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Western Mindanao State University College of Nursing Zamboanga City

Curative and Rehabilitative Nursing Care Management 102 A

Disturbances in Fluids and Electrolytes and Acid Base Balance

Antonio D. Patio Jr. Level III Faculty

2 After completing this chapter, you will be able to: 1 Discuss the functions and regulatory mechanisms that maintain water and electrolyte balance in the body. 2 Compare and contrast the causes, effects, and care of the client with fluid volume or electrolyte imbalance. 3 Describe the pathophysiology and manifestations of imbalances of sodium, potassium, calcium, magnesium, and phosphorus. 4 Identify laboratory and diagnostic tests used to diagnose and monitor treatment of fluid, electrolyte, and acid-base disorders. 5 Discuss the causes and effects of acid-base imbalances 6 Recognize normal and abnormal values of electrolytes in the blood. 7 Use arterial blood gas findings to identify the type of acid base imbalance present in a client. 8 Provide teaching about diet and medications used to treat or prevent electrolyte disorders. 9 Use the nursing process as a framework to provide individualized nursing care to clients with fluid, electrolyte, and acid-base disorders. Illness & Trauma often results in changes in the normal distribution & composition of body fluids These changes affects: 1 fluid balance of the intracellular and extracellular compartments of the body 2 the concentration of electrolytes within fluid compartments 3 the bodys hydrogen ion concentration (pH). Normal Physiologic Processes Depend on a: 1 relatively stable state in the internal environment of the body. 2 the fluid volume, electrolyte composition, and pH of both intracellular 3 extracellular spaces must remain constant within a relatively narrow range to maintain health and life. Homeostasis is the bodys tendency to maintain a state of physiologic balance in the presence of constantly changing conditions. 1 Homeostasis is necessary if the body is to function optimally at a cellular level and as a total organism. 2 Homeostasis depends on multiple factors in both the external and internal environments, = such as available oxygen in the air, nutrients in food = as well as normal body temperature, respiration, and digestive processes. 1 The normal volume, composition, distribution, and pH of body fluids reflect a state of homeostasis. The GOAL in managing fluid, electrolyte, and acid-base imbalances is to: Reestablish & Maintain a Normal Balance Nursing Care Includes: 1 assessing clients who are likely to develop imbalances 2 monitoring clients for early manifestations 3 implementing collaborative and nursing interventions to prevent or correct imbalances. Effective Nursing Interventions Requires: 1 an understanding of the multiple processes that maintain fluid, electrolyte, and acid-base balance 2 an understanding of the causes and treatment of imbalances that occur. 3 mechanisms that maintain normal fluid and electrolyte balance are discussed first, followed by sections on fluid imbalances and electrolyte imbalances. 4 discussion of normal acid-base balance precedes discussion of acid-base imbalances. 5 case studies related to selected fluid, electrolyte, and acid-base disorders are found throughout the chapter. Overview of Normal Fluid & Electrolytes Balance 1 Fluid and electrolyte balance in the body involves regulatory mechanisms that maintain the composition, distribution, and movement of fluids and electrolytes.

What is Your Understanding of the Concept: FLUID BALANCE The term Fluid Balance Means Several Things To say that the body is in a state of fluid balance is to say: That the total amount of water in the body is normal and remains relatively constant What Else?

3 Fluid Balance Means: Relatively constancy of the distribution of water in the bodys three fluid compartments: 1. Volume of water inside the cells 2. Volume of water in the interstitial spaces 3. Volume of water in the blood cells Fluid Imbalance Means: total volume of in one or more of its compartments have increased or decreased beyond normal limits Cardinal Principle about Fluid Balance 1. Fluid Balance can only be maintained if intake equals output 2. Devices for varying output so that it equal intake constitute the most crucial mechanism for maintaining fluid balance: mechanism for adjusting intake or output also operate (such aldosterone mechanism) Hormones that Influences Fluid & Electrolytes Balance 1. Antidiuretics Hormone [ADH] or Vasopressin 1 When posterior pituitary glands fails to secrete ADH water absorption in the distal segments of the renal tubular system is greatly decreased thus allowing urine output to increase as much as three to ten folds condition known as diabetes insipidus: - despite this increase in urine output blood volume normally normally does not decrease enough to be measurable WHY? - the thirst mechanism simply causes the person to drink enough water to make up the differences ADH secreted in tremendous amount as in syndrome of inappropriate ADH secretion, the chronic state of the condition is the blood volume increases imperceptibly -un noticed perhaps 3 to 5 percent! Why minute increase? The slight volume increase that does occur increases the arterial pressure enough to - overcome the antidiuretic hormone effects on the kidney of causing water retention Arterial pressure Stress exerted by the circulating blood on the arteries as a result of the product of cardiac output and vascular resistance 2. Aldosterone: increases renal absorption of sodium and water thus regulating the ECF volume - hormone [one of the mineralocorticoids] releases by cortex of the adrenal gland.- regulates salt [sodium and potassium] and water balance in the body causes excessive salt reabsorption from the distal tubules, collecting tubules and collecting duct of the kidneys causes osmotic reabsorption of water 3. Thyroid Hormone: Thyroxine(T4) and Triiodothyronine (T3) maintain adequate cardiac output to adequate perfuse the kidney over 90% of the thyroid hormones being release by the thyroid gland is the thyroxine ,T4 less than 10% is Triodothyroxine T3 Once these two enters the peripheral tissues cells: T3 is about 4 times as potent in stimulating metabolism and causing other intracellular effects than T3 T4 duration of action is four or more times as long as than T3 SO: the integrated effect of the two is the same as per action per unit mass of delivered hormones Function: increases the metabolic activities of almost all the tissues of the body with few notable exception: brain, retina, spleen, testes and lungs 4. Parathyroid Hormones: maintain calcium level - Parathyroid gland causes rapid absorption of calcium salts form the bones which resulted to hypercalcemia in the extracellular fluid and hypofunction causes hypocalcemia often resulting to tetany B. BODY FLUIDS COMPOSITION

I. Water
1 2 3 4 5 6 7 Water is the primary component of body fluids. It functions in several ways to maintain normal cellular function. Provides a medium for the transport and exchange of nutrients and other substances such as oxygen, carbon dioxide, and metabolic wastes to and from cells. Provides a medium for metabolic reactions within cells. Assists in regulating body temperature through the evaporation of perspiration. Provides form for body structure and acts as a shock absorber. Provides insulation and acts as a lubricant.

4 Total body water constitutes about 60% of the total body weight, but this amount varies with age, gender,and the amount of body fat. Total body water decreases with aging; = infants at 70-80% of their body weight = adults at 60% of their body weight = in people over age 65, body water may decrease to 45% to 50% of total body weight Fat cells contain comparatively little water: = in person who is obese, the proportion of water to total body weight is less than in the person of average weight = in a person who is very thin, the proportion of water to total body weight is greater than in the person of average weight. The so-called lean body mass, which means a body stripped of fat, contains 0.69 parts of water (69%) of the total body weight in all persons. - Such high values are observed in the newborn and in extremely fit athletes with minimal body fat. - Babies have a tenfold higher water turnover per kg of body weight than adults do. As an average females have a low body water % compared to males. - Such differences show sex dependency, but the important factor is the relative content of body fat, since fat tissue contains significantly less water (only 10%) than muscle and other tissues (70%). - This is why the relative water content depends upon the relative fat content. The average for most healthy persons is 60% of the body weight. Sedentary, overweight persons contain only 50-55 % water dependent on the body fat content. The relative content of body fat rises with increasing age and body weight, and the relative mass of muscle tissue becomes less. Consequently, the body water fraction falls with increasing body weight and age. Aging implies loss of cells, but the Extra Cellular Volume is remarkably constant through life and under disease conditions. To Maintain Normal Fluid Balance Body Water Intake & Output Should Be Approximately Equal. The average fluid intake and output usually is about 2500 mL over a 24-hour period. Daily Loss of Water in Millimeters Normal Temp Prolong Hot Weather Heavy Exercise 350 250 350 650

Insensible Losses
5. Skin 6. Respirator Tract Sensible Losses Urine Sweat Feces Total = 350 350

1,400 100 100 2300

1,200 1,400 100 3,300

500 5,000 100 6,600

II. Electrolytes
Body fluids contain both water molecules and chemical compounds, these chemical compounds can either remain intact in solution or separate (dissociate) into discrete particles. Electrolytes : Are substances that dissociate in solution to form charged particles called ions. Cations - are positively charged electrolytes; Anions - are negatively charged electrolytes.

Membrane Potentials
1.Diffusion of ions through cell membrane as a result of difference of concentration between the two sides of membrane creating an imbalance of negative & positive charges on the two sides 2. Active transport of ions through the membrane thus creating an imbalance of charges Sodium Potassium Pump Generally, very minute excess of negative ions [anion] accumulates immediately inside the cell membrane & along its surface & equal number of positive ions [cation] accumulates outside the membrane

Membrane Potential

Fluids in & out of cells are electrolyte @ 150-160 mEg/L of positive & same negative ions

Another Method Membrane Potentials Can Be Develop


Active Transport: Sodium Potassium Electronic Pump

Pumps 3 Sodium Ion OUT

Pumps 2 Potassium Ion IN

Each cycle of the pump

Results to

Nerve fibers losses one POSITIVE charge ion inside

Membrane becomes NEGATIVELY charge on the inside

Creating a membrane Potential called Electrogenic Pump

Na- K Pump Continually

Na to the exterior causing reduced Na concentration inside nerve fiber

Potassium ions to the interior helps establish the high concentration of K inside the cell

After many nerve impulses has been transmitted

Both Na & K gradients decreases diffusion of ions through membrane during the ACTION POTENTIAL

Na-K pump will soon re-establish the appropriate concentration gradient

The Nerve Action Potential

Action Potential transfer & conduct nerve signal along the nerve fiber until it comes to the fibers end

Action Potential initiate change from normal resting NEGATIVE potential to POSITIVE membrane potential & ends with an almost equally rapid change back to negative

The Successive Stages of the Action Potential


Resting Stage: Resting membrane potential before the action potential occurs Polarized large NEGATIVE membrane present Depolarization Stage: Membrane suddenly becomes permeable to sodium allowing tremendous numbers of sodium ion to flow into the interior of axon potential rising rapidly in the POSITIVE direction

Repolarization Stage: Within a few 10,000ths of a second after the membrane becomes highly permeable to sodium the sodium channel close almost as rapidly as they had opened the rapid diffusion of potassium ion to the exterior re-establishes the normal NEGATIVE resting membrane potential

Electrolytes Undertaking. 1 Assist in regulating water balance. 2 Help regulate and maintain acid-base balance. 3 Contribute to enzyme reactions. 4 Are essential for neuromuscular activity. 5 The concentration of electrolytes in body fluids generally is measured in milliequivalents per liter of water (mEq/L).

Extracellular fluid (ECF) is located outside of cells. It accounts for approximately 20% of the total body weight. Extracellular Fluid is classified by location. Interstitial fluid is located in the spaces between most of the cells of the body. = accounts for approximately 15% of total body weight. Intravascular fluid, called plasma- noncellular portion of the blood; part of ECF & communicates with the interstitial fluid via capillary pores is contained within the arteries, veins, and capillaries. = accounts for approximately 5% of total body weight.

Effects of Adding Water to Extracellular Fluid


Injection to the blood stream/beneath the skin or by ingesting water followed by absorption from the GIT

Dilutes the Extracellular fluid causing it to become hypotonic with respect to the Intracellular fluid

Osmosis begins at cell membranes with large amount passing to the interior of the cell

Water becomes distributed evenly among all the Extracellular Fluid & Intracellular Fluid compartments

Transcellular fluid includes urine; digestive secretions; perspiration; and cerebrospinal, pleural, synovial, intraocular, gonadal, and pericardial fluids A trace amount of water is found in bone, cartilage, and other dense connective tissues; this water is not exchangeable with other body fluids. ECF is the transport medium that carries oxygen and nutrients to and waste products from the cells. Example: = plasma transports oxygen from the lungs and glucose from the digestive system to the tissues and kidneys for elimination = these solutes diffuse through the capillary wall into the interstitial space, and from there across the cell membrane into the cells. = waste products of metabolism: carbon dioxide & hydrogen ion diffuse from the intracellular space into the interstitial space, and from there into plasma via the capillary walls.

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C. Body Fluid Movement


Four chemical and physiologic processes controls: 1 the movement of fluid, electrolytes, 2 other molecules across membranes between = intracellular and interstitial space = interstitial space and plasma. 1. Osmosis Diffusion, 3. Filtration 2. Diffusion 4. Active Transport. 1.Osmosis. The process by which water moves across a selectively permeable membrane from an area of lower solute concentration to an area of higher solute concentration Osmosis continues until the solute concentration on both sides of the membrane is equal. Example, = if pure water and a sodium chloride solution are separated by a selectively permeable membrane, then water molecules will move across the membrane to the sodium chloride solution. Osmosis is the primary process that controls body fluid movement between the ICF and ECF compartments.

Osmolarity & Osmolality


The concentration of a solution may be expressed as the osmolarity or osmolality of the solution. Osmolarity refers : - to the amount of solutes per liter of solution (by volume), it is reported in milliosmoles per liter (mOsm/L) in a solution. Osmolality refers: - to the number of solutes per kilogram of water (by weight), it is reported in milliosmoles per kilogram (mOsm/kg). The normal osmolality of both ICF and ECF ranges between 275 and 295 mOsm/kg.

Osmotic Pressure and Tonicity.


Osmotic Pressure of the solution - the power of a solution to draw water across a membrane Importance: maintaining fluid balance between the interstitial and intravascular spaces thus helping hold water within the vascular system. The composition of interstitial fluid and intravascular plasma is essentially the same: except for a higher concentration of proteins in the plasma. These proteins (especially albumin) exert osmotic pressure, pulling fluid from the interstitial space into the intravascular compartment.

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Tonicity refers:
- To the effect a solutions osmotic pressure has on water movement across the cell membrane of cells within that solution. Isotonic solutions have the same concentration of solutes as plasma. Cells placed in an isotonic solution will neither shrink nor swell as there is no net gain or loss of water within the cell, and no change in cell volume : does not upset the osmotic equilibria b/w fluids outside & inside the cells Normal saline (0.9% sodium chloride solution) is an example of an isotonic solution.

Hypertonic solutions have a greater concentration of solutes than plasma. In their presence, water is drawn out of a cell, causing it to shrink = sodium chloride solution of greater than 0.9% concentration is hypertonic

Hypotonic solutions have a lower solute concentration than plasma When red blood cells are placed in a hypotonic solution, water moves into the cells, causing them to swell and rupture (hemolyze). = any solution less than 0.9% sodium chloride

The concepts of osmotic draw and tonicity are important in understanding the pathophysiologic changes that occur with fluid & electrolyte imbalances, as well as treatment measures. For example: An increased sodium concentration of extracellular fluid causes water to shift from the ICF compartment to the ECF compartment. In this case, administering a hypotonic intravenous solution will facilitate water movement back into the intracellular space. 2.DIFFUSION. The process by which solute molecules move from an area of high solute concentration to an area of low solute concentration to become evenly distributed.

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3. FILTRATION.
The process by which water and dissolved substances (solutes) move from an area of high hydrostatic pressure to an area of low hydrostatic pressure, usually occurs across glomerulus of the kidneys and arterial end capillary membranes. Hydrostatic pressure is created- by the pumping action of the heart and gravity against the capillary wall A balance of hydrostatic (filtration) pressure and osmotic pressure regulates the movement of water between the intravascular and interstitial spaces in the capillary beds of the body. Hydrostatic pressure within the interstitial space opposes this movement to some degree Arterial end of capillaries - hydrostatic pressure within the arterial end of the capillary pushes water into the interstitial space. At the venous end of the capillary, the osmotic force of plasma proteins draws fluid back into the capillary

4. ACTIVE TRANSPORT. Allows molecules to move across cell membranes and epithelial membranes against a concentration gradient. This movement requires energy: A. Adenosine Triphosphate (ATP) is the main usable energy source found in all living things. ATP fuels most cell activities, including muscle movement, protein synthesis, cell division, and nerve signal transmission The sodium-potassium pump is an important example of active transport

D. Body Fluid Regulation


Homeostasis requires several regulatory mechanisms and processes to maintain the balance between fluid intake and excretion w/c includes: A. thirst D. Antidiuretic hormone B. the kidneys E. Atrial natiuretic factor C. renin-angiotensin aldosterone mechanism, These mechanisms affect the volume, distribution, and composition of body fluids. A. Thirst : Thirst is the primary regulator of water intake. - plays an important role in maintaining fluid balance and preventing dehydration. - The thirst center, located in the brain, is stimulated when the blood volume drops because of water losses or when serum osmolality (solute concentration) increases The thirst mechanism is highly effective in regulating extracellular sodium levels. Increased Sodium in ECF Increase Serum Osmolality Stimulating the Thirst Center Fluid intake in turn reduces the sodium concentration of ECF and lowers serum osmolality. Conversely, a drop in serum sodium and low serum osmolality inhibit the thirst center.

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PRACTICE ALERT The thirst mechanism declines with aging, making older adults more vulnerable to dehydration and hyperosmolality (high serum osmolality). Clients with an altered level of consciousness or who are unable to respond to thirst also are at risk. B. Kidneys The kidneys are primarily responsible for regulating fluid volume and electrolyte balance in the body. they regulate the volume and osmolality of body fluids by controlling the excretion of water and electrolytes. In adults, about 170 L of plasma are filtered through the glomeruli every day. - by selectively reabsorbing water and electrolytes, the kidneys maintain the volume and osmolality of body fluids. The sodium-potassium pump. Sodium and potassium ions are moved across the cell membranes against their concentration gradients. This active transport process is fueled by energy from adenosine triphosphate (ATP). Fluid balance between the intravascular and interstitial spaces is maintained in the capillary beds by a balance of filtration at the arterial end and osmotic draw at the venous end.

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C. Renin-Angiotensin-Aldosterone System (RAAS)


Maintains intravascular fluid balance and blood pressure: Decrease blood flow & pressure to the kidneys Stimulates specialized receptors juxtaglomerular cells of the nephrons produce an enzyme renin Renin converts Angiotensinogen (a plasma protein) in the circulating blood into Angiotensin I. Angiotensin I travels through the bloodstream to the lungs & with an Angiotensin converting enzyme Converted to Angiotensin II Angiotensin II is a potent vasoconstrictor; it raises the blood pressure. It also stimulates the thirst mechanism to promote fluid intake and acts directly on the kidneys, causing them to retain sodium and water. Angiotensin II Stimulates Adrenal Cortex Releases Aldosterone. Sodium & Water Retention (distal nephron of the kidney) Restoring Blood Volume

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D. Antidiuretic Hormone
Antidiuretic hormone (ADH) regulates water excretion from the kidneys. Increase serum osmolality/decrease blood volume Osmoreceptors in the Hypothalamus Respond Stimulating ADH Production Acts on the Distal Tubules of the Kidney More permeable to water and thus increasing water reabsorption. Urine output falls, blood volume is restored, and serum osmolality drops as the water dilutes body fluids

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ADH RELEASE AND EFFECT

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Fluids and Electrolytes Imbalances I. Extracellular Fluid Volume Deficit = dehydration II. Extracellular Fluid Volume Excess = hyper or overhydration,third spacing = hypervolemia III. Extracellular Fluid Volume Shift = third spacing IV. Intracellular Fluid Volume Deficit = cell dehydration VI. Intracellular Fluid Volume Excess = water intoxication/potassium imbalances

CLIENT WITH EXTRACELLULAR FLUID VOLUME DEFICIT (Isotonic Volume Deficit)


Extracellular Fluid Volume Deficit (FVD) commonly referred to as Dehydration Is a decrease in: 1. intravascular 2. interstitial, and/or 3. intracellular fluid in the body. FVD may be due: 1. to excessive fluid losses 2. failure of regulatory mechanisms 3. insufficient fluid intake 4. fluid shifts within the body. Etiology and Pathophysiology Isotonic Fluid Loss Fluid and solute lost in proportional amounts, thus serum osmolality remains normal and no osmotic force is created Intracellular water not disturbed and fluid losses are primarily ECF (especially the vascular volume), which can quickly lead to shock Primarily an extracellular fluid loss that requires extra-cellular fluid replacement, with emphasis on the vascular volume Types of Extracellular Fluid Volume Deficit I. Hyperosmolar Fluid Volume Deficit - Water loss is greater than electrolytes loss II. Iso - Osmolar Fluid Volume Deficit - Water & electrolytes losses are equal III. Hypotonic Fluid Volume Deficit - Electrolytes loss is greater than the fluid loss (rare case)

Pathophysiolgy The most common cause of FVD is excessive loss of GIT from: A. vomiting C. gastrointestinal suctioning E. intestinal drainage B. diarrhea D. intestinal fistulas Other causes of fluid losses include: A. excessive renal losses of water and sodium from diuretic therapy, B. renal disorders, or endocrine disorders and hemorrhage C. water and sodium losses during sweating from excessive exercise or increased environmental temperature. D chronic abuse of laxatives and/or enemas. E. inadequate fluid intake may result from lack of access to fluids, inability to request or to swallow fluids, oral trauma, or altered thirst mechanisms

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Regulation of Body Fluids

HYPERVOLEMIA Excess Fluid Volume Inhibits

HYPOVOLEMIA Decreased Fluid Volume Stimulates

ADH Aldosterone release release inhibited inhibited Contribute to Increased Urination of dilute urine

Thirst inhibited

Thirst ADH release stimulated stimulated

Aldosterone release stimulated

Contribute to Decreased Urination concentrated urine

Normal Fluid Volume Restored


Third Spacing: - is a shift of fluid from the vascular space into an area where it is not available to support normal physiologic processes and is a volume loss: Trapped fluid may be: a. may be sequestered in the abdomen or bowel, or in such other actual or potential body spaces as the pleural or peritoneal space. b. trapped within soft tissues following trauma or burns. Assessing the extent of fluid volume deficit resulting from third spacing is difficult. Note: It may not be reflected by changes in weight or intake-and-output records, and it may not become apparent until after organ malfunction occurs Manifestations With a rapid fluid loss (such as hemorrhage or uncontrolled vomiting), manifestations of hypovolemia develop rapidly. When the loss of fluid occurs more gradually, the clients fluid volume may be very low before symptoms develop. Rapid weight loss is a good indicator of fluid volume deficit. = each liter of body fluid weighs about 1 kg (2.2 lb). Loss of interstitial fluid causes skin turgor to diminish. = when pinched ,the skin of a client with FVD remains elevated. = loss of skin elasticity with aging makes this assessment finding less accurate in older adults. Tongue turgor is not generally affected by age; therefore, assessing the size, dryness, and longitudinal furrows of the tongue may be a more accurate indicator of fluid volume deficit. Postural or orthostatic hypotension is a sign of hypovolemia. A drop of more than 15 mmHg in systolic blood pressure when changing from a lying to standing position often indicates loss of intravascular volume. Venous pressure falls , causing: A. flat neck veins, even when the client is recumbent. B. loss of intravascular fluid causes the hematocrit to increase. Compensatory Mechanisms to conserve water and sodium and maintain circulation account for many of the manifestations of fluid volume deficit: = such as tachycardia; pale, cool, skin (vasoconstriction); and decreased urine output. = the specific gravity of urine increases as water is reabsorbed in the tubules.

19 The systemic effects of fluid volume deficit are illustrated

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FLUID VOLUME ASSESSMENT DATA

Assessment Data Thirst in mentally alert people Poor skin turgor-forehead & upper chest. In severe deficit-pinched skin remains in pinch position for several seconds Dryness of the skin & mucous membranes. In severe case- tongue is dry & furrowed Eyeballs soft and in severe case - sunken Elevated body temperature

Pathophysiologic Basis Cells shrinks, stimulating the thirst osmo receptors Loss of normal elasticity of the skin

Cells of the skin and mucous membranes dries out

Water tension in eyeball decreases

Regulation of body temperature is disturbed by lack of water Normal temperature control requires 800 ml of water

Apprehension and restlessness; coma in severe case Concentrated urine: Specific gravity above 1.030 In severe dehydrationrenal shutdown: hypernatremia plus hypovolemia

Cellular dehydration in brain due to shift of water from cells to exctracellular fluid compartment ADH released in response to increase osmolality of body fluids

Decreased plasma volume resulting to decrease in blood flow to kidneyoliguria & anuria

21 The primary goals of care related to fluid volume deficit 1 prevent deficits in clients at risk and to correct deficits and their underlying causes. 2 depending on the acuity of the imbalance, treatment may include replacement of fluids and electrolytes by the intravenous, oral, or enteral route. 3 when possible, the oral or enteral route is preferred for administering fluids. 4 in acute situations, however, intravenous fluid administration is necessary.

Diagnostic Tests 1 Laboratory and diagnostic tests may be ordered when FVDt is suspected. Such tests measure: 1. Serum Electrolytes. In an isotonic fluid deficit, sodium levels are within normal limits; when the loss is water only, sodium levels are high. Decreases in potassium are common. 2. Serum Osmolality. - To help differentiate isotonic fluid loss from water loss. - With water loss, osmolality is high; it may be within normal limits with an isotonic fluid loss. 3. Serum Hemoglobin and Hematocrit. The hematocrit often is elevated due to loss of intravascular volume and hemo concentration. 4. Urine Specific Gravity and Osmolality. As the kidneys conserve water, both the specific gravity and osmolality of urine increase. 5 Central Venous Pressure (CVP) . The CVP measures the mean pressure in the superior vena cava or right atrium, providing an accurate assessment of fluid volume status. CVP is a hemodynamic monitoring method for evaluating fluid volume status. 1 It measures mean right atrial pressure by means of a catheter. 2 The CVP catheter is inserted by a physician, most often at the clients bedside, into the antecubital, internal jugular, or Subclavian vein

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Nursing Responsibilities in Measuring CVP: 1. Explain to the client and family what is being done. 2. Prior to the first measurement: a. take baseline vital signs b. measure the level of the right atrium on the clients thorax. = this is usually at the fourth intercostal space on the lateral chest wall, midway between the anterior and posterior chest. = this site is marked and used as the reference point for all measurements. 3. Place the bed in the same position for each reading, usually with the client supine and the head of the bed flat. 4. Use a carpenters level to check the level of the measuring device to make sure the 0 on the manometer is level with the reference point on the clients chest Continuation: CVP 5. Remove any air bubbles in the line. 6. = Turn the stopcock on the manometer so that fluid flows into the manometer, filling it a few centimeters above the expected reading. = Then turn the stopcock to open the line between the manometer and the client. = The fluid level will fall and then reach a point at which it fluctuates with the clients respirations. = This point is recorded as the CVP. 7. After the measurement is taken, turn the stopcock so that the fluid can again flow from the fluid source to the client. Normal Values When CVP is measured by a manometer, normal values range from 2 to 8 cm water. 1 A low CVP indicates inadequate venous return from fluid deficit and hypovolemia or due to peripheral vasodilation. 1 A high CVP indicates fluid overload, cardiac problems that decrease cardiac contractility, or pulmonary disorders that increase pulmonary vascular resistance.

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Parenteral Fluid Therapy Purpose: - to provide water, electrolytes and nutrients to meet daily requirements - to replace water and correct electrolytes deficits - to administer medications and blood products Types of IV Solutions: Isotonic, Hypotonic, Hypertonic Electrolytes solutions are considered isotonic if total electrolytes content [anion + cations] is approximately 310 mEg/L Hypotonic total electrolytes content is less than 250 mEg/L Hyepertonic total electrolytes content is exceeds 375 mEg/L Isotonic D5W has an osmolality of 252 mOsm/L once administered: glucose is rapidly metabolized and this initially isotonic solutions can easily disperses as an hyptonic solutions: 1/3 extracellular and 2/3 intracellular

total osmolality close to that of ECF and do not cause red blood cells to shrinks or swell expands the ECF volume: 1 L of solutions expands ECF by 1 L, but expands the plasma by 0.25 because of its crystalloid fluid and diffuses quickly into the ECF compartments 3 L of isotonic solutions is needed to replace 1 L of blood loss Because these fluid expands the intravascular space patient with hypertension and heart failure must be closely monitored for signs of circulatory overload

24 Essential to remember this action: especially for patient at risk for increased intracranial pressure - during resuscitation : do not use causes hypeglycemia - therefore used D5W mainly to supply water and to correct an increased serum osmolality - 1 L of D5W provides fewer than 200 ml kcal and a minor source of calories for bodys daily requirements Normal Saline Solution [0.9% sodium chloride]: has a total osmolality of 308 mOsm/L - entrire osmolality contributed by electrolytes solutions remains with ECF THUS: normal saline solutions is often used to correct an extracellualr volume deficit - although referred to as NORMAL contains only sodium and chloride and does not actually simulate [replicate] the ECF - use in blood transfusion and to replace large sodium losses as in burn injuries - does not supply calories - not to use in heart failure, pulmonary edema, renal impairment or sodium retention Other isotonic solutions: - Lactated Ringer solutions contains potassium and calcium and in addition to sodium chloride - Used to correct dehydration and sodium depletion and replace GI loses - Lactated Ringers contains bicarbonate precursors Hypotonic solutions - Half-strength saline [.45% sodium chloride osmolality at 154 mOsm/L] - one purpose of hypotonic solutions: replace cellular fluid because it is a hypotonic solutions as compared with plasma - provide free water for excretion of body waste - used to treat hypernatremia and other hyperosmolar conditions Excessive hypotonic infusion: - leads to intravascular fluid depletion, decreased blood pressure, cellular edema and cell damage Hypertonic solution: - when normal saline or lactated ringer solutions contains 5% dextrose total osmolality exceeds that of ECF - dextrose is quickly metabolized

Factors Affecting Flow: Governed by the same principles that govern fluid movements in general: - flow is directly proportional to the height of the liquid column raising the height of the infusion container may improves sluggish flow - flow is directly proportional to the diameter of the tubing. The clamp on IV tubing regulates the flow by changing the tubing diameter. In addition, the flow is faster through large-gauge rather than small-gauge cannula - flow is inversely proportional to the length of the tubing. Adding extension tubing to an IV line will decrease the flow - flow is inversely proportional to the viscosity of a fluid. Viscous IV solutions, such as blood, require a larger cannula than do water or saline solutions

25 Solution HYPOTONIC 5%Dextrose in Water (D5W) Contents 50 g dextrose No electrolyte Uses Replace deficits of total body water Not used alone to expand ECF volume because dilution of electrolytes can occur Comments Supplies 170kcal/L & free water. Distilled water can not be given IV coz it would cause hemolysis Dextrose is metabolized in liver leaving solution of water w/out hemolytic problem Not used for routine administration of IV fluids because it contains more Na than ECF(140 mEg of NaCl & 103 mEg of CL). Expands plasma & Interstitial volume & does not enter the cells Solution is roughly isotonic to plasma but does not contain magnesium or phosphate

ISOTONIC .9 Na CL (Normal Saline solution: NS.0.9%NS)

154 mEg/L of Na and CL

ECF deficits in patients with low serum levels of Na or CL & metabolic alkalosis Before & after the infusion of blood product

ISOTONIC Lactated Ringers Solution (LR)

130mEg/L Na 4 mEg/L K 3 mEg/Ca 109 mEg/CL 28 mg/el lactate

ECF deficits such as fluid loss with burns and bleeding, dehydration from loss of bile or diarrhea

HYPERTONIC Lactated Ringers Solution with 5% Dextrose

50 g dextrose 130 mEg/L Na 4 mEg/L K 3 mEg/L Ca 109 mEg/L CL 28 mEg/L lactate

Lactate is equivalent to bicarbonate and can be used to treat many forms of acidosis ECF deficits, such as This solution is fluid loss with burns hypertonic because it & bleeding & is the combination of dehydration from loss two solution : of bile or diarrhea D5W & LR Provides modest calories -170 kcal ECF deficits in patients with low serum levels of Na or CI & metabolic alkalosis Before & after blood infusion pf blood products This solution is hypertonic because its a combination of two solutions: D5W & LR

Cont. Hypertonic 5% Dextrose & Normal Saline D5/0.9 NS

50 g Dextrose 77 mEg/L Na & Cl

26 Cont.Hypertonic 5% Dextrose & 0.45% 50g Dextrose Normal Saline 34 mEg/L D5/1/2 NS NaCl

5% Dextrose & 50 g Dextrose 0.225% Normal Saline 34 mEg/L Na & CL D5 /0.2 NS, D5 NS

Can be used as initial Commonly used as fluid for hydration maintenance of fluid because it provides more water than sodium

Health Promotion Health promotion activities focus on teaching clients to prevent fluid volume deficit. Discuss the importance of maintaining adequate fluid intake, particularly when exercising and during hot weather. Advise clients to use commercial sports drinks to replace both water and electrolytes when exercising during warm weather. Instruct clients to maintain fluid intake when ill, particularly during periods of fever or when diarrhea is a problem. Teach older adults (and their caretakers) that thirst decreases with aging and urge them to maintain a regular fluid intake of about 1500 mL per day, regardless of perception of thirst. Carefully monitor clients at risk for abnormal fluid losses through routes such as : a. vomiting d. nasogastric suction, b. fever e. increased urine output c. diarrhea f. wounds Monitor fluid intake in clients: a. decreased level of cons. c. physical limitations b. disorientation d. nausea & anorexia Discuss the increased risk for fluid volume deficit with older adults and provide information about prevention. Nursing Care of the Older Adult The older adult is at risk for fluid volume deficit from a variety of factors. Physical changes include the following: The perception of thirst decreases with aging. As muscle tissue declines with aging, the amount of total body water decreases. Renal blood flow and glomerular filtration decline with aging, and the ability to concentrate urine decreases. Body temperature regulation is less effective with aging. Functional changes of aging also affect fluid balance: fear of incontinence can lead to self-limiting of fluid intake. physical disabilities associated with age-related illnesses, such as arthritis or stroke, may limit access to fluids. cognitive impairments can interfere with recognition of thirst and the ability to respond to it. older adults who have self-care deficits, or who are confused, depressed, tube fed, on bed rest, or taking medications (such as sedatives, tranquilizers, diuretics, and laxatives) are at greatest risk for fluid volume deficits. older adults without air conditioning are at risk during extremely hot weather. Assessment Health History: Risk factors such as: A. medications B. endocrine disease

C. acute or chronic renal

27 Precipitating factors such as: A. hot weather, B. extensive exercise D. lack of access to fluids C. recent illness (especially if accompanied by fever, vomiting, and/or diarrhea); onset and duration of symptoms. Physical Assessment: weight; vital signs including orthostatic blood pressure and pulse; peripheral pulses and capillary refill; jugular neck vein distention; skin color, temperature, turgor; level of consciousness and mentation; urine output. Nursing Diagnoses and Interventions The focus for nursing diagnoses & interventions for the client with fluid volume deficit is on: Managing the Effects of the Deficit & Preventing Complications. I. Deficient Fluid Volume Clients with fluid volume deficit due to abnormal losses, inadequate intake, or impaired fluid regulation require close monitoring as well as immediate and ongoing fluid replacement. 1. Assess intake and output accurately, monitoring fluid balance. = In acute situations, hourly intake and output may be indicated. Urine output should be 30 to 60 mL per hour (unless renal failure is present). Urine output of less than 30 mL per hour indicates inadequate renal perfusion and an increased risk for acute renal failure and inadequate tissue perfusion. 2. Assess vital signs, CVP, and peripheral pulse volume at least every 4 hours. Hypotension, tachycardia, low CVP, and weak, easily obliterated peripheral pulses indicate hypovolemia. 3. Weigh daily under standard conditions (time of day, clothing, and scale). In most instances (except third spacing), changes in weight accurately reflect fluid balance. 4. Administer and monitor the intake of oral fluids as prescribed. Identify beverage preferences and provide these on a schedule. Oral fluid replacement is preferred when the client is able to drink and retain fluids. 5. Administer intravenous fluids as prescribed using an electronic infusion pump. Monitor for indicators of fluid overload if rapid fluid replacement is ordered: A. dyspnea D. tachypnea, B. tachycardia, E. increased CVP, C. jugular vein distension F. edema Rapid fluid replacement may lead to hypervolemia, resulting in pulmonary edema and cardiac failure, particularly in clients with compromised cardiac and renal function. 6. Monitor laboratory values: electrolytes, serum osmolality, BUN, and hematocrit. Rehydration may lead to changes in serum electrolytes,osmolality, BUN, and hematocrit. In some cases, electrolyte replacement may be necessary during rehydration. II. Ineffective Tissue Perfusion A fluid volume deficit can lead to decreased perfusion of renal, cerebral, and peripheral tissues. Inadequate renal perfusion can lead to acute renal failure. Decreased cerebral perfusion leads to changes in mental status and cognitive function, causing restlessness, anxiety, agitation, excitability, confusion, vertigo, fainting, and weakness. 1.Monitor for changes in level of consciousness and mental status. Restlessness, anxiety, confusion, and agitation may indicateinadequate cerebral blood flow and circulatory collapse. 2. Monitor serum creatinine, BUN, and cardiac enzymes, reporting elevated levels to the physician. Elevated levels may indicate impaired renal function or cardiac perfusion related to circulatory failure.

28 PRACTICE ALERT Report a urine output of less than 30 mL per hour to the primary health care provider. 3. Turn at least every 2 hours. Provide good skin care and monitor for evidence of skin or tissue breakdown. Impaired circulation to peripheral tissues increases the risk of skin breakdown. Turn frequently to relieve pressure over bony prominences. Keep skin clean, dry, and moisturized to help maintain integrity. III. Risk for Injury The client with fluid volume deficit is at risk for injury because of dizziness and loss of balance resulting from decreased cerebral perfusion secondary to hypovolemia. 1. Institute safety precautions, including keeping the bed in a low position, using side rails as needed, and slowly raising the client from supine to sitting or sitting to standing position. Using safety precautions and allowing time for the blood pressure to adjust to position changes reduce the risk of injury. 2. Teach client and family members how to reduce orthostatic hypotension: a. Move from one position to another in stages; for example, raise the head of the bed before sitting up, and sit for a few minutes before standing. Continuation; Nsg Dx.: Risk for Injury b. Avoid prolonged standing. c. Rest in a recliner rather than in bed during the day. d. Use assistive devices to pick up objects from the floor rather than stooping. Teaching measures to reduce orthostatic hypotension reduces the clients risk for injury. Prolonged bed rest increases skeletal muscle weakness and decreases venous tone, contributing to postural hypotension. Prolonged standing allows blood to pool in the legs, reducing venous return and cardiac output. Home Care Depending on the severity of the fluid volume deficit, the client may be managed in the home or residential facility, or may be admitted to an acute care facility. Assess the clients understanding of the cause of the deficit and the fluids necessary for providing replacement. Address the following topics when preparing the client and family for home care. 1. The importance of maintaining adequate fluid intake (at least 1500 mL per day; more if extra fluid is being lost through perspiration, fever, or diarrhea) 2. Manifestations of fluid imbalance, and how to monitor fluid balance 3 How to prevent fluid deficit: Avoid exercising during extreme heat. Increase fluid intake during hot weather. If vomiting, take small frequent amounts of ice chips or clear liquids, such as weak tea, flat cola, or ginger ale. Reduce intake of coffee, tea, and alcohol, which increase urine output and can cause fluid loss. 4. Replacement of fluids lost through diarrhea with fruit juices or bouillon, rather than large amounts of tap water 5. Alternate sources of fluid (such as gelatin, frozen juices, or ice cream) for effective replacement of lost Fluids CLIENT WITH EXTRACELLULAR FLUID VOLUME EXCESS Etiology : Fluid Volume Excess [FVE] a. when both water and sodium are retained in the body. b. caused by fluid overload (excess water and sodium intake) c. impairment of the mechanisms that maintain homeostasis.

29 The excess fluid can lead to Excess Intravascular Fluid [HYPERVOLEMIA] Excess Interstitial Fluid [EDEMA] Pathophysiology FVE usually results from conditions that cause retention of both sodium and water. These conditions include: a. Heart failure d. adrenal gland disorders b. cirrhosis of the liver e. corticosteroid administration, c. renal failure f. stress conditions causing the release of ADH and aldosterone. Other causes include an excessive a. intake of sodium-containing foods, drugs that cause sodium retention b. the administration of excess amounts of sodium-containing intravenous fluids ( 0.9% NaCl or Ringers solution). d. this iatrogenic cause of fluid volume excess primarily affects clients with impaired regulatory mechanisms. In FVE, both water and sodium are gained together in about the same proportions as normally exists in extracellular fluid. The total body sodium content is increased which in turn causes an increase in total body water. Because the increase in sodium and water is isotonic, the serum sodium and osmolality remain normal, and the excess fluid remains in the extracellular space. Manifestation and Complications I. Excess extracellular fluid leads : a. hypervolemia b. circulatory overload. The following manifestations of FVE which relate to both the excess fluid and its effects on circulation. The increase in total body water causes weight gain (more than 5% of body weight) over a short period. Circulatory overload causes manifestations such as: = A full bounding pulse = Distended neck and peripheral veins. Increased central venous pressure (> 1112 cm of water). Cough, dyspnea (labored or difficult breathing) Orthopnea (difficulty breathing when supine). Moist crackles (rales) in the lungs; pulmonary edema (excess fluid in pulmonary interstitial spaces and alveoli) if severe. Increased urine output (polyuria). Ascites (excess fluid in the peritoneal cavity). Peripheral edema, or if severe, anasarca (severe, generalized edema). Dilution of plasma by excess fluid causes a decreased hematocrit and BUN. Possible cerebral edema (excess water in brain tissues) can lead to altered mental status and anxiety. Heart failure is not only a potential cause of fluid volume excess, but it is also a potential complication of the condition if the heart is unable to increase its workload to handle the excess blood volume. Severe fluid overload and heart failure can lead to pulmonary edema, a medical emergency. II. Excess extracellular fluid leads : EDEMA Mechanism of Edema Formation A. Fluid Overload B. Decreased Plasma & Albumin C. Lymphatic Obstruction D. Tissue Injury

30

A.

Fluid Overload

Increased Hydrostatic Pressure in Arterial End of Capillary

Increased Peripheral Vascular Resistance

Fluid Movement Into Tissue

Increased Left Ventricular Pressure

EDEMA

Increased Arterial Pressure

Pulmonary Edema

31

B. Decreased Serum &Albumin


Decreased Production of Plasma Protein

Decreased Capillary Oncotic Pressure

Decreased Reabsorption at Venous Blood

EDEMA

C. Lymphatic Obstruction
Lymphatic Obstruction Decrease Absorption of Interstitial Fluid

Decreased Transport of Capillary Filtered Protein

Increased Tissue Oncotic Pressure Which Pulls Fluid Toward It

EDEMA

32

D. Tissue Injury
Increased Capillary Permeability

Movement Of Plasma Protein Into Tissues

Increased Tissue Oncotic Pressure

EDEMA

Diagnostic Tests The following laboratory tests may be ordered. Serum electrolytes and serum osmolality are measured. = serum sodium and osmolality usually remain within normal limits. Serum hematocrit and hemoglobin often are decreased due to plasma dilution from excess extracellular fluid. Additional tests of renal and liver function (such as serum creatinine, BUN, and liver enzymes) may be ordered to help determine the cause of fluid volume excess if it is unclear. Medications Diuretics are commonly used to treat fluid volume excess. They inhibit sodium and water reabsorption, increasing urineoutput. The three major classes of diuretics, each of which acts on a different part of the kidney tubule, are as follows: 1. Loop diuretics act in the ascending loop of Henle. 2. Thiazide-type diuretics act on the distal convoluted tubule. 3. Potassium-sparing diuretics affect the distal nephron. Diuretics for Fluid Volume Excess Nursing Implications Diuretics increase urinary excretion of water and sodium. Diuretics are used to enhance renal function and to treat vascular fluid overload and edema. Common side effects include orthostatic hypotension, dehydration, electrolyte imbalance, and possible hyperglycemia. Diuretics should be used with caution in the older adult. Examples of each major type follow 1. Loop Diuretics Furosemide (Lasix) Ethacrynic Acid (Edecrin) Bumetanide (Bumex) Torsemide (Demadex) Loop diuretics inhibit sodium and chloride re- absorption in the ascending loop of Henle As a result, loop diuretics promote the excretion of sodium, chloride, potassium, and water.

33 2. Thiazide and Thiazide - Like Diuretics Bendroflumethiazide (Naturetin) Polythiazide (Renese) Chlorothiazide (Diuril) Chlorthalidone (Hygroton) Hydrochlorothiazide Trichlormethiazide (HydroDIURIL,Oretic) (Naqua) Metolazone (Zaroxolyn) Indapamide (Lozol) Thiazide and thiazide - like diuretics promote the excretion of sodium, chloride, potassium, and water by decreasing absorption in the distal tubule. 3. POTASSIUM-SPARING DIURETICS Spironolactone (Aldactone) Amiloride HCl (Midamor) Triamterene (Dyrenium) Potassium-sparing diuretics promote excretion of sodium and water by inhibiting sodium-potassium exchange in the distal tubule. Client and Family Teaching 1. The drug will increase the amount and frequency of urination. 2. The drugs must be taken even when you feel well. 3. Take the drugs in the morning and afternoon to avoid having to get up at night to urinate. 4. Change position slowly to avoid dizziness. 5. Report the following to your primary health care provider: - dizziness; trouble breathing; or swelling of face, hands, or feet. 6. Weigh yourself every day, and report sudden gains or losses. 7. Avoid using the salt shaker when eating. 8. If the drug increases potassium loss, eat foods high in potassium, such as orange juice and bananas. 9. Do not use salt substitute if you are taking a potassium-sparing diuretic. Assessment 1. Health History: Risk factors such as : a. medications, heart failure c. renal disease b. acute or chronic d. endocrine disease Precipitating factors such as: a. recent illness b. changes in diet and in medication Recent weight gain; complaints of persistent cough, shortness of breath, swelling of feet and ankles, or difficulty sleeping when lying down. Physical assessment: Weight; vital signs; peripheral pulses and capillary refill; jugular neck vein distention; edema; lung sounds (crackles or wheezes), dyspnea, cough, and sputum; urine output; mental status. Medical Management 1. Fluid Management Fluid intake may be restricted in clients who have fluid volume excess. The amount of fluid allowed per day is prescribed by the primary care provider. All fluid intake must be calculated, including meals and that used to administer medications orally or intravenously.

34

2. Dietary Management Because sodium retention is a primary cause of fluid volume excess, a sodium restricted diet often is prescribed. The primary dietary sources of sodium are the salt shaker, processed foods, and foods themselves A mild sodium restriction can be achieved by: A. instructing the client and primary food preparer in the household to reduce the amount of salt in recipes by half B. avoid using the salt shaker during meals, and avoid foods that contain high levels of sodium (either naturally or because of processing). In moderate and severely sodium-restricted diets, salt is avoided altogether, as are all foods containing significant amounts of sodium.

35

Nursing Care Health Promotion Health promotion related to fluid volume excess focuses on teaching preventive measures to clients who are at risk (e.g., clients who have heart or kidney failure). Discuss the relationship between sodium intake and water retention. Provide guidelines for a low-sodium diet, and teach clients to carefully read food labels to identify hidden sodium, particularly in processed foods. Instruct clients at risk to weigh themselves on a regular basis, using the same scale, and to notify their primary care provider if they gain more than 5 lb in a week or less. Carefully monitor clients receiving intravenous fluids for signs of hypervolemia. Reduce the flow rate and promptly report manifestations of fluid overload to the physician. Nursing Diagnoses and Interventions Diagnoses and interventions for the client with fluid volume excess focus on the multisystem effects of the fluid overload.

36 Nursing Diagnosis # 1 Excess Fluid Volume Nursing care for the client with fluid volume excess includes collaborative interventions such as: A. administering diuretics B. maintaining a fluid restriction C. monitoring the status and effects of the fluid volume excess. This is particularly critical in older clients because of the age-related decline in cardiac and renal compensatory responses. Continuation: Nsg Dx: Excess Fluid Volume 1. Assess vital signs, heart sounds, CVP, and volume of peripheral arteries. Hypervolemia can cause hypertension, bounding peripheral pulses, a third heart sound (S3) due to the volume of blood flow through the heart, and high CVP readings. 2. Assess for the presence and extent of edema, particularly in the lower extremities, the back, sacral, and periorbital areas. Initially, edema affects the dependent portions of the body the lower extremities of ambulatory clients and the sacrum in bedridden clients. Periorbital edema indicates more generalized edema.

3. Obtain daily weights at the same time of day, using approximately the same clothing and a balanced scale. Daily weights are one of the most important gauges of fluid balance. Acute weight gain or loss represents fluid gain or loss. Weight gain of 2 kg is equivalent to 2 L of fluid gain. 4. Administer oral fluids cautiously, adhering to any prescribed fluid restriction. 5. Discuss the restriction with the client and significant others, including the total volume allowed, the rationale, and the importance of reporting all fluid taken. All sources of fluid intake, including ice chips, are recorded to avoid excess fluid intake. 6. Provide oral hygiene at least every 2 hours. Oral hygiene contributes to client comfort and keeps mucous membranes intact; it also helps relieve thirst if fluids are restricted. 7. Teach client and significant others about the sodium-restricted diet, and emphasize the importance of checking before bringing foods to the client. Excess sodium promotes water retention; a sodium-restricted diet is ordered to reduce water gain. 8. Administer prescribed diuretics as ordered, monitoring the clients response to therapy. Loop or high-ceiling diuretics such as furosemide can lead to rapid fluid loss and signs of hypovolemia and electrolyte imbalance. Nursing Diagnosis # 2 Risk for Impaired Skin Integrity - Tissue edema decreases oxygen and nutrient delivery to the skin and subcutaneous tissues, increasing the risk of injury. 1. Frequently assess skin, particularly in pressure areas and over bony prominences. Skin breakdown can progress rapidly when circulation is impaired. 2. Reposition the client at least every 2 hours. Provide skin care with each position change. Frequent position changes minimize tissue pressure and promote blood flow to tissues. 3. Provide an eggcrate mattress or alternating pressure mattress, foot cradle, heel protectors, and other devices to reduce pressure on tissues. These devices, which distribute pressure away from bony prominences, reduce the risk of skin breakdown.

37 Nursing Diagnosis # 3 Risk for Impaired Gas Exchange - With fluid volume excess, gas exchange may be impaired by edema of pulmonary interstitial tissues. Acute pulmonary edema is a serious and potentially life-threatening complication of pulmonary congestion. 1.Auscultate lungs for presence or worsening of crackles and wheezes; auscultate heart for extra heart sounds. Crackles and wheezes indicate pulmonary congestion and edema. A gallop rhythm (S3) may indicate diastolic overloading of the ventricles secondary to fluid volume excess. 2. Place in Fowlers position if dyspnea or orthopnea is present. Fowlers position improves lung expansion by decreasing the pressure of abdominal contents on the diaphragm. 3, Monitor oxygen saturation levels and arterial blood gases (ABGs) for evidence of impaired gas exchange (SaO2 < 92%95%; PaO2 < 80 mmHg). Administer O2 as indicated. Supplemental oxygen promotes gas exchange across the alveolar- capillary membrane, improving tissue oxygenation. Edema of interstitial lung tissues can interfere with gas exchange and delivery to body tissues. Home Care Teaching for home care focuses on managing the underlying cause of fluid volume excess and preventing future episodes of excess fluid volume. Address the following topics when preparing the client and family for home care. 1. Signs and symptoms of excess fluid and when to contact the care provider 2. Prescribed medications: when and how to take, intended and adverse effects, what to report to care provider 3. Recommended or prescribed diet; ways to reduce sodium intake; how to read food labels for salt and sodium content; use of salt substitutes, if allowed. (see Box 55) 4. If restricted, the amount and type of fluids to take each day; how to balance intake over 24 hours 5. Monitoring weight; changes reported to care provider 6. Ways to decrease dependent edema: a. Change position frequently b. Avoid restrictive clothing. c. Avoid crossing the legs when sitting. d. Wear support stockings or hose. e. Elevate feet and legs when sitting. 7. How to protect edematous skin from injury: a. Do not walk barefoot. b. Buy well-fitting shoes; shop in the afternoon when feet are more likely to be swollen. Using additional pillows or a recliner to sleep, to relieve orthopnea

38

CLIENT WITH EXTRACELLULAR - FLUID VOLUME SHIFT THIRD SPACING


Extracellualr Fluid Volume Shift = A fluid volume shift where a change in the location of ECF between the Intravascular & Insterstitial spaces = results not only from pathologic condition but also reflects an inability of the lymphatic system to compensate Lymph Circulation Of the approximately 23 litres (42 pints) of fluid that pass from the bloodstream to bodily tissues every day carrying oxygen and nutrients, only 20 litres (36 pints) return with carbon dioxide and cellular waste to the capillaries. The remaining 3 litres (6 pints) pass into the vessels of the lymphatic system and are filtered through the closely packed cells of the lymph nodes, relieving the cells of fats, protein, and other debris. Lymph, which also transports disease-fighting white blood cells (lymphocytes), circulates only as a result of muscle movement there is no heart-like central pump.

39

Etiology Fluids move into interstitial space because of : 1. Increased Capillary Permeability [permeability - rate substance passes through porous medium] = any pathologic process that increases capillary permeability can cause third spacing = any tissue injury can lead to fluid shift = massive fluid shift from the vascular to the interstitial spaces can be seen in crush injuries, major tissue trauma, major surgery, extensive burns, acid-base imbalance, bowel obstruction sepsis permeability can also be altered by ischemia 2. Decreases Serum Protein Levels = decrease protein intake, production, or storage can lead to hypoalbumineria [seen in protein-calorie malnutrition] = bowel disorder that reduces protein absorption can cause reduce serum level = conditions such as kidney ,liver disease, large draining wounds burns depletes proteins storage Note: Protein anabolism: healing phases of wounds & fracture Protein catabolism : fever, infection or sepsis and malignancy 3. Obstruction of the venous portions of the capillary = lymphatic obstruction & venous thrombosis can slow fluid returning though the venous system. 4. Non functional lymphatic drainage system

40

Pathophysiology
Tissue Injury

Histamine

Bradykinin

Increased Capillary Permeability

Allows More Fluid, Protein and Other Solutes to Move into Interstitial Space

Phases of Fluid Shift associated with tissue injury I. Vascular to Interstitial Space: = leads to a fluid volume deficit hypovolemia = severe hypovolemia may lead to vascular collapse and death = if cellular damage is severe, a toxic response may occur from intracellular ions potassium which leads into the vascular spaces II. Interstitial to Vascular = leads to fluid volume excess hypervolemia = if severe, may lead to heart failure WHY & HOW ? Intracellular potassium ions shift back into the cell during this phase which increases the risk from

Hypokalemia
Clinical Manifestations Manifestations of fluid shift from vascular to interstitial are similar with Hypovolemic Shock, due to fluid that is not within the vascular system = pallor, cold limbs, weak and rapid pulse, hypotension, oliguria, poor skin turgor and decreased level of consciousness If fluids collect and obstruct an organ, what are the manifestations? If fluid obstruct blood vessels or nerves: = extremities may be pale, cool and pulseless If intestinal tract is obstructed: = bowel sounds may change through out the abdomen Laboratory results: = elevated hematocrit, BUN & Urine elevated specific gravity When fluid returns to blood vessels: Signs are similar with Fluid Overload = bounding pulse, crackles, engorgement of peripheral & jugular veins, increase in BP Labaoratory Results: = decrease in hematocrit and BUN

41 Management Note: as with FVD & FVE, Third Spacing is only a manifestation, therefore it is crucial: = underlying cause must be identified for appropriate intervention, thru: 1. thorough history 2. thorough physical examination TS due to pericarditis pericardiocentesis TS due to bowel obstruction - paracentesis Replace Fluids: Hypovolemia as a result from tissue injury [ burns, crash injury] = large volume of Isosmolar or Isotonic fluid adminstration is required to replace the intravascular volume. = maintenance of IV is essential to maintain kidney perfusion and fluids are to titrate to maintain adequate blood pressure What is the cardinal sign or evidence of capillary sealing? Cardinal Sign of Capillary Sealing: Increase urine output without additional fluid Note: = when capillary walls regains integrity; fluids shifts from the tissue spaces back into the vessels: if fluid replacement is aggressive during this phase a fluid overload can result! Nursing Management Assess VS every shift, if with shock like symptoms: g hour Assess signs of fluid overload: pulmonary crackles, difficulty in breathing, neck vein engorgement TS at abdomen monitor the girth q 8 hrs. TS at limb monitor leg circumferences and peripheral pulses q 8 hrs. Monitor Urine output less 30ml/hr and if persisted for more than 2 hours, refer immediately Urine output is decrease during tissue injury due to fluid shift One to three days after tissue injury, fluids returns to normal circulation and excess fluid is excreted by the kidney: Anticipate : monitoring of renal function like laboratory exams to check BUN and Creatinine

Client with Intracellular Fluid Volume Deficit


Dehydration can become so severe that the cells become dehydrated Compensatory attempts to combat the fluid deficit have the same physiologic effect as in ECFD. Thirst & oliguria are the most common compensatory mechanism Cellular manifestations are due to the dysfunction in the cerebral cells & include fever & central nervous system changes such as confusion, coma & cerebral hemorrhage

Desired Outcome Restoration of fluid volume which is addressed through IV replacement Once stable focus is on correction or control of the underlying cause Focus of nursing management Prevention or early detection of complication secondary to the pathology or treatment. Interdisciplinary communication is critical to the achievement of positive outcome

Client with Intracellular Fluid Volume Excess [Water Intoxication]


Intracellular Fluid Volume Excess Results from either: I. Water Excess - number of solutes is normal but they are diluted by excessive water II. Solute Deficit - amount of water is normal but there are too few particles per liter of water

42

Etiology & Pathopysiology I. Administration of excessive amount of hyposmolar IV fluids such as

0.45% Saline solution or 5% Dextrose in Water [D5W]


Hyposomolar fluids in the vessels move by OSMOSIS to the region of higher concentration of sodium in the cells in an attempt to maintain equilibrium

ICVFE cell ECFVE - tissue

Too much fluids accumulates in the cells

Cerebral cells absorb hypososmolar fluid more quickly than do other Cells this cellular change causes the fluid shift

Cellular Edema

All neurological sings are due to increase Intracranial Pressure which are mostly Cephalocaudal early signs are cortical Pupillary then changes in Vital Signs

Brain Cells - very vulnerable to Fluid Excess or Deficit First priority reduce increase ICP thru steroid & osmotic diuretics Identifying & addressing the cause of the fluid excess Brain tissue has a very narrow margin in which life sustained frequent monitoring & early intervention are critical: - perform nuerologic check every hours if cranial nerves changes are present: level of consciousness, reflexes, Vital signs, pupillary responses - Blood Pressure, especially systolic drops too less than 100 mmHg or too greater than 150mmHg : Indicative of Altered Cerebral Perfusion Behavioral Changes: Confusion & Disorientation Provide Safety Measures: Keep bed in low position with bedside rails raised Keep suction apparatus at bedside in anticipation of seizures , turn client to one side to display the tongue and remain at the bedside and monitor /document stages of seizures If signs of increased ICP are improving indicative of less risks of complication TIME EQUALS BRAIN CELL SURVIVAL Longer manifestation of increased ICP persist; the more serious they are & the graver the prognosis II. People with psychiatric disorder such as schizophrenia : compulsive water consumption behavior. - Monitor for compulsive water consumption with history or with current manifestations or organic psychiatric disorder III. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) also leads to ICFVE regardless of whether it is caused by CNS trauma, stress of surgery, pain or narcotic use Early administration of IV fluids containing Sodium Chloride Saline solution D5/0.45% NaCl - increases the osmolality of vascular fluid and prevent or help correct hyposomolality

43 Administer antiemetic prophylactically as appropriate: To promote food and fluid ingestion and retention and to prevent the risk of vomiting which will worsen the increased ICP Monitor weight daily Monitor Intake and Output daily Polyuria is a good sign: - -Why - - Why - - Why? Serves as an indicator that fluid has shifted to the vascular space and to the renal tubules where it can be excreted

Clients with Electrolytes Imbalances Sodium


Continuation: sodium imbalance Sodium is the most plentiful electrolyte in ECF, with normal serum sodium levels ranging : from 135 to 145 mEq/L. Sodium is the primary regulator of the volume, osmolality, and distribution of ECF. It also is important to maintain neuromuscular activity. Because of the close interrelationship between sodium and water balance, disorders of fluid volume and sodium balance often occur together. Sodium imbalances affect the osmolality of ECF and water distribution between the fluid compartments. When sodium levels are low (hyponatremia), water is drawn into the cells of the body, causing them to SWELL. In contrast, high levels of sodium in ECF (hypernatremia) draw water out of body cells, causing them to SHRINK. OVERVIEW OF NORMAL SODIUM BALANCE Most of the bodys sodium comes from dietary intake. Although a sodium intake of 500 mg per day is usually sufficient to meet the bodys needs, the average intake of sodium by adults in the is about 6 to 15 g per day Other sources of sodium include prescription drugs and certain self-prescribed remedies. Sodium is primarily excreted by the kidneys. A small amount is excreted through the skin and the gastrointestinal tract. Continuation: overview of sodium balance The kidney is the primary regulator of sodium balance in the body. The kidney excretes or conserves sodium in response to changes in vascular volume. A fall in blood volume prompts several mechanisms that lead to sodium and water retention. HOW ?

44

Fall in Blood Volume

Renin-Angiotensin-Aldosterone System Stimulates Angiotensin II

Prompts renal tubules to reabsorb sodium & causes vasoconstriction to slow down blood flow to kidney & reduces glomurular filtration

Further reduces amount of sodium excreted

Angiotensin II promotes the release of Aldosterone from Adrenal Cortex

Aldosterone more Na reabsorbed in the kidney & more K eliminates in the urine

Renin -Angiotensin- Aldosterone System

45

Posterior Pituitary Gland releases Antidiuretic Hormone


ADH promotes Na & Water reabsorbtion In the distal tubules of the kidney, reducing Output & expanding blood volume

When blood volume expand Na & water elimination by kidney increases

The glomerular filtration rate increases allowing more water and sodium to be filtered and excreted. Atrial natriuretic peptide (ANP) is released by cells in the atria of the heart

ANP increases sodium excretion by the kidneys.


ADH release from the pituitary gland is inhibited.

ADH Release & Effect

46

Client with Hyponatremia


Hyponatremia is a serum sodium level of less than 135 mEq/L. Pathophysiology Remember most Na is outside the cell & less is available to move across excitable membrane resulting in delayed membrane depolarization Most pathophysiologic changes results from the decreased excitability of the membranes from a loss of sodium and changes in water volume Excitable tissue vary in their response to decrease Sodium The cells most sensitive to change are the CNS cells

ECF Na concentration decreases

ECF & ICF gradient difference decrease

When extracellular Na falls

ECF becomes hypoosmolar[ there is Osmotic shift]

Leads to intracellular edema

Compensatory Mechanism Water moves into the cell to the area of greater concentration to rebalance Water concentration Intracellular osmolality is reduced through decreasing the amount of Intracellular ions: Na, K & Amino Acids

ETIOLOGY & MANIFESTATIONS Excess Sodium Loss Can Occur Through: A. Kidneys: 1. Diuretic medications 2. Kidney diseases 3. Adrenal insufficiency with impaired aldosterone and cortisol production can lead to excessive sodium excretion in urine. B. Skin. 1. Excessive sweating or loss of skin surface ( as in extensive burn) can also cause excessive sodium loss. C. Gastrointestinal Tract: 1. Vomiting and diarrhea 2. Gastrointestinal suction are common causes of excess sodium loss through the GI tract. 3. Sodium may also be lost when gastrointestinal tubes are irrigated with water instead of saline, or when repeated tap water enemas are administered

47 Clinical Manifestation I. Nuerologic Early nuerologic signs such as headache & apprehension are from increased fluid shift into the cerebral cells As the intracranial pressure rises and plasma Na drops to 115 mEg/L: severe nuerologic changes occur: = confusion, hallucination, behavioral changes, and seizure disorder Early manifestations of hyponatremia include muscle cramps, weakness, and fatigue from its effects on muscle cells. II. Cardiovascular Decrease systolic & diastolic, orthosthatic hypotension, weak & thready [sounding thin and lacking in power and tone] pulse due to decrease in vascular volume secondary to Na and water loss.

O2, CO2, hydrogen ion is affected Chemoreceptors in the aortic arch & bodies Triggers a response releasing Catecholamine by the sympathetic nervous system Dopamine & Adrenaline Tachycardia

III. Lungs

Increase fluid pressure in the pulmonary Capillaries

Fluid shift into the alveoli

crackles

48

Increased Left Ventricular Fluid Pressure Leads to Increase Pressure in the Left Atrium & Pulmonary Blood Vessel Arrangement

Presence of fluid in the alveoli

Alters O2 & CO2 level

Change in Respiratory Rate & Difficulty in Breathing

Alteration in respiratory pattern

Increase intracranial pressure Tachypnea, dyspnea, orthopnea, shortness of breath

Cheyne-stoke respiration-abnormal
[Shallow breathing & heavy breathing signs of impending death]

Nuerogenic hyperventilation Apneustic breathing or Ataxic breathing[ inability to control muscle]

Types of Hyponatremia Hypovolemic hyponatremia

Euvolemic Hyponatremia

Clinical Condition& Disorder Renal loss of sodium from diuretic use, diabetic glycosuria, aldosterone deficiency, intrinsic renal disease Extrarenal loss of sodium from vomiting, diarrhea, increased sweating, burns, high-volume ileostomy. Sodium deficit resulting from SIADH or the continuous secretion of ADH due to pain, emotion, medications; cancers: CNS disorders. Edematous disorders resulting in sodium deficits; congestive heart failure, cirrhosis of the liver, nephrotic syndrome, acute & chronic renal failure. Pseudohyponatremia, hyperglycemia, hyperlipidemia

Hypervolemic Hyponatremia

Redistributive Hyponatremia

49 Assessment data related to hyponatremia includes: I. Health history: = Current manifestations, including : 1. nausea and vomiting 3. muscle weakness 2. abdominal discomfort 4. headache = Other symptoms; duration of symptoms and any precipitating factors such as 1 heavy perspiration 2. vomiting or diarrhea 3. chronic diseases such as heart or renal failure, cirrhosis of the liver, or endocrine disorders; current medications. Physical Assessment: Complete History of Risk Factors/Presenting Manifestation: - emphasize on diet, medication - including OTC Client and family members should be assess about behavioral changes, headache, increased weakness sleepiness, dizziness & palpitation Calculate ideal body weight used height, weight & body frame Assess I&O, mental status & level of consciousness; vital signs including orthostatic vitals and peripheral pulses; presence of edema or weight gain. Diagnostic Tests The following laboratory tests may be ordered. Serum sodium are decreased < 135 mEg/L Osmolality are decreased < 275 mOsm/Kg A24-hour urine specimen is obtained to evaluate sodium excretion. In conditions associated with normal or increased extracellular volume (such as SIADH), urinary sodium is increased; In conditions resulting from losses of isotonic fluids (e.g., sweating, diarrhea, vomiting, and third-space fluid accumulation), by contrast, urinary sodium is decreased. Medications When both sodium and water have been lost (hyponatremia with hypovolemia), sodium-containing fluids are given to replace both water and sodium. These fluids may be given by mouth, nasogastric tube, or intravenously. Isotonic Ringers solution or isotonic saline (0.9% NaCl) solution may be administered. Cautious administration of intravenous 3% or 5% NaCl solution may be necessary in clients who have very low plasma sodium levels (110 to 115 mEq/L). Loop diuretics are administered to clients who have hyponatremia with normal or excess ECF volume. Loop diuretics promote an isotonic diuresis and fluid volume loss without hyponatremia Thiazide diuretics are avoided because they cause a relatively greater sodium loss in relation to water loss. In addition, drugs to treat the underlying cause of hyponatremia may be administered. Fluid and Dietary Management If hyponatremia is mild, increasing the intake of foods high in sodium may restore normal sodium balance Fluids often are restricted to help reduce ECF volume and correct hyponatremia ( Box 53).

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Health Promotion At risk for mild hyponatremia include those who participate in activities that increase fluid loss through excessive perspiration (diaphoresis) and then replace those losses by drinking large amounts of water. = athletes = people who do heavy labor in high environmental temperatures = older adults living in non-air-conditioned settings during hot weather. Teach the following to clients who are at risk. Manifestations of mild hyponatremia, including nausea, abdominal cramps, and muscle weakness The importance of drinking liquids containing sodium and other electrolytes at frequent intervals when perspiring heavily, when environmental temperatures are high, and/or if watery diarrhea persists for several days

52 Nursing Diagnosis I. Risk for Imbalanced Fluid Volume Because of its role in maintaining fluid balance, sodium imbalances often are accompanied by water imbalances. In addition, treatment of hyponatremia can affect the clients fluid balance. For additional nursing interventions that may apply to the client with hyponatremia, review the discussions of fluid volume deficit and fluid volume excess. 1. Monitor intake and output, weigh daily, and calculate 24- hour fluid balance. Fluid excess or deficit may occur with hyponatremia. 2. Use an intravenous flow control device to administer hypertonic saline (3% and 5% NaCl) solutions; carefully monitor flow rate and response. Hypertonic solutions can increase the risk of pulmonary and cerebral edema due to water retention. Careful monitoring is vital to prevent these complications and possible permanent damage. 4. If fluids are restricted, explain the reason for the restriction, the amount of fluid allowed, and how to calculate fluid intake. Teaching increases the clients sense of control & compliance. II. Risk for Decreased Intracranial

Severe hyponatremia Experiences fluid shifts Increase in intracellular fluid volume Cause brain cells to swell Increasing pressure within the cranial vault
1. Monitor serum electrolytes and serum osmolality and report abnormal results to the care provider. As serum sodium levels fall, the manifestations and neurologic effects of hyponatremia become increasingly severe. 2. Assess for neurologic, mental status and orientation: Serum sodium levels of 115 to 120 mEq/L: > headache, confusion and convulsion > lethargy, and decreased responsiveness Sodium levels less than 110 to 115 mEq/L > may cause seizures and coma. 3. Assess muscle strength and tone, and deep tendon reflexes. Increasing muscle weakness and decreased deep tendon reflexes are manifestations of increasing hyponatremia. PRACTICE ALERT : Carefully monitor clients receiving sodium-containing intravenous solutions for signs of hypervolemia: 1. increased blood pressure and CVP 2. achypnea, tachycardia, 3. gallop rhythm, shortness of breath, crackles). Hypertonic saline solutions can lead to hypervolemia, particularly in clients with cardiovascular or renal disease. PRACTICE ALERT Maintain a quiet environment, and institute seizure precautions in clients with severe hyponatremia. Severe hyponatremia can lead to seizures. A quiet environment reduces neurologic stimulation. Safety precautions, such as ensuring that side rails are up and having an airway readily available, reduce risk of injury from seizure.

53 Home Care Teaching for home care focuses on the underlying cause of the sodium deficit and often on prevention. Teach clients who have experienced hyponatremia and those who are at risk for developing hyponatremia about the following: Manifestations of mild and more severe hyponatremia to report to the primary care provider The importance of regular serum electrolyte monitoring if taking a potent diuretic or on a low-sodium diet Types of foods and fluids to replace sodium orally if dietary sodium is not restricted

Client with Hypernatremia


Hypernatremia is a serum sodium level greater than 145 mEq/L. It may develop when sodium: 1. gained in excess of water 2. when water is lost in excess of sodium. Either fluid volume deficit or fluid volume excess often accompany hypernatremia.

Pathophysiology

Rise in Na level Osmotic shift of H2O from cells to the ECF as an attempt to dilute the Hyperosmolar state

Heart is sensitive Ca moves for cardiac contraction

Create a Crisis Cellular Dehydration In Hypernatremia,Na molecules compete with Ca slowing down myocardial contractility In hypernatremia evolves slowly or chronic,brain develops own osmotic particles idiogenic osmolesto prevent fluid shift into & outof brain cells

Body compensatory mechanism: suppressing the effects of Aldosterone and Anti Diuretic Hormone: to increase renal blood flow and cause excretion of Sodium and Water

Water deprivation is a cause of hypernatremia in clients who: unable to respond to thirst due to altered mental status or physical disability. Excess water loss may occur with watery diarrhea or increased insensible losses (due to fever, hyperventilation, excessive perspiration, or massive burns). Unless water is adequately replaced, clients with diabetes insipidus also may develop hypernatremia. Excess sodium intake can result from ingestion of excess salt or hypertonic intravenous solutions. Clients who experience near-drowning in seawater are at risk for hypernatremia, as are clients with heatstroke. Hypernatremia causes hyperosmolality of ECF.

54 As a result: Water is drawn out of cells, leading to cellular dehydration. Most serious effects of cellular dehydration are seen in the brain

Brain Cells Contract and Shrink Develop Neurological Manifestations Causing Mechanical Traction on Cerebral Vessel Vessels May Tear and Bleed
NOTE: Although the brain rapidly adapts to hyperosmolality to minimize the water loss, acute hypernatremia can cause widespread cerebral vascular bleeding Major Protective Mechanism Against Hypernatremia: 1. Thirst 2. Renal water conservation stimulated by ADH when serum sodium concentration increases Types of Hypernatremia Renal losses: osmotic diuresis, severe hyperglycemia External losses: profuse diaphoresis, decreased thirst, diarrhea occuring w/ inadequate volume replacemnt or fluid repalcement w/ hyperosmolar solutions, burns

Hypovelemic Hypernatremia

Euvolemic Hypernatremia

Excess fluid losses from the skin & lungs, hypodipsia in elderly & infant, diabetes insipidus Administration of concnetrated saline slutions, hypertonic feedings, excess minerralocorticoids Accidental or intentional salt ingestion, commercially prepared soups & canned vegetables

Hypervolemic Hyprnatremia

Clinical Manifestation Early Stages of Hypernatremia - Signs are nonspecific due to two thirds of body water is intracellular, primary water losses tend to cause only modest effects on circulating blood volume Early Manifestation: - Polyuria followed by oliguria - Anorexia, nausea & vomiting due to increase fluid retention in the gastric cells Early Nuerologic Manifestations: - restless, agitation, irritability, muscle weakness due to sensitivity of brain cells to fluid shifting When Sodium level reaches 155 mEg/L or more, cells shrinks because of the increased ECF osmolality More severe neurologic changes occur: confusion, seizures, or coma & in some cases irreversible brain damage Altered nueromuscular contractility & irritability lead to muscle twitching, tremor, hyperflexia & seizures The development of rigid paralysis is a grave sign

55 Kidney Hypervolemic state: kidneys excrete some of the excess water Hypovolemic state: oliguria is a method or renal compensation As fluid level decreases in the interstitial area: = skin becomes dry & flushed, mucous membrane becomes dry & sticky & tongue furrows develop = experience increasing thirst & fever as a result of decrease lack of fluid available for dissipitating or diminish heat Cardiovascular Hypovelemic Hypernatremia: = orthostatic hypotension with compensatory tachycardia occurs Hypervolemic Hypernatremia: = signs of hypertension, jugular veins distention, prolong peripheral veins emptying, extra heart sound [gallop] & generalized weight gain & edema Lungs Hypervolemic Hypernatremia = crackles, dyspnea & pleural effusion due to increase hydrostatic pressure Diagnostic Findings Diagnosis of hypernatremia is validated through the plasmas: Sodium Concentration - above 145 mEg/L Serum Osmolality above 295 mOsm/kg Since Chloride is the major ECF ion that balances sodium above 106 mEg/L Nursing Management Assessment 1. Thorough diet & medication history, including the use of corticosteroids & OTC such as cough medicine, food flavoring & spices salt 2. Asses VS & peripheral vein feelings q 4-8 & monitor body weight 3. Monitor changes in serum level & osmolality 4. Report early signs of altered mental status to prevent the progression of hypernatremia 5. Monitor lung sounds q 2 to 4 hrs. to check for pulmonary overload Nursing Outcomes and Interventions Outcomes: the nurse will maintain a high index of suspicion for high risk group clients and will monitor plasma sodium & chloride levels & clinical manifestation of hypernatremia Interventions : - Monitor client for response to IV fluid replacement of hyposmolar electrolytes solution, absence of clinical manifestation of hypernatremia, & return of normal sodium level - Maintain prescribed rate use of IV pump - Initiate safety & seizure precaution if with weakness or cerebral changes - Consult with dietitian , teach client and family members the food items that should be restricted and their rational for their restriction - Initiate gastric feeding slowly & increase rate if client tolerates - Evidence of no diarrhea, with residual less than half the amount of the feeding per hour or up to 100 ml - Provide oral care every 2 hours with non alcoholic mouthwash, avoid lemon-glycerin swab because it dries mucous membrane - Dilute saline & alcoholic mouthwash, use soft toothbrush, moisten client lips q 2 hrs. - Offer cool, nonacidic fluids such as apple juice - Limit ice chips may decrease discomfort from dry oral membrane Medical Management Goal: Correction of body water osmolality, with restoration of cell volume by decreasing the ration of sodium to water in the ECF Minor manifestation from hypovolemia or euvolemic hypernatremia: = focus is on correcting the underlying disorder & giving oral fluid replacement = with cardiovascular, pulmonary & neurologic requires hospitalization

56 To Decrease Total Body Sodium & Replace Fluid Loss = either a hypososmolar electrolytes solution such as 0.2% or 0.45% NaCl/5% Water is given = these solutions do not cause a considerable dilutions of body sodium, instead, the plasma sodium level gradually decrease as an excess sodium is excreted = dietary sodium restriction is useful in preventing hypernatemia in high-risk client ,it cannot bring a high sodium level down to normal = in hypervolemic hypernatremia, fluid must be restricted & drinking excess water defeats the purpose of medication POTASSIUM helps regulate intracellular osmolality & promotes the transmission and conduction of nerve impulses and the contraction of skeletal, cardiac and smooth muscle Promotes enzymes action for cellular metabolism & glycogen storage in the liver Fosters acid-base balance through cellular exchange with hydrogen K is plentiful in cells - 96% or 150 mEg/L is in ICF - 4% or 5 mEg/L is in intravascular fluid Because the greatest amount is intracellular, the plasma range is narrow Normal values range from 3.5 to 5.0 mEg/L Life-threatening changes occurs at plasma concentration level of less than 2.5 or greater than 7.0 mEg/L

Hypokalemia
Define as plasma Potassium level of less than 3.5 mEg/L. Etiology & Risk Factors: body does not conserve potassium; thus, its deficit is commonly results from inadequate potassium intake People at risk are those debilitated, confused, restrained, or lacking access to dietary sources for financial or other reasons, client who are malnourished, anorexic, bulimic, older people This significant difference in the potassium concentrations of ICF and ECF helps maintain the resting membrane potential of nerve and muscle cells. Either a deficit or an excess of potassium can adversely affect neuromuscular and cardiac function. To maintain its balance, potassium must be replaced daily, normally, potassium is supplied in food virtually all foods contain potassium The kidneys eliminate potassium very efficiently Even when potassium intake is stopped, the kidneys continue to excrete it. However, because the kidneys are the principal organs involved in the elimination of potassium, renal failure can lead to potentially serious elevations of serum potassium. Aldosterone helps regulate potassium elimination by the kidneys. An increased potassium concentration in ECF stimulates aldosterone production by the adrenal gland. The kidneys respond to aldosterone by increasing potassium excretion.

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Pathophysiology

K level decrease

Decrease in plasma Gradient b/w ECF & the plasma causing the resting membrane potential to increase its excitability

Making cell membrane more responsive to stimuli

NOTE: Almost all of the manifestation that occurs with hypokalemia are secondary to the changes in nueronal excitability and its consequent effect on muscle function

Potassium intake may be inadequate in clients who are unable or unwilling to eat for prolonged periods. Hospitalized clients are at risk, especially those on extended parenteral fluid therapy with solutions that do not contain potassium. Clients with anorexia nervosa or alcoholism may develop hypokalemia due to both inadequate intake and loss of potassium through vomiting, diarrhea, or laxative or diuretic use. Hypokalemia Influence 1. the transmission of nerve impulses 2. interfering with the contractility of smooth, skeletal, and cardiac muscle 3. the regulation and transmission of cardiac impulses. The most serious cardiac effect is an increased risk of atrial and ventricular dysrhythmias (abnormal rhythms).

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Normal ECG

Characteristic ECG changes of hypokalemia includes: Flattened or inverted T waves, the development of U waves, and a depressed ST segment Hypokalemia affects both the resting membrane potential and intracellular enzymes in skeletal and smooth muscle cells. This causes skeletal muscle weakness and slowed peristalsis of the gastrointestinal tract. Muscles of the lower extremities are affected first, then the trunk and upper extremities. Severe hypokalemia can lead to rhabdomyolysis, a condition in which muscle fibers disintegrate. Hypokalemia also can affect kidney function, particularly the ability to concentrate urine. The multisystem effects of hypokalemia are summarized on next slide

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Nursing Diagnoses and Interventions I. Activity Intolerance Muscle cramping and weakness are common early manifestations of hypokalemia. The lower extremities are usually affected initially. This muscle weakness can cause the client to fatigue easily, particularly with activity. Monitor skeletal muscle strength and tone, which are affected by moderate hypokalemia. Increasing weakness, paresthesias, or paralysis of muscles or progression of affected muscles to include the upper extremities or trunk can indicate a further drop in serum potassium levels. Monitor respiratory rate, depth, and effort; heart rate and rhythm; and blood pressure at rest and following activity. - Tachypnea, dyspnea, tachycardia, and/or a change in blood pressure may indicate decreasing ability to tolerate activities. - Report changes to the care provider. Assist with self-care activities as needed. Increasing muscle weakness can lead to fatigue and affect the ability to meet self-care needs. II. Decreased Cardiac Output Hypokalemia affects the strength of cardiac contractions and can lead to dysrhythmias that further impair cardiac output. Hypokalemia also alters the response to cardiac drugs, such as digitalis and the antidysrhythmics. Monitor serum potassium levels, particularly in clients at risk for hypokalemia (those with excess losses due to drug therapy, gastrointestinal losses, or who are unable to consume a normal diet). Report abnormal levels to the care provider. Potassium must be replaced daily, as the body is unable to conserve it. Either lack of intake or abnormal losses of potassium in the urine or gastric fluids can lead to hypokalemia. Monitor vital signs, including orthostatic vitals and peripheral pulses. As cardiac output falls, the pulse becomes weak and thready. Orthostatic hypotension may be noted with decreased cardiac output. Monitor bowel sounds and abdominal distention. Hypokalemia affects smooth muscle function and can lead to slowed peristalsis and paralytic ileus.

62 III. Acute Pain Discomfort is common when intravenous potassium chloride at a concentration of more than 40 mEq/L is given into a peripheral vein. When possible, administer intravenous KCl through a central line The rapid blood flow through central veins dilutes the KCl solution, decreasing discomfort. Spread the total daily dose of KCl over 24 hours to minimize the concentration of intravenous solutions. High concentrations of KCl are irritating to vein walls, particularly if inflammation is present. Discuss with the physician using a small amount of lidocaine prior to or with the infusion. Both a lidocaine bolus given at the infusion site and a small amount of lidocaine in the intravenous infusion have been shown to at least partially relieve discomfort associated with concentrated potassium solutions IV. Home Care The focus in preparing the client with or at risk for hypokalemia is prevention. Discharge planning focuses on teaching self-care practices. Include the following topics when preparing the client and family for home care. Recommended diet, including a list of potassium-rich foods Prescribed medications and potassium supplements, their use, and desired and unintended effects Using salt substitutes (if recommended) to increase potassium intake; avoiding substitutes if taking a potassium supplement or potassium-sparing diuretic HYPERKALEMIA Elevation of the Potassium level above 5.0 mEg/L Etiology & Risk Factor 3 major causes which limits kidney to excrete excess K 1. Retention of potassium by the body because of decreased or inadequate urine output 2. Excessive release of potassium from the cells during the first 24 72 hrs. after traumatic injury or burns or from cell lysis or acidosis 3. Excess infusion of IV solution that contains potassium or excessive oral intake, especially in a person who has renal disease Kidneys accounts for 80-90% of potassium excretion, once decreases its function, ultimately be the underlying cause of hypernatremia People with 5% glomerular function can maintain normal potassium levels if urine output is at least 1L/day. Shock compounds the problem low volume of circulating vascular fluids & diminished kidney function Other routes for excretion are less effective to rid off potassium such GIT & skin to compensate for an acute state of hyperkalemia Note : Since potassium is inside the cell any conditions that destroy cells releases potassium into the circulation - People with fast-growing cancers such as Non-Hodgkins lyphomas, acute leukemia, small cells carcinoma and some metastastic cancer are at risk for developing tumor lysis syndrome [TLS]consequences of rapid cell destruction as a result of chemotherapy or radiation. - Can also result from burns, crush injury or severe infection involving extensive cells destruction Pathophysiology Hyperkalemia increases the cell membranes excitation threshold, causing the cells to become less excitable resulting decreased irritability or excitability of nerve and muscle results As hyperkalemia becomes more severe, muscles become weak, flaccid and paralyzed Hyperkalemia alters the cell membrane potential, affecting the heart, skeletal muscle function, and the gastrointestinal tract. The most harmful consequence of hyperkalemia is its effect on cardiac function. The cardiac conduction system is affected first, with slowing of the heart rate, possible heart blocks, and prolonged depolarization. ECG changes include peaked T waves, a prolonged PR interval, and widening of the QRS complex . Ventricular dysrhythmias develop, and cardiac arrest may occur.

63 The seriousness of hyperkalemia is based on the serum potassium (K+) level and ECG changes. Mild hyperkalemia: serum K+ between 5 and 6.5 ECG changes limited to peaked T wave Moderate hyperkalemia: serum K+ between 6.5 and 8 ECG changes limited to peaked T wave. Severe hyperkalemia: serum K+ greater than 8 - ECG shows absent P waves and widened QRS pattern. - Severe hyperkalemia decreases the strength of myocardial contractions.

ECG in Hyperkalemia

The manifestations of hyperkalemia result from its effects on the heart, skeletal, and smooth muscles. Early manifestations include diarrhea, colic (abdominal cramping), anxiety, paresthesias, irritability, and muscle tremors and twitching. As serum potassium levels increase, muscle weakness develops, progressing to flaccid paralysis. The lower extremities are affected first, progressing to the trunk and upper extremities. Diagnostic Tests The following laboratory and diagnostic tests may be ordered. Serum electrolytes show a serum potassium level greater than 5.0 mEq/L. Low calcium and sodium levels may increase the effects of hyperkalemia; therefore, these electrolytes are usually measured as well. ABGs are measured to determine if acidosis is present. In acidosis, excess hydrogen ions enter the cells, causing potassium to shift into the extracellular space. The extent of this shift is greater with metabolic acidosis than with respiratory acidosis An ECG is obtained and continuous ECG monitoring is instituted to evaluate the effects of hyperkalemia on cardiac conduction and rhythm. Medical Management Hyperkalemia Diuretic Potassium-wasting diuretics, such as furosemide (Lasix), may be used to enhance renal excretion of potassium.

64 Nursing Responsibilities Monitor serum electrolytes. Monitor and record weight at regular intervals under standard conditions (same time of day, balanced scale, same clothing). Monitor intake and output. Insulin, Hypertonic Dextrose,& Sodium Bicarbonate Insulin, hypertonic dextrose (10% to 50%), and sodium bicarbonate are used in the emergency treatment of moderate to severe hyperkalemia. Insulin: - promotes the movement of potassium into the cell, and glucose prevents hypoglycemia. - the onset of action of insulin and hypertonic dextrose occurs within 30 minutes and is effective for approximately 4 to 6 hours. Sodium Bicarbonate: - elevates the serum pH; potassium is moved into the cell in exchange for hydrogen ion. - Sodium bicarbonate is particularly useful in the client with metabolic acidosis. Onset of effects occurs within 15 to 30 minutes and is effective for approximately 2 hours. Nursing Responsibilities Administer intravenous insulin and dextrose over prescribed interval of time using an infusion pump. Administer sodium bicarbonate as prescribed. It may be administered as an intravenous bolus or added to a dextrose-in-water solution and given by infusion. In clients receiving sodium bicarbonate, monitor for sodium overload, particularly in clients with hypernatremia, heart failure, and renal failure. Monitor the ECG pattern closely. Monitor serum electrolytes (K+,Na+, Ca2+,Mg2+) frequently during treatment. Sodium Bicarbonate: - elevates the serum pH; potassium is moved into the cell in exchange for hydrogen ion. - Sodium bicarbonate is particularly useful in the client with metabolic acidosis. Onset of effects occurs within 15 to 30 minutes and is effective for approximately 2 hours. Nursing Responsibilities Administer intravenous insulin and dextrose over prescribed interval of time using an infusion pump. Administer sodium bicarbonate as prescribed. It may be administered as an intravenous bolus or added to a dextrose-in-water solution and given by infusion. In clients receiving sodium bicarbonate, monitor for sodium overload, particularly in clients with hypernatremia, heart failure, and renal failure. Monitor the ECG pattern closely. Monitor serum electrolytes (K+,Na+, Ca2+,Mg2+) frequently during treatment. Calcium Gluconate & Calcium Chloride Intravenous calcium gluconate or calcium chloride is used as a temporary emergency measure to counteract the toxic effects of potassium on myocardial conduction and function. Nursing Responsibilities Closely monitor the ECG of the client receiving intravenous calcium, particularly for bradycardia. Calcium should be used cautiously in clients receiving digitalis, because calcium increases the cardiotonic effects of digitalis and may precipitate digitalis toxicity, leading to dysrhythmias. Sodium Polystyrene Sulfonate (Kayexalate) & Sorbitol Sodium polystyrene sulfonate (Kayexalate) is used to treat moderate or severe hyperkalemia. Categorized as a cation exchange resin, Kayexalate exchanges sodium or calcium for potassium in the large intestine. Sorbitol is given with Kayexalate to promote bowel elimination. Kayexalate and sorbitol may be administered orally, through a nasogastric tube, or rectally as a retention enema. The usual dosage is 20 g three or four times a day with 20 mL of 70% sorbitol solution. Nursing Responsibilities Because Kayexalate contains sodium, monitor clients with heart failure and edema closely for water retention. Monitor serum electrolytes (K+,Na+, Ca2+,Mg2+) frequently during therapy. Restrict sodium intake in clients who are unable to tolerate increased sodium load (e.g., those with CHF or hypertension).

65 Nursing Diagnosis Risk for Imbalanced Fluid Volume Renal failure is a major cause of hyperkalemia. Clients with renal failure also are at risk for fluid retention and other electrolyte imbalances. Closely monitor serum potassium, BUN, and serum creatinine. Notify the physician if serum potassium level is greater than 5 mEq/L, or if serum creatinine and BUN levels are increasing. Serum creatinine and BUN are the primary indicators of renal function. Levels of these substances rise rapidly in acute renal failure, more slowly in chronic renal failure Maintain accurate intake and output records. Report an imbalance of 24-hour totals and/or urine output less than 30 mL/hour. Oliguria (scant urine) or anuria (no urine output) may indicate renal failure and an increased risk for hyperkalemia and fluid volume excess. Monitor clients receiving sodium bicarbonate for fluid volume excess. Increased sodium from injection of a hypertonic sodium bicarbonate solution can cause a shift of water into the extracellular space. Monitor clients receiving cation exchange resins and sorbitol for fluid volume excess. The resin exchanges potassium for sodium or calcium in the bowel. Excessive sodium and water retention may occur. Home Care Preventing future episodes of hyperkalemia is the focus when preparing the client for home care. Include the family, a significant other, or a caregiver when teaching the following topics. Recommended diet and any restrictions including salt substitutes and foods high in potassium Medications to be avoided, including over-the-counter and fitness supplements Follow-up appointments for lab work and evaluation

Calcium

an extracellular & intracellular cation and has a normal plasma range of 4.5 to 5.5 mEg/L or 9 to 11 mg/dl. 99% of the bodys calcium is in bones/teeth 1% only in tissues & intravascular half of calcium in the blood is bound to protein mostly albumin & remaining half is free is free

Calcium Has Many Function Act as catalyst in the transmission & conduction of nerve impulses Stimulates the contraction of skeletal, smooth and cardiac muscle Maintain normal cellular permeability: Increased level - decrease cellular permeability Decreased level - increase cellular permeability Promotes coagulation of blood in all phases but mostly in the prothrombin to thrombin phase Promotes absorption & utilization of Vit. B12, promotes strong & durable bones & teeth; Vit. D is needed to absorb calcium from the GI tract

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Calcium Level Normal = 9-11 mg/dl Increased in Ca level Decreased in Ca level

Decreased PTH Secretion

Increased PTH Secretion

Increase in urinary Ca excretion Decrease in GI absorption Decrease bone in reabsorption

Decrease in urinary Ca Excretion Increase in Bone reabsorption Increase in GI absorption

Resulting to Restored Normal Level of Serum Calcium

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The Client with Hypocalcemia Hypocalcemia is a total serum calcium level of less than 8.5mg/dL. Hypocalcemia can result from decreased total body calcium stores or low levels of extracellular calcium with normal amounts of calcium stored in bone. The systemic effects of hypocalcemia are caused by decreased levels of ionized calcium in extracellular fluid. RISK FACTORS Certain populations are at greater risk for hypocalcemia: People who have had a parathyroidectomy & parathyroid disease has low level of parathyroid hormone A deficiency in PTH results in drop in plasma calcium secondary to decrease bone reaborption and GI absorption and increased urinary excretion of calcium Older adults (especially women), people with lactose intolerance, and those with alcoholism. Older women are at particular risk after menopause because of reduced estrogen levels. Intolerance to lactose (found in milk and milk products) causes diarrhea and often limits the intake of milk and milk products, leading to possible calcium deficiency. Ethanol, or drinking alcohol, has a direct effect on calcium balance, reduces its intestinal absorption, and interferes with other processes involved in regulating serum calcium levels GI diseases , liver disease, alcoholism, anorexia and bulimia Decreased intake for several days such as those with NPO status, or longer period as in high- protein and other weight-reduction diets Older adults also may be less active, promoting calcium loss from bones,they are more likely to be taking drugs that interfere with calcium absorption or promote calcium excretion (e.g., furosemide). Older adults often consume less milk and milk products (good sources of calcium) and may have less exposure to the sun (a source of vitamin D)

68 Vitamin D must be activated by exposure to the sun, caution are those who experience prolonged institutionalization Encourage few minutes exposure each week of arms and face - is enough to promote vitamin D synthesis Open wounds are associated with calcium loss Excess sodium as seen in Cushings disease promotes calcium excretion Client receiving multiple transfusions of stored blood are at risk binding of the preservative citrate with the calcium Several medications have been linked with hypocalcemia Magnesium sulfate, colchicine, and neomycin inhibits PTH secretion Aspirin, anticonvulsants, estrogen alters vitamin D metabolism Phosphate preparations impair reabsorption of calcium Steroids decrease calcium mobilization Loop diuretics reduces calcium reabsorption Antacids and laxatives decrease calcium reabsorption from the intestine

Decreased Calcium level

Smaller stimulus to initiate cells threshold potentials

Partial depolarization of nerves & muscles

Increased neuronal excitability/irritability in the motor & sensory nerves GIT- irritability of smooth muscle of intestinal wall -increase peristalsis

Muscular - tetany

Myocardium:- weakened myocardial contraction, decreased cardiac output leading to weak pulse, hypotension, dysrrythmias
Clinical Manifestation Mild Hypocalcemia - mostly neuromuscular hyperexcitabilty - numbness & tingling of the hands, toes ,lips - emotional lability [instability & anxiety] Severe Hypocalcemia -cardiac insifficiency, hypotension, dysarrhytmias, prolonged QT intervals,

69 Trousseaus & Chovosteks signs and prolonged bleeding time All these abnormalities may progress to: seizures, laryngeal stridor, tetany [tonic muscular spasm], hemorrhage, cardiac collapse & eventually death

Trousseau's Sign

Chvosteks Sign

70 Prolonged Hypocalcemia Cataracts increased uptake of sodium & water by the lens Tropic changes such as: dry & sparse hair & rough skin Spontaneous fracture can occur when bone is depleted with calcium Tetany can cause bronchial muscle spasms, simulating an asthma attack Visceral muscle spasms, producing acute abdominal pain. Cardiovascular manifestations include hypotension, possible bradycardia (slow heart rate), and ventriculardysrhythmias. Serious complications of hypocalcemia includes: 1.airway obstruction and possible respiratory arrest from laryngospasm, 2.ventricular dysrhythmias and cardiac arrest, heart failure, and convulsions. Diagnostic Tests The following laboratory and diagnostic tests may be ordered when hypocalcemia is known or suspected. Measurements include: Total serum calcium is the amount of ionized (active) calcium available usually is estimated. In critically ill clients, however, ionized calcium may be directly measured using ionselective electrodes. Direct measurement of ionized calcium requires special handling of the blood specimen, including placing the specimen on ice and analyzing it immediately. Serum Albumin, because the albumin level affects serum calcium results. when the albumin level is low (hypoalbuminemia), the amount of ionized calcium may remain normal even though the total calcium level is low. Serum Magnesium, because hypocalcemia is often associated with hypomagnesemia (serum magnesium <1.6 mg/dL). In this case, normal magnesium levels must be restored to correct the hypocalcemia. Serum Phosphate hyperphosphatemia (serum phosphate > 4.5 mg/dL) can lead to hypocalcemia because of the inverse relationship between phosphorus and calcium (as phosphatelevels rise, calcium levels fall). Parathyroid Hormone (PTH), to identify the possible diagnoses of hyperparathyroidism. An ECG, to evaluate the effects of hypocalcemia on the heart, such as a prolonged ST segment. Medical Management : Restore Calcium Balance I. Diet : Chronic or mild hypocalcemia can be treated in part by having the client consume a diet high in calcium High-Calcium Foods Dairy Products - All type of Cheese ,Ice Cream, Milk, Yogurt Other Foods - Oatmeal , instant cup , spinach Low- Calcium Foods - Apple, banana, chicken breast baked, oatmeal cooked, pasta, vegetable juice II. If secondary to parathyroid deficiency - Avoid high-phosphate foods such as milk products & carbonated beverages & excess protein binds with available Calcium - Maintenance needs are met through Calium & Vitamin D supplement Medication Hypocalcemia is treated with oral or intravenous calcium. Oral calcium preparations (calcium carbonate, calcium gluconate, or calcium lactate) are used to treat chronic, asymptomatic hypocalcemia. Calcium supplements may be combined with vitamin D, or vitamin D may be given alone to increase gastrointestinal absorption of calcium. Nursing Responsibilities Oral calcium salts Administer 1 to 1.5 hours after meals and at bedtime. Give calcium tablets with a full glass of water. The client with severe hypocalcemia is treated with intravenous calcium to prevent life-threatening problems such as airway obstruction. The most common IV calcium preparations include Calcium Chloride and Calcium Gluconate. More irritating to the veins and may cause venous sclerosis (hardening of the vein walls) if given into a peripheral vein.

71 Intravenous calcium preparations can cause necrosis and sloughing of tissue if they extravasate into subcutaneous tissue. Rapid drug administration can lead to bradycardia and possible cardiac arrest due to overcorrection of hypocalcemia with resulting hypercalcemia. Intravenous Calcium Salts Assess IV site for patency. Do not administer calcium if there is a risk of leakage into the tissues. May be given by slow IV push (dilute with sterile normal saline for injection prior to administering) or added to compatible parenteral fluids such as NS, lactated Ringers solution, or D5W. Administer into the largest available vein; use a central line if available. Continuously monitor ECG when administering IV calcium to clients taking digitalis due to increase risk of digitalis toxicity. Frequently monitor serum calcium levels and response to therapy. Client and Family Teaching Take calcium tablets with a full glass of water 1 to 2 hours after meals. Do not take with food or milk. If possible, do not take within 1 to 2 hours of other medications. Maintain adequate vitamin D intake through diet or exposure to the sun to promote calcium absorption. Calcium carbonate can cause constipation. Eat a high-fiber diet and maintain a generous fluid intake to prevent constipation. Nursing Diagnoses and Interventions I. Risk for Injury The client with hypocalcemia is at risk for injury from possible laryngospasm, cardiac dysrhythmias, or convulsions. In addition, too rapid administration of intravenous calcium or extravasation of the medication into subcutaneous tissues can lead to injury. Frequently monitor airway and respiratory status. Report changes such as respiratory stridor (a high-pitched, harsh inspiratory sound indicative of upper airway obstruction) or increased respiratory rate or effort to the physician. These changes may indicate laryngeal spasm due to tetany. Monitor cardiovascular status including heart rate and rhythm, blood pressure, and peripheral pulses. Hypocalcemia decreases myocardial contractility, causing reduced cardiac output and hypotension. It also can cause bradycardia or ventricular dysrhythmias. Cardiac arrest may occur in severe hypocalcemia. Assess the clients cardiac status: Monitor ECG, especially apical heart rate & rhythm @ 1-2 hours Assess CMMS: color, warm, motion & sensation & peripheral pulses data for peripheral cardiac output evaluation Monitor for bleeding in the gums & petechiae or ecchymosis in the skin Assess for changes in the clarity of urine microscopic bleeding causes clear urine to be cloudy before frank bleeding is apparent Tetany a disorder usually caused by disorder of calcium metabolism: muscle twitching, cramps, convulsions, also with vitamin D deficiency IV Calcium Chloride or Calcium Gluconate Use D5W solutions when dilution is necessary, avoid saline solutions they promote calcium loss Nursing Management Thorough history of the clients current & chronic illnesses, diet intake, & medication including OTC Assist in identifying risks for Calcium deficit & guides interventions for health promotion & maintenance Monitor IV sites for infiltration or phlebitis, if it happen, notify physician, change IV site To prevent pathologic fracture, use caution by obtaining adequate help to turn or move patient Use gait belts & extra personnel to walk or transfer the client to & from bed Instruct client about food rich in Calcium such as milk, cheese, yogurt & green leafy vegetables Encourage to take calcium supplements before meals & with Vitamin D for better absorption Advised to ingest protien for better bindiogs of calcium

72

Hypercalcemia
Hypercalcemia is defined as plasma level over 5.5 mEg/L, can occur in any age group. It is a common electrolyte disorder that can have serious physical complications. Etiology & Risk Factor Three most common causes of hypercalcemia (1) Metastatic malignancy (2) Hyperparathyroidism (3) Thiazide diuretic therapy. The most common cancers that cause hypercalcemia are malignancies lung, breast, ovary, prostate, bladder bone (multiple myeloma, leukemia) kidney, head and neck, and lymph tissues. Malignancy - induced hypercalcemia is the result of either bone destruction or an increases secretion of ectopic PTH.

Pathophysiology
Malignancies Hyperparathyroidism Prolonged Immobility/lack of weight bearing Excess PTH is Produced

Bone destruction by tumor

Cause Ca to be released from bones & increased absorption in the intestine & retention of Ca in kidney Hypercalcemia results from increased RESORPTION of Calcium from the bones

Thiazide & renal failure interfere w/ elimination of Ca by kidney causing high Ca level ability to concentrate is impaired causing excess Na & water loss & increased thirst

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NUEROMUSCULAR JUNCTION -increase nueromuscular excitability leading to muscle weakness, fatigue & depressed deep tendon reflex BRAIN - Increased Ca in CSF leads to behavioral changes such as personality changes to confusion, impaired memory, acute psychosis, lethargy & coma

HEART- strengthen contraction & reducing heart rate bradycardia & heart block dysrhythmias, ECG changes, and possible hypertension. GIT- overuse of calcium-antacids containing or excess milk Ingestion leading to increase absorption of Ca reducing GIT motility gastrointestinal manifestations such as anorexia, nausea, vomiting, and constipation

Manifestations and Complications


Cardiovascular effects include Hypercalcemia causes polyuria, and, as a result, increased thirst. Complications of Hypercalcemia Can affect several different organ systems. Peptic ulcer disease may develop due to increase gastric acid secretion. Pancreatitis can occur as a result of calcium deposits in pancreatic ducts. Excess calcium can precipitate to form kidney stones. Hypercalcemic crisis, an acute increase in the serum calcium level, can lead to cardiac arrest. Diagnostic Tests The laboratory and diagnostic tests that may be ordered and the resultant findings are as follows: Serum electrolytes show a total serum calcium greater than 10.0 mg/dL. Serum PTH levels are measured to identify or rule out hyperparathyroidism as the cause of hypercalcemia. ECG changes in hypercalcemia include a shortened QT interval, shortened and depressed ST segment, and widened T wave. Medications Measures to promote calcium elimination by the kidneys and reduce calcium resorption from bone are used to treat hypercalcemia. In acute hypercalcemia, intravenous fluids are given with a loop diuretic such as furosemide to promote elimination of excess calcium. Calcitonin, which promotes the uptake of calcium into bones, also may be used to rapidly lower serum calcium levels. A number of drugs that inhibit bone resorption are available. The bisphosphonates (pamidronate and etidronate) are commonly used to treat hypercalcemia associated with malignancies. These drugs also are used to prevent and treat osteoporosis. When a bisphosphonate drug is ineffective to correct hypercalcemia, mithramycin, a chemotherapeutic agent, may be used.

74 Glucocorticoid drugs may be used in combination with other therapies to lower serum calcium levels by inhibiting intestinal calcium absorption and bone resorption. Rapid reversal of hypercalcemia in emergency situations may be accomplished by intravenous administration of : Sodium Phosphate or Potassium Phosphate. - Ca binds to phosphate, and serum calcium levels thereby decrease. - complications of this therapy can include fatal hypocalcemia resulting from binding of the ionized calcium and soft tissue calcifications. Other drug therapies include the use of intravenous plicamycin (Mithracin) to inhibit bone resorption. Glucocorticoids (cortisone), which compete with vitamin D, and a low calcium diet may be prescribed to decrease gastrointestinal absorption of calcium and to increase urinary calcium excretion. Also, calcitonin may be prescribed to decrease skeletal mobilization of calcium and phosphorus and to increase renal output of calcium and phosphorus. Fluid Management Intravenous fluids, usually isotonic saline, are administered to clients with severe hypercalcemia to restore vascular volume and promote renal excretion of calcium. Isotonic saline is used because sodium excretion is accompanied by calcium excretion. Careful assessment of cardiovascular and renal function is done prior to fluid therapy; the client is carefully monitored for evidence of fluid overload during treatment. Nursing Diagnoses and Interventions I. Risk for Injury Clients with hypercalcemia are at risk for injury due to changes in mental status, the effects of hypercalcemia on muscle strength, and loss of calcium from bones. Institute safety precautions if confusion or other changes in mental status are noted. - Changes in mental status may impair judgment and the clients ability to maintain own safety. Closely monitor intake and output. - A loop diuretic such as furosemide may be necessary if urinary output does not keep up with fluid administration. Frequently assess vital signs, respiratory status, and heart sounds. - Increasing pulse rate, dyspnea, adventitious lung sounds, and an S3 on auscultation of the heart may indicate excess fluid volume and potential heart failure. Place in semi-Fowlers to Fowlers position. - Elevating the head of the bed improves lung expansion and reduces the work of breathing. Administer diuretics as ordered, monitoring response. - Loop diuretics may be ordered to help eliminate excess fluid and calcium. If the client has confusion, lethargy, or coma: institute precautions, including low bed position To prevent injury, turn & move client with extreme caution & w/ adequate assistance Gait belts, back braces, tripod canes, & walkers may be used to facilitate safer ambulation Assist w/ resistive range of motion & weight-bearing activities to decrease calcium loss from the bone Report clinical manifestations of fracture immediately such as bone pain or ecchymosis Health Promotion Identify and monitor clients at risk for hypercalcemia. Promote mobility in clients when possible. Ambulate hospitalized clients as soon as possible. In the home setting, discuss the benefits of weightbearing activity with clients, families, and caregivers. Encourage a generous fluid intake of up to 3 to 4 quarts per day. Encourage clients at risk to limit their intake of milk and milk products, as well as calcium-containing antacids and supplements.

75

76 Magnesium Second most abundant intracellular cation & half of it is stored in bone - 49% at ICF, 1% in the plasma, 30% is bound to protein, 15% combined w/ anion, 55% is in free, ionized form Absorbed from small intestine at same site where Ca is absorbed & excreted in urine Malabsorption affects electrolytes Functions of Magnesium Thru its effect on more than 300 enzymes system : Transmission & conduction of nerve impulses Contraction of skeletal, smooth & cardiac muscle Transportation of Sodium & Potassium across cell membrane (Na-K pump) Synthesis & release of PTH deficit can lead to hypocalcemia & hypokalemia Influences the use of potassium, sodium, Calcium, & phosphate Activates enzymes that are necessary for the metabolism of carbohydrates, proteins, lipids & vitamin B 12. Promotes vasodilation of peripheral arteries & arterioles NOTE: Increased Calcium or Phosphorous intake can decrease Magnesium absorption from the intestine Conversely, a low Calcium level increases Magnesium absorption from the intestine

Risk Factors Loss of gastrointestinal fluids, particularly from diarrhea, an ileostomy, or intestinal fistula is a major risk factor for hypomagnesemia. Disruption of nutrient absorption in the small intestine also increases the risk. Chronic alcoholism is the most common cause of deficient magnesium levels Multiple factors associated with alcoholism contribute to hypomagnesemia: - deficient nutrient intake , impaired absorption - increased gastrointestinal losses, and increased renal excretion. Other risk factors for hypomagnesemia include: Protein-calorie malnutrition or starvation. Endocrine disorders including diabetic ketoacidosis. Drugs such as loop or thiazide diuretics, - aminoglycoside antibiotics - amphotericin B, and cyclosporine. Rapid administration of citrated [citric acid derivatives] blood (banked blood). Kidney disease

77

Pathophysiology
MAGNESIUM deficiency usually occurs along with low serum POTASSIUM and low CALCIUM level Its effects will relate also to Hypokalemia & Hypocalcemia

Deficient intracellular Magnesium in the Myocardium

CNS - Increased Nueral Excitability

Gastrointestinal Tract Increased Nueromuscular Excitability

Manifestations and Complications Neuromuscular manifestations of hypomagnesemia include - tremors, hyperreactive reflexes, - positive Chvosteks and Trousseaus signs, - tetany, paresthesias, and seizures. CNS effects include - confusion, mood changes (apathy, depression, agitation), hallucinations, and possible psychoses. Cardiovascular - an increased heart rate and ventricular dysrhythmias are - common, especially when hypokalemia is present or the client is taking digitalis,cardiac arrest and sudden death may occur. Gastrointestinal manifestations include - nausea, vomiting, anorexia, diarrhea, and abdominal distention. Diagnosis and Treatment Hypomagnesemia is diagnosed by measuring serum electrolyte levels. The ECG shows a prolonged PR interval, widened QRS complex, and depression of the ST segment with T wave inversion. Treatment is directed toward prevention and identification of an existing deficiency. In clients able to eat, a mild deficiency may be corrected by increasing the intake of foods rich in magnesium or with oral magnesium supplements. Foods High in Magnesium Green, leafy vegetables , Oranges Seafood , Grapefruit Meat , Chocolate Wheat bran , Molasses Milk , Coconut Legumes , Refined sugar Bananas

78 Magnesium Sulfate Magnesium sulfate is used to prevent or treat hypomagnesemia. It also is used as an anticonvulsant in severe eclampsia or preeclampsia. It may be given intravenously or by intramuscular injection. Oral magnesium supplements may cause diarrhea, however, limiting their use. Clients with manifestations of hypomagnesemia are treated with parenteral magnesium sulfate. Nursing Responsibilities Assess serum magnesium levels and renal function tests (BUN and serum creatinine) prior to administering. Notify the care provider if magnesium levels are above normal limits or renal function is impaired. Frequently monitor neurologic status and deep tendon reflexes during therapy. Withhold magnesium and notify the care provider if deep tendon reflexes are hypoactive or absent. Monitor intake and output. Administer IM doses deep into the ventral or dorsal gluteal sites. Intravenous magnesium sulfate may be given by direct IV push or by continuous infusion. Client and Family Teaching Explain purpose and duration of treatment. Discuss reason for frequent neurologic and reflex assessments. Nursing Diagnoses and Interventions Nursing care for clients with hypomagnesemia focuses on careful monitoring of manifestations and responses to treatment, promoting safety, client and family teaching, and administering prescribed medications. Risk for Injury Monitor serum electrolytes, including magnesium, potassium, and calcium. - Magnesium deficiency often is accompanied by deficiencies of potassium and calcium. Monitor gastrointestinal function, including bowel sounds and abdominal distention. - Hypomagnesemia reduces gastrointestinal motility. Initiate cardiac monitoring, reporting and treating (as indicated) ECG changes and dysrhythmias. In clients receiving digitalis, monitor for digitalis toxicity. - Low magnesium levels can precipitate ventricular dysrhythmias, including lethal dysrhythmias such as ventricular fibrillation. Assess deep tendon reflexes frequently during intravenous magnesium infusions and prior to each intramuscular dose. - Depressed tendon reflexes indicate a high serum magnesium level. Maintain a quiet, darkened environment. Institute seizure precautions. - Increased neuromuscular and CNS irritability can lead to seizures. A quiet, dark environment reduces stimuli. The Client with Hypermagnesemia Hypermagnesemia Magnesium level greater than 2.6 mg/dL. Contributory Factor: May occur with renal insufficiency Excessive use of magnesium- containing antacids or laxatives In severe dehydration from ketoacidosis Overuse of IV magnesium sulfate for controlling premature labor or pregnancy induced hypertension Magnesium - Containing Medications Antacids Laxatives Gelusil Milk of Magnesia Maalox No. 1 Magnesium Oxide Maalox Plus Haleys M-O Riopan Magnesium Citrate Milk of Magnesia Epsom Salts Mylanta Gaviscon Di-Gel

79 Pathophysiology Clinical manifestations are related to blocked release of acetycholine from the neuromuscular junction resulting to decrease in muscle cell activity Acetycholine is being secreted by neurons and as a transmitter it has an excitatory effect. Mild Hypermagnesemia Peripheral vessels dilates causing hypotension ECG changes includes prolonged PR & QT intervals Extreme Hypermagnesemia Profound sedative effects on the nueromuscular system leading to severe muscle weakness, lethargy, drowsiness, loss of deep tendon reflexes, respiratory paralysis & loss of conciousness Cardiac Signs Delayed myocardial conduction manifested on ECG & elevated T wave, heart block & Premature Ventricular Contraction Management The management of hypermagnesemia focuses on identifying and treating the underlying cause. All medications or compounds containing magnesium (such as antacids, intravenous solutions, or enemas) are withheld. In the client with renal failure, hemodialysis or peritoneal dialysis is instituted to remove the excess magnesium. The client may require mechanical ventilation to support respiratory function, and a pacemaker to maintain adequate cardiac output. Decreasing the use of magnesium sulfate enhancing the elimination of magnesium A saline solution with a diuretics increases renal elimination Note: Treatment may cause loss of Calcium & Hypocalcemia will intensify Hypermagnesemia {Calcium antagonizes Magnesium} - Thus IV calcium salt is being used in the treatment of hypermagnesemia Calcium gluconate is administered intravenously to reversethe neuromuscular and cardiac effects of hypermagnesemia. Nursing Care Includes Measures to prevent and identify hypermagnesemia in clients at risk, monitoring for critical effects of hypermagnesemia, and providing measures to ensure the clients safety. Consider the following Nursing Diagnoses for the client with hypermagnesemia. Decreased cardiac output related to altered myocardial conduction Risk for ineffective breathing pattern related to respiratory depression Risk for injury related to muscle weakness and altered level of consciousness Risk for ineffective health maintenance related to lack of knowledge about use of magnesium-containing supplements, antacids, laxatives, and enemas

80

Regulation of Acid-Base Disturbances


When one speaks of the regulation of acid-base balance: It is the regulation of hydrogen ion concentration in the body fluids is actually meant. The hydrogen ion concentration in different solution can vary from less than 10 - 14 equivalent /L to higher than 10 o which means a total variation of more than quadrillion fold Logarithmic basis hydrogen ion concentration is approximately midway between these two extremes NOTE: only slight changes in hydrogen ion concentration from the normal value can cause marked alterations in e rates of chemical reaction in the cells: some depressed others accelerated For this reason: regulation of hydrogen ion concentration is one of the most important aspects of homeostasis Overall effects of high concentration acidosis people with acidosis dies in coma Overall effects of low concentration alkalosis people with alkalosis dies of tetany or convulsions Normal range 7.35 7.45 Defense Against Changes in Hydrogen Ion Concentration 1. All body fluids are supplied with acid-base buffer[shock absorber] systems that immediately combine with any acid or alkali and thereby prevent excessive changes in the hydrogen ion concentration Actions: within a fraction of a second to prevent excessive changes in hydrogen ion concentration 2. If the hydrogen ion concentration does not change measurably, the respiratory centers is immediately stimulated to alter the rate of breathing Resulting to: - rate of carbon dioxide removal from the body is automatically changed, and for this reason causes hydrogen ion concentration return towards normal Action: takes 1 to 5 minutes to readjust the hydrogen ion concentration 3. When the hydrogen ion concentration changes from normal - the kidney excrete either acid or alkaline urine thereby also helping readjust the hydrogen ion concentration of the body fluids to normal - requires many minutes to several days to readjust but providing the most powerful of all acid-base regulatory mechanism Buffer System Hydrogen Ion are buffered by both intracellular and extracellular buffers The bodys major extracellular buffer system is: BICARBONATE CARBONIC ACID Bicarbonate [ HCO3] 20 Parts : Carbonic Acid [ H2CO3] 1 Part : if this ration will altered, the pH will change NOTE: It is the ratio of HCO2 to H2CO3 that is important in maintaining the pH - Carbon Dioxide [CO2 ] is a potential acid: when dissolved in water it becomes carbonic acid - When CO2 is increased, the carbonic acid is increased or vice versa Kidneys: - regulates bicarbonate levels in the ECF, they can regenerate bicarbonate ions as well reabsorb them from the renal tubule Lungs - under control of medulla, control the CO2 and thus carbonic acid is content with the ECF - HOW? adjusting ventilation in response to the amount of CO2 in the blood - A rise in partial pressure of carbon dioxide in the arterial blood {PaO2] is a powerful stimulant to respiration

Respiratory Acidosis
a compromise in any essential part of breathing: ventilation, perfusion, or diffusion may lead to respiratory acidosis pulmonary system cant rid the body of enough carbon dioxide (CO2) to maintain healthy pH balance may be acute in which pH falls abnormally low : less than 7.35 may be chronic, I which pH stays within normal limits (7.34 7.45) because the kidneys have time to compensate for the imbalance

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Respiratory Acidosis

Step 1 Pulmonary Ventilation Decreases: Retained CO2, combines with water to form carbonic acid [H2CO3] H2CO3 dissociates to release free Hydrogen Ions {H+} and Bicarbonate Excess H2CO3 causes pH to drop [Look for a Pac\CO2 level greater than 45 mmHg and pH level less than 7.35]

Step 2: As the pH levels falls, 2,3 diphosphoglycerate [2,3 DPG] increases in the RBC Causes changes in hemoglobin and makes hemoglobin releases oxygen [Look for a decreased arterial O2]

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Step 3: When ever PaCO2 increases, CO2 builds up in all tissues and fluids to include CSF and the respiratory center in the medulla The CO2 reacts with H2O to form H2CO3 ions which then breaks into free H+ and HCO3 Ions The increased amount of CO2 and free H+ stimulates the respiratory center to increase respiratory rate Increased respiratory rate expels more CO2 and helps reduce the CO2 level in the blood and other tissues [look for rapid shallow respirations and decreasing PaCO2]

Step 4 Eventually, CO2 and H+ causes cerebral blood vessels to dilate, which increases blood flow to the brain Increased blood flow can cause cerebral edema and depresses CNS activity

83

[Look for headache, confusion, lethargy, nausea and vomiting]

Step 5 As respiratory mechanism falls, increasing PaCO2 Stimulates the kidneys to conserve HCO3 ions, Na and to excrete H+ partially in the form of Ammonium {NH4] The additional HCO3 and Na combine to form extra NaHO3 able to buffer more H+ [look for increased in acid content in urine, increasing in serum pH and HCO3, levels and shallow, depressed respirations]

Step 6 As the concentration of H+ overwhelms the body compensatory mechanism, the H+ moves into the cells and K+ moves out Concurrent lack of O2 causes an aerobic production of lactic acid which further skews the acid base balance and critically depressed neurologic and cardiac functions [look for hyperkalemia, arrythmias, increased PaCO2, decreased pH and decreased LOC]

84 What causes it? A. Neuromuscular Problems Guillain Bare Syndrome Myasthenia Gravis Poliomyelitis Spinal Cord Injury B. Respiratory Center Depression Central Nervous System Trauma Brain Lesion Obesity Primary Hypoventilation Use of Certain Drugs - Anesthesia: enflurance, halothane, isoflurane, nitrous oxide - Opiods: buthorphanol, meperidine, morphine, nalbuphine - Sedatives: amobarbital, lorazepam, secobarbital, triazolam, pentobarbital C. Lung Diseases Respiratory infection COPD Acute Asthma Attacks Chronic bronchitis Pulmonary Edema Chest Wall Trauma Acute Respiratory Distress Syndrome D Airway Obstruction Retained Secretions Tumors Anphylaxis Laryngeal Spasm Lung Diseases that Alter Alveolar Ventilation What to look for? Tachypnea Dyspnea with rapid, shallow breathing Nausea and Vomiting Decreased Deep Tendon Reflexes Warm Flushed Skin Diaphoresis Confusion and Decreased Level of Consciousness What Test shows: I. Chest X- Rays - evidence of COPD - evidence of pneumonia, pneumothorax, or other causes II. Electrolytes levels - potassium level greater than 5 mEg/L III. Other blood test - drug screening that may detect overdose IV. Arterial Blood Gas [ABG}analysis - can help assess breathing effectiveness and acid base balance - test that will help monitor patients response to treatment - when interpreting the ABG values: follows a consistent sequences to analyze information 3 cardinal features for assessing ABG pH - 7.4 NOTE: only slight changes in hydrogen ion concentration from the normal value can cause marked alterations in e rates of chemical reaction in the cells: some depressed others accelerated For this reason: regulation of hydrogen ion concentration is one of the most important aspects of homeostasis Overall effects of high concentration acidosis people with acidosis dies in coma Overall effects of low concentration alkalosis people with alkalosis dies of tetany or convulsions Normal range 7.35 7.45 PaCO2 40mm Hg [ partial pressure of CO2] - A rise in partial pressure of carbon dioxide in the arterial blood {PaO2] is a powerful stimulant to respiration HCO3 24 mEg/l [bicarbonate]

Tremors Restlessness Apprehension

85

Steps in Evaluating Arterial Blood Gas Values First Step: Determine pH Check pH first serves as a basis

Acidosis Less than 7.35

Alkalosis Greater than 7.45

Second Step

Determine the cause if Respiratory or Metabolic

Respiratory: PaCO2 Acidosis > 40 mmHg - hypoventilates: retains too much CO2 Alkalosis < 40 mmHg Patient hyperventilates and blows off too much CO2

Metabolic: HCO3 Acidosis - < 24 mEg/L - bicarbonate levels drops: loss of bicarbonate or lactic acid / ketones gains Alkalosis - > 24 mEg/L Body gains too much bicarbonate, an alkaline substance

Third Step: Determine if Compensation has begun pH 1) 7.20 PaCO2 60 mm Hg HCO3 27 mEg/L Normal without Compensation

Acute Respiratory Acidosis

High

2) 7. 40

60 mm Hg

34 mEg/L

Chronic Respiratory Acidosis

Elevated to appropriate level to balance high PaCO2 and produces normal pH with compensation

86 How its treated - maintain a patent airways - give bronchodilator to open constricted airways - administer supplemental oxygen as needed - expect to use a lower O2 concentration for a patient with COPD : such patient , the medulla is accustomed to high CO2 levels and a lack of O2 stimulates breathing. Therefore administering too much O2 can diminish the stimulation of breathing and depress respiratory efforts - give drugs to treat hyperkalemia - give antibiotics to treat infection - perform chest physiotherapy to remove secretions from the lungs - perform tracheal suctioning, incentives spirometry, postural drainage, and assist with coughing and deep breathing as needed - monitor for changes in the patients cardiac rhythm and respiratory patterns - closely observe the patients neurologic status and report significant changes - promote fluid intake and carefully track fluid intake and output

Respiratory Alkalosis
results from alveolar hyperventilation pH is greater than 7.45, partial pressure of arterial carbon dioxide [PaCO2] is less than 35 mm Hg may be cause resulting from a sudden increase in ventilation, or chronic, which may be difficult to identify because of renal compensation any condition that increases respiratory rate or depth can cause the lungs to eliminate too much CO2. because CO2 is an acid, eliminating it decreasese PaCO2 and increases pH

87

Respiratory Alkalosis

Step1. When Pulmonary Ventilation Increases Above the Amount Needed to Maintain Normal CO2 Levels, Excessive Amount of CO2 are Exhaled Hypocapnia [Fall in PaCO2] leads to : Reduction of H2CO3, Loss of H+ and HCO3 and Subsequently Rise in pH [Look for pH greater than 7.45, PaCO2 , 35 mEg/L and H2CO3 , 22 mEg/L]

Step 2 In defense against rising pH H+ is pulled out of cells and into the blood in exchange of K+ The H+ entering the blood combines with HCO2 ions Forming H2CO3 lowering the pH [Look for further decrease in HCO3, fall in pH and fall in serum K levels- hypokalemia]

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Step 3 Hypocapnia Stimulates the Carotid and Aortic Bodies and the Medulla Causes an Increase in Heart Rate without an Increase in Blood Pressure [Look for Angina, ECG Changes, Restlessness, and Anxiety

Step 4 Simultaneously, Hypocapina Produces Vasoconstriction Prompting a Reduction in Cerebral Blood Flow, Overexcites the Medulla, Pons and Other Parts of the Autonomic Nervous System [Look for increasing anxiety, diaphoresis, dyspnea, alternating period of apnea and hyperventilation, dizziness, tingling in the Fingers or Toes]

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Step 5 When Hypercapnia lasts more than 6 hours Kidneys Increases Secretion of HCO3 and Reduces Excretion of H+. Periods of Apnea May Result if the pH Remains High and PaCo2 Remains Low [Look for slowing of respiratory rate, hypoventilation, and Cheyne-Stokes Respirations]

Step 6 Continues Low PaCO2 Increases Cerebral and Peripheral Hypoxia from Vasoconstriction Severe Alkalosis Inhibits Ca++ Ionization, Which in Turns Causes Increased Level of Nerve Excitability and Muscles Contractions. Eventually, the Alkalosis Overwhelms the Central Nervous System and the Heart [Look for deceasing level of consciousness, hyperreflexia, carpopedal spasms, tetany, arrhythmias, seizures and coma]

90 What causes it? Hyperventilation - pain anxiety salicylate intoxication, use of certain drugs Drugs Catecholamine Salicylate Xanthines - Dobutamine - Aspirin - Aminiphyline - Dopamine - Aspirin-containing compound - Oxtrriphyline - Epinephrine - Diflunisal - Theophyline - Isoproterenol Others - nicotine - Norepinephrine Hypermetabolic - fever liver failure sepsis Conditions that affects the respiratory control center Other causes - acute hypoxia secondary to high altitude - severe anemia - hypotension - pulmonary disease - pulmonary embolus What to look for Tachycardia syncope diaphoresis hyperreflexia Dyspnea and increased respiratory rate and depth paresthesia Tetany anxiety confusion restlessness What tests shows 1. ABG Analysis ABG Uncompensated Compensated pH > 7.45 normal PaCO2 < 35 mmHg < 35 mmHg HCO3 Normal < 22 mEg/L 2. ECG changes - arrythmias - characteristics indications of hypokalemia or hypocalcemia 3. Electrolytes levels - serum calcium level below normal - serum potassium level below normal 4. Other blood test - toxicology screening with evidence of salicylate poisoning How its treated: - correct underlying cause: treat salicylate poisoning - administer supplemental Oxygen if needed - give sedative if anxiety is the cause - counteract hyperventilate by instructing the patient to breath into a paper bag forces him to breath exhaled CO2 and raises CO2 level - if the cause is iatrogenic adjust ventilator setting - monitor vital signs and report changes in neurologic, neuromuscular, or cardiovascular functioning - monitor ABG and serum electrolyte levels, and immediately report any changes - institute seizure precautions as needed

Metabolic Acidosis
metabolic acidosis is characterized by a pH level less than 7.35, HCO3 < than 22 mEG/L metabolic acidosis depresses the CNS and, if untreated, can lead to arrhythmias, coma, and cardiac arrest Generally, metabolic acidosis is caused by HCO3 loss from extracellular fluid, metabolic acid accumulation or both Remember : Plasma pH is an indicator of hydrogen ion [H+] concentration Homeostatic mechanism keeps pH within normal range [7.35 7.45] has to consider the buffer system: Lungs and Kidneys H+ concentration is extremely important: greater concentration more acidic lower concentration more alkaline higher pH [ pH range compatible: 6.8 7.8]: tenfold difference in H+ concentration in plasma -

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Step 1 As H+ starts to accumulate in the body Chemical buffers (plasma HCO3 and proteins) in the cells and extracellular fluid binds with them [No signs are detectable at this stage]

Step 2 If excess H+ Cant Bind to the Buffers, pH Decreases Stimulating the Chemoreceptors in the Medulla to Increase the Respiratory Rate Increased Respiratory Rate Lowers the PaCO2 Allows More H+ to Bind with HCO3 Ions Respiratory Compensation Occurs Within Minutes but NOT Sufficient to the Imbalances [ look for pH < 7.35, HCO3 < than 22 mEg/L, < PaCO2, rapid, deeper respirations]

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Step 3 Healthy Kidneys Try to Compensate for Acidosis by Secreting Excess H+ into the Renal Tubules the Ions are Buffered by Phosphate or Ammonia Then are Excreted Into the Urine in the Form of a Weak Acid [Look for Acidic Urine]

Step 4 Each Time a H+ Ion is Secreted Into the Renal Tubules A Na+ Ion and HCO3 Ions are Absorbed from the Tubules and Returned to the Blood [Look for pH and HCO3 levels that return slowly to normal]

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Step 5 Excess H+ in the Extracellular Fluid Diffuses Into Cells To maintain the Balance of the Charge Across the membrane Cells Releases Potassium into the Blood [look for S&Sx of hyperkalemia, colic diarrhea, weakness or flaccid paralysis, tingling or numbness in the extremities, bradycardia, a tall T wave, prolonged PR interval and wide QRS complex]

Step 6 Excess H+ Alters the Normal Balance of K, Na and Ca Leading to Reduce Excitability of Nerve Cells [Look for S&Sx of Progressive CNC Depression, Including Lethargy, Dull Headache, Confusion, Stupor and Coma]

94 What causes it? 1. Ketone Overproduction - ketones are end product of fats metabolism - diabetes mellitus - starvation - chronic alcoholism - hyperthyroidism - severe malnutrition - severe infection with fever 2. Lactic Acidosis - shock - hepatic disorder - heart failure - seizures - pulmonary disease - strenuous exercise 3. Kidney Disorder - renal insufficiency - renal failure with acute tubular necrosis 4. GI Disorders - diarrhea - urinary diversion to the ileum - intestinal malabsorption - hyperaldosteronism - pancreatic or hepatic fistula 5. Drugs Potassium Sparring- Diuretics - acetazolamide amiloride sprironolactone triamterene Other Drugs and Substances [with poisoning or toxicity] - ammonium chloride aspirin or other salicylate hydrochloric acid What to look for? 1. Signs and Symptoms of Hyperkalemia - abdominal cramps - diarrhea and muscle weakness 2. Weakness 3. Decreased DTRs 4. Hypotension

5. Lethargy 6. Anorexia, nausea and vomiting 7. Confusion and decreasing LOC 7. Kussmaul [rapid, deep] breathing 9. Warm Dry skin

What tests shows 1. ABG Analysis ABG Uncompensated Compensated pH < 7.35 Normal PaCO2 Normal < 35 mmHg HCO3 < 22 mEg/L < 22 mEg/L 2. ECG changes characteristic of hyperkalemia: Tall T wave, Prolonged PR intervals, wide QRS interval 3. Electrolytes levels - K above normal, if with lactic acidosis expect plasma lactate level above normal 4. Other blood tests - blood glucose and serum ketones greater than normal in diabetic ketoacidosis How it is treated? 1. promote respiratory compensation by providing mechanical ventilator as an example 2. administer rapid-acting insulin to reverse DKA and more potassium back into cells 3. monitor patients potassium level 4. administer sodium-potassium bicarbonate {NaHCO3] IV to neutralize blood acidity if pH is is less than 7.1 5. flush IV line with normal saline solution before and after administering NaHCO3: it might inactivate or cause precipitation of other drugs 6. too much NaHCO3 can cause metabolic acidosis and pulmonary edema 7. begin dialysis for a patient with renal failure or a toxic drug reaction 8. if dopamine does not rise blood pressure, check patients blood pH pH < than 7.1 causes resistance to vasopressors such as dopamine, to make effective correct patients pH level 9. give an antidiarrheal drug if the HCO3 loss has been caused by diarrhea 10. closely monitor patients neurologic status to detect changes in LOC and CNS deterioration

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Metabolic Alkalosis
characterized by a blood pH > than7.45 and HCO3 > 26 mEg/L if untreated, this condition can lead into coma, arrhythmias and death generally it results fro a loss of H+ [acidic] and a gain of HCO3 ions or both

Step 1

As HCO3 Ions Starts to Accumulate in the Body Chemical Buffers [ in the extracellular fluid and cells] Bind with the Ion [ No signs are detectable at this stage]

Step 2. Excess HCO3 Ions that DONT Bind with Chemical Buffers Elevate Serum pH levels Which in turn Depresses Chemoreceptor in the Medulla Depression of these Chemoreceptors Causes a Decrease in Respiratory Rate Increases the PaCO2 Additional CO2 Combines with H2O to Form H2CO3 Note: lowered O2 levels limit Respiratory Compensation [ look for serum pH > than 7.45, HCO3 > than 25 mEg/L, Rising PaCO2, shallow Respiration]

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Step 3

When the HCO3 levels Exceeds 28 mEg/L [normal is 26] Renal Glomeruli Can No Longer Reabsorb Excess HCO3 Excess HCO3 is Excreted in the Urine [Look for Alkaline Urine and pH and HCO3 levels that Returns Slowly to Normal]

Step 4.

To Maintain Electrochemical Balance Kidneys Excrete Excess Na, H2O and HCO3 [Look for polyuria initially, then S & Sx of hypovolemia including thirst and dry mucous membranes]

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Step 5

Lowered H+ Levels in the Extracellular Fluid Causes the Ions to Diffuse Out of the Cells To Maintain the Balance of Charge Across the Cell Membrane,

Extra K+ Moves into the Cells {Look for S & Sx of hypokalemia, including anorexia, muscle weakness and loss of reflexes]

Step 6.

As H+ ion Declines, Ca Ionization Decreases Decrease in Ionization Makes Nerves Cells More permeable to Na Na Moving into Verve Cells Stimulates Neural Impulses and Produces Overexcitability of the Peripheral and Central Nervous System [Look for tetany, irritability, disorientation and seizures]

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What causes it?


1. Hypokalemia: Use of diuretics Use of Drugs Antacids Loop Diuretics Thiazide Diuretics Calcium carbonate Bumetadine Chlorothiazide Sodium Bicarbonate Furosemide Hydrochlorothiazide 2. Excessive Acid Loss from the GI tract Vomiting Pyloric Stenosis Nasogastric [NG] suctioning 3. Other Causes Cushing syndrome: disorder cause by excessive production of cortisol by adrenal gland or by prolong administration of cortisol drugs as in rheumatism [moon face, mental disturbances, abnormal growth of facial and body hair in women] Overcorrection of acidosis Kidney disease such as renal artery stenosis Multiple transfusion

What to look for?


Hypotension Cyanosis Nausea and vomiting Anorexia Polyuria Weakness, Paresthesia Hyperactive Reflexes Muscle twitching and tetany Apathy and Confusion

What Tests shows?


1. ABG Analysis ABG Uncompensated pH > 7.45 PaCO2 Normal HCO3 >25mEg/L 2. ECG Low T waves that merge with P waves 3. Electrolytes Serum K. calcium and chloride levels below normal Compensated Normal > 45 mmHg > 26 mEg/L

How its treated? 1. for severe metabolic alkalosis, administer ammonium chloride IV 2. infuse 0.9% ammonium chloride no faster than 1 L over 4 hours. Causes hemolysis of RBS and never give this drug to patient with hepatic or renal disease 3. discontinue thiazide diuretics and NG suctioning 4. give an antiemetic to treat underlying nausea and vomiting 5. give acetazolamide to increase renal excretion of HCO3 6. administer supplemental oxygen as needed to correct hypoxemia 7. institute seizures precautions as needed 8. administer a diluted potassium solution using infusion pump 9. irrigate ab NG tube with normal saline solutions instead of tap water to prevent loss of gastric electrolytes 10. monitor patients closely for muscle weakness, tetany or deceased muscular activity

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