencer (project manager) NQCFE – D N O S A J J M A M F J
Digital Composition Services 07 06 05 10 9 8 7 6 5 4 3 2 1
Diane Paluba (manager), Joyce Rossi Biletz,
Donna S. Morris
Library of Congress Cataloging-in-Publication Data
Patricia K. Dorshaw (director), Beth J. Welsh Nurse’s quick check. Fluids & electrolytes.
p. ; cm.
Editorial Assistants Includes bibliographical references and index.
Megan Aldinger, Karen Kirk, Linda Ruhf 1. Water-electrolyte imbalances—Nursing—Handbooks,
manuals, etc. 2. Water-electrolyte balance (Physiology)—
Indexer Handbooks, manuals, etc. I. Lippincott Williams &
Barbara Hodgson Wilkins. II. Title: Fluids & electrolytes. [DNLM: 1. Water-
Electrolyte Imbalance—nursing—Handbooks. 2. Nursing
Care—Handbooks. WY 49 N97423 2006]
RC630.N87 2006
ISBN 1-58255-414-5 (alk. paper) 2004031001
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Contributors and consultants vii

Foreword ix

Part one
Essential concepts 1

Part two
Disorders related to
fluid and electrolyte
imbalance (in alphabetical order) 43

Common fluid and electrolyte

imbalances in pediatric patients 286
Common fluid and electrolyte
imbalances in elderly patients 287
NANDA II taxonomy codes 288
Herbs that affect fluids and electrolytes 291
Selected references 294
Index 296

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and consultants

Marguerite Ambrose, RN, DNSc, APRN, BC Shelba Durston, RN, MSN, CCRN
Faculty, Department of Nursing Adjunct Faculty
Immaculata University San Joaquin Delta College
Immaculata, Pa. Stockton, Calif.
Staff Nurse
Patricia Laing Arie, RN, BSEd San Joaquin General Hospital
Coordinator, Practical Nursing French Camp, Calif.
Central Technology Center
Drumright, Okla. Helen Fu, MSN, FNP
Family Nurse Practitioner
Margaret W. Bellak, RN, MN Soteria Family Health Center
Associate Professor Plymouth, Minn.
Indiana University of Pennsylvania
Indiana, Pa. Margaret M. Gingrich, RN, MSN
Associate Professor
Mary Ann Boucher, RN, ND, APRN, BC Harrisburg Area Community College
Assistant Professor, Nursing Harrisburg, Pa.
University of Massachusetts Dartmouth
Dartmouth, Mass. David J. Hartman, MSN, CRNP
Nurse Practitioner
Cheryl L. Brady, RN, MSN University of Pennsylvania Health System
Adjunct Faculty Philadelphia
Kent State University
East Liverpool, Ohio Angela R. Irvin, RN, BSN, FNP student
Clinical Instructor
Shari Regina Cammon, RN, MSN, CCRN Western Kentucky University
Clinical Risk Management & Safety Surveillance Bowling Green, Ky.
Merck & Co., Inc. Kathy J. Keister, RN, MS
West Point, Pa. Assistant Professor
Miami University
Lillian Craig, MSN, FNP, CS Middletown, Ohio
Family Nurse Practitioner
Veterans’ Administration Medical Center Linda Kucher, RN, MSN
Amarillo, Texas Assistant Professor of Nursing
Gordon College
Peggy A. Davis, RN, MSN, CNS Barnesville, Ga.
Assistant Professor of Nursing
University of Tennessee Ellen Marcolongo, RN, MSN, CRNP
Martin, Tenn. Clinical Nurse Specialist
North Philadelphia Health System
Philadelphia, Pa.

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Dawna Martich, RN, BSN, MSN Bruce Austin Scott, MSN, APRN, BC
Clinical Trainer Instructor
American Healthways San Joaquin Delta College
Pittsburgh, Pa. Stockton, Calif.
Clinical Nurse
Lakshmi McRae, RNC, BA University of California, Davis Medical Center
Staff Nurse Sacramento, Calif.
Doctor’s Outpatient Surgical Center
Pasadena, Texas Patricia Weiskittel, RN, MSN, CNN, APRN, BC
Primary Care Nurse Practitioner, Internal Medicine
Valerie Mignatti, RN, BSN Veterans Administration Hospital
Cardiovascular Clinical Nurse Cincinnati, Ohio
University of Pennsylvania Medical Center
Philadelphia Sharon Wing, RN, MSN
Assistant Professor
Sharon D. O’Kelley, ADN, OCN Cleveland State University
Clinical Nurse III Cleveland, Ohio
Duke University Hospital
Durham, N.C. Denise York, RNC, CNS, MS, MEd
Associate Professor
Sherry A. Parmenter, RD, LD Columbus State Community College
Clinical Dietitian Columbus, Ohio
Fairfield Medical Center
Lancaster, Ohio

Clare Petrotta, RN, PHN, BSN

Nursing Instructor
Pacific College
Costa Mesa, Calif.

Abby Plambeck, RN, BSN

Freelance Writer
Milwaukee, Wis.

Theresa Pulvano, RN, BSN

Practical Nursing Instructor
Ocean County Vocational Technical School
Lakehurst, N.J.

Monica Narvaez Ramirez, RN, MSN

University of the Incarnate Word School of Nursing &
Health Professions
San Antonio, Texas

Lisa A. Salamon, MSN, RNBC, ET

Clinical Nurse Specialist
Cleveland Clinic Foundation
Cleveland, Ohio

Barbara K. Scheirer, RN, BS, MSN

Assistant Professor
Grambling State University
Grambling, La.

viii Contributors and consultants

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For students and practicing nurses alike, there’s one fluid movement, volume shifts, major cations and an-
physiologic concept that intimidates nearly everyone: ions, acid-base balance, fluid and electrolyte replace-
fluids and electrolytes. Many disorders can cause or ment, parenteral nutrition, and dialysis.
influence fluid shifts, electrolyte imbalances, acid-base Throughout the book, you’ll find special icons de-
imbalances, and metabolic problems. In some cases, signed to direct your attention to important details:
these changes can be life-threatening. An A LERT icon highlights crucial information, and an
What’s more, many treatments influence fluid and AGE AWARE icon points out information particular to
electrolyte status. Take just one example: I.V. therapy. A certain age groups.
patient with an I.V. line may be receiving parenteral The fact is that nurses are the patient’s first and last
maintenance to replace fluids, electrolytes, or both. line of defense when it comes to overall care. Clearly,
The fluid may be serving as a carrier for parenterally that care must encompass issues of acid-base balance,
administered drugs. It may contain additives that sig- fluid volume composition, and interpretation of the
nificantly affect the patient’s fluid and electrolyte bal- laboratory values that reveal the patient’s fluid and
ance. And it may be running into a patient whose in- electrolyte status. I’ve heard many a nurse say in frus-
nate ability to maintain homeostasis is compromised tration, head bent over a patient’s lab report, “If only I
by a disease, an injury, or an imbalance. had a quick key or refresher to help me understand
To care for your patients appropriately, you need a the imbalances I’m seeing here, I’d feel so much more
solid foundation of understanding fluids and elec- confident.” Of course, they have laboratory books,
trolytes, acids and bases, pH, buffering mechanisms, medical-surgical books, and pathophysiology books,
and more. Plus, you need to be able to weave your but not at their fingertips, not on the unit, and not in a
knowledge about disorders together with your knowl- format that allows a quick check.
edge about treatments to help predict and manage Understanding the intricacies of fluid and electrolyte
their combined effects on fluids and electrolytes. balance can be intimidating, but it’s crucial to good
To many nurses, that seems like a tall order. That’s nursing care — not just for patients receiving infusion
why I’m so pleased with Nurse’s Quick Check: Fluids therapy, but for all patients. In my view, Nurse’s Quick
& Electrolytes. Written by expert nurses, it offers suc- Check: Fluids & Electrolytes offers practical, time-
cinct, two-page entries on all the major disorders that saving help with this complex area of nursing care. I
affect fluid and electrolyte balance. Each entry includes recommend it highly.
information designed especially to cover what nurses
need to know. You’ll find a description of the disorder Patricia N. Allen, RN, MSN, APRN
followed by a brief review of its pathophysiology, caus- Clinical Instructor, School of Nursing
es, prevalence, and complications. You’ll find essential Indiana University
elements of assessment, including history, physical
findings, and test results. And you’ll find a review of
nursing diagnoses, outcomes, interventions, patient
teaching, and discharge planning.
The best part is that all the material is presented in
scan-and-go bulleted lists that spare you the laborious
reading most books require.
To provide even more help, the book opens with a
quick refresher course in fluid and electrolyte basics
that’s presented in the same time-saving format as the
main part of the book. It covers such crucial topics as

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Part one
Essential concepts

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Fluid types solution until the two solutions have equal concen-
trations of solutes.
Hypertonic solutions
Fluid tonicity ❍ A hypertonic solution has a higher solute concentra-
tion than another solution to which it's being com-
Isotonic solutions pared.
❍ A solute is a substance that's dissolved in a solvent. ❍ For instance, say one solution contains a large
Together, they make a solution. amount of sodium and a second solution contains
❍ An isotonic solution has the same solute concentra- much less sodium. The first solution is hypertonic
tion as another solution to which it's being com- compared with the second solution.
pared. ❍ Dextrose 5% in normal saline solution is an example
❍ Normal saline solution is an example of an isotonic of a hypertonic solution because the concentration
solution; its concentration of sodium nearly equals of solutes in the solution is greater than the concen-
the concentration of sodium in blood. (See Under- tration of solutes in blood.
standing isotonic, hypotonic, and hypertonic so- ❍ Because the body seeks equilibrium, fluid from the
lutions.) less concentrated solution will move into the hyper-
❍ If two fluids in adjacent compartments have equal tonic solution until the two solutions contain equal
concentrations of a certain solute — if they're iso- concentrations of solutes.
tonic, in other words — the fluid in each compart-
ALERT Fluid shifts can have important impli-
ment stays where it is.
cations for your nursing care. For instance, if
❍ A balanced solute concentration means no net shift
you give a hypotonic fluid to a patient, it may cause
in fluid.
too much fluid to shift out of the veins (where the flu-
Hypotonic solutions id is delivered) and into the cells, and the cells can
swell. Conversely, if you give a hypertonic solution to
❍ A hypotonic solution has a lower solute concentra-
a patient, it may cause too much fluid to shift out of
tion than another solution to which it's being com-
the cells and into the bloodstream, and the cells can
❍ If one solution contains only a little sodium and an-
other solution contains more sodium, the first solu-
tion is hypotonic compared with the second solution. Fluid locations
❍ Half-normal saline solution is an example of a hypo-
tonic solution; its concentration of sodium is lower Intracellular fluid
than the concentration of sodium in blood. ❍ Intracellular fluid is the fluid that's inside cells.
❍ The body constantly seeks to maintain a state of bal- ❍ In a typical adult, intracellular fluid averages about
ance, or equilibrium. As a result, fluid from the hy- 40% of body weight, or about 28 L.
potonic solution shifts into the more concentrated

Understanding isotonic, hypotonic, and hypertonic solutions

Isotonic solution Hypotonic solution Hypertonic solution
There's no net fluid shift between iso- When a less concentrated, or hypo- If one solution has more solutes than
tonic solutions because the solutions tonic, solution is placed next to a more an adjacent solution, it has less fluid
contain equal concentrations of concentrated solution, fluid shifts relative to the adjacent solution. Fluid
solutes. from the hypotonic solution into the will move out of the less concentrated
more concentrated compartment to solution into the more concentrated,
equalize concentrations. or hypertonic, solution until both solu-
tions have the same amount of solutes
and fluid.

Hypotonic Semipermeable Hypertonic Semipermeable
solution membrane solution membrane

Isotonic Isotonic
solution solution Fluid shift Fluid shift

2 Fluid types
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Fluid compartments
This illustration shows the main body's fluid compart-
ments: intracellular and extracellular, the latter of which is
further divided into interstitial and intravascular. Capillary
walls and cell membranes separate intracellular fluids
from extracellular fluids.



❍ Capillary walls and cell membranes separate intra-

cellular fluid from fluid that exists outside the cells.
❍ Fluid inside and outside the cells must stay in bal-
Extracellular fluid
❍ Extracellular fluid is the fluid that's outside the cells,
either in the interstitial space (interstitial fluid) or in
blood vessels (intravascular fluid). (See Fluid com-
❍ Interstitial fluid surrounds the cells.
❍ Intravascular fluid, or plasma, is the liquid portion
of blood.
❍ In a typical adult, extracellular fluid averages about
20% of the person’s body weight, or about 14 L.
❍ Extracellular fluid must be balanced with intracellu-
lar fluid.
Transcellular fluid
❍ Transcellular fluid is found in the cerebrospinal col-
umn, pleural cavity, lymph system, joints, and eyes.
❍ Usually, transcellular fluids don't undergo significant
gains and losses throughout the day.
AGE AWARE The distribution of fluid in the
body changes with age. In a typical young
adult, interstitial fluid makes up about 15% of body
weight; that percentage decreases progressively with
age. In contrast, plasma makes up about 5% of total
fluid volume, a percentage that remains stable
throughout life.

Fluid types 3
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Fluid movement ❍ ATP is stored in all cells, and it supplies energy for
solute movement in and out of cells. (See Under-
standing active transport.)
❍ Some solutes, such as sodium and potassium, use
Diffusion ATP to move in and out of cells in a form of active
transport called the sodium-potassium pump.
❍ In this type of fluid movement, solutes shift from an ❍ Other solutes that cross cell membranes by active
area of higher concentration to an area of lower transport include calcium ions, hydrogen ions,
concentration. amino acids, and certain sugars.
❍ Eventually, solute concentrations equalize between
ALERT In the vascular system, only capillaries
the two areas.
have walls thin enough to let solutes pass
❍ Diffusion is a form of passive transport because no
through. The movement of fluids and solutes through
energy is needed to make it happen. (See Under-
the capillary walls plays a critical role in fluid bal-
standing diffusion and osmosis.)

Capillary filtration
❍ Osmosis refers to the movement of fluid across a
membrane from an area of lower solute concentra- ❍ The movement of fluids through capillaries — a
tion and comparatively more fluid into an area of process called capillary filtration — results from
higher solute concentration and comparatively less blood pushing against the walls of the capillary. That
fluid. pressure, called hydrostatic (or fluid-pushing) pres-
❍ Like diffusion, osmosis is a passive process; it re- sure, forces fluids and solutes through the capillary
quires no energy expenditure. wall.
❍ Osmosis stops when enough fluid has moved ❍ When the hydrostatic pressure inside a capillary ex-
through the membrane to equalize the solute con- ceeds the pressure in the surrounding interstitial
centration on both sides of the membrane. space, fluids and solutes inside the capillary are
forced out into the interstitial space.
❍ When pressure outside of a capillary exceeds pres-
Active transport sure inside it, fluids and solutes move back into the
❍ In active transport, solutes move from an area of
lower concentration to an area of higher concentra-
tion. Reabsorption
❍ This process requires energy because it goes against
the body's natural tendency to equalize concentra- ❍ Reabsorption prevents too much fluid from leaving
tions. the capillaries no matter how much hydrostatic pres-
❍ The energy needed for a solute to move against a sure is inside them.
concentration gradient comes from a substance ❍ When fluid filters through a capillary, the protein al-
called adenosine triphosphate (ATP). bumin stays behind in the shrinking volume of water.

Understanding diffusion and osmosis

In diffusion, solutes move from an area of higher concentra- until the concentration is equal in both areas. Both
tion to an area of lower concentration, as shown on the left, processes are passive; that is, they need no energy. Just
until the concentration is equal in both areas. In osmosis, remember that, in diffusion, solutes move; in osmosis,
fluid moves from an area of lower solute concentration to an fluid moves.
area of higher solute concentration, as shown on the right,

Semipermeable membrane
Semipermeable membrane

Lower concentration
Higher concentration
concentration Solutes shift.

Fluid shifts.

4 Fluid movement
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Understanding active transport

During active transport, energy
from a molecule called adenosine AREA OF HIGHER AREA OF LOWER
solutes against the gradient,
from an area of lower concentra-
Energy from ATP
tion to an area of higher concen-
pushes against
tration. Sodium and potassium concentration gradient.
are examples of two solutes
moved by active transport.

Semipermeable membrane

❍ Albumin is a large molecule that normally can’t pass

through capillary membranes.
❍ As the concentration of albumin inside a capillary in-
creases, fluid begins to move back into the capillar-
ies by osmosis.
❍ The osmotic, or pulling, force of albumin in the in-
travascular space is called plasma colloid osmotic
❍ Plasma colloid osmotic pressure in capillaries aver-
ages about 25 mm Hg.
❍ As long as hydrostatic pressure exceeds plasma col-
loid osmotic pressure, water and solutes can leave
the capillaries and enter interstitial fluid. If hydrosta-
tic pressure falls below plasma colloid osmotic pres-
sure, water and diffusible solutes return to the capil-
❍ Normally, hydrostatic pressure exceeds plasma col-
loid osmotic pressure in the arteriole end and falls
below it in the venule end. As a result, capillary fil-
tration occurs along the first half of the vessel and
reabsorption occurs along the second half.
❍ As long as hydrostatic pressure and plasma albumin
levels remain normal, the amount of water moving
into the capillaries equals the amount moving out.
❍ Occasionally, extra fluid filters out of the capillary.
When that happens, excess fluid shifts into lymphatic
vessels located just outside the capillaries and even-
tually returns to the heart for recirculation.

Fluid movement 5
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Fluid balance Balancing systems

Renal system
Types of fluid loss ❍ The kidneys play a vital role in fluid balance. If they
aren’t working properly, the body has great difficulty
Sensible loss controlling fluid balance.
❍ Sensible loss is fluid loss that can be measured. ❍ The nephron is the part of the kidney that forms
❍ It includes fluid lost through urination, defecation, urine. (See Parts of a nephron.)
bleeding, wound drainage, gastric drainage, and ❍ A nephron consists of a glomerulus and a tubule.
vomiting. (See Tracking fluid intake and output.) – The glomerulus is a cluster of capillaries that fil-
❍ A typical adult loses 100 to 200 ml/day of fluid ters blood.
through defecation. In severe diarrhea, losses may – Surrounding the glomerulus like a vascular cradle
exceed 5,000 ml/day. is Bowman's capsule.
❍ Gastric, intestinal, pancreatic, and biliary secretions – The tubule, sometimes convoluted, ends in a col-
are almost completely reabsorbed and aren’t usually lecting duct.
counted in daily fluid gains and losses. ❍ Capillary blood pressure forces fluid through the
capillary walls and into Bowman’s capsule at the
Insensible loss proximal end of the tubule.
❍ Insensible loss is fluid loss that can't be measured. ❍ Along the tubule, water and electrolytes are either
❍ It includes fluid lost through skin (perspiration) and excreted or retained according to the body’s needs.
lungs (respiration). – If the body needs more fluid, it retains more.
– If the body needs less fluid, less is reabsorbed and
AGE AWARE The body surface area of an in-
more is excreted.
fant is greater than that of an adult relative to
❍ Electrolytes, such as sodium and potassium, are ei-
their respective weights. As a result, infants typically
ther filtered or reabsorbed throughout the same
lose a greater proportion of water from their skin
area. The resulting filtrate, which eventually be-
than adults do.
comes urine, flows through the tubule into the col-
❍ Changes in humidity levels affect the amount of fluid lecting ducts and eventually into the bladder as
lost through the skin. urine.
❍ Changes in respiratory rate and depth affect the ❍ Nephrons filter about 125 ml of blood every minute,
amount of fluid lost through the lungs. In tachypnea, or about 180 L/day. That rate, called the glomerular
for example, water loss increases; in bradypnea, it filtration rate, leads to the production of 1 to 2 L of
decreases. urine per day. The nephrons reabsorb the remaining
❍ Fever increases insensible losses from both the skin 178 L or more of fluid.
and lungs.
AGE AWARE Infants and young children ex-
crete urine at a higher rate than adults be-
cause their higher metabolic rates produce more
waste. Also, an infant's kidneys can’t concentrate
urine until about age 3 months, and they remain less
Tracking fluid intake and output efficient than an adult’s kidney until about age 2
Each day the body gains and loses fluid through several years.
processes. The main ones are shown here. The body's Antidiuretic hormone
processes work together to balance output with intake.
DAILY TOTAL INTAKE ❍ Antidiuretic hormone (ADH) is a water-retaining
(2,600 ML) hormone also known as vasopressin.
Liquids 1,500 ml ❍ When the hypothalamus senses a low blood volume
Solid foods 800 ml
and increased serum osmolality, it signals the pitu-
Water of oxidation 300 ml
itary gland.
❍ The posterior pituitary gland, which stores ADH, se-
DAILY TOTAL OUTPUT cretes it into the bloodstream.
(2,600 ML) ❍ ADH prompts the kidneys to retain water, which in-
Lungs 400 ml creases blood volume, decreases serum osmolality,
Skin 600 ml and increases the concentration of urine.
❍ Decreased serum osmolality or increased blood vol-
Urine 1,500 ml
ume inhibits the release of ADH and causes less wa-
Feces 100 ml ter to be reabsorbed, making the urine less concen-

6 Fluid balance
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❍ The amount of ADH released varies throughout the Parts of a nephron

day, depending on the body’s needs. The nephron filters blood, produces urine, and excretes
excess solutes, electrolytes, fluids, and metabolic waste
Renin-angiotensin-aldosterone system products while keeping the blood composition and volume
❍ Juxtaglomerular cells near each glomerulus secrete constant.
renin to help balance sodium and water and main-
tain blood volume and pressure. Bowman’s
– Renin is an enzyme. capsule Proximal tubule
– Through a complex series of steps, renin leads to
production of angiotensin II. Distal tubule
❍ Angiotensin II causes peripheral vasoconstriction, Glomerulus
which increases blood pressure.
Ascending limb
❍ Angiotensin II also stimulates the adrenal glands to Descending
produce aldosterone.
Collecting duct
– Aldosterone is a hormone.
Loop of Henle
– It cues the kidneys to retain sodium and water,
thus increasing blood pressure and volume.
❍ As soon as blood pressure reaches a normal level,
the body stops releasing renin, and this feedback – decreasing vascular resistance by causing vasodi-
loop of renin to angiotensin to aldosterone stops. lation.
❍ The amount of renin secreted depends on blood flow ❍ The amount of ANP that atria release rises in re-
and the level of sodium in the bloodstream. sponse to many conditions, including chronic renal
– If blood flow to the kidneys declines (as in a hem- failure and heart failure.
orrhage) or the amount of sodium reaching the
ALERT Anything that causes atrial stretching
glomerulus drops, juxtaglomerular cells secrete
can increase ANP release, including orthostatic
more renin, which causes vasoconstriction and in-
changes, atrial tachycardia, high sodium intake, sodi-
creases blood pressure.
um chloride infusions, and use of drugs that cause
– If blood flow to the kidneys increases or the
amount of sodium reaching the glomerulus in-
creases, juxtaglomerular cells secrete less renin,
which reduces vasoconstriction and keeps blood Thirst
pressure from rising. ❍ Perhaps the simplest mechanism for maintaining flu-
❍ Aldosterone acts as well when blood volume drops. id balance is the thirst mechanism.
– It starts the active transport of sodium from the ❍ Thirst arises after even small fluid losses.
distal tubules and the collecting ducts into the ❍ Losing body fluids or eating salty foods leads to an
bloodstream. increase in extracellular fluid osmolality.
– When sodium is forced into the bloodstream, ❍ This increase dries the mucus membranes in the
more water is reabsorbed and blood volume ex- mouth, which stimulates the thirst center in the hy-
pands. pothalamus.
Atrial natriuretic peptide AGE AWARE In an elderly person, the thirst
mechanism is less effective than it is in a
❍ A cardiac hormone called atrial natriuretic peptide
younger person, leaving the older person more prone
(ANP) also helps maintain fluid balance.
to dehydration.
– ANP is stored in the cells of the atria.
– It's released when atrial pressure increases.
❍ ANP opposes the renin-angiotensin-aldosterone sys-
– If blood volume and pressure rise, the atrial walls
stretch, prompting release of ANP.
– ANP shuts off the renin-angiotensin-aldosterone
system, thus decreasing blood pressure and re-
ducing intravascular blood volume.
❍ ANP has several key functions:
– suppressing serum renin levels
– decreasing aldosterone release from the adrenal
– increasing glomerular filtration, which increases
urinary excretion of sodium and water
– decreasing ADH release from the posterior pitu-
itary gland

Fluid balance 7
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Hypovolemia – Hemorrhage (frank or occult)

– Nasogastric drainage
– Renal failure (with increased urination)
Overview – Vomiting
❍ Third-space fluid shifts
– Acute intestinal obstruction
Description – Acute peritonitis
❍ Isotonic fluid loss (which includes loss of fluids and – Burns (during the initial phase)
solutes) from the extracellular space – Crush injuries
❍ Subtle initial signs and symptoms as the body tries to – Hip fracture
compensate for reduced circulating blood volume – Hypoalbuminemia
– Pleural effusion
❍ Fluid circulating in the blood decreases, lowering Complications
cardiac output and leading to hypotension and im- ❍ Acute respiratory distress syndrome
paired tissue perfusion. ❍ Acute tubular necrosis and renal failure
❍ Tissue anoxia prompts a shift in cellular metabolism ❍ Disseminated intravascular coagulation
from aerobic to anaerobic pathways; lactic acid ac- ❍ Multiple organ dysfunction
cumulates, and metabolic acidosis may develop.
❍ Third-space fluid shifts may occur from increased
permeability of the capillary membrane or de- Assessment
creased plasma colloid osmotic pressure.
Risk factors ❍ Presence of one of the above causes
❍ Adrenal insufficiency ❍ Restlessness
❍ Coma ❍ Anxiety
❍ Diabetes insipidus ❍ Confusion
❍ Hemorrhage ❍ Thirst
❍ Osmotic diuresis ❍ Weight loss
❍ Third-space fluid shift
Physical assessment
Causes ❍ Increased heart rate
❍ Fluid loss from the extracellular compartment ❍ Orthostatic hypotension
– Abdominal surgery ❍ Delayed capillary refill
– Diabetes mellitus (with increased urination) ❍ Cool, pale, clammy skin over the arms and legs
– Diarrhea ❍ Decreased urine output (See Danger signs of hypo-
– Excessive diuretic therapy volemia.)
– Excessive laxative use
– Excessive sweating Test results
– Fever Laboratory
– Fistula ❍ Decreased hemoglobin level, hematocrit, and red
blood cell count
❍ Increased serum potassium, sodium, lactic dehydro-
Danger signs of hypovolemia genase, creatinine, and blood urea nitrogen levels
❍ Increased urine specific gravity and urine osmolality
Watch for these signs and symptoms of hypovolemia and
❍ Positive occult blood test (if the patient has gastroin-
impending hypovolemic shock:
● deterioration in mental status (from restlessness and testinal bleeding)
anxiety to unconsciousness) Diagnostic procedures
● thirst ❍ Invasive hemodynamic monitoring shows reduced
● tachycardia central venous pressure (CVP), pulmonary artery
● delayed capillary refill pressure (PAP), right atrial pressure, pulmonary
● orthostatic hypotension progressing to marked artery wedge pressure (PAWP), and cardiac output.
hypotension ❍ Gastroscopy may identify an internal bleeding site.
● urine output initially more than 30 ml/minute and then
dropping below 10 ml/hour
● cool, pale skin over arms and legs Nursing diagnoses
● weight loss
❍ Decreased cardiac output
● flat jugular veins
● decreased central venous pressure ❍ Ineffective tissue perfusion: cardiopulmonary, renal,
● weak or absent peripheral pulses. cerebral

8 Hypovolemia
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❍ Impaired gas exchange

❍ Deficient fluid volume
Key outcomes
The patient will:
❍ maintain adequate cardiac output
❍ maintain hemodynamic stability
❍ maintain adequate ventilation
❍ regain adequate fluid volume.

❍ Identification of cause of fluid loss
❍ Oxygen administration
❍ Bed rest
❍ Isotonic I.V. fluids, such as normal saline solution or
Ringer’s solution
❍ Surgery (possibly) to control underlying problem
❍ Maintain the patient's airway.
❍ Give prescribed I.V. fluids or blood products.
❍ Insert an indwelling urinary catheter.
❍ Provide emotional support to the patient and family.
Drug therapy
❍ Oxygen
❍ Vasopressors
❍ Vital signs
❍ Airway patency
❍ Intake and output
❍ Weight
❍ I.V. site patency
❍ Hemodynamic values (cardiac output, CVP, PAP,
❍ Cardiac rhythm
❍ Signs of bleeding
❍ Signs of transfusion reaction if giving blood products
❍ Signs of impeding shock
❍ Laboratory values: complete blood count, electrolyte
levels, blood urea nitrogen level, creatinine level
❍ Arterial blood gas levels
Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment plan
❍ all procedures and their purposes
❍ the risks of blood transfusion
❍ the purpose of all equipment, including cardiac
❍ warning signs of hypovolemia and when to report
❍ prescribed drugs and their possible adverse effects.

Hypovolemia 9
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Hypervolemia – Hyperaldosteronism
– Low intake of dietary protein
❍ Fluid shift from interstitial to intravascular space
Overview – Remobilization of fluids after burn treatment
– Delivery of hypertonic fluids, such as mannitol or
hypertonic saline solution
Description – Use of plasma proteins, such as albumin
❍ Excess isotonic fluid (water and sodium) in the ex- – Acute or chronic renal failure with low urine out-
tracellular compartment put
❍ Fluid and solutes gained in equal proportion, leaving
osmolality unaffected Complications
❍ Signs and symptoms if compensatory mechanisms ❍ Heart failure
fail ❍ Pulmonary edema

Pathophysiology Assessment
❍ Increased extracellular fluid volume in either the in- History
terstitial or intravascular compartments prompts the ❍ Weight gain
body to try to compensate and restore fluid balance. ❍ Edema of limbs
❍ It adjusts circulating levels of aldosterone, antidi- ❍ Shortness of breath
uretic hormone, and atrial natriuretic peptide to
make the kidneys release additional water and sodi- Physical assessment
um. ❍ Rapid and bounding pulse
❍ If hypervolemia is prolonged or severe or the patient ❍ Increased blood pressure, central venous pressure
has poor heart function, the body can’t compensate (CVP), pulmonary artery pressure (PAP), and pul-
for the extra volume. monary artery wedge pressure (PAWP)
❍ Fluid is forced out of the blood vessels and into the ❍ Decreased blood pressure and cardiac output as the
interstitial space, causing edema. heart fails
❍ An S3 gallop with heart failure
ALERT Elderly patients and patients with im- ❍ Distended veins, especially in the hands and neck
paired renal or cardiovascular function are es-
❍ Edema
pecially prone to hypervolemia.
– Visible first in dependent areas, such as sacrum
and buttocks when the patient is lying down and
Causes legs and feet when the patient is standing
❍ Excessive sodium or fluid intake – Becomes generalized (See Evaluating pitting
– I.V. replacement therapy using normal saline solu- edema.)
tion or lactated Ringer’s solution ❍ Crackles with lung auscultation
– Blood or plasma replacement ❍ Tachypnea
– Excessive intake of dietary sodium ❍ Frothy cough
❍ Fluid or sodium retention
– Heart failure Test results
– Cirrhosis of the liver Laboratory
– Nephrotic syndrome ❍ Decreased hematocrit
– Corticosteroid therapy

Evaluating pitting edema

Edema can be evaluated using a scale of +1 to +4.
Press your fingertip firmly into the skin over a bony
surface for a few seconds. Then note the depth of the
imprint your finger leaves. A slight imprint indicates
+1 pitting edema, as shown on the left. A deep im-
print, with the skin slow to return to its original con-
tour, indicates +4 pitting edema, as shown in the cen-
ter. If you leave no imprint because the skin is dis-
tended so much that fluid can't be displaced, the
patient has brawny edema, as shown on the right.

10 Hypervolemia
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❍ Normal serum sodium level but decreased serum Patient teaching

potassium and blood urea nitrogen levels Be sure to cover:
❍ Decreased oxygen level (with early tachypnea, possi- ❍ the disorder, diagnosis, and treatment plan
ble decreased partial pressure of arterial carbon ❍ all procedures and their purposes
dioxide, decreased pH, and respiratory alkalosis) ❍ the purpose of all equipment, including cardiac
Imaging monitoring
❍ Chest X-rays reveal pulmonary congestion. ❍ prescribed drugs and their possible adverse effects
Diagnostic procedures ❍ fluid and sodium restrictions
❍ Invasive hemodynamic monitoring shows increased ❍ warning signs of hypervolemia and when to report
CVP, PAP, right atrial pressure, PAWP, and cardiac them.

Nursing diagnoses
❍ Impaired gas exchange
❍ Ineffective airway clearance
❍ Excess fluid volume
❍ Anxiety
Key outcomes
The patient will:
❍ maintain adequate ventilation
❍ maintain a patent airway
❍ regain fluid balance
❍ verbalize decreased anxiety and fear.

❍ Restriction of sodium and fluid intake
❍ Oxygen therapy
❍ Identification and treatment of cause
❍ Bed rest
❍ Give prescribed drugs.
❍ Maintain the patient's airway and ventilation.
❍ Watch for distended veins in the neck and hands.
❍ Restrict fluids.
❍ Offer emotional support to the patient and family.
Drug therapy
❍ Digoxin
❍ Diuretics
❍ Morphine
❍ Nitroglycerin
❍ Oxygen
❍ Arterial blood gas values
❍ Heart sounds (for an S3)
❍ Intake and output
❍ Oxygenation
❍ Respiratory status
❍ Serum potassium level
❍ Vital signs
❍ Weight

Hypervolemia 11
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Electrolyte basics ALERT The anion gap is a useful test for dis-
tinguishing types and causes of acid-base im-
balances because it reflects the serum anion-cation
Charges balance.

❍ An electrical charge makes cells function normally.

Ions ❍ Electrolytes exist in extracellular and intracellular
❍ Electrolytes are substances that, when in solution, fluid compartments.
separate (or dissociate) into electrically charged ❍ Individual electrolytes differ in concentration, but
particles called ions. the totals balance to reach a neutral electrical
❍ Some ions carry a positive charge. Others carry a charge. This balance is called electroneutrality.
negative charge. ❍ Most electrolytes interact with hydrogen ions to
❍ Several pairs of oppositely charged ions are so maintain acid-base balance. The major electrolytes
closely linked that a problem with one ion causes a also have specialized functions that contribute to
problem with the other. Examples include the metabolism and fluid and electrolyte balance.
sodium-chloride pair and the calcium-phosphorus
Electrolyte locations
Anions and cations
❍ Anions are electrolytes that generate a negative Extracellular electrolytes
charge. ❍ Sodium, chloride, calcium, and bicarbonate are
❍ Chloride, phosphorus, and bicarbonate are anions. mainly in extracellular fluid.
(See Understanding electrolytes.) ❍ Sodium affects serum osmolality (solute concentra-
❍ Cations are electrolytes that generate a positive tion in 1 L of water) and extracellular fluid volume.
charge. It also helps nerve and muscle cells interact.
❍ Sodium, potassium, calcium, and magnesium are

Understanding electrolytes
Electrolytes help regulate water distribution, govern acid-base balance, and transmit nerve impulses. They also contribute to
energy generation and blood clotting. You'll find summaries of the body's major electrolytes below. Check the illustration to
see how electrolytes are distributed in and around the cell.

Potassium (K+) Chloride (Cl–)

● The main intracellular fluid (ICF) cation ● The main ECF anion
● Regulates cell excitability ● Helps maintain normal ECF osmolality
● Permeates cell membranes, thereby affecting the cell’s ● Affects the body's pH
electrical status ● Plays a vital role in maintaining acid-base balance; com-
● Helps control ICF osmolality and, consequently, ICF bines with hydrogen ions to produce hydrochloric acid
osmotic pressure Calcium (Ca+)
Magnesium (Mg++) ● A major cation in teeth and bones
● A leading ICF cation ● Found in fairly equal concentrations in ICF and ECF
● Contributes to many enzymatic and metabolic processes, ● Also found in cell membranes, where it helps cells
particularly protein synthesis adhere to one another and maintain their shape
● Modifies nerve impulse transmission and skeletal muscle ● Acts as an enzyme activator in cells (muscles must have
response (unbalanced Mg++ concentrations dramatically Ca+ to contract)
affect neuromuscular processes) ● Aids coagulation
Phosphorus (P+) ● Affects cell membrane permeability and firing level
● The main ICF anion Bicarbonate (HCO3–)
● Promotes energy storage and carbohydrate, protein, and ● Present in ECF
fat metabolism ● Functions mainly to regulate acid-base balance
● Acts as a hydrogen buffer
Sodium (Na+)
● The main extracellular fluid (ECF) cation
● Helps govern normal ECF osmolality (A shift in Na+ con-
centration triggers a fluid volume change to restore
Ca + P+ K+ Ca+ Na+

normal solute and water ratios.)

Cl –
Ca+ Mg ++
● Helps maintain acid-base balance HCO3–
● Activates nerve and muscle cells
● Influences water distribution (with chloride)

12 Electrolyte basics
414501.qxd 18/8/08 12:11 PM Page 13

❍ Chloride helps maintain osmotic (water-pulling) ❍ Results for many laboratory tests are reported in mil-
pressure. Gastric mucosal cells need chloride to liequivalents per liter (mEq/L), which is a measure
produce hydrochloric acid. of the ion’s chemical activity or its power.
❍ Calcium is the major cation involved in the structure
ALERT Although serum electrolyte levels re-
and function of bones and teeth and also helps to:
main fairly stable throughout a person’s life
– stabilize the cell membrane and reduce its perme-
span, understanding which levels are normal and
ability to sodium
which are abnormal is critical to reacting quickly and
– transmit nerve impulses
appropriately to an imbalance. If you see an abnor-
– contract muscles
mal laboratory test result, consider it in the context
– coagulate blood.
of what you know about the patient. For instance, a
❍ Bicarbonate plays a vital role in acid-base balance.
serum potassium level of 7 mEq/L for a patient with
Intracellular electrolytes previously normal serum potassium levels and no ap-
parent reason for the increase may be an inaccurate
❍ Potassium, phosphate, and magnesium are among
result. Perhaps the patient’s blood sample was he-
the most abundant electrolytes inside the cell.
molyzed from trauma to the cells.
❍ Potassium plays an important role in several
– cell excitability regulation
– nerve impulse conduction
– resting membrane potential
– muscle contraction and myocardial membrane re-
– intracellular osmolality control.
❍ Phosphorus occurs in the body as phosphate salts.
Sometimes the words phosphorus and phosphate are
used interchangeably. Phosphate is essential for en-
ergy metabolism. Combined with calcium, it plays a
key role in bone and tooth mineralization. It also
helps maintain acid-base balance.
❍ Magnesium acts as a catalyst for enzyme reactions. It
– regulates neuromuscular contraction
– promotes normal functioning of the nervous and
cardiovascular systems
– aids in protein synthesis and sodium and potassi-
um ion transportation.

Electrolyte movement and

❍ Although electrolytes are concentrated in one com-
partment or another, they aren’t locked or frozen in
these areas. Like fluids, electrolytes move about try-
ing to maintain balance and electroneutrality.
❍ Fluid intake and output, acid-base balance, hormone
secretion, and normal cell functioning all influence
electrolyte balance.
❍ Because electrolytes function both with other elec-
trolytes and individually, imbalances in one elec-
trolyte can affect the balance of others.

Electrolyte measurement
❍ Only levels of extracellular electrolytes are mea-
❍ The patient’s condition determines how often elec-
trolyte levels are checked.

Electrolyte basics 13
414501.qxd 18/8/08 12:12 PM Page 14

Potassium ❍ Extracellular fluid also gains potassium when cells

are destroyed and release intracellular potassium
and when potassium shifts out of intracellular fluid
and into extracellular fluid.
Overview ❍ About 80% of ingested potassium is excreted in
urine, with each liter of urine containing 20 to
❍ Potassium is the major cation (ion with a positive 40 mEq of potassium. Any remaining potassium is
charge) in intracellular fluid. excreted in feces and sweat.
❍ About 98% of the body's potassium is found in intra- ❍ Extracellular potassium also is lost when it moves
cellular fluid; about 2% is found in extracellular from extracellular fluid into intracellular fluid and
fluid. when cells undergo anabolism.
❍ Three more factors that affect potassium levels in-
ALERT Potassium levels are affected by dis-
clude the sodium-potassium pump, renal regulation,
ease, injury, drugs, and treatments. Small un-
and pH level.
treated changes in the serum potassium level can
seriously affect neuromuscular and cardiac func-
tioning. Balance
❍ Potassium directly affects cell, nerve, and muscle
function by: ❍ The sodium-potassium pump is an active transport
– maintaining the electrical neutrality and osmolality mechanism that moves ions across cell membranes
of cells against a concentration gradient.
– aiding neuromuscular transmission of nerve im- ❍ The pump moves sodium from the cell into extracel-
pulses lular fluid and maintains high intracellular potassi-
– assisting skeletal and cardiac muscle contraction um levels by pumping potassium into the cell.
and electrical conductivity ❍ The body discards excess potassium via the kidneys.
– affecting acid-base balance in relationship to hy- As serum potassium levels rise, the renal tubules ex-
drogen, another cation. (See Potassium’s role in crete more of it, leading to increased potassium loss
acid-base balance.) in the urine.
❍ Potassium levels normally range from 3.5 to 5 mEq/L ❍ Sodium and potassium have a reciprocal relation-
in serum and typically are 140 mEq/L in cells (a lev- ship. The kidneys reabsorb sodium and excrete
el usually not measured). potassium when the hormone aldosterone is se-
❍ Potassium must be ingested daily because the body creted.
can’t conserve it. ❍ The kidneys have no effective way to combat potassi-
❍ Recommended daily potassium requirement for um loss and may excrete it even when the serum
adults is about 40 mEq; average daily intake is 60 to potassium level is low.
100 mEq.

Potassium’s role in acid-base balance

Normal balance Acidosis Alkalosis
Under normal conditions, the potas- In acidosis, the hydrogen ion content In alkalosis, more hydrogen ions are
sium ion (K+) content in intracellular in extracellular fluid increases and the present in intracellular fluid than in the
fluid is much greater than in extracel- ions move into the intracellular fluid. extracellular fluid. Therefore, hydrogen
lular fluid. Hydrogen ion (H+) concen- To keep the intracellular fluid electri- ions move from the intracellular fluid
tration is low in both compartments. cally neutral, an equal number of into the extracellular fluid. To keep the
potassium ions leave the cell, which intracellular fluid electrically neutral,
causes hyperkalemia. potassium ions move from the extra-
cellular fluid into the intracellular fluid,
which causes hypokalemia.

H+ K +
+ K+ K+
K + K + K+
K+ H+ H+ K+ K+
H H+ + K
H+ K+ K+ K K+H K
+ + +
K+ H H+ K+
K+ H
+ K +
K+ H K
+ K+ +
K+ K + K K
+ + H+ +
K+ H K +
H+ H+ H+ KK+
K+ K+ K+
K+ K +
+ K+ +
H H+ H H+ KK+
H+ K+ K+ H+

14 Potassium
414501.qxd 18/8/08 12:12 PM Page 15

❍ A change in pH may affect serum potassium levels

because hydrogen ions and potassium ions freely ex-
change across plasma cell membranes.
❍ In acidosis, excess hydrogen ions move into cells
and push potassium into the extracellular fluid,
which may lead to hyperkalemia as potassium moves
out of the cell to maintain balance.
❍ In alkalosis, potassium moves into the cell to main-
tain balance, which may lead to hypokalemia.
ALERT Potassium is gained by intake and lost
by excretion. If either is altered, hyperkalemia
or hypokalemia may result.

Dietary sources
❍ The Food and Nutrition Board of the National Acade-
my of Sciences recommends 2,000 mg as the mini-
mum daily potassium requirement for men and
women older than age 18.
❍ A good food source of potassium contains at least
200 mg of potassium in a serving size.
❍ Potassium is lost in cooking; therefore, foods should
be cooked in a minimum of water and for the short-
est possible time.
❍ Major sources of potassium include:
– bread, cereals, and other grain products
– chocolate
– dried fruit
– fruits, such as oranges, bananas, apricots, can-
taloupe, watermelon, peaches, and prunes
– meat and fish
– milk
– nuts
– seeds
– vegetables, such as squash, potatoes, mushrooms,
tomatoes, lima beans, and cauliflower.

Potassium 15
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Sodium Balance
❍ Sodium levels stay fairly constant because the more
sodium a person takes in, the more sodium the kid-
Overview neys excrete.
❍ Sodium is also excreted through the gastrointestinal
❍ Sodium is one of the most important elements in the tract and in sweat.
body. ❍ The normal range of serum sodium levels reflects
❍ It accounts for 90% of extracellular fluid cations the relationship between sodium and water. If sodi-
(positively charged ions) and is the most abundant um intake suddenly increases, extracellular fluid
solute in extracellular fluid. Almost all sodium in the concentration also rises, and vice versa.
body is found in this fluid. ❍ The body makes adjustments when the sodium level
❍ Sodium attracts fluid and helps preserve the extra- rises. Increased serum sodium levels cause thirst
cellular fluid volume and fluid distribution in the and prompt the posterior pituitary gland to release
body. It's needed to maintain proper extracellular antidiuretic hormone (ADH).
fluid osmolality (concentration). ❍ ADH cues the kidneys to retain water, which dilutes
❍ Sodium helps transmit impulses in nerve and muscle the blood and normalizes serum osmolality.
fibers and combines with chloride and bicarbonate ❍ When serum osmolality decreases and thirst and
to regulate acid-base balance. ADH secretion decline, the kidneys excrete more wa-
❍ Because the electrolyte compositions of serum and ter to maintain normal osmolality. (See Regulating
interstitial fluid are essentially equal, the sodium sodium and water balance.)
concentration in extracellular fluid is measured in ❍ Aldosterone also regulates extracellular sodium bal-
serum levels. ance via a feedback loop. The adrenal cortex se-
❍ Normally, the sodium level ranges from 135 to cretes aldosterone, which stimulates the renal
145 mEq/L. The amount of sodium inside the cells is tubules to conserve water and sodium when the
10 mEq/L. sodium level is low, thus helping to normalize extra-
cellular fluid sodium levels.

Regulating sodium and water balance

This flowchart show two of the body's mechanisms for maintaining and restoring sodium and water balance.

Serum sodium
sodium level
level decreases
decreases Serum sodium level increases
(water excess).
excess). (water deficit).

Serum osmolality
Serum falls decreases
sodium level to less than Serum osmolality
Serum sodium rises
level to more than
280 mOsm/kg.
(water excess). 300 mOsm/kg.
(water excess).

Thirst decreases,
Serum sodiumleading to decreased
level decreases Thirst increases,
Serum sodiumleading to increased
level decreases
water excess).
(water intake. water excess).
(water intake.

Antidiuretic hormone
Serum sodium level(ADH) release
decreases Serum
is suppressed. ADHsodium
releaselevel decreases
(water excess). (water excess).

Renal sodium
water level decreases
excretion increases. Serum sodium level decreases
Renal water excretion decreases.
(water excess). (water excess).

Serum sodium level decreases

Serum osmolality normalizes.
(water excess).

16 Sodium
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Sodium-potassium pump
Here's how the sodium-potassium pump works. Normally, return to their original positions through the cell wall by be-
more sodium (Na+) ions exist outside cells than inside, and ing linked with a carrier molecule, as shown on the right.
more potassium (K+) ions exist inside the cells than outside, Energy for the ions' return trip comes from adenosine
as shown on the left. When something increases the mem- triphosphate (ATP), magnesium (Mg++), and an enzyme
brane's permeability, sodium ions diffuse inward and potas- commonly found in cells.
sium ions diffuse outward, as shown in the middle. Ions

Na +
Na + Na + Na + Na+
+ Na +
Na Na + Na K+
+ K+ + +
+ K K K+ K K+
+ Na
K +
K K+ Cell ATP
K Mg++

Heat Energy
Cell membrane Cold
Electrical stimulation

❍ Normally, extracellular sodium levels are much high- – processed foods to which sodium chloride (salt),
er than intracellular levels. An active transport mech- benzoate, or phosphate has been added
anism called the sodium-potassium pump helps – salt added while cooking or eating
maintain normal sodium levels. (See Sodium-potas- – salted meats.
sium pump.)
❍ The sodium-potassium pump allows the body to car-
ry out its essential functions and helps prevent cellu-
lar swelling from too many ions inside the cell at-
tracting excessive amounts of water. The pump also
creates an electrical charge in the cell from the
movement of ions, permitting transmission of neuro-
muscular impulses.

Dietary sources
❍ The Food and Nutrition Board of the National Acade-
my of Sciences recommends a minimum daily sodi-
um requirement of 2,300 mg for men and women
older than age 18.
❍ Sodium may need to be restricted because the aver-
age American diet provides at least 6 g of sodium
daily. Dietary restrictions should be recommended
by a doctor.
❍ Salt is 40% sodium by weight. One teaspoon of salt
contains 2,400 mg of sodium.
❍ Major sources of sodium:
– butter
– cheese
– cold cuts
– ketchup
– margarine
– nuts

Sodium 17
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Magnesium AGE AWARE Magnesium levels in newborns

and children are different from those of adults.
In newborns, magnesium levels range from 1.4 to
2.9 mEq/L; in children, 1.6 to 2.6 mEq/L.
Overview ❍ More than half of circulating magnesium moves in a
free, ionized form. Another 30% binds with a protein
❍ After potassium, magnesium is the most abundant (mostly albumin), and the remainder binds with oth-
cation (positively charged ion) in intracellular fluid. er substances.
❍ About 60% of the body’s magnesium is contained in ❍ Ionized magnesium is physiologically active and
bones, less than 1% in extracellular fluid, and the must be regulated to maintain homeostasis. Howev-
rest in intracellular fluid. er, this form alone can’t be measured, so the mea-
❍ Magnesium performs the following functions in the sured level reflects the total amount of circulating
body: magnesium.
– It promotes enzyme reactions in the cells during
ALERT Magnesium levels are linked to albu-
carbohydrate metabolism.
min levels. A patient with a low serum albu-
– It helps the body produce and use adenosine
min level will have a low total serum magnesium
triphosphate for energy.
level — even if the level of ionized magnesium re-
– It takes part in protein synthesis.
mains unchanged. That's why serum albumin levels
– It influences vasodilation, helping the cardiovascu-
need to be measured with serum magnesium levels.
lar system function normally.
– It helps sodium and potassium ions cross cell ❍ Serum calcium and certain other laboratory values
membranes (which explains why magnesium af- also come into play when assessing and treating
fects sodium and potassium ion levels both inside magnesium imbalances. Because magnesium is
and outside the cell). mainly an intracellular electrolyte, changes in the
– It regulates muscle contractions by acting on the levels of other intracellular electrolytes, such as
myoneural junctions — the sites where nerve and potassium and phosphorus, can affect serum magne-
muscle fibers meet — and affecting the irritability sium levels, too.
and contractility of cardiac and skeletal muscle.
– It influences the body’s calcium level through its
effect on parathyroid hormone, which maintains a Balance
constant calcium level in extracellular fluid.
❍ Normally, the total serum magnesium level is 1.6 to ❍ The gastrointestinal (GI) and urinary systems regu-
2.6 mEq/L. However, the measured level may not ac- late magnesium through absorption, excretion, and
curately reflect magnesium stores. That’s because retention — that is, through dietary intake and out-
most magnesium is found in cells, where it measures put in urine and feces.
about 40 mEq/L. In serum, magnesium levels are ❍ The body tries to adjust to any changes in magne-
relatively low. sium level.
– If the serum magnesium level drops, the GI tract
may absorb more magnesium.
– If the serum magnesium level rises, the GI tract ex-
Effects of hypomagnesmia cretes more magnesium in the feces.
❍ The kidneys balance magnesium by altering its reab-
Dysfunction Effects
sorption at the proximal tubule and loop of Henle.
Cardiovascular Arrhythmias – If serum magnesium levels climb, the kidneys ex-
Hypertension (occasionally) crete the excess in the urine. Diuretics heighten
Vasomotor changes (vasodila- this effect.
tion and hypotension) – If serum magnesium levels fall, the kidneys con-
serve magnesium. That conservation is so efficient
Neurologic Confusion
that the daily loss of circulating ionized magne-
Hallucinations sium may be no more than 1 mEq.
Seizures ❍ If magnesium levels become deficient, a range of
clinical effects results. (See Effects of hypomagne-
Neuromuscular Chvostek's sign (facial muscle semia.)
spasms when branches of
the facial nerve are tapped)
Leg and foot cramps
Dietary sources
❍ The Food and Nutrition Board of the National Acade-
my of Sciences recommends a minimum daily mag-

18 Magnesium
414501.qxd 18/8/08 12:12 PM Page 19

nesium requirement of 310 to 420 mg for men and

women older than age 18.
❍ Major sources of magnesium include:
– chocolate
– dry beans and peas
– fruits, such as avocados, bananas, and kiwi
– green vegetables, such as spinach
– meats
– nuts
– seafood
– seeds
– whole grains.

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Calcium About half is ionized (or free) calcium, the only ac-
tive form of calcium.
AGE AWARE Children have higher serum calci-
Overview um levels than adults. These levels can rise as
high as 7 mg/dl during periods of increased growth. In
❍ Calcium is a positively charged ion, or cation, found
contrast, elderly people have a decreased normal
in both extracellular fluid and intracellular fluid.
range. For elderly men, the range is 2.3 to 3.7 mg/dl;
❍ About 99% of the body’s calcium is found in the
for elderly women, it's 2.8 to 4.1 mg/dl.
bones and the teeth. Only 1% is found in serum and
soft tissue. That 1% is what matters when measuring ALERT Because nearly half of all calcium is
calcium levels in the blood. bound to the protein albumin, serum protein
❍ Calcium functions in the following ways: abnormalities can influence total serum calcium lev-
– It’s responsible for the formation and structure of els. For example, in hypoalbuminemia, the total
bones and teeth. serum calcium level decreases. However, ionized cal-
– It helps maintain cell structure and function. cium levels — the more important of the two — re-
– It plays a role in cell membrane permeability and main unchanged. So when considering total serum
impulse transmission. calcium levels, you should also consider serum albu-
– It affects the contraction of cardiac muscle, min levels. (See Calculating calcium and albumin lev-
smooth muscle, and skeletal muscle. els.)
– It participates in the blood-clotting process.
❍ Calcium can be measured in two ways: Balance
– total serum calcium level, which measures the to-
tal amount of calcium in the blood ❍ Both intake of dietary calcium and existing stores of
– ionized calcium level, which measures the various calcium affect calcium levels in the body.
forms of calcium in extracellular fluid. ❍ Calcium is absorbed in the small intestine and is ex-
❍ The normal range for total serum calcium level is creted in the urine and feces.
8.9 to 10.1 mg/dl. ❍ When serum calcium levels are low, the parathyroid
❍ The normal range for ionized calcium level is 4.5 to glands release parathyroid hormone (PTH).
5.1 mg/dl. – PTH draws calcium from the bones and promotes
❍ Ionized calcium carries out most of the ion’s physio- the transfer of calcium (and phosphorus) into the
logic functions. plasma, a process that increases serum calcium
❍ About 41% of extracellular calcium is bound to pro- levels.
tein; 9% is bound to citrate or other organic ions. – PTH also promotes reabsorption of calcium by the
kidneys and stimulates absorption by the intes-
tines. Phosphorus is excreted at the same time. In
Calculating calcium and albumin levels hypercalcemia, the body suppresses PTH release.
❍ Calcitonin also helps to regulate calcium levels. A
For every 1 g/dl that a noncritically ill patient’ s serum hormone, calcitonin is produced in the thyroid gland
albumin level drops, his total calcium level decreases by
and acts as an antagonist to PTH.
0.8 mg/dl. To see what your patient’s calcium level would
be if his serum albumin level were normal — and to help
– High levels of calcitonin inhibit bone resorption,
determine if treatment is justified — just do a little math. which decreases the amount of calcium available
from bone and, in turn, decreases the serum calci-
Correcting a level um level.
The normal albumin level is 4 g/dl. The formula for cor- – Calcitonin also decreases absorption of calcium
recting a patient’s calcium level is: and enhances its excretion by the kidneys.
❍ Vitamin D also influences calcium levels.
Total serum calcium level + 0.8 (4 – albumin level) = – Vitamin D is ingested with foods, particularly dairy
corrected calcium level products.
– Skin exposed to ultraviolet light synthesizes vita-
Sample problem min D.
For example, if a patient’s serum calcium level is 8.2 mg/dl – The active form of vitamin D promotes calcium ab-
and his albumin level is 3 g/dl, what would his corrected sorption through the intestines, resorption from
calcium be? bone, and kidney reabsorption, all of which raise
the serum calcium level. (See Calcium in bal-
8.2 + 0.8 (4 – 3) = 9 mg/dl ance.)
❍ Phosphorus also affects serum calcium levels.
The corrected calcium level is in the normal range and – Phosphorus inhibits calcium absorption in the in-
probably wouldn’t be treated. testines, the opposite effect of vitamin D.

20 Calcium
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– When calcium levels are low and the kidneys re- Calcium in balance
tain calcium, phosphorus is excreted. Normally, several interrelated processes maintain extracel-
ALERT Calcium and phosphorus exist in in- lular calcium levels by moving calcium ions into and out of
verse relationship. When calcium levels rise, extracellular fluid. Calcium enters the extracellular space
through resorption of calcium ions from bone, absorption
phosphorus levels drop. When calcium levels drop,
of dietary calcium in the gastrointestinal (GI) tract, and re-
phosphorus levels rise. absorption of calcium by the kidneys. Calcium leaves ex-
❍ Serum pH has an inverse relationship with the ion- tracellular fluid by being excreted in feces and urine and
ized calcium level. If serum pH level rises (the blood deposited in bone. This illustration shows how calcium
becomes alkaline), more calcium binds with protein moves through the body.
and the ionized calcium level drops. Thus, a patient
with alkalosis typically has hypocalcemia. Bone
❍ The opposite is true for acidosis. When the pH level
drops, less calcium binds to protein, and the ionized GI tract
calcium level rises. When all those regulatory efforts
fail to control the level of calcium in the body, one of Kidney
two conditions may result: hypocalcemia or hyper-
Dietary sources fluid

❍ For adults, the recommended daily calcium require- Calcium loss

(feces) Calcium loss (urine)
ment is 800 to 1,200 mg. Recommendations vary for
children, pregnant women, and patients being treat-
ed for osteoporosis.
❍ Major sources of calcium include:
– beans
– bonemeal
– dairy products, such as milk, cheese, and yogurt
– fish with edible bones, such as sardines
– green, leafy vegetables
– legumes
– molasses
– nuts
– orange juice fortified with calcium
– whole grains.

Calcium 21
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Phosphorus ❍ Most ingested phosphorus is absorbed through the

❍ The kidneys excrete about 90% of phosphorus as
they regulate serum levels. The gastrointestinal (GI)
Overview tract excretes the rest.
❍ If dietary intake of phosphorus increases, the kid-
❍ Phosphorus is the main anion, or negatively charged neys increase excretion to maintain normal levels of
ion, in intracellular fluid. phosphorus. A low-phosphorus diet causes the kid-
❍ It’s also known as phosphate. neys to reabsorb more phosphorus in the proximal
❍ About 85% of phosphorus is in bone and teeth, com- tubules in order to conserve it.
bined in a 1:2 ratio with calcium. About 14% is in ❍ The parathyroid gland controls hormonal regulation
soft tissue, and less than 1% is in extracellular fluid. of phosphorus levels by affecting the activity of
❍ An essential element of all body tissues, phosphorus parathyroid hormone (PTH). (See Parathyroid hor-
is vital to various body functions. It plays a crucial mone and phosphorus.)
role in: – Changes in calcium levels, rather than changes in
– cell membrane integrity (phospholipids make up phosphorus levels, affect the release of PTH.
cell membranes) – Normally, calcium and phosphorus have an in-
– muscle function verse relationship: If one is elevated, the other is
– neurologic function decreased.
– metabolism of carbohydrate, fat, and protein – When the serum calcium level is low, the phospho-
– buffering of acids and bases rus level is high.
– promotion of energy transfer to cells through the – PTH release increases calcium and phosphorus
formation of energy-storing substances such as resorption from bone, raising both calcium and
adenosine triphosphate phosphorus levels. Phosphorus absorption from
– white blood cell phagocytosis the intestines is also increased. (Activated vitamin
– platelet function. D — calcitriol — also enhances its absorption in
❍ Phosphorus is a primary ingredient in 2,3-diphos- the intestines.)
phoglycerate, a compound in red blood cells (RBCs) – PTH then acts on the kidneys to increase excretion
that facilitates oxygen delivery from RBCs to the tis- of phosphorus.
sues. – Reduced PTH levels allow for phosphorus reab-
❍ Normally, serum phosphorus levels range from sorption by the kidneys. As a result, serum levels
2.5 to 4.5 mg/dl (or 1.8 to 2.6 mEq/L) in adults. The rise.
normal cellular level is 100 mEq/L. ❍ Certain conditions cause phosphorus to shift in and
❍ Because phosphorus is located mainly inside the out of cells.
cells, serum levels may not always reflect the total – Insulin moves not only glucose but also phospho-
amount of phosphorus in the body. rus into the cell.
– Alkalosis results in the same kind of phosphorus
AGE AWARE Elderly patients are at risk for al-
tered electrolyte levels for two main reasons.
❍ The total amount of phosphorus in the body is relat-
First, they have a lower ratio of lean body weight to
ed to dietary intake, hormonal regulation, kidney ex-
total body weight, which places them at risk for water
cretion, and transcellular shifts.
deficits. Second, their thirst response and renal func-
tion are decreased, which makes maintaining elec-

Parathyroid hormone and phosphorus

This illustration shows how
parathyroid hormone (PTH) af- PTH
fects serum phosphorus (P+)
levels — by increasing phospho-
rus release from bone, increas-
ing phosphorus absorption from
the intestines, and decreasing
phosphorus reabsorption in the
renal tubules.
P+ P+ P+
Release Absorption Reabsorption

22 Phosphorus
414501.qxd 18/8/08 12:12 PM Page 23

trolyte balance more difficult. Age-related renal

changes affects renal blood flow and glomerular fil-
tration rate. Drugs also may alter electrolyte levels by
affecting phosphate absorption. Ask all elderly pa-
tients if they take over-the-counter medications, such
as antacids, laxatives, herbs, and teas.

Dietary sources
❍ The recommended daily phosphorus requirement is
800 to 1,200 mg for adults.
❍ Phosphorus is readily absorbed through the GI tract,
and the amount absorbed is proportional to the
amount ingested.
❍ Major dietary sources of phosphorous include:
– cheese
– dried beans
– eggs
– fish
– milk products
– nuts
– organ meats, such as brain and liver
– poultry
– seeds
– whole grains.

Phosphorus 23
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Chloride ❍ Chloride levels remain relatively stable with age. Be-

cause chloride balance relates closely to sodium bal-
ance, the levels of both electrolytes usually change in
direct proportion to one another.
Overview ❍ Three types of diuertics increase the risk of chloride
❍ Chloride is the most abundant anion (negatively – loop diuretics, such as furosemide
charged ion) in extracellular fluid. – osmotic diuretics, such as mannitol
❍ High chloride levels are found in cerebrospinal fluid – thiazide diuretics, such as hydrochlorothiazide.
(CSF), but the anion can also be found in bile and in
gastric and pancreatic juices.
❍ It moves into and out of cells with sodium and potas- Balance
❍ Chloride combines with major cations (positively ❍ Chloride regulation depends on intake and excretion
charged ions) to form sodium chloride, hydrochlo- of chloride and reabsorption of chloride ions in the
ric acid, potassium chloride, calcium chloride, and kidneys.
other important compounds. ❍ Most chloride is absorbed in the intestines, with only
❍ Because of its negative charge, chloride travels with a small portion lost in the feces.
positively charged sodium and helps maintain serum ❍ Chloride is produced mainly in the stomach as hy-
osmolality and water balance. drochloric acid, so chloride levels can be influenced
❍ Chloride and sodium also work together to form CSF. by gastrointestinal disorders.
The choroid plexus, a tangled mass of tiny blood ves- ❍ Because chloride and sodium are closely linked, a
sels in the ventricles of the brain, depends on these change in one electrolyte level causes a comparable
two electrolytes to attract water and to form the fluid change in the other.
component of CSF. ❍ Chloride levels can be indirectly affected by aldos-
❍ In the stomach, chloride is secreted by the gastric terone secretion, which causes the renal tubules to
mucosa as hydrochloric acid, creating the acid envi- reabsorb sodium.
ronment conducive to digestion and enzyme activa- – As positively charged sodium ions are reabsorbed,
tion. negatively charged chloride ions are passively re-
❍ Chloride helps maintain acid-base balance and as- absorbed because of their electrical attraction to
sists in carbon dioxide transport in red blood cells. sodium.
❍ Serum chloride levels have a normal range of 96 to ❍ Regulation of chloride levels also involves acid-base
106 mEq/L. The chloride level in cells is 4 mEq/L. balance.
– Chloride is reabsorbed and excreted in direct op-
AGE AWARE Patients between ages 60 and 90
position to bicarbonate.
have chloride levels between 98 and 107 mEq/L;
– When chloride levels change, the body attempts to
patients age 90 and older, between 98 and 111 mEq/L.
keep its positive-negative balance by making cor-
responding changes in levels of bicarbonate (an-
other negatively charged ion) in the kidneys.
Chloride and bicarbonate – When chloride levels decrease, the kidneys retain
Chloride and bicarbonate have an inverse relationship. bicarbonate, and bicarbonate levels increase.
When the level of one goes up, the level of the other goes – When chloride levels increase, the kidneys excrete
down. bicarbonate, and bicarbonate levels decrease.
– Changes in chloride and bicarbonate levels can
lead to acidosis or alkalosis. (See Chloride and

HCO3- CI- Dietary sources

❍ The daily chloride requirement for adults is 750 mg.
❍ Most diets provide sufficient chloride, usually as
sodium chloride (table salt) in the same foods that
contain sodium.

24 Chloride
414501.qxd 18/8/08 12:12 PM Page 25

❍ Major sources of chloride include:

– canned vegetables
– fruits
– processed meats
– salty foods
– table salt
– vegetables.

Chloride 25
414501.qxd 18/8/08 12:12 PM Page 26

Acid-base balance base, neutralizing harmful effects until other regu-

lators take over.
– The respiratory system uses hypoventilation or hy-
Overview perventilation to regulate excretion or retention of
acids within minutes of a change in pH.
– The kidneys excrete or retain more acids or bases
pH as needed to restore a normal hydrogen ion con-
❍ pH is a calculation based on the percentage of hy- centration within hours or days.
drogen ions in a solution and the amount of acids
and bases in the solution. (See Normal pH.) Chemical buffers
❍ A solution with a pH below 7 is an acid. ❍ The bicarbonate-buffer system is the body’s primary
❍ A solution with a pH above 7 is a base. buffer system and works mainly in blood and inter-
❍ A patient’s acid-base balance can be assessed if you stitial fluid.
know the pH of his blood. – This system relies on a series of chemical reac-
❍ Arterial blood is usually used to measure pH. tions in which pairs of weak acids and bases (such
❍ If the hydrogen ion concentration of the blood in- as carbonic acid and bicarbonate) combine with
creases or the bicarbonate level decreases, pH may stronger acids (such as hydrochloric acid) and
decrease. A decrease in pH below 7.35 signals aci- bases to weaken them.
dosis. – Decreasing the strength of potentially damaging
❍ If the bicarbonate level increases or the hydrogen acids and bases reduces the danger those chemi-
ion concentration of the blood decreases, pH may cals pose to pH balance.
increase. An increase in pH above 7.45 signals alka- – The kidneys assist the bicarbonate-buffer system in
losis. regulating production of bicarbonate.
– The lungs assist by regulating production of car-
Acids bonic acid, which results from combining carbon
❍ Acids are molecules that can give up hydrogen ions dioxide and water.
to other molecules. ❍ Like the bicarbonate-buffer system, the phosphate-
❍ Carbonic acid is an acid that occurs naturally in the buffer system also depends on a series of chemical
body. reactions to minimize pH changes.
❍ A solution that contains more acid than base has – Phosphate buffers react with either acids or bases
more hydrogen ions, so it has a lower pH. to form compounds that slightly alter pH, which
can provide extremely effective buffering.
Bases – This system proves especially effective in renal
❍ Bases are molecules that can accept hydrogen ions tubules, where phosphates exist in greater concen-
❍ Bicarbonate is one example of a base. trations.
❍ A solution that contains more base than acid has ❍ Protein buffers, the most plentiful buffers in the
fewer hydrogen ions, so it has a higher pH. body, work inside and outside cells.
– These buffers are made up of hemoglobin and oth-
ALERT A change in pH can compromise es-
er proteins.
sential body processes, including electrolyte
– Protein buffers bind with acids and bases to neu-
balance, the activity of critical enzymes, muscle con-
tralize them. In red blood cells, for instance, he-
traction, and basic cellular function.
moglobin combines with hydrogen ions to act as a
Regulatory systems Respiratory buffers
❍ The body responds to acid-base imbalances by acti- ❍ The respiratory system serves as the second line of
vating compensatory mechanisms that minimize pH defense against acid-base imbalances.
changes. ❍ The lungs regulate blood levels of carbon dioxide, a
❍ If the body compensates only partially for an imbal- gas that combines with water to form carbonic acid.
ance, pH will still be outside the normal range. If the Increased levels of carbonic acid decrease pH.
body compensates fully or completely, pH will be ❍ Chemoreceptors in the medulla of the brain sense
back to normal. pH changes and vary the rate and depth of breathing
❍ Returning the pH to a normal or near-normal level to compensate.
mainly involves changes in the component — meta-
ALERT Breathing faster or deeper eliminates
bolic or respiratory — not primarily affected by the
more carbon dioxide from the lungs, which de-
creases the amount of carbonic acid made. As a re-
❍ When pH rises or falls, three regulatory systems
sult, pH rises. The body normalizes such a pH change
come into play:
by breathing slower or less deeply, reducing carbon
– Chemical buffers act immediately to protect tissues
dioxide excretion.
and cells. They combine with the offending acid or

26 Acid-base balance
414501.qxd 18/8/08 12:12 PM Page 27

❍ To assess the effectiveness of ventilation, look at the Normal pH

partial pressure of carbon dioxide in arterial blood This illustration shows that the blood pH normally stays
(PaCO2). Normally, PaCO2 is 35 to 45 mm Hg. PaCO2 slightly alkaline, between 7.35 and 7.45, a point at which
values reflect carbon dioxide levels in the blood. As the amount of acid (H) is balanced with the amount of
those levels increase, so does PaCO2. base (bicarbonate). Typically, pH is maintained in a ratio of
❍ As a buffer, the respiratory system can maintain acid- 20 parts bicarbonate to 1 part carbonic acid. A pH below
base balance twice as effectively as can chemical 7.35 is abnormally acidic; a pH above 7.45, abnormally
buffers because it can handle twice the amount of alkaline. A pH below 6.8 or above 7.8 typically is fatal.
acids and bases. pH
AGE AWARE The respiratory system of an older 14
adult may be compromised and less able to
regulate acid-base balance. ALKALINE H < BICARBONATE

❍ Although the respiratory system responds to pH 7.45

changes within minutes, it can restore normal pH 7.35
only temporarily. The kidneys are responsible for 7
long-term adjustments to pH.
ALERT If a lack of bicarbonate causes acido-
sis, the rate of breathing increases, which ACIDIC
blows off carbon dioxide and helps to raise the pH to
normal. If an excess of bicarbonate causes alkalosis,
the rate of breathing decreases, which retains carbon
dioxide and helps lower the pH.
❍ If the blood contains more base and less acid, pH
Renal buffers rises. The kidneys compensate by excreting bicar-
❍ The kidneys maintain acid-base balance by reab- bonate and retaining more hydrogen ions. Urine be-
sorbing acids and bases or excreting them into comes more alkaline, and the blood bicarbonate lev-
urine. el drops. Conversely, if the blood contains less
❍ They can also produce bicarbonate to replenish lost bicarbonate and more acid, the pH drops.
supplies. Such adjustments to pH take the kidneys
ALERT If the respiratory system disturbs the
hours to days to complete.
acid-base balance, the kidneys can compen-
❍ The kidneys also regulate the bicarbonate level,
sate by altering levels of bicarbonate and hydrogen
which reflects the metabolic component of acid-base
ions. When the PaCO2 is high (acidosis), the kidneys
retain bicarbonate and excrete more acid to raise the
– The bicarbonate level typically is reported with ar-
pH. When the PaCO2 level is low (alkalosis), the kid-
terial blood gas results.
neys excrete bicarbonate and hold on to more acid to
– A normal bicarbonate level is 22 to 26 mEq/L.
lower the pH.
– Bicarbonate is also reported with serum elec-
trolyte levels as total serum carbon dioxide con-
❍ If the blood contains too much acid or not enough
base, the pH drops and the kidneys reabsorb sodium
❍ The kidneys also excrete hydrogen along with phos-
phate or ammonia. Although urine tends to be acidic
because the body usually produces slightly more
acids than bases, in such situations urine becomes
more acidic than normal.
AGE AWARE Because ammonia production de-
creases with age, the kidneys of an older adult
can’t handle excess acid as well as the kidneys of a
younger adult.
❍ The reabsorption of bicarbonate and the increased
excretion of hydrogen causes more bicarbonate to
be formed in the renal tubules and eventually re-
tained in the body. The bicarbonate level in the
blood then rises to a more normal level, increasing

Acid-base balance 27
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Fluid and electrolyte – They move from the bloodstream into the cell,
causing the cell to swell.
replacement ❍ Hypotonic fluids have an osmolality of less than
275 mOsm/L.
❍ Examples of hypotonic fluids include half-normal
Isotonic solutions saline solution, 0.33% sodium chloride solution, and
dextrose 2.5% in water.
❍ Hypotonic solutions should be given cautiously be-
❍ Isotonic crystalloids cause fluid moves from the extracellular space into
– These solutions contain about the same concentra- cells, causing them to swell and increasing the risk
tion of osmotically active particles as extracellular of cardiovascular collapse from vascular fluid deple-
fluid. tion.
– Fluid doesn’t shift between the extracellular and ❍ These solutions also can cause increased intracra-
intracellular areas. nial pressure (ICP) from fluid shifting into brain
❍ Dextrose 5% in water (D5W) cells.
– D5W has an osmolality (or concentration) of – They shouldn't be given to a patient at risk for in-
275 to 295 mOsm/L. creased ICP — for example, a patient who has had
– The dextrose metabolizes quickly, acting like a hy- a cerebrovascular accident, head trauma, or neu-
potonic solution and leaving water behind. rosurgery.
– Large amounts of D5W may cause hyperglycemia. – Signs of increased ICP include a change in the pa-
❍ Normal saline solution tient’s level of consciousness; motor or sensory
– This solution contains only the electrolytes sodium deficits; and changes in pupil size, shape, or re-
and chloride. sponse to light.
❍ Other isotonic fluids ❍ Hypotonic solutions also shouldn’t be used for pa-
– These fluids are more like extracellular fluid. tients who have abnormal fluid shifts into the inter-
– Ringer’s solution contains sodium, potassium, cal- stitial space or the body cavities — for example, as a
cium, and chloride. result of liver disease, a burn, or trauma.
– Lactated Ringer’s solution contains those elec-
trolytes plus lactate, which the liver converts to bi-
carbonate. Hypertonic solutions
❍ Hypertonic crystalloids
Hypotonic fluids – These solutions are more highly concentrated than
extracellular fluid.
❍ Hypotonic crystalloids – Fluid moves into the bloodstream from the cells,
– These solutions are less concentrated than extra- causing the cells to shrink. (See Comparing fluid
cellular fluid. tonicity.)

Comparing fluid tonicity

The illustrations below show the effects of different types of I.V. fluids on fluid movement and cell size.

Isotonic fluids Hypertonic fluids Hypotonic fluids

These fluids have a concentration of These fluids have a tonicity greater than These fluids have a tonicity less than
dissolved particles, or tonicity, equal to that of intracellular fluid, so osmotic that of intracellular fluid. Osmotic pres-
that of intracellular fluid. Osmotic pres- pressure is unequal inside and outside sure draws water into the cells from the
sure is therefore the same inside and the cells. Dehydration or rapidly infused extracellular fluid. Half-normal saline
outside the cells, so they neither shrink hypertonic fluids, such as 3% saline or solution is an example of a hypotonic
nor swell with fluid movement. Normal 50% dextrose, draws water out of the fluid. Severe electrolyte losses or inap-
saline solution is an example of an iso- cells into the more highly concentrated propriate use of I.V. fluids can make
tonic solution. extracellular fluid. body fluids hypotonic.

Normal cell Cell shrinks Cell swells

28 Fluid and electrolyte replacement

414501.qxd 18/8/08 12:12 PM Page 29

❍ Hypertonic solutions have an osmolality greater than

295 mOsm/L.
❍ Examples of hypertonic solutions include:
– dextrose 5% in half-normal saline solution
– dextrose 5% in normal saline solution
– dextrose 5% in lactated Ringer’s solution
– dextrose 10% in water.
❍ A hypertonic solution draws fluids from the intracel-
lular space, causing cells to shrink and the extracel-
lular space to expand.
ALERT Patients with cardiac or renal disease
may be unable to tolerate extra fluid. Watch
for fluid overload and pulmonary edema.
❍ Because hypertonic solutions draw fluids from cells,
patients at risk for cellular dehydration (those with
diabetic ketoacidosis, for example) shouldn’t receive

❍ A colloid is a large molecule, such as albumin, that
normally doesn't cross the capillary membrane. A
crystalloid is a solute, such as sodium or glucose,
that crosses the capillary membrane in solution.
❍ The use of colloids over crystalloids is controversial.
Still, a colloid — also known as a plasma expander
— may be prescribed if your patient’s blood volume
doesn’t improve with crystalloids.
❍ Examples of colloids include:
– albumin (available in 5% solutions, which are os-
motically equal to plasma, and 25% solutions,
which draw about four times their volume in inter-
stitial fluid into the circulation within 15 minutes)
– plasma protein fraction
– dextran
– hetastarch.
❍ Colloids pull fluid into the bloodstream. The effects
of colloids last several days if the lining of the capil-
laries is normal.
❍ The patient needs to be closely monitored during a
colloid infusion for increased blood pressure, dysp-
nea, and bounding pulse, which are all signs of hy-
❍ If neither crystalloids nor colloids are effective in
treating the imbalance, the patient may need a blood
transfusion or other treatment.

Fluid and electrolyte replacement 29

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Blood products and posed to Rh-positive blood. The first exposure usual-
ly causes sensitization, but the second exposure may
transfusions result in a fatal hemolytic reaction. These reactions
can occur during transfusions or pregnancy.
HLA group
Compatibility ❍ HLA is located on the surface of circulating platelets,
white blood cells (WBCs), and most tissue cells.
❍ Blood contains various antigens that affect whether ❍ It causes febrile reactions in patients receiving a
one person’s blood is compatible with another’s. transfusion that contains platelets from several
❍ Antigens include: donors. The antigen-antibody reaction causes
– ABO blood group platelet destruction, making the patient less respon-
– rhesus (Rh) factor sive to platelet transfusions.
– human leukocyte antigen (HLA) blood group. ❍ Giving HLA-matched platelets greatly decreases the
❍ These characteristics — especially Rh factor and risk of such antigen-antibody reactions.
ABO blood type — are crossmatched to ensure com- ❍ In general, HLA tests benefit patients who receive
patibility between donor and recipient before trans- multiple transfusions over a long period or frequent
fusion. transfusions during a short-term illness.
ABO group
❍ The ABO method of typing blood identifies two anti- Blood products
gens on red blood cells (RBCs).
– A person may have both A and B antigens (type AB Whole blood
blood). ❍ Whole blood is available in 500-ml bags and may be
– He may have only one antigen (either type A blood used to treat hemorrhage, trauma, or major burns.
or type B blood). ❍ You'll rarely use it unless the patient has lost more
– He may have neither antigen (type O blood). than 25% of total blood volume.
❍ In the United States, 85% of the population has ei- ❍ ABO compatibility and Rh matching are required be-
ther type A or type O blood (with type O being the fore administration.
most common), 10% has type B, and 5% has type ❍ Avoid whole blood if fluid overload is a concern.
AB. ❍ Stored whole blood is high in potassium.
❍ A person with A antigens has anti-B antibodies in his ❍ After 24 hours, the viability and function of RBCs de-
plasma. If he has B antigens, he has anti-A antibodies crease.
in his plasma. Receiving a blood type for which he
has antibodies may cause a transfusion reaction. Packed red blood cells
❍ People with type AB blood are called universal recip- ❍ Packed RBCs are prepared by removing about 90%
ients. They have no antibodies and, therefore, can of the plasma surrounding the cells and adding an
receive blood of any type without a reaction. anticoagulant preservative.
❍ People with type O blood are universal donors. Their ❍ A 250-ml bag of packed RBCs can help restore or
blood may be transfused into a person with any maintain the oxygen-carrying capacity of the blood in
blood type. However, because type O blood contains patients with anemia or can correct blood losses
both anti-A and anti-B antibodies, people with this during or after surgery.
blood type may receive only type O blood safely. ❍ About 70% of the leukocytes in packed cells have
❍ If a patient’s blood type is available, he should re- been removed, which reduces the risk of febrile,
ceive blood that’s compatible with his own blood nonhemolytic reactions.
type to keep transfusion reactions to a minimum. ❍ ABO compatibility and Rh matching are still required
(See Identifying compatible blood types.) for these transfusions.
❍ In an emergency, when waiting for a crossmatch
would be dangerous, blood from a universal donor White blood cells
or plasma volume expanders may be given. Perfluo- ❍ Granulocyte, or WBC, transfusions are rarely indicat-
rocarbons — milky, white emulsions that act like ed; however, they may be used to treat gram-negative
plasma but carry oxygen like RBCs — may provide sepsis or progressive soft-tissue infection unrespon-
an alternative in some hospitals. sive to antimicrobial drugs.
❍ HLA compatibility tests are preferable, and Rh
Rh factor matching is required.
❍ About 85% of the U.S. population is Rh-positive,
which means their blood contains the Rh antigen Fresh frozen plasma
on the membranes of RBCs. ❍ Fresh frozen plasma is prepared by separating the
❍ No natural antibodies to Rh exist. However, Rh- plasma from the RBCs and freezing it within 6 hours
negative people may develop an Rh antibody if ex- of collection.

30 Blood products and transfusions

414501.qxd 18/8/08 12:12 PM Page 31

❍ The solution contains plasma proteins, water, fib- Identifying compatible blood types
rinogen, some clotting factors, electrolytes, glucose, A transfusion most likely will be safe if the donor and
vitamins, minerals, hormones, and antibodies. recipient have compatible blood types. This illustration
❍ Fresh frozen plasma is used to treat hemorrhage, ex- provides a key to blood-type compatibility.
pand plasma volume, correct undetermined coagula-
tion factor deficiencies, replace specific clotting fac-
tors, and correct factor deficiencies caused by liver
❍ ABO compatibility testing isn't needed; Rh matching
is preferred.
❍ Large-volume transfusions of fresh frozen plasma Recipient’s blood type Compatible donor type
A A, O
may require correction for hypocalcemia because B B, O
citric acid in the transfusion binds with and depletes AB A, B, AB, O
the patient’s serum calcium level. O O

❍ Cryoprecipitate (also called factor VIII) is the insolu-
ble portion of plasma recovered from fresh frozen
❍ It’s used to treat von Willebrand’s disease, hypofib-
rinogenemia, factor VIII deficiency (antihemophilic
factor), hemophilia A, and disseminated intravascu-
lar coagulation.
❍ ABO compatibility testing isn't needed. – bacterial contamination
– febrile
Albumin – hemolytic
❍ Albumin, which comes in an isotonic 5% solution – plasma protein incompatibility.
and a hypertonic 25% solution, is extracted from ❍ Exogenous transfusion reactions (those caused by
plasma and contains globulin and other proteins. external factors in administered blood) include:
❍ It’s used for patients with acute liver failure, burns, – bleeding tendencies
or trauma; patients who have had surgery; and – circulatory overload
neonates with hemolytic disease when crystalloids – hypocalcemia
prove ineffective. – hypothermia
❍ As a colloidal solution, albumin’s large molecules in- – potassium intoxication.
crease plasma oncotic pressure, moving fluid from ❍ With human immunodeficiency virus (HIV)–
the interstitial space across capillary membranes and antibody testing being done on all donated blood
into the intravascular space. and stringent criteria being used to exclude high-risk
❍ Albumin may actually do more harm than good in blood donors, studies now show that HIV transmis-
patients with shock by leaking through damaged sion through infusion is rare.
capillary membranes and dragging intravascular flu- ❍ Testing for hepatitis B and hepatitis C viruses has be-
id along to worsen interstitial edema. come more specific, which has helped to make the
❍ Albumin is also used to treat hypoproteinemia with blood supply safer.
or without edema.
❍ ABO matching isn't needed.
❍ Platelets are given to patients with platelet dysfunc-
tion or thrombocytopenia and to those who have had
multiple transfusions of stored blood, acute leuke-
mia, or bone marrow abnormalities.
❍ Platelet transfusion may cause febrile or mild aller-
gic reactions.
❍ Rh matching is preferred.

Transfusion reactions
❍ Endogenous transfusion reactions (those caused by
antigen-antibody reactions) include:
– allergic

Blood products and transfusions 31

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Total parenteral – drugs. (See Understanding common TPN addi-

Lipid emulsions
Solution components ❍ Lipid emulsions supply essential fatty acids and calo-
❍ Total parenteral nutrition (TPN) formulas provide ❍ These thick solutions assist in wound healing, red
nutritional supplementation tailored to the patient’s blood cell production, and prostaglandin synthesis.
specific needs. ❍ Although they’re typically given with TPN, they may
❍ Nutritional support teams consisting of nurses, doc- be given alone through a peripheral or central ve-
tors, pharmacists, and dietitians assess, prescribe nous line, or they may be mixed with amino acids
for, and monitor patients receiving TPN. and dextrose in one container (providing a three-in-
❍ TPN solutions may contain: one-system) and infused over 24 hours.
– protein (amino acids in a 2.5% to 8.5% solution), ❍ Lipid emulsions should be given cautiously to pa-
with varying types available for patients with renal tients with hepatic or pulmonary disease, anemia, or
or liver failure a coagulation disorder and to patients at risk for fat
– dextrose (15% to 50% solution) embolism.
– fat emulsions (10% to 20% solution) ❍ These emulsions shouldn’t be given to patients who
– electrolytes have conditions that disrupt normal fat metabolism,
– vitamins such as pathologic hyperlipidemia, lipid nephrosis,
– trace element mixtures and acute pancreatitis.

Understanding common TPN additives Adverse reactions

Common components of total parenteral nutrition (TPN)
solutions — such as dextrose 5% in water (D5W), amino ❍ Signs and symptoms of electrolyte imbalances
acids, and other additives — are used for specific pur- caused by TPN administration include:
poses. For instance, D5W provides calories for metabo- – abdominal cramps
lism. Here’s a list of other common additives and the pur- – lethargy
poses each serves. (Lipids may be infused separately.) – confusion
Electrolytes – malaise
● Calcium promotes development of bones and teeth and – muscle weakness
aids in blood clotting. – tetany
● Chloride regulates acid-base balance and maintains os- – seizures
motic pressure. – cardiac arrhythmias.
● Magnesium helps the body absorb carbohydrates and ❍ Acid-base imbalances can also occur as a result of
protein. the patient’s condition or the contents of the TPN.
● Phosphorus is essential for cellular energy and calcium ❍ Other complications may include:
– heart failure or pulmonary edema from fluid and
● Potassium is needed for cellular activity and cardiac
electrolyte administration, conditions that can lead
● Sodium helps control water distribution and maintain
to tachycardia, lethargy, confusion, weakness, and
normal fluid balance. labored breathing
– hyperglycemia from infusing dextrose too quickly,
● Folic acid is needed for DNA formation and promotes
a condition that may require adjustment of the pa-
growth and development.
tient’s insulin dosage
● Vitamin B complex helps the final absorption of carbo- – adverse reactions to drugs in the TPN solution —
hydrates and protein. such as hypoglycemia from added insulin, which
● Vitamin C helps in wound healing. can cause confusion, restlessness, lethargy, pallor,
● Vitamin D is essential for bone metabolism and mainte- and tachycardia
nance of serum calcium levels. – complications from I.V. cannulas and central ve-
● Vitamin K helps prevent bleeding disorders. nous catheters.
Other additives ❍ Immediate or early adverse reactions from lipid
● Acetate prevents metabolic acidosis. emulsions may include:
● Micronutrients (such as zinc, cobalt, and manganese) – back and chest pain
help in wound healing and red blood cell synthesis. – cyanosis
● Amino acids provide the proteins needed for tissue re- – diaphoresis or flushing
pair. – dyspnea
– headache

32 Total parenteral nutrition

414501.qxd 18/8/08 12:12 PM Page 33

– hypercoagulability
– irritation at the site
– lethargy or syncope
– nausea or vomiting
– slight pressure over the eyes
– thrombocytopenia.
❍ Delayed complications from prolonged use of lipid
emulsions may include:
– blood dyscrasias
– fatty liver syndrome
– hepatomegaly
– jaundice
– splenomegaly.

Total parenteral nutrition 33

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Hemodialysis basics ❍ Is usually performed in hemodialysis unit by special-

ly trained staff
❍ May be done at bedside in intensive care unit if pa-
tient is acutely ill and unstable
Overview ❍ May be available for use at home (special hemodial-
ysis units)
❍ Is performed to remove toxic wastes from the blood
of patients in renal failure
❍ Removes blood from the body, circulates it through a Contraindications
purifying dialyzer, and then returns the blood to the
body ❍ Hemodynamic instability
❍ May be delivered through various types of access
sites, although long-term treatment typically is deliv-
ered via an arteriovenous (AV) fistula (See Hemo- Special considerations
dialysis access sites.)
❍ Works on the principle of differential diffusion ❍ Obtain blood samples from the patient, as ordered,
across a semipermeable membrane, which extracts usually before hemodialysis starts.
byproducts of protein metabolism, such as urea and
ALERT To avoid pyrogenic reactions and bac-
uric acid, as well as creatinine and excess water
teremia with septicemia resulting from conta-
❍ Restores or maintains balance of the body’s buffer
mination, use strict sterile technique when preparing
system and electrolyte level, promoting rapid return
the dialysis machine.
to normal serum values and preventing complica-
tions of uremia ❍ Immediately report any machine malfunction or
❍ Provides temporary support for patients with acute equipment defect.
reversible renal failure ❍ Avoid unnecessary handling of hemodialysis tubing.
❍ Is used for regular long-term treatment of patients ❍ Assess the catheter insertion site for signs of infec-
with chronic end-stage renal disease tion, such as purulent drainage, inflammation, and
❍ Is performed less commonly for acute poisoning, tenderness.
such as barbiturate or analgesic overdose
ALERT Make sure you complete each step in
❍ Depends on patient’s condition (rate of creatinine
the dialysis procedure correctly to avoid un-
accumulation and weight gain) for number and du-
necessary blood loss or inefficient treatment from
ration of treatments

Hemodialysis access sites

Hemodialysis requires vascular access. The site and type of access may vary with the expected duration of dialysis, the sur-
geon’s preference, and the patient’s condition.

Subclavian vein catheterization Femoral vein catheterization

Using the Seldinger technique, a doctor or surgeon inserts Using the Seldinger technique, a doctor or surgeon inserts
an introducer needle into the subclavian vein, inserts a an introducer needle into the left or right femoral vein, in-
guidewire through the serts a guidewire through the introducer needle, and re-
introducer needle, and moves the needle. Using the guidewire, he then threads a 5"
removes the needle. Us- to 12" plastic or Teflon
ing the guidewire, he catheter into the vein
then threads a 5" to 12" with a Y hub or two
(12.5- to 30.5-cm) plas- catheters, one for in-
tic or Teflon catheter flow and another
(with a Y hub) into the placed about 1/2" (1.3
patient’s vein. cm) distal to the first
Native arteriovenous fistula for outflow.
To create a native arteriovenous (AV) fistula, the surgeon Prosthetic arteriovenous fistula
makes an incision into the patient’s wrist or lower forearm, To create an AV fistula with synthetic material, the surgeon
a small incision in the side of an artery, and another small makes an incision in the patient’s forearm, upper arm, or
incision in the side of a thigh. He then tun-
vein. He sutures the nels a synthetic
edges of the incisions graft under the skin
together to make a and sutures the dis-
common opening 3 to tal end to an artery
7 mm long. and the proximal
end to a vein.

34 Hemodialysis basics
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poor clearances or inadequate fluid removal. For ex-

❍ Time blood specimens were taken for testing, the test
ample, allowing a saline solution bag to run dry while
priming and soaking the dialyzer can cause air to en- results, and treatment for complications
❍ Time the treatment was completed
ter the patient portion of the dialysate system. Ulti-
❍ Patient’s response to treatment
mately, failure to perform accurate hemodialysis
❍ Condition of vascular access site and site care
therapy can lead to patient injury and even death.
❍ If bleeding continues after you remove an AV fistula
needle, apply just enough pressure with a sterile, ab-
sorbable gelatin sponge or topical thrombin solution
to stop the bleeding.
❍ Monitor the patient's vital signs throughout he-
modialysis at least hourly or as often as every 15
minutes, if needed.
❍ After dialysis is complete, assess the patient’s weight,
vital signs, and mental status, and compare the find-
ings with your predialysis assessment.
❍ Perform periodic tests of clotting time on the pa-
tient’s blood samples and samples from the dialyzer.
❍ If the patient receives meals during treatment, make
sure they’re light.
❍ Continue needed drug therapy during dialysis unless
the drug would be removed in the dialysate; if so,
give the drug after dialysis.
❍ Provide emotional support.

❍ Air embolism
❍ Angina
❍ Cardiac arrhythmias
❍ Dialysis disequilibrium syndrome
❍ Exsanguination
❍ Fever
❍ Hemolysis
❍ Hyperglycemia
❍ Hypernatremia
❍ Hyperosmolarity
❍ Hyperthermia
❍ Hypotension
❍ Hypovolemia
❍ Stenosis of AV fistula
❍ Thrombosis of AV fistula

Patient teaching
Be sure to cover:
❍ how to care for the vascular access site at home
❍ how to perform hemodialysis at home if possible —
usually a complex process requiring 2 to 3 months
to feel comfortable and be competent
❍ the telephone number of the dialysis center.

❍ Time treatment began
❍ Any problems with treatment
❍ Vital signs and weight before and during treatment

Hemodialysis basics 35
414501.qxd 18/8/08 12:12 PM Page 36

Managing hemodialysis ❍

Clean gloves
Sterile gloves
❍ Normal saline solution
Hemodialysis of all types ❍

Alcohol pads
Heparin flush solution
❍ Luer-lock injection caps
Equipment ❍ Transparent occlusive dressing
❍ Hemodialysis machine with appropriate dialyzer
❍ I.V. solution Essential steps
❍ Administration sets, lines, and related equipment Starting hemodialysis
❍ Dialysate ❍ If extension tubing isn’t already clamped, clamp it to
❍ Optional: heparin, 3-ml syringe with needle, medica- prevent air from entering the catheter.
tion label ❍ Clean each catheter extension tube, clamp, and Luer-
❍ Hemostats lock injection cap with povidone-iodine pads to re-
move contaminants.
Equipment preparation ❍ Place a sterile 4  4 gauze pad under the exten-
❍ Prepare the hemodialysis equipment according to sion tubing, and place two 5-ml syringes and two
manufacturer’s instructions and hospital protocol. sterile gauze pads on the drape.
❍ Test the dialyzer and dialysis machine for residual ❍ Prepare the anticoagulant regimen as ordered.
disinfectant after rinsing, and test all the alarms. ❍ Identify arterial and venous blood lines, and place
them near the drape.
Essential steps ❍ To remove clots and ensure catheter patency, remove
❍ Wash your hands thoroughly before all procedures. catheter caps, attach syringes to each catheter port,
❍ If the patient is having hemodialysis for the first time, open the clamp, aspirate 1.5 to 3 ml of blood, close
explain the procedure in detail. the clamp, and flush each port with 5 ml of heparin
❍ Maintain sterile technique to prevent pathogens from flush solution.
entering the patient’s bloodstream during dialysis. ❍ To gain patient access, remove the syringe from the
❍ Wear appropriate personal protective equipment, as arterial port, attach the line to the arterial port, and
needed, during all procedures. give the heparin according to protocol to prevent
❍ Weigh the patient and compare it to his weight after clotting in the extracorporeal circuit.
the last dialysis and his target weight to determine ul- ❍ Grasp the venous blood line and attach it to the ve-
trafiltration needs. nous port, open the clamps on the extension tubing,
❍ Record baseline vital signs, taking blood pressure and secure the tubing to the patient’s limb with tape
while the patient’s sitting and standing; auscultate the to reduce tension on the tube and minimize trauma
heart for rate, rhythm, and abnormalities; assess the to the insertion site.
patient for edema; observe respiratory rate, rhythm, ❍ Begin hemodialysis according to your facility’s pro-
and quality; and check the patient’s mental status. tocol.
❍ Assess the condition and patency of the access site. Stopping hemodialysis
❍ Check for problems since the last dialysis session, ❍ Clamp the extension tubing to prevent air from en-
and evaluate previous laboratory data. tering the catheter.
❍ Help the patient into a comfortable position (supine ❍ Clean all connection points on the catheter and
or sitting in a reclining chair with feet elevated). blood lines as well as the clamps to reduce the risk
❍ Support the access site and rest it on a clean drape. of systemic or local infections.
❍ Place a clean drape under the catheter, and place
two sterile 4  4 gauze pads on the drape be-
Hemodialysis with neath the catheter lines.
a double-lumen catheter ❍ Soak the pads with povidone-iodine solution.
❍ Prepare the catheter flush solution with normal
saline or heparin flush solution, as ordered.
Equipment ❍ Put on clean gloves.
Starting hemodialysis ❍ Grasp each blood line with a gauze pad and discon-
❍ Povidone-iodine pads nect each line from the catheter.
❍ Two sterile 4  4 gauze pads ❍ Flush each port with saline solution to clean the ex-
❍ Two 3-ml and two 5-ml syringes tension tubing and catheter of blood.
❍ Tape ❍ Give additional heparin flush solution as ordered to
❍ Heparin bolus syringe ensure catheter patency. Then attach Luer-lock injec-
❍ Clean gloves tion caps to prevent entry of air or loss of blood.
Stopping hemodialysis ❍ Clamp the extension tubing.
❍ Sterile gauze pads ❍ Re-dress the catheter insertion site; also re-dress it if
❍ Povidone-iodine pads it’s occluded, soiled, or wet.

36 Managing hemodialysis
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❍ During the dressing change, position the patient in a ❍ Put on clean gloves.
supine position with his face turned away from the ❍ Remove the fistula needle guard and squeeze the
insertion site so that he doesn’t contaminate the site wing tips firmly together.
by breathing on it. ❍ Insert the arterial needle at least 1 (2.5 cm) above
❍ Change gloves after washing your hands, and remove the anastomosis, being careful not to puncture the
the outer occlusive dressing. fistula.
❍ Put on sterile gloves, remove the old inner dressing, ❍ Release the tourniquet and flush the needle with he-
and discard the gloves and the inner dressing. parin flush solution to prevent clotting.
❍ Set up a sterile field, and observe the site for ❍ Clamp the arterial needle tubing with a hemostat,
drainage, obtaining a drainage sample for culture if and secure the wing tips of the needle to the skin
needed. with adhesive tape to prevent it from dislodging in-
❍ Notify the doctor if the suture seems to be missing. side the vein.
❍ Put on sterile gloves and clean the insertion site with ❍ Perform another venipuncture with the venous nee-
an alcohol pad to remove skin oils. dle a few inches above the arterial needle.
❍ Clean the site with a povidone-iodine pad and allow ❍ Flush the venous needle with heparin flush solution.
it to air dry. ❍ Clamp the venous needle tubing, and secure the wing
❍ Place a precut gauze dressing under the catheter, tips of the venous needle as you did with the arterial
and place another gauze dressing over the catheter. needle.
❍ Apply a skin barrier preparation to the skin sur- ❍ Remove the syringe from the end of the arterial tub-
rounding the gauze dressing and cover the gauze and ing, uncap the arterial line from the hemodialysis
catheter with a transparent occlusive dressing. machine, and connect the two lines.
❍ Apply a 4 to 5 (10- to 12.5-cm) piece of 2 tape ❍ Tape the connection securely to prevent it from sepa-
over the cut edge of the dressing to reinforce the rating during the procedure.
lower edge. ❍ Remove the syringe from the end of the venous tub-
ing, uncap the venous line from the hemodialysis
machine, and connect the two lines.
Hemodialysis with ❍ Tape the connection securely to prevent it from sepa-
an AV fistula rating during the procedure.
❍ Release the hemostats and start hemodialysis.
Equipment Stopping hemodialysis
❍ Turn the blood pump on the hemodialysis machine
Starting hemodialysis to 50 to 100 ml/minute.
❍ Two winged fistula needles (each attached to a 10-ml ❍ Put on clean gloves and remove the tape from the
syringe filled with heparin flush solution) connection site of the arterial lines.
❍ Linen-saver pad ❍ Clamp the needle tubing with the hemostat and dis-
❍ Povidone-iodine pads connect the lines. The blood in the machine’s arteri-
❍ Sterile 4  4 gauze pads al line will continue to flow toward the dialyzer, fol-
❍ Tourniquet lowed by a column of air. Just before the blood
❍ Clean gloves reaches the point where the saline solution enters
❍ Adhesive tape the line, clamp the blood line with another hemostat.
❍ Hemostats ❍ Unclamp the saline solution to allow a small amount
Stopping hemodialysis to flow through the line.
❍ Clean gloves ❍ Unclamp the hemostat on the machine line to allow
❍ Hemostats all blood to flow into the dialyzer where it passes
❍ Sterile gauze pads through the filter and back to the patient through the
❍ Two adhesive bandages venous line.
❍ After the blood is retransfused, clamp the venous
Essential steps needle tubing and the machine’s venous line with he-
Starting hemodialysis mostats and turn off the blood pump.
❍ Flush the fistula needles using attached syringes with ❍ Remove the tape from the connection site of the ve-
heparinized saline solution, and set them aside. nous lines and disconnect the lines.
❍ Place a linen-saver pad under the patient’s arm. ❍ Remove the venipuncture needle and apply pressure
❍ Using sterile technique, clean a 3  10 (8  to the site with a folded 4  4 gauze pad until all
25 cm) area of skin over the fistula with povidone- bleeding stops, usually within 10 minutes.
iodine pads. If the patient is sensitive to iodine, use ❍ Apply an adhesive bandage.
chlorhexidine gluconate or alcohol instead. ❍ Repeat the procedure on the arterial line.
❍ Discard each pad after one wipe. ❍ Disinfect and rinse the delivery system according to
❍ Apply a tourniquet above the fistula to distend the the manufacturer’s instructions.
veins and facilitate venipuncture, making sure you
don't occlude the fistula.

Managing hemodialysis 37
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Peritoneal dialysis Essential steps

❍ Explain all procedures to the patient.
Overview ❍

Maintain asepsis throughout all procedures.
Wash your hands and close the door to the room.
❍ Is indicated for patients with chronic renal failure ❍ Wear appropriate personal protective equipment
who can't tolerate hemodialysis during all procedures.
❍ Also is indicated for patients who prefer it or who ❍ Assess and record vital signs, weight, and abdominal
refuse hemodialysis girth to establish baseline levels.
❍ May be indicated for patients who prefer home dialy- ❍ Place the patient in a supine position if tolerated and
sis but have no one trained for home hemodialysis have him put on a sterile face mask.
❍ Is performed by instilling dialysate into the perito-
ALERT Whenever the dialysis system is opened
neal cavity by catheter (inserted surgically) to draw
or entered, everyone in the room should be
waste products, excess fluid, and electrolytes from
wearing a mask.
the blood across the peritoneal membrane
❍ Requires dialysate to be drained from the peritoneal ❍ Inspect the warmed dialysate, which should appear
cavity after prescribed period, removing impurities clear and colorless.
with it ❍ Put on a sterile face mask.
❍ Is repeated with new dialysate each time until waste ❍ Add prescribed drugs to the dialysate, using strict
removal is complete and fluid, electrolyte, and acid- sterile technique, immediately before the solution is
base balance is restored hung and used.
❍ Disinfect multiple-dose vials by soaking them in
Contraindications and cautions ❍
povidone-iodine solution for 5 minutes.
Prepare the dialysis administration set. (See Setup
❍ Peritonitis for peritoneal dialysis.)
❍ Documented loss of peritoneal function or extensive ❍ Close the clamps on all lines.
abdominal adhesions that limit dialysate flow ❍ Place the drainage bag below the patient to facilitate
❍ Uncorrectable mechanical defects gravity drainage and connect the drainage line to it.
❍ Fresh intra-abdominal foreign bodies ❍ Connect the dialysate infusion lines to the bottles or
❍ Peritoneal leaks bags of dialysate.
❍ Intolerance to volumes needed to reach an adequate ❍ Hang the bottles or bags on the I.V. pole at the pa-
peritoneal dialysis dose tient’s bedside.
❍ Inflammatory or ischemic bowel disease ❍ Open the infusion lines and let the solution flow until
❍ Abdominal wall or skin infection all lines are primed; then close all clamps.
❍ Morbid obesity ❍ Connect the catheter to the administration set.
❍ Severe malnutrition ❍ Unclamp the lines to the patient and instill the pre-
❍ Frequent episodes of diverticulitis scribed amount of dialysate into the peritoneal cavity
to test the catheter’s patency.
Equipment ❍

Clamp the lines to the patient.
As soon as the dialysate container empties, clamp the
❍ Must be sterile lines to the patient immediately to prevent air from
❍ Commercially packaged dialysis kits or trays entering the tubing.
❍ Prescribed dialysate (in 1- or 2-L bottles or bags) ❍ Let the solution dwell in the peritoneal cavity for the
❍ Warmer, heating pad, or water bath prescribed time.
❍ Face masks ❍ Warm the solution for the next infusion.
❍ Dialysis administration set with drainage bag ❍ At the end of the prescribed dwell time, unclamp the
❍ Two pairs of sterile gloves line to the drainage bag and let solution drain from
❍ I.V. pole the peritoneal cavity (usually 20 to 30 minutes).
❍ Fenestrated sterile drape ❍ Repeat the infuse-dwell-drain cycle as prescribed
(usually 4 to 5 times daily).
Equipment preparation
ALERT To reduce the risk of peritonitis, use
❍ Wash your hands thoroughly before all procedures.
strict sterile technique during catheter inser-
❍ Bring all equipment to the patient’s bedside.
tion, dialysis, and dressing changes.
❍ Make sure the dialysate is at body temperature to re-
duce discomfort and reduce vasoconstriction of the ❍ Change the dressing at least every 24 hours or when-
peritoneal capillaries. ever it becomes wet or soiled.
❍ Place the container in a warmer or a water bath, or ❍ To prevent respiratory distress, position the patient
wrap it in a heating pad set at 98.6 F (37 C) for 30 for maximal lung expansion, turn the patient often,
to 60 minutes to warm the solution. and encourage deep-breathing exercises.

38 Peritoneal dialysis
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ALERT If the patient develops severe respira- Setup for peritoneal dialysis
tory distress during the dwell phase of dialysis, The proper setup for peritoneal dialysis is shown below.
drain the peritoneal cavity and notify the doctor.

Special considerations
❍ To prevent protein depletion, the doctor may order a Dialysate
high-protein diet or a protein supplement and moni-
Drip chamber
toring of serum albumin levels.
❍ Dialysate is available in three concentrations: 4.25% Roller clamp
dextrose, 2.5% dextrose, and 1.5% dextrose. If your
Administration tubing
patient receives the 4.25% dextrose solution, watch
for excess fluid loss and hyperglycemia. Peritoneal dialysis
Drainage catheter
❍ Patients with low serum potassium levels may need
potassium in the dialysate to prevent further losses.
❍ To help prevent fluid imbalance, monitor fluid vol- Drip
ume balance, blood pressure, and pulse and notify chamber
the doctor if the patient retains 500 ml or more of
fluid for three consecutive cycles or loses at least Drainage bag
1 L of fluid for three consecutive cycles.
❍ Weigh the patient at the same time each day to assess
how much fluid is being removed during dialysis.
❍ If inflow and outflow are slow or absent, check the
tubing for kinks, raise the I.V. pole, reposition the
patient, or apply manual pressure to the lateral as- ❍ Electrolyte imbalances
pects of the patient’s abdomen. If these maneuvers ❍ Hyperglycemia
fail, notify the doctor. ❍ Hypotension and shock
❍ Normally, outflow fluid (effluent) is clear or pale yel- ❍ Peritonitis and sclerosing encapsulating peritonitis
low, but pink-tinged effluent may appear during the ❍ Protein depletion
first three or four cycles. ❍ Respiratory distress
❍ If the effluent is pink-tinged or grossly bloody, sus- ❍ Tunnel abscess (in continuous ambulatory peri-
pect bleeding into the peritoneal cavity and notify the toneal dialysis)
❍ If the outflow contains feces, which suggests bowel Patient teaching
perforation, or if it’s cloudy, which suggests peritoni-
tis, notify the doctor and obtain a sample for culture Be sure to cover:
and Gram’s stain. ❍ performing the procedure using sterile technique
❍ If the patient has pain during the procedure, deter- ❍ dressing changes and skin care
mine when it occurs, its quality and duration, and ❍ signs and symptoms of peritonitis and other compli-
whether it radiates, and notify the doctor. cations to report
❍ the need to record weight and blood pressure daily
ALERT Pain during infusion usually results ❍ the importance of keeping accurate intake records
from dialysate that’s too cool or acidic. It also
❍ name and telephone number of a person to call for
may result from rapid inflow; slowing the inflow rate
assistance and questions.
may reduce the pain. Severe, diffuse pain with re-
bound tenderness and cloudy effluent may indicate
peritoneal infection. Pain that radiates to the shoul- Documentation
der commonly results from air accumulation under
❍ Date and time of dialysis
the diaphragm. Severe, persistent perineal or rectal
❍ Exchange number
pain can result from improper catheter placement.
❍ Volume of dialysate infused and drained
❍ To minimize the patient’s discomfort, perform daily ❍ Infusion, dwell, and drain times
care during the drain phase of the cycle, when the ❍ Drugs added to the solution
patient’s abdomen is less distended. ❍ Color and character of effluent
❍ Complications and treatment
Complications ❍

Daily weight
Vital signs before, during, and after dialysis
❍ Abdominal or pericatheter infection ❍ Patient teaching
❍ Amyloidosis ❍ Total fluid balance after each exchange
❍ Bladder perforation ❍ Pericatheter skin assessment
❍ Bowel perforation

Peritoneal dialysis 39
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Continuous renal – Simple technology using a semipermeable mem-

brane and an extracorporeal circuit
replacement therapy – Uses arterial pressure to move blood through the
extracorporeal circuit and semipermeable mem-
Overview – High risk for blood loss from clotting in the circuit
– High risk for bleeding from arterial cannulation
❍ Continuous arteriovenous hemodiafiltration
Description – Same procedure as CAVH
❍ Is used to manage fluid and electrolyte imbalance in – Uses dialysate to promote waste removal
hemodynamically unstable patients. ❍ Continuous venovenous hemofiltration (CVVH)
❍ Removes toxins from the blood – Blood flow through a semipermeable fiber filter
❍ Doesn't cause dramatic changes in blood pressure, and an extracorporeal circuit
as hemodialysis may, because fluid exits slowly – Uses a pump to propel blood through the circuit
❍ Is performed by a specially trained nurse in a critical and semipermeable membrane
care setting – Decreased risk of clotting because pump rotates to
❍ Requires special equipment, supplies, and staff train- move the blood
ing – Decreased risk of blood loss from a double-
lumen, large-bore venous catheter to gain access
Types of continuous renal to the patient’s blood
replacement therapy – Alarms on the equipment to signal machine or pa-
❍ Continuous arteriovenous hemofiltration (CAVH) tient problem
❍ Continuous venovenous hemodialysis (CVVHD)
– Same procedure as CVVH
Following the circuit of continuous renal – Uses dialysate to increase solute removal
replacement therapy ❍ Continuous venovenous hemofiltration
– Same procedure as CVVHD
In continuous renal replacement therapy (CRRT), a dual-
lumen venous catheter provides access to the patient’s
– Uses a replacement solution to maximize uremic
blood. A pulsatile pump propels the blood through the toxin removal through convective clearance (See
tubing circuit. Following the circuit of continuous renal re-
This illustration shows the standard setup for one type placement therapy.)
of CRRT called continuous venovenous hemofiltration.
The patient’s blood enters the hemofilter from a line con- Contraindications
nected to one lumen of the venous catheter, flows ❍ Coagulopathy
through the hemofilter, and returns to the patient through ❍ Liver disease
the second lumen of the catheter. ❍ Life-threatening hyperkalemia
At the first pump, an anticoagulant may be added to
the blood. A second pump moves dialysate through the Cautions
hemofilter. A third pump adds replacement fluid if
❍ The patient needs to be in an intensive care unit.
needed. The ultrafiltrate (plasma water and toxins) re-
❍ Access must be secure and functional.
moved from the blood drains into a collection bag.
❍ The nurse performing CRRT must have specialized
knowledge of the machine and the procedure.
Replacement ❍ The patient has limited mobility during treatment.
Dialysate fluid
Blood Pump
Pump ❍ Dialysis machine at the patient’s bedside
❍ Access, such as a femoral catheter, internal arteri-
ovenous (AV) graft, or AV shunt
To patient
❍ Hemofilter for the dialysis machine, made up of
Convection across about 5,000 hollow fiber capillaries, which filters the
pressure gradient blood at about 250 ml/minute
Dialysate and
ultrafiltrate ❍ Dialysate solution
Blood From patient
❍ Flush solution
❍ Heparin, if ordered
Pump ❍ Collection bag

Ultrafiltrate in Equipment preparation

collection bag Anticoagulant
❍ May be prepared by dialysis nurse, based on facility

40 Continuous renal replacement therapy

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Essential steps
❍ Consult with the nephrologist.
❍ Establish access for dialysis.
❍ Set up equipment for the appropriate type of CRRT.
❍ Monitor the patient's response to therapy.

Special considerations
❍ Requires one-to-one nursing care
❍ Requires continuous monitoring of vital signs, car-
diac rhythm, fluid status, electrolyte balance, mental
status, and signs of bleeding
❍ Requires certification of nurse performing CRRT
❍ Requires meticulous documentation of intake and

❍ Bradycardia
❍ Dyspnea
❍ Electrolyte and acid-base imbalance
❍ Fluid volume overload
❍ Hypotension
❍ Hypothermia
❍ Hypovolemia
❍ Removal of drugs across the semipermeable mem-
brane (may need to increase doses of cardiac drugs
and antibiotics)
❍ Uncontrolled bleeding

Patient teaching
Be sure to cover:
❍ the need for CRRT
❍ equipment needed for procedure
❍ how the procedure is performed
❍ precautions needed during the procedure
❍ length of treatment (days to weeks).

❍ Use specialized flowsheets for accurate documenta-
tion of intake and output.
❍ Document vital signs, hemodynamic parameters, and
laboratory values according to facility policy.
❍ Note the patient's response to the procedure.

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Part two
Disorders related to
fluid and electrolyte

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Acute poststreptococcal
Renal disease in which the glomeruli become in-
Relatively common
Usually occurs after an infection, commonly a strep-
tococcal infection of the respiratory tract or, less
commonly, a skin infection such as impetigo

Decreased urination
Smoky or coffee-colored urine
Untreated respiratory streptococcal infection within
previous 1 to 3 weeks
Physical assessment
❍ Bibasilar crackles (with heart failure)
❍ Full recovery in up to 95% of children and 70% of ❍ Generalized edema
adults ❍ Hematuria
❍ May lead to chronic renal failure within months in ❍ Mild to moderate periorbital edema
geriatric patients ❍ Mild to severe hypertension
❍ Also called acute glomerulonephritis ❍ Oliguria
Pathophysiology Test results
❍ Antigen-antibody complexes are produced in re- Laboratory
sponse to group A beta-hemolytic Streptococcus in- ❍ Electrolyte imbalances
fection. ❍ Elevated blood urea nitrogen (BUN) and creatinine
❍ Antigen-antibody complexes are trapped and collect levels
in the glomerular capillary membranes. ❍ Decreased serum protein levels
❍ Inflammatory damage results, impeding glomerular ❍ RBCs, white blood cells, mixed cell casts, and pro-
function. tein in urine (indicate renal failure)
❍ Immune complement may further damage the ❍ High levels of fibrin-degradation products and C3
glomerular membrane. protein
❍ Damaged and inflamed glomeruli lose the ability to
AGE AWARE If the patient is elderly, expect the
be selectively permeable.
proteinuria to be less pronounced than it
❍ Red blood cells (RBCs) and proteins filter through
would be in a younger patient.
as glomerular filtration rate decreases.
❍ Uremic poisoning may result. ❍ Decreased serum complement levels and increased
antistreptolysin-O (80% of patients), streptozyme,
Risk factors and anti-DNase B titers, which verify recent strepto-
❍ Group A beta-hemolytic Streptococcus infection of coccal infection
the respiratory tract ❍ Group A beta-hemolytic streptococci in throat cul-
❍ Impetigo ture
Causes ❍ Kidney-ureter-bladder X-rays show bilateral kidney
❍ Immune system reaction to untreated group A beta- enlargement.
hemolytic Streptococcus infection, especially of the ❍ Chest X-rays may show central venous congestion in
respiratory tract a hilar pattern.
Diagnostic procedures
Prevalence ❍ Renal biopsy or assessment of renal tissue shows in-
❍ Most common in boys ages 4 to 6 flammatory changes, which confirm the diagnosis.
❍ May occur at any age
❍ Actual prevalence unknown
Nursing diagnoses
❍ Anemia ❍ Acute pain
❍ Hypertension ❍ Decreased cardiac output
❍ Progressive deterioration of renal function ❍ Fatigue
❍ Risk for imbalanced fluid volume
❍ Risk for infection
❍ Risk for injury

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Key outcomes
The patient will:
❍ maintain fluid balance
❍ report increased comfort
❍ identify risk factors that worsen the condition and
modify lifestyle accordingly
❍ maintain hemodynamic stability.

❍ Correction of electrolyte imbalances (possibly with
❍ Fluid restriction
❍ High-calorie, low-protein, low-sodium, low-
potassium diet
❍ Bed rest
❍ Give prescribed drugs.
❍ Encourage the patient to talk.
❍ Provide support.
Drug therapy
❍ Antibiotics if appropriate
❍ Antihypertensives
❍ Loop diuretics, such as metolazone or furosemide
❍ Creatinine clearance
❍ Daily weight
❍ Electrolyte values
❍ Intake and output
❍ Serum creatinine and BUN levels
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ the importance of follow-up examinations to monitor
renal function
❍ drug regimen, dosages, and possible adverse effects.

Discharge planning
❍ Refer the patient to appropriate resources for infor-
mation and support.

Acute poststreptococcal glomerulonephritis 45

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Acute pyelonephritis ❍

❍ Hematuria
Overview ❍

Pain over one or both kidneys
❍ Symptoms that develop rapidly over a few hours or a
Description few days
❍ Inflammation of the kidney ❍ Urinary frequency
❍ Affects mainly interstitial tissue and renal pelvis, oc- ❍ Urinary urgency
casionally renal tubules ❍ Vomiting
❍ May affect one or both kidneys
❍ Rarely causes extensive permanent damage Physical assessment
❍ Good prognosis ❍ Ammonia-like or fishy odor to urine
❍ Also called acute infective tubulointerstitial nephritis ❍ Cloudy urine
❍ Fever of 102° F (38.9° C) or higher
Pathophysiology ❍ Pain with flank palpation
❍ Infection spreads from bladder to ureters to kidneys, ❍ Shaking chills
commonly through vesicoureteral reflux.
❍ Vesicoureteral reflux may result from congenital Test results
weakness at the junction of the ureter and bladder. Laboratory
❍ Bacteria refluxed to intrarenal tissues may create ❍ Pyuria
colonies of infection in 24 to 48 hours. ❍ Significant bacteriuria
❍ Low urine specific gravity and osmolality
Risk factors ❍ Slightly alkaline urine pH
❍ Female sex ❍ Elevated white blood cell count
❍ Genitourinary obstruction ❍ Elevated neutrophil count
❍ Hematogenic infection, such as septicemia ❍ Elevated erythrocyte sedimentation rate
❍ Neurogenic bladder ❍ Proteinuria, glycosuria, and ketonuria (less com-
❍ Pregnancy in women mon)
❍ Renal disease Imaging
❍ Renal procedures that involve instrumentation, such ❍ Kidney-ureter-bladder X-rays show calculi, tumors,
as cystoscopy or cysts in the kidneys or urinary tract.
❍ Sexual activity in women ❍ Excretory urography shows asymmetrical kidneys,
which may indicate frequent infection.
❍ Bacterial infection of the kidneys
Nursing diagnoses
❍ Community-acquired form: 15 cases per 100,000 ❍ Acute pain
people per year ❍ Decreased cardiac output
❍ Hospital-acquired form: 7 cases per 10,000 people ❍ Fatigue
per year ❍ Risk for imbalanced fluid volume
❍ More common in women than men because of dif- ❍ Risk for infection
ference in anatomy ❍ Risk for injury
Complications Key outcomes
❍ Chronic pyelonephritis The patient will:
❍ Multisystem infection ❍ maintain fluid balance
❍ Renal abscess ❍ report increased comfort
❍ Renal calculi ❍ identify risk factors that worsen the condition, and
❍ Renal failure modify lifestyle accordingly
❍ Septic shock ❍ maintain hemodynamic stability.

Assessment Interventions
History General
❍ Anorexia ❍ Identification and correction of predisposing factors
❍ Burning during urination to infection, such as obstruction or calculi
❍ Diarrhea

46 Acute pyelonephritis
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❍ Short courses of therapy for uncomplicated infection

❍ Increased fluid intake
❍ Give prescribed drugs.
Drug therapy
❍ Antibiotics
❍ Urinary analgesics, such as phenazopyridine
❍ Characteristics of urine
❍ Daily weight
❍ Intake and output
❍ Pattern of urination
❍ Renal function studies
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ hygienic toileting practices that reduce the risk of
bacterial contamination, such as wiping the peri-
neum from front to back after bowel movements for
❍ proper technique for collecting a clean-catch urine
❍ drug regimen, dosages, and possible adverse effects
ed checkups if the patient has a history of uri-
nary tract infections
❍ signs and symptoms of recurrent infection.

Discharge planning
❍ Refer the patient to a nephrologist for recurring in-
fections, as needed.

Acute pyelonephritis 47
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Acute respiratory ❍ 85% probability in people who have three of the
distress syndrome causes listed
Overview ❍

Cardiac arrest
Metabolic acidosis
❍ Multiple organ dysfunction syndrome
Description ❍ Respiratory acidosis
❍ Severe form of alveolar injury or acute lung injury
❍ A form of pulmonary edema
❍ May be difficult to recognize Assessment
❍ Hypoxemia despite increased supplemental oxygen
(hallmark sign) History
❍ Occurs in four stages that may rapidly progress to fa- ❍ Causative factor (one or more)
tal hypoxemia ❍ Dyspnea, especially on exertion
❍ Little or no permanent lung damage in patients who
recover Physical assessment
❍ May coexist with disseminated intravascular coagula- Stage I
tion (DIC) ❍ Dyspnea, especially on exertion
❍ Also known as adult respiratory distress syndrome ❍ Normal to increased respiratory and pulse rates
and shock, stiff lung, white lung, wet lung, or Da ❍ Reduced breath sounds
Nang lung Stage II
❍ Anxiety
Pathophysiology ❍ Basilar crackles
❍ Increased permeability of the alveolocapillary mem- ❍ Bloody, sticky secretions
branes allows fluid to accumulate in the lung inter- ❍ Cool, clammy skin
stitium, alveolar spaces, and small airways, causing ❍ Dry cough with thick, frothy sputum
the lungs to stiffen. ❍ Increased blood pressure
❍ Impaired ventilation reduces oxygenation of pul- ❍ Pallor
monary capillary blood. ❍ Respiratory distress
❍ Elevated capillary pressure increases interstitial and ❍ Restlessness
alveolar edema. ❍ Tachycardia
❍ Alveolar closing pressure exceeds pulmonary pres- ❍ Tachypnea
sures. ❍ Use of accessory muscles for respiration
❍ Alveoli collapse. Stage III
❍ Labile blood pressure
Risk factors ❍ Pale, cyanotic skin
❍ Chronic disease ❍ Possible crackles and rhonchi
❍ Old age ❍ Productive cough
❍ Respiratory rate exceeding 30 breaths/minute
Causes ❍ Tachycardia with arrhythmias
❍ Acute miliary tuberculosis Stage IV
❍ Anaphylaxis ❍ Acute respiratory failure with severe hypoxia
❍ Aspiration of gastric contents ❍ Bradycardia with arrhythmias
❍ Coronary artery bypass grafting ❍ Deteriorating mental status (possible coma)
❍ Diffuse pneumonia (especially viral) ❍ Hypotension
❍ Drug overdose ❍ Lack of spontaneous respirations
❍ Hemodialysis ❍ Metabolic and respiratory acidosis
❍ Idiosyncratic drug reaction ❍ Pale, cyanotic skin
❍ Indirect or direct lung trauma (most common)
❍ Inhalation of noxious gases Test results
❍ Leukemia Laboratory
❍ Near-drowning ❍ Initial arterial blood gas (ABG) analysis: partial pres-
❍ Oxygen toxicity sure of arterial oxygen (PaO2) below 60 mm Hg and
❍ Pancreatitis partial pressure of arterial carbon dioxide (PaCO2)
❍ Thrombotic thrombocytopenic purpura below 35 mm Hg
❍ Uremia ❍ Later ABG analysis: PaO2 decreased despite oxygen
❍ Venous air embolism therapy, PaCO2 above 45 mm Hg, and bicarbonate
levels below 22 mEq/L

48 Acute respiratory distress syndrome

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❍ Infectious organism seen with Gram's stain, sputum ❍ Provide alternative nonverbal means of communica-
culture and sensitivity testing, or blood cultures tion.
❍ Drug overdose revealed by toxicology tests
❍ Increased serum amylase in pancreatitis Drug therapy
Imaging ❍ Bronchodilators
❍ Early chest X-rays may show bilateral infiltrates. ❍ Diuretics
❍ Later chest X-rays show a ground-glass appearance ❍ Humidified oxygen
and, eventually, “whiteouts” of both lung fields. For mechanical ventilation
Diagnostic procedures ❍ Antimicrobials if the patient has nonviral infection
❍ Pulmonary artery catheterization may find a pul- ❍ Fluids and vasopressors if the patient is hypotensive
monary artery wedge pressure of 12 to 18 mm Hg. ❍ Neuromuscular blocking drugs
❍ Opioids
Nursing diagnoses ❍ Sedatives
❍ Short course of high-dose corticosteroids if the pa-
❍ Anxiety tient has fatty emboli or chemical injury
❍ Deficient fluid volume ❍ Sodium bicarbonate if the patient has severe meta-
❍ Impaired gas exchange bolic acidosis
❍ Ineffective tissue perfusion: cardiopulmonary
❍ Risk for impaired skin integrity Monitoring
❍ Complications, such as cardiac arrhythmias, DIC,
Key outcomes gastrointestinal (GI) bleeding, infection, malnutri-
The patient will: tion, or pneumothorax
❍ maintain adequate ventilation ❍ Daily weight
❍ maintain a patent airway ❍ Hemodynamics
❍ maintain fluid volume balance ❍ Intake and output
❍ use effective coping strategies ❍ Laboratory studies
❍ maintain skin integrity ❍ Level of consciousness
❍ report feelings of increased comfort. ❍ Mechanical ventilator settings
❍ Nutritional status
❍ Respiratory status (breath sounds, ABG results)
Interventions ❍ Response to treatment
❍ Sputum characteristics
General ❍ Vital signs and pulse oximetry
❍ Correction of electrolyte and acid-base imbalances A LERT Because PEEP may lower cardiac out-
❍ Possible tracheotomy put, check for hypotension, tachycardia, and
❍ Treatment of the underlying cause decreased urine output. To maintain PEEP, suction
For mechanical ventilation only as needed.
❍ Bed rest
❍ Fluid restriction For mechanical ventilation
❍ Low tidal volumes ❍ Complications of mechanical ventilation
❍ Plateau pressures less than or equal to 40 cm H 2O ❍ Cuff pressure
❍ Positive end-expiratory pressure (PEEP) as needed ❍ Endotracheal tube position and patency
❍ Tube feedings or parenteral nutrition ❍ Signs and symptoms of stress ulcer
❍ Use of increased respiratory rates ❍ Ventilator settings

Nursing Patient teaching

❍ Give prescribed drugs.
❍ Maintain a patent airway. Be sure to cover:
❍ Perform tracheal suctioning, as needed. ❍ the disorder, diagnosis, and treatment
❍ Ensure adequate humidification. ❍ drug regimen and possible adverse reactions
❍ Reposition the patient often. ❍ when to contact a doctor
❍ Consider prone positioning for alveolar recruitment. ❍ complications, such as GI bleeding, infection, and
❍ Give tube feedings or parenteral nutrition, as or- malnutrition
dered. ❍ recovery time.
❍ Allow periods of uninterrupted sleep.

Perform passive range-of-motion exercises. Discharge planning
Provide meticulous skin care.
❍ Reposition the endotracheal tube according to facili- ❍ Refer the patient to a pulmonary rehabilitation pro-
ty policy. gram, if needed.
❍ Provide emotional support.

Acute respiratory distress syndrome 49

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Acute respiratory ❍

Metabolic acidosis
failure ❍

❍ Precipitating event
Overview ❍

Pulmonary emboli
Description Physical assessment
❍ Inadequate ventilation resulting from the inability of ❍ Ashen skin
the lungs to maintain arterial oxygenation or elimi- ❍ Asymmetrical chest movement
nate carbon dioxide ❍ Cold, clammy skin
❍ Crackles (in pulmonary edema)
Pathophysiology ❍ Cyanosis of the oral mucosa, lips, and nail beds
❍ If respiratory failure is mainly hypercapnic, it results ❍ Decreased tactile fremitus over an obstructed
from inadequate alveolar ventilation. bronchus or pleural effusion
❍ If respiratory failure is mainly hypoxemic, it results ❍ Hyperresonance
from inadequate oxygen exchange between the alve- ❍ Increased tactile fremitus over consolidated lung
oli and capillaries. tissue
❍ Many people with respiratory failure have combined ❍ Nasal flaring
hypercapnic and hypoxemic failure. ❍ Pursed-lip breathing
❍ Rapid breathing
Risk factors ❍ Reduced or absent breath sounds
❍ Any condition that increases the work of breathing ❍ Rhonchi (in bronchitis)
and decreases the respiratory drive of patients with ❍ Wheezes (in asthma)
chronic obstructive pulmonary disease ❍ Yawning and use of accessory muscles
Causes Test results
❍ Accumulated secretions from cough suppression Laboratory
❍ Airway irritants ❍ Hypercapnia and hypoxemia in ABG analysis
❍ Bronchospasm ❍ Increased serum white blood cell count if the patient
❍ Central nervous system depression has a bacterial infection
❍ Gas exchange failure ❍ Decreased oxygen-carrying capacity as revealed by
❍ Endocrine or metabolic disorders serum hemoglobin level and hematocrit
❍ Heart failure ❍ Hypokalemia
❍ Myocardial infarction (MI) ❍ Hypochloremia
❍ Pulmonary emboli ❍ Pathogen present in blood cultures, Gram's stain, or
❍ Respiratory tract infection sputum culture
❍ Thoracic abnormalities Imaging
❍ Ventilatory failure ❍ Chest X-rays may show underlying pulmonary disor-
ders, such as emphysema, atelectasis, lesions, pneu-
Prevalence mothorax, infiltrates, or effusion.
❍ Occurs in patients with hypercapnia and hypoxemia Diagnostic procedures
❍ Occurs in patients who have an acute deterioration ❍ Electrocardiography may show arrhythmias, cor pul-
in arterial blood gas (ABG) values monale, or myocardial ischemia.
❍ Pulse oximetry may show decreased arterial oxygen
Complications saturation.
❍ Chronic respiratory acidosis ❍ Pulmonary artery catheterization may show pulmo-
❍ Metabolic alkalosis nary or cardiovascular changes that could cause
❍ Respiratory and cardiac arrest acute respiratory failure.
❍ Tissue hypoxia
Nursing diagnoses
❍ Anxiety
History ❍ Impaired gas exchange
❍ Cough suppression and resulting accumulated pul- ❍ Ineffective coping
monary secretions ❍ Ineffective tissue perfusion: cardiopulmonary
❍ Exposure to irritants (smoke or fumes) ❍ Risk for imbalanced fluid volume
❍ Heart failure ❍ Risk for impaired skin integrity

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Key outcomes ❍ Histamine-receptor antagonists

The patient will: ❍ Positive inotropic drugs
❍ maintain a patent airway ❍ Vasopressors
❍ maintain adequate ventilation
❍ use a support system to assist with coping Monitoring
❍ maintain skin integrity ❍ Cardiac rate and rhythm
❍ express feelings of increased comfort ❍ Chest X-rays
❍ modify lifestyle to minimize the risk of decreased tis- ❍ Complications
sue perfusion ❍ Daily weight
❍ maintain fluid volume balance. ❍ Intake and output
❍ Laboratory studies
❍ Respiratory status (breath sounds and ABG results)
Interventions ❍ Signs and symptoms of infection
❍ Sputum quality, consistency, and color
General ❍ Vital signs and pulse oximetry
❍ Activity as tolerated For mechanical ventilation
❍ Fluid restriction if the patient has heart failure ❍ Complications of mechanical ventilation
❍ High-frequency ventilation if the patient doesn’t re- ❍ Cuff pressures
spond to conventional mechanical ventilation ❍ ET tube position and patency
❍ Mechanical ventilation with an endotracheal or a tra- ❍ Signs and symptoms of stress ulcers
cheostomy tube ❍ Ventilator settings
❍ Possible tracheostomy
Nursing Patient teaching
❍ Give prescribed drugs.
❍ Orient the patient often. Be sure to cover:
❍ Give oxygen. ❍ the disorder, diagnosis, and treatment
❍ Maintain a patent airway. ❍ drug regimen and possible adverse reactions
❍ Encourage pursed-lip breathing. ❍ when to contact a doctor
❍ Encourage the use of an incentive spirometer. ❍ smoking cessation, if appropriate
❍ Reposition the patient every 1 to 2 hours. ❍ communication techniques, if intubated
❍ Help clear the patient’s secretions with postural ❍ signs and symptoms of respiratory infection.
drainage and chest physiotherapy.
❍ Assist with or perform oral hygiene.
❍ Position the patient for comfort and optimal gas ex- Discharge planning
❍ Maintain normothermia. ❍ Refer the patient to a smoking-cessation program, if
❍ Schedule care to provide frequent rest periods. applicable.
For mechanical ventilation
❍ Obtain blood samples for ABG analysis, as ordered.
❍ Suction the trachea after hyperoxygenation, as
❍ Provide humidification.
❍ Secure the endotracheal (ET) tube according to fa-
cility policy.
❍ Prevent infection.
❍ Prevent tracheal erosion.
❍ Maintain skin integrity.
❍ Provide alternative nonverbal means of communica-
❍ Provide sedation, as needed.

Drug therapy
❍ Antacids
❍ Antibiotics
❍ Bronchodilators
❍ Cautious oxygen therapy to increase partial pressure
of arterial oxygen
❍ Corticosteroids
❍ Diuretics

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Acute tubular necrosis ❍ Low urine output (less than 400 ml in 24 hours)
Physical assessment
Overview ❍

Cardiac arrhythmia, if the patient is hyperkalemic
Dry mucous membranes
❍ Dry, pruritic skin
Description ❍ Evidence of bleeding abnormalities, such as petechi-
❍ Injury to the tubular segment of the nephron result- ae and ecchymosis
ing from ischemic or nephrotoxic injury ❍ Muscle weakness
❍ Causes renal failure and uremic syndrome ❍ Uremic breath
❍ Also known as acute tubulointerstitial nephritis
Test results
Pathophysiology Laboratory
❍ Ischemic injury — as from circulatory collapse, se- ❍ Red blood cells (RBCs) and casts in urine sediment
vere hypotension, traumatic injury, hemorrhage, de- ❍ Decreased urine specific gravity
hydration, cardiogenic or septic shock, surgery, ❍ Decreased urine osmolality (less than
anesthetics, or a transfusion reaction — may disrupt 400 mOsm/kg)
blood flow to the kidneys. ❍ Increased urine sodium level (40 to 60 mEq/L)
❍ Nephrotoxic injury may result from a hypersensitivity ❍ Increased blood urea nitrogen and serum creatinine
reaction in the kidneys, or it may follow ingestion of levels
certain chemicals, such as contrast medium or an ❍ Anemia
antibiotic. ❍ Defects in platelet adherence
❍ Metabolic acidosis
Risk factors ❍ Hyperkalemia
❍ Diabetic nephropathy Diagnostic procedures
❍ Liver disease ❍ Electrocardiography may show arrhythmias and,
with hyperkalemia, a widening QRS complex, disap-
Causes pearing P waves, and tall, peaked T waves.
❍ Diseased tubular epithelium
❍ Ischemic injury to glomerular epithelial cells or vas-
cular endothelium Nursing diagnoses
❍ Obstructed urine flow
❍ Acute pain
Prevalence ❍ Decreased cardiac output
❍ Accounts for about 3 in 4 cases of acute renal failure ❍ Fatigue
❍ The most common cause of acute renal failure in ❍ Risk for imbalanced fluid volume
critically ill patients ❍ Risk for infection
❍ Risk for injury
❍ Anemia Key outcomes
❍ Anorexia The patient will:
❍ Heart failure ❍ maintain fluid balance
❍ Intractable vomiting ❍ report increased comfort
❍ Poor wound healing from debilitation ❍ identify risk factors that worsen the condition and
❍ Pulmonary edema modify lifestyle accordingly
❍ Uremic lung ❍ maintain hemodynamic stability.
❍ Uremic pericarditis
A LERT Fever and chills may signal the onset of
an infection, the leading cause of death in pa-
tients with acute tubular necrosis.
Acute phase
Assessment ❍ Vigorous supportive measures until normal kidney
function resumes
❍ Diagnosis is usually delayed until the condition has Long-term management
progressed to an advanced stage. ❍ Daily replacement of projected fluid loss (including
insensible loss)
History ❍ Peritoneal dialysis or hemodialysis if the patient is
❍ Fever and chills catabolic or if hyperkalemia and fluid volume over-
❍ Ischemic or nephrotoxic injury load aren’t controlled by other measures

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❍ Fluid restriction
❍ Low-sodium, low-potassium diet
❍ Rest periods when fatigued
❍ Give prescribed drugs and blood products.
❍ Restrict high-sodium and high-potassium foods.
❍ Use aseptic technique, particularly when handling
❍ Perform passive range-of-motion exercises.
❍ Provide good skin care.
Drug therapy
❍ Antibiotics
❍ Diuretics
❍ Emergency I.V. administration of 50% glucose, regu-
lar insulin, and sodium bicarbonate (with hyper-
❍ Epoetin alfa
❍ Sodium polystyrene sulfonate with sorbitol by mouth
or enema (with hyperkalemia)
❍ Transfusion of packed RBCs
❍ Complications
❍ Intake and output
❍ Laboratory studies
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ signs of infection and when to report them to a doc-
❍ dietary restrictions
❍ how to set goals that are realistic for the patient’s

Discharge planning
❍ Refer the patient to appropriate supportive services
or social service.

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Adrenal hypofunction Primary hypofunction
❍ Autoimmune process in which circulating antibodies
Overview react specifically to adrenal tissue
❍ Bilateral adrenalectomy
❍ Family history of autoimmune disease, which may
Description predispose the patient to Addison’s disease and other
Primary hypofunction endocrinopathies
❍ Originates in the adrenal gland ❍ Hemorrhage into the adrenal gland
❍ Characterized by decreased secretion of mineralo- ❍ Infection, such as histoplasmosis and cytomegalo-
corticoids, glucocorticoids, and androgens virus
❍ Also known as Addison's disease ❍ Neoplasm
Secondary hypofunction ❍ Tuberculosis (once the chief cause, now responsible
❍ Originates in a process outside the adrenal gland, for less than 20% of adult cases)
such as impaired pituitary secretion of corticotropin Secondary hypofunction
❍ Characterized by decreased glucocorticoid secretion ❍ Abrupt withdrawal of long-term corticosteroid
Adrenal crisis therapy
❍ A critical deficiency of mineralocorticoids and gluco- ❍ Hypopituitarism
corticoids ❍ Removal of a corticotropin-secreting tumor
❍ Typically follows acute stress, sepsis, traumatic in- Adrenal crisis
jury, surgery, or the omission of corticosteroid thera- ❍ Exhausted body stores of glucocorticoids in a patient
py in a patient with chronic adrenal insufficiency with adrenal hypofunction after traumatic injury,
❍ A medical emergency that needs immediate, vigorous surgery, or other physiologic stress
❍ Also known as addisonian crisis Prevalence
Primary hypofunction
Pathophysiology ❍ Relatively uncommon
❍ Adrenal hypofunction results from partial or com- ❍ May occur at any age and in both sexes
plete destruction of the adrenal cortex. Autoimmune Addison’s disease
❍ Levels of corticotropin and corticotropin-releasing ❍ Most common in white women, probably from ge-
hormone increase with destruction of the adrenal netic predisposition
cortex. ❍ More common in patients with a familial predisposi-
❍ Addison’s disease involves all zones of the cortex and tion to autoimmune endocrine diseases
causes deficient secretion of adrenocortical hor-
AGE AWARE Addison’s disease usually is diag-
mones, glucocorticoids, androgens, and mineralo-
nosed when the patient is between ages 20
and 50.
❍ Symptoms reflect deficient production of the adreno-
cortical hormones cortisol, aldosterone, and andro- Complications
❍ Cortisol deficiency decreases liver gluconeogenesis ❍ Hyperpyrexia
(formation of glucose from noncarbohydrate mole- ❍ Inadequate or excessive corticosteroid treatment
cules); as a result, blood glucose levels may become ❍ Profound hypoglycemia
dangerously low in patients who take insulin ❍ Psychotic reactions
routinely. ❍ Shock
❍ Aldosterone deficiency increases renal sodium loss ❍ Ultimate vascular collapse, renal shutdown, coma,
and potassium reabsorption. and death (if untreated)
❍ Hypotension may result from sodium excretion.
❍ Production of angiotensin II increases because of
low plasma volume and arteriolar pressure. Assessment
❍ Androgen deficiency may decrease hair growth in ax-
illary and pubic areas (less noticeable in men) and History
on the limbs of women. ❍ Adrenal surgery
❍ Amenorrhea (in women)
Risk factors ❍ Craving for salty food
❍ Autoimmune disease ❍ Decreased tolerance for stress
– Graves' disease ❍ Dehydration
– Hypoparathyroidism ❍ Fatigue
– Hypopituitarism ❍ Gastrointestinal disturbances
– Myasthenia gravis ❍ Impotence (in men)
– Type 1 diabetes ❍ Muscle weakness

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❍ Recent infection ❍ Arrange for a diet that maintains sodium and potassi-
❍ Use of synthetic steroids um balances; if the patient is anorexic, suggest six
❍ Weight loss small meals daily to increase calorie intake.
❍ Watch for cushingoid signs, such as fluid retention
Physical assessment around the eyes and face.
❍ Areas of vitiligo ❍ Check for petechiae.
❍ Bronze coloration of the skin, darkening of scars ❍ If the patient receives glucocorticoids alone, watch
❍ Decreased axillary and pubic hair (in women) for orthostatic hypotension or electrolyte abnormali-
❍ Hypotension ties.
❍ Increased pigmentation of mucous membranes
❍ Poor coordination Drug therapy
❍ Weak, irregular pulse ❍ Hydrocortisone
❍ I.V. saline and glucose solutions (for adrenal crisis)
Test results ❍ Lifelong corticosteroid replacement, usually with
Laboratory cortisone or hydrocortisone
❍ Increased corticotropin level in rapid corticotropin ❍ Oral fludrocortisone
stimulation test (primary disorder)
❍ Decreased corticotropin level in rapid corticotropin Monitoring
stimulation test (secondary disorder) ❍ Blood glucose levels
❍ Decreased plasma cortisol level (less than 10 mcg/dl ❍ Cardiac rhythm
in the morning) ❍ Daily weight
❍ Decreased serum sodium level ❍ Hyperkalemia before treatment
❍ Decreased fasting blood glucose level ❍ Hypokalemia after treatment
❍ Increased serum potassium, calcium, and blood ❍ Intake and output
urea nitrogen levels ❍ Signs of shock (decreased level of consciousness
❍ Elevated hematocrit and urine output)
❍ Increased lymphocyte and eosinophil counts ❍ Vital signs
❍ Chest X-ray shows a small heart.
❍ Computed tomography scan of the abdomen shows Patient teaching
adrenal calcification if the cause is infectious.
Be sure to cover:
❍ lifelong need for corticosteroid therapy
Nursing diagnoses ❍ symptoms of corticosteroid overdose (swelling,
weight gain) and underdose (lethargy, weakness)
❍ Decreased cardiac output ❍ possible need for increased dosage during times of
❍ Ineffective coping stress or illness (when the patient has a cold, for ex-
❍ Risk for imbalance fluid volume ample)
❍ Risk for infection ❍ risk of adrenal crisis during infection, injury, or pro-
fuse sweating in hot weather
Key outcomes ❍ the importance of wearing or carrying medical iden-
The patient will: tification showing that the patient takes a cortico-
❍ maintain stable vital signs steroid, including the drug name and dosage
❍ maintain an adequate fluid balance ❍ procedure for giving a hydrocortisone injection
❍ remain free from signs and symptoms of infection ❍ need to keep an emergency kit containing hydrocor-
❍ develop adequate coping skills. tisone in a prepared syringe available for use in
times of stress
❍ stress management techniques.
General Discharge planning
❍ I.V. fluids
❍ Periods of rest ❍ Refer the patient to the National Adrenal Diseases
❍ Small, frequent, high-protein meals Foundation for support and information.
❍ Until onset of mineralocorticoid effect, encourage
fluids to replace excessive fluid loss.

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Adrenogenital ❍ Altered growth, external genitalia, and sexual

syndrome ❍ Hyperkalemic infertility
❍ Hypertension
Salt-losing congenital adrenal hyperplasia
Overview ❍ Cardiac arrest
❍ Cardiovascular collapse

❍ A group of disorders resulting from hyperplasia of Assessment
the adrenal cortex
❍ May be inherited, as in congenital adrenal hyperpla- History
sia (CAH) Simple virilizing congenital adrenal
❍ May be acquired, usually from an adrenal tumor hyperplasia
(adrenal virilism) ❍ Failure to start menstruation (girls)
❍ May cause fatal adrenal crisis in neonates (salt- ❍ Frequent erections at an early age (boys)
losing CAH) Salt-losing congenital adrenal hyperplasia
❍ Apathy, failure to eat, and diarrhea (infants)
Pathophysiology ❍ Symptoms of adrenal crisis in the first week after
❍ Deficiencies occur in the enzymes needed for birth (vomiting, dehydration from hyponatremia, hy-
adrenocortical secretion of cortisol and possibly al- perkalemia)
❍ Compensatory corticotropin secretion produces Physical assessment
varying degrees of adrenal hyperplasia. ❍ Pseudohermaphroditism in girls
Simple virilizing congenital adrenal ❍ Precocious puberty in either sex
hyperplasia Salt-losing congenital adrenal hyperplasia
❍ Deficiency of the enzyme 21-hydroxylase results in ❍ May be taller than other children of the same age
underproduction of cortisol. ❍ Progressive virilization at an early age: early appear-
❍ Cortisol deficiency causes increased secretion of ance of pubic and axillary hair, deep voice, acne, fa-
corticotropin, producing large amounts of cortisol cial hair
precursors and androgens that don’t require 21- ❍ Small testes
hydroxylase for synthesis.
Salt-losing congenital adrenal hyperplasia Test results
❍ 21-hydroxylase is almost completely absent. Laboratory
❍ Corticotropin secretion increases, causing excessive ❍ Elevated levels of plasma 17-ketosteroids (17-KS),
production of cortisol precursors, including salt- which can be suppressed with oral dexamethasone
wasting compounds. ❍ Elevated urinary levels of hormone metabolites, par-
❍ Plasma cortisol and aldosterone levels — both de- ticularly pregnanetriol
pendent on 21-hydroxylase — fall precipitously and, ❍ Elevated plasma 17-hydroxyprogesterone level
combined with excessive production of salt-wasting ❍ Normal or decreased urinary levels of 17-hydroxy-
compounds, precipitate acute adrenal crisis. corticosteroids
❍ Corticotropin hypersecretion stimulates adrenal an-
AGE AWARE Adrenal hypofunction or adrenal
drogens and produces masculinization.
crisis in the first week after birth suggests salt-
Causes losing CAH. Hyperkalemia, hyponatremia, and hypo-
chloremia with excessive urinary 17-KS and preg-
❍ Transmitted as an autosomal recessive trait
nanetriol and decreased urinary aldosterone levels
Prevalence confirm it.
❍ Rare (acquired adrenal virilism) Diagnostic procedures
❍ Affects twice as many female as male children ❍ Gonadal biopsy and chromosomal studies confirm
AGE AWARE CAH is the most prevalent adrenal ❍ Sex chromatin and karyotype studies determine the
disorder in infants and children; simple viriliz-
genetic sex of patients with ambiguous genitalia.
ing CAH and salt-losing CAH are the most common
Complications Nursing diagnoses
❍ Adrenal crisis ❍ Decreased cardiac output
❍ Adrenal tumor ❍ Deficient knowledge: adrenal hypofunction
❍ Risk for imbalanced fluid volume

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Key outcomes ❍ the importance of not stopping drugs suddenly

The patient will: because life-threatening adrenal hypofunction will
❍ maintain stable vital signs result
❍ maintain adequate fluid balance ❍ need to report stress and infection, which warrant
❍ have normal laboratory test results increased corticosteroid dosages
❍ express understanding of the disorder and treat- ❍ the importance of wearing or carrying medical iden-
ment, as will his family. tification showing that the patient takes a cortico-
steroid, including the drug name and dosage.
Interventions Discharge planning
General ❍ Refer the patient for psychological counseling to
❍ No activity restriction help accept this disorder.
❍ Reconstructive surgery based on the determined sex
and external genitalia
❍ Well-balanced diet
❍ Maintain I.V. access, infuse fluids, and give cortico-
steroids, as ordered.
❍ Watch for cyanosis, hypotension, tachycardia, tachy-
pnea, and signs of shock.
❍ Minimize external stressors.
❍ If a child is receiving maintenance therapy with cor-
ticosteroid injections, rotate I.M. injection sites to
prevent atrophy, and tell the parents to do the same.
Drug therapy
Simple virilizing congenital adrenal
❍ Cortisone or hydrocortisone given daily
Salt-losing congenital adrenal hyperplasia
with adrenal crisis
❍ Desoxycorticosterone I.M.
❍ Hydrocortisone I.V.
❍ Immediate I.V. infusion of sodium chloride and glu-
❍ Maintenance: mineralocorticoid replacement (des-
oxycorticosterone, fludrocortisone, or both) and
glucocorticoid replacement (cortisone or hydrocor-
❍ Blood pressure
❍ Body weight
❍ Edema, weakness, and hypertension if the patient re-
ceives desoxycorticosterone or fludrocortisone
❍ Serum electrolyte levels

Patient teaching
Be sure to cover:
❍ possible adverse effects (cushingoid symptoms) of
long-term therapy
❍ need for lifelong maintenance therapy with hydro-
cortisone, cortisone, or the mineralocorticoid flu-

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Test results
Alport’s syndrome Laboratory
❍ Immunoglobulins and complement components in
Overview blood studies
❍ Proteinuria
❍ Pyuria
Description ❍ Red cell casts in urine
❍ Hereditary nephritis Diagnostic procedures
❍ Characterized by recurrent gross or microscopic ❍ Audiology reveals hearing loss.
hematuria ❍ Electron microscopy reveals characteristic changes
❍ Accompanied by deafness, albuminuria, and variably in basement membrane and confirms diagnosis.
progressive azotemia ❍ Renal biopsy confirms the diagnosis when electron
microscopy shows basement membrane changes.
AGE AWARE Symptoms of Alport’s syndrome in
❍ Genetic mutations lead to abnormalities in the base-
children almost always include hearing loss
ment membrane of the glomerulus.
and such ocular defects as lenticonus, posterior poly-
❍ Abnormalities lead to hematuria and glomeruloscle-
morphous corneal dystrophy, and retinal flecks.
Risk factors Nursing diagnoses
❍ Genetic predisposition
❍ Deficient knowledge: Alport’s syndrome
Causes ❍ Impaired urinary elimination
❍ Genetic transmission as an X-linked, autosomal ❍ Ineffective coping
Key outcomes
Prevalence The patient will:
❍ Usually arises during childhood ❍ express understanding of the disorder, diagnostic
❍ Affects males more often and more severely than fe- testing, and treatment
males ❍ show appropriate coping mechanisms
❍ use available support systems
AGE AWARE Many men with hematuria and ❍ regain or maintain adequate renal function.
proteinuria from Alport's syndrome develop
end-stage renal disease in their 30s or 40s.
A LERT Respiratory infection commonly caus- Interventions
es recurrent bouts of hematuria in those with
Alport’s syndrome. General
❍ Dialysis
❍ Eyeglasses or contact lenses
Assessment ❍ Hearing aid
❍ Kidney transplantation
History ❍ Supportive and symptomatic care
❍ Deafness (especially to high-frequency sounds)
❍ Family history of recurrent hematuria and renal fail- Nursing
ure (especially in men) ❍ Provide emotional support.
❍ Flank pain ❍ Pursue an effective communication system.
❍ Recurrent hematuria, which typically appears during
early childhood Drug therapy
❍ Antibiotics
Physical assessment ❍ Antihypertensives
❍ Deafness
❍ Flank pain Monitoring
❍ Hematuria ❍ Blood pressure
❍ Hypertension (commonly related to progressive re- ❍ Laboratory values
nal failure) ❍ Urine color
❍ Ocular changes, possibly including cataracts and, ❍ Urine output
less commonly, keratoconus, myopia, retinitis pig-
mentosa, and nystagmus

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Patient teaching
Be sure to cover:
❍ the diagnosis, testing, and treatment
❍ the need to monitor urine function
❍ when to contact a doctor.

Discharge planning
❍ Refer the patient and family for genetic counseling as

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Amyloidosis Assessment
Overview ❍ Usually asymptomatic until organs are affected
❍ Constipation or diarrhea
❍ A rare, chronic disease characterized by accumula- Physical assessment
tion of an abnormal fibrillar scleroprotein (amyloid) ❍ Variable signs and symptoms based on system
that infiltrates organs and soft tissues affected
❍ May be primary or secondary Renal system
❍ May affect the inner coats of blood vessels (periretic- ❍ Edema
ular type) ❍ Low urine output
❍ May affect the outer coats of blood vessels and the Cardiac system
parenchyma (pericollagen type) ❍ Faint heart sounds
❍ Variable prognosis based on type and on site and ex- ❍ Irregular heartbeat
tent of involvement ❍ Shortness of breath
❍ Sometimes causes permanent — possibly life-threat- Gastrointestinal (GI) system
ening — organ damage ❍ Abdominal pain
❍ Sometimes linked to a Mediterranean ethnic origin ❍ Clay-colored stools
(familial Mediterranean fever [FMF]), although only ❍ GI bleeding
50% of those with FMF have a family history of the ❍ Signs of malnutrition
disorder ❍ Stiffness and enlargement of the tongue
❍ Sometimes diagnosed as multiple myeloma Skin
❍ Papules
Pathophysiology ❍ Purpura
❍ Accumulation and infiltration of amyloid causes Respiratory system
pressure on and atrophy of nearby cells. ❍ Trouble breathing
❍ Some types of amyloidosis cause reticuloendothelial ❍ Wheezing
cell dysfunction and abnormal immunoglobulin syn- Neurologic system
thesis. ❍ Carpal tunnel symptoms
❍ Muscle weakness
Risk factors ❍ Numbness and tingling
❍ Age older than 50
❍ Chronic infection or inflammatory disease Test results
❍ Increased protein in diet Laboratory
❍ Multiple myeloma ❍ Proteinuria
❍ Histologic confirmation, via polarizing or electron
Causes microscope, of aspirated tissue from rectal mucosa
❍ Primary amyloidosis: no apparent cause and abdominal fat pad (less hazardous than kidney
❍ Secondary amyloidosis: disorders that cause chronic or liver biopsy) or possibly from gingiva, skin, or
inflammation, such as tuberculosis, Crohn’s disease, nerves
rheumatoid arthritis, Hodgkin’s disease, and syphilis Imaging
❍ May accompany Alzheimer’s disease ❍ A chest X-ray may show an enlarged heart and con-
❍ Linked to type 2 diabetes mellitus gestive heart failure.
❍ Ethnic origin in the Mediterranean area (hereditary Diagnostic procedures
form) ❍ Electrocardiography may show low-voltage and con-
duction or rhythm abnormalities resembling those of
Prevalence a myocardial infarction.
❍ In the United States, evidence of amyloidosis in 0.5%
of autopsies
❍ Difficult to determine actual occurrence Nursing diagnoses
Complications ❍ Deficient knowledge: amyloidosis
❍ Heart failure ❍ Ineffective airway clearance
❍ Nephrotic syndrome ❍ Ineffective coping
❍ Renal failure ❍ Risk for impaired skin integrity

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Key outcomes
The patient will:
❍ show effective coping mechanisms
❍ use available support systems
❍ express understanding of the disorder and its treat-
❍ maintain a patent airway
❍ avoid a break in skin integrity.

❍ Elimination of the underlying cause
❍ Supportive care based on symptoms
❍ Total parenteral nutrition
❍ Transplantation of affected organ, although this ac-
tion doesn't halt the disorder
❍ Offer emotional support.
❍ Provide care as needed based on symptoms.
❍ Supply meticulous mouth care if the tongue is in-
❍ Establish an alternate nonverbal means of communi-
cation if the patient can’t talk.
❍ Regularly assess airway patency if the patient's
tongue is involved, and prevent respiratory tract
compromise with gentle and adequate suctioning, if
needed. Keep a tracheostomy tray at bedside.
Drug therapy
❍ Analgesics
❍ Antibiotics
❍ Colchicine
❍ Laxatives
❍ Complications
❍ Intake and output
❍ Laboratory values
❍ Nutritional status

Patient teaching
Be sure to cover:
❍ the disorder, diagnostic tests, and treatment
❍ when to contact a doctor
❍ drug regimen, dosages, and adverse effects.

Discharge planning
❍ Refer the patient for speech therapy, if needed.

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Physical assessment
Anaphylaxis ❍ Angioedema
❍ Apprehension, restlessness
Overview ❍

Cool and clammy skin
❍ Diarrhea
Description ❍ Dizziness, drowsiness
❍ Dramatic, acute atopic reaction to an allergen ❍ Edema
❍ Marked by sudden onset of rapidly progressive ur- ❍ Erythema
ticaria and respiratory distress ❍ Headache
❍ Severity greater as time between exposure to the ❍ Hoarseness or stridor
antigen and appearance of signs and symptoms de- ❍ Hypotension, shock
creases ❍ Nausea
❍ May include vascular collapse, systemic shock, and ❍ Seizures
possibly death if reaction is severe ❍ Severe abdominal cramps
❍ Tachypnea
Pathophysiology ❍ Urinary urgency and incontinence
❍ After initial exposure to an antigen, the immune sys- ❍ Urticaria
tem produces immunoglobulin (Ig) antibodies in the ❍ Wheezing
lymph nodes. Helper T cells enhance the process. ❍ Angina and cardiac arrhythmias (less common)
❍ IgE antibodies bind to membrane receptors on mast
cells and basophils. Test results
❍ When the antigen reappears, the IgE antibodies, or ❍ Not needed, although skin testing may help identify a
cross-linked IgE receptors, recognize the antigen as particular allergen
foreign, activating the release of powerful chemical ❍ Diagnosis established by signs, symptoms, and
mediators that produce signs and symptoms of an history
allergic reaction.
❍ IgG or IgM antibodies take part in the reaction and
activate the release of complement factors. Nursing diagnoses
Risk factors ❍ Acute pain
❍ History of allergies ❍ Decreased cardiac output
❍ History of asthma ❍ Impaired gas exchange
❍ Previous anaphylactic reaction ❍ Ineffective airway clearance
❍ Ineffective tissue perfusion (renal)
Causes ❍ Risk for injury
❍ Systemic exposure to sensitizing drugs, foods, insect
venom, or other specific antigens Key outcomes
The patient will:
Prevalence ❍ maintain a patent airway
❍ Most common anaphylaxis-causing antigen: peni- ❍ maintain adequate ventilation
cillin, which causes a reaction in 1 to 4 of every ❍ express feelings of increased comfort and decreased
10,000 patients treated pain
❍ maintain normal cardiac output and normal heart
Complications rate
❍ Respiratory obstruction ❍ identify causative allergen
❍ Systemic vascular collapse ❍ maintain fluid balance.
❍ Death
History ❍ Airway establishment and maintenance
❍ Complaints of shortness of breath and chest tightness ❍ Bed rest until stable
❍ Complaints of sweating and weakness ❍ Cardiopulmonary resuscitation if needed
❍ Immediately after exposure, complaints of a feeling ❍ Nothing by mouth until stable
of impending doom or fright
❍ Reports of sneezing and nasal itching Nursing
❍ Reports of a lump in the throat (angioedema) ❍ Provide supplemental oxygen and prepare to assist
with insertion of an endotracheal tube, if needed.

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❍ Insert a peripheral I.V. line.

❍ Continually reassure the patient, and explain all tests
and treatments.
❍ If the patient has skin or scratch testing, watch for
signs of a serious allergic response. Keep emergency
resuscitation equipment readily available.
A LERT If a patient must receive a drug to
which he’s allergic, prevent a severe reaction
by making sure he either receives corticosteroids be-
fore the allergenic drug or he undergoes careful de-
sensitization with gradually increasing doses of the
antigen. Monitor the patient closely, and keep resus-
citation equipment and epinephrine readily avail-
Drug therapy
❍ Aminophylline I.V.
❍ Antihistamines
❍ Corticosteroids
❍ Diphenhydramine I.V.
❍ Dopamine
❍ Immediate injection of epinephrine 1:1,000 aqueous
solution, 0.1 to 0.5 ml S.C. or I.V.
❍ Norepinephrine
❍ Vasopressors
❍ Volume expander infusions, as needed
❍ Adverse reactions to radiographic contrast media
❍ Complications
❍ Degree of edema
❍ Neurologic status
❍ Respiratory status
❍ Response to treatment
❍ Serious allergic response after skin or scratch testing
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the risk of delayed symptoms and the importance of
reporting them immediately
❍ the need to avoid exposure to known allergens
❍ the importance of carrying and knowing how to use
an anaphylaxis kit
❍ the need to wear medical identification jewelry to
identify the allergy.

Discharge planning
❍ Refer the patient to an allergist or pulmonary spe-
cialist as indicated.

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Aneurysm, ❍ Possible abdominal pain from bleeding into the peri-

abdominal aortic Physical assessment
Intact aneurysm
Overview ❍ Gnawing, generalized, steady abdominal pain
❍ Lower back pain unaffected by movement
❍ Gastric or abdominal fullness
Description ❍ Sudden onset of severe abdominal pain or lumbar
❍ Abnormal dilation in the arterial wall of the aorta, pain with radiation to flank and groin
commonly between the renal arteries and iliac ❍ Possible pulsating mass in the periumbilical area
branches A LERT If the patient has a pulsating mass in
❍ May be fusiform (spindle-shaped), saccular (pouch- the periumbilical area, don't palpate it.
like), or dissecting
Ruptured aneurysm
Pathophysiology ❍ Absent distal peripheral pulses
❍ Degenerative changes develop into a focal weakness ❍ Decreased level of consciousness
in the tunica media layer of the aorta, which allows ❍ Diaphoresis
the tunica intima and tunica adventitia layers to ❍ Distended abdomen
stretch outward. ❍ Ecchymosis or hematoma in the abdominal, flank, or
❍ Pressure from blood in the aorta progressively weak- groin area
ens vessel walls and enlarges the aneurysm. ❍ Gastrointestinal bleeding with massive hematemesis
and melena with rupture into the duodenum
Risk factors ❍ Hypotension
❍ Age older than 50 ❍ Mottled skin from poor distal perfusion
❍ Atherosclerosis ❍ Oliguria
❍ Caucasian ❍ Paraplegia if rupture reduces blood flow to the spine
❍ Diabetes ❍ Severe, persistent abdominal and back pain with
❍ Family history of abdominal aortic aneurysm rupture in to the peritoneal cavity
❍ History of smoking ❍ Systolic bruit over the aorta
❍ Hypertension ❍ Tachycardia
❍ Increased cholesterol level ❍ Tenderness over the affected area
❍ Male sex
Test results
Causes Imaging
❍ Arteriosclerosis or atherosclerosis (95%) ❍ Anteroposterior and lateral abdominal X-rays can
❍ Infection detect aortic calcification, which outlines the mass at
❍ Syphilis least 75% of the time.
❍ Traumatic injury ❍ Computed tomography scan may be used to deter-
mine the effect of the aneurysm on nearby organs.
Prevalence Diagnostic procedures
❍ Seven times more common in hypertensive men than ❍ Abdominal ultrasonography or echocardiography
in women may determine the size, shape, and location of the
❍ Most common in whites ages 50 to 80 aneurysm.
❍ Aortography shows the condition of vessels proximal
Complications and distal to the aneurysm and the extent of the
❍ Dissection aneurysm.
❍ Hemorrhage
A LERT Aortography may underestimate the
❍ Shock diameter of an aneurysm because it shows
only the flow channel and not the surrounding clot.
History Nursing diagnoses
❍ Asymptomatic until the aneurysm enlarges and com-
presses surrounding tissue ❍ Acute pain
❍ Syncope when aneurysm ruptures ❍ Anxiety
❍ Possible resolution of symptoms when a clot forms ❍ Decreased cardiac output
and bleeding stops ❍ Deficient fluid volume
❍ Deficient knowledge: abdominal aortic aneurysm

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❍ Ineffective tissue perfusion: cardiopulmonary ❍ Maintain the patient's blood pressure in the pre-
scribed range using fluids and drugs.
Key outcomes
A LERT Assess the patient for severe back pain,
The patient will: which may indicate that the graft is tearing.
❍ maintain adequate cardiac output
❍ maintain hemodynamic stability ❍ Have the patient cough, or suction the endotracheal
❍ maintain palpable pulses distal to the aneurysm site tube, as needed.
❍ maintain adequate urine output (equivalent to in- ❍ Turn the patient often, and assist with ambulation as
take) soon as the patient is able.
❍ express feelings of increased comfort and decreased
pain Drug therapy
❍ relate an understanding of the disease process and ❍ Analgesics
treatment. ❍ Antibiotics
❍ Antihypertensives
❍ Beta blockers
General ❍ Abdominal dressings
Small, asymptomatic aneurysm ❍ Arterial blood gas values, as ordered
❍ Activity, as tolerated ❍ Cardiac rhythm and hemodynamics
❍ Careful control of hypertension ❍ Daily weight
❍ Fluid and blood replacement ❍ Fluid status
❍ Low-fat diet ❍ Intake and output hourly
❍ Weight reduction, if appropriate ❍ Laboratory studies
Large or symptomatic aneurysm ❍ Nasogastric intubation for patency, amount, and type
❍ Bypass if perfusion distal to aneurysm is poor of drainage
❍ Endovascular grafting ❍ Neurologic status
❍ Repair and graft replacement for a ruptured ❍ Pulse oximetry
aneurysm ❍ Respirations and breath sounds at least every hour
❍ Surgical resection ❍ Vital signs
❍ Wound site for infection
In a nonacute situation
❍ Let the patient express his fears and concerns. Patient teaching
❍ Identify effective coping strategies.
❍ Offer the patient and his family psychological sup- Be sure to cover:
port. ❍ surgical procedure and expected postoperative care
❍ Before elective surgery, weigh the patient, insert an ❍ importance of taking all prescribed drugs and carry-
indwelling urinary catheter and an I.V. line, and as- ing a list of these drugs at all times, in case of an
sist with insertion of the arterial line and pulmonary emergency
artery catheter to monitor hemodynamic balance. ❍ physical activity restrictions until the patient is
❍ Give prescribed preventive antibiotics. cleared by the doctor
In an acute situation ❍ the need for regular examinations and ultrasound
❍ Insert an I.V. line with at least a 14G needle to facili- checks to monitor progression of the aneurysm if the
tate blood replacement. patient didn't have surgery.
❍ Obtain blood samples for laboratory tests, as or-
❍ Give prescribed drugs. Discharge planning
A LERT Watch carefully for signs of rupture,
which may be immediately fatal. If an ❍ Refer the patient for follow-up visits with a cardiolo-
aneurysm ruptures, the patient will need surgery im- gist as appropriate.
mediately. Medical antishock trousers may be used
during transport.
After surgery
❍ Assess peripheral pulses for graft failure or occlu-
❍ Watch for signs of retroperitoneal bleeding from the
graft site.

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Aneurysm, ❍ Increasing area of flatness over the heart, suggesting

cardiac tamponade and hemopericardium
thoracic aortic ❍ Pallor
❍ Transient paralysis
❍ Weak legs
Overview Dissecting ascending aneurysm
❍ Boring, tearing, or ripping pain in the thorax or the
right anterior chest that may extend to the neck,
Description shoulders, lower back, and abdomen
❍ Abnormal widening of the ascending, transverse, or ❍ Diastolic murmur of aortic insufficiency
descending part of the aorta ❍ Normal or significantly increased blood pressure,
❍ May be saccular (outpouching), fusiform (spindle- with a large difference in systolic blood pressure be-
shaped), or dissecting tween the right and left arms
❍ Usually an emergency with a poor prognosis ❍ Pain most intense at onset
❍ Pericardial friction rub if the patient has hemoperi-
Pathophysiology cardium
❍ Circumferential or transverse tear of the aortic wall Dissecting descending aneurysm
intima, usually in the medial layer ❍ Carotid and radial pulses present and equal bilater-
Risk factors ❍ Possible bilateral crackles and rhonchi if the patient
❍ Hypertension has pulmonary edema
❍ Cigarette smoking ❍ Sharp, tearing pain between the shoulder blades that
usually radiates to the chest
Causes ❍ Systolic blood pressure that’s equal bilaterally
❍ Atherosclerosis Dissecting transverse aneurysm
❍ Bacterial infections, usually at an atherosclerotic ❍ Dry cough
plaque ❍ Dysphagia
❍ Blunt chest trauma ❍ Dyspnea
❍ Coarctation of the aorta ❍ Hoarseness
❍ Marfan syndrome ❍ Sharp, boring, tearing pain that radiates to the shoul-
❍ Rheumatic vasculitis ders
❍ Syphilis ❍ Throat pain

Prevalence Test results

❍ Ascending thoracic aorta the most common site Laboratory
❍ Occurs mainly in hypertensive men younger than ❍ Possible decreased hemoglobin level from blood
age 60 loss through a leaking aneurysm
❍ Descending thoracic aortic aneurysms most com- Imaging
mon in younger people who have had chest trauma ❍ Posteroanterior and oblique chest X-rays may show
widening of the aorta and mediastinum.
Complications ❍ Magnetic resonance imaging and computed tomog-
❍ Cardiac tamponade raphy may be used to confirm and locate a dissec-
❍ Dissection tion.
❍ Death Diagnostic procedures
❍ Electrocardiography will show no evidence of a myo-
cardial infarction.
Assessment ❍ Aortography may be used to determine the lumen,
size, and location of the aneurysm.
History ❍ Echocardiography may be used to identify a dissect-
❍ No signs and symptoms until aneurysm expands and ing aneurysm of the aortic root.
begins to dissect ❍ Transesophageal echocardiography may be used to
❍ Sudden pain and possibly syncope measure an aneurysm in the ascending and descend-
ing aorta.
Physical assessment
❍ Abrupt loss of radial and femoral pulses and right
and left carotid pulses Nursing diagnoses
❍ Abrupt onset of intermittent neurologic deficits
❍ Cyanosis ❍ Acute pain
❍ Diaphoresis ❍ Decreased cardiac output
❍ Dyspnea ❍ Deficient fluid volume

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❍ Ineffective gas exchange Patient teaching

❍ Risk for infection
Be sure to cover:
Key outcomes ❍ diagnosis
The patient will: ❍ procedure and expected postoperative care, if
❍ maintain adequate cardiac output and hemodynamic surgery is scheduled
stability ❍ compliance with antihypertensive therapy, including
❍ maintain adequate ventilation the need for drugs and their expected adverse effects
❍ express feelings of increased comfort and decreased ❍ monitoring of blood pressure
pain ❍ the need to call a doctor if the patient has any sharp
❍ show no signs or symptoms of infection pain in the chest or back of the neck.
❍ maintain adequate fluid volume.

Discharge planning
❍ Refer the patient to a smoking-cessation program, if
General indicated.
❍ I.V. fluids and whole blood transfusions, if needed
❍ Low-fat diet
❍ No activity restrictions unless the patient has surgery
❍ Surgical resection with a Dacron or Teflon graft
❍ Weight reduction, if appropriate
❍ In a nonemergency situation, give the patient time to
express his fears and concerns and to identify and
use effective coping strategies.
❍ Offer the patient and his family psychological sup-
❍ Give prescribed analgesics to relieve pain.
After repair of a thoracic aneurysm
❍ Maintain blood pressure in the prescribed range us-
ing fluids and drugs.
❍ Give prescribed analgesics.
❍ After stabilization of vital signs, encourage and assist
the patient in turning, coughing, and deep breathing.
❍ Help the patient walk as soon as he’s able.
❍ Assist the patient with range-of-motion leg exercises.

Drug therapy
❍ Analgesics
❍ Antibiotics
❍ Antihypertensives
❍ Beta blockers
❍ Negative inotropic drugs
❍ Chest tube drainage
❍ Distal pulses
❍ Heart and lung sounds
❍ I.V. therapy and intake and output
❍ Laboratory results
❍ Level of consciousness and pain
❍ Signs of infection
❍ Vital signs and hemodynamics
A LERT After surgical repair, watch for signs
and symptoms similar to those of the initial
dissecting aneurysm; they suggest a tear at the graft

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Test results
Aneurysm, ventricular Imaging
❍ If the aneurysm is large, a chest X-ray may show an
Overview abnormal bulge that distorts the heart’s contour
(may be normal if the aneurysm is small).
Diagnostic procedures
Description ❍ Electrocardiography may show persistent ST–T wave
❍ An outpouching of a ventricle, almost always the left, elevations.
that produces ventricular wall dysfunction ❍ Two-dimensional echocardiography shows abnormal
❍ May develop days to weeks after myocardial infarc- motion in the left ventricular wall.
tion (MI) or may be delayed for years ❍ Left ventriculography may be used to show left ven-
tricular enlargement with an area of akinesia or
Pathophysiology dyskinesia (during cineangiography) and diminished
❍ When an MI destroys a large section of muscle in the cardiac function.
left ventricle, necrosis reduces the ventricular wall to ❍ Noninvasive nuclear cardiology may indicate the site
a thin sheath of fibrous tissue. of infarction and the area of aneurysm.
❍ Under intracardiac pressure, the thin sheath stretch-
es and forms a separate noncontractile sac.
❍ The affected ventricular wall moves abnormally. Nursing diagnoses
❍ During systolic ejection, abnormal muscle wall
movements cause the remaining normal myocardial ❍ Acute pain
fibers to contract more forcefully to maintain stroke ❍ Anxiety
volume and cardiac output. ❍ Decreased cardiac output
❍ At the same time, a portion of the stroke volume is ❍ Deficient fluid volume
lost to passive distention of the noncontractile sac. ❍ Fatigue
Risk factors Key outcomes
❍ History of MI The patient will:
❍ maintain adequate cardiac output
Causes ❍ maintain hemodynamic stability
❍ MI ❍ maintain adequate fluid balance
❍ express feelings of increased energy and decreased
Prevalence fatigue
❍ Occurs in about 20% of patients who have an MI ❍ express feelings of decreased anxiety.

❍ Cerebral embolization Interventions
❍ Heart failure
❍ Ventricular arrhythmias General
❍ Depends on the size of the aneurysm and the pres-
ence of complications
Assessment ❍ Aneurysmectomy with myocardial revascularization
❍ Embolectomy
History ❍ Low-fat diet
❍ Dyspnea ❍ May warrant only routine medical examination to
❍ Fatigue follow the patient’s condition
❍ Previous MI ❍ May warrant aggressive measures, such as cardiover-
sion, defibrillation, and endotracheal intubation
Physical assessment ❍ No activity restrictions unless the patient undergoes
❍ Arrhythmias, such as premature ventricular contrac- surgery
tions ❍ Weight reduction, if appropriate
❍ Crackles and rhonchi
❍ Distended jugular veins, if heart failure is present Nursing
❍ Double, diffuse, or displaced apical impulse ❍ Give prescribed drugs.
❍ Edema ❍ Prepare the patient for surgery, if indicated.
❍ Gallop rhythm ❍ Provide psychological support for the patient and his
❍ Irregular peripheral pulse rhythm family.
❍ Pulsus alternans A LERT Stay alert for sudden changes in senso-
❍ Visible or palpable systolic precordial bulge rium, which may indicate cerebral emboliza-
tion, and for signs that suggest renal failure or an MI.

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Drug therapy
❍ Analgesics
❍ Antiarrhythmics
❍ Anticoagulants
❍ Antihypertensives
❍ Cardiac glycosides
❍ Diuretics
❍ Fluid and electrolyte replacement
❍ Nitrates
Heart failure
❍ Cardiac rhythm, especially for ventricular arrhyth-
❍ Blood urea nitrogen and serum creatinine levels
❍ Fluid and electrolyte balance
❍ Intake and output
❍ Vital signs and heart sounds
After surgery
❍ Pulmonary artery catheter pressures
❍ Signs and symptoms of infection
❍ Type and amount of chest tube drainage

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ prescribed drugs and their potential adverse reac-
❍ when to contact a doctor
❍ expected postoperative care, if the patient is sched-
uled to undergo resection
❍ how to monitor pulse irregularity and rate changes.

Discharge planning
❍ Refer the patient (or his family) to a community-
based cardiopulmonary resuscitation training pro-
❍ Refer the patient to a weight-reduction program, if
❍ Refer the patient to a smoking-cessation program, if

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Anorexia nervosa ❍

Suicide attempts
Tooth and gum erosion and dental caries
❍ Death
❍ A psychological disorder of self-imposed starvation History
❍ Results from a distorted body image and an intense ❍ Amenorrhea
and irrational fear of gaining weight ❍ Angry disposition
❍ Loss of appetite (rare) ❍ Compulsion to be thin
❍ May occur with bulimia nervosa ❍ Constipation or diarrhea
❍ Fatigue
Pathophysiology ❍ Infertility
❍ Decreased calorie intake depletes body fat and pro- ❍ Intolerance to cold
tein stores. ❍ Loss of libido
❍ Lack of lipid substrate for synthesis causes estrogen ❍ Loss of 15% or more of body weight for no known
deficiency and amenorrhea in women. reason
❍ Testosterone levels fluctuate in men, decreasing ❍ Morbid fear of being fat (See Criteria for diagnos-
erectile function and sperm count. ing anorexia nervosa.)
❍ Increased use of fat as energy leads to ketoacidosis. ❍ Ritualistic personality
❍ Sleep alterations
Risk factors ❍ Tendency to minimize weight loss
❍ Compulsive personality
❍ High achievement goals Physical assessment
❍ Feeling of pressure to achieve ❍ Atrophy of breast tissue
❍ Issues with dependence and independence ❍ Blotchy or sallow skin
❍ Low self-esteem ❍ Bradycardia
❍ Sexual abuse ❍ Dryness or loss of scalp hair
❍ Social attitudes that equate slimness with beauty ❍ Emaciated appearance
❍ Stress caused by multiple responsibilities ❍ Hypotension
❍ Lanugo on the face and body
Causes ❍ Loss of fatty tissue
❍ Exact cause unknown ❍ Skeletal muscle atrophy
❍ Subconscious need to exert personal control over With bulimia
life or to protect oneself from dealing with issues ❍ Abrasions or scars on the dorsum of the hand
surrounding sexuality, dependence, achievement ❍ Bowel distention
❍ Calluses of the knuckles
Prevalence ❍ Dental caries
❍ Affects 5% to 10% of the American population ❍ Oral or pharyngeal abrasions
❍ Affects females in more than 90% of cases ❍ Painless salivary gland enlargement
❍ Slowed reflexes
AGE AWARE Anorexia nervosa occurs mainly
in adolescents and young adults but also may Test results
affect older women and occasionally men.
❍ Decreased hemoglobin level, platelet count, and
Complications white blood cell count
❍ Amenorrhea ❍ Prolonged bleeding time
❍ Anemia ❍ Decreased erythrocyte sedimentation rate
❍ Decreased cardiac output ❍ Decreased levels of serum creatinine, blood urea ni-
❍ Decreased left ventricular muscle mass and chamber trogen, uric acid, cholesterol, total protein, albumin,
size sodium, potassium, chloride, calcium, and fasting
❍ Dehydration blood glucose
❍ Electrocardiogram changes ❍ Elevated levels of alanine aminotransferase and as-
❍ Electrolyte imbalances partate aminotransferase in severe starvation states
❍ Esophageal erosion, ulcers, tears, and bleeding ❍ Elevated serum amylase levels
❍ Heart failure ❍ In women, decreased levels of serum luteinizing hor-
❍ Hypotension mone and follicle-stimulating hormone
❍ Increased susceptibility to infection ❍ Decreased triiodothyronine levels
❍ Malnutrition ❍ Dilute urine

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Diagnostic procedures Criteria for diagnosing anorexia nervosa

❍ Electrocardiography may show nonspecific changes According to the Diagnostic and Statistical Manual of
in ST interval and T wave, a prolonged PR interval, Mental Disorders, 4th edition (text revision), these criteria
and possible ventricular arrhythmias. must be documented before a patient can be diagnosed
with anorexia nervosa:
● Refusal to maintain or achieve normal weight for age
Nursing diagnoses and height
● Intense fear of gaining weight or becoming fat, even
❍ Chronic low self-esteem though underweight
❍ ● Disturbed perception of body weight, size, or shape
Deficient fluid volume
● In women, the absence of at least three consecutive
❍ Delayed growth and development
menstrual cycles when otherwise expected to occur.
❍ Disturbed body image
❍ Imbalanced nutrition: less than body requirements
Key outcomes
The patient will: ❍ the need for the patient to avoid discussions about
❍ acknowledge a change in body image food with her family.
❍ express positive feelings about self
❍ achieve and maintain an expected body weight
❍ achieve an expected state of wellness Discharge planning
❍ maintain fluid volume balance.
❍ Refer the patient to support services.
❍ Balanced diet with a normal eating pattern
❍ Behavior modification
❍ Curtailed activity if needed for cardiac arrhythmias
❍ Gradual increase in physical activity with weight gain
and stabilization
❍ Group, family, or individual psychotherapy
❍ Parenteral nutrition, if needed
❍ Support the patient’s efforts to achieve a target
❍ Negotiate an adequate food intake with the patient.
❍ Supervise the patient one-on-one during meals and
for 1 hour afterward.
Drug therapy
❍ Vitamin and mineral supplements
❍ Activity for compulsive exercise
❍ Electrolyte levels and complete blood count
❍ Intake and output
❍ Vital signs
❍ Weight on a regular schedule
A LERT Monitor the patient for 1 hour after
meals to rule out self-induced vomiting.

Patient teaching
Be sure to cover:
❍ nutrition
❍ the importance of keeping a food journal

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Aortic insufficiency ❍

Bisferious pulse
Corrigan’s pulse
❍ Diffuse, hyperdynamic apical impulse, displaced lat-
Overview ❍
erally and inferiorly
Head bobbing with each heartbeat
❍ High frequency, blowing, early-peaking, diastolic de-
Description crescendo murmur best heard with the patient sitting
❍ A heart condition in which blood flows back into the down, leaning forward, and in deep fixed expiration
left ventricle, causing excess fluid volume (See Identifying the murmur of aortic insuffi-
❍ Also called aortic regurgitation ciency.)
❍ Pulsating nail beds and Quincke’s sign
Pathophysiology ❍ S3 gallop with increased left ventricular end-diastolic
❍ Blood flows backward into the left ventricle during pressure
diastole, increasing left ventricular diastolic pres- ❍ Systolic thrill at base or suprasternal notch
sure. ❍ Tachycardia, peripheral vasoconstriction, and pul-
❍ This process causes volume overload, dilation, and, monary edema if severe
eventually, hypertrophy of the left ventricle. ❍ Water-hammer pulse
❍ Excess fluid volume also eventually increases left ❍ Wide pulse pressure
atrial pressure and pulmonary vascular pressure.
Test results
Risk factors Imaging
❍ History of any condition that weakens the aortic valve ❍ Chest X-rays may show left ventricular enlargement
and pulmonary vein congestion.
Causes Diagnostic procedures
❍ Aortic aneurysm ❍ Echocardiography may show left ventricular enlarge-
❍ Aortic dissection ment, increased motion of the septum and posterior
❍ Connective tissue diseases wall, thickening of valve cusps, prolapse of the valve,
❍ Hypertension flail leaflet, vegetations, or dilation of the aortic root.
❍ Idiopathic valve calcification ❍ In severe disease, electrocardiography shows sinus
❍ Infective endocarditis tachycardia, left axis deviation, left ventricular hyper-
❍ Primary disease of the aortic valve leaflets, the wall trophy, and left atrial hypertrophy.
or the aortic root, or both ❍ Cardiac catheterization shows the presence and de-
❍ Rheumatic fever gree of aortic insufficiency, left ventricular dilation
❍ Traumatic injury and function, and coexisting coronary artery disease.
❍ Occurs most commonly among males Nursing diagnoses
❍ When accompanied by mitral valve disease, more
common among females ❍ Activity intolerance
❍ Decreased cardiac output
Complications ❍ Ineffective tissue perfusion: cardiopulmonary
❍ Left-sided heart failure ❍ Excess fluid balance
❍ Myocardial ischemia ❍ Impaired gas exchange
❍ Pulmonary edema ❍ Ineffective coping
Key outcomes
Assessment The patient will:
❍ carry out activities of daily living without excess fa-
History tigue or decreased energy
❍ Angina, especially nocturnal ❍ maintain cardiac output, hemodynamic stability, and
❍ Exertional dyspnea, orthopnea, paroxysmal noctur- absence of arrhythmias
nal dyspnea ❍ maintain adequate fluid balance
❍ Fatigue ❍ maintain adequate ventilation
❍ Palpitations, head pounding ❍ use available support systems.
❍ Sensation of a forceful heartbeat, especially when
❍ Symptoms of heart failure (late stages) Interventions
Physical assessment General
❍ Austin Flint murmur ❍ Low-sodium diet

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❍ Medical control of hypertension Identifying the murmur of

❍ Periodic noninvasive monitoring of aortic insuffi- aortic insufficiency
ciency and left ventricular function with echocardio- Aortic insufficiency is characterized by a high-pitched,
gram blowing decrescendo murmur that radiates from the aortic
❍ Planned rest periods to avoid fatigue valve area to the left sternal as shown here.
❍ Valve replacement
S1 S2 S1 S2
❍ Give prescribed drugs.
❍ If the patient needs bed rest, stress its importance,
and provide a bedside commode.
❍ Alternate periods of activity and rest.
❍ Allow the patient to express his concerns about the
effects of activity restrictions on his responsibilities
and routines.
❍ Keep the patient’s legs elevated while he sits in a
❍ Place the patient in an upright position, if needed,
and give oxygen. ❍ when to contact a doctor
❍ Keep the patient on a low-sodium diet in consulta- ❍ the need for periodic rest periods in the patient’s
tion with a dietitian. daily routine
❍ After surgery, watch for hypotension, arrhythmias, ❍ the need to elevate the legs whenever the patient sits
and thrombus formation. ❍ diet restrictions
❍ signs and symptoms of heart failure
Drug therapy ❍ the importance of consistent follow-up care
❍ Antiarrhythmics ❍ how to monitor pulse rate and rhythm
❍ Antihypertensives ❍ blood pressure control.
❍ Cardiac glycosides
❍ Diuretics
❍ Infective endocarditis prophylaxis Discharge planning
❍ Vasodilators
❍ Refer the patient to an outpatient cardiac rehabilita-
A LERT Avoid using beta blockers in patients
with aortic insufficiency because these drugs tion program, if indicated.
❍ Refer the patient to a smoking-cessation program, if
have negative inotropic effects.
❍ Refer the patient to a weight-reduction program, if
Monitoring needed.
❍ Adverse reactions to drug therapy
❍ Complications
❍ Pulmonary edema
❍ Signs and symptoms of heart failure
After surgery
❍ Arterial blood gas levels
❍ Blood chemistry studies, prothrombin time, and In-
ternational Normalized Ratio values
❍ Chest tube drainage
❍ Chest X-ray results
❍ Daily weight
❍ Heart sounds
❍ Intake and output
❍ Neurologic status
❍ Pulmonary artery pressures
❍ Vital signs and cardiac rhythm

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ prescribed drugs and their potential adverse reac-

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Aortic stenosis ❍

Diminished carotid pulses with delayed upstroke
Distinct lag between carotid artery pulse and apical
Overview ❍ Harsh, rasping, mid- to late-peaking systolic murmur
best heard at the base that may radiate to carotids
and apex (See Identifying the murmur of aortic
Description stenosis.)
❍ Narrowing of the aortic valve that affects blood flow ❍ Orthopnea
in the heart ❍ Peripheral edema
❍ Classified as either acquired or rheumatic ❍ Prominent jugular vein A waves
❍ Prominent S4
Pathophysiology ❍ Small, sustained arterial pulses that rise slowly
❍ Stenosis of the aortic valve impedes forward blood ❍ Split S2 as stenosis becomes more severe
flow. ❍ Suprasternal thrill
❍ The left ventricle must exert greater pressure to open
AGE AWARE An early systolic ejection murmur
the aortic valve.
may be present in children and adolescents
❍ The increased workload increases myocardial oxy-
who have noncalcified valves. The murmur is low-
gen demand.
pitched, rough, and rasping and is loudest at the base
❍ Reduced cardiac output reduces coronary artery
in the second intercostal space.
blood flow.
❍ Left ventricular hypertrophy and failure result.
Test results
Risk factors Imaging
❍ Diabetes mellitus ❍ Chest X-rays show valvular calcification, left ventricu-
❍ Hypercholesterolemia lar enlargement, pulmonary vein congestion and, in
later stages, left atrial, pulmonary arterial, right atri-
Causes al, and right ventricular enlargement.
❍ Atherosclerosis Diagnostic procedures
❍ Congenital aortic bicuspid valve ❍ Echocardiography shows a decreased valve area, in-
❍ Idiopathic fibrosis and calcification creased gradient, and increased thickness of the left
❍ Rheumatic fever ventricular wall.
❍ Electrocardiography may show left ventricular hyper-
Prevalence trophy, atrial fibrillation, or another arrhythmia.
❍ May be asymptomatic until age 50 to 70, even though ❍ Cardiac catheterization shows an increased pressure
stenosis has been present since childhood gradient across the aortic valve, increased left ven-
❍ Affects men in about 80% of cases tricular pressures, and the presence of coronary
artery disease.
❍ Cardiac arrhythmias, especially atrial fibrillation
❍ Infective endocarditis Nursing diagnoses
❍ Left-sided heart failure
❍ Left ventricular hypertrophy ❍ Activity intolerance
❍ Right-sided heart failure ❍ Decreased cardiac output
❍ Sudden death ❍ Excess fluid volume
❍ Impaired physical mobility
❍ Ineffective coping
Assessment ❍ Ineffective tissue perfusion: cardiopulmonary
History Key outcomes
❍ Angina The patient will:
❍ Dyspnea on exertion ❍ perform activities of daily living without excess fa-
❍ Exertional syncope tigue or exhaustion
❍ Fatigue ❍ avoid complications
❍ May be asymptomatic ❍ maintain cardiac output
❍ Palpitations ❍ show hemodynamic stability
❍ Paroxysmal nocturnal dyspnea ❍ keep a balanced fluid status
❍ maintain joint mobility and range of motion
Physical assessment ❍ develop and use adequate coping skills.
❍ Apex of the heart may be displaced inferiorly and

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Identifying the murmur of aortic stenosis

Aortic stenosis is characterized by a low-pitched, harsh,
General crescendo-decrescendo murmur that radiates from the
aortic valve area to the carotid artery as shown here.
❍ In adults, valve replacement after symptoms begin
and hemodynamic evidence suggests severe obstruc- SYSTOLE DIASTOLE SYSTOLE
S1 S2 S1 S2
❍ In children without calcified valves, simple commis-
surotomy under direct visualization
❍ Lifelong treatment and management of congenital
aortic stenosis
❍ Low-sodium, low-fat, low-cholesterol diet
❍ Percutaneous balloon aortic valvuloplasty
❍ Periodic noninvasive evaluation of the severity of
valve narrowing
❍ Planned rest periods
❍ Ross procedure in patients younger than age 5
❍ prescribed drugs and their potential adverse reac-
Nursing tions
❍ Give prescribed drugs. ❍ when to contact a doctor
❍ Maintain a low-sodium diet in consultation with a di- ❍ the need for rest periods in the patient’s daily routine
etitian. ❍ the need to elevate the legs when the patient sits
❍ If the patient needs bed rest, stress its importance; ❍ diet and fluid restrictions
provide a bedside commode. ❍ the importance of consistent follow-up care
❍ Alternate periods of activity and rest. ❍ signs and symptoms of heart failure
❍ Keep the patient’s legs elevated while he sits in a ❍ prevention of infective endocarditis
chair. ❍ pulse rate and rhythm
❍ Place the patient in an upright position and give oxy- ❍ monitoring methods for atrial fibrillation and other
gen, as needed. arrhythmias.
❍ Allow the patient to express his fears and concerns.
Drug therapy Discharge planning
❍ Antibiotics to prevent infective endocarditis
❍ Cardiac glycosides ❍ Refer the patient to a weight-reduction program, if
A LERT The use of diuretics and vasodilators ❍ Refer the patient to a smoking-cessation program, if
in patients with aortic stenosis may lead to hy-
potension and an inadequate stroke volume.

❍ Arrhythmias
❍ Daily weight
❍ Intake and output
❍ Respiratory status
❍ Signs and symptoms of heart failure
❍ Signs and symptoms of progressive aortic stenosis
❍ Vital signs
After surgery
❍ Arterial blood gas results
❍ Blood chemistry results
❍ Chest X-rays
❍ Hemodynamics
❍ Signs and symptoms of thrombus formation

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment

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Asbestosis Assessment
Overview ❍ Chest pain
❍ Cough
Description ❍ Exertional or resting dyspnea
❍ Lung disease characterized by diffuse interstitial pul- ❍ Exposure to asbestos fibers
monary fibrosis ❍ Recurrent respiratory tract infections
❍ Results from prolonged exposure to airborne as-
bestos particles Physical assessment
❍ May develop 15 to 20 years after regular exposure to ❍ Characteristic dry crackles in the lung bases
asbestos ceases ❍ Clubbing of the fingers
❍ Causes pleural plaques and mesotheliomas of the ❍ Tachypnea
pleura and the peritoneum
❍ A form of pneumoconiosis Test results
❍ Also known as mesothelioma Laboratory
❍ Decreased partial pressures of arterial oxygen and
Pathophysiology carbon dioxide in arterial blood gas analysis
❍ Inhaled asbestos fibers travel down the airway and Imaging
penetrate respiratory bronchioles and alveolar walls. ❍ Chest X-rays may show fine, irregular, and linear dif-
❍ Goblet cells and mucus production are stimulated to fuse infiltrates; a honeycomb or ground-glass ap-
protect the airway and aid in expectoration. pearance in the lungs; and pleural thickening, pleur-
❍ Fibers become encased in a brown, iron-rich, pro- al calcification, bilateral obliteration of costophrenic
teinlike sheath and are called asbestosis bodies. angles, and an enlarged heart with a “shaggy” bor-
❍ Chronic irritation by the fibers continues, causing der.
edema of the airways. Diagnostic procedures
❍ Fibrosis develops in response to the chronic irrita- ❍ Pulmonary function tests may show decreased vital
tion. capacity, forced vital capacity (FVC), and total lung
capacity; decreased or normal forced expiratory vol-
Risk factors ume in 1 second (FEV1); a normal ratio of FEV1 to
❍ Asbestos exposure FVC; and a reduced diffusing capacity for carbon
❍ Cigarette smoking monoxide.
❍ Prolonged inhalation of asbestos fibers from such in- Nursing diagnoses
dustries as mining and milling, construction, fire-
proofing, and textiles ❍ Deficient knowledge: asbestosis
❍ Production of paints, plastics, and brake and clutch ❍ Fatigue
linings ❍ Imbalanced nutrition: less than body requirements
❍ Exposure to fibrous dust shaken off workers’ cloth- ❍ Impaired gas exchange
ing ❍ Risk of imbalanced fluid volume
❍ Exposure to fibrous dust or waste piles from nearby
asbestos plants Key outcomes
The patient will:
Prevalence ❍ maintain adequate ventilation
❍ Commonly becomes symptomatic between ages 40 ❍ maintain adequate calorie intake
and 75 ❍ express understanding of the illness
❍ Affects males more commonly than females ❍ identify measures to prevent or reduce fatigue
❍ maintain fluid volume balance.
❍ Cor pulmonale
❍ Pulmonary fibrosis Interventions
❍ Pulmonary hypertension
❍ Respiratory failure General
❍ Activity, as tolerated
❍ At least 3 qt (3 L) of fluids daily
❍ Controlled coughing and postural drainage with
chest percussion and vibration
❍ High-calorie, high-protein, low-sodium diet

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❍ Lung transplantation in severe disease

❍ Give prescribed drugs.
❍ Provide supportive care.
❍ Provide chest physiotherapy.
❍ Provide high-calorie, high-protein, low-sodium
foods in small, frequent meals.
❍ Encourage oral fluid intake.
❍ Provide frequent rest periods.
Drug therapy
❍ Antibiotics
❍ Cardiac glycosides
❍ Diuretics
❍ Inhaled mucolytics
❍ Supplemental oxygen
❍ Complications
❍ Daily weight
❍ Intake and output
❍ Mentation
❍ Respiratory status (breath sounds, arterial blood gas
❍ Sputum production
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ prescribed drugs and their potential adverse reac-
❍ transtracheal catheter care, if applicable
❍ prevention of infection
❍ signs and symptoms of infection
❍ the need for influenza and pneumococcus immu-
❍ home oxygen therapy, if needed
❍ the importance of follow-up care
❍ the need for chest physiotherapy
❍ the need for a high-calorie, high-protein, low-
sodium diet
❍ the need for adequate oral fluid intake
❍ energy conservation techniques.

Discharge planning
❍ Refer the patient to a smoking-cessation program, if

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Asphyxia ❍ Erythema and petechiae on the upper chest (from

❍ Intercostal rib retractions
Overview ❍

Little or no air movement
Pale skin
❍ Prominent neck muscles
Description ❍ Wheezing and stridor
❍ A condition of insufficient oxygen and accumulating
carbon dioxide in the blood and tissues Test results
❍ Without prompt treatment, leads to cardiopulmonary Laboratory
arrest and death ❍ Decreased partial pressure of arterial oxygen (less
than 60 mm Hg) and increased partial pressure of
Pathophysiology arterial carbon dioxide (more than 50 mm Hg) on
❍ Asphyxia is an interference with respiration that arterial blood gas (ABG) analysis
causes an insufficient oxygen intake. ❍ Toxicology tests showing drugs, chemicals, or an ab-
❍ Carbon dioxide accumulates as a result. normal hemoglobin level
❍ Hypoxemia arises. Imaging
❍ Tissue perfusion is inadequate. ❍ Chest X-rays may detect a foreign body, pulmonary
edema, or atelectasis.
Risk factors Diagnostic procedures
❍ Opioid abuse ❍ Pulmonary function tests may indicate respiratory
❍ Spinal cord injury muscle weakness.
❍ Bronchoscopy can be used to locate a foreign body.
❍ Opioid abuse
❍ Airway obstruction Nursing diagnoses
❍ Aspiration
❍ Carbon monoxide poisoning ❍ Decreased cardiac output
❍ Near drowning ❍ Impaired gas exchange
❍ Pulmonary edema ❍ Ineffective airway clearance
❍ Respiratory muscle paralysis ❍ Risk for aspiration
❍ Smoke inhalation ❍ Risk for deficient fluid volume
❍ Strangulation ❍ Risk for suffocation
❍ Trauma to airway
❍ Tumor Key outcomes
The patient will:
Prevalence ❍ maintain a patent airway
❍ Can occur at any age ❍ maintain adequate ventilation
❍ maintain an acceptable cardiac output
Complications ❍ demonstrate knowledge of safety measures to pre-
❍ Neurologic damage vent suffocation
❍ Death ❍ maintain fluid volume balance.

Assessment Interventions
History General
❍ Possibly an obvious cause ❍ Activity based on outcome of interventions
❍ Variable causes of signs and symptoms ❍ Established airway and ventilation
❍ Nothing by mouth until airway is protected
Physical assessment ❍ Treatment for the underlying cause
❍ Altered respiratory rate ❍ Tumor removal
❍ Anxiety or agitation
❍ Cherry-red mucous membranes (carbon monoxide Nursing
poisoning) ❍ Perform abdominal thrust maneuver if the patient
❍ Confusion has an airway obstruction.
❍ Cyanosis in mucous membranes, lips, and nail beds ❍ Maintain a patent airway.
❍ Decreased or absent breath sounds ❍ Begin cardiopulmonary resuscitation, if needed.
❍ Dyspnea ❍ Insert a nasogastric tube or an Ewald tube for lavage
(for opioid abuse).

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❍ Give prescribed drugs.

❍ Reassure the patient and his family.
❍ Ensure I.V. access.
Drug therapy
❍ Narcan (if caused by opioid abuse)
❍ Oxygen
❍ ABG levels, pulse oximetry
❍ Cardiac status
❍ Neurologic status
❍ Respiratory status
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the cause of asphyxia
❍ ways to prevent recurrence (with patient and family
members) if appropriate
❍ safety measures if the patient is a child.

Discharge planning
❍ Refer the patient to the proper authorities, if crimi-
nal intent was involved.
❍ Refer the patient to resource and support services, if

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Asthma ❍

Hereditary predisposition
❍ Psychological stress
Overview ❍

Sensitivity to allergens or irritants such as pollutants
❍ Viral infections
❍ A chronic reactive airway disorder involving episod- Prevalence
ic, reversible airway obstruction caused by broncho- ❍ Can occur at any age
spasm, increased mucus secretion, and mucosal ❍ Affects children younger than age 10 in about 50% of
edema cases
❍ Signs and symptoms that range from mild wheezing ❍ Affects twice as many boys as girls
and dyspnea to life-threatening respiratory failure ❍ Onset between ages 10 and 30 in about one-third of
❍ Possibly persistent signs and symptoms of bronchial patients
airway obstruction between acute episodes ❍ Also occurs in at least one immediate family member
about one-third of the time
Pathophysiology ❍ Occurs as both intrinsic and extrinsic asthma in
❍ Tracheal and bronchial linings overreact to various many people
stimuli, causing episodic smooth-muscle spasms that
severely constrict the airways. Complications
❍ Mucosal edema and thick secretions further block ❍ Respiratory failure
the airways. ❍ Status asthmaticus
❍ Immunoglobulin E (IgE) antibodies, attached to hist- ❍ Death
amine-containing mast cells and receptors on cell
membranes, initiate intrinsic asthma attacks.
❍ When exposed to an antigen such as pollen, the IgE Assessment
antibodies combine with the antigen. With later ex-
posure to that antigen, mast cells degranulate and History
release mediators. ❍ Exposure to a particular allergen followed by a sud-
❍ The mediators cause the bronchoconstriction and den onset of dyspnea, wheezing, chest tightness, and
edema of an asthma attack. cough with thick, clear, or yellow sputum
❍ During an asthma attack, expiratory airflow decreas- ❍ Irritants, emotional stress, fatigue, endocrine
es, trapping gas in the airways and causing alveolar changes, temperature and humidity variations, and
hyperinflation. exposure to noxious fumes
❍ Atelectasis may develop in some lung regions. ❍ Possibly dramatic simultaneous onset of severe, mul-
❍ The increased airway resistance leads to labored tiple symptoms, or possibly a gradual increase in
breathing. respiratory distress
❍ Previous severe respiratory tract infection (intrinsic
Risk factors asthma), especially in adults
❍ Air pollution
❍ Occupational exposure to irritants Physical assessment
❍ Second-hand tobacco smoke ❍ Ability to speak only a few words before pausing for
Causes ❍ Cyanosis, confusion, and lethargy (at onset of life-
❍ Sensitivity to specific external allergens or internal, threatening status asthmaticus and respiratory fail-
nonallergenic factors ure)
Extrinsic asthma (atopic asthma) ❍ Diaphoresis
❍ Animal dander ❍ Diminished breath sounds
❍ Food additives containing sulfites and any other sen- ❍ Hyperresonance
sitizing substance ❍ Increased anteroposterior thoracic diameter
❍ House dust or mold ❍ Inspiratory and expiratory wheezes
❍ Kapok or feather pillows ❍ Mild systolic hypertension
❍ Pollen ❍ Prolonged expiratory phase of respiration
Intrinsic asthma (nonatopic asthma) ❍ Tachycardia
❍ Emotional stress ❍ Tachypnea
❍ Genetic factors ❍ Use of accessory respiratory muscles
Bronchoconstriction ❍ Visible dyspnea
❍ Cold air
❍ Drugs, such as aspirin, beta blockers, and non-
steroidal anti-inflammatory drugs

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Test results ❍ Treat the patient’s dehydration with I.V. or oral flu-
Laboratory ids, as tolerated.
❍ Hypoxemia on arterial blood gas (ABG) analysis ❍ Anticipate bronchoscopy or bronchial lavage.
❍ Increased serum IgE levels from an allergic reaction ❍ Keep the room temperature comfortable.
❍ Increased eosinophil count on complete blood count ❍ Use an air conditioner or a fan in hot, humid
with differential weather.
❍ Chest X-rays may show hyperinflation with areas of Drug therapy
focal atelectasis. ❍ Antibiotics
Diagnostic procedures ❍ Anticholinergic bronchodilators
❍ Pulmonary function studies may show decreased ❍ Bronchodilators
peak flows and forced expiratory volume in 1 sec- ❍ Corticosteroids
ond, low-normal or decreased vital capacity, and in- ❍ Heliox trial (before intubation)
creased total lung and residual capacities. ❍ Histamine antagonists
❍ Skin testing may identify specific allergens. ❍ I.V. magnesium sulfate (controversial)
❍ Bronchial challenge testing shows the practical sig- ❍ Leukotriene antagonists
nificance of allergens identified by skin testing. ❍ Low-flow oxygen
❍ Pulse oximetry may show decreased oxygen satura-
A LERT The patient with increasingly severe
tion. asthma that doesn’t respond to drug therapy is
usually admitted for treatment with corticosteroids,
Nursing diagnoses epinephrine, and sympathomimetic aerosol sprays.
The patient may need endotracheal intubation and
mechanical ventilation.
❍ Fear
❍ Impaired gas exchange
❍ Ineffective airway clearance Monitoring
❍ Ineffective breathing pattern ❍ ABG results
❍ Ineffective coping ❍ Breath sounds
❍ Risk for deficient fluid volume ❍ Complications of corticosteroids
❍ Intake and output
Key outcomes ❍ Level of anxiety
The patient will: ❍ Pulmonary function test results
❍ maintain adequate ventilation ❍ Pulse oximetry
❍ maintain a patent airway ❍ Response to treatment
❍ use effective coping strategies ❍ Signs and symptoms of theophylline toxicity
❍ report feelings of comfort ❍ Vital signs
❍ maintain fluid volume balance.

Patient teaching
Be sure to cover:
General ❍ the disorder, diagnosis, and treatment
❍ Activity as tolerated ❍ prescribed drugs and their potential adverse reac-
❍ Desensitization to specific antigens tions
❍ Establishment and maintenance of a patent airway ❍ when to contact a doctor
❍ Fluid replacement ❍ the need to avoid known allergens and irritants
❍ Identification and avoidance of precipitating factors ❍ how to use a metered-dose or dry powder inhaler
❍ pursed-lip and diaphragmatic breathing
Nursing ❍ use of a peak flow meter
❍ Give prescribed drugs. ❍ effective coughing techniques
❍ Place the patient in high Fowler’s position. ❍ maintaining adequate hydration.
❍ Encourage pursed-lip and diaphragmatic breathing.
❍ Give prescribed humidified oxygen.
❍ Adjust the oxygen according to the patient’s vital Discharge planning
signs and ABG values.
❍ Assist with intubation and mechanical ventilation, if ❍ Refer the patient to a local asthma support group.
❍ Perform postural drainage and chest percussion, if
❍ Suction an intubated patient, as needed.

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Atelectasis Assessment
Overview ❍ CNS depression
Description ❍ Mechanical ventilation
❍ Incomplete expansion of alveolar clusters or lung ❍ Prolonged immobility
segments leading to partial or complete lung col- ❍ Recent abdominal surgery
lapse ❍ Rib fractures, tight chest dressings
❍ May be chronic or acute ❍ Smoking
❍ Good prognosis with prompt removal of airway ob-
struction, relief of hypoxia, and reexpansion of the Physical assessment
collapsed lung ❍ Anxiety
❍ Cyanosis
Pathophysiology ❍ Decreased chest wall movement
❍ Incomplete expansion removes certain regions of the ❍ Decreased fremitus
lung from gas exchange. ❍ Decreased or absent breath sounds
❍ Unoxygenated blood passes unchanged through ❍ Diaphoresis
these regions and produces hypoxia. ❍ Dullness or flatness over lung fields
❍ Alveolar surfactant causes increased surface tension, ❍ End-inspiration crackles
permitting complete alveolar deflation. ❍ Mediastinal shift to the affected side
❍ Substernal or intercostal retractions
Risk factors ❍ Tachycardia
❍ Anesthesia
❍ Lung disease Test results
❍ Prolonged bed rest Laboratory
❍ Hypoxia on arterial blood gas analysis
Causes Imaging
❍ Bed rest in a supine position ❍ Chest X-rays show characteristic horizontal lines in
❍ Bronchial occlusion the lower lung zones and characteristic dense shad-
❍ Bronchiectasis ows.
❍ Bronchogenic carcinoma Diagnostic procedures
❍ Cystic fibrosis ❍ Bronchoscopy may show an obstructing neoplasm,
❍ External compression foreign body, or pneumonia.
❍ General anesthesia ❍ Pulse oximetry shows decreased oxygen saturation.
❍ Idiopathic respiratory distress syndrome of the
❍ Inflammatory lung disease Nursing diagnoses
❍ Oxygen toxicity
❍ Pleural effusion ❍ Acute pain
❍ Pulmonary edema ❍ Impaired gas exchange
❍ Pulmonary embolism ❍ Ineffective coping
❍ Sarcoidosis ❍ Ineffective airway clearance
❍ Risk for deficient fluid volume
❍ Common after upper abdominal or thoracic surgery Key outcomes
❍ More common with prolonged immobility, mechani- The patient will:
cal ventilation, and central nervous system (CNS) de- ❍ maintain a patent airway
pression ❍ maintain adequate ventilation
❍ Increased predisposition in patients who smoke and ❍ report feelings of increased comfort
in those with chronic obstructive pulmonary disease ❍ use support systems to manage anxiety and fear
(COPD) ❍ maintain fluid volume balance.

❍ Acute respiratory failure Interventions
❍ Hypoxemia
❍ Pneumonia General
❍ Activity (not bed rest) as tolerated
❍ Bronchoscopy if other measures fail

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❍ Chest percussion
❍ Diet based on patient’s condition, as tolerated
❍ Frequent coughing and deep breathing
❍ Humidity
❍ Incentive spirometry
❍ Increased fluids
❍ Intermittent positive-pressure breathing therapy
❍ Possibly radiation for an obstructing neoplasm
❍ Postural drainage
❍ Surgery for an obstructing neoplasm
❍ Give prescribed drugs.
❍ Encourage coughing and deep breathing.
❍ Reposition the patient often.
❍ Encourage and assist with ambulation as soon as
❍ Help the patient use an incentive spirometer.
❍ Humidify inspired air.
❍ Encourage adequate fluid intake.
❍ Loosen secretions with postural drainage and chest
❍ Provide suctioning, as needed.
❍ Offer reassurance and emotional support.
Drug therapy
❍ Analgesics after surgery
❍ Bronchodilators
❍ Intake and output
❍ Pulse oximetry
❍ Respiratory status (breath sounds, arterial blood gas
❍ Vital signs

Patient teaching
Be sure to cover:
❍ use of an incentive spirometer
❍ postural drainage and percussion
❍ coughing and deep-breathing exercises
❍ the importance of splinting an incision
❍ energy conservation techniques
❍ stress reduction strategies
❍ the importance of mobilization.

Discharge planning
❍ Refer the patient to a smoking-cessation program, if
❍ Refer the patient to a weight-reduction program, if

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B Blood transfusion

A hemolytic reaction caused by transfusion of mis-
matched blood
Accompanies or follows I.V. delivery of blood com-
Mediated by immune or nonimmune factors
Varies from mild to severe

A LERT Double-check the patient’s name,
identification number, blood type, and Rh sta-
tus before giving blood. If you find any discrepancy,
don’t start the transfusion. Notify the blood bank im-
mediately, and return the unopened unit.

❍ Mild reactions: 1% to 2% of transfusions
❍ Acute tubular necrosis leading to acute renal failure
Anaphylactic shock
Disseminated intravascular coagulation
Vascular collapse
❍ Recipient’s antibodies — immunoglobulin (Ig) G or Assessment
IgM — bind to donor red blood cells (RBCs), lead-
ing to widespread clumping and destruction of the History
recipient’s RBCs. ❍ Chest or back pain
❍ Transfusion with Rh-incompatible blood triggers a ❍ Chest tightness
less serious reaction, known as Rh isoimmunization, ❍ Chills
within several days to 2 weeks. (See Understanding ❍ Nausea
the Rh system.) ❍ Transfusion of blood or blood product
❍ A febrile nonhemolytic reaction — the most common ❍ Vomiting
type — develops when cytotoxic or agglutinating an-
tibodies in the recipient’s plasma attack antigens on Physical assessment
transfused lymphocytes, granulocytes, or plasma ❍ Angioedema
cells. ❍ Apprehension
❍ Dyspnea
Causes ❍ Fever
❍ Transfusion of incompatible blood or blood prod- ❍ Hypotension
ucts ❍ Tachycardia
❍ Urticaria
❍ Wheezing
❍ In a surgical patient: blood oozing from mucous
Understanding the Rh system membranes or the incision site
❍ In a hemolytic reaction:
The Rh system contains more than 30 antibodies and – Fever
antigens. About 85% of people are Rh-positive, which – Unexpected decrease in serum hemoglobin level
means that their red blood cells carry the D or Rh antigen.
– Frank blood in urine
Everyone else is Rh-negative; they don’t have this antigen.
– Jaundice
Effects of sensitization
When an Rh-negative person receives Rh-positive blood Test results
for the first time, he becomes sensitized to the D antigen Laboratory
but shows no immediate reaction to it. If he receives Rh-
❍ Decreased serum hemoglobin level
positive blood a second time, he’ll have a massive
❍ Increased serum bilirubin level
hemolytic reaction.
For example, an Rh-negative mother who delivers an ❍ Increased indirect bilirubin level
Rh-positive baby is sensitized by the baby’s Rh-positive ❍ Hemoglobinuria in urinalysis
blood. During her next Rh-positive pregnancy, her ❍ Serum anti-A or anti-B antibodies in indirect
sensitized blood will cause a hemolytic reaction in the fetal Coombs’ test or serum antibody screen
circulation. ❍ Increased prothrombin time
Preventing sensitization ❍ Decreased fibrinogen level
To prevent the formation of antibodies against Rh-positive ❍ Increased blood urea nitrogen level
blood in her next pregnancy, an Rh-negative mother ❍ Increased serum creatinine level
should receive Rho(D) immune globulin (human)
(RhoGAM) I.M. within 72 hours after delivering an Rh-
positive baby.

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Nursing diagnoses Patient teaching

❍ Acute pain Be sure to cover:
❍ Decreased cardiac output ❍ before the transfusion, the type of transfusion
❍ Impaired gas exchange needed
❍ Impaired tissue integrity ❍ signs and symptoms of a reaction
❍ Powerlessness ❍ after recovery, the type of reaction that occurred.
❍ Risk for imbalanced body temperature
❍ Risk for imbalanced fluid volume
❍ Risk for injury Discharge planning
Key outcomes ❍ Urge the patient to inform other health care
The patient will: providers about the transfusion reaction.
❍ maintain hemodynamic stability
❍ show no signs of active bleeding
❍ maintain adequate ventilation
❍ express understanding of the reaction
❍ maintain adequate fluid volume.

❍ Bed rest
❍ Dialysis (may be needed if acute tubular necrosis
❍ Diet, as tolerated
❍ Immediate halt of transfusion
❍ Stop the transfusion.
❍ Maintain a patent I.V. line with normal saline solu-
❍ Insert an indwelling urinary catheter.
❍ Report early signs of complications.
❍ Cover the patient with blankets to ease chills.
❍ Give supplemental oxygen, as needed.
❍ Document the transfusion reaction on the patient’s
chart, noting the duration of the transfusion and the
amount of blood absorbed.
❍ Follow your facility’s blood transfusion policy and
Drug therapy
❍ Antipyretics
❍ Corticosteroids
❍ Diphenhydramine
❍ Epinephrine
❍ I.V. normal saline solution
❍ I.V. vasopressors
❍ Osmotic or loop diuretics
❍ Intake and output
❍ Laboratory test results
❍ Signs of shock
❍ Vital signs

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Bronchitis, chronic Assessment

Overview ❍ Cough
– Initially more common in winter
Description – Gradually becoming year-round
❍ Inflammation of the lining of the bronchial tubes ❍ Exertional dyspnea
❍ A form of chronic obstructive pulmonary disease ❍ Frequent upper respiratory tract infections
❍ Excessive production of tracheobronchial mucus ❍ Increasingly severe coughing episodes
❍ A cough lasting 3 or more months each year for ❍ Longtime smoker
2 consecutive years ❍ Productive cough
❍ Severity linked to amount of cigarette smoke or oth- ❍ Worsening dyspnea
er pollutants inhaled and duration of inhalation
❍ Respiratory tract infections that typically worsen the Physical assessment
cough and related symptoms ❍ Accessory respiratory muscle use
❍ Significant airway obstruction in some patients ❍ Cough that produces copious gray, white, or yellow
Pathophysiology ❍ Cyanosis
❍ Bronchial mucous glands undergo hypertrophy and ❍ Neck vein distention
hyperplasia. ❍ Pedal edema
❍ Goblet cells increase. ❍ Prolonged expiratory time
❍ Cilia are damaged. ❍ Rhonchi
❍ Columnar epithelium undergoes squamous meta- ❍ Substantial weight gain
plasia. ❍ Tachypnea
❍ Bronchial walls are chronically infiltrated by leuko- ❍ Wheezing
cytes and lymphocytes.
❍ Additional effects include widespread inflammation, Test results
narrowing of the airways, and mucus in the airways. Laboratory
❍ All effects produce resistance in the small airways ❍ Decreased partial pressure of oxygen in arterial
and, in turn, a severe ventilation-perfusion imbal- blood gas (ABG) analysis
ance. (See What happens in chronic bronchitis.) ❍ Normal or increased partial pressure of carbon
dioxide in ABG analysis
Causes ❍ Microorganisms and neutrophils in sputum culture
❍ Cigarette smoking Imaging
❍ Environmental pollution ❍ Chest X-ray may show hyperinflation and increased
❍ Organic or inorganic dust bronchovascular markings.
❍ Exposure to noxious gas Diagnostic procedures
❍ Possibly genetic predisposition ❍ Electrocardiography may show abnormalities:
– atrial arrhythmias
Prevalence – peaked P waves in leads II, III, and aVF
❍ About 20% of men – right ventricular hypertrophy.
❍ More prevalent in women than men ❍ Pulmonary function tests show:
❍ Diagnosed in more than 8.8 million Americans – increased residual volume
yearly – decreased vital capacity
❍ Increased risk among children of parents who – decreased forced expiratory flow
smoke – normal static compliance and diffusing capacity.
❍ Acute respiratory failure Nursing diagnoses
❍ Cor pulmonale
❍ Pulmonary hypertension ❍ Anxiety
❍ Right ventricular hypertrophy ❍ Deficient knowledge (chronic bronchitis)
❍ Fatigue
❍ Imbalanced nutrition: less than body requirements
❍ Impaired gas exchange
❍ Ineffective breathing patterns
❍ Risk for deficient fluid volume

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What happens in chronic bronchitis

In chronic bronchitis, irritants inhaled
for a prolonged period inflame the
inflammation leads to increased BRONCHIAL TREE CHRONIC BRONCHITIS
mucus production and a narrowed or
Cilia Cilia
blocked airway.
As inflammation continues, the
mucus-producing goblet cells
hypertrophy, as do the ciliated
epithelial cells that line the respiratory
tract. Hypersecretion from the goblet
cells blocks the free movement of cilia,
which normally sweep irritants, dust,
and mucus from the airways.
As a result, the airway stays
blocked, and mucus and debris Goblet cell Epithelial cell Goblet cell Epithelial cell
accumulate in the respiratory tract.

Key outcomes ❍ Diuretics

The patient will: ❍ Oxygen
❍ maintain adequate ventilation
❍ identify measures to prevent or reduce fatigue Monitoring
❍ express understanding of the illness ❍ Breath sounds
❍ maintain a patent airway ❍ Daily weight
❍ maintain fluid volume balance. ❍ Edema
❍ Intake and output
❍ Respiratory status
Interventions ❍ Response to treatment
❍ Sputum production
General ❍ Vital signs
❍ Activity as tolerated with frequent rest periods
❍ Adequate fluid intake
❍ Avoidance of air pollutants Patient teaching
❍ Chest physiotherapy
❍ High-calorie, protein-rich diet Be sure to cover:
❍ Smoking cessation ❍ the disorder, diagnosis, and treatment
❍ Tracheostomy in advanced disease ❍ prescribed drugs and their possible adverse effects
❍ Ultrasonic or mechanical nebulizer treatments ❍ when to contact a doctor
❍ infection control practices
Nursing ❍ influenza and pneumococcus immunizations
❍ Give prescribed drugs. ❍ home oxygen therapy, if needed
❍ Encourage expression of fears and concerns. ❍ postural drainage and chest percussion
❍ Include the patient and his family in care decisions. ❍ coughing and deep-breathing exercises
❍ Perform chest physiotherapy. ❍ use of an inhaler
❍ Provide a high-calorie, protein-rich diet. ❍ the need for high-calorie, protein-rich meals
❍ Offer small, frequent meals. ❍ the need for adequate hydration
❍ Encourage energy conservation techniques. ❍ avoidance of inhaled irritants
❍ Ensure adequate oral fluid intake. ❍ prevention of bronchospasm.
❍ Perform frequent mouth care.
❍ Encourage daily activity.
❍ Provide diversional activities, as appropriate. Discharge planning
❍ Arrange frequent rest periods.
❍ Refer the patient to a smoking-cessation program, if
Drug therapy needed.
❍ Antibiotics ❍ Refer the patient to the American Lung Association
❍ Bronchodilators for information and support.
❍ Corticosteroids

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Bulimia nervosa ❍

Maladaptive learned behavior
Struggle for control or self-identity
❍ Cultural overemphasis on physical appearance
Overview ❍ Parental obesity
Description ❍ Affects women about 80% of the time
❍ Behavioral disorder ❍ Affects 1% to 3% of adolescent and young women
❍ Binge eating ❍ 5% to 15% of adolescent and young women have
– More food in a measured time (usually 2 hours) some symptoms of the disorder
than an ordinary person would eat
AGE AWARE Bulimia typically starts in ado-
– Feeling of lack of control over eating
lescence or early adulthood.
❍ Inappropriate behaviors to compensate for binges
– Self-induced vomiting
– Misuse of laxatives or enemas Complications
– Misuse of diuretics ❍ Arrhythmia
– Strict dieting or fasting ❍ Cardiac failure
❍ Extreme concern about body image and weight ❍ Death
❍ Dehydration
Pathophysiology ❍ Dental caries
❍ Patient's behaviors and attitudes suggest that weight ❍ Electrolyte imbalance
and body image are primary concerns. ❍ Erosion of tooth enamel
❍ Patient eats large amounts of food without gaining ❍ Esophageal tear
weight. ❍ Gastric rupture
❍ Patient creates complex schedules to hide binge- ❍ Gum infection
purge episodes. ❍ Intestinal mucosal damage
❍ Patient visits the bathroom often, particularly after ❍ Parotitis
meals. ❍ Sudden death
❍ Patient may withdraw from usual friends and activi- ❍ Suicide
❍ Bulimia commonly is accompanied by evidence of
depression. Assessment
Causes History
❍ Exact cause unknown ❍ Childhood trauma or abuse
❍ Family disturbance or conflict ❍ Continued eating until abdominal pain, sleep, or an-
❍ Sexual abuse other person interrupts
❍ Depression
❍ Episodic binge eating
Criteria for diagnosing bulimia nervosa ❍ Exaggerated sense of guilt
❍ Parental obesity
According to the Diagnostic and Statistical Manual of ❍ Possible depression (Beck Depression Inventory)
Mental Disorders, 4th edition (text revision), these criteria ❍ Preferred food usually sweet, soft, high-calorie, high-
must be documented before a patient can be diagnosed carbohydrate
with bulimia nervosa:
❍ Unsatisfactory sexual relationships
● Recurrent episodes of binge eating during which the
person eats substantially more than most people would
in the same period and during which the person feels a Physical assessment
lack of control over what or how much is eaten ❍ Abdominal and epigastric pain
● Recurrent inappropriate compensatory behaviors to
prevent weight gain, which may include self-induced ❍ Abnormal use of diuretics, laxatives, vomiting, and
vomiting; misuse of laxatives, diuretics, other drugs, exercise (See Criteria for diagnosing bulimia ner-
or enemas; fasting; or excessive exercise vosa.)
● Binges and compensatory behaviors that occur, on ❍ Amenorrhea
average, at least twice weekly for 3 months and not
only during episodes of anorexia nervosa ❍ Calluses, abrasions, or scars on knuckles or back of
● Undue concern over body image and weight. the hand
Bulimia may be categorized as the purging type or the ❍ Eroded tooth enamel
nonpurging type. In the former, the patient uses vomiting ❍ Hoarseness
or misuses laxatives, diuretics, or enemas. In the latter, ❍ Normal weight or slightly overweight
the patient uses mostly fasting or excessive exercise to ❍ Painless swelling of salivary glands
compensate for binges. ❍ Throat irritation or lacerations
❍ Unusual swelling of cheeks or jaw area

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Test results
Laboratory Patient teaching
❍ Increased bicarbonate level
❍ Decreased potassium level Be sure to cover:
❍ Decreased sodium level ❍ the importance of keeping a food journal
❍ risks of self-induced vomiting
❍ risks of laxative and diuretic abuse
Nursing diagnoses ❍ risks of fasting and excessive exercise
❍ assertiveness training
❍ Chronic low self-esteem ❍ prescribed drugs, dosages, and possible adverse ef-
❍ Constipation fects.
❍ Disturbed body image
❍ Disturbed sleeping pattern
❍ Imbalanced nutrition: less than body requirements Discharge planning
❍ Ineffective coping
❍ Risk for deficient fluid volume ❍ Refer the patient to support services or specialized
inpatient care.
Key outcomes ❍ Refer the patient for psychological counseling.
The patient will:
❍ acknowledge a change in body image
❍ participate in decision-making about her care
❍ express positive feelings about self
❍ achieve an expected state of wellness
❍ maintain fluid volume balance.

❍ Balanced diet
❍ Drug rehabilitation
❍ Inpatient or outpatient psychotherapy
❍ Monitoring of activity
❍ Monitoring of eating pattern
❍ Self-help groups
❍ Supervise the patient during and for a specified peri-
od after meals, usually up to 1 hour.
❍ Set a time limit for each meal.
❍ Provide a pleasant, relaxed environment for eating.
❍ Use behavior modification techniques.
❍ Establish a food contract, specifying the amount and
type of food to be eaten at each meal.
❍ Encourage verbalization, and provide support.
Drug therapy
❍ Antidepressants
❍ Vitamin supplements
❍ Activity
❍ Complications
❍ Eating patterns
❍ Elimination patterns
❍ Response to treatment
❍ Suicide potential

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Physical assessment
Burns ❍ Depth and size of the burn
❍ Severity of the burn
Overview – Major burn: affects more than 10% of adult's or
20% of child’s body surface area (BSA)
– Moderate burn: 3% to 10% of adult's or 10% to
Description 20% of child’s BSA
❍ Heat or chemical injury to tissue – Minor burn: less than 3% of adult's or less than
❍ May be permanently disfiguring and incapacitating 10% of child’s BSA
First-degree burns
Pathophysiology ❍ Blanching
First-degree burns ❍ Chills
❍ Superficial, partial thickness ❍ Erythema
❍ Not life-threatening ❍ Headache
Second-degree burns ❍ Localized pain
❍ Deep, partial thickness ❍ Nausea and vomiting
❍ Destruction of epidermis and some dermis Second-degree burns
❍ Thin-walled, fluid-filled blisters ❍ Mild to moderate pain
❍ Painful open nerve endings when blisters break ❍ Thin-walled, fluid-filled blisters
❍ Lost barrier function of skin ❍ White, waxy appearance in damaged area
Third- and fourth-degree burns Third- and fourth-degree burns
❍ Painless; full thickness into subcutaneous tissue ❍ No blisters
❍ Every body system and organ affected ❍ No pain
❍ Damage to muscle, bone, and interstitial tissues ❍ Pale, white, brown, or black leathery tissue
❍ Edema from interstitial fluids ❍ Visible thrombosed vessels
❍ Immediate immunologic response Electrical burns
❍ Risk of wound sepsis ❍ Cardiac arrest
❍ Hearing impairment
Causes ❍ Muscle contractions
❍ Fires ❍ Numbness and tingling
❍ Traffic accidents ❍ Respiratory failure
❍ Improper use or storage of flammable materials ❍ Seizures
❍ Malfunction of electrical devices ❍ Silver colored, raised area at contact site
❍ Contact with faulty electrical wiring ❍ Unconsciousness
❍ Chewing of electric cords ❍ Weakness
❍ Contact with high-voltage power lines Mucosal burns
❍ Scalding accidents ❍ Coughing, wheezing
❍ Contact with or ingestion, inhalation, or injection of ❍ Darkened sputum
acids, alkali, or vesicants ❍ Sores in mouth or nose
❍ Friction or abrasion ❍ Voice changes
❍ Sun exposure
Test results
Prevalence Laboratory
❍ Affects more than 2 million people each year ❍ Evidence of smoke inhalation, decreased alveolar
❍ 70,000 hospitalizations, 20,000 in burn units function, possible hypoxia in arterial blood gas tests
❍ Decreased hemoglobin level and hematocrit in com-
Complications plete blood count if patient loses blood
❍ Anemia ❍ Abnormal electrolyte levels from fluid loss and shifts
❍ Hypovolemic shock ❍ Increased blood urea nitrogen level with fluid loss
❍ Malnutrition ❍ Decreased glucose level in children because of limit-
❍ Multiple organ dysfunction syndrome ed glycogen storage
❍ Respiratory complications ❍ Myoglobinuria and hemoglobinuria in urinalysis
❍ Sepsis ❍ Increased carboxyhemoglobin level
Diagnostic procedures
❍ Electrocardiography may show myocardial ischemia,
Assessment injury, or arrhythmias, especially in electrical burns.
❍ Fiber-optic bronchoscopy may show airway edema.
❍ Cause of the burn
❍ Existing medical conditions

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Fluid replacement after a burn

Nursing diagnoses For a burned adult, use one of the following formulas:

❍ Acute pain First 24 hours

❍ Anxiety EVA N S
❍ Deficient fluid volume ● 1 ml  patient’s weight in kg  % total body surface
area (TBSA) burn (0.9% normal saline solution)
❍ Deficient knowledge (burns) ● 1 ml  patient’s weight in kg  % TBSA burn (colloid
❍ Disturbed body image solution)
❍ Hypothermia BROOKE
❍ Imbalanced nutrition: less than body requirements ● 1.5 ml  patient’s weight in kg  % TBSA burn
❍ Impaired gas exchange (lactated Ringer’s solution)
❍ Impaired physical mobility ● 0.5 ml  patient’s weight in kg  % TBSA burn
(colloid solution)
❍ Impaired skin integrity
❍ Ineffective coping PA R K LA N D
● 4 ml  patient’s weight in kg  % TBSA burn
❍ Ineffective protection (lactated Ringer’s solution). Give half of volume in first
❍ Ineffective tissue perfusion: all 8 minutes; then infuse remainder over 16 minutes.
❍ Risk for infection Second 24 hours
Key outcomes EVA N S
● 50% of first 24-hour replacement (0.9% normal saline
The patient will: solution)
❍ report increased comfort and decreased pain ● 2,000 ml (dextrose 5% in water [D5W])
❍ attain the highest degree of mobility possible BROOKE
❍ maintain fluid balance in an acceptable range ● 50% to 75% of first 24-hour replacement (lactated
❍ maintain a patent airway Ringer’s solution)
● 2,000 ml (D5W)
❍ use effective coping techniques.
● 30% to 60% of calculated plasma volume
Interventions (25% albumin)
● Volume to maintain desired urine output (D5W)

❍ Stopping the burn source
❍ Securing the airway
Drug therapy
❍ Preventing hypoxia ❍ Analgesics
❍ Giving I.V. fluids through a large-bore I.V. line (See ❍ Anxiolytics
Fluid replacement after a burn.) ❍ Antibiotics
– Adult: urine output 30 to 50 ml/hour ❍ Booster of tetanus toxoid
– Child less than 30 kg (66 lb): urine output 1
ml/kg/hour Monitoring
❍ Nasogastric tube and urinary catheter insertion ❍ Vital signs
❍ Wound care ❍ Respiratory status
❍ Nothing by mouth until severity of burn is estab- ❍ Signs of infection
lished; then high-protein, high-calorie diet ❍ Intake and output
❍ Increased hydration with high-calorie, high-protein ❍ Hydration and nutritional status
drinks, not free water
❍ Total parenteral nutrition if unable to eat
❍ Activity limited based on extent and location of burn Patient teaching
❍ Physical therapy
❍ Loose tissue and blister debridement Be sure to cover:
❍ Escharotomy ❍ the injury, diagnosis, and treatment
❍ Skin grafting ❍ appropriate wound care
❍ prescribed drugs and possible adverse effects
Nursing ❍ developing a dietary plan
❍ Apply immediate, aggressive burn treatment. ❍ signs and symptoms of complications.
❍ Use strict sterile technique.
❍ Remove constricting items and smoldering clothes.
❍ Perform appropriate wound care. Discharge planning
❍ Provide adequate hydration.
❍ Weigh the patient daily. ❍ Refer the patient to rehabilitation, if appropriate.
❍ Encourage verbalization and provide support. ❍ Refer the patient for psychological aid, if needed.
❍ Refer the patient to resource and support services.

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Cardiomyopathy, dilated

Disease of the heart muscle fibers
Also called congestive cardiomyopathy

Extensively damaged myocardial muscle fibers re-
duce contractility in the left ventricle. (See Under-
standing dilated cardiomyopathy.)
As systolic function declines, cardiac output falls.

Gradual onset of shortness of breath, orthopnea,
dyspnea on exertion, paroxysmal nocturnal dyspnea,
fatigue, dry cough at night, palpitations, and vague
chest pain
Possible history of a disorder that can cause cardio-
Physical assessment
Irregular cardiac rhythms, diffuse apical impulses,
❍ The sympathetic nervous system is stimulated to in- pansystolic murmur
crease heart rate and contractility. ❍ Jugular vein distention
❍ When compensatory mechanisms can no longer ❍ Narrow pulse pressure
maintain cardiac output, the heart begins to fail. ❍ Peripheral cyanosis
❍ Peripheral edema
Causes ❍ Pulmonary crackles
❍ Cardiotoxic effects of drugs or alcohol ❍ Pulsus alternans in late stages
❍ Chemotherapy ❍ S3 and S4 gallop rhythms
❍ Drug hypersensitivity ❍ Splenomegaly
❍ Hypertension ❍ Tachycardia even at rest
❍ Ischemic heart disease A LERT Dilated cardiomyopathy may need to
❍ Peripartum syndrome related to toxemia be differentiated from other types of cardiomy-
❍ Valvular disease opathy. (See Assessment findings in cardiomyopathies.)
❍ Viral or bacterial infection
Prevalence Test results
❍ Most common among middle-age men but can occur Imaging
in any age group ❍ Chest X-rays show moderate to marked cardiomegaly
and possible pulmonary edema.
Complications ❍ Echocardiography may show ventricular thrombi,
❍ Arrhythmias global hypokinesis, and the degrees of left ventricu-
❍ Emboli lar dilation and systolic dysfunction.
❍ Intractable heart failure ❍ Gallium scans may identify patients with dilated car-
diomyopathy and myocarditis.
Diagnostic procedures
❍ Electrocardiography evaluates ischemic heart dis-
Understanding dilated cardiomyopathy ease and identifies arrhythmias and intraventricular
conduction defects.
❍ Cardiac catheterization can show left ventricular di-
lation and dysfunction, elevated left (and often right)
ventricular filling pressures, and diminished cardiac
❍ Angiography rules out ischemic heart disease.
❍ Transvenous endomyocardial biopsy may help deter-
mine the underlying disorder.

Nursing diagnoses
● Greatly increased chamber size ❍ Activity intolerance
● Thinning of left ventricular muscle
❍ Anxiety
● Increased atrial chamber size
❍ Decreased cardiac output
● Increased myocardial mass
❍ Deficient knowledge: dilated cardiomyopathy
● Normal ventricular inflow resistance
● Decreased contractility ❍ Excess fluid volume
❍ Fatigue

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Assessment findings in cardiomyopathies

Type Assessment findings
Dilated cardiomyopathy ● Generalized weakness, fatigue
● Chest pain, palpitations
● Syncope
● Tachycardia
● Narrow pulse pressure
● Pulmonary congestion, pleural effusions
● Jugular vein distention, peripheral edema
● Paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion

Hypertrophic cardiomyopathy ● Angina, palpitations

● Syncope
● Orthopnea, dyspnea with exertion
● Pulmonary congestion
● Loud systolic murmur
● Life-threatening arrhythmias
● Sudden cardiac arrest

Restrictive cardiomyopathy ● Generalized weakness, fatigue

● Bradycardia
● Dyspnea
● Jugular vein distention, peripheral edema
● Liver congestion, abdominal ascites

❍ Hopelessness ❍ Let the patient and family express their fears and
❍ Ineffective tissue perfusion: cardiopulmonary concerns, and help them identify effective coping
Key outcomes
The patient will: Drug therapy
❍ maintain adequate cardiac output and hemodynamic ❍ Angiotensin-converting enzyme inhibitors
stability ❍ Antiarrhythmics
❍ maintain adequate ventilation ❍ Anticoagulants
❍ develop no complications of excess fluid volume ❍ Beta blockers
❍ recognize and accept limitations of chronic illness ❍ Cardiac glycosides
❍ express feelings of increased energy and decreased ❍ Diuretics
fatigue. ❍ Oxygen
❍ Vasodilators
Interventions Monitoring
❍ Daily weight
General ❍ Evidence of progressive heart failure
❍ No ingestion of alcohol if cardiomyopathy results ❍ Hemodynamics
from alcoholism ❍ Intake and output
❍ Low-sodium diet with vitamin supplements ❍ Vital signs
❍ Rest periods
❍ Heart transplantation
❍ Possible cardiomyoplasty Patient teaching
AGE AWARE A woman of childbearing age
Be sure to cover:
who has dilated cardiomyopathy should avoid
❍ the disorder, diagnosis, and treatment
❍ prescribed drugs and potential adverse reactions
❍ when to contact a doctor
Nursing ❍ sodium and fluid restrictions
❍ Alternate periods of rest with required activities of ❍ evidence of worsening heart failure.
daily living.
❍ Provide active or passive range-of-motion exercises.
❍ Consult with a dietitian to provide a low-sodium diet. Discharge planning
❍ Give oxygen, as needed.
❍ Check serum potassium levels for hypokalemia, es- ❍ Refer family members to community cardiopul-
pecially if therapy includes a cardiac glycoside. monary resuscitation classes.
❍ Offer support, and let the patient express his feel-

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Cardiomyopathy, ❍ Heart failure
hypertrophic ❍

Pulmonary hypertension
Ventricular arrhythmias

Overview Assessment
Description History
❍ Primary disease of cardiac muscle characterized by ❍ Usually, no discernible features until disease is well
left ventricular hypertrophy advanced
❍ Also known as idiopathic hypertrophic subaortic ❍ Blood flow to left ventricle abruptly reduced by atrial
stenosis, hypertrophic obstructive cardiomyopathy, dilation and, sometimes, atrial fibrillation
and muscular aortic stenosis ❍ Possible family history of hypertrophic cardiomy-
Pathophysiology ❍ Orthopnea
❍ The hypertrophied ventricle becomes stiff, noncom- ❍ Dyspnea on exertion
pliant, and unable to relax during ventricular filling. ❍ Angina
❍ Tachycardia develops, reducing ventricular filling ❍ Fatigue
time. ❍ Syncope, even at rest
❍ Reduced ventricular filling time leads to low cardiac
output. (See Understanding hypertrophic cardio- Physical assessment
myopathy.) ❍ Rapidly rising carotid arterial pulse possible
❍ Pulsus biferiens
Causes ❍ Double or triple apical impulse, possibly displaced
❍ Transmission by autosomal dominant trait (about laterally
half of all cases) ❍ Bibasilar crackles if the patient has heart failure
❍ Associated with hypertension ❍ Harsh systolic murmur heard after S 1 at the apex
near the left sternal border
Prevalence ❍ Possible S4
❍ More common in men than women A LERT Hypertrophic cardiomyopathy may
❍ Affects 5 to 8 people per 100,000 in the United States need to be differentiated from other types of
❍ More common in Blacks than in other races cardiomyopathy.

Test results
Understanding hypertrophic ❍ Chest X-rays may show mild to moderate increase in
heart size.
❍ Echocardiography shows left ventricular hypertrophy
(a thick, asymmetrical intraventricular septum in the
obstructive form or hypertrophy in various ventricu-
lar areas in the nonobstructive form).
❍ Thallium scan usually reveals myocardial perfusion
Diagnostic procedures
❍ Electrocardiography usually shows left ventricular
hypertrophy, ST-segment and T-wave abnormalities,
left anterior hemiblock, left axis deviation, ventricu-
lar arrhythmias, atrial arrhythmias, and Q waves in
leads II, III, aVF, and V4 to V6 (from hypertrophy,
not infarction).
● Normal right and decreased left chamber size
❍ Cardiac catheterization reveals elevated left ventricu-
● Left ventricular hypertrophy
● Thickened interventricular septum (hypertrophic lar end-diastolic pressure and, possibly, mitral insuf-
obstructive cardiomyopathy) ficiency.
● Atrial chamber size increased on left side ❍ Angiography reveals a dilated, diffusely hypokinetic
● Increased myocardial mass left ventricle.
● Increased ventricular inflow resistance
● Increased or decreased contractility

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Nursing diagnoses ❍ Hemodynamics
❍ Intake and output
❍ Activity intolerance ❍ Vital signs
❍ Anxiety
❍ Decreased cardiac output
❍ Deficient knowledge: hypertrophic cardiomyopathy Patient teaching
❍ Excess fluid volume
❍ Fatigue Be sure to cover:
❍ Hopelessness ❍ the possibility that propranolol can cause depression
❍ Ineffective tissue perfusion: cardiopulmonary and the need to notify the doctor if symptoms occur
❍ instructions to take drugs as ordered
Key outcomes ❍ the need to tell all doctors that the patient shouldn’t
The patient will: receive nitroglycerin, digoxin, or diuretics because
❍ maintain adequate cardiac output and hemodynamic they can worsen obstruction
stability ❍ the need for antibiotic prophylaxis before dental
❍ develop no complications of excess fluid volume work or surgery to prevent infective endocarditis
❍ carry out activities of daily living without excess fa- ❍ warnings against strenuous activity, which may cause
tigue or decreased energy syncope or sudden death
❍ express feelings of comfort and decreased pain ❍ the need to avoid Valsalva’s maneuver or sudden po-
❍ develop adequate coping mechanisms. sition changes.

Interventions Discharge planning

General ❍ Refer family members to community cardiopul-
❍ Cardioversion for atrial fibrillation monary resuscitation classes.
❍ Low-fat, low-salt diet
❍ Fluid restrictions
❍ Avoidance of alcohol
❍ Activity limitations as needed
❍ Bed rest, if needed
❍ Ventricular myotomy alone or with mitral valve
❍ Heart transplantation
❍ Alternate periods of rest with required activities and
❍ Provide personal care, as needed, to prevent fatigue.
❍ Provide active or passive range-of-motion exercises.
A LERT If propranolol is being stopped, don’t
do so abruptly. Rebound effects could cause
myocardial infarction or sudden death.
❍ Offer support, and let the patient express his feel-
❍ Let the patient and family express their fears and
concerns and identify effective coping strategies.
Drug therapy
❍ Amiodarone, unless the patient has atrioventricular
❍ Antibiotic prophylaxis
❍ Beta blockers
❍ Calcium channel blockers
A LERT Angiotensin-converting enzyme in-
hibitors, nitrates, and digoxin are contraindi-
cated in hypertrophic cardiomyopathy.

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Cholera ❍

Thready or absent peripheral pulses
Decreased blood pressure
❍ Fever
Overview ❍ Inaudible, hypoactive bowel sounds
Test results
Description Laboratory
❍ Acute enterotoxin-mediated gastrointestinal infection ❍ A culture of V. cholerae from feces or vomitus
❍ Transmitted through food and water contaminated ❍ Rapidly moving bacilli (like shooting stars) with mi-
with the feces of carriers or people with active infec- croscopic examination of fresh feces
tions ❍ Group- and type-specific antisera in agglutination
❍ Food poisoning caused by Vibrio parahaemolyti- testing
cus, a similar bacterium
❍ Also known as Asiatic cholera or epidemic cholera
Nursing diagnoses
❍ Humans are the only hosts and victims of Vibrio ❍ Diarrhea
cholerae, a motile, aerobic organism. ❍ Impaired urinary elimination
❍ Risk for imbalanced fluid volume
Risk factors
❍ Deficiency or absence of hydrochloric acid Key outcomes
The patient will:
Causes ❍ regain and maintain adequate fluid and electrolyte
❍ The gram-negative bacillus V. cholerae balance
❍ have normal elimination patterns
Prevalence ❍ have stable vital signs
❍ Most common in Africa, Southern and Southeast ❍ produce adequate urine volume.
Asia, and the Middle East, although outbreaks have
occurred in Japan, Australia, and Europe
❍ Occurs during warm months, usually among lower Interventions
socioeconomic groups
❍ Common among children ages 1 to 5 in India, but General
equally distributed among all age groups in other ❍ Enteric precautions
endemic areas ❍ Supportive care
❍ Increased fluid intake
❍ Dehydration Nursing
❍ Hypovolemic shock ❍ Wear a gown and gloves when handling feces-
❍ Metabolic acidosis contaminated articles.
❍ Uremia ❍ Carefully observe neck veins.
❍ Coma and death ❍ Auscultate the lungs frequently.
Drug therapy
Assessment ❍ Rapid I.V. infusion of large amounts (50 to 100 ml/
minute) of isotonic saline solution, alternating with
History isotonic sodium bicarbonate or sodium lactate
❍ Profuse, watery diarrhea ❍ Tetracycline
❍ Vomiting
❍ Intense thirst Monitoring
❍ Weakness ❍ Intake and output
❍ Muscle cramps (especially in the limbs) ❍ I.V. infusion
❍ Laboratory test results
Physical assessment ❍ Neck veins
❍ Stools containing white flecks of mucus (rice-water ❍ Vital signs
❍ Loss of skin turgor, wrinkled skin, sunken eyes
❍ Pinched facial expression
❍ Cyanosis
❍ Tachycardia, tachypnea

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Patient teaching
Be sure to cover:
❍ administration of cholera vaccine to travelers in en-
demic areas
❍ proper hand-washing technique
❍ need for increased fluid intake.

Discharge planning
❍ Explain the use of oral tetracycline to family mem-
❍ If the doctor orders a cholera vaccine, tell the pa-
tient that he’ll need a booster 3 to 6 months later for
continuing protection.

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Chronic ❍ Signs of uremia

– Fatigue
glomerulonephritis – Loss of appetite
– Nausea
– Peripheral neuropathy
Overview – Pruritus
– Reversal of sleep pattern
– Seizures
Description – Vomiting
❍ A slowly progressive disease characterized by inflam- – Weakness
mation of the glomeruli
❍ Causes sclerosis, scarring, and eventual renal failure Physical assessment
❍ Usually subclinical until the progressive phase be- ❍ Hypertension
gins, marked by proteinuria, cylindruria (presence ❍ Jugular vein distension
of granular tube casts), and hematuria ❍ Pulmonary crackles
❍ Usually irreversible ❍ Mild to severe edema
Pathophysiology Test results
❍ Injury to the kidney reduces the size of the nephron. Laboratory
❍ The glomerular filtration rate decreases. ❍ Proteinuria
❍ The remaining nephron develops hypertrophy and ❍ Hematuria
hyperfiltration. ❍ Cylindruria
❍ Intraglomerular hypertension develops. ❍ Red blood cell casts in urinalysis
❍ Glomerulosclerosis eventually occurs, along with ❍ Increased blood urea nitrogen level
further nephron loss, leading to renal failure. ❍ Increased serum creatinine level
❍ Increased potassium level
Causes ❍ Anemia
❍ Focal glomerulosclerosis Imaging
❍ Goodpasture’s syndrome ❍ X-ray or ultrasound shows smaller kidneys.
❍ Hemolytic uremic syndrome Diagnostic procedures
❍ Lupus erythematosus ❍ Kidney biopsy identifies underlying disease.
❍ Membranoproliferative glomerulonephritis
❍ Membranous glomerulopathy
❍ Poststreptococcal glomerulonephritis Nursing diagnoses
❍ Primary renal disorders
❍ Rapidly progressive glomerulonephritis ❍ Excess fluid volume
❍ Fatigue
Prevalence ❍ Imbalanced nutrition: less than body requirements
❍ Third leading cause of end-stage renal disease in the ❍ Impaired skin integrity
United States ❍ Ineffective tissue perfusion: renal
❍ Risk for infection
❍ Cardiac hypertrophy Key outcomes
❍ End-stage renal failure The patient will:
❍ Heart failure ❍ maintain fluid balance
❍ Metabolic acidosis ❍ report increased comfort
❍ Pericarditis ❍ identify risks that worsen decreased tissue perfusion
❍ Pulmonary edema and modify lifestyle appropriately
❍ Severe anemia ❍ maintain hemodynamic stability
❍ Severe hypertension ❍ avoid or minimize complications
❍ have increased energy and decreased fatigue.

❍ Causative factor General
❍ Possibly no symptoms for many years ❍ Activity as tolerated
❍ Leg cramps ❍ Correction of fluid and electrolyte imbalances
❍ Shortness of breath through restrictions and replacement
❍ Chest pain ❍ Dialysis

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❍ Kidney transplantation
❍ Sodium-restricted, low-protein diet
❍ Symptomatic care
❍ Give drugs as prescribed.
❍ Watch for signs of fluid, electrolyte, and acid-base
❍ Provide skin care (because of pruritus and edema)
and oral hygiene.
❍ Provide emotional support.
Drug therapy
❍ Antibiotics for symptomatic urinary tract infection
❍ Antihypertensives
❍ Diuretics
❍ Daily weight
❍ Evidence of heart failure
❍ Intake and output
❍ Laboratory test results
❍ Vital signs

Patient teaching
Be sure to cover:
❍ disease process, diagnostic tests and procedures,
and treatment plan
❍ the need for low-sodium, high-calorie meals with ad-
equate protein.
❍ prescribed drugs, dosages, and possible adverse ef-
❍ when to contact a doctor
❍ how to assess ankle edema
❍ signs of infection, particularly urinary tract infection,
and the need to avoid contact with infected persons.

Discharge planning
❍ Encourage follow-up examinations to assess renal

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Cirrhosis ❍

Prolonged biliary tract obstruction or inflammation
Viral hepatitis
Early stage
Overview ❍ Abdominal pain
❍ Diarrhea, constipation
❍ Fatigue
Description ❍ Muscle cramps
❍ Chronic hepatic disease ❍ Nausea, vomiting
❍ Several types ❍ Vague signs and symptoms
Later stage
Pathophysiology ❍ Bleeding tendency, such as frequent nosebleeds, easy
❍ Hepatic cells undergo diffuse destruction and bruising, and bleeding gums
fibrotic regeneration. ❍ Chronic dyspepsia
❍ Necrotic tissue yields to fibrosis. ❍ Constipation
❍ Liver structure and vasculature are altered. ❍ Pruritus
❍ Blood and lymph flow are impaired. ❍ Weight loss
❍ Hepatic insufficiency develops.
Physical assessment
Causes ❍ Anemia
❍ Alcoholism ❍ Ascites
❍ Biliary obstruction ❍ Asterixis
❍ Hepatitis ❍ Clubbed fingers
❍ Metabolic disorders ❍ Distended abdominal blood vessels
❍ Toxins ❍ Ecchymosis
Laënnec’s or micronodular cirrhosis ❍ Enlarged spleen
(alcoholic or portal cirrhosis) ❍ Gynecomastia
❍ Chronic alcoholism ❍ Jaundice
❍ Malnutrition ❍ Menstrual irregularities
Postnecrotic or macronodular cirrhosis ❍ Palmar erythema
❍ Complication of viral hepatitis ❍ Palpable, large, firm liver with a sharp edge (early
❍ Possible after exposure to such liver toxins as ar- finding)
senic, carbon tetrachloride, and phosphorus ❍ Slurred speech, paranoia, hallucinations
Biliary cirrhosis ❍ Spider angiomas on the face, neck, arms, and trunk
❍ Prolonged biliary tract obstruction or inflammation ❍ Telangiectasis on the cheeks
Idiopathic cirrhosis (cryptogenic) ❍ Testicular atrophy
❍ No known cause ❍ Thigh and leg edema
❍ Chronic inflammatory bowel disease ❍ Umbilical hernia
❍ Sarcoidosis
Test results
Prevalence Laboratory
❍ Tenth most common cause of death in the United ❍ Increased levels of liver enzymes, such as alanine
States aminotransferase, aspartate aminotransferase, total
❍ Most common among those ages 45 to 75 serum bilirubin, and indirect bilirubin
❍ Occurs in twice as many men as women ❍ Decreased total serum albumin and protein levels
❍ Prolonged prothrombin time
Complications ❍ Decreased serum electrolyte levels, hemoglobin
❍ Bleeding esophageal varices level, and hematocrit
❍ Death ❍ Vitamins A, C, and K deficiency
❍ Hepatic encephalopathy ❍ Increased urine levels of bilirubin and urobilinogen
❍ Hepatorenal syndrome ❍ Decreased fecal urobilinogen levels
❍ Portal hypertension Imaging
❍ Abdominal X-rays show liver and spleen size and
cysts or gas in the biliary tract or liver; liver calcifi-
Assessment cation; and massive ascites.
❍ Computed tomography and liver scans determine liv-
History er size, identify liver masses, and reveal hepatic
❍ Chronic alcoholism blood flow and obstruction.
❍ Exposure to liver toxins such as arsenic and certain ❍ Radioisotope liver scans show liver size, blood flow,
drugs and obstruction.
❍ Malnutrition

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Diagnostic procedures Monitoring

❍ Liver biopsy is the definitive test for cirrhosis, reveal- ❍ Abdominal girth
ing hepatic tissue destruction and fibrosis. ❍ Ammonia level
❍ Esophagogastroduodenoscopy reveals bleeding ❍ Bleeding tendencies
esophageal varices, stomach irritation or ulceration, ❍ Changes in mentation, behavior
and duodenal bleeding and irritation. ❍ Hydration and nutritional status
❍ Laboratory test results
❍ Skin integrity
Nursing diagnoses ❍ Vital signs
❍ Weight
❍ Activity intolerance
❍ Excess fluid volume
❍ Hopelessness Patient teaching
❍ Imbalanced nutrition: less than body requirements
❍ Risk for impaired skin integrity Be sure to cover:
❍ Risk for injury ❍ the disorder, diagnosis, and treatment
❍ over-the-counter medications that may increase
Key outcomes bleeding tendencies
The patient will: ❍ diet modifications
❍ maintain caloric intake, as needed ❍ the need to avoid infections and abstain from alcohol
❍ maintain normal fluid volume ❍ the need to avoid sedatives and acetaminophen
❍ incur no injuries (hepatotoxic)
❍ have no bleeding ❍ the need for a high-calorie diet and small, frequent
❍ maintain intact skin. meals.

Interventions Discharge planning

General ❍ Refer the patient to Alcoholics Anonymous, if appro-
❍ Blood transfusion priate.
❍ Esophageal balloon tamponade ❍ Refer the patient for psychological counseling, if
❍ Frequent rest periods, as needed needed.
❍ High-calorie diet
❍ I.V. fluids
❍ No alcohol intake
❍ Paracentesis
❍ Peritoneovenous shunt, if needed, to divert ascites
into venous circulation
❍ Portal-systemic shunt
❍ Removal or alleviation of underlying cause
❍ Restricted fluid intake
❍ Restricted sodium consumption
❍ Sclerotherapy
❍ Give prescribed I.V. fluids and blood products.
❍ Give prescribed drugs.
❍ Encourage verbalization and provide support.
❍ Provide appropriate skin care.
Drug therapy
❍ Ammonia detoxicant
❍ Antacids
❍ Antiemetics
❍ Beta blockers
❍ Potassium-sparing diuretics
❍ Vasopressin
❍ Vitamin and nutritional supplements

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Crohn’s disease Assessment

Overview ❍ Diarrhea that may worsen after emotional upset or
ingestion of poorly tolerated foods, such as milk, fat-
Description ty foods, and spices
❍ Inflammatory bowel disease that may affect any part ❍ Fatigue and weakness
of the gastrointestinal (GI) tract ❍ Fever, flatulence, nausea
❍ Commonly involves the terminal ileum ❍ Gradual onset of signs and symptoms, marked by pe-
❍ Affects colon and small bowel in 50% of cases; ter- riods of remission and exacerbation
minal ileum in 33%; colon alone in 10% to 20% ❍ Steady, colicky or cramping abdominal pain that
❍ Extends through all layers of the intestinal wall usually occurs in the right lower abdominal quad-
❍ May involve regional lymph nodes and mesentery rant
❍ Weight loss
❍ Crohn’s disease involves slow, progressive inflamma- Physical assessment
tion of the bowel. ❍ Bloody diarrhea
❍ Enlarged lymph nodes cause lymphatic obstruction. ❍ Hyperactive bowel sounds
❍ Edema, mucosal ulceration, fissures, and abscesses ❍ Perianal and rectal abscesses
develop. ❍ Possible abdominal mass, indicating adherent loops
❍ Elevated patches of closely packed lymph follicles of bowel
(Peyer’s patches) develop in the small intestinal ❍ Possible soft or semiliquid stool, usually without
lining. gross blood
❍ Fibrosis thickens the bowel wall and causes stenosis. ❍ Right lower abdominal quadrant tenderness or dis-
❍ Inflamed bowel loops adhere to other diseased or tention
normal loops.
❍ The diseased bowel becomes thicker, shorter, and Test results
narrower. Laboratory
❍ Occult blood in stools
Risk factors ❍ Decreased hemoglobin level and hematocrit
❍ History of allergies ❍ Increased white blood cell count and erythrocyte
❍ Immune disorders sedimentation rate
❍ Genetic predisposition ❍ Decreased serum potassium, calcium, and magne-
– One or more affected relatives in 10% to 20% of sium levels
patients with the disease ❍ Hypoglobulinemia from intestinal protein loss
– Sometimes occurs in monozygotic twins ❍ Vitamin B12 and folate deficiency
Causes ❍ Small bowel X-rays may show irregular mucosa, ul-
❍ Exact cause unknown ceration, and stiffening.
❍ Lymphatic obstruction and infection among con- ❍ Barium enema reveals the string sign (segments of
tributing factors stricture separated by normal bowel) and may also
show fissures and narrowing of the lumen.
Prevalence Diagnostic procedures
❍ Occurs equally in males and females ❍ Sigmoidoscopy and colonoscopy show patchy areas
❍ More common in Jewish people of inflammation and may also reveal the characteris-
❍ Onset usually before age 30 tic coarse irregularity (cobblestone appearance) of
the mucosal surface.
Complications ❍ Biopsy reveals granulomas in up to half of speci-
❍ Anal fistula mens.
❍ Fistulas of the bladder or vagina or to the skin in an
old scar area
❍ Intestinal obstruction Nursing diagnoses
❍ Nutritional deficiencies caused by malabsorption and
maldigestion ❍ Chronic pain
❍ Perforation ❍ Deficient knowledge (Crohn’s disease)
❍ Perineal abscess ❍ Diarrhea
❍ Disturbed body image
❍ Imbalanced nutrition: less than body requirements
❍ Ineffective coping

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❍ Ineffective tissue perfusion: GI

❍ Risk for deficient fluid volume
Patient teaching
❍ Risk for impaired skin integrity
Be sure to cover:
Key outcomes ❍ information about the disease, symptoms, and com-
The patient will: plications
❍ maintain adequate caloric intake ❍ ordered diagnostic tests and pretest guidelines
❍ maintain normal fluid volume ❍ the importance of adequate rest
❍ regain normal bowel movements ❍ ways to identify and reduce sources of stress
❍ verbalize understanding of the disease process and ❍ prescribed diet changes
treatment regimen ❍ prescribed drugs, dosages, and possible adverse re-
❍ use adequate coping mechanisms and seek appro- actions.
priate sources of support
❍ express feelings of comfort.
Discharge planning
Interventions ❍ Refer the patient to a smoking-cessation program, if
General ❍ Refer the patient to an enterostomal therapist, if
❍ Adequate caloric, protein, and vitamin intake indicated.
❍ Avoidance of foods that worsen diarrhea
❍ Avoidance of raw fruits and vegetables if blockage
❍ Colectomy with ileostomy
❍ Parenteral nutrition, if needed
❍ Reduced physical activity
❍ Stress reduction
❍ Provide emotional support to the patient and family.
❍ Provide meticulous skin care after each bowel move-
❍ Schedule patient care to include rest periods
throughout the day.
❍ Assist with diet modification.
❍ Give prescribed iron supplements and blood transfu-
❍ Give prescribed analgesics.
Drug therapy
❍ Antibacterial and antiprotozoal drugs
❍ Antidiarrheals
❍ Anti-inflammatory drugs
❍ Antispasmodics
❍ Corticosteroids
❍ Immunosuppressants
❍ Opioids
❍ Sulfonamides
❍ Vitamin supplements
❍ Abdominal pain and distention
❍ Bleeding, especially with corticosteroid use
❍ Daily weight
❍ Intake and output, including amount of stool
❍ Serum electrolyte, glucose, and hemoglobin levels,
and stools for occult blood
❍ Signs of infection or obstruction
❍ Vital signs

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Cushing’s syndrome Assessment

Overview ❍ Amenorrhea
❍ Decreased libido
Description ❍ Fatigue
❍ Evidence of glucocorticoid excess, particularly cor- ❍ Frequent infections
tisol ❍ Headache
❍ May also reflect excess secretion of mineralocorti- ❍ Impotence
coids and androgens ❍ Irritability; emotional instability
❍ Classified as primary, secondary, or iatrogenic, de- ❍ Muscle weakness
pending on etiology ❍ Polyuria
❍ Prognosis dependent on early diagnosis, identifica- ❍ Sleep disturbances
tion of underlying cause, and effective treatment ❍ Symptoms resembling those of hyperglycemia
❍ Thirst
Pathophysiology ❍ Use of synthetic corticosteroids
❍ Normal feedback inhibition by cortisol is lost. ❍ Water retention
❍ Elevated cortisol levels don’t suppress hypothalamic
and anterior pituitary secretion of corticotropin Physical assessment
releasing hormone and adrenocorticotropic hor- ❍ Acne
mone (ACTH). ❍ Buffalo hump
❍ The result is excessive levels of circulating cortisol. ❍ Central obesity
❍ Delayed wound healing
Causes ❍ Hirsutism
❍ Corticotropin-producing tumor in another organ ❍ Hypertension
❍ Cortisol-secreting adrenal tumor ❍ Moon-shaped face
❍ Excess production of corticotropin ❍ Muscle wasting and weakness
❍ Long-term use of synthetic glucocorticoids or corti- ❍ Petechiae, ecchymoses, and purplish striae
cotropin ❍ Swollen ankles
❍ Pituitary microadenoma ❍ Thin hair
❍ Thin limbs
AGE AWARE In neonates, the usual cause of
Cushing’s syndrome is adrenal carcinoma. Test results
Prevalence ❍ Increased salivary free cortisol level
❍ More common in females than males ❍ Decreased ACTH level in adrenal disease; increased
❍ Can affect a person at any age ACTH level with excessive pituitary or ectopic secre-
Complications ❍ Hypernatremia
❍ Diabetes mellitus ❍ Hypokalemia
❍ Dyslipidemia ❍ Hypocalcemia
❍ Frequent infections ❍ Increased blood glucose level
❍ Heart failure ❍ Increased free cortisol level in urine
❍ Hypertension ❍ Increased serum cortisol level in the morning
❍ Impaired glucose tolerance ❍ Glycosuria
❍ Ischemic heart disease Imaging
❍ Menstrual disturbances ❍ Ultrasonography, computed tomography scan, and
❍ Osteoporosis and pathologic fractures magnetic resonance imaging may show the location
❍ Peptic ulcer of a pituitary or adrenal tumor.
❍ Psychiatric problems ranging from mood swings to Diagnostic procedures
psychosis ❍ A low-dose dexamethasone suppression test shows
❍ Sexual dysfunction that plasma cortisol levels aren't suppressed.
❍ Slow wound healing
❍ Suppressed inflammatory response
Nursing diagnoses
❍ Activity intolerance
❍ Deficient knowledge (Cushing’s syndrome)

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❍ Disturbed body image A LERT Giving glucocorticoids on the morning

❍ Excess fluid volume of surgery can help prevent acute adrenal in-
❍ Impaired skin integrity sufficiency during surgery. Cortisol therapy is essen-
❍ Ineffective coping tial during and after surgery to help the patient toler-
❍ Risk for infection ate the physiologic stress caused by removal of the
pituitary or adrenal glands.
Key outcomes
The patient will: Monitoring
❍ maintain skin integrity ❍ Daily weights
❍ remain free from infection ❍ Intake and output
❍ perform activities of daily living as tolerated within ❍ Serum electrolyte results
the confines of the disorder ❍ Vital signs
❍ express positive feelings about self After bilateral adrenalectomy and
❍ express understanding of disorder. hypophysectomy
❍ Adrenal hypofunction
❍ Bowel sounds
Interventions ❍ Hemorrhage and shock
❍ Hypopituitarism
General ❍ Increased ICP
❍ Management to restore hormone balance and re- ❍ Neurologic and behavioral status
verse Cushing’s syndrome, including radiation, drug ❍ Severe nausea, vomiting, and diarrhea
therapy, or surgery ❍ Transient diabetes insipidus
❍ High-protein, high-potassium, low-calorie, low- After hypophysectomy with transsphenoidal
sodium diet approach
❍ Activity, as tolerated ❍ Cerebrospinal fluid leak
❍ Possible hypophysectomy or pituitary irradiation
❍ Bilateral adrenalectomy
❍ Excision of nonendocrine, corticotropin-producing Patient teaching
tumor, followed by drug therapy
Be sure to cover:
Nursing ❍ the disorder, diagnosis, and treatment
❍ Give prescribed drugs. ❍ prescribed drugs, dosages, and potential adverse re-
❍ Consult a dietitian. actions
❍ Apply protective measures to reduce the patient's ❍ when to contact a doctor
risk of infection. ❍ lifelong corticosteroid replacement
❍ Use meticulous hand-washing technique. ❍ signs and symptoms of adrenal crisis
❍ Schedule adequate rest periods. ❍ the need for medical identification
❍ Institute safety precautions. ❍ prevention of infection
❍ Provide meticulous skin care. ❍ stress reduction strategies.
❍ Encourage verbalization of feelings.
❍ Offer emotional support.
❍ Help the patient develop effective coping strategies. Discharge planning
After hypophysectomy with transsphenoidal
approach ❍ Refer the patient to a mental health professional for
❍ Keep the head of the bed elevated at least 30 de- additional counseling, if needed.
❍ Maintain nasal packing.
❍ Provide frequent mouth care.
❍ Avoid activities that increase intracranial pressure
Drug therapy
❍ Aminoglutethimide
❍ Antifungals
❍ Antihypertensives
❍ Antineoplastic antihormone drugs
❍ Diuretics
❍ Glucocorticoids
❍ Potassium supplements

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Cystic fibrosis ❍ Arthritis
❍ Atelectasis
Overview ❍

Azoospermia in males
Biliary disease
❍ Bronchiectasis
Description ❍ Cardiac arrhythmias
❍ Chronic, progressive, inherited, incurable disease ❍ Clotting problems
affecting exocrine (mucus-secreting) glands ❍ Cor pulmonale
❍ Transmitted as an autosomal recessive trait ❍ Death
❍ Genetic mutation that involves chloride transport ❍ Dehydration
across epithelial membranes (more than 100 muta- ❍ Delayed sexual development
tions of the gene identified) ❍ Diabetes
❍ Characterized by major aberrations in sweat gland, ❍ Distal intestinal obstructive syndrome
respiratory, and gastrointestinal (GI) functions ❍ Electrolyte imbalances
❍ Accounts for almost all cases of pancreatic enzyme ❍ Gastroesophageal reflux
deficiency in children ❍ Hepatic disease
❍ May be apparent soon after birth or take years to de- ❍ Malnutrition
velop ❍ Pneumonia
❍ Death typically from pneumonia, emphysema, or at- ❍ Potentially fatal shock
electasis ❍ Retarded bone growth
❍ Secondary amenorrhea in females
❍ Viscosity of bronchial, pancreatic, and other mucous
gland secretions increases, obstructing glandular Assessment
❍ Accumulation of tenacious secretions in bronchioles History
and alveoli causes respiratory changes and eventual- ❍ Abdominal distention, vomiting, constipation
ly severe atelectasis and emphysema. ❍ Dry, nonproductive cough
❍ Disease also causes characteristic GI effects in the ❍ Frequent, bulky, foul-smelling, and pale stool with a
intestines, pancreas, and liver. high fat content
❍ Obstruction of pancreatic ducts causes trypsin, amy- ❍ Hematemesis
lase, and lipase deficiency, which prevents conver- ❍ Nasal polyps and sinusitis
sion and absorption of fat and protein in the intesti- ❍ Poor growth
nal tract and interferes with the digestion of food and ❍ Poor weight gain
absorption of fat-soluble vitamins. ❍ Ravenous appetite
❍ In the pancreas, fibrotic tissue, multiple cysts, thick ❍ Recurring bronchitis and pneumonia
mucus, and fat replace the acini, producing signs of ❍ Shortness of breath
pancreatic insufficiency. ❍ Wheezing
Causes AGE AWARE Neonates may have meconium
ileus and symptoms of intestinal obstruction:
❍ Autosomal recessive mutation of gene on chromo-
abdominal distention, vomiting, constipation, dehy-
some 7
dration, and electrolyte imbalance.
❍ Causes of symptoms: increased viscosity of
bronchial, pancreatic, and other mucous gland se-
cretions and consequent destruction of glandular Physical assessment
ducts ❍ Barrel chest
❍ Bibasilar crackles and hyperresonance
Prevalence ❍ Cyanosis
❍ Most common fatal genetic disease of white children ❍ Clubbing of fingers and toes
❍ Twenty-five percent chance of transmission with each ❍ Delayed sexual development
pregnancy when both parents are carriers of the re- ❍ Distended abdomen
cessive gene ❍ Dry, nonproductive, paroxysmal cough
❍ Highest occurrence in people of northern European ❍ Dyspnea
ancestry ❍ Failure to thrive
❍ Less common in Blacks, Native Americans, and peo- ❍ Hepatomegaly
ple of Asian ancestry ❍ Neonatal jaundice
❍ Equally common in both sexes ❍ Rectal prolapse
❍ Sallow skin with poor turgor
❍ Tachypnea

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❍ Thin limbs ❍ Activity, as tolerated

❍ Wheezy respirations ❍ Heart-lung transplantation
Test results Nursing
Laboratory ❍ Give prescribed drugs.
❍ Absence of trypsin in stool specimen ❍ Give pancreatic enzymes with meals and snacks.
❍ Delta F 508 deletion in deoxyribonucleic acid tests ❍ Perform chest physiotherapy and postural drainage.
❍ Possible hepatic insufficiency in liver enzyme tests ❍ Give oxygen therapy, as needed.
❍ Possible organisms — such as Pseudomonas and ❍ Provide a well-balanced, high-calorie, high-protein
Staphylococcus — in sputum cultures diet; include adequate fats.
❍ Decreased serum albumin level ❍ Provide vitamin A, D, E, and K supplements, if indi-
❍ Possible hypochloremia cated.
❍ Possible hyponatremia ❍ Ensure adequate oral fluid intake.
❍ Hypoxemia in arterial blood gas studies ❍ Provide exercise and activity periods.
Imaging ❍ Encourage breathing exercises.
❍ Chest X-rays may show early signs of lung obstruction. ❍ Provide a young child with play periods.
❍ High-resolution chest computed tomography scan ❍ Enlist the help of physical and play therapists, if
shows bronchial wall thickening, cystic lesions, and available.
bronchiectasis. ❍ Provide emotional support.
Diagnostic procedures ❍ Include family members in all phases of the child’s
❍ Sweat tests using pilocarpine solution show positive care.
results — increased sodium or chloride levels.
❍ Pulmonary function tests show decreased vital ca- Drug therapy
pacity, elevated residual volume, and decreased ❍ Antibiotics
forced expiratory volume in 1 second. ❍ Bronchodilators
❍ Dornase alfa, a pulmonary enzyme given by aerosol
Nursing diagnoses ❍ Oral pancreatic enzymes
❍ Oxygen therapy, as needed
❍ Anxiety ❍ Prednisone
❍ Deficient knowledge (cystic fibrosis) ❍ Vitamin A, D, E, and K supplements
❍ Disabled family coping
❍ Imbalanced nutrition: less than body requirements Monitoring
❍ Impaired gas exchange ❍ Daily weight
❍ Ineffective airway clearance ❍ Hydration
❍ Ineffective breathing patterns ❍ Intake and output
❍ Ineffective tissue perfusion: cardiopulmonary ❍ Pulse oximetry
❍ Risk for deficient fluid volume ❍ Respiratory status
❍ Vital signs
Key outcomes
The patient will:
❍ maintain a patent airway and adequate ventilation Patient teaching
❍ consume adequate calories daily
❍ use a support system to assist with coping Be sure to cover:
❍ express an understanding of the illness ❍ the disorder, diagnosis, and treatment
❍ maintain fluid balance. ❍ drugs and potential adverse reactions
❍ when to contact a doctor
❍ aerosol therapy
Interventions ❍ chest physiotherapy
❍ evidence of infection
General ❍ complications.
❍ Based on organ systems involved
❍ Chest physiotherapy, nebulization, and breathing ex-
ercises several times daily Discharge planning
❍ Postural drainage
❍ Gene therapy (experimental) ❍ Refer family members for genetic counseling, as ap-
❍ Annual influenza vaccination propriate.
❍ Salt supplements ❍ Refer patient and family to a local support group,
❍ High-fat, high-protein, high-calorie diet such as the Cystic Fibrosis Foundation.

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Physical assessment
Cystinuria ❍ Hematuria
❍ Tenderness in the costovertebral angle or over the
Overview kidneys
Test results
Description Laboratory
❍ An autosomal recessive disorder ❍ Cystine crystals in calculi
❍ An inborn error of amino acid transport in the kid- ❍ Hexagonal, flat cystine crystals in urine, visible by
neys and intestine that allows excessive urinary ex- microscope
cretion of cystine and other dibasic amino acids ❍ Cystine crystals that resemble benzene rings when
❍ Causes recurrent cystine renal calculi glacial acetic acid is added to chilled urine
❍ The most common defect of amino acid transport ❍ Increased serum white blood cell count
❍ Good prognosis with proper treatment ❍ Increased clearance of cystine, lysine, arginine, and
Pathophysiology ❍ Aminoaciduria with cystine, lysine, arginine, and or-
❍ Impaired renal tubular reabsorption of dibasic nithine
amino acids (cystine, lysine, arginine, and ornithine) ❍ Usually a urine pH less than 5
results in excessive amino acid concentration and ❍ Positive cyanide-nitroprusside test
excretion in the urine. Imaging
❍ Cystine concentration exceeds its solubility and pre- ❍ Kidney-ureter-bladder X-rays determine the size and
cipitates and forms crystals, precursors of cystine location of calculi.
calculi. Diagnostic procedures
❍ Excretory urography determines renal function.
❍ Inherited as an autosomal recessive defect
Nursing diagnoses
❍ About 1 in 15,000 live births ❍ Acute pain
❍ More prevalent in persons of short stature, for un- ❍ Deficient knowledge (cystinuria)
known reasons ❍ Impaired urinary elimination
❍ Affects both sexes ❍ Risk for infection
❍ More severe in males
Key outcomes
Complications The patient will:
❍ Obstruction and destruction of kidney and ureter ❍ maintain urine specific gravity within designated
tissue limits
❍ report increased comfort
❍ identify risk factors that worsen decreased tissue
Assessment perfusion, and modify lifestyle accordingly
❍ avoid or minimize complications.
AGE AWARE The effects of cystinuria result
from cystine or mixed cystine calculi, which
typically develop between ages 10 and 30. Interventions
History General
❍ Abdominal distention ❍ Increasing fluid intake to maintain a minimum
❍ Dull flank pain 24-hour urine volume of 4,000 ml (5,000 to
❍ Family history of renal disease or calculi 7,000 ml is optimal)
❍ Nausea ❍ Alkaline-ash diet (high in vegetables and fruit, low in
❍ Signs of secondary infection protein) to alkalinize urine, increasing cystine solu-
– Chills bility, although this may increase the risk of calcium
– Fever phosphate calculi
– Burning, itching, or pain on urination ❍ Surgical removal of calculi
– Urinary frequency
– Foul-smelling urine Nursing
❍ Vomiting ❍ Give prescribed drugs.
❍ Encourage increased oral fluid intake.
❍ Provide emotional support.

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Drug therapy
❍ Antibiotics for secondary infection
❍ Penicillamine (cautiously, because of toxic adverse
effects and risk of allergic reaction)
❍ Sodium bicarbonate
❍ Intake and output
❍ Serum bicarbonate level
❍ Signs of infection
❍ Urine pH

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ the need to maintain increased, evenly spaced fluid
intake, even through the night
❍ signs of renal calculi and urinary tract infection
❍ prescribed drugs, dosages, and possible adverse ef-

Discharge planning
❍ Refer the patient to a nephrologist for follow-up

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Diabetes insipidus ❍

❍ Hypovolemia
Overview ❍ Loss of consciousness

Description Assessment
❍ Disorder of water balance regulation characterized
by excessive fluid intake and hypotonic polyuria History
❍ Failure of vasopressin secretion in response to nor- ❍ Abrupt onset of extreme polyuria
mal physiologic stimuli ❍ Extreme thirst
❍ Two types: primary and secondary ❍ Extraordinarily large oral fluid intake
❍ May occur only during pregnancy, usually after the ❍ Weight loss
fifth or sixth month of gestation ❍ Dizziness, weakness, fatigue
❍ Good prognosis if uncomplicated ❍ Constipation
❍ Variable prognosis if complicated by underlying dis- ❍ Nocturia
order, such as cancer
AGE AWARE In children, reports of enuresis,
❍ Increased risk of complications with impaired or ab-
sleep disturbances, irritability, anorexia, thirst,
sent thirst mechanism
and decreased weight gain and linear growth are
Pathophysiology common.
❍ Vasopressin (antidiuretic hormone) is synthesized in
the hypothalamus and stored by the posterior pitu- Physical assessment
itary gland. ❍ Decreased muscle strength
❍ Once released into the general circulation, vaso- ❍ Dyspnea
pressin acts on the distal and collecting tubules of ❍ Fever
the kidneys. ❍ Hypotension
❍ Vasopressin increases permeability of the tubules to ❍ Pale, voluminous urine
water and causes water reabsorption. ❍ Poor skin turgor
❍ Absence of vasopressin allows filtered water to be ❍ Signs of dehydration
excreted in the urine instead of being reabsorbed. ❍ Tachycardia
Causes Test results
❍ Certain drugs, such as lithium Laboratory
❍ Congenital malformation of the central nervous sys- ❍ Colorless urine with low osmolality and specific
tem (CNS) gravity
❍ Damage to hypothalamus or pituitary gland ❍ Increased serum sodium level
❍ Failure of the kidneys to respond to vasopressin, ❍ Increased serum osmolality
called nephrogenic diabetes insipidus (DI) ❍ Decreased serum vasopressin level
❍ Familial ❍ Decreased specific gravity and increased volume in
❍ Granulomatous disease 24-hour urine test
❍ Idiopathic ❍ Increased blood urea nitrogen (BUN) and creatinine
❍ Infection levels
❍ Neurosurgery, skull fracture, or head trauma Diagnostic procedures
❍ Pregnancy (gestational DI) ❍ Dehydration test or water deprivation test shows an
❍ Psychogenic increase in urine osmolality exceeding 9% after va-
❍ Trauma sopressin administration.
❍ Tumors
❍ Vascular lesions
Nursing diagnoses
❍ Affects men and women equally ❍ Deficient fluid volume
❍ Primary DI in 50% of patients ❍ Deficient knowledge (diabetes insipidus)
❍ Delayed growth and development
Complications ❍ Fear
❍ Bladder distention ❍ Impaired oral mucous membrane
❍ Circulatory collapse ❍ Impaired urinary elimination
❍ CNS changes ❍ Ineffective coping
❍ Hydronephrosis

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Key outcomes ❍ intake and output

The patient will: ❍ use of a hydrometer to measure urine specific gravity
❍ demonstrate balanced fluid volume ❍ need for medical identification
❍ display adaptive coping behaviors ❍ need for ongoing medical care.
❍ avoid complications
❍ have normal laboratory test results.
Discharge planning
Interventions ❍ Refer the patient to a mental health professional for
additional counseling as indicated.
❍ Identification and treatment of underlying cause
❍ Control of fluid balance
❍ Dehydration prevention
❍ Free access to oral fluids
❍ With nephrogenic DI, low-sodium diet
❍ Give prescribed drugs.
❍ Provide meticulous skin and mouth care.
❍ Encourage verbalization of feelings.
❍ Offer encouragement while providing a realistic as-
sessment of the situation.
❍ Help the patient develop effective coping strategies.
A LERT Use caution when giving vasopressin
to a patient with coronary artery disease
because it can cause coronary artery constriction.

Drug therapy
❍ I.V. fluids
– Dextrose 5% in water if serum sodium level
exceeds 150 mEq/L
– Normal saline solution if serum sodium level is
less than 150 mEq/L
❍ Synthetic vasopressin analogue
❍ Thiazide diuretics in nephrogenic DI
❍ Vasopressin
❍ Vasopressin stimulant

❍ Cardiac rhythm
❍ Daily weight
❍ Evidence of hypovolemic shock
❍ Intake and output
❍ Mental or neurologic status
❍ Serum electrolyte and BUN levels
❍ Urine specific gravity
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ drugs, dosages, and possible adverse reactions
❍ when to contact a doctor
❍ evidence of dehydration
❍ daily weight

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Diabetes mellitus ❍

Impaired resistance to infection
❍ Nephropathy
Overview ❍

Peripheral vascular disease
Retinopathy, blindness
Description AGE AWARE If a diabetic mother's glucose
levels aren't well controlled before and during
❍ Chronic disease of absolute or relative insulin defi-
pregnancy, her neonate has two to three times the
ciency or resistance
risk of congenital malformations and fetal distress.
❍ Characterized by disturbances in carbohydrate, pro-
tein, and fat metabolism
❍ Two primary forms Assessment
– Type 1, characterized by absolute insufficiency
– Type 2, characterized by insulin resistance with
varying degrees of insulin secretory defects History
❍ Dehydration
Pathophysiology ❍ Dry, itchy skin
❍ The effects of diabetes mellitus result from insulin ❍ Dry mucous membranes
deficiency or resistance to endogenous insulin. ❍ Frequent skin and urinary tract infections
❍ Insulin allows glucose transport into the cells for use ❍ Nocturnal diarrhea
as energy or storage as glycogen. ❍ Numbness or pain in hands or feet
❍ Insulin also stimulates protein synthesis and free fat- ❍ Polydipsia
ty acid storage in adipose tissue. ❍ Polyuria, nocturia
❍ Insulin deficiency compromises the body's access to ❍ Poor skin turgor
essential nutrients for fuel and storage. ❍ Postprandial feeling of nausea or fullness
❍ Sexual problems
Risk factors ❍ Weakness, fatigue
❍ Certain drugs ❍ Weight loss and hunger
– Adrenal corticosteroids ❍ Vision changes
– Hormonal contraceptives Type 1
– Thiazide diuretics ❍ Rapidly developing symptoms
❍ Obesity (type 2) Type 2
❍ Physiologic or emotional stress ❍ Family history of diabetes mellitus
❍ Pregnancy ❍ Other endocrine diseases
❍ Sedentary lifestyle (type 2) ❍ Pregnancy
❍ Viral infection (type 1) ❍ Recent stress or trauma
❍ Severe viral infection
Causes ❍ Use of drugs that increase blood glucose levels
❍ Autoimmune disease (type 1) ❍ Vague, long-standing symptoms that develop
❍ Genetic factors gradually
Prevalence Physical assessment
Type 1 ❍ Characteristic “fruity” breath odor in ketoacidosis
❍ Usually occurs before age 30, although it may occur ❍ Cool skin temperature
at any age ❍ Decreased peripheral pulses
❍ More common in men ❍ Diminished deep tendon reflexes
Type 2 ❍ Dry mucous membranes
❍ Occurrence increases with age ❍ Muscle wasting and loss of subcutaneous fat (type 1)
❍ Usually occurs in obese adults older than age 30, al- ❍ Obesity, particularly in the abdominal area (type 2)
though it may occur in obese North American youths ❍ Orthostatic hypotension
of African-American, Native American, or Hispanic ❍ Poor skin turgor
descent ❍ Possible hypovolemia and shock in ketoacidosis and
❍ Affects about 8% of the United States' population hyperosmolar hyperglycemic state
❍ About one-third of patients undiagnosed ❍ Retinopathy or cataract formation
❍ Skin changes, especially on the legs and feet
❍ Cardiovascular disease Test results
❍ Cognitive dysfunction Laboratory
❍ Diabetic dermopathy ❍ Fasting plasma glucose level greater than or equal to
❍ Hyperosmolar, hyperglycemic syndrome 126 mg/dl on at least two occasions

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❍ Random blood glucose level greater than or equal to ❍ Offer emotional support.
200 mg/dl ❍ Help to develop effective coping strategies.
❍ Two-hour postprandial blood glucose level greater
than or equal to 200 mg/dl Drug therapy
❍ Increased glycosylated hemoglobin level ❍ Exogenous insulin (type 1 or possibly type 2)
❍ Possible acetone or glucose in urine ❍ Oral antihyperglycemics (type 2)
Diagnostic procedures
❍ Ophthalmic examination may show diabetic Monitoring
retinopathy. ❍ Cardiovascular status
❍ Daily weight
❍ Intake and output
Nursing diagnoses ❍ Renal status
❍ Serum glucose
❍ Deficient fluid volume ❍ Signs and symptoms of developing problems
❍ Imbalanced nutrition: less than body requirements – Hypoglycemia
❍ Imbalanced nutrition: more than body requirements – Hyperglycemia
❍ Impaired skin integrity – Hyperosmolar coma
❍ Ineffective coping – Urinary tract and vaginal infections
❍ Ineffective tissue perfusion: renal, cardiovascular, – Diabetic neuropathy
peripheral ❍ Urine acetone
❍ Risk for infection ❍ Vital signs
❍ Sexual dysfunction
Key outcomes Patient teaching
The patient will:
❍ maintain optimal body weight Be sure to cover:
❍ remain free from infection ❍ the disorder, diagnosis, and treatment
❍ avoid complications ❍ prescribed drugs, dosages, and possible adverse re-
❍ verbalize understanding of the disorder and treat- actions
ment ❍ methods of administering drugs
❍ demonstrate adaptive coping behaviors. ❍ when to contact a doctor
❍ prescribed meal plan
❍ prescribed exercise program
Interventions ❍ signs and symptoms of problems
– infection
General – hypoglycemia
❍ American Diabetes Association recommendations to – hyperglycemia
reach target glucose, glycosylated hemoglobin, lipid, – diabetic neuropathy
and blood pressure levels ❍ self-monitoring of blood glucose level
❍ Exercise and diet control ❍ complications of hyperglycemia
❍ Modest calorie restriction for weight loss or mainte- ❍ foot care
nance ❍ annual ophthalmologic examinations
❍ Pancreas transplantation ❍ safety precautions
❍ Regular aerobic exercise ❍ management of diabetes during illness.
❍ Tight glycemic control to prevent complications
Nursing Discharge planning
❍ Give prescribed drugs.
❍ Give rapidly absorbed carbohydrates for hypo- ❍ Refer the patient to a dietitian.
glycemia or, if the patient is unconscious, glucagon ❍ Refer the patient to a podiatrist if needed.
or I.V. dextrose, as ordered. ❍ Refer the patient to an ophthalmologist.
❍ Give I.V. fluids and insulin replacement for hyper- ❍ Refer an adult diabetic patient who is planning a
glycemic crisis, as ordered. family for preconception counseling.
❍ Provide meticulous skin care, especially to the feet ❍ Refer the patient to the Juvenile Diabetes Research
and legs. Foundation, the American Association of Diabetes
❍ Treat all injuries, cuts, and blisters immediately. Educators, and the American Diabetes Association to
❍ Avoid constricting hose, slippers, or bed linens. obtain additional information.
❍ Encourage adequate fluid intake.
❍ Encourage verbalization of feelings.

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Physical assessment
Diabetic ketoacidosis ❍ Acetone breath
❍ Evidence of acidosis
Overview – Abdominal pain
– Altered level of consciousness
– Shallow rapid breathing (Kussmaul's respirations)
Description ❍ Evidence of dehydration
❍ Acute complication of diabetes mellitus
❍ Life-threatening Test results
❍ Increased serum ketone and blood glucose levels Laboratory
❍ Decreased serum pH (below 7.2) ❍ Glucose and ketones in urine
❍ Blood glucose level higher than 250 mg/dl
Pathophysiology ❍ Ketones in serum
❍ Absolute or relative insulin deficiency causes an in- ❍ Metabolic acidosis
crease in counter-regulatory hormones. ❍ Increased serum potassium level
❍ Hepatic glyconeogenesis, glycogenolysis, and lipoly- ❍ Decreased serum sodium, chloride, and phosphorus
sis occurs, causing hyperglycemia and an increase in levels
serum free fatty acids. ❍ Increased white blood cell count (even without in-
❍ Ketonemia and ketonuria occur, resulting in meta- fection)
bolic acidosis and osmotic diuresis. Diagnostic procedures
❍ Hypoglycemia may then occur. ❍ Electrocardiography may show T-wave changes that
reflect disturbed potassium levels.
❍ Uncontrolled type 1 diabetes mellitus
– New diagnosis Nursing diagnoses
– Noncompliance
– Concurrent illness ❍ Deficient fluid volume
– Medication ❍ Deficient knowledge (diabetes mellitus and diabetic
– Stress (physical or psychological) ketoacidosis)
– Idiopathic ❍ Imbalanced nutrition: less than body requirements
❍ Occasionally uncontrolled type 2 diabetes mellitus ❍ Impaired gas exchange
❍ Ineffective coping
Prevalence ❍ Ineffective tissue perfusion: renal, cardiovascular,
❍ Accounts for 50% of diabetes-related hospital admis- peripheral
sions in young people
❍ Exact prevalence unknown Key outcomes
❍ More common among Whites, as is diabetes mellitus The patient will:
❍ Affects women slightly more than men ❍ have adequate respirations and ventilation
❍ be hemodynamically stable
AGE AWARE Diabetic ketoacidosis occurs ❍ remain free from infection
more often in children and adolescents than in
❍ avoid complications
❍ verbalize understanding of the disorder and treat-
Complications ment
❍ demonstrate adaptive coping behaviors.
❍ Cardiac arrhythmia
❍ Cerebral edema
❍ Hypoglycemia Interventions
❍ Myocardial infarction
❍ Pulmonary edema General
❍ Serial laboratory tests and arterial blood gas (ABG)
Assessment ❍ Adequate oxygenation
❍ I.V. fluids
❍ Fatigue Nursing
❍ Increased thirst ❍ Give prescribed drugs.
❍ Increased urination ❍ Give oxygen as ordered.
❍ Nausea ❍ Evaluate respiratory and neurologic status continu-
❍ Possible history of diabetes mellitus ously.
❍ Vomiting

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❍ Provide emotional support.

❍ Encourage compliance with treatment program.
Drug therapy
❍ Antibiotics (if infection present)
❍ Correction of electrolyte imbalances
❍ Insulin
❍ Sodium bicarbonate
❍ ABG analysis
❍ Cardiac rhythm
❍ Intake and output
❍ Laboratory test results
❍ Neurologic status
❍ Respiratory status
❍ Serial blood glucose levels
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ prescribed drugs, dosages, and possible adverse ef-
❍ signs of hyperglycemia and hypoglycemia and effec-
tive immediate treatment
❍ when to contact a doctor or seek medical attention
❍ how to test blood glucose levels at home.

Discharge planning
❍ Refer the patient to a diabetic teaching class for
more information.
❍ Refer the patient to the Juvenile Diabetes Research
Foundation, the American Association of Diabetes
Educators, and the American Diabetes Association to
obtain additional information.

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Disseminated Assessment
intravascular History
coagulation ❍ Abnormal bleeding (possibly at all body orifices)
without a history of a serious hemorrhagic disorder
❍ Possible bleeding from surgical or invasive proce-
Overview ❍
dure sites, such as incisions or venipuncture sites
Possible gastrointestinal (GI) bleeding, hematuria
❍ Possible nausea and vomiting; severe muscle, back,
Description and abdominal pain; chest pain; hemoptysis; epi-
❍ Syndrome of activated coagulation characterized by staxis; seizures; and oliguria
bleeding or thrombosis ❍ Possible presence of a disorder that causes DIC
❍ Complicates diseases and conditions that accelerate ❍ Possible signs of bleeding into the skin, such as cu-
clotting taneous oozing, petechiae, ecchymoses, or hema-
– occlusion of small blood vessels tomas
– organ necrosis
– depletion of circulating clotting factors and Physical assessment
platelets ❍ Acrocyanosis
– activation of the fibrinolytic system ❍ Dyspnea, tachypnea
❍ Also known as DIC, consumption coagulopathy, and ❍ Mental status changes, including confusion
defibrination syndrome ❍ Petechiae
Pathophysiology Test results
❍ Typical accelerated clotting results in generalized ac- Laboratory
tivation of prothrombin and a consequent excess of ❍ Decreased serum platelet count (less than
thrombin. 150,000/mm3)
❍ Excess thrombin converts fibrinogen to fibrin, pro- ❍ Decreased serum fibrinogen level (less than
ducing fibrin clots in the microcirculation. 170 mg/dl)
❍ This process consumes exorbitant amounts of coag- ❍ Prolonged prothrombin time (more than 19 sec-
ulation factors (especially platelets, factor V, pro- onds)
thrombin, fibrinogen, and factor VIII), causing ❍ Prolonged activated partial thromboplastin time
thrombocytopenia, deficiencies in factors V and VIII, (more than 40 seconds)
hypoprothrombinemia, and hypofibrinogenemia. ❍ Increased FDPs (commonly greater than 45 mcg/ml,
❍ Circulating thrombin activates the fibrinolytic system, or positive at less than 1:100 dilution)
which lyses fibrin clots into fibrinogen degradation ❍ Positive D-dimer test (specific fibrinogen test for
products (FDPs). DIC) at less than 1:8 dilution
❍ The hemorrhage that occurs may result largely from ❍ Prolonged thrombin time
the anticoagulant activity of FDPs and depletion of ❍ Decreased levels of blood clotting factors V and VIII
plasma coagulation factors. ❍ Decreased hemoglobin levels (less than 10 g/dl)
❍ Increased levels of blood urea nitrogen (greater
Causes than 25 mg/dl) and serum creatinine (greater than
❍ Disorders that produce necrosis, such as extensive 1.3 mg/dl)
burns and trauma
❍ Infection, sepsis
❍ Neoplastic disease Nursing diagnoses
❍ Obstetric complications
❍ Other disorders, such as acute respiratory distress ❍ Acute pain
syndrome, cardiac arrest, cardiopulmonary bypass, ❍ Anxiety
diabetic ketoacidosis, drug reactions, heatstroke, in- ❍ Fatigue
compatible blood transfusion, pulmonary embolism, ❍ Fear
sickle cell anemia, and shock ❍ Impaired gas exchange
❍ Ineffective tissue perfusion: GI, cerebral, renal
Prevalence ❍ Risk for deficient fluid volume
❍ Depends on the cause
Key outcomes
The patient will:
❍ maintain balanced intake and output
❍ maintain adequate ventilation

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❍ express feelings of increased comfort and decreased

Patient teaching
❍ have laboratory values return to normal
❍ use available support systems to assist in coping with Be sure to cover (for the patient and his family):
fears. ❍ an explanation of the disorder
❍ evidence of the problem, diagnostic procedures
needed, and treatment that the patient is to receive.
General Discharge planning
❍ Treatment for underlying condition
❍ Possibly supportive care alone if the patient isn’t ac- ❍ Refer the patient for follow-up care with a hematolo-
tively bleeding gist if appropriate.
❍ Activity, as tolerated
A LERT Focus on early recognition of signs of
abnormal bleeding, prompt treatment of the
underlying disorders, and prevention of further
❍ Provide emotional support.
❍ Provide adequate rest periods.
❍ Give prescribed drugs, including analgesics.
❍ Reposition the patient every 2 hours, and provide
meticulous skin care.
❍ Give prescribed oxygen therapy.
A LERT To prevent clots from dislodging and
causing fresh bleeding, don’t vigorously rub
the affected areas when bathing.
❍ Protect the patient from injury.
❍ If bleeding occurs, use pressure and topical hemo-
static agents to control bleeding.
❍ Limit venipunctures whenever possible.
❍ Watch for transfusion reactions and signs of fluid
❍ Measure the amount of blood lost, weigh dressings
and linen, and record drainage.
❍ Weigh the patient daily, particularly if there is renal
Drug therapy
In active bleeding
❍ Antithrombin III and gabexate
❍ Blood, fresh frozen plasma, platelets, or packed red
blood cells
❍ Cryoprecipitate
❍ Fluid replacement

❍ Intake and output, especially when giving blood
❍ Results of serial blood studies
❍ Signs of shock
❍ Vital signs

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Electric shock ❍

Nervous irritability
Physical assessment
Overview ❍ Apnea
❍ Burns
Description ❍ Cold skin
❍ Electric current passing through body ❍ Cyanosis
❍ Physical damage varies ❍ Determined by voltage exposure
– Intensity of current ❍ Entrance and exit injuries
– Resistance of tissues it passes through ❍ Local tissue coagulation
– Type of current ❍ Markedly decreased blood pressure
– Frequency and duration of current flow ❍ Numbness or tingling or sensorimotor deficits
❍ Classified as lightning, low-voltage (less than 600 ❍ Unconsciousness
volts [V]), and high-voltage (more than 600 V)
Test results
Pathophysiology Laboratory
❍ Electrical energy alters the resting potential of cell ❍ Laboratory test results to evaluate internal damage
membranes, causing depolarization in muscles and and guide treatment:
nerves. – Arterial blood gas analysis to determine
❍ Electric shock alters normal electrical activity of the respiratory status
heart and brain. – Urine analysis and urine myoglobin tests to
❍ High-frequency current generates more heat in tis- evaluate tissue damage
sues than a low-frequency current, resulting in burns – Complete blood count
and local tissue coagulation and necrosis. – Electrolyte status to show imbalances
❍ Electric shock causes muscle tetany, tissue destruc- – Blood urea nitrogen and creatinine levels to show
tion, and coagulative necrosis. kidney damage
Causes ❍ Chest X-rays, if chest injury or shortness of breath
❍ Accidental contact with an exposed part of an electri- occurred, reveal internal damage.
cal appliance or wiring Diagnostic procedures
❍ Lightning ❍ Electrocardiography (ECG) reveals arrhythmias, al-
❍ Flash of electric arcs from high-voltage power lines lows evaluation of internal damage, and guides treat-
or machines ment.
❍ Causes more than 500 deaths annually Nursing diagnoses
❍ More common in men ages 20 to 40
❍ Acute pain
Complications ❍ Anxiety
❍ Cardiac dysfunction ❍ Decreased cardiac output
❍ Death ❍ Impaired skin integrity
❍ Electrolyte abnormalities ❍ Ineffective breathing pattern
❍ Neurologic dysfunction ❍ Ineffective tissue perfusion: cardiopulmonary
❍ Peripheral nerve injuries ❍ Risk for imbalanced fluid volume
❍ Psychiatric dysfunction ❍ Risk for post-trauma syndrome
❍ Renal failure
❍ Sepsis Key outcomes
❍ Thrombi The patient will:
❍ Vascular disruption ❍ maintain stable cardiac rhythm
❍ maintain cardiac output
❍ regain skin integrity
Assessment ❍ have wounds and incisions that appear clean, pink,
and free from purulent drainage
History ❍ maintain adequate fluid volume.
❍ Exposure to electricity or lightning
❍ Loss of consciousness
❍ Muscle pain
❍ Fatigue

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❍ Activity based on outcome of interventions
❍ Cardiopulmonary resuscitation if needed
❍ Emergency stabilizing measures
❍ No dietary restrictions if swallowing ability intact
❍ Separation of victim from source of electrical
❍ Stabilization of cervical spine
❍ Treatment of acid-base imbalance
❍ Vigorous fluid replacement
❍ Turn off the electricity to separate the victim from the
source of current.
❍ Provide emergency treatment.
❍ Give rapid I.V. fluid infusion.
❍ Obtain a 12-lead ECG.
❍ Give prescribed drugs.
Drug therapy
❍ Osmotic diuretic
❍ Tetanus prophylaxis
❍ Cardiac rhythm (continuously)
❍ Intake and output (hourly)
❍ Neurologic status
❍ Peripheral neurovascular status
❍ Sensorimotor deficits

Patient teaching
Be sure to cover:
❍ information about the injury, diagnosis, and treat-
❍ how to avoid electrical hazards at home and at work
❍ electrical safety for children.

Discharge planning
❍ Refer the patient to rehabilitation and specialist care
in keeping with his injury and recovery.

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Emphysema ❍

Distant heart sounds
❍ Inspiratory wheeze
Overview ❍ Prolonged expiratory phase with grunting respira-
❍ Pursed-lip breathing
Description ❍ Tachypnea
❍ Chronic lung disease characterized by exertional ❍ Use of accessory muscles
dyspnea and permanent enlargement of air spaces
distal to the terminal bronchioles Test results
❍ One of several diseases usually labeled collectively as Laboratory
chronic obstructive pulmonary disease or chronic ❍ Decreased partial pressure of oxygen on arterial
obstructive lung disease blood gas analysis
❍ Normal partial pressure of carbon dioxide until late
Pathophysiology in the disease
❍ Recurrent inflammation caused by the release of ❍ Increased hemoglobin level late in the disease
proteolytic enzymes from lung cells causes abnor- Imaging
mal, permanent enlargement of the air spaces distal ❍ Chest X-rays may show several changes:
to the terminal bronchioles. – Flattened diaphragm
❍ This enlargement leads to the destruction of alveolar – Reduced vascular markings at the lung periphery
walls, which results in a breakdown of elasticity. – Overaeration of the lungs
(See What happens in emphysema.) – Vertical heart
– Enlarged anteroposterior chest diameter
Causes – Large retrosternal air space.
❍ Cigarette smoking Diagnostic procedures
❍ Genetic deficiency of alpha1-antitrypsin ❍ Pulmonary function tests show typical changes:
– Increased residual volume and total lung capacity
Prevalence – Reduced diffusing capacity
❍ Most common cause of death from respiratory dis- – Increased inspiratory flow.
ease in the United States ❍ Electrocardiography may show changes:
❍ More common in men than women – Tall, symmetrical P waves in leads II, III, and aVF
❍ About 2 million Americans affected – Vertical QRS axis
❍ 1 in 3,000 neonates affected – Signs of right ventricular hypertrophy late in the
❍ Cor pulmonale
❍ Peptic ulcer disease Nursing diagnoses
❍ Pneumomediastinum
❍ Recurrent respiratory tract infections ❍ Activity intolerance
❍ Respiratory failure ❍ Anxiety
❍ Spontaneous pneumothorax ❍ Deficient knowledge (emphysema)
❍ Fatigue
❍ Impaired gas exchange
Assessment ❍ Ineffective airway clearance
❍ Ineffective breathing pattern
❍ Anorexia and weight loss Key outcomes
❍ Chronic cough The patient will:
❍ Malaise ❍ maintain a patent airway and adequate ventilation
❍ Shortness of breath ❍ use energy conservation techniques
❍ Smoking ❍ express understanding of the illness
❍ demonstrate effective coping strategies.
Physical assessment
❍ Barrel chest
❍ Clubbed fingers and toes Interventions
❍ Crackles
❍ Cyanosis General
❍ Decreased breath sounds ❍ Activity, as tolerated
❍ Decreased chest expansion ❍ Adequate hydration
❍ Decreased tactile fremitus ❍ Chest physiotherapy

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❍ Chest tube insertion for pneumothorax What happens in emphysema

❍ High-protein, high-calorie diet In a patient with emphysema, recurrent pulmonary inflam-
❍ Possible transtracheal catheterization and home oxy- mation damages and eventually destroys the alveolar
gen therapy walls, creating large air spaces and a reduced surface area
for gas exchange. Damage to the alveoli leaves them
Nursing unable to recoil normally after expanding, which traps air
❍ Give prescribed drugs. in the lungs. The patient must exhale forcefully to remove
❍ Provide supportive care. air from the lungs, which compresses the airways and
❍ Help the patient adjust to lifestyle changes caused by may cause them to collapse.
a chronic illness. Associated pulmonary capillary destruction usually
allows a patient with severe emphysema to match venti-
❍ Encourage the patient to express fears and concerns.
lation to perfusion and thus avoid cyanosis.
❍ Perform chest physiotherapy.
❍ Provide a high-calorie, protein-rich diet.
❍ Give small, frequent meals. NORMAL ALVEOLI
❍ Encourage daily activity and diversional activities.
❍ Provide frequent rest periods.
Drug therapy Bronchiole
❍ Antibiotics
❍ Anticholinergics Alveoli
❍ Bronchodilators
❍ Corticosteroids
❍ Mucolytics

❍ Activity tolerance Bronchiole
❍ Complications
❍ Daily weight
❍ Intake and output Alveoli
❍ Respiratory status
❍ Vital signs

Discharge planning
Patient teaching
❍ Refer the patient to a smoking-cessation program if
Be sure to cover: indicated.
❍ the disorder, diagnosis, and treatment ❍ Refer the patient for influenza and pneumococcal
❍ prescribed drugs, dosages, and possible adverse re- pneumonia immunizations as needed.
actions ❍ Refer the family of patients with familial emphysema
❍ when to contact a doctor for alpha1-antitrypsin deficiency screening.
❍ the need to avoid smoking and areas where smoking
is permitted
❍ the need to avoid crowds and people with infections
❍ home oxygen therapy, if indicated
❍ transtracheal catheter care, if needed
❍ coughing and deep-breathing exercises
❍ proper use of handheld inhalers
❍ high-calorie, protein-rich diet
❍ adequate oral fluid intake
❍ avoidance of respiratory irritants
❍ signs and symptoms of pneumothorax.
A LERT Urge the patient to notify a doctor if he
experiences a sudden onset of worsening
dyspnea or sharp pleuritic chest pain worsened by
chest movement, breathing, or coughing.

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Esophageal cancer Assessment

Overview ❍ Anorexia, vomiting, and regurgitation of food
❍ Dysphagia of varying degrees depending on the ex-
Description tent of disease
❍ Malignant esophageal tumor ❍ Feeling of fullness, pressure, indigestion, or subster-
– Squamous cell carcinoma nal burning
– Adenocarcinoma ❍ Hoarseness
❍ Usually fungating and infiltrating ❍ Pain on swallowing or pain that radiates to the back
❍ Commonly metastasizes to liver and lungs ❍ Weight loss
❍ Nearly always fatal
❍ 5-year survival in fewer than 5% of cases Physical assessment
❍ Death common within 6 months of diagnosis ❍ Cachexia and dehydration
❍ Chronic cough (possibly from aspiration)
❍ Most esophageal cancers are poorly differentiated Test results
squamous cell carcinomas, with 50% occurring in Imaging
the lower portion of the esophagus, 40% in the mid- ❍ X-rays of the esophagus, with barium swallow and
dle portion, and 10% in the upper or cervical esoph- motility studies, are used to delineate structural and
agus. filling defects and detect reduced peristalsis.
❍ Adenocarcinomas are less common and are con- ❍ Computed tomography scan may help diagnose and
tained to the lower third of the esophagus. monitor esophageal lesions.
❍ The tumor partially constricts the lumen of the ❍ Magnetic resonance imaging permits evaluation of
esophagus. esophagus and adjacent structures.
❍ Regional metastasis occurs early by way of submu- Diagnostic procedures
cosal lymphatics, often fatally invading adjacent vital ❍ Esophagoscopy, punch and brush biopsies, and exfo-
intrathoracic organs. liative cytologic tests confirm esophageal tumors.
❍ If the patient survives primary extension, the liver ❍ Bronchoscopy (usually performed after an esoph-
and lungs are the usual sites of distant metastases; agoscopy) may reveal tumor growth in the tracheo-
unusual metastasis sites include the bone, kidneys, bronchial tree.
and adrenal glands. ❍ Endoscopic ultrasonography of the esophagus com-
bines endoscopy and ultrasound technology to mea-
Risk factors sure the depth of penetration of the tumor.
❍ Chronic irritation from heavy smoking
❍ Excessive use of alcohol
❍ Nutritional deficiency, as in untreated sprue and Nursing diagnoses
Plummer-Vinson syndrome
❍ Previous head and neck tumors ❍ Acute pain
❍ Stasis-induced inflammation, as in achalasia or ❍ Anxiety
stricture ❍ Fatigue
❍ Fear
Causes ❍ Deficient fluid volume
❍ Unknown ❍ Imbalanced nutrition: less than body requirements
❍ Impaired swallowing
Prevalence ❍ Risk for aspiration
❍ Most common in men older than age 60
❍ Occurs worldwide, but most common in Japan, Rus- Key outcomes
sia, China, the Middle East, and the Transkei region The patient will:
of South Africa ❍ maintain weight
❍ keep fluid volume in the normal range
Complications ❍ avoid aspiration
❍ Direct invasion of adjoining structures ❍ express feelings of increased comfort and decreased
❍ Inability to control secretions pain.
❍ Loss of lower esophageal sphincter control (may re-
sult in aspiration pneumonia)
❍ Obstruction of the esophagus

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❍ Surgery and other treatments to relieve disease
❍ Palliative therapy to keep esophagus open
– Dilation of the esophagus
– Laser therapy
– Radiation therapy
– Installation of prosthetic tubes (such as Celestin’s
❍ Liquid to soft diet, as tolerated
❍ High-calorie supplements
❍ Radical surgery to excise tumor and resect esopha-
gus or stomach and esophagus
❍ Gastrostomy or jejunostomy
❍ Endoscopic laser treatment and bipolar electrocoag-
❍ Provide support and encourage verbalization.
❍ Position the patient properly to prevent aspiration.
❍ Provide tube feedings, as ordered.
❍ Give prescribed drugs.
Drug therapy
❍ Chemotherapy and radiation therapy
❍ Analgesics
❍ Electrolyte levels
❍ Hydration and nutritional status
❍ Intake and output
❍ Pain control
❍ Postoperative complications
❍ Swallowing ability
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disease process, treatment, and postoperative
❍ dietary needs
❍ the need to rest between activities.

Discharge planning
❍ Arrange for home care follow-up after discharge.
❍ Refer the patient to the American Cancer Society.

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F Fanconi’s syndrome

Hereditary renal disorder producing malfunctions of
the proximal tubules
Leads to electrolyte losses and, eventually, retarded
growth and development, rickets, and osteomalacia
In children, onset usually during the first 6 months
May be secondary to another illness: acquired Fan-
coni’s syndrome
Also known as de Toni-Fanconi syndrome
AGE AWARE An infant with Fanconi’s syn-
drome appears normal at birth, although birth
weight may be low.
Infants (at about age 6 months)
❍ Anorexia
❍ Constipation
❍ Failure to thrive
❍ Slow linear growth
❍ Vomiting
❍ Weakness
Pathophysiology ❍ Osteomalacia
❍ Characteristic changes occur in the proximal renal ❍ Weakness
tubules, including shortening of the connection to
the glomeruli by an abnormally narrow segment Physical assessment
called a swan’s neck. Infants
❍ Changes result from the atrophy of epithelial cells ❍ Cystine crystals in corneas and conjunctiva
and loss of proximal tubular mass volume. ❍ Peripheral retinal pigment degeneration
❍ Changes in proximal renal tubules decrease tubular ❍ Signs of dehydration
resorption of glucose, phosphate, amino acid, bicar- ❍ Yellow skin
bonate, potassium, and, occasionally, water. Adults
❍ Muscle weakness and paralysis
Causes ❍ Signs of hypokalemia, hypophosphatemia, and glu-
❍ Congenital cosuria
❍ Idiopathic ❍ Signs of metabolic acidosis
Acquired Fanconi’s syndrome
❍ Certain drugs Test results
❍ Cystinosis Laboratory
❍ Dysproteinemias ❍ Excessive amounts of glucose, phosphate, amino
❍ Exposure to a toxic substance (heavy metal poison- acids, bicarbonate, and potassium in 24-hour urine
ing) specimen
❍ Galactosemia ❍ Increased serum phosphate and androgen levels
❍ Kidney transplant ❍ Increased alkaline phosphatase level (with rickets)
❍ Lowe’s disease ❍ Hyperchloremia
❍ Wilson’s disease ❍ Hypokalemia

AGE AWARE Cystinosis is the most common

cause of Fanconi’s syndrome in children. Nursing diagnoses
Prevalence ❍ Activity intolerance
❍ Most prevalent in children ❍ Anticipatory grieving
❍ Affects both sexes equally ❍ Impaired urinary elimination
❍ Risk for deficient fluid volume
Complications ❍ Risk for injury
❍ Aminoaciduria
❍ Bicarbonate wasting Key outcomes
❍ End-stage renal disease The patient will:
❍ Glycosuria ❍ remain free from injury
❍ Hyperkalemia ❍ maintain adequate fluid volume
❍ Hypernatremia ❍ keep electrolyte levels within normal limits
❍ Phosphaturia ❍ use positive coping mechanisms and available sup-
❍ Retarded growth and development port systems
❍ Rickets ❍ maintain or achieve optimal activity level.
❍ Uricosuria

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❍ Dialysis
❍ Symptomatic treatment to replace the patient’s spe-
cific deficiencies
❍ With acquired Fanconi’s syndrome, treatment of the
underlying cause
❍ Give prescribed electrolytes, mineral replacements,
and drugs.
❍ Provide a nutritious diet.
❍ Maintain fluid therapy, as ordered.
❍ Provide adequate rest periods.
❍ Provide emotional support.
Drug therapy
❍ Cysteamine (for cystinosis)
❍ Dietary supplements
❍ D-penicillamine (for Wilson’s disease)
❍ Electrolyte replacement
❍ Intake and output
❍ Laboratory test results
❍ Renal function
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment plan
❍ dietary changes
❍ need to comply with treatment
❍ possible need for dialysis.

Discharge planning
❍ Refer patient and family for appropriate counseling.

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G Gastric cancer

Cancer of the gastrointestinal (GI) tract
Classified according to gross appearance
– Diffuse
– Polypoid
– Ulcerating
– Ulcerating and infiltrating
❍ 5-year survival rate about 15%
❍ Prognosis based on stage of disease at time of diag-

Vague feeling of fullness, heaviness, and moderate
abdominal distention after meals
Weight loss, nausea, vomiting
Weakness and fatigue
Physical assessment
❍ Abdominal distention
Palpable lymph nodes, especially supraclavicular
and axillary nodes
Palpable mass
Other assessment findings corresponding to extent of
disease and location of metastasis
Test results
nosis Laboratory
❍ Iron-deficiency anemia
Pathophysiology ❍ Possible elevated liver function studies with metasta-
❍ The most commonly affected areas of the stomach sis to liver
are the pylorus and antrum. ❍ Possible elevated carcinoembryonic antigen radioim-
❍ Other affected areas in order of descending frequen- munoassay
cy are: Imaging
– lesser curvature of the stomach ❍ Barium X-rays of the GI tract with fluoroscopy show
– cardia changes that suggest gastric cancer, including a tu-
– body of the stomach mor or filling defect in the outline of the stomach,
– greater curvature of the stomach. loss of flexibility and distensibility, and abnormal
❍ Cancer metastasizes rapidly to regional lymph nodes, gastric mucosa with or without ulceration.
omentum, liver, and lungs. Diagnostic procedures
❍ Gastroscopy with fiber-optic endoscopy helps rule
Risk factors out other diffuse gastric mucosal abnormalities by
❍ Excessive alcohol consumption allowing direct visualization.
❍ Family history of gastric cancer ❍ Gastroscopic biopsy permits evaluation of gastric
❍ Gastritis with gastric atrophy mucosal lesions.
❍ Smoked foods, pickled vegetables, and salted fish ❍ Gastric acid stimulation test discloses whether the
and meat in the diet stomach secretes acid properly.
❍ Smoking
❍ Type A blood (10% increased risk)
Nursing diagnoses
❍ Unknown ❍ Acute pain
❍ Anxiety
Prevalence ❍ Fatigue
❍ Common worldwide in all races ❍ Fear
❍ More common in men older than age 40 ❍ Imbalanced nutrition: less than body requirements
❍ Mortality high in Japan, Iceland, Chile, and Austria ❍ Impaired oral mucous membrane
❍ Occurrence decreased 50% over the past 25 years ❍ Impaired swallowing
❍ Death rate one-third the death rate of 30 years ago ❍ Risk for deficient fluid volume
❍ Risk for infection
❍ GI obstruction Key outcomes
❍ Iron-deficiency anemia The patient will:
❍ Malnutrition ❍ lose no more weight
❍ Metastasis ❍ express feelings of increased energy
❍ report feeling less tension and pain
❍ avoid aspiration
Assessment ❍ maintain fluid balance.

❍ Back, epigastric, or retrosternal pain not relieved by
over-the-counter analgesics

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❍ Excision of lesion with appropriate margins (in
more than one-third of patients)
❍ Gastroduodenostomy
❍ Gastrojejunostomy
❍ Partial gastric resection
❍ Total gastrectomy (including omentum and spleen if
metastasis has occurred)
❍ Radiation therapy with chemotherapy (not before
surgery because it may damage viscera and impede
❍ Diet based on the patient's condition
❍ Parenteral feeding if patient can't consume adequate
❍ Provide a high-protein, high-calorie diet with dietary
❍ Give prescribed drugs.
❍ Provide parenteral nutrition as appropriate.
❍ After surgery, provide supportive care.
Drug therapy
❍ Antiemetics
❍ Chemotherapy
❍ Opioid analgesics
❍ Sedatives and tranquilizers
❍ Effects of prescribed drugs
❍ Hydration and nutritional status
❍ Nasogastric tube function and drainage
❍ Pain control
❍ Postoperative complications
❍ Vital signs
❍ Wound site

Patient teaching
Be sure to cover (with the patient or his family):
❍ the disorder, diagnosis, and treatment
❍ prescribed drugs, dosages, and possible adverse
❍ the diet plan
❍ effective pulmonary toilet
❍ the need to avoid crowds and people with infections
❍ relaxation techniques.

Discharge planning
❍ Direct the patient and his family to support services.
❍ Refer the patient for home services if needed.
❍ Refer the patient for physical or occupational thera-
py if needed.

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Gastritis ❍ Increased presence of H. pylori in people older than

age 60
❍ 8 of 1,000 people affected by acute gastritis
Overview ❍ 2 of 10,000 people affected by chronic gastritis
Description ❍ Gastric cancer
❍ Inflammation of the gastric mucosa ❍ Hemorrhage
❍ May be acute or chronic ❍ Obstruction
❍ Most common stomach disorder (acute form) ❍ Perforation
❍ Peritonitis
Acute gastritis
❍ The protective mucosal layer is altered. Assessment
❍ Acid secretion produces mucosal reddening, edema,
and superficial surface erosion. History
Chronic gastritis ❍ Anorexia
❍ The gastric mucosa undergoes progressive thinning ❍ Coffee-ground emesis or melena with GI bleeding
and degeneration. ❍ Cramping
❍ Epigastric discomfort
Risk factors ❍ Indigestion
❍ Age older than 60 years ❍ Nausea, hematemesis, and vomiting
❍ Exposure to toxic substances ❍ Presence of one or more causative factors
❍ Hemodynamic disorder ❍ Rapid onset of symptoms (acute gastritis)
Causes Physical assessment
Acute gastritis ❍ Abdominal distention, tenderness, and guarding
❍ Complication of acute illness ❍ Grimacing
❍ Drugs ❍ Hypotension
– Antimetabolites ❍ Normoactive to hyperactive bowel sounds
– Aspirin and other nonsteroidal anti-inflammatory ❍ Pallor
agents (in large doses) ❍ Possible normal appearance
– Caffeine ❍ Restlessness
– Corticosteroids ❍ Tachycardia
– Cytotoxic drugs
– Indomethacin Test results
– Phenylbutazone Laboratory
❍ Endotoxins released from infecting bacteria, such as ❍ Occult blood in vomitus, stool, or both if the patient
staphylococci, Escherichia coli, and salmonella has gastric bleeding
❍ Ingested poisons ❍ Decreased hemoglobin level and hematocrit
– Ammonia Diagnostic procedures
– Carbon tetrachloride ❍ Urea breath test shows the presence of H. pylori.
– Corrosive substances ❍ Upper-GI endoscopy reveals gastritis when per-
– Dichloro-diphenyl-trichloroethane (commonly formed within 24 hours of bleeding.
known as DDT) ❍ Biopsy reveals inflammatory process.
– Mercury
❍ Long-term ingestion of irritating foods and alcohol
Chronic gastritis Nursing diagnoses
❍ Diabetes mellitus
❍ Helicobacter pylori infection (common cause of ❍ Acute pain
nonerosive gastritis) ❍ Deficient knowledge (gastritis)
❍ Pernicious anemia ❍ Imbalanced nutrition: less than body requirements
❍ Recurring exposure to irritating substances, such as ❍ Ineffective coping
drugs, alcohol, cigarette smoke, and environmental ❍ Risk for deficient fluid volume
❍ Renal disease Key outcomes
The patient will:
Prevalence ❍ express feelings of increased comfort
❍ Occurs equally in men and women ❍ maintain weight
❍ May occur at any age ❍ express concerns about current condition

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❍ maintain adequate fluid balance

❍ verbalize understanding of the disorder and treat-
ment regimen.

❍ Elimination of cause
❍ For massive bleeding, blood transfusion, iced saline
lavage, angiography with vasopressin
❍ Nothing by mouth if bleeding occurs
❍ Elimination of irritating foods
❍ Activity, as tolerated (encourage mobilization)
❍ If conservative treatment fails, vagotomy, pyloroplas-
ty, or partial or total gastrectomy (rarely)
❍ Provide physical and emotional support.
❍ Give prescribed drugs and I.V. fluids.
❍ Assist the patient with diet modification.
❍ If surgery is needed, prepare the patient beforehand
and provide appropriate postoperative care.
❍ Consult a dietitian as needed.
Drug therapy
❍ Antacids
❍ Histamine (H2) blockers
❍ Proton pump inhibitors
❍ Prostaglandins
❍ Vitamin B12
❍ Triple therapy — two antibiotics and bismuth subsal-
❍ Dual therapy — antibiotic and proton pump in-
❍ Electrolyte and hemoglobin levels
❍ Fluid intake and output
❍ Pain control
❍ Response to drug therapy
❍ Returning symptoms as food is reintroduced
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ lifestyle and diet modifications
❍ preoperative teaching if surgery is needed
❍ stress-reduction techniques
❍ drugs, dosages, and possible adverse effects.

Discharge planning
❍ Refer the patient to a smoking-cessation program if

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Gastroenteritis ❍

Food allergens
Ingestion of toxins, such as poisonous plants and
Overview ❍ Parasites, such as Ascaris, Enterobius, and
Trichinella spiralis
❍ Viruses, such as adenoviruses, echoviruses, and cox-
Description sackieviruses
❍ Self-limiting inflammation of the stomach and small
intestine Prevalence
❍ Also known as intestinal flu, traveler’s diarrhea, viral ❍ Occurs at any age
enteritis, and food poisoning (See Preventing trav- ❍ Major cause of illness and death in developing na-
eler’s diarrhea.) tions
❍ Ranks second to common cold as cause of lost work
Pathophysiology time in the United States
❍ The bowel reacts to the various causes of gastroen- ❍ Fifth most common cause of death among young
teritis with increased luminal fluid that can’t be ab- children
sorbed. ❍ May be life-threatening in elderly and debilitated pa-
❍ This results in severe diarrhea with abdominal pain, tients
vomiting, and depletion of intracellular fluid.
❍ Dehydration and electrolyte loss develop. Complications
❍ Electrolyte imbalance
Causes ❍ Severe dehydration
❍ Amoebae, especially Entamoeba histolytica
❍ Bacteria, such as Staphylococcus aureus, Salmo-
nella, Shigella, Clostridium botulinum, Clostridi- Assessment
um perfringens, and Escherichia coli
❍ Drug reactions from antibiotics History
❍ Enzyme deficiencies ❍ Abdominal pain and discomfort
❍ Acute onset of diarrhea
❍ Exposure to contaminated food
Preventing traveler’s diarrhea ❍ Malaise and fatigue
❍ Nausea, vomiting
If your patient travels, especially to developing nations, ❍ Recent travel
discuss precautions he can take to reduce his risk of
traveler’s diarrhea. Explain that this condition is caused by Physical assessment
ingestion of bacteria-contaminated food or water in areas ❍ Decreased blood pressure
of inadequate sanitation. Organisms attach to the lining of
❍ Hyperactive bowel sounds
the small intestine, where they release a toxin that causes
❍ Poor skin turgor (with dehydration)
cramps and diarrhea. To minimize this risk, advise taking
the following steps. ❍ Slight abdominal distention
● Drink water only if it’s chlorinated or bottled.
Chlorination protects water from bacterial contaminants
Test results
such as Escherichia coli. Brush your teeth with Laboratory
chlorinated water as well. ❍ Causative bacteria revealed by Gram's stain, stool
● Don’t drink out of glasses that may have been washed culture (by direct rectal swab), or blood culture
in contaminated water.
● Don’t use ice cubes that may have been made from
contaminated water.
● Drink only beverages made with boiled water, such as
Nursing diagnoses
coffee and tea, or those in bottles or cans.
❍ Acute pain
● Sanitize impure water by adding 2% tincture of iodine
❍ Diarrhea
(5 drops/L of clear water; 10 drops/L of cloudy water)
or by adding liquid laundry bleach (about 2 drops/L of ❍ Imbalanced nutrition: less than body requirements
clear water; 4 drops/L of cloudy water) ❍ Risk for deficient fluid volume
● Don’t eat uncooked vegetables, unpeeled fresh fruits,
salads, unpasteurized milk, and other dairy products. Key outcomes
● Don’t eat foods offered by street vendors. The patient will:
● If traveler’s diarrhea occurs despite precautions, try ❍ maintain weight without further loss
relieving the symptoms by taking loperamide ❍ express feelings of increased comfort
(Imodium), bismuth subsalicylate (Pepto Bismol), or ❍ maintain adequate fluid volume
diphenoxylate with atropine (Lomotil). ❍ maintain normal vital signs.

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❍ Activity, as tolerated (encourage mobilization)
❍ Avoidance of milk products
❍ Electrolyte solutions
❍ Initially, clear liquids as tolerated
❍ Rehydration
❍ Supportive treatment for nausea, vomiting, and
❍ Allow uninterrupted rest periods.
❍ Replace lost fluids and electrolytes through diet or
I.V. fluids.
❍ Give prescribed drugs.
Drug therapy
❍ Antidiarrheal therapy
❍ Antiemetics
❍ Antibiotics
❍ I.V. fluids
❍ Electrolytes
❍ Intake and output
❍ Signs of dehydration
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ diet modifications
❍ prescribed drugs, dosages, and possible adverse ef-
❍ preventive measures
❍ how to perform warm sitz baths three times daily to
relieve anal irritation.

Discharge planning
❍ Refer the patient for dietary follow-up as needed.

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Goodpasture’s ❍ Possible red blood cells and cellular casts in urine,

which typify glomerular inflammation
syndrome ❍ Possible proteinuria and granular casts in urine
❍ Chest X-rays reveal pulmonary infiltrates in a diffuse,
Overview nodular pattern.
Diagnostic procedures
❍ Immunofluorescence of the alveolar basement mem-
Description brane shows linear deposition of immunoglobulins
❍ Pulmonary-renal syndrome characterized by hemop- as well as C3 and fibrinogen.
tysis and rapidly progressive glomerulonephritis ❍ Immunofluorescence of the GBM shows linear depo-
sition of immunoglobulins.
Pathophysiology ❍ Lung biopsy shows interstitial and intra-alveolar
❍ Abnormal production and deposition of antibodies hemorrhage with hemosiderin-laden macrophages.
against glomerular basement membrane (GBM) and ❍ Renal biopsy usually shows focal necrotic lesions
alveolar basement membrane activate the comple- and cellular crescents.
ment and inflammatory responses.
❍ Glomerular and alveolar tissue damage result.
Nursing diagnoses
❍ Unknown ❍ Activity intolerance
❍ May be related to exposure to hydrocarbons or type ❍ Anxiety
II hypersensitivity reaction ❍ Excess fluid volume
❍ Possible genetic predisposition ❍ Fatigue
❍ Impaired gas exchange
Prevalence ❍ Impaired oral mucous membrane
❍ Occurs at any age ❍ Impaired urinary elimination
❍ Most common in men between ages 20 and 30 ❍ Ineffective airway clearance
❍ Ineffective breathing pattern
Complications ❍ Risk for injury
❍ Pulmonary edema and hemorrhage
❍ Renal failure Key outcomes
The patient will:
❍ maintain a patent airway and adequate ventilation
Assessment ❍ maintain adequate fluid balance
❍ express feelings of increased energy
History ❍ maintain intact mucous membranes
❍ Possible complaint of malaise, fatigue, and pallor ❍ avoid complications
❍ Possible pulmonary bleeding for months or years be- ❍ use available support systems.
fore developing overt hemorrhage and signs of renal
Physical assessment
❍ Decreased urine output General
❍ Dyspnea, tachypnea, orthopnea ❍ Activity, as tolerated
❍ Hematuria ❍ Dialysis
❍ Hemoptysis, ranging from a cough with blood-tinged ❍ Low-protein, low-sodium diet
sputum to frank pulmonary hemorrhage ❍ Kidney transplantation
❍ Pulmonary crackles and rhonchi ❍ Plasmapheresis
❍ Restlessness
Test results ❍ Elevate the head of the bed, and give humidified oxy-
Laboratory gen, as ordered.
❍ Circulating serum anti-GBM antibodies, which distin- ❍ Encourage the patient to conserve energy.
guish Goodpasture’s syndrome from other pul- ❍ Assist with range-of-motion exercises.
monary-renal syndromes, such as Wegener’s granu- ❍ Assist with activities of daily living, and provide fre-
lomatosis, polyarteritis, and systemic lupus quent rest periods.
erythematosus ❍ Transfuse blood and give corticosteroids, as or-
❍ Increased serum creatinine and blood urea nitrogen dered. Watch closely for adverse reactions.
(BUN) levels (typically two to three times normal)

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Drug therapy
❍ High-dose I.V. corticosteroids
❍ Arterial blood gas levels
❍ Creatinine clearance, BUN, and serum creatinine
❍ Daily weight
❍ Hematocrit and coagulation studies
❍ Intake and output
❍ Respiratory status
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ the importance of conserving energy
❍ the possible need for fluid restriction
❍ prescribed drugs, dosages, and possible adverse ef-
❍ how to deep-breathe and cough
❍ how to recognize respiratory and genitourinary
bleeding and the need to report them to the doctor
at once.

Discharge planning
❍ If the patient needs dialysis or kidney transplanta-
tion, refer him to a renal support group.
❍ Encourage regular follow-up care.

Goodpasture’s syndrome 133

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Gout ❍ Secondary gout that develops with other diseases

– Diabetes mellitus
– Hypertension
Overview – Leukemia
– Myeloma
Description – Obesity
– Polycythemia
❍ Inflammatory arthritis caused by uric acid and crys- – Renal disease
tal deposits – Sickle cell anemia
❍ Red, swollen, acutely painful joints ❍ Secondary gout that follows treatment with drugs
❍ Mostly affects feet, great toe, ankle, and midfoot – Hydrochlorothiazide
Primary gout – Pyrazinamide
❍ Patient symptom-free for years between attacks
❍ Sudden first acute attack that peaks quickly Prevalence
❍ Delayed attacks with olecranon bursitis ❍ Primary gout typically in men older than age 30 and
Chronic polyarticular gout postmenopausal women who take diuretics
❍ Final, unremitting stage of the disease marked by
persistent painful polyarthritis Complications
❍ Atherosclerotic disease
Pathophysiology ❍ Cardiovascular lesions
❍ Uric acid crystallizes in blood or body fluids, and the ❍ Cerebrovascular accident
precipitate accumulates in connective tissue, creat- ❍ Coronary thrombosis
ing tophi. ❍ Hypertension
❍ Crystals trigger an immune response. ❍ Infection when tophi rupture
❍ Neutrophils secrete lysosomes for phagocytosis. ❍ Renal calculi
❍ Lysosomes damage tissue and worsen the immune
❍ Decreased renal excretion of uric acid History
❍ Exact cause unknown ❍ Sedentary lifestyle
❍ Genetic defect in purine metabolism (hyper- ❍ Hypertension
uricemia) ❍ Renal calculi
❍ Waking during the night with pain in great toe
❍ Initial moderate pain that grows intense
Recognizing gouty tophi ❍ Chills, mild fever
In advanced gout, urate crystal deposits develop into hard, Physical assessment
irregular, yellow-white nodules called tophi. These bumps
❍ Swollen, dusky red or purple joint
commonly protrude from the great toe and ear.
❍ Limited movement of joint
❍ Tophi, especially in the outer ears, hands, and feet
(See Recognizing gouty tophi.)
❍ Skin over tophi that may ulcerate and release chalky
white exudate or pus
❍ Secondary joint degeneration
❍ Erosions, deformity, and disability
❍ Warmth over joint
❍ Extreme tenderness
❍ Fever
❍ Hypertension
Test results
Tophi ❍ Increased serum uric acid levels during an attack
❍ Increased white blood cell count during acute attack
❍ Increased urine uric acid level in 20% of patients
❍ X-ray of articular cartilage and subchondral bone
shows evidence of chronic gout.

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Diagnostic procedures ❍ Nonsteroidal anti-inflammatory drugs

❍ Needle aspiration of synovial fluid shows needlelike ❍ Probenecid or sulfinpyrazone
intracellular crystals.
❍ For 24 to 96 hours after surgery, development of
Nursing diagnoses acute gout attacks
❍ Intake and output
❍ Acute pain ❍ Serum uric acid levels
❍ Anxiety
❍ Deficient knowledge: gout
❍ Impaired physical mobility Patient teaching
❍ Risk for imbalanced fluid volume
❍ Risk for injury Be sure to cover:
❍ the disorder, diagnosis, and treatment
Key outcomes ❍ the need to drink plenty of fluids (up to 2 L daily)
The patient will: ❍ relaxation techniques
❍ express feelings of increased comfort and decreased ❍ prescribed drugs, dosages, and possible adverse ef-
pain fects
❍ maintain joint mobility and range of motion ❍ compliance with prescribed drug regimen
❍ perform activities of daily living within the confines ❍ dietary adjustments
of the disease ❍ the need to control hypertension.
❍ express knowledge of the condition and treatment
❍ maintain adequate fluid volume.
Discharge planning
Interventions ❍ Refer the patient to a weight-reduction program if
Initial interventions
❍ Termination of acute attack
❍ Bed rest in acute attack
❍ Immobilization of joint
❍ Local application of cold
❍ Protection of inflamed, painful joints
Ongoing interventions
❍ Avoidance of alcohol
❍ Prevention of recurrent gout
❍ Prevention of renal calculi
❍ Sparing consumption of purine-rich foods (such as
anchovies, liver, and sardines)
❍ Treatment for hyperuricemia
❍ Weight loss program, if indicated

❍ Institute bed rest.
❍ Use a bed cradle, if appropriate.
❍ Apply cold packs to affected areas.
❍ Give analgesics as needed.
❍ Give anti-inflammatories and other drugs as pre-
❍ Identify techniques and activities that promote rest
and relaxation.
❍ Allow adequate time for self-care.
❍ Provide a purine-poor diet.
Drug therapy
❍ Allopurinol
❍ Analgesics
❍ Colchicine

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Graft rejection Assessment

syndrome History
❍ Signs and symptoms that vary markedly with type of
Overview rejection, underlying illnesses, and type of organ
Description Physical assessment
❍ Rejection of a donated organ when the host’s im- ❍ Kidney transplant: oliguria and increasing serum
mune responses are directed against the graft creatinine and blood urea nitrogen levels
❍ Three subtypes based on time of onset and mecha- ❍ Liver transplant: increased transaminase levels, de-
nisms involved: creased albumin levels, and hypocoagulability
– Hyperacute rejection ❍ Heart transplant: hypotension, heart failure, and
– Acute rejection edema
– Chronic rejection
Test results
Pathophysiology Laboratory
❍ Hyperacute rejection occurs minutes to hours after ❍ Hyperacute rejection: large numbers of polymor-
graft transplantation. phonuclear leukocytes in the graft blood vessels,
❍ Circulating host antibodies recognize and bind to widespread microthrombi, platelet accumulation,
graft antigens. and interstitial hemorrhage, with little or no intersti-
❍ Binding of these antibodies starts the complement tial inflammation
cascade, recruitment of neutrophils, platelet activa- Diagnostic procedures
tion, damage to graft endothelial cells, and stimula- ❍ Biopsy of the transplanted tissue confirms rejection.
tion of coagulation reactions.
❍ Acute rejection may occur hours, days, or even
weeks after transplantation. Nursing diagnoses
❍ Alloantigen-reactive T cells from the host infiltrate
the graft and are activated by contact with foreign, ❍ Activity intolerance
graft-related proteins on antigen-presenting cells. ❍ Disturbed body image
❍ These T cells may damage graft tissue. ❍ Fatigue
❍ In chronic rejection, blood vessel lumens become ❍ Imbalanced nutrition: less than body requirements
occluded through progressive thickening of the inti- ❍ Impaired urinary elimination
mal layers of medium and large arterial walls. ❍ Ineffective coping
❍ Large amounts of intimal matrix are produced, lead- ❍ Interrupted family processes
ing to increasingly occlusive vessel wall thickening. ❍ Risk for deficient fluid volume
❍ A slowly progressing reduction in blood flow results ❍ Risk for infection
in regional tissue ischemia, cell death, and tissue fi-
brosis. Key outcomes
The patient will:
Causes ❍ experience no fever, chills, or other evidence of ill-
❍ Immune system response to a graft ness
❍ use support systems to assist with coping
Prevalence ❍ express his feelings about the condition
❍ Hyperacute rejection: rare; affects less than 1% of ❍ comply with the treatment regimen
transplant recipients ❍ maintain fluid volume balance.
❍ Acute rejection: occurs in 50% of transplant pa-
tients; loss of graft in 10%
❍ Chronic rejection: occurs in 50% of transplant pa- Interventions
tients within 10 years after transplantation
Complications ❍ Activity, as tolerated
❍ Rapid thrombosis ❍ Close monitoring of function of grafted organ
❍ Loss of graft function ❍ Diet restrictions based on organ system affected
❍ Surveillance, with preventive measures against op-
portunistic infections

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❍ Give prescribed antibiotics for infection.
❍ Give prescribed antirejection therapies.
❍ Give prescribed immunosuppressants.
Drug therapy
❍ Antibiotics
❍ Antirejection therapies
❍ Immunosuppressants
❍ Function of the transplanted organ
❍ Signs and symptoms of infection
❍ Signs and symptoms of rejection
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ prescribed drugs, dosages, and possible adverse ef-
❍ how to recognize organ dysfunction
❍ the need to immediately report fever, chills, and oth-
er symptoms of infection
❍ the need for lifelong compliance with the drug regi-

Discharge planning
❍ Refer the patient and his family to social support, in-
cluding psychological support services, as indicated.

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Guillain-Barré ❍ Occurs equally in both sexes
syndrome ❍ Occurs between ages 30 and 50
Overview ❍

❍ Life-threatening respiratory and cardiac compromise
Description ❍ Muscle wasting
❍ A form of polyneuritis ❍ Pressure ulcers
❍ Acute, rapidly progressive, and potentially fatal ❍ Respiratory tract infections
❍ Three phases ❍ Thrombophlebitis
– Acute: beginning from first symptom, ending in 1
to 3 weeks
– Plateau: lasting several days to 2 weeks Assessment
– Recovery: coincides with remyelination and axon-
al process regrowth and typically lasts 4 months to History
3 years, although recovery may never be complete ❍ Minor febrile illness 1 to 4 weeks before current
Pathophysiology ❍ Paresthesia in the legs
❍ Peripheral nerves undergo segmented demyelina- ❍ Progression of symptoms to arms, trunk and, finally,
tion, preventing normal transmission of electrical face
impulses. ❍ Stiffness and pain in the calves
❍ Sensorimotor nerve roots are affected; autonomic
nerve transmission also may be affected. (See Un- Physical assessment
derstanding sensorimotor nerve degeneration.) ❍ Difficulty talking, chewing, and swallowing
❍ Diminished or absent deep tendon reflexes
Risk factors ❍ Loss of position sense
❍ Hodgkin’s or some other malignant disease ❍ Muscle weakness (the major neurologic sign)
❍ Lupus erythematosus ❍ Paralysis of ocular, facial, and oropharyngeal mus-
❍ Rabies or swine influenza vaccination cles
❍ Surgery ❍ Sensory loss, usually in the legs (spreads to arms)
❍ Viral illness
Test results
Causes Laboratory
❍ Unknown ❍ Normal white blood cell count and increased protein
level in cerebrospinal fluid
❍ Increased cerebrospinal fluid pressure in severe dis-
Understanding sensorimotor nerve ease
degeneration Diagnostic procedures
❍ Electromyography may show repeated firing of the
Guillain-Barré syndrome attacks the peripheral nerves,
same motor unit instead of widespread sectional
disrupting the transmission of messages to the brain.
Here’s what goes wrong:
● The myelin sheath degenerates for unknown reasons. ❍ Nerve conduction studies show marked slowing of
This sheath covers the nerve axons and conducts nerve conduction velocities.
electrical impulses along the nerve pathways.
● With degeneration come inflammation, swelling, and
patchy demyelination. Nursing diagnoses
● As this disorder destroys myelin, the nodes of Ranvier
(at the junctures of the myelin sheaths) widen. This ❍ Anxiety
delays and impairs impulse transmission along the ❍ Fear
dorsal and ventral nerve roots. ❍ Imbalanced nutrition: less than body requirements
● The dorsal nerve roots are responsible for sensory ❍ Impaired gas exchange
function, so the patient may experience tingling,
❍ Impaired physical mobility
numbness, or other sensations when the nerve root is
❍ Impaired urinary elimination
● The ventral nerve roots are responsible for motor ❍ Impaired verbal communication
function, so the patient may experience varying ❍ Ineffective breathing pattern
amounts of weakness, immobility, and paralysis when ❍ Ineffective coping
the nerve root is impaired. ❍ Risk for imbalanced fluid volume

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Key outcomes ❍ effective means of communication

The patient will: ❍ the appropriate home care plan
❍ maintain a patent airway and adequate ventilation ❍ prescribed drugs, dosages, and possible adverse
❍ develop alternate means of communication effects.
❍ maintain required caloric intake daily
❍ maintain joint mobility and range of motion
❍ develop and use effective coping mechanisms Discharge planning
❍ use available support systems
❍ maintain adequate fluid volume. ❍ Refer the patient to physical rehabilitation as needed.
❍ Refer the patient to occupational and speech rehabil-
itation resources as indicated.
Interventions ❍ Refer the patient to the Guillain-Barré Syndrome
❍ Adequate caloric intake
❍ Emotional support
❍ Exercise program to prevent contractures
❍ Fluid volume replacement
❍ Maintenance of skin integrity
❍ Plasmapheresis
❍ Possible endotracheal intubation or tracheotomy
❍ Possible gastrostomy or jejunotomy feeding tube in-
❍ Possible tracheostomy
❍ Possible tube feedings with endotracheal intubation
❍ Supportive measures
❍ Establish a means of communication before the pa-
tient needs intubation, if possible.
❍ Turn and reposition the patient.
❍ Encourage coughing and deep breathing.
❍ Provide meticulous skin care.
❍ Perform passive range-of-motion exercises.
❍ In case of facial paralysis, provide eye and mouth
❍ Provide emotional support.
❍ Give prescribed drugs.
Drug therapy
❍ I.V. beta blockers
❍ I.V. immune globulin
❍ Parasympatholytics
❍ Arterial blood gas measurements
❍ Level of consciousness
❍ Pulse oximetry
❍ Respiratory status
❍ Response to drug therapy
❍ Signs of thrombophlebitis
❍ Signs of urine retention
❍ Skin integrity
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment

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H Heart failure

Fluid buildup in the heart because the myocardium
can’t provide sufficient cardiac output
Usually occurs in a damaged left ventricle
May occur mainly in right ventricle
May be secondary to left-sided heart failure
Left-sided heart failure

Peripheral edema
Sense of abdominal fullness (particularly in right-
sided heart failure)
Substance abuse (alcohol, drugs, tobacco)
Physical assessment
Cool, clammy, pale skin
Cough that produces pink, frothy sputum
Cyanosis of the lips and nail beds
Decreased pulse oximetry
❍ The pumping ability of the left ventricle fails and car- ❍ Decreased pulse pressure
diac output falls. ❍ Decreased urinary output
❍ Blood backs up into the left atrium and lungs, caus- ❍ Diaphoresis
ing pulmonary congestion. ❍ Hepatomegaly and, possibly, splenomegaly
Right-sided heart failure ❍ Jugular vein distention
❍ Ineffective contraction of the right ventricle leads to ❍ Moist, bibasilar crackles, rhonchi, and expiratory
blood backing up into the right atrium and peripher- wheezing
al circulation. ❍ Peripheral edema
❍ Peripheral edema results, along with engorgement of ❍ Pulsus alternans
the kidneys and other organs. ❍ S3 and S4 heart sounds
❍ Tachycardia
❍ Anemia Test results
❍ Arrhythmias Laboratory
❍ Atherosclerosis with myocardial infarction ❍ Elevated B-type natriuretic peptide immunoassay
❍ Constrictive pericarditis Imaging
❍ Emotional stress ❍ Chest X-rays show increased pulmonary vascular
❍ Hypertension markings, interstitial edema, or pleural effusion and
❍ Increased salt or water intake cardiomegaly.
❍ Infection Diagnostic procedures
❍ Mitral or aortic insufficiency ❍ Electrocardiography reflects heart strain, enlarge-
❍ Mitral stenosis secondary to rheumatic heart disease, ment or ischemia. It also may reveal atrial enlarge-
constrictive pericarditis, or atrial fibrillation ment, tachycardia, extrasystole, or atrial fibrillation.
❍ Myocarditis ❍ Pulmonary artery pressure monitoring typically
❍ Pregnancy shows elevated pulmonary artery and pulmonary
❍ Pulmonary embolism artery wedge pressures, left ventricular end-diastolic
❍ Thyrotoxicosis pressure in left-sided heart failure, and elevated right
❍ Ventricular and atrial septal defects atrial or central venous pressure in right-sided heart
❍ Affects 1% of people older than age 50
❍ Affects 10% of people older than age 80 Nursing diagnoses
Complications ❍ Activity intolerance
❍ Myocardial infarction ❍ Decreased cardiac output
❍ Pulmonary edema ❍ Excess fluid volume
❍ Organ failure, especially the brain and kidneys ❍ Fatigue
❍ Imbalanced nutrition: less than body requirements
❍ Ineffective gas exchange
Assessment ❍ Ineffective tissue perfusion: cardiopulmonary
History Key outcomes
❍ A disorder or condition that can cause heart failure The patient will:
❍ Anorexia ❍ maintain hemodynamic stability
❍ Dyspnea or paroxysmal nocturnal dyspnea ❍ maintain adequate cardiac output

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❍ carry out activities of daily living without excess fa-

tigue or decreased energy
Patient teaching
❍ maintain adequate ventilation
❍ maintain adequate fluid balance. Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ signs and symptoms of worsening heart failure
Interventions ❍ when to contact a doctor
❍ prescribed drugs, dosages, potential adverse effects,
General and monitoring needs
❍ Activity, as tolerated ❍ the need to avoid high-sodium foods
❍ Antiembolism stockings ❍ the need to avoid fatigue
❍ Calorie restriction, if indicated ❍ instructions about fluid restrictions
❍ Elevation of legs ❍ the need to weigh himself every morning, at the same
❍ Fluid restriction time, before eating, and after urinating; keeping a
❍ Heart transplantation record of his weight, and reporting a weight gain of
❍ Low-fat diet, if indicated 3 to 5 lb (1.5 to 2.5 kg) in 1 week
❍ Sodium-restricted diet ❍ the importance of smoking cessation, if appropriate
❍ Stent placement ❍ weight reduction, as needed
❍ Surgical replacement (valvular dysfunction with re- ❍ the importance of follow-up care.
current acute heart failure)
❍ Ventricular assist device
❍ Walking program Discharge planning
Nursing ❍ Encourage follow-up care.
❍ Place the patient in Fowler’s position, and give sup- ❍ Refer the patient to a smoking-cessation program, if
plemental oxygen. appropriate.
❍ Provide continuous cardiac monitoring during acute
and advanced stages.
❍ Assist the patient with range-of-motion exercises.
❍ Apply antiembolism stockings. Check for calf pain
and tenderness.
Drug therapy
❍ Anticoagulants
❍ Angiotensin-converting enzyme inhibitors
❍ Angiotensin receptor blockers
❍ Beta blockers
❍ Cardiac glycosides
❍ Diuretics
❍ Inotropic drugs
❍ Oxygen
❍ Potassium supplements
❍ Vasodilators
❍ Blood urea nitrogen and serum creatinine, potassi-
um, sodium, chloride, and magnesium levels
❍ Cardiac rhythm
❍ Daily weight for peripheral edema and other signs
and symptoms of fluid overload
❍ Intake and output
❍ Mental status
❍ Peripheral edema
❍ Response to treatment
❍ Vital signs
A LERT Auscultate for abnormal heart and
breath sounds, and report changes immedi-

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Heat syndrome ❍

Cardiogenic shock
Disseminated intravascular coagulation
❍ Hepatic failure
❍ Hypovolemic shock
Overview ❍ Renal failure
❍ Heat exhaustion — acute heat injury with hyperther- Assessment
mia caused by dehydration
❍ Heatstroke — extreme hyperthermia with ther- History
moregulatory failure Heat exhaustion
❍ Fatigue
Pathophysiology ❍ Headache
❍ Normally, temperature is regulated by evaporation ❍ Muscle cramps
(30% of body’s heat loss) or vasodilation. ❍ Nausea and vomiting
❍ When heat is generated or gained by the body faster ❍ Prolonged activity in a very warm or hot environ-
than it can dissipate, the thermoregulatory mecha- ment
nism is stressed and eventually fails. ❍ Thirst
❍ Hyperthermia accelerates. ❍ Weakness
❍ Cerebral edema and cerebrovascular congestion oc- Heatstroke
curs. ❍ Same signs as heat exhaustion
❍ Cerebral perfusion pressure increases and cerebral ❍ Blurred vision
perfusion decreases. ❍ Confusion
❍ Tissue damage occurs when temperature exceeds ❍ Decreased muscle coordination
107.6° F (42° C), resulting in tissue necrosis, organ ❍ Exposure to high temperatures and humidity without
dysfunction, and failure. air circulation
❍ Hallucinations
Risk factors ❍ Syncope
❍ Age
❍ Alcohol use Physical assessment
❍ Obesity Heat exhaustion
❍ Poor physical condition ❍ Cool, moist skin
❍ Salt and water depletion ❍ Decreased blood pressure
❍ Socioeconomic status ❍ Hyperventilation
❍ Impaired judgment
Causes ❍ Irritability
❍ Behavior ❍ Pale skin
❍ Dehydration ❍ Rectal temperature over 100° F (37.8° C)
❍ Drugs, such as phenothiazines, anticholinergics, and ❍ Syncope
amphetamines ❍ Thready, rapid pulse
❍ Endocrine disorders Heatstroke
❍ Excessive clothing ❍ Altered mental status
❍ Excessive physical activity ❍ Anhydrosis (late sign)
❍ Heart disease ❍ Cheyne-Stokes respirations
❍ Hot environment without ventilation ❍ Decreased blood pressure in later stages
❍ Illness ❍ Gray, dry, hot skin in later stages
❍ Inadequate fluid intake ❍ Hyperpnea
❍ Infection (fever) ❍ Rectal temperature of at least 104° F (40° C)
❍ Lack of acclimatization ❍ Red, diaphoretic, hot skin in early stages
❍ Neurologic disorder ❍ Signs of central nervous system dysfunction
❍ Sudden discontinuation of Parkinson’s disease med- ❍ Slightly elevated blood pressure in early stages
ications ❍ Tachycardia

Prevalence Test results

❍ Affects men and women equally Laboratory
❍ More common among elderly patients and neonates ❍ Elevated serum electrolyte levels
during excessively hot summer days ❍ Possible hyponatremia and hypokalemia
❍ Possible respiratory alkalosis on arterial blood gas
Complications measurements
❍ Cardiac arrhythmias ❍ Leukocytosis

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❍ Thrombocytopenia
❍ Increased bleeding and clotting times
Patient teaching
❍ Possible concentrated urine
❍ Possible proteinuria with tubular casts and myoglo- Be sure to cover:
binuria ❍ the disorder, diagnosis, and treatment
❍ Possible increased blood urea nitrogen level ❍ how to avoid reexposure to high temperatures
❍ Possible decreased serum calcium level ❍ the need to maintain adequate fluid intake
❍ Possible decreased serum phosphorus level ❍ the need to wear loose clothing
❍ limiting activity in hot weather.

Nursing diagnoses
Discharge planning
❍ Decreased cardiac output
❍ Deficient fluid volume ❍ Refer the patient to social services, if appropriate.
❍ Deficient knowledge (heat syndrome)
❍ Hyperthermia
❍ Impaired gas exchange
Key outcomes
The patient will:
❍ maintain adequate ventilation
❍ maintain a normal body temperature
❍ prevent recurrent episodes of hyperthermia
❍ express understanding of the need to maintain ade-
quate fluid intake.

Heat exhaustion
❍ Cool environment
❍ Oral or I.V. fluid administration
❍ Avoidance of caffeine and alcohol
❍ Evaporation, hypothermia blankets, and ice packs to
the groin, axillae, and neck
❍ Increased hydration; cool liquids only
❍ Lowering body temperature as rapidly as possible
❍ Rest periods, as needed
❍ Supportive respiratory and cardiovascular measures

❍ Perform rapid cooling procedures.
❍ Provide supportive measures.
❍ Provide adequate fluid intake.
❍ Give prescribed drugs.
❍ Cardiac rhythm
❍ Complications
❍ Intake and output
❍ Level of consciousness
❍ Myoglobin test results
❍ Pulse oximetry readings
❍ Vital signs

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Hemolytic uremic Physical assessment

Early symptoms
syndrome ❍ Bloody stool
❍ Diarrhea
❍ Fever
❍ Irritability
Overview ❍ Lethargy
❍ Vomiting
Description ❍ Weakness
❍ Syndrome characterized by acute renal failure, he- Later symptoms
molytic anemia, fever and thrombocytopenia ❍ Anuria
❍ Usually affects children ❍ Bruising
❍ Decreased consciousness
Pathophysiology ❍ Jaundice
❍ A toxin produced by Escherichia coli, Shigella ❍ Low urine output
dysenteriae, or a virus (such as varicella) causes ❍ Pallor
endothelial damage. ❍ Petechiae
❍ Microvascular lesions develop with microthrombi. ❍ Seizures (rare)
❍ Arterioles and capillaries in the renal microvascula-
ture become occluded. Test results
❍ Thrombocytopenia and microangiopathic hemolytic Laboratory
anemia develop. ❍ Schistocytes and giant platelets in peripheral smear
❍ Increased lactate dehydrogenase level
Risk factors ❍ Increased indirect bilirubin level
❍ Eating rare hamburger ❍ Increased blood urea nitrogen level
❍ Visiting a petting zoo ❍ Increased creatinine level
❍ Visiting someone with diarrhea ❍ Red blood cells in urine
❍ Proteinuria
Causes ❍ Disseminated intravascular coagulation panel within
❍ Prodromal infectious disease normal range
❍ Upper respiratory infection ❍ Increased reticulocyte count

AGE AWARE Hemolytic uremic syndrome usu-
Nursing diagnoses
ally affects children 6 months to 4 years of age.
❍ Acute pain
❍ In adults, usually women who take oral contracep- ❍ Impaired urinary elimination
tives, recently gave birth, or have obstetric complica- ❍ Risk for imbalanced fluid volume
❍ More common among patients who have received Key outcomes
chemotherapy with 5-fluorouracil The patient will:
❍ maintain hemodynamic stability
Complications ❍ maintain balanced electrolytes and fluid status
❍ Acute renal failure ❍ express understanding of disorder and treatment.
❍ Cerebrovascular accident
❍ Disseminated intravascular coagulation
❍ Chronic renal failure Interventions
❍ Hypertension
❍ Neurologic deficits General
❍ Dialysis
❍ Initially, fluid replacement
Assessment ❍ Plasmapheresis
❍ Supportive care
❍ Acute diarrhea a few weeks before the onset of Nursing
symptoms ❍ Give fluids as prescribed.
❍ Bloody stool ❍ Give prescribed drugs.
❍ Decreased urine output ❍ Provide emotional support.
❍ Fatigue ❍ Antibiotics may be avoided.

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Drug therapy
❍ Antihypertensives
❍ Intake and output
❍ Laboratory test results
❍ Renal status
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ the need to refrain from eating rare beef
❍ the need to wash hands thoroughly.

Discharge planning
❍ Encourage follow-up care with a nephrologist and

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Hepatorenal syndrome Test results

❍ Increased serum creatinine level
❍ Creatinine clearance less than 40 ml/minute in
Overview 24-hour urine test
❍ Proteinuria
Description ❍ Low urine sodium level
❍ Renal failure in patients with chronic liver disease ❍ Bacteria in ascites fluid
❍ Liver disease progressed to portal hypertension and
❍ Two types Nursing diagnoses
– Type 1: rapid and progressive renal impairment
caused by spontaneous bacterial peritonitis ❍ Anticipatory grieving
– Type 2: moderate and stable reduction in the ❍ Anxiety
glomerular filtration rate ❍ Deficient knowledge (hepatorenal syndrome)
❍ Impaired urinary elimination
Pathophysiology ❍ Ineffective coping
❍ Advanced liver disease causes vasoconstriction in the ❍ Risk for imbalanced fluid volume
renal circulation and intense systemic arteriolar va-
sodilatation. Key outcomes
❍ This results in reduced systemic vascular resistance The patient will:
and arterial hypotension. ❍ maintain adequate fluid balance
❍ Renal perfusion is affected. ❍ express understanding of the disease process and
❍ Renal failure eventually occurs. treatment
❍ use positive coping mechanisms
Causes ❍ use available support systems
❍ Chronic liver disease with marked sodium and water ❍ express desires for end-of-life care.
Prevalence Interventions
❍ Affects both sexes equally
❍ Ages 40 to 80 in most adults with chronic liver General
failure ❍ Liver transplant
❍ Low-sodium diet
Complications ❍ Peritoneovenous shunting (type 2)
❍ Death ❍ Supportive care
❍ Surgical shunts
Assessment Nursing
❍ Give drugs and fluids as prescribed.
History ❍ Provide supportive care.
❍ Chronic liver disease ❍ Provide emotional support.
❍ Decreased urine output ❍ Encourage a low-sodium diet.
❍ Fatigue
❍ Malaise Drug therapy
❍ Antibiotics
Physical assessment ❍ Antioxidants
❍ Clubbing ❍ Plasma expanders
❍ Decreased urine output ❍ Vasoconstrictors
❍ Evidence of chronic advanced liver disease ❍ Vasodilators
– Asterixis ❍ Vasopressin analogues
– Scleral icterus
– Muscle wasting Monitoring
– Spider nevi ❍ Intake and output
– Ascites ❍ Laboratory test results
– Peripheral edema ❍ Renal status
❍ Vital signs

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Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ low-sodium diet
❍ liver transplantation
❍ end-of-life issues.

Discharge planning
❍ Refer the patient to social services for appropriate

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Hydronephrosis ❍

Change in voiding pattern
❍ Dysuria
❍ Hematuria
Overview ❍ No symptoms or only mild pain and slightly de-
creased urine flow
Description ❍ Pain on urination
❍ Abnormal dilation of the renal pelvis and calyces of ❍ Possibly no initial symptoms, but eventual renal dys-
one or both kidneys function as pressure increases behind the obstruc-
❍ Caused by obstruction of urine flow in the genitouri- tion
nary tract ❍ Pyuria
❍ May be acute or chronic ❍ Severe, colicky, renal pain or dull flank pain that ra-
diates to the groin
Pathophysiology ❍ Nausea
❍ With obstruction in the urethra or bladder, hydro- ❍ Urinary hesitancy
nephrosis is usually bilateral. ❍ Varies with cause of obstruction
❍ With obstruction in a ureter, hydronephrosis is usu- ❍ Vomiting
ally unilateral.
❍ Obstruction distal to the bladder causes the bladder Physical assessment
to dilate, acting as a buffer zone, delaying hydro- ❍ Costovertebral angle tenderness
nephrosis. ❍ Distended bladder
❍ Total obstruction of urine flow with dilation of the ❍ Hematuria
collecting system ultimately causes complete cortical ❍ Leg edema
atrophy, and glomerular filtration ceases. ❍ Palpable kidney
❍ Pyuria
Causes ❍ Urinary tract infection
❍ Benign prostatic hyperplasia (BPH)
❍ Bladder, ureteral, or pelvic tumors Test results
❍ Blood clots Laboratory
❍ Congenital abnormalities ❍ Abnormal results on renal function study
❍ Gram-negative infection ❍ Inability to concentrate urine
❍ Neurogenic bladder ❍ Decreased glomerular filtration rate
❍ Renal calculi ❍ Pyuria if infection is present
❍ Strictures or stenosis of the ureter or bladder outlet ❍ Leukocytosis, indicating infection
❍ Tuberculosis Imaging
❍ Ureterocele ❍ Radionuclide scan may show the site of obstruction.
❍ Urethral strictures ❍ Computed tomography may indicate the cause.
Diagnostic procedures
Prevalence ❍ Excretory urography, retrograde pyelography, and
❍ About 1 in 100 people affected by unilateral hydro- renal ultrasonography confirm diagnosis.
nephrosis ❍ I.V. urogram may show site of obstruction.
❍ About 1 in 200 people affected by bilateral hydro- ❍ On a nephrogram, the apearance of contrast materi-
nephrosis al may be delayed.
❍ Infection Nursing diagnoses
❍ Obstructive nephropathy
❍ Paralytic ileus ❍ Acute pain
❍ Pyelonephritis ❍ Anxiety
❍ Renal calculi ❍ Deficient fluid volume
❍ Renal failure ❍ Imbalanced nutrition: less than body requirements
❍ Renovascular hypertension ❍ Impaired urinary elimination
❍ Sepsis ❍ Risk for infection
Key outcomes
Assessment The patient will:
❍ avoid or minimize complications
History ❍ maintain fluid balance
❍ Abdominal fullness ❍ report increased comfort
❍ Alternating oliguria and polyuria, anuria

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❍ maintain hemodynamic stability

❍ demonstrate skill in managing urinary elimination.

❍ Dilatation for urethral stricture
❍ For inoperable obstructions, decompression and
drainage of the kidney using a nephrostomy tube
placed temporarily or permanently in the renal
❍ If renal function affected, low-protein, low-sodium,
and low-potassium diet
❍ Placement of percutaneous nephrostomy tube
❍ Prostatectomy for BPH
❍ Urinary catheterization
❍ Give prescribed drugs.
❍ Give prescribed I.V. fluids.
❍ Allow the patient to express his fears and anxieties.
Drug therapy
❍ Analgesics
❍ Antibiotic therapy
❍ Oral alkalinization therapy (for uric acid calculi)
❍ Corticosteroid therapy (for retroperitoneal fibrosis)
❍ Fluid and electrolyte status
❍ Intake and output
❍ Nephrostomy tube function and drainage, if appro-
❍ Renal function studies
❍ Vital signs
❍ Wound site (postoperatively)

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ the procedure and postoperative care, if surgery is
❍ nephrostomy tube care, if appropriate
❍ prescribed drugs, dosages, and possible adverse ef-
❍ diet changes
❍ how to recognize and when to report hydronephro-
sis symptoms.

Discharge planning
❍ Follow-up imaging studies may be required to evalu-
ate the patient’s recovery.
❍ Follow-up laboratory studies may be needed to as-
sess renal function.

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Hyperaldosteronism Assessment
Overview ❍ Fatigue
❍ Headaches
Description ❍ Nocturnal polyuria
❍ Hypersecretion of the mineralocorticoid aldosterone ❍ Polydipsia
by the adrenal cortex ❍ Vision disturbances
❍ Excessive reabsorption of sodium and water
❍ Excessive renal excretion of potassium Physical assessment
❍ May be primary (uncommon) or secondary ❍ High blood pressure
❍ Intermittent flaccid paralysis
Pathophysiology ❍ Muscle weakness
Primary hyperaldosteronism (Conn’s ❍ Paresthesia
❍ Chronic excessive secretion of aldosterone is inde- Test results
pendent of the renin-angiotensin system and sup- Laboratory
presses plasma renin activity. ❍ Persistently low serum potassium levels
❍ This aldosterone excess enhances sodium and water ❍ Low plasma renin level that fails to increase appro-
reabsorption and potassium loss by the kidneys, priately during volume depletion (upright posture,
which leads to mild hypernatremia and, simultane- sodium depletion) and a high plasma aldosterone
ously, hypokalemia and increased extracellular fluid level during volume expansion by salt loading (con-
volume. firmation of primary hyperaldosteronism in a hyper-
❍ Expansion of intravascular fluid volume results in tensive patient without edema)
volume-dependent hypertension and increased car- ❍ Increased serum bicarbonate level
diac output. ❍ Markedly increased urine aldosterone level
❍ Increased plasma aldosterone level
A LERT Excessive consumption of English
black licorice or licorice-like substances can ❍ Increased plasma renin level (secondary)
produce a syndrome similar to primary hyperaldos- ❍ Suppression test to differentiate between primary
teronism because of the mineralocorticoid action of and secondary hyperaldosteronism
glycyrrhizic acid. Imaging
❍ Chest X-rays show left ventricular hypertrophy from
Secondary hyperaldosteronism chronic hypertension.
❍ An extra-adrenal abnormality stimulates the adrenal Diagnostic procedures
gland to increase aldosterone production. ❍ Electrocardiography shows signs of hypokalemia
(ST-segment depression and U waves).
Causes ❍ Adrenal angiography or computed tomography scan
❍ Bartter’s syndrome localize tumor.
❍ Benign aldosterone-producing adrenal adenoma (in
70% of patients)
❍ Bilateral adrenocortical hyperplasia (in children) or Nursing diagnoses
carcinoma (rarely)
❍ Conditions that produce a sodium deficit (Wilms’ tu- ❍ Acute pain
mor) ❍ Decreased cardiac output
❍ Conditions that reduce renal blood flow and extra- ❍ Deficient knowledge (hyperaldosteronism)
cellular fluid volume (renal artery stenosis) ❍ Impaired urinary elimination
❍ Heart failure ❍ Ineffective coping
❍ Hepatic cirrhosis with ascites ❍ Ineffective tissue perfusion: renal
❍ Nephrotic syndrome
Key outcomes
Prevalence The patient will:
❍ Most common between ages 30 and 50 ❍ maintain hemodynamic stability
❍ Three times more common in women than in men ❍ express feelings of increased comfort
❍ maintain adequate fluid balance
Complications ❍ express understanding of the condition and treat-
❍ Left ventricular hypertrophy, heart failure, death ment.
❍ Metabolic alkalosis, nephropathy, azotemia
❍ Neuromuscular irritability, tetany, paresthesia
❍ Seizures

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❍ Treatment of underlying cause (secondary)
❍ Low-sodium, high-potassium diet
❍ Unilateral adrenalectomy (primary)
❍ Watch for signs of tetany (muscle twitching,
Chvostek’s sign, Trousseau’s sign).
❍ Give potassium replacement, and keep I.V. calcium
gluconate available.
❍ After adrenalectomy, watch for weakness, hypona-
tremia, rising serum potassium levels, and signs of
adrenal hypofunction, especially hypotension.
Drug therapy
❍ Potassium-sparing diuretics (primary)
❍ Cardiac arrhythmias
❍ Intake and output
❍ Serum electrolyte levels
❍ Vital signs
❍ Weight

Patient teaching
Be sure to cover:
❍ adverse effects of spironolactone, including hyper-
kalemia, impotence, and gynecomastia, if needed
❍ the importance of wearing medical identification
jewelry while taking steroid hormone replacement

Discharge planning
❍ Refer the patient to an endocrinologist as needed.

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Hypercalcemia Physical assessment

❍ Confusion
❍ Decreased muscle tone (See Effects of hypercal-
Overview cemia.)
❍ Hyporeflexia
❍ Muscle weakness
❍ Excessive serum calcium level Test results
Pathophysiology ❍ Serum calcium levels greater than 10.5 mg/dl
❍ Together with phosphorus, calcium is responsible ❍ Ionized calcium levels less than 5.3 mg/dl
for the formation and structure of bones and teeth. Imaging
❍ Calcium helps maintain cell structure and function. ❍ Electrocardiogram shows a shortened QT interval
❍ It plays a role in cell membrane permeability and and ventricular arrhythmias.
impulse transmission.
❍ It affects the contraction of cardiac muscle, smooth
muscle, and skeletal muscle. Nursing diagnoses
❍ It participates in the blood-clotting process.
❍ Decreased cardiac output
Causes ❍ Deficient knowledge (hypercalcemia)
❍ Certain cancers ❍ Impaired gas exchange
❍ Certain drugs (See Drugs that cause hypercal- ❍ Ineffective tissue perfusion: cardiopulmonary
❍ Hyperparathyroidism Key outcomes
❍ Hypervitaminosis D The patient will:
❍ Multiple fractures ❍ maintain stable vital signs
❍ Prolonged immobilization ❍ maintain adequate cardiac output
❍ express an understanding of the disorder and treat-
Prevalence ment regimen.
❍ Considerably more common in women than in men
❍ No gender predominance when related to cancer
❍ Increases with age Interventions
Complications General
❍ Cardiac arrest ❍ Activity, as tolerated
❍ Coma ❍ Treatment of the underlying cause
❍ Renal calculi
❍ Provide safety measures.
Assessment ❍ Institute seizure precautions, if appropriate.
❍ Give prescribed I.V. solutions.
History ❍ Watch for evidence of heart failure.
❍ Anorexia
❍ Constipation Drug therapy
❍ Lethargy ❍ Loop diuretics
❍ Nausea, vomiting ❍ Normal saline solution
❍ Polyuria
❍ Underlying cause Monitoring
❍ Weakness ❍ Calcium levels
❍ Cardiac rhythm
❍ Seizures
Drugs that cause hypercalcemia
These drugs can cause or contribute to hypercalcemia:
● antacids that contain calcium
Patient teaching
● calcium preparations (oral or I.V.)
● lithium
Be sure to cover:
❍ the need to avoid over-the-counter drugs that are
● thiazide diuretics
● vitamin A high in calcium
● vitamin D. ❍ the need to increase fluid intake
❍ the need to follow a low-calcium diet.

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Effects of hypercalcemia
Body system Effects
Cardiovascular ● Cardiac arrest
● Hypertension
● Signs of heart block

Gastrointestinal ● Anorexia
● Constipation
● Dehydration
● Nausea and vomiting
● Polydipsia

Musculoskeletal ● Bone pain

● Muscle flaccidity
● Pathologic fractures
● Weakness

Neurologic ● Confusion
● Depression or apathy
● Drowsiness
● Headaches
● Irritability
● Lethargy

Other ● Eventual azotemia

● Flank pain
● Renal polyuria

Discharge planning
❍ Refer the patient to a dietitian and social services, if

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Hyperchloremia ❍

❍ Loss of pancreatic secretion
❍ Metabolic acidosis
Overview ❍ Prolonged diarrhea
❍ Renal tubular acidosis
❍ Excessive serum levels of the chloride anion Complications
❍ Usually accompanied by sodium and water retention ❍ Coma
❍ Chloride accounts for two-thirds of all serum anions. Assessment
❍ Chloride is secreted by the stomach mucosa as hy-
drochloric acid; it provides an acid medium that History
aids digestion and activates enzymes. ❍ Altered level of consciousness
❍ Chloride helps to maintain acid-base and body water
balances, influences the osmolality or tonicity of ex- Physical assessment
tracellular fluid, plays a role in the exchange of oxy- ❍ Agitation
gen and carbon dioxide in red blood cells, and helps ❍ Dyspnea
activate salivary amylase (which, in turn, activates ❍ Hypertension
digestion). ❍ Pitting edema
❍ An inverse relationship exists between chloride and ❍ Rapid deep breathing (Kussmaul’s respirations)
bicarbonate. (See Anion gap and metabolic acido- ❍ Tachypnea
sis.) ❍ Weakness
Risk factors Test results
❍ Therapy with drugs known to increase the chloride Laboratory
level ❍ Serum chloride level above 108 mEq/L
❍ With metabolic acidosis, serum pH below 7.35,
Causes serum carbon dioxide level below 22 mEq/L, and
❍ Certain drugs (See Drugs that cause hyper- normal anion gap
chloremia.) ❍ Serum sodium level above 145 mEq/L

Anion gap and metabolic acidosis

Nursing diagnoses
The anion gap is the difference between measurements of
cations and anions. Because concentrations of positive ❍ Anxiety
and negative electrolytes balance in the body, you might ❍ Deficient fluid volume
think the difference should be zero. However, because not ❍ Deficient knowledge (hyperchloremia)
all electrolytes are routinely measured, there’s an anion ❍ Ineffective breathing pattern
gap. Plus, the patient may have small amounts of ❍ Ineffective tissue perfusion: cardiopulmonary
anions — such as lactate, phosphates, sulfates, and
proteins — in his blood. Usually, the anion gap is Key outcomes
considered normal if it’s 8 to 16 mEq/L if potassium is
included in the calculation (8 to 12 mEq/L if it’s isn’t). The patient will:
The anion gap can be used to help identify metabolic ❍ maintain adequate cardiac output
acidosis. That’s because, as acids accumulate in the ❍ maintain stable vital signs
bloodstream, bicarbonate levels decline to regulate blood ❍ maintain adequate fluid volume
pH. When bicarbonate levels decline, the anion gap ❍ avoid complications.
increases. That’s why metabolic acidosis usually is
reflected in an increased anion gap. Metabolic alkalosis
usually is reflected in a decreased anion gap. Interventions
Hyperchloremia relates to the anion gap because
chloride and bicarbonate have an inverse relationship. As General
chloride levels rise, bicarbonate levels decline. If a patient
❍ Activity, as tolerated
with metabolic acidosis has a normal anion gap, the
❍ Restoration of fluid, electrolyte, and acid-base bal-
acidosis probably results from a loss of bicarbonate ions
by the kidneys or the gastrointestinal tract. Or the acidosis ance
could result from an accumulation of chloride ions as ❍ Restricted sodium and chloride intake
acidifying salts. In these cases, chloride ion levels rise, ❍ Treatment of underlying cause
causing hyperchloremia — with a normal anion gap.

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Drugs that cause hyperchloremia

These drugs can cause or contribute to hyperchloremia:
● acetazolamide
● ammonium chloride
● phenylbutazone
● salicylates (overdose)
● sodium polystyrene sulfonate (Kayexalate)
● triamterene.

❍ Provide a safe environment.
❍ Give prescribed I.V. fluids.
❍ Evaluate muscle strength.
❍ Adjust activity level.
❍ Reorient a confused patient when needed.
Drug therapy
❍ Diuretics
❍ Lactated Ringer’s solution
❍ Sodium bicarbonate I.V.
❍ Arterial blood gas levels
❍ Cardiac rhythm
❍ Intake and output
❍ Neurologic status
❍ Respiratory status
❍ Serum electrolyte levels
❍ Signs of metabolic alkalosis

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ dietary or fluid restrictions, as indicated
❍ prescribed drugs, dosages, and possible adverse ef-

Discharge planning
❍ Refer the patient to a nutritionist for diet restrictions
as appropriate.

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Hyperkalemia Assessment
Overview ❍ Abdominal cramps
❍ Diarrhea
Description ❍ Irritability
❍ Excessive serum levels of the potassium anion ❍ Muscle weakness
❍ Commonly induced by other treatments ❍ Nausea
❍ Paresthesia
❍ Potassium facilitates contraction of skeletal and Physical assessment
smooth muscles, including myocardial contraction. ❍ Hypotension
❍ Potassium figures prominently in nerve impulse con- ❍ Irregular heart rate
duction, acid-base balance, enzyme action, and cell ❍ Possible cardiac arrhythmia (See Effects of hyper-
membrane function. kalemia.)
❍ Slight changes in serum levels can produce pro-
found clinical consequences. Test results
❍ Potassium imbalance can lead to muscle weakness Laboratory
and flaccid paralysis because of an ionic imbalance ❍ Serum potassium levels greater than 5 mEq/L
in neuromuscular tissue excitability. ❍ Decreased arterial pH
Causes ❍ Electrocardiogram shows a tall, tented T wave.
❍ Adrenal gland insufficiency
❍ Burns
❍ Certain drugs (See Drugs that cause Nursing diagnoses
❍ Crush injuries ❍ Decreased cardiac output
❍ Decreased urinary excretion of potassium ❍ Deficient knowledge (hyperkalemia)
❍ Dehydration
❍ Diabetic acidosis
❍ Increased potassium intake Effects of hyperkalemia
❍ Large quantities of transfused blood
❍ Renal dysfunction or failure Type of dysfunction Effects
❍ Severe infection
❍ Acid-base balance ● Metabolic acidosis
Use of potassium-sparing diuretics, such as tri-
amterene, by patients with renal disease Cardiovascular ● Cardiac arrest (with
levels > 7.0 mEq/L)
Prevalence ● Electrocardiogram
❍ Affects males and females equally changes (tented and
elevated T waves,
❍ Diagnosed in up to 8% of hospitalized patients in the widened QRS complex,
United States prolonged PR interval,
flattened or absent P
Complications waves, depressed ST
❍ Cardiac arrest ● Tachycardia and later
❍ Cardiac arrhythmia bradycardia
❍ Metabolic acidosis
Gastrointestinal ● Abdominal cramps
● Diarrhea
● Nausea
Genitourinary ● Anuria
Drugs that cause hyperkalemia
● Oliguria
These drugs may increase potassium levels: Musculoskeletal ● Flaccid paralysis
● angiotensin-converting enzyme inhibitors ● Muscle weakness
● antibiotics
● beta blockers Neurologic ● Flaccid paralysis
● chemotherapeutic drugs ● Hyperreflexia progressing
● nonsteroidal anti-inflammatory drugs to weakness
● potassium (in excessive amounts) ● Numbness
● Tingling
● spironolactone.

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Avoiding false results

Discharge planning
When your patient gets a laboratory test result indicating
a high potassium level, and the result doesn’t make sense,
make sure it’s a true result. If the sample was drawn using ❍ Refer the patient to a nutritionist for a low-potassium
poor technique, the results may be falsely high. Some of diet as appropriate.
the causes of falsely high potassium levels are:
● drawing the sample above the site of an I.V. infusion
that contains potassium
● using a recently exercised arm or leg for the veni-
puncture site
● causing hemolysis (cell damage) as the specimen is

❍ Diarrhea
❍ Fluid volume deficit
Key outcomes
The patient will:
❍ maintain hemodynamic stability
❍ maintain a normal potassium level
❍ understand potential adverse effects of prescribed

❍ Activity, as tolerated
❍ Hemodialysis or peritoneal dialysis
❍ Treatment of the underlying cause
❍ Check the serum sample. (See Avoiding false re-
❍ Give prescribed drugs.
❍ Insert an indwelling urinary catheter.
❍ Implement safety measures.
❍ Be alert for signs of hypokalemia after treatment.
Drug therapy
❍ Insulin and 10% to 50% glucose I.V.
❍ Rapid infusion of 10% calcium gluconate (decreases
myocardial irritability)
❍ Sodium polystyrene sulfonate with 70% sorbitol
❍ Cardiac rhythm
❍ Intake and output
❍ Serum potassium levels

Patient teaching
Be sure to cover:
❍ prescribed drugs and potential adverse effects
❍ the need to monitor intake and output
❍ preventing future episodes of hyperkalemia
❍ the need for a potassium-restricted diet.

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Hypermagnesemia Prevalence
❍ Rarely occurs in the United States
Overview ❍ Cardiac arrest
❍ Cardiac arrhythmia
Description ❍ Respiratory depression
❍ Excessive serum levels of the magnesium cation
Pathophysiology Assessment
❍ Magnesium enhances neuromuscular integration
and stimulates parathyroid hormone secretion, thus History
regulating intracellular fluid calcium levels. ❍ Confusion
❍ Magnesium may also regulate skeletal muscles ❍ Drowsiness
through its influence on calcium utilization by de- ❍ Nausea
pressing acetylcholine release at synaptic junctions. ❍ Vomiting
❍ Magnesium activates many enzymes needed for car-
bohydrate and protein metabolism, aids in cell me- Physical assessment
tabolism and the transport of sodium and potassium ❍ Flushed appearance
across cell membranes, and influences sodium, ❍ Hyporeflexia (See Effects of hypermagnesemia and
potassium, calcium, and protein levels. Testing the patellar reflex.)
❍ About one-third of magnesium consumed is ab- ❍ Hypotension
sorbed through the small intestine and eventually is ❍ Muscle weakness
excreted in the urine; the remaining unabsorbed ❍ Weak pulse
magnesium is excreted in stool.
Test results
Risk factors Laboratory
❍ Advanced age ❍ Serum magnesium levels greater than 2.5 mEq/L
❍ Pregnancy Diagnostic procedures
❍ Neonates whose mothers received magnesium sul- ❍ Electrocardiogram (ECG) shows prolonged PR inter-
fate during labor val, widened QRS complex, and tall T waves.
❍ Receiving magnesium sulfate to control seizures
Causes Nursing diagnoses
❍ Addison’s disease
❍ Adrenocortical insufficiency ❍ Anxiety
❍ Chronic renal insufficiency ❍ Deficient knowledge (hypermagnesemia)
❍ Overcorrection of hypomagnesemia ❍ Impaired gas exchange
❍ Overuse of magnesium-containing antacids ❍ Ineffective tissue perfusion: renal
❍ Severe dehydration (resulting oliguria can cause ❍ Risk for deficient fluid volume
magnesium retention)
❍ Untreated diabetic ketoacidosis
❍ Use of magnesium-containing laxatives (magnesium Effects of hypermagnesemia
sulfate, Milk of Magnesia, and magnesium citrate so-
Body system Effects
lutions), especially with renal insufficiency (See
Drugs and supplements that cause hypermagne- Cardiovascular ● Bradycardia
semia.) ● Cardiac arrest
● Heart block
● Hypotension
● Weak pulse
Drugs and supplements that cause
hypermagnesemia Neurologic ● Confusion
● Diminished sensorium
● Drowsiness
Monitor your patient’s magnesium level closely if he’s ● Flushing
receiving: ● Lethargy
● an antacid (Di-Gel, Gaviscon, Maalox)
● a laxative (Milk of Magnesia, Haley’s M-O, magnesium Neuromuscular ● Diminished reflexes
citrate) ● Flaccid paralysis
● a magnesium supplement (magnesium oxide, ● Muscle weakness
● Respiratory muscle
magnesium sulfate). paralysis that may cause
respiratory compromise

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Testing the patellar reflex

One way to gauge your patient’s Sitting Supine position
magnesium status is to test his Test the reflex with the patient sitting Test the reflex after flexing the pa-
patellar reflex, one of the deep tendon on the side of the bed, legs dangling tient’s knee at a 45-degree angle with
reflexes affected by magnesium level. freely, as shown here. nondominant hand behind it for
To test the reflex, strike the patellar support.
tendon just below the patella with the
patient sitting or lying in a supine
position, as shown. Look for leg
extension or contraction of the
quadriceps muscle in the front of
the thigh.
If the patellar reflex is absent, notify
the doctor immediately. This finding
may mean your patient’s magnesium
level is 7 mEq/L or higher.

Key outcomes Patient teaching

The patient will:
❍ maintain hemodynamic stability Be sure to cover:
❍ attain and maintain a normal magnesium level ❍ the need not to abuse laxatives and antacids contain-
❍ understand the causes of high magnesium levels ing magnesium, particularly by the elderly or pa-
❍ have a normal ECG tients with compromised renal function
❍ maintain fluid volume balance. ❍ hydration requirements
❍ prescribed drugs.

Discharge planning
❍ Identification and correction of the underlying cause None.
❍ Increased fluid intake
❍ Peritoneal dialysis or hemodialysis
❍ Provide sufficient fluids for adequate hydration and
maintenance of renal function.
❍ Give prescribed drugs.
❍ Report abnormal serum electrolyte levels immedi-
❍ Watch patients receiving both a cardiac glycoside
and calcium gluconate because calcium excess en-
hances the cardiac glycoside.
Drug therapy
❍ Calcium gluconate (10%)
❍ Loop diuretics, such as furosemide, with impaired
renal function
❍ Cardiac rhythm
❍ Electrolyte levels
❍ Intake and output
❍ Level of consciousness
❍ Magnesium levels
❍ Neuromuscular system
❍ Respiratory status
❍ Vital signs

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Hypernatremia Complications
❍ Coma
❍ Permanent neurologic damage
Overview ❍ Seizures

Description Assessment
❍ Excessive serum levels of the sodium cation relative
to body water History
❍ Disorientation
Pathophysiology ❍ Fatigue
❍ Sodium is the major cation (90%) in extracellular ❍ Lethargy
fluid; potassium, the major cation in intracellular ❍ Restlessness, agitation
fluid. ❍ Weakness
❍ During repolarization, the sodium-potassium pump
continually shifts sodium into the cells and potassi- Physical assessment
um out of the cells; during depolarization, it does ❍ Dry, swollen tongue
the reverse. ❍ Flushed skin
❍ Sodium cation functions include maintaining tonicity ❍ Hypertension, dyspnea (with hypervolemia)
and concentration of extracellular fluid, acid-base ❍ Low-grade fever
balance (reabsorption of sodium ion and excretion ❍ Orthostatic hypotension and oliguria (with hypo-
of hydrogen ion), nerve conduction and neuromus- volemia) (See Effects of hypernatremia.)
cular function, glandular secretion, and water bal- ❍ Sticky mucous membranes
ance. ❍ Twitching
❍ Increased sodium causes high serum osmolality (in-
creased solute concentrations in the body), which Test results
stimulates the hypothalamus to create the sensation Laboratory
of thirst. ❍ Serum sodium level greater than 145 mEq/L
❍ Urine sodium level less than 40 mEq/24 hours, with
Risk factors high serum osmolality
❍ Inability to drink voluntarily
Causes Nursing diagnoses
❍ Antidiuretic hormone deficiency (diabetes insipidus)
❍ Certain drugs (See Drugs that cause hypernatre- ❍ Deficient knowledge (hypernatremia)
mia.) ❍ Disturbed thought processes
❍ Decreased water intake ❍ Ineffective tissue perfusion: cardiopulmonary
❍ Excess adrenocortical hormones, as in Cushing’s ❍ Risk for deficient fluid volume
syndrome ❍ Risk for injury
❍ Excessive I.V. administration of sodium solutions
❍ Salt intoxication (less common), which may be pro- Key outcomes
duced by excessive consumption of table salt The patient will:
❍ maintain adequate fluid volume
Prevalence ❍ maintain a normal sodium level
❍ Occurs in about 1% of hospitalized patients ❍ maintain stable vital signs
❍ Usually occurs in elderly patients ❍ remain alert and oriented to the environment.
❍ Affects males and females equally

Drugs that cause hypernatremia

Ask your patient if he has received or is taking any of General
these drugs, all of which can elevate his sodium level: ❍ Activity, as tolerated
● anatacids with sodium bicarbonate ❍ Administration of salt-free solutions (such as dex-
● antibiotics, such as ticarcillin disodium–clavulanate trose in water) followed by infusion of half-normal
potassium (Timentin)
saline solution to prevent hyponatremia
● I.V. sodium chloride preparations
❍ Discontinuation of drugs that promote sodium reten-
● salt tablets
● sodium bicarbonate injections (such as those given
during cardiac arrest) ❍ Sodium-restricted diet
● sodium polystyrene sulfonate (Kayexalate). ❍ Treatment of underlying cause

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Effects of hypernatremia
Body system Effects
Cardiovascular ● Excessive weight gain
● Hypertension
● Pitting edema
● Tachycardia

Gastrointestinal ● Dry, sticky membranes

● Flushed skin

Genitourinary ● Intense thirst

● Rough, dry tongue

Musculoskeletal ● Oliguria

Neurologic ● Agitation
● Fever
● Restlessness
● Seizures

Respiratory ● Death (from dramatic rise

in osmotic pressure)
● Dyspnea
● Respiratory arrest

❍ Obtain a drug history to check for drugs that pro-
mote sodium retention.
❍ Assist with oral hygiene.
❍ Watch for signs of cerebral edema during fluid re-
placement therapy.
Drug therapy
❍ Diuretics
❍ Vasopressin if the patient has diabetes insipidus.
❍ Intake and output
❍ Neurologic status
❍ Serum sodium levels

Patient teaching
Be sure to cover:
❍ the disorder and treatment
❍ the importance of sodium restriction
❍ low-sodium diet
❍ prescribed drugs, dosages, and possible adverse ef-
❍ signs and symptoms of hypernatremia
❍ the need to avoid over-the-counter drugs that contain

Discharge planning
❍ Refer the patient to a nutritionist or dietitian for diet
restrictions as appropriate.

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Hyperosmolar ❍

Negative ketone test
pH usually above 7.25
hyperglycemic ❍

Increased urine specific gravity
nonketotic syndrome ❍ Possible evidence of urinary tract infection

Overview Nursing diagnoses

❍ Deficient fluid volume
Description ❍ Deficient knowledge (hyperosmolar hyperglycemic
❍ Metabolic condition characterized by hyperglycemia nonketotic syndrome)
and hyperosmolarity without ketoacidosis ❍ Disturbed thought processes
❍ Occurs in adult-onset diabetes mellitus ❍ Ineffective coping
❍ Risk for injury
❍ Fluid intake decreases in a diabetic patient, usually Key outcomes
because of a secondary illness. The patient will:
❍ Hyperglycemia and hyperosmolarity lead to osmotic ❍ maintain adequate fluid volume
diuresis and intracellular dehydration. ❍ express understanding of disorder
❍ Ketoacidosis doesn’t occur, for unknown reasons. ❍ remain safe from injury
❍ remain alert and oriented
Causes ❍ use positive coping mechanisms and available sup-
❍ Certain drugs (such as diuretics and beta blockers) port systems.
❍ Illness in a person with diabetes mellitus
❍ Noncompliance with diabetic drug therapy
❍ Stress Interventions
Prevalence General
❍ Occurs slightly more in women than men ❍ Airway maintenance
❍ Mean age of occurrence is the early 40s ❍ I.V. fluids
❍ Supportive care
Complications ❍ Treatment for concurrent illness
❍ Coma
❍ Give drugs and I.V. fluids as ordered.
Assessment ❍ Provide emotional support.
History Drug therapy
❍ Diabetes mellitus ❍ Antibiotics (if infection present)
❍ Drowsiness ❍ Insulin
❍ Secondary illness, acute or chronic
❍ Seizures Monitoring
❍ Sensory deficits ❍ Blood glucose levels
❍ Visual changes ❍ Intake and output
❍ Hydration status
Physical assessment ❍ Neurological status
❍ Hypotension ❍ Vital signs
❍ Signs of dehydration
❍ Signs of infection (See Comparing hyperosmolar
hyperglycemic nonketotic syndrome and diabetic Patient teaching
❍ Tachycardia Be sure to cover:
❍ the disorder, diagnosis, and treatment
Test results ❍ the need to follow the appropriate diabetic diet
Laboratory ❍ when to notify the doctor
❍ Increased serum glucose level ❍ prescribed drugs, and possible adverse effects.
❍ Abnormal sodium level
❍ Elevated blood urea nitrogen and creatinine levels
❍ Increased serum osmolarity

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Comparing hyperosmolar hyperglycemic nonketotic syndrome and diabetic ketoacidosis

Hyperosmolar hyperglycemic nonketotic syndrome (HHNS) and diabetic ketoacidosis (DKA), both acute complications of
diabetes, share some similarities, but they’re two distinct conditions. Use this flowchart to help determine which condition
your patient is experiencing.

History of diabetes mellitus


Type 1 NO Type 2


Rapid onset NO Slow onset

● Coma
YES ● Drowsiness YES
● Extreme volume depletion
● Polyuria
● Stupor

● Acetone breath odor ● Blood glucose level

● Blood glucose level slightly markedly elevated
above normal ● Hypernatremia
● Hyperkalemia initially and ● Negative or small serum ke-
then hypokalemia tones
● Hyperventilation ● Lack of acidosis
● Metabolic acidosis ● No breath odor
● Mild hyponatremia NO ● Normal serum potassium
● Positive or large serum ● Serum osmolality markedly
ketones elevated
● Serum osmolality slightly ● Slightly rapid respirations


Suspect DKA Suspect HHNS

Discharge planning
❍ Refer the patient for diabetic teaching if needed.

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Hyperparathyroidism Assessment
Overview ❍ Abdominal pain
❍ Anemia
Description ❍ Anorexia, nausea, and vomiting
❍ Increased secretion of parathyroid hormone (PTH) ❍ Cataracts
❍ Classified as either primary or secondary ❍ Chronic lower back pain
❍ Constant, severe epigastric pain that radiates to the
Pathophysiology back
❍ Primary: One or more of the parathyroid glands en- ❍ Constipation
larges, increasing PTH secretion and elevating serum ❍ Depression
calcium levels; or an adenoma secretes PTH, unre- ❍ Easy fracturing
sponsive to negative feedback of serum calcium. ❍ Hematuria
❍ Secondary: Excessive compensatory production of ❍ Lethargy
PTH stems from a hypocalcemia-producing abnor- ❍ Muscle weakness, particularly in the legs
mality outside the parathyroid gland that isn’t re- ❍ Osteoporosis
sponsive to PTH, such as decreased intestinal ab- ❍ Overt psychosis
sorption of calcium or vitamin D. ❍ Personality disturbances
❍ Increased PTH levels act directly on bone and renal ❍ Polydipsia
tubules, increasing extracellular calcium levels. ❍ Polyuria
❍ Renal excretion and uptake into the soft tissues or ❍ Recurring nephrolithiasis
skeleton can’t compensate for increased calcium.
Physical assessment
Causes ❍ Muscle weakness and atrophy
❍ Adenoma ❍ Psychomotor disturbances
❍ Certain drugs, such as phenytoin ❍ Stupor, possibly coma
❍ Chronic renal failure ❍ Skin necrosis
❍ Decreased intestinal absorption of vitamin D or cal- ❍ Subcutaneous calcification
❍ Dietary vitamin D or calcium deficiency Test results
❍ Genetic disorders Primary disease
❍ Idiopathic ❍ Increased alkaline phosphatase level
❍ Laxative use ❍ Increased osteocalcin level
❍ Multiple endocrine neoplasia ❍ Increased tartrate-resistant acid phosphatase level
❍ Osteomalacia ❍ Increased serum PTH level
❍ Increased serum calcium level
Prevalence ❍ Decreased serum phosphorus level
❍ More common in women than men ❍ Increased urine and serum calcium level
❍ More common in postmenopausal women ❍ Increased serum chloride level
❍ Onset usually between ages 35 and 65 ❍ Possible increased creatinine level
❍ Possible increased basal acid secretion
Complications ❍ Possible increased serum amylase level
❍ Cardiac arrhythmias Secondary disease
❍ Cholelithiasis ❍ Normal or slightly decreased serum calcium level
❍ Depression ❍ Variable serum phosphorus level
❍ Heart failure ❍ Increased serum PTH level
❍ Muscle atrophy ❍ Changes on imaging tests
❍ Osteoporosis – X-rays show diffuse bone demineralization, bone
❍ Peptic ulcers cysts, outer cortical bone absorption, and sub-
❍ Renal calculi and colic periosteal erosion of the phalanges and distal clav-
❍ Renal insufficiency and failure icles in primary disease.
❍ Subchondral fractures – X-ray spectrophotometry shows increased bone
❍ Traumatic synovitis turnover in primary disease.
❍ Vascular damage – Esophagography, thyroid scan, parathyroid ther-
mography, ultrasonography, thyroid angiography,
computed tomography scan, and magnetic reso-
nance imaging may show the location of parathy-
roid lesions.

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signs of tetany, so keep I.V. calcium gluconate or cal-

Nursing diagnoses cium chloride available for emergency use.

❍ Activity intolerance
Drug therapy
❍ Decreased cardiac output Primary disease
❍ Disturbed body image ❍ Bisphosphonates
❍ Disturbed thought processes ❍ Calcitonin
❍ Excess fluid volume ❍ Oral sodium or potassium phosphate
❍ Fear ❍ Plicamycin if primary disease is metastatic
❍ Imbalanced nutrition: less than body requirements Secondary disease
❍ Aluminum hydroxide
Key outcomes ❍ Glucocorticoids
The patient will: ❍ Vitamin D therapy
❍ maintain current weight After surgery
❍ express feelings of increased comfort ❍ I.V. magnesium and phosphate
❍ maintain adequate cardiac output ❍ Sodium phosphate
❍ maintain balanced fluid volume status ❍ Supplemental calcium
❍ perform activities of daily living without excessive ❍ Vitamin D or calcitriol
❍ express positive feelings about self. Monitoring
❍ Cardiovascular status
❍ Intake and output
Interventions ❍ Respiratory status
❍ Serum calcium levels
General ❍ Vital signs
❍ Activity, as tolerated After parathyroidectomy
❍ Increased oral fluid intake ❍ Chvostek’s sign
❍ In renal failure, dialysis ❍ Complications
❍ In primary disease, treatment to decrease calcium ❍ Increased neuromuscular irritability
levels ❍ Neck edema
❍ In primary disease, removal of adenoma or all but ❍ Trousseau’s sign
half of one gland
❍ In secondary disease, treatment to correct underly-
ing cause of parathyroid hypertrophy Patient teaching
Nursing Be sure to cover:
❍ Obtain baseline serum potassium, calcium, phos- ❍ the disorder, diagnosis, and treatment
phate, and magnesium levels before treatment. ❍ prescribed drugs, dosages, and possible adverse ef-
❍ Provide at least 3 L of fluid daily. fects
❍ Institute safety precautions. ❍ when to notify a doctor
❍ Schedule frequent rest periods. ❍ the signs and symptoms of tetany, respiratory dis-
❍ Provide comfort measures. tress, and renal dysfunction
❍ Give prescribed drugs. ❍ the need for periodic blood tests
❍ Help the patient turn and reposition every 2 hours. ❍ avoidance of calcium-containing antacids and thi-
❍ Support affected limbs with pillows. azide diuretics
❍ Offer emotional support. ❍ the need for medical identification.
❍ Help the patient develop effective coping strategies.
After parathyroidectomy
❍ Keep a tracheotomy tray and endotracheal tube set- Discharge planning
up at the bedside.
❍ Maintain seizure precautions. ❍ Refer the patient to an endocrinologist, as appro-
❍ Place the patient in semi-Fowler’s position. priate.
❍ Support the patient’s head and neck with sandbags.
❍ Have the patient ambulate as soon as possible.
A LERT Listen for complaints of tingling in the
hands and around the mouth. If these symp-
toms don’t subside quickly, they may be prodromal

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Hyperphosphatemia Complications
❍ Acute hyopcalcemia
❍ Tetany
❍ Calcium-phosphate deposits in major organs, bones,
Overview joints, subcutaneous tissue, soft tissue, or eyes
❍ Excessive serum phosphate levels Assessment
❍ Reflects the kidney’s inability to excrete excess phos-
phorus History
❍ Anorexia
Pathophysiology ❍ Decreased mental status
❍ Phosphorus exists mainly in inorganic combination ❍ Nausea and vomiting
with calcium in teeth and bones.
❍ In extracellular fluid, phosphate ions support several Physical assessment
metabolic functions: use of B vitamins, acid-base ❍ Abdominal spasm
homeostasis, bone formation, nerve and muscle ac- ❍ Conjunctivitis
tivity, cell division, transmission of hereditary traits, ❍ Hyperreflexia
and metabolism of carbohydrates, proteins, and fats. ❍ Hypocalcemic electrocardiogram changes
❍ Renal tubular reabsorption of phosphate is inversely ❍ Muscle weakness and cramps
regulated by calcium levels — an increase in phos- ❍ Papular eruptions
phorus causes a decrease in calcium. An imbalance ❍ Paresthesia
causes hypophosphatemia or hyperphosphatemia. ❍ Presence of Chvostek’s or Trousseau’s sign
❍ Tetany
Risk factors ❍ Visual impairment
❍ Chemotherapy
❍ Heatstroke Test results
❍ Infection Laboratory
❍ Muscle necrosis ❍ Serum phosphorus level higher than 4.5 mg/dl
❍ Trauma ❍ Serum calcium level lower than 8.9 mg/dl
❍ Increased blood urea nitrogen level
Causes ❍ Increased creatinine level
❍ Acid-base imbalance Imaging
❍ Certain drugs (See Drugs and supplements that ❍ X-ray studies may reveal skeletal changes caused by
cause hyperphosphatemia.) osteodystrophy in chronic hyperphosphatemia.
❍ Hypervitaminosis D Diagnostic procedures
❍ Hypocalcemia ❍ Electrocardiography may show changes characteris-
❍ Hypoparathyroidism tic of hypercalcemia.
❍ Overuse of laxatives with phosphates or phosphate
❍ Renal failure Nursing diagnoses
Prevalence ❍ Anxiety
❍ Occurs most commonly in children, who tend to ❍ Deficient knowledge (hyperphosphatemia)
consume more phosphorus-rich foods and bever- ❍ Impaired gas exchange
ages than adults ❍ Risk for deficient fluid volume
❍ More common in children and adults with renal in-
sufficiency Key outcomes
The patient will:
❍ maintain a patent airway
Drugs and supplements that cause ❍ maintain adequate vital signs
hyperphosphatemia ❍ have a normal phosphorus level
These drugs may cause hyperphosphatemia: ❍ express understanding of the condition and treat-
● enemas, such as Fleet enemas ment
● laxatives that contain phosphorus or phosphate ❍ maintain a low-phosphorus diet
● oral phosphorus supplements ❍ maintain fluid volume balance.
● parenteral phosphorus supplements (sodium
phosphate, potassium phosphate)
● vitamin D supplements.

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Foods high in phosphorus

Discharge planning
These foods have a high phosphorus content:
● beans
● bran ❍ Refer the patient to a dietitian and social services, if
● cheese indicated.
● chocolate
● dark-colored sodas
● ice cream
● lentils
● milk
● nuts
● peanut butter
● seeds
● yogurt.

❍ Activity, as tolerated
❍ Discontinuation of drugs linked to hyperphos-
❍ I.V. saline solution
❍ Low-phosphorus diet
❍ Peritoneal dialysis or hemodialysis (if severe)
❍ Treatment of the underlying cause
❍ Provide safety measures.
❍ Be alert for signs of hypocalcemia.
❍ Give prescribed drugs.
❍ Give antacids with meals to increase their effective-
❍ Prepare the patient for dialysis, if appropriate.
❍ Assist with selecting a low-phosphorus diet.
Drug therapy
❍ Aluminum
❍ Calcium gel
❍ Magnesium
❍ Phosphate-binding antacids
❍ Calcium and phosphorus levels
❍ Intake and output
❍ Renal studies
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder and treatment
❍ prescribed drugs, dosages, and possible adverse ef-
❍ avoidance of products that contain phosphorus
❍ avoidance of high-phosphorus foods. (See Foods
high in phosphorus.)

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Hypertension Prevalence
❍ Affects 15% to 20% of adults in the United States
❍ Essential hypertension: 90% to 95% of cases
Overview Complications
❍ Blindness
Description ❍ Cardiac disease
❍ Intermittent or sustained increase in systolic blood ❍ Cerebrovascular accident
pressure, diastolic blood pressure, or both ❍ Renal failure
❍ Usually begins as benign disease, slowly progressing
to accelerated or malignant state
❍ Two major types Assessment
– Essential hypertension, also called primary or id-
iopathic hypertension History
– Secondary hypertension, which results from renal ❍ Commonly no symptoms
disease or another identifiable cause ❍ Discovered incidentally during evaluation for anoth-
❍ Occurs in stages er disorder or during a routine blood pressure
– Prehypertension: systolic blood pressure 120 to screening program
139 mm Hg or diastolic blood pressure 80 to ❍ Symptoms that reflect the effect of hypertension on
89 mm Hg the organ systems
– Stage 1: systolic blood pressure 140 to 159 mm ❍ Awakening with a headache in the occipital region,
Hg or diastolic blood pressure 90 to 99 mm Hg which subsides spontaneously after a few hours
– Stage 2: systolic blood pressure 160 mm Hg or ❍ Dizziness, fatigue, confusion
higher or diastolic blood pressure 100 mm Hg or ❍ Palpitations, chest pain, dyspnea
higher ❍ Epistaxis
❍ Malignant hypertension ❍ Hematuria
– A medical emergency ❍ Blurred vision
– A severe, fulminant form of hypertension
– Commonly arises from essential and secondary hy- Physical assessment
pertension ❍ Bounding pulse
❍ Bruits over the abdominal aorta and femoral arteries
Pathophysiology or the carotids
❍ Several theories: ❍ Elevated blood pressure readings on at least two
– Changes in the arteriolar bed increase peripheral consecutive occasions after initial screenings
vascular resistance. ❍ Hemorrhages, exudates, and papilledema of the eye
– Abnormally increased tone in the sympathetic ner- in late stages if hypertensive retinopathy present
vous system (originating in the vasomotor system ❍ Peripheral edema (late stages)
centers) increases peripheral vascular resistance. ❍ Pulsating abdominal mass, suggesting an abdominal
– Renal or hormonal dysfunction causes increased aneurysm
blood volume. ❍ S4 sound
– An increase in arteriolar thickening (caused by
genetic factors) increases peripheral vascular re- Test results
sistance. Laboratory
– Abnormal renin release causes formation of an- ❍ Protein, red blood cells, or white blood cells in
giotensin II, which constricts arterioles and in- urine, suggesting renal disease
creases blood volume. ❍ Glucose in urine, suggesting diabetes mellitus
❍ Serum potassium levels less than 3.5 mEq/L, possi-
Risk factors bly indicating adrenal dysfunction (primary hyperal-
❍ Aging dosteronism)
❍ Excessive alcohol intake A LERT If the patient has serum potassium
❍ Family history levels less than 3.5 mEq/L, monitor electrocar-
❍ High-sodium, high–saturated-fat diet diogram tracings because these levels may potentiate
❍ Hormonal contraceptive use cardiac arrhythmias.
❍ Obesity
❍ Sedentary lifestyle ❍ Blood urea nitrogen levels normal or higher than
❍ Smoking 20 mg/dl, suggesting renal disease
❍ Stress ❍ Serum creatinine levels normal or higher than
1.5 mg/dl, suggesting renal disease
❍ Unknown

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Imaging Monitoring
❍ Excretory urography may reveal renal atrophy, indi- ❍ Adverse effects of antihypertensive drugs
cating chronic renal disease; one kidney more than ❍ Complications
5/8 (1.6 cm) shorter than the other suggests unilat- ❍ Signs and symptoms of target end-organ damage
eral renal disease. ❍ Response to treatment
❍ Chest X-rays may show cardiomegaly. ❍ Risk factor modification
Diagnostic procedures ❍ Vital signs, especially blood pressure
❍ Electrocardiography may show left ventricular hyper-
trophy or ischemia.
❍ Renal arteriography may show renal artery stenosis. Patient teaching
❍ An oral captopril challenge may be done to test for
renovascular hypertension. Be sure to cover:
❍ Ophthalmoscopy reveals arteriovenous nicking and, ❍ the disorder, diagnosis, and treatment
in hypertensive encephalopathy, edema. ❍ how to use a self-monitoring blood pressure cuff
and record the reading in a journal for review by a
Nursing diagnoses ❍ importance of compliance with antihypertensive
therapy and establishing a daily routine for taking
❍ Decreased cardiac output prescribed drugs
❍ Ineffective tissue perfusion: cardiopulmonary, pe- ❍ the need to report adverse drug effects
ripheral, renal, cerebral, gastrointestinal ❍ the need to avoid high-sodium antacids and over-
❍ Noncompliance with medication regimen the-counter cold and sinus medications containing
❍ Risk for activity intolerance vasoconstrictors
❍ examining and modifying lifestyle, including diet
Key outcomes ❍ the need for a routine exercise program, particularly
The patient will: aerobic walking
❍ maintain adequate cardiac output ❍ dietary restrictions
❍ maintain hemodynamic stability ❍ the importance of follow-up care.
❍ develop no arrhythmias
❍ express feelings of increased energy
❍ comply with the therapy regimen. Discharge planning
❍ Refer the patient to stress-reduction therapies, sup-
Interventions port groups, and smoking cessation programs as
General ❍ Refer the patient to a nutritionist, if indicated.
❍ For a patient with secondary hypertension, correc-
tion of the underlying cause and control of hyperten-
sive effects
❍ Diet containing adequate calcium, magnesium, and
❍ Diet low in saturated fat and sodium
❍ Lifestyle modification, such as weight control, limit-
ing alcohol, regular exercise, and smoking cessation
❍ Give prescribed drugs.
❍ Encourage dietary changes, as needed.
❍ Help the patient identify risk factors and modify his
lifestyle, as appropriate.
Drug therapy
❍ Aldosterone antagonist
❍ Alpha blockers
❍ Angiotensin-converting enzyme inhibitors
❍ Angiotensin II–receptor blockers
❍ Beta blockers
❍ Calcium channel blockers
❍ Diuretics
❍ Vasodilators

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Hypocalcemia Complications
❍ Cardiac arrhythmia
❍ Laryngeal spasm
Overview ❍

Respiratory arrest
❍ Calcium level below 8.9 mg/dl or ionized calcium Assessment
level below 4.5 mg/dl
Pathophysiology ❍ Anxiety
❍ Together with phosphorous, calcium is responsible ❍ Brittle nails, dry skin and hair
for the formation and structure of bones and teeth. ❍ Diarrhea
❍ Calcium helps maintain cell structure and function. ❍ Fractures
❍ It plays a role in cell membrane permeability and ❍ Irritability
impulse transmission. ❍ Muscle cramps
❍ It affects the contraction of cardiac muscle, smooth ❍ Seizures
muscle, and skeletal muscle. ❍ Underlying cause
❍ It also participates in the blood-clotting process.
Physical assessment
Causes ❍ Carpopedal spasm
❍ Hypomagnesemia ❍ Confusion
❍ Hypoparathyroidism ❍ Hypotension
❍ Inadequate dietary intake of calcium and vitamin D ❍ Perioral paresthesia
❍ Malabsorption or loss of calcium from the gastroin- ❍ Positive Chvostek’s and Trousseau’s signs (See
testinal tract Checking for Trousseau’s and Chvostek’s signs.)
❍ Overcorrection of acidosis ❍ Tetany
❍ Pancreatic insufficiency ❍ Twitching
❍ Renal failure
❍ Severe infections or burns Test results
❍ Drugs such as calcitonin and mithramycin that de- Laboratory
crease calcium resorption from the bone ❍ Serum calcium levels less than 8.5 mg/dl
❍ Ionized calcium levels less than 4.5 mg/dl
Prevalence Diagnostic procedures
❍ Occurs equally in males and females ❍ Depending on cause, electrocardiography may show
❍ Affects all ages arrhythmias.

Checking for Trousseau’s and Chvostek’s signs

Trousseau’s and Chvostek’s signs can aid in the diagnosis of tetany and hypocalcemia. Here’s how to assess your patient for
these important signs.
Trousseau’s sign Chvostek’s sign
To check for Trousseau’s sign, apply a blood pressure cuff You can induce Chvostek’s sign by tapping the patient’s
to the patient’s upper arm and inflate it to 20 mm Hg above facial nerve next to the ear. A brief contraction of the upper
the patient’s systolic pressure. Trousseau’s sign may appear lip, nose, or side of the face indicates Chvostek’s sign.
after 1 to 4 minutes. The patient will experience an adducted
thumb, flexed wrist and metacarpophalangeal joints, and
extended interphalangeal joints (with fingers together) —
carpopedal spasm — indicating tetany, a major sign of

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Nursing diagnoses Patient teaching

❍ Acute confusion Be sure to cover:
❍ Anxiety ❍ taking calcium supplements 1 to 11⁄2 hours after
❍ Decreased cardiac output meals
❍ Disturbed thought process ❍ the need to follow a high-calcium diet
❍ Risk for deficient fluid volume ❍ foods high in calcium
❍ Risk for falls ❍ warning signs and symptoms and when to report
Key outcomes ❍ the importance of exercise to prevent calcium loss
The patient will: from bones.
❍ maintain stable vital signs
❍ maintain adequate cardiac output
❍ express an understanding of the disorder and its Discharge planning
❍ maintain fluid volume balance. ❍ Refer the patient to a nutritionist and social services,
if indicated.
❍ Treatment of the underlying cause
❍ Diet high in calcium and vitamin D
AGE AWARE A breast-fed infant may have
low calcium and vitamin D levels if his moth-
er’s intake is inadequate. Assess the mother for ade-
quate intake and exposure to sunlight.
❍ Activity, as tolerated
❍ Provide safety measures.
❍ Institute seizure precautions, if appropriate.
❍ Reorient the patient as needed.
❍ Give prescribed calcium replacement.
A LERT Dilute I.V. calcium preparations in
dextrose 5% in water because normal saline
solution can increase renal calcium loss. Dilution in
a bicarbonate solution will cause precipitation. Give
calcium slowly because rapid delivery may cause syn-
cope, hypotension, and arrhythmias.

❍ Assess I.V. sites if giving calcium I.V. because infiltra-

tion causes necrosis and sloughing.
❍ Assess the patient’s ability to perform activities of
daily living, and assist as needed.
Drug therapy
❍ Calcium gluconate I.V.
❍ Oral calcium and vitamin D supplements
❍ Cardiac rhythm
❍ Respiratory status
❍ Seizures
❍ Serum calcium levels

Hypocalcemia 171
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Hypochloremia AGE AWARE Chloride-deficient formula can

be a cause of this disorder in infants.
❍ Untreated diabetic ketoacidosis
Overview Prevalence
❍ Depends on underlying cause
❍ Serum chloride levels below 98 mEq/L Complications
❍ Possible changes in levels of sodium, potassium, cal- ❍ Coma
cium, and other electrolytes ❍ Respiratory arrest
❍ Possible metabolic alkalosis if bicarbonate levels ❍ Seizures
rise to compensate for decreased chloride levels
(See How hypochloremia can lead to metabolic
alkalosis.) Assessment
Pathophysiology History
❍ Chloride accounts for two-thirds of all serum anions. ❍ Agitation
❍ Chloride is secreted by the stomach’s mucosa as hy- ❍ Irritability
drochloric acid; it provides an acid medium that ❍ Risk factors for low chloride levels
aids digestion and activation of enzymes.
❍ It helps maintain acid-base and body water balances, Physical assessment
influences the osmolality or tonicity of extracellular ❍ Cardiac arrhythmias, tachycardia
fluid, plays a role in the exchange of oxygen and car- ❍ Hyperactive deep tendon reflexes
bon dioxide in red blood cells, and helps activate ❍ Muscle cramps
salivary amylase (which, in turn, activates the diges- ❍ Muscle weakness and twitching
tive process). ❍ Shallow, depressed breathing (with metabolic
Risk factors ❍ Tetany
❍ Cystic fibrosis
❍ Draining fistula Test results
❍ Heart failure Laboratory
❍ Ileostomy ❍ Serum chloride level less than 98 mEq/L
❍ Pyloric obstruction ❍ Serum sodium level below 135 mEq/L
❍ pH above 7.45
Causes ❍ Carbon dioxide level above 32 mEq/L
❍ Addison’s disease
❍ Administration of dextrose I.V. without electrolytes
❍ Certain drugs Nursing diagnoses
❍ Loss of hydrochloric acid in gastric secretions from
vomiting, gastric suctioning, or gastric surgery ❍ Decreased cardiac output
❍ Prolonged diarrhea or diaphoresis ❍ Impaired gas exchange
❍ Prolonged use of mercurial diuretics ❍ Ineffective breathing pattern
❍ Salt-restricted diets

How hypochloremia can lead to metabolic alkalosis

Cl– HCO3–
HCO3– pH

Nasogastric suctioning can Kidneys retain sodium Bicarbonate ions An excess of bicarbonate
deplete chloride ions. and bicarbonate ions to accumulate in ions raises the pH and
balance chloride loss. extracellular fluid. leads to hypochloremic
metabolic alkalosis.

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❍ Risk for deficient fluid volume

❍ Risk for falls
Key outcomes
The patient will:
❍ maintain adequate cardiac output
❍ maintain adequate fluid volume
❍ maintain stable vital signs
❍ avoid complications.

❍ Activity, as tolerated
❍ High-sodium diet
❍ Treatment of metabolic acidosis or electrolyte imbal-
❍ Treatment of underlying condition
❍ Offer foods high in chloride.
❍ Ensure a safe environment.
❍ Give prescribed I.V. fluids, drugs, and supplements.
Drug therapy
❍ Ammonium chloride
❍ Normal saline solution I.V.
❍ Potassium chloride (for metabolic acidosis)
❍ Arterial blood gas levels
❍ Cardiac rhythm
❍ Level of consciousness
❍ Muscle strength and movement
❍ Respiratory status
❍ Serum electrolyte levels
❍ Signs of metabolic alkalosis
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ signs and symptoms of electrolyte imbalance
❍ dietary supplements
❍ prescribed drugs.

Discharge planning
❍ Refer the patient to a physical therapist and nutri-
tionist, as needed.

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Hypokalemia A LERT Before giving digoxin, check the pa-

tient’s serum digoxin and potassium levels.
Hypokalemia can potentiate digoxin toxicity.
❍ Serum potassium level less than 3.5 mEq/L History
❍ Narrow normal range for serum potassium level: 3.5 ❍ Abdominal cramps
to 5 mEq/L ❍ Anorexia
❍ Constipation
A LERT A slight decrease in potassium levels
❍ Muscle weakness
can have profound clinical consequences.
❍ Nausea, vomiting
❍ Paresthesia
Pathophysiology ❍ Polyuria
❍ Potassium facilitates contraction of skeletal and
smooth muscles, including myocardial muscle. Physical assessment
❍ This anion figures prominently in nerve impulse ❍ Decreased bowel sounds
conduction, acid-base balance, enzyme action, and ❍ Hyporeflexia
cell membrane function. ❍ Orthostatic hypotension
❍ Potassium imbalance can lead to muscle weakness ❍ Weak, irregular pulse
and flaccid paralysis because of an ionic imbalance
in neuromuscular tissue excitability. Test results
Causes ❍ Serum potassium levels less than 3.5 mEq/L
❍ Acid-base imbalances ❍ Increased pH and bicarbonate levels
❍ Certain drugs ❍ Slightly increased serum glucose level
– Corticosteroids Diagnostic procedures
– Potassium-wasting diuretics ❍ Characteristic electrocardiogram changes include a
– Some sodium-containing antibiotics (such as car- flattened T wave, depressed ST segment, and U wave.
❍ Chronic renal disease and tubular potassium wasting
❍ Cushing’s syndrome Nursing diagnoses
❍ Excessive ingestion of licorice
❍ Excessive gastrointestinal or urinary losses ❍ Constipation
– Anorexia ❍ Decreased cardiac output
– Chronic laxative abuse ❍ Nausea
– Dehydration ❍ Risk for activity intolerance
– Diarrhea ❍ Risk for deficient fluid volume
– Gastric suction
– Vomiting Key outcomes
❍ Hyperglycemia The patient will:
❍ Low-potassium diet ❍ maintain hemodynamic stability
❍ Primary hyperaldosteronism ❍ maintain a normal potassium level
❍ Prolonged potassium-free I.V. therapy ❍ understand potential adverse effects of medications
❍ Severe serum magnesium deficiency ❍ express understanding of high-potassium foods
❍ Trauma, as from injury, burns, or surgery ❍ maintain fluid volume balance.

❍ Affects up to 20% of hospitalized patients (significant Interventions
in about 4% to 5% of these patients)
❍ Affects up to 14% of outpatients mildly General
❍ Affects about 80% of patients who receive diuretics ❍ Activity, as tolerated
❍ Males and females affected equally ❍ High-potassium diet
❍ Treatment of the underlying cause
❍ Cardiac arrest Nursing
❍ Cardiac arrhythmia ❍ Give prescribed drugs.
❍ Digoxin toxicity ❍ Implement safety measures.
❍ Rhabdomyolysis

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Guidelines for I.V. potassium administration

Following are some guidelines for giving I.V. potassium and for monitoring patients receiving it. Remember that potassium
only needs to be replaced I.V. if hypokalemia is severe or the patient can’t take oral potassium supplements.

Administration Patient monitoring

● When adding the potassium preparation to an I.V. ● Monitor the patient’s cardiac rhythm during rapid I.V.
solution, mix it well. Don’t add it to a hanging container; potassium delivery to prevent toxic effects from
the potassium will pool, and the patient will receive a hyperkalemia. Report any irregularities immediately.
highly concentrated bolus. Use premixed potassium ● Evaluate the results of treatment by checking serum
when possible. potassium levels and assessing the patient for evidence
● To prevent or reduce toxic effects, I.V. infusion of a toxic reaction, such as muscle weakness and
concentrations shouldn’t exceed 40 to 60 mEq/L. Rates paralysis.
are usually 10 mEq/hour. More rapid infusions may be ● Watch the I.V. site for evidence of infiltration, phlebitis,
used in severe cases; they demand closer monitoring of or tissue necrosis.
the patient’s cardiac status. The maximum adult dose ● Monitor the patient’s urine output, and notify the doctor
typically shouldn’t exceed 200 mEq/24 hours unless if volume is inadequate. To avoid hyperkalemia, urine
prescribed. output should exceed 30 ml/hour.
● Use an infusion device to control the flow rate.
● Never give potassium by I.V. push or bolus; doing so
can cause cardiac arrhythmias and cardiac arrest.

❍ Be alert for signs of hyperkalemia after treatment.

❍ Give I.V. fluids.
Drug therapy
❍ Potassium chloride (I.V. or P.O.)
A LERT I.V. potassium supplements must be
diluted and given with caution to prevent seri-
ous complications, such as cardiac arrest. (See Guide-
lines for I.V. potassium administration.)
A LERT A patient taking a potassium-wasting
diuretic may be switched to a potassium-
sparing diuretic to prevent excessive urinary loss of

❍ Cardiac rhythm
❍ Intake and output
❍ Respiratory status
❍ Serum potassium levels
❍ Vital signs

Patient teaching
Be sure to cover:
❍ the disorder, diagnosis, and treatment
❍ prescribed drugs, dosages, and possible adverse ef-
❍ monitoring of intake and output
❍ prevention of future episodes of hypokalemia
❍ need for and components of a high-potassium diet
❍ warning signs and symptoms to report to the doctor.

Discharge planning
❍ Refer the patient to a nutritionist, if needed.

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Hypomagnesemia ❍

Occurs in 30% to 80% of alcoholics
Affects males and females equally
Overview ❍ Cardiac arrest
❍ Cardiac arrhythmia
Description ❍ Laryngeal stridor
❍ Serum magnesium levels less than 1.5 mEq/L ❍ Respiratory depression
❍ Seizures
❍ Magnesium enhances neuromuscular integration
and stimulates parathyroid hormone secretion, thus Assessment
regulating intracellular fluid calcium levels.
❍ It also may regulate skeletal muscles through its in- History
fluence on calcium use by depressing acetylcholine ❍ Altered level of consciousness
release at synaptic junctions. ❍ Anorexia
❍ Magnesium activates many enzymes for carbohydrate ❍ Drowsiness
and protein metabolism, aids in cell metabolism and ❍ Dysphagia
the transport of sodium and potassium across cell ❍ Leg and foot cramps
membranes, and influences sodium, potassium, cal- ❍ Nausea
cium, and protein levels. ❍ Vomiting
❍ About one-third of magnesium taken into the body is
absorbed through the small intestine and is eventual- Physical assessment
ly excreted in urine; the remaining unabsorbed mag- ❍ Cardiac arrhythmia
nesium is excreted in stool. ❍ Chvostek’s and Trousseau’s signs
❍ Hyperactive deep tendon reflexes
Causes ❍ Hypertension
❍ Administration of parenteral fluids without magne- ❍ Muscle weakness, tremors, twitching
sium salts ❍ Tachycardia
❍ Certain drugs
– Aminogluc