Fluid And Electrolytes

Fluid and Electrolytes (relates to Chapter 16, “Fluid, Electrolyte, and Acid-Base Imbalances,” in the textbook)

Homeostasis  State of equilibrium in internal environment of body,

naturally maintained by adaptive responses that promote healthy survival  Body fluids and electrolytes play an important role

Water Content of the Body  Accounts for 60% of body weight in adult  70-80% of body weight in infant  Varies with gender, body mass, and age

{See Figure 16-1 in the textbook} Compartments  Intracellular fluid (ICF)  Extracellular fluid (ECF)  Intravascular (plasma)  Interstitial  Transcellular

{See Figure 16-2 in the textbook} Intracellular Fluid (ICF)  Fluid located within cells  42% of body weight

 Most prevalent cation is potassium (K+)  Most prevalent anion is phosphate (PO4-)

Extracellular Fluid (ECF)  Fluid spaces between cells (interstitial fluid) and the plasma

space Extracellular Fluid  Interstitial  Most prevalent anion is chloride (Cl-)  Most prevalent cation is sodium (Na+)  Expands and contracts  2/3 of ECF in interstitium

Extracellular Fluid (ECF)  Intravascular (IV)  Within vascular space  Measured with blood tests  1/3 of ECF

Transcellular Fluid  Small but important fluid compartment  Approximately 1L

Transcellular Fluid  Includes fluid in  Cerebrospinal fluid  Gastrointestinal (GI) tract  Pleural spaces

 Synovial spaces  Peritoneal fluid spaces

Mechanisms Controlling Fluid and Electrolyte Movement  Diffusion  Facilitated diffusion  Active transport  Osmosis  Hydrostatic pressure  Oncotic pressure

Diffusion  Movement of molecules from an area of high concentration

to low concentration  Occurs in liquids, solids, and gases  Membrane separating two areas must be permeable to

substance for diffusion to occur Diffusion Facilitated Diffusion  Very similar to diffusion  Specific carrier molecules involved to accelerate diffusion

Active Transport  Process in which molecules move against concentration

gradient  Example: sodium-potassium pump  ATP is energy source

Sodium-Potassium Pump

Osmosis  Movement of water between two compartments by a

membrane permeable to water but not to a solute  Water moves from area of low solute concentration to area

of high solute concentration  Requires no energy

{See Figure 16-6 in the textbook} Osmotic Pressure  Amount of pressure required to stop osmotic flow of water  Water will move from less concentrated to more

concentrated side  Determined by concentration of solutes in solution

Hydrostatic Pressure  Force within a fluid compartment  Major force that pushes water out of vascular system at

capillary level Oncotic Pressure  Osmotic pressure exerted by colloids in solution  Protein is major colloid in vascular system

Fluid Movement in Capillaries  Amount and direction of movement determined by  Capillary hydrostatic pressure  Plasma oncotic pressure  Interstitial hydrostatic pressure  Interstitial oncotic pressure

{See Figure 16-8 in the textbook} Fluid Shifts  Plasma to interstitial fluid shift results in edema  Elevation of hydrostatic pressure  Decrease in plasma oncotic pressure  Elevation of interstitial oncotic pressure

Fluid Shifts  Interstitial fluid to plasma  Fluid drawn into plasma space whenever there is increase in

plasma osmotic or oncotic pressure  Wearing of compression stockings or hose is a therapeutic

action on this effect Fluid Movement Between Extracellular and Intracellular  Water deficit (increased ECF) is associated with symptoms

that result from cell shrinkage as water is pulled into vascular system  Water excess (decreased ECF) develops from gain or

retention of excess water Fluid Spacing  First spacing  Normal distribution of fluid in ICF and ECF  Second spacing  Abnormal accumulation of interstitial fluid  Third spacing  Fluid accumulation in part of body where it is not easily

exchanged with ECF

Electrolytes  Cations (+) and anions (-) are paired 

Most powerful cation is H+

 If one electrolyte is disturbed, others are likely disturbed

Regulation of Water Balance  Hypothalamic regulation  Pituitary regulation  Adrenal cortical regulation  Renal regulation  Cardiac regulation  Gastrointestinal regulation  Insensible water loss

Hypothalamic Regulation  Osmoreceptors in hypothalamus sense fluid deficit or

increase in plasma osmolality  Stimulates thirst and antidiuretic hormone (ADH) release  Result in increased free water and decreased plasma

osmolarity Pituitary Regulation  Under control of hypothalamus, posterior pituitary releases

ADH  Stress, nausea, nicotine, and morphine also stimulate ADH

release Adrenal Cortical Regulation  Adrenal cortex releases hormones to regulate both water

and electrolytes

 Glucocorticoids  Mineralcorticoids  Aldosterone is a mineralocorticoid with potent sodium-

retaining and potassium excreting capability Factors Affecting Aldosterone Secretion Effects of Stress on F&E Balance Renal Regulation  Kidneys are primary organs for regulating fluid and

electrolyte balance  Selective reabsorption of water and electrolytes  Excretion of electrolytes occurs  Renal tubules are sites of action of ADH and aldosterone

Cardiac Regulation  Atrial natriuretic factor (ANF) is released by the cardiac

atria in response to increased atrial pressure  ANF causes vasodilation and increased urinary excretion of

sodium and water Gastrointestinal Regulation  Gastrointestinal tract accounts for most of the water intake  Small amounts of water are eliminated by GI tract in feces

Insensible Water Loss  Invisible vaporization from lungs and skin  Approximately 900 ml per day is lost  No electrolytes are lost with insensible water loss  Excessive sweating, not insensible loss, leads to loss of

water and electrolytes

Sodium  Imbalances typically associated with parallel changes in

osmolality  Plays a major role in  ECF volume and concentration  Generation and transmission of nerve impulses  Acid-base balance

Hypernatremia  Elevated serum sodium occurring with water loss or sodium

gain  Causes hyperosmolality leading to cellular dehydration  Primary protection is thirst from hypothalamus

Differential Assessment of ECF Volume Imbalances in ECF Volume Hypernatremia  Manifestations include thirst, lethargy, agitation, seizures,

and coma  If secondary to water deficiency, it often results of impaired

LOC  Can be produced by clinical states such as central or

nephrogenic diabetes insipidus Hypernatremia  Management includes  Treat underlying cause  If oral fluids cannot be ingested, IV solution of 5% dextrose

in water or hypotonic saline

 Diuretics  Serum sodium levels must be reduced gradually to avoid

cerebral edema Nursing Management Nursing Diagnosis  Risk for injury

Hyponatremia  Results from loss of sodium-containing fluids or from water

excess  Clinical manifestations include confusion, nausea, vomiting,

seizures, and coma Hyponatremia  If caused by water excess, fluid restriction is needed  If severe symptoms (seizures) occur, small amount of

intravenous hypertonic saline solution (3% NaCl) is given Hyponatremia  If associated with abnormal fluid loss, fluid replacement

with sodium-containing solution is needed Nursing Management Nursing Diagnosis  Risk for injury

Extracellular Fluid Volume Imbalances  Hypovolemia can occur with loss of normal body fluids

(diarrhea, fistula drainage, hemorrhage), decreased intake, or plasma-to-interstitial fluid shift  Hypervolemia may result from excessive intake of fluids,

abnormal retention of fluids (CHF), or interstitial-to-plasma fluid shift Extracellular Fluid Volume Imbalances

 Treatment for hypovolemia is balanced IV solutions, isotonic

chloride, or blood  Treatment for hypervolemia is use of diuretics, fluid

restriction, and sodium restriction Nursing Management Nursing Diagnoses  Hypervolemia:  Excess fluid volume  Ineffective airway clearance  Risk for impaired skin integrity  Disturbed body image  Potential complications: pulmonary edema, ascites

Nursing Management Nursing Diagnoses  Hypovolemia  Deficient fluid volume  Decreased cardiac output  Potential complication: hypovolemic shock

Nursing Management Nursing Implementation 

I&O



Monitor cardiovascular changes



Assess respiratory status and monitor changes



Daily weights



Skin assessment

Nursing Management Nursing Implementation  Neurologic function  LOC  PERLA  Voluntary movement of extremities  Muscle strength  Reflexes

Potassium  Potassium major ICF cation  Potassium is necessary for  Transmission and conduction of nerve impulses  Maintenance of normal cardiac rhythms  Skeletal muscle contraction  Acid-base balance

Potassium  Critical to action membrane potential  Sources  Fruits  Salt

and vegetables (bananas and oranges)

substitutes

 Potassium  Stored

medications (PO, IV)

blood

Hyperkalemia  Causes

 Increased retention  Renal

failure

 Potassium

sparing diuretics

 Increased intake  Mobilization from ICF  Tissue

destruction

 Acidosis

Hyperkalemia Clinical Manifestations 

Skeletal muscles weak or paralyzed



Ventricular fibrillation or cardiac standstill



Cardiac depolarization is impaired



Repolarization occurs more quickly



Abdominal cramping or diarrhea

Nursing Management Nursing Diagnoses  Risk for injury  Potential complication: arrhythmias

Nursing Management Nursing Implementation  Eliminate oral and parenteral K intake  Increase elimination of K (diuretics, dialysis, Kayexalate)  Force K from ECF to ICF by IV insulin or sodium bicarbonate  Reverse membrane effects of elevated ECF potassium by

administering calcium gluconate IV

Hypokalemia  Causes  Increased loss  Aldosterone  Loop  GI

diuretics

losses

 Associated

with Mg deficiency

 Movement

into cells

Hypokalemia Clinical Manifestations  Potentially lethal ventricular arrhythmias  Impaired repolarization  Increased digoxin toxicity in those taking the drug  Skeletal muscle weakness and paralysis  Muscle cell breakdown  Leads to myoglobin in plasma and urine

Hypokalemia Clinical Manifestations 

Decreased GI motility



Altered airway responsiveness



Impaired regulation of arterial blood flow



Diuresis



Hyperglycemia

Nursing Management Nursing Diagnoses

 Risk for injury  Potential complication: arrhythmias

Nursing Management Nursing Implementation  Replacement PO or IV  Never push IV  Painful in peripheral veins  Never give with anuric renal failure  Teach prevention methods

Calcium  Obtained from ingested foods  More than 99% combined with phosphorus and concentrated

in skeletal system  Inverse relationship with phosphorus  Bones readily available store of calcium

Calcium  Calcium blocks sodium transport and stabilizes cell

membrane  Functions include transmission of nerve impulses,

myocardial contractions, blood clotting, formation of teeth and bone, and muscle contractions  Only ionized form of calcium is biologically active

Calcium  Controlled by  Parathyroid hormone  Calcitonin

 Vitamin D

Hypercalcemia  High serum calcium levels  Causes include  Hyperparathyroidism  Malignancy  Vitamin D overdose  Prolonged immobilization

Hypercalcemia  Clinical manifestations include  decreased memory  confusion  disorientation  fatigue

Hypercalcemia  Management includes  loop diuretic  hydration with isotonic saline infusion  synthetic calcitonin  mobilization

Nursing Management Nursing Diagnosis  Risk for injury  Potential complication: arrhythmias

Hypocalcemia  Low serum calcium levels  Causes include  Decreased production of PTH  Acute pancreatitis  Multiple drug transfusions  Alkalosis  Decreased intake

Hypocalcemia  Clinical manifestations include positive Trousseau’s sign and

Chvostek’s sign  Others include laryngeal stridor, dysphagia, numbness, and

tingling around the mouth or in the extremities {See Figure 16-15 in the textbook} Hypocalcemia  Management  Treat cause  Oral or IV calcium supplements  Treatment of pain and anxiety to prevent hyperventilation-

induced respiratory alkalosis Summary Electrolyte Disorders Signs and Symptoms Electrolyte Disorders Signs and Symptoms Phosphate

 Phosphorus is primary anion in ICF  Essential to function of muscle, red blood cells, and nervous

system  Deposited with calcium for bone and tooth structure

Phosphate  Involved in acid-base buffering system, ATP production, and

cellular uptake of glucose  Maintenance requires adequate renal functioning  Essential to function muscle, RBCs, and nervous system

Hyperphosphatemia 

Causes include



Acute or chronic renal failure



Chemotherapy



Excessive ingestion of milk or phosphate containing laxatives



Large intakes of vitamin D

Hyperphosphatemia Clinical Manifestations  Hypocalcemia  Muscle problems (tetany)  Deposition of calcium-phosphate precipitates in skin, soft

tissue, cornea, viscera, and blood vessels Hyperphosphatemia  Management  Identifying and treating underlying cause

 Restricting foods and fluids containing phosphorus  Adequate hydration and correction of hypocalcemic

conditions  Sevelamer (Renagel)

Hypophosphatemia  Causes include  Malnourishment/malabsorption  Alcohol withdrawal  Use of phosphate-binding antacids  During parenteral nutrition with inadequate replacement

Hypophosphatemia Clinical Manifestations 

CNS depression



Confusion



Muscle weakness and pain



Arrhythmias



Cardiomyopathy

Hypophosphatemia  Management  Oral supplementation  Ingestion of foods high in phosphorus  May require IV administration of sodium or potassium

phosphate Magnesium  50-60% contained in bone

 A coenzyme in metabolism of protein and carbohydrates  Factors that regulate calcium balance appear to influence

magnesium balance Magnesium  Acts directly on myoneural junction  Important for normal cardiac function

Hypermagnesemia  Causes include  Increased intake or ingestion of products containing

magnesium when renal insufficiency or failure is present Hypermagnesemia Clinical Manifestations  Lethargy  Drowsiness  N/V  Reflexes impaired  Somnolence  Respiratory and cardiac arrest can occur

Hypermagnesemia  Management  Prevention  IV CaCl or calcium gluconate  Fluids

Hypomagnesemia  Causes include

 Prolonged fasting or starvation  Chronic alcoholism  Fluid loss

Hypomagnesemia  Prolonged parenteral nutrition without supplementation  Diuretics  Osmotic diuretics from high glucose levels

Hypomagnesemia Clinical Manifestations  Hyperactive deep tendon reflexes  Tremors  Seizures  Cardiac arrhythmias  Confusion

Hypomagnesemia  Management  Oral supplements  Increase dietary intake  If severe, parenteral IV or IM magnesium

Protein Imbalances  Plasma proteins, particularly albumin, are significant

determinants of plasma volume  Hyperproteinemia is rare, but occurs with dehydration-

induced hemoconcentration Hypoproteinemia

 Caused by  Anorexia  Malnutrition  Starvation  Fad dieting  Poorly balanced vegetarian diets

Hypoproteinemia Poor absorption can occur in certain GI malabsorptive diseases 

Protein can shift out of intravascular space with inflammation 



Hemorrhage



Nephrotic syndrome

Hypoproteinemia Clinical Manifestations  Edema  Slow healing  Anorexia  Fatigue  Anemia  Muscle loss  Ascites

Hypoproteinemia  Management

 High-carbohydrate, high-protein diet  Dietary protein supplements  Enteral nutrition or total parenteral nutrition

IV Fluids Purposes  Maintenance  When

oral intake is not adequate

 Replacement  When

losses have occurred

IV Fluids  IV fluids will cause electrolyte imbalances if not corrected  Imbalances classified as deficits or excesses  Sodium plays major role in homeostasis of ECF

D5W  Isotonic  Provides 170 kcal/L  Free water  Moves into ICF  Increases renal solute excretion

D5W  Prevents ketosis  Supports edema formation  Decreased chance of IV fluid overload

 Usually compatible with medications

Normal Saline (NS)  Isotonic  No calories  More NaCl than ECF  30% stays in IV (most)  70% moves out of IV

Normal Saline (NS) 

Expands IV volume



Preferred fluid for immediate response



Risk for fluid overload higher



Does not change ICF Volume



Blood products



Compatible with most medications

Lactated Ringer’s 

Isotonic



More similar to plasma than NS



Has less Na Cl



Has K, Ca, PO4, lactate (metabolized to HCO3)



Expands ECF, IV



Common replacement fluid

D5 ½ NS  Hypertonic

 Common maintenance fluid  KCl added for maintenance or replacement

D5 ½ NS  Provides calories  Prevents ketosis  Moves into ICF  Usually compatible with medications

D10W  Hypertonic  Provides 340 kcal/L  Free water  Limit of dextrose concentration may be infused peripherally

Plasma Expanders  Pull fluid into IV from interstitium  Colloids  Packed RBCs  Albumin  Plasma