1 - Chap13-Fluid and Electrolyte - Balance and Disturbance 2017

Fluid and Electrolytes: Balance and
Disturbance
Dr. Ahmad Aqel, 2017

The University of Jordan/School of Nursing
Brunner & Suddarth’s Textbook of Medical-Surgical Nursing 13 th ed. Chapter 13. (p 237)
Introduction:
 Necessary for life.
 Homeostasis: maintenance of a constant internal
equilibrium (involves positive and negative feedback
mechanisms).
 Disorders of fluid and electrolyte balance occur with
every disorder.
 Nursing role: prevent, identify, respond to, and treat
fluid and electrolyte disturbances.
Dr. Ahmad Aqel 2017 2

 ≈ 60% of adult is fluid
– Varies with age, gender, and body fat.
 Intracellular fluid (2/3) [skeletal muscle mass].
 Extracellular fluid (1/3) [transports electrolytes; carries other
substances, such as enzymes and hormones].
– Intravascular (plasma) [3L of the average 6 L of blood volume
is made up of plasma] The remaining 3L is erythrocytes,
leukocytes, and thrombocytes].
– Interstitial (fluid surround the cells 11-12L)
– Transcellular (1L) [contained within epithelial lined spaces]
(eg. cerebrospinal, pericardial, synovial, intraocular, and
pleural fluids).
 Active chemicals that carry
– positive electrical charges (cations),
• Major cations: sodium, potassium, calcium, magnesium,
hydrogen ions
– negative electrical charges (anions) (mEq/L)
• Major anions: chloride, bicarbonate, phosphate, sulfate,
and proteinate ions
 Electrolyte concentrations differ in fluid
compartments

 Movement of fluid through capillary walls
depends on
– Hydrostatic pressure: exerted on walls of blood
vessels
– Osmotic pressure: exerted by protein in plasma
 Direction of fluid movement depends on
differences of hydrostatic, osmotic pressure

 Osmosis: area of low solute concentration to area of
high solute concentration
 Osmotic pressure is the amount of hydrostatic
pressure needed to stop the flow of water by
osmosis.
 Osmotic diuresis is the increase in urine output
caused by the excretion of substances
 Oncotic pressure is the osmotic pressure exerted by
proteins (eg, albumin).

 Diffusion: solutes move from area of higher
concentration to one of lower concentration
 Filtration: movement of water, solutes occurs

from area of high hydrostatic pressure to area
of low hydrostatic pressure

 Active transport: physiologic pump that
moves fluid from area of lower concentration
of one of higher concentration
– Movement against concentration gradient
– Sodium-potassium pump: maintains higher
concentration of extracellular sodium, intracellular
potassium
– Requires adenosine (ATP) for energy

• Osmolality is the concentration of fluid that
affects the movement of water between fluid
compartments by osmosis.
– Serum osmolality primarily reflects the concentration
of sodium, blood urea nitrogen (BUN) and glucose.
– Urine osmolality is determined by urea, creatinine,
and uric acid.
– serum osmolality is 280 to 300 mOsm/kg, and normal
urine osmolality is 200 to 800 mOsm/kg
– Urine specific gravity measures the kidneys’ ability to
excrete or conserve water (1.010 to 1.025).
Laboratory Tests for Evaluating Fluid
Status
 BUN is made up of urea, which is an end
product of the metabolism of protein by the
liver. (10 to 20 mg/dL).
 Creatinine is the end product of muscle
metabolism. (0.7 to 1.4 mg/dL).
 Hematocrit measures the volume percentage
of red blood cells (erythrocytes) in whole
blood and normally ranges from 42% to 52%
for males and 35% to 47% for females.

 Gain
– Dietary intake of fluid, food or enteral feeding
– Parenteral fluids
 Loss
– Kidney: urine output
– Skin loss: sensible, insensible losses
– Lungs
– GI tract

 Hypothalamic regulation
 Pituitary regulation
 Adrenal cortical regulation
 Renal regulation
 Cardiac regulation
 Gastrointestinal regulation
 Insensible water loss

 Osmoreceptors in hypothalamus sense fluid
deficit or increase in plasma osmolality
 Stimulates thirst and antidiuretic hormone

(ADH) release
 Result in increased free water and decreased

plasma osmolarity
 Under control of hypothalamus, posterior
pituitary releases ADH
 Stress, nausea, nicotine, and morphine also

stimulate ADH release

 Adrenal cortex releases hormones to regulate
both water and electrolytes
1. Glucocorticoids
2. Mineralcorticoids
 Aldosterone is a mineralocorticoid with potent

sodium-retaining and potassium excreting
capability

 Kidneys are primary organs for regulating fluid
and electrolyte balance
 Selective reabsorption of water and
electrolytes
 Excretion of electrolytes occurs
 Renal tubules are sites of action of ADH and
aldosterone

 Atrial natriuretic factor (ANF) is released by
the cardiac atria in response to increased
atrial pressure
 ANF causes vasodilation and increased urinary

excretion of sodium and water

 Gastrointestinal tract accounts for most of the
water intake
 Small amounts of water are eliminated by GI

tract in feces

 Invisible vaporization from lungs and skin
 Approximately 900 ml per day is lost
 No electrolytes are lost with insensible water

loss
– Excessive sweating, not insensible loss, leads to
loss of water and electrolytes

• Reduced homeostatic mechanisms: cardiac,
renal, respiratory function
• Decreased body fluid percentage

• Fluid volume deficit (FVD): hypovolemia
• Fluid volume excess (FVE): hypervolemia

 Loss of extracellular fluid exceeds intake ratio
of water
– Electrolytes lost in same proportion as they exist
in normal body fluids
 Dehydration: loss of water along with
increased serum sodium level
– May occur in combination with other imbalances

Causes:
vomiting, diarrhea, GI suctioning, sweating,
decreased intake, inability to gain access to fluid
Risk factors: diabetes insipidus, adrenal
insufficiency, osmotic diuresis, hemorrhage, coma

• Manifestations:
– rapid weight loss
– decreased skin turgor, cool clammy skin due to vasoconstriction
– oliguria, concentrated urine
– postural hypotension
– flattened neck veins
– rapid weak pulse
– increased temperature
– thirst
– nausea
– muscle weakness, cramps
• Laboratory data: elevated BUN in relation to serum creatinine,
increased hematocrit
– Serum electrolyte changes may occur

 Medical management: provide fluids to meet
body needs
– Oral fluids
– IV solutions

 I&O, VS
 Monitor for symptoms: skin and tongue
turgor, mucosa, UO, mental status
 Measures to minimize fluid loss
 Oral care
 Administration of oral fluids
 Administration of parenteral fluids

What is a major indicator of extracellular FVD?
– Full and bounding pulse
– Drop in postural blood pressure
– polyuria
– Pitting edema of lower extremities

Manifestations:
Edema, distended neck veins Increased pulse, BP, pulse
pressure and CVP,
abnormal lung sounds increased weight and urine

(crackles), shortness of breath output
and wheezing
Medical management:
Treat the cause
Restriction of fluids and sodium
Administration of diuretics
 I&O and daily weights; assess lung sounds, edema,
other symptoms; monitor responses to diuretics
 Promote adherence to fluid restrictions, patient
teaching related to sodium and fluid restrictions
 Monitor, avoid sources of excessive sodium,
including medications
 Promote rest
 Semi-Fowler’s position for orthopnea
 Skin care, positioning/turning
 Sodium: hyponatremia, hypernatremia
 Potassium: hypokalemia, hyperkalemia
 Calcium: hypocalcemia, hypercalcemia
 Magnesium: hypomagnesemia,
hypermagnesemia
 Phosphorus: hypophosphatemia,
hyperphosphatemia
 Chloride: hypochloremia, hyperchloremia
Hyponatremia
Definition <135mEq/L
Normal value 135 to 145 mEq/L
Common food Butter, Canned food, Cheese,

sources Ketchup, meat , Milk, Table salt,
White and whole-wheat, bread

CAUSES adrenal insufficiency, water intoxication,
SIADH or losses by vomiting, diarrhea,
sweating, diuretics
MANIFESTATIONS poor skin turgor, dry mucosa, headache,
decreased salivation, decreased BP, nausea,
abdominal cramping, neurologic changes
MEDICAL water restriction, sodium replacement
MANAGEMENT
NURSING assessment and prevention, dietary sodium
MANAGEMENT and fluid intake, identify and monitor at-risk
patients, effects of medications (diuretics)
DEFINITION Serum sodium >145mEq/L
CAUSES excess water loss, excess sodium administration,

diabetes insipidus, heat stroke, hypertonic IV
solutions
MANIFESTATIONS thirst; elevated temperature; dry, swollen
tongue; sticky mucosa; neurologic symptoms;
 Note: thirst may
restlessness; weaknessin elderly or the ill
be impaired
MEDICAL hypotonic electrolyte solution or D5W
MANAGEMENT
NURSING assessment and prevention, assess for OTC
MANAGEMENT sources of sodium, offer and encourage fluids to
meet patient needs, provide sufficient water
with tube feedings
HYPOKALEMIA
1. Hypokalemia is a serum potassium <3.5 mEq/L.
2. Its life-threatening because all body system is affected.
B. Causes
1. Actual total body potassium loss
• Excessive use of medications such as diuretics or corticosteroids
• Increased secretion of aldosterone, such as in Cushing’s
syndrome
• Vomiting, diarrhea
• Wound drainage, particularly gastrointestinal
• Prolonged nasogastric suction
• Excessive diaphoresis
• Renal disease impairing reabsorption of potassium
Continue… Causes of hypokalemia
2. Inadequate potassium intake: NPO
3. Movement of potassium from the extracellular fluid
to the intracellular fluid
a. Alkalosis
b. Hyperinsulinism
4. Dilution of serum potassium
a. Water intoxication
b. IV therapy with potassium-poor solutions

 Manifestations:
 fatigue, anorexia, nausea, vomiting, dysrhythmias,
muscle weakness and cramps, paresthesias, glucose
intolerance, decreased muscle strength, DTRs
 Medical management:
 increased dietary potassium, potassium
replacement, IV for severe deficit
 Nursing management:
 assessment, severe hypokalemia is life-threatening,
monitor ECG and ABGs, dietary potassium, nursing
care related to IV potassium administration

Cautions
• Oral potassium supplements may cause nausea and
vomiting and they should not be taken on an empty
stomach
– if the client complains of abdominal pain, distention, nausea,
vomiting, diarrhea, or gastrointestinal bleeding, the
supplement may need to be discontinued.
• Liquid potassium chloride has an unpleasant taste and

should be taken with juice or another liquid.

• Potassium is never administered by IV push,
intramuscular, or subcutaneous routes.
• IV potassium is always diluted and

administered using an infusion device!

 Serum potassium >5.0 mEq/L
 Causes:
 usually treatment related, impaired renal function,
hypoaldosteronism, tissue trauma, acidosis
 Manifestations:
 cardiac changes and dysrhythmias, muscle weakness with
potential respiratory impairment, paresthesias, anxiety, GI
manifestations
 Medical management:
 monitor ECG, limit K diet, cation-exchange resin (Kayexalate),
IV sodium bicarbonate , IV calcium gluconate, regular insulin
and hypertonic dextrose IV, -2 agonists, dialysis
Precautions with Intravenously
Administered Potassium
• Potassium is never given by intravenous (IV push, IM,
SQ) route.
• A dilution of no more than 1 mEq/10 mL of solution is
recommended.
• After adding potassium to an IV solution, rotate and
invert the bag to ensure that the potassium is
distributed evenly throughout the IV solution.
• IV bag containing potassium: properly labeled.
• The maximum recommended infusion rate is 5 to 10
mEq/hr, never to exceed 20 mEq/hr
• A client receiving more than 10 mEq/hr should be
placed on a cardiac monitor and infusion device.
• Potassium infusion can cause phlebitis; therefore the

nurse should assess the IV site frequently for signs of
phlebitis or infiltration.
– If either occurs, the infusion should be stopped
immediately.
• The nurse should assess renal function before

administering potassium, and monitor intake and
output during administration
Electrocardiographic Changes in
HYPO/HYPERKALEMIA
Hypokalemia
– ST depression
– Shallow, flat, or inverted T wave
– Prominent U wave
Hyperkalemia
– Tall peaked T waves
– Flat P waves
– Widened QRS complex
– Prolonged PR interval

Nursing management:
assess potassium levels
Mix IVs containing K+ well
Monitor medication affects
Restrict dietary potassium /dietary teaching for patients
at risk
Hemolysis of blood specimen or drawing of blood above
IV site may result in false laboratory result
Potassium-sparing diuretics may cause elevation of
potassium
– Should not be used in patients with renal dysfunction

 Serum level less than 8.5 mg/dL, must be
considered in conjunction with serum albumin
level
 Causes: hypoparathyroidism, malabsorption,
pancreatitis, alkalosis, massive transfusion of
citrated blood, renal failure, medications, other
 Manifestations: tetany, circumoral numbness,
paresthesias, hyperactive DTRs, Trousseau’s sign,
Chovstek's sign, seizures, respiratory symptoms
of dyspnea and laryngospasm, abnormal clotting,
anxiety

 Medical management: IV of calcium
gluconate, calcium and vitamin D
supplements; diet
 Nursing management: assessment, severe
hypocalcemia is life-threatening, weight-
bearing exercises to decrease bone calcium
loss, patient teaching related to diet and
medications, and nursing care related to IV
calcium administration

 Serum level above 10.5 mg/dL
 Causes: malignancy and hyperparathyroidism, bone loss
related to immobility
 Manifestations: muscle weakness, incoordination,
anorexia, constipation, nausea and vomiting, abdominal
and bone pain, polyuria, thirst, ECG changes,
dysrhythmias
 Medical management: treat underlying cause, fluids,
furosemide, phosphates, calcitonin, biphosphonates
 Nursing management: assessment, hypercalcemic crisis
has high mortality, encourage ambulation, fluids of 3 to 4
L/d, provide fluids containing sodium unless
contraindicated, fiber for constipation, ensure safety

Electrocardiographic Changes in
HYPO/HYPERCALCEMIA
• Hypocalcemia
– Prolonged ST interval
– Prolonged QT interval
• Hypercalcemia
– Shortened ST segment
– Widened T wave

 Serum level less than 1.8 mg/dL, evaluate in
conjunction with serum albumin (hypokalemia and
hypocalcemia)
 Causes: alcoholism, GI losses, enteral or parenteral
feeding deficient in magnesium, medications, rapid
administration of citrated blood; contributing
causes include diabetic ketoacidosis, sepsis, burns,
hypothermia
 Manifestations: neuromuscular irritability, muscle
weakness, tremors, athetoid movements, ECG
changes and dysrhythmias, alterations in mood and
level of consciousness
 Medical management: diet, oral magnesium,
magnesium sulfate IV

 Nursing management: assessment, ensure safety,
patient teaching related to diet, medications,
alcohol use, and nursing care related to IV
magnesium sulfate
 Hypomagnesemia often accompanied by
hypocalcemia
– Need to monitor, treat potential hypocalcemia
 Dysphasia common in magnesium-depleted
patients
– Assess ability to swallow with water before
administering food or medications

 Serum level more than 2.7 mg/dL
 Causes: renal failure, diabetic ketoacidosis, excessive
administration of magnesium, adrenocortical insufficiency,
soft-tissue injury, decreased GI motility.
 Manifestations: flushing, lowered BP, nausea, vomiting,
hypoactive reflexes, drowsiness, muscle weakness, depressed
respirations, ECG changes, dysrhythmias, dysarthria, lethargy,
delayed thrombin formation
 Medical management: IV calcium gluconate, loop diuretics, IV
NS of RL, hemodialysis
 Nursing management: assessment, do not administer
medications containing magnesium, patient teaching regarding
magnesium containing OTC medications

 Serum level below 2.5 mg/DL
 Causes: alcoholism, refeeding of patients after starvation, pain, heat
stroke, respiratory alkalosis, hyperventilation, diabetic ketoacidosis,
hepatic encephalopathy, major burns, hyperparathyroidism, low
magnesium, low potassium, diarrhea, vitamin D deficiency, use of
diuretic and antacids
 Manifestations: neurologic symptoms, confusion, muscle weakness,
tissue hypoxia, muscle and bone pain, increased susceptibility to
infection , bleeding
 Medical management: oral or IV phosphorus replacement
 Nursing management: assessment, encourage foods high in
phosphorus, gradually introduce calories for malnourished patients
receiving parenteral nutrition
 Serum level above 4.5 mg/DL
 Causes: renal failure, excess phosphorus, excess vitamin
D, acidosis, hypoparathyroidism, chemotherapy
 Manifestations: few symptoms; soft-tissue calcifications,
symptoms occur due to associated hypocalcemia
 Medical management: treat underlying disorder, vitamin-
D preparations, calcium-binding antacids, phosphate-
binding gels or antacids, loop diuretics, NS IV, dialysis
 Nursing management: assessment, avoid high-
phosphorus foods; patient teaching related to diet,
phosphate-containing substances, signs of hypocalcemia

 Serum level less than 96 mEq/L
 Causes: GI tube drainage, severe vomiting and diarrhea,
Administration of chloride-deficient IV solutions, low
sodium intake, decreased serum sodium levels, metabolic
alkalosis, massive blood transfusions, diuretic therapy,
burns, fever, aldosterone, ACTH, corticosteroids,
bicarbonate.
 Manifestations: (Alkalosis, hypokalemia, hyponatremia)
Hyperexcitability of muscles, tetany, hyperactive DTRs,
weakness, twitching, and muscle cramps, dysrhythmias
 Medical management: replace chloride-IV NS or 0.45%
NS
 Nursing management: assessment, avoid free water,
encourage high-chloride foods, patient teaching related
to high-chloride foods
 Serum level more than 108 mEq/L
 Causes: excess sodium chloride infusions with water loss, head
injury, hypernatremia, dehydration, respiratory alkalosis,
metabolic acidosis, hyperparathyroidism, medications
 Manifestations: (metabolic acidosis: hypervolemia and
hypernatremia) tachypnea, lethargy, weakness, rapid, deep
respirations, hypertension, cognitive changes
 Normal serum anion gap
 Medical management: restore electrolyte and fluid balance,
LR, sodium bicarbonate, diuretics
 Nursing management: assessment, patient teaching related to
diet and hydration

 Normal plasma pH 7-35-7.45: hydrogen ion
concentration
 Major extracellular fluid buffer system;
bicarbonate-carbonic acid buffer system
 Kidneys regulate bicarbonate in ECF
 Lungs under control of medulla regulate CO2,
carbonic acid in ECF

 Other buffer systems
– ECF: inorganic phosphates, plasma proteins
– ICF: proteins, organic, inorganic phosphates
– Hemoglobin

 Low pH <7.35
 Low bicarbonate <22 mEq/L
 Most commonly due to renal failure
 Manifestations: headache, confusion, drowsiness,
increased respiratory rate and depth, decreased blood
pressure, decreased cardiac output, dysrhythmias, shock;
if decrease is slow, patient may be asymptomatic until
bicarbonate is 15 mEq/L or less
 Correct underlying problem, correct imbalance
– Bicarbonate may be administered

 With acidosis, hyperkalemia may occur as
potassium shifts out of cell
 As acidosis is corrected, potassium shifts back
into cell, potassium levels decrease
 decreases the CO2 level as a compensatory
action.
 Monitor potassium levels
 Serum calcium levels may be low with chronic
metabolic acidosis
– Must be corrected before treating acidosis

Metabolic Acidosis
(cont’d)
 Causes: diarrhea, lower intestinal fistulas,
ureterostomies, and use of diuretics; early
renal insufficiency; excessive administration of
chloride; and the administration of parenteral
nutrition without bicarbonate or
bicarbonateproducing solutes (eg, lactate).

 High pH >7.45
 High bicarbonate >26 mEq/L
 Most commonly due to vomiting or gastric
suction
 May also be due to medications, especially long-term
diuretic use
 Hypokalemia will produce alkalosis
 Manifestations: symptoms related to decreased
calcium, respiratory depression, tachycardia,
symptoms of hypokalemia

 Correct underlying disorder, supply chloride to
allow excretion of excess bicarbonate, restore
fluid volume with sodium chloride solutions

 Low pH <7.35
 PaCO2 >42 mm Hg
 Always due to respiratory problem with
inadequate excretion of CO2
 With chronic respiratory acidosis, body may
compensate, may be asymptomatic
– Symptoms may be suddenly increased pulse,
respiratory rate and BP, mental changes, feeling of
fullness in head, cloudiness, Hyperkalemia

 Potential increased intracranial pressure
 Treatment aimed at improving ventilation

 High pH >7.45
 PaCO2 <35 mm Hg
 Always due to hyperventilation
 Manifestations: lightheadedness, inability to
concentrate, numbness and tingling, tinnitus,
sometimes loss of consciousness
 Correct cause of hyperventilation,
hypokalemia, hypocalcemia
 changes in the PaCO2 and plasma HCO3–
concentration (cardiac and respiratory arrest).

 The pulmonary and renal systems compensate
for each other to return the pH to normal.
 The lungs compensate for metabolic
disturbances by changing CO2 excretion.
 The kidneys compensate for respiratory
disturbances by altering bicarbonate retention
and H secretion.

 pH 7.35 - (7.4) - 7.45
 PaCO2 35 - (40) - 45 mm Hg
 HCO3ˉ 22 - (24) - 26 mEq/L
 Assumed average values for ABG interpretation
 PaO2 80 to 100 mm Hg
 Oxygen saturation >94%
 Base excess/deficit ±2 mEq/L

 IV solutions contain dextrose or electrolytes
mixed in various proportions with water.
 Purpose:
 To provide water, electrolytes, and nutrients to
meet daily requirements
 To replace water and correct electrolyte deficits
 To administer medications and blood products

 Classified according to whether their total
osmolality is the same as, less than, or greater
than that of blood.
 Isotonic:310 mOsm/L
 Hypotonic: less than 250 mOsm/L
 Hypertonic: greater than 375 mOsm/L

 do not cause red blood cells to shrink or swell.
 Isotonic fluids expand the ECF volume.
 3 L of isotonic fluid is needed to replace 1 L of
blood loss.
 Fluid over load (hypertension and heart
failure)

 D5W: to supply water and to correct an
increased serum osmolality.
 Normal Saline: to correct an extracellular
volume deficit and to replace large sodium
losses.
 Lactated Ringer’s: similar to the ECF in
composition, contains sodium chloride,
potassium and calcium and bicarbonate
precursors.
It is used to correct dehydration and sodium
depletion and replace GI losses.

 Hypotonic Fluids (Half strength saline: to
replace cellular fluid, to provide free water for
excretion of body wastes, to treat
hypernatremia and other hyperosmolar
conditions.
 Excessive infusions: intravascular fluid
depletion, decreased blood pressure, cellular
edema, and cell damage.

 Hypertonic Fluids (normal saline + D5W): draw
water from the ICF to the ECF and cause cells
to shrink.
 extracellular volume excess and precipitate
circulatory overload and dehydration.
 Higher hypertonic solution must be
admonestered by central venous catheter.

 Choosing an Intravenous Site (The metacarpal,
cephalic, basilic, and median veins are recommended
sites because of their size and ease of access).
 Leg veins (thromboembolism), veins distal to a
previous IV infiltration or phlebitic area, sclerosed or
thrombosed veins, an arm with an arteriovenous shunt
or fistula, and an arm affected by edema, infection,
blood clot, deformity, severe scarring, or skin
breakdown, the side of a mastectomy (impaired
lymphatic flow), sites interfer with motion ability.
 Central vein (subclavian and internal jugular veins).

 Vein ch-ch: firm, elastic, engorged, and round
—not hard, flat, or bumpy.
 For flushing (should be at least twice the
volume capacity of the catheter).
 gtt/mL of infusion set/60 (min in 1 hr) * total
hourly volume= gtt/min
 electronic infusion devices
 Volumetric pumps

 Fluid overload: increased blood pressure
and central venous pressure, crackles on
auscultation of the lungs, edema, weight
gain, dyspnea, and rapid, shallow
respirations.
 treatment includes decreasing the IV
rate, monitoring vital signs frequently,
assessing breath sounds, and placing the
patient in a high Fowler’s position.
 Complication: heart failure, and
pulmonary edema.
Air embolism:
•Manifestations: palpitations, dyspnea, and
cyanosis; hypotension; weak, rapid pulse; loss of
consciousness; and chest, shoulder, and low back
pain.
•Treatment: clamping the cannula, placing the
patient on the left side in the Trendelenburg position,
assessing vital signs and breath sounds, and
administering oxygen.
•Prevention: filling all tubing with solution, and using
an air detection alarm.
Septicemia, other infections:
•Manifistation: fever, backache, headache,
increased pulse and respiratory rate, nausea
and vomiting, diarrhea, chills and shaking, and
general malaise, vascular collapse and septic
shock.
Infiltration: administration of a nonvesicant solution or
medication into surrounding tissue.
Extravasation: administration of vesicant or irritant
solution or medication into the surrounding tissue.
•Causes IV cannula dislodges or perforates the wall of the
vein.
•Ch-ch:redness, pain, edema around the insertion site,
leakage of IV fluid from the insertion site, discomfort and
coolness in the area of infiltration, and decrease in the flow
rate.
•pain, burning, redness at the site, Blistering,
inflammation, and necrosis of tissues (extravasation)
•Treatment: stop infusion, sterile dressing, warm compress
or cold compress , elevate affected extremity, antidotes.
Phlebitis: inflammation of a vein.
•Chemical (irritating medication or solution, rapid infusion rates,
and medication incompatibilities.)
•Mechanical (long periods of cannulation, catheters in flexed
areas, catheter gauges larger than the vein lumen, and poorly
secured catheters).
•Bacterial (poor hand hygiene, lack of aseptic technique, failure
to check all equipment before use, and failure to recognize early
signs and symptoms of phlebitis.
•S&S: reddened, warm area around the insertion site or along
the path of the vein, pain or tenderness at the site or along the
vein, and swelling.
•warm, moist compress to the affected site.
• Thrombophlebitis: the presence of a clot plus
inflammation in the vein.
– S&S: localized pain, redness, warmth, and
swelling around the insertion site or along the
path of the vein, immobility of the extremity
because of discomfort and swelling, sluggish
flow rate, fever, malaise, and leukocytosis.
– Treatment: discontinuing the IV infusion; cold
compress (to decrease the flow of blood and
increase platelet aggregation), followed by a
warm compress; elevating the extremity.
• Hematoma: blood leaks into tissues surrounding the IV
insertion site.
– Causes: needle slips out of the vein, or insufficient
pressure is applied to the site after removal of the
needle or cannula.
– S&S: ecchymosis, immediate swelling at the site, and
leakage of blood at the insertion site.
– Treatment: light pressure with a sterile, dry
dressing; applying ice for 24 hours to the site to
avoid extension of the hematoma; elevating the
extremity; assessing the extremity for any
circulatory, neurologic, or motor dysfunction.
• Clotting, obstruction:
– Causes: kinked IV tubing, a very slow infusion rate,
an empty IV bag, or failure to flush the IV line.
– signs are decreased flow rate and blood backflow into
the IV tubing.
– Management: discontinued fliude, change cannula,
The tubing should not be irrigated or milked. Neither
the infusion rate nor the solution container should be
raised,
 Review patient history
• history of transfusions and health problems
 Obtain baseline assessment and VS
 Perform patient teaching and obtain consent
 Procedure to identify patient and blood product
 Monitoring of patient and VS
 Nursing management is directed toward preventing
complications, promptly recognizing complications if
they develop, and promptly initiating measures to
control complications.
Febrile nonhemolytic reaction:
caused by antibodies to donor leukocytes that
remain in the unit of blood or blood
component.
exposure to multiple antigens from previous
blood products
The signs and symptoms: chills (minimal to
severe) muscle stiffness, fever typically begins
within 2 hours after the transfusion.
Complications
Acute hemolytic reaction: the donor blood is
incompatible with that of the recipient (ABO
incompatibility.)
•Symptoms consist of fever, chills, low back pain,
nausea, chest tightness, dyspnea, anxiety,
hemoglobinuria, Hypotension, bronchospasm, and
vascular collapse, Diminished renal perfusion, and
DIC.
•Treatment goals include maintaining blood volume
and renal perfusion and preventing and managing
DIC.
•Prevention: check detail in labeling blood samples
Complications
Allergic reaction: a sensitivity reaction to a
plasma protein within the blood component
being transfused.
•Symptoms: urticaria, itching, and flushing.
•Rarely, the allergic reaction is severe, with
bronchospasm, laryngeal edema, and shock.
•Prevention: blood components are washed to
remove any remaining plasma proteins.
Complications
Circulatory overload: too much blood is infused too quickly.
•PRBCs are safer to use than whole blood.
•If the administration rate is sufficiently slow, circulatory
overload may be prevented.
•diuretics are administered after the transfusion.
•Signs: dyspnea, orthopnea, tachycardia, anxiety, Jugular vein
distention, crackles, increase in blood pressure, pulmonary
edema (as manifested by severe dyspnea and coughing of pink,
frothy sputum).
•overload is mild: continue transfusion at slow rate and
administering diuretics.
•Sever case: place patient in an upright position with the feet in
a dependent position, the transfusion is discontinued, and the
physician is notified.
Complications
Bacterial contamination: often results from organisms
on the donor’s skin. (low risk with PRBCs and high risk with
platelet).
•Prevention: Transfusion should be administered within a
4-hour period.
•The signs are fever, chills, and hypotension.
•Complication septic shock.
•Management: discontinue transfusion, send blood for
testing and culture.
Complications
Transfusion related acute lung injury:
•Signs and symptoms include acute shortness of breath,
hypoxia (arterial oxygen saturation [SaO2] less than 90%),
hypotension, fever, and eventual pulmonary edema
•Diagnostic criteria include hypoxemia, bilateral pulmonary
infiltrates (seen on chest x-ray), and no evidence of cardiac
cause for the pulmonary edema
Complications
Delayed hemolytic reaction: occur within 14 days after
transfusion
•Signs and symptoms: fever, anemia, increased bilirubin
level, decreased or absent haptoglobin, and possibly
jaundice.
Complications
Disease acquisition:
Complications of long-term transfusion therapy:

(Iron overload)
1. pH 7.48 PaCO2 32 HCO3 24
2. pH 7.32 PaCO2 48 HCO3 25
3. pH 7.30 PaCO2 40 HCO3 18
4. pH 7.38 PaCO2 48 HCO3 28
5. pH 7.49 PaCO2 40 HCO3 30
6. pH 7.35 PaCO2 48 HCO3 27
7. pH 7.45 PaCO2 47 HCO3 29
8. pH 7.31 PaCO2 38 HCO3 15
9. pH 7.30 PaCO2 50 HCO3 24
10. pH 7.48 PaCO2 40 HCO3 30
1. Respiratory alkalosis
2. Respiratory acidosis
3. Metabolic acidosis
4. Compensated Respiratory acidosis
5. Metabolic alkalosis
6. Compensated Respiratory acidosis
7. Compensated Metabolic alkalosis
8. Metabolic acidosis
9. Respiratory acidosis
10. Metabolic alkalosis

1 - Chap13-Fluid and Electrolyte - Balance and Disturbance 2017

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Fluid and Electrolytes: Balance and

Dr. Ahmad Aqel, 2017

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 Filtration: movement of water, solutes occurs

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 Stimulates thirst and antidiuretic hormone

 Result in increased free water and decreased

 Stress, nausea, nicotine, and morphine also

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 Aldosterone is a mineralocorticoid with potent

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 ANF causes vasodilation and increased urinary

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 Small amounts of water are eliminated by GI

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 Approximately 900 ml per day is lost

 No electrolytes are lost with insensible water

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abnormal lung sounds increased weight and urine

Normal value 135 to 145 mEq/L

Common food Butter, Canned food, Cheese,

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CAUSES excess water loss, excess sodium administration,

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• Liquid potassium chloride has an unpleasant taste and

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• IV potassium is always diluted and

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• Potassium infusion can cause phlebitis; therefore the

• The nurse should assess renal function before

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