Fluid and Electrolyte Physiology
A. Total Body Water
1. Total body water (TBW) is the percentage of total body weight that is water, and varies with gender, age, and body fat content. TOTAL BODY WATER IN RELATION TO BODY WEIGHT Body build TBW (%) Adult male TBW (%) Adult female TBW (%) Infant Normal Lean Obese 60 70 50 50 60 45 70 80 60 2. Fat contains less water than muscle a. Fat is essentially water-free b. More susceptible to dehydration B. Fluid Compartments 1. Cell membrane separates total body fluids into two major compartments. a. Intracellular fluid (ICF): All fluid contained within cells (1) 2/3 of total body water (TBW) (2) Major electrolytes: K+, Mg++, and PO4- b. Extracellular fluid (ECF): All body fluid outside the cell (1) 1/3 TBW (2) Two compartments (a) Intravascular fluid/ plasma volume (25% of ECF) (b) Interstitial fluid (75% of ECF) (3) Transcellular fluid (1%) - includes lymph, CSF, synovial fluid (4) Major electrolytes: Na+, Cl , and HC03- FLUID DISTRIBUTION FOR THE 70 KG MALE VOLUME (L) % BODY Wt Intracellular Fluid 32 L 47 % Extracellular Fluid 16 L 23 % Plasma 4 L (6 %) Interstitial fluid 12 L (17 %) Total Body Water (70%) 48 L 70 % c. Pediatric Fluid Distribution (1) Infancy - majority of body water in the ECF. (2) Beyond infancy - same distribution as adults 2. Compartment membranes a. Cell membrane (1) Permeable to water, BUN, oxygen, CO2, small uncharged molecules (2) Electrolytes transported via “pumps” and transport mediators (3) Glucose generally requires insulin (4) Maintains stable internal environment that differs from ECF through transport mechanisms C. Transport Mechanisms of Solutes 1. Fluids and solutes move constantly within the body to maintain homeostasis. 2. Solutes and fluids within the various compartments move through the membranes separating those compartments using a variety of mechanisms. a. Semipermeable – allow water & some solutes to pass through the membrane b. Solutes are small dissolved particles (1) Nonelectrolyte (a) Do not dissociate; no electrical charge (b) Includes glucose, urea, bilirubin, and creatinine (2) Electrolytes (approximately 95% of solutes in body water) (a) Electrically charged ions when placed in solution (c) Cations have a positive charge (move toward the negative pole or cathode) Include Na+, K+, Ca++, Mg + (d) Anions have a negative charge (move toward the positive pole or anode) Include Cl-, HCO3-,, and PO4- (e) Anions and cations are always present in equal amounts because positive and negative charges must be equal except in polarized cells (f) Measured in mEq/L or mg/dL 3. Passive Transport: Simple Diffusion a. Molecules and ions flow from an area of higher solute concentration to an area of lower concentration. b. Diffusion rate is determined by: (a) Concentration gradient (b) Temperature – affects velocity of kinetic motion (c) Number and size of openings in the membrane (d) Lipid solubility – cell membrane is made up of lipid molecule (e) Molecular weight - water is small and uncharged so diffuses rapidly. Other lipid insoluble molecules can pass same way as water if they are small enough. (f) Distance the molecules have to travel (wall thickness) (g) Cross-sectional area of the container or chamber 4. Active Transport - process of moving a substance against a concentration, electrical, or pressure gradient. a. Requires energy – ATP, which is available in large quantities inside the cell b. Faster than simple diffusion c. High degree of specificity d. Almost all active transport occurs in the cell membrane. e. Nearly all electrolytes cross the cell membrane by active transport. f. Sodium-Potassium Pump (1) For every molecule of ATP hydrolyzed: three molecules of Na+ are transported out of the cell and two molecules of K+ move into the cell (2) Results in an electrical potential (Cell inside is more negative than outside) D. Water Transport 1. Unlike electrolytes and other solutes, water freely crosses all body membranes. 2. Two forces control the movement of water between various fluid compartments: osmotic and hydrostatic pressures. 3. Osmotic Forces a. Osmosis: passive (without energy, or ATP) movement of water across a semipermeable membrane from an area of lower solute concentration (dilute) to an area of higher solute concentration (concentrated) b. Osmolality (1) Measure of the number of milliosmoles of solutes per kilogram of water (solute concentration per weight of water) (2) Controls movement of water between body compartments. (3) Normal serum osmolality is 275 to 297 mOsm/kg (= in IF & ECF) (4) Reflects hydration (not volume) status (5) determined by three primary solutes: Na+, glucose, and urea and their relationship to 1-kg (1 liter) of plasma water. (6) Formula (memorize): Gluc BUN osmo = 2 (Na+) + 18 + 2.8 (8) With a change in the ICF or ECF osmolarity, cells will strive to restore osmotic equilibrium by moving water (osmosis) into or out of the cell. (9) IV fluids are used to restore osmolality. (a) Isotonic solutions (e.g., 0.9% NS; LR) 1) Same concentration of particles as the ICF and ECF (285 mOsm). 2) No net movement of water (b) Hypertonic solutions (e.g., 3% NS) 1) Have a concentration greater than 295 mOsm. 2) Net water movement out of cells (c) Hypotonic solutions (e.g., 0.45% NS) 1) Less concentrated or is more dilute than ICF and ECF. 2) Net movement of water into cells 4. Oncotic Pressure a. Colloid oncotic pressure is the drawing/pulling force for water exerted by proteins. (Osmotic pressure is due to solutes as Na+, glucose, BUN) b. Proteins are the greatest factor in oncotic pressure and do not readily diffuse through capillary membranes, therefore they exert oncotic/colloid osmotic pressure in the vasculature 5. Hydrostatic Pressure a. Mechanical force in mmHg pushing against a membrane b. In the vascular system, this is equivalent to B/P generated by ? contraction 6. Filtration: a. Fluid movement between vascular and interstitial space based on the balance between oncotic and the capillary arterial and venous hydrostatic pressures b. Net filtration by Starling’s forces: Filtration = forces favoring filtration minus forces opposing filtration c. Capillary hydrostatic pressure (CHP) favors filtration on the arterial end d. Capillary oncotic pressure (COP) opposes filtration, results in reabsorption on the venous end e. If venous hydrostatic pressure rises, reabsorption decreases resulting in interstitial edema, a form of third spacing f. Capillary permeability is essential for maintenance of balance between filtration and reabsorption. (1) If permeability increases protein is lost to the interstitial space (? vascular COP and ? interstitial oncotic pressure) (2) Effect is interstitial edema formation or third spacing E. Water Regulating Mechanisms 1. Water input and output are normally equal 2. Sources of fluid gains: a. Drinking oral fluids b. Solid food c. Oxidative metabolism 3. Fluid loss a. Insensible Losses (1) Skin - through evaporation and perspiration (? in stress and fever) (2) Lungs - through expiration (3) Stool b. Kidneys (normal adult UOP 0.5-1 ml/kg/hr) (pediatric: 1-1.5 ml/kg/hr) NORMAL WATER GAINS AND LOSSES (70 kg man) INTAKE OUTPUT Drinking 1400 - 1800 cc Water in food 700 – 1000 cc Water from oxidation 300 – 400 cc Urine 1400 – 1800 cc Stool 100 cc Skin 300 – 500 cc Lungs 600 – 800 cc 4. Control a. ? plasma osmolarity: “osmoreceptors” in the hypothalmus shrink and cause thirst and antidiuretic hormone (ADH) release? water reabsorption in the distal tubules b. Renal regulation. (1) of Na+ and H2O constitutes the most important mechanism for volume regulation in the body (2) ? Renal perfusion ? ? glomerular filtration rate (GFR) ? renin ? angiotensin I ? II? * aldosterone release by adrenals ? renal sodium reabsorption and therefore water retention * ADH release by hypothalamus ? water reabsorption is released in response to hypovolemia, RAAS, and increased serum osmolarity ? water reabsorption in the distal tubules c. Atrial natriuretic factor (ANF) –Released by atria when stretched, as would occur in volume overload. ANF ? kidneys to inhibit Na+ reabsorption ? salt-diuresis. 5. REMEMBER: Where Na+ goes, water generally follows. F. Fluid Volume Deficit 1. Definition: deficit in ECF compartment 2. May be isotonic (water + Na+ loss) or hypertonic (water loss > Na+ loss) 3. Etiology a. Increased excretion and secretion (diuretics, fever, V, D, DM, DI, renal salt wasting, tubes, drains, fistulas, wounds) b. GI tract is most common route of loss c. Third spacing (1) Abnormal fluid accumulation in peritoneum, pleural space, pericardial space, spinal space, interstitial space (2) Symptoms of fluid loss without weight loss d. Surgical loss – open abdomen GI loss in OR is 1 liter/hr e. Decreased intake 4. Symptoms a. 10% ECF decrease (2% body weight) (1) Thirst (2) Tachycardia (3) Postural hypotension b. 20% ECF loss (4% body weight) (1) Decreased skin turgor (2) Hypotension (3) Prolonged capillary refill c. 30% ECF loss (6% body weight) (1) Life threatening (2) Compromising BP (3) Compromising renal functions, AEB ? UOP (provided renal function WNL) to < 25 ml/hr 5. Treatment - replace volume G. Fluid Excess 1. Definition: excess of fluid in the ECF compartment 2. May be isotonic (water + Na gain) or hypotonic (water gain > Na+ gain) 3. Etiology a. Generally associated with an increase in total body sodium content. b. Excessive water administration c. Water absorption from colon, wounds treated with hypotonic wet dressings d. Heart failure, cirrhosis, renal insufficiency, hypoalbuminemia, SIADH 3. Symptoms: a. Weight gain b. Serum Na+ normal or ? c. Dilution of serum proteins d. JVD e. Dyspnea f. Stupor (water intoxication) g. Edema – excess accumulation of interstitial fluid 4. Treatment a. Restrict fluids and sodium b. Diuretics H. Sodium Imbalances (Normal range 137 – 145 mEq/L) 1. Major role a. Promotes normal volume distribution by osmolarity b. Enhances conduction and transmission of electrical activity in skeletal muscle, nerve impulses, and myocardium 2. Regulation a. Aldosterone: renal reabsorption b. ANF: renal excretion 3. Hyponatremia (hypo-osmolarity) ? cells swell a. Etiology (1) Excessive free water relative to sodium (a) Replacing loss of isotonic fluid with hypotonic or free water fluids (b) Water intoxication, tap water enemas, IVPB in D5W (c) SIADH (too much ADH) (d) Hyperglycemia (HHNK): resulting in water being pulled into vascular space from cells (2) Actual loss of Na+ – secondary to insufficient aldosterone or cortisol (adrenal insufficiency), kidneys unable to retain sodium, intestinal loss. b. Signs/symptoms (1) Water moves into the cell causing intracellular edema (especially brain cells) resulting in twitching, irritability, disorientation, convulsions, coma, and death. (2) Weakness, muscular twitching, anorexia, N/V (3) When too much water causes sodium deficit will have wt gain, ? BP and edema c. Treatment (1) Replace with NaCl (2) Severe hyponatremia (a) < 120 mEq/L is associated with a 50% mortality rate (b) Rapid correction may precipitate central nervous system injury (c) Increase Na+ by 1-2 mEq/L per hour until level = 125-135 mEq/L 4. Hypernatremia (hyperosmolarity) ? cells shrink a. Etiology (1) Loss of free water (a) Loss of body fluids (except small bowel and pancreatic secretions that contain sodium) (b) Diabetes insipidus - not enough ADH (c) Excessive diuresis, fever, ? evaporative loss (2) Too much sodium (a) Cushing’s syndrome (hyperaldosteronism), steroids (b) Excessive hypertonic solution IV (e.g., NaHCO3) (c) Near salt-water drowning b. Signs/symptoms (1) Water moves out of cell and into vascular compartment; ICF dehydration results. (a) Thirst, dry “fuzzy” tongue (b) Apprehension, restlessness, coma (c) Dry skin and mucus membranes; soft, sunken eyeballs (2) If ? total body Na+ and water results in ? Na+? hypervolemia (3) If ? Na+ is caused by not having enough free water, patient is hypovolemic c. Treatment: (1) Replace vascular fluid loss with isotonic saline (2) Free water deficit (cell volume) replaced after vascular volume replaced (3) Rule of thumb - gradually decrease sodium over 48 hours with 0.45% saline. I. Crystalloid and Colloid Administration - use normal fluid distribution to anticipate where IV fluid expands Interstitial Space 12L (75% ECF) IV Space 4L (25% ECF) Intracellular Space Extracellular Space 16L (1/3 TBW) 32L (2/3 TBW) Total Body Water 48L 1. Crystalloids a. Normal Saline - stays in the ECF space (75% IS space, 25% plasma) (1) Excellent replacement, ideal for hypovolemic shock (2) 1L = 750 cc’s interstitial space, 250 cc’s remains in the IV space. (3) Can cause hypokalemia, hypernatremia and hyperchloremic acidosis b. Lactated Ringers - Distributed the same as 0.9% saline (1) Used to replace body fluids (2) Buffers acidosis (lactate converted to HCO3- in the liver) c. D5W - glucose metabolized and becomes free water (1) Free water, expands all compartments (2) 1L = expands IV space by only 80 cc’s (3) Useful for free water losses with ? Na+ d. 0.45% Normal saline (500 cc’s NS, 500 cc’s free water) (1) Hypotonic solutions have no role in fluid resuscitation (2) Readily moves into the IS space (only 165 cc’s stay in the blood vessel) e. Hypertonic saline 1.5 - 24% (Usually 3%) (1) IVS expands from interstitial and intracellular spaces (2) Increases IVS while minimizing edema f. Advantages: inexpensive, long shelf life, readily accessible, reaction free/safe, decreases blood viscosity g. Disadvantages: edema, ? COP (dilutes plasma proteins), electrolyte imbalances 2. Colloids a. Relatively impermeable to vascular membrane b. ? COP c. Albumin (natural agent) - Produced in the liver (1) Obtained from human donor plasma and processed for viral inactivation (2) 1 Gm intravascular albumin binds 18 mls H2O by osmotic activity (100 mls of 25% albumin [25 G] expands plasma volume by 450 cc’s because an additional 350 cc’s is pulled from the IS space). (3) IV volume replacement, ? COP d. Others: Dextran, Hespan e. Disadvantages: cost, pulmonary edema (requires intact capillary), ? ionized Ca++, which could theoretically decrease heart contractility and cause clotting difficulties, anaphylaxis (0.47 - 1.53%) 3. Fluid Bolus/ Fluid Challenge a. Crystalloid: give 500 cc/5 minutes - increases IV volume by 100 – 150 cc b. Monitor patient response: J. Normal Electrolyte Panel (KNOW) Na+ 137 - 145 Cl- 98 - 107 BUN 10-20 K+ 3.8 - 5.2 CO2 22 - 30 Creatinine O.8 – 1.5 K. Electrolytes 1. Electrolytes made easy a. “Golden rules” (1) Anions (negative charge) are part of acid-base regulation (2) Cations (positive charge) have roles in electrical activity (a) Cardiac conduction/dysrhythmias (b) Nervous system function/conduction: seizures, spasm, etc. (c) Muscle contraction: weakness, paralytic ileus, cardiac contractility, etc. (3) When Mg+ is low, Ca+ and K+ are generally also low (4) Consider how the electrolyte is regulated (e.g., hormone, pH, renal, etc), its excretion, and where it comes from (e.g., oral intake, bone mobilization, intracellular release, concentration in various body fluids) b. Regulation of electrolytes (1) Hypothalmus (2) Pituitary (3) Adrenal cortex (4) Kidneys (5) GI tract 2. Potassium (3.8-5.2 mEq/L) a. Major roles and regulations (1) Primary intracellular cation (a) Intracellular osmolality (b) Major determinant of resting membrane potentials in the nervous system, skeletal and smooth muscles and the heart (2) Acid-base balance (a) H+ and K+ exchange across cell membrane if excess or deficit of either ion (b) Serum K+ is high in acidosis and low in alkalosis (3) Cell metabolism - (a) K+ transported into the cell with glucose (b) K+ required for amino acid metabolism (4) Aldosterone control: causes renal K+ excretion b. Hypokalemia (1) Etiology (a) Low intake (dietary deficiency) (b) Increased loss (diuretics, GI losses, ?aldosterone, ?catecholamines) (c) Alkalosis (b) Glucose and amino acid mobilization (treatment of DKA, TPN) (2) Symptoms (a) Skeletal muscle weakness, aching (b) Decreased bowel tone - abdominal distention, paralytic ileus (c) Altered electrical activity of heart (can be life threatening) (d) Increased digitalis effect (3) Treatment (a) IV - use infusion pump. Recommended dose no > 20 mEq/hr. (b) Oral replacement c. Hyperkalemia (1) Etiology (a) Decreased excretion (renal failure, potassium sparing diuretics) (b) Overzealous replacement therapy (check K+, BUN and creatinine) (c) Acidosis (d) Tissue trauma releases intracellular K+ release (2) Symptoms (a) Skeletal muscles: same as hypokalemia (b) Increased GI irritability (c) Electrically depresses the heart (can cause asystole) (3) Emergent treatment (a) CaCl 10% - give 5 - 10 ml in 20 min. (cardiac stimulant) (b) Move K+ into cells * Sodium bicarbonate * Glucose and insulin * Cation exchange resin (Kayexelate, Sorbitol) (c) Dialysis (4) Non-emergency treatment (if K+ < 6.5 mEq/L and no EKG changes): Stop potassium and give diuretics 3. Calcium imbalances (8.5 – 10.5 mEq/L) a. Major roles (1) Conduction of electrical impulses (2) Required for myocardial contraction (3) Coenzyme in blood coagulation b. Ionized and un-ionized calcium (1) Total calcium in the serum (on the electrolyte lab report) is sum of ionized (40%) and unionized (40-50%) calcium components (a) Ionized calcium is physiologically active (b) Unionized calcium is bound to albumin (2) Since the lab reports protein bound plus the ionized calcium: (a) A low calcium with hypoalbuminemia may not be hypocalcemia secondary to availability of more ionized calcium. (b) For every gram that the albumin is below its normal (3.5-5.5). correct the calcium up by 0.8 (know this one). (3) Ionized Ca++ goes to blood gas lab on ice. c. Hormonal control - parathyroid (1) Intestinal absorption and secretion (2) Exchange between ECF, bones, kidneys (3) Above are regulated by: vitamin D, parathyroid, growth hormone, thyrocalcitonin, glucocorticoids, and phosphorus d. Hypocalcemia (1) Etiology (a) Protein losses (b) Alkalosis (promotes protein binding) (c) Renal failure (d) Blood transfusions (citrate preservative binds with ionized calcium) (e) Parathyroidectomy (f) Decreased absorption (e.g., small bowel resection, Chron’s disease) (g) Increased excretion (e.g., diuretics, overuse of antacids or laxatives) (2) Symptoms R/T less calcium being available to repel sodium entry into the cell ? repetitive depolarization ? neuromuscular irritability (a) Depressed cardiac mechanical muscle contraction, also arterioles ? decreased stroke volume, cardiac output and B/P (b) Paresthesia of fingers (c) Tetany, muscle spasm, carpopedal spasm, bronchospasm, laryngospasm, dyspnea, (d) Chvostek s sign and Trousseau s sign (3) Treatment: (a) Treat underlying cause (b) CaCl or Ca-gluconate (? sensitivity to Digoxin) (c) PO meds or diet e. Hypercalcemia (1) Etiology (a) Bone demineralization from malignant tumors, hyperparathyroidism, (b) ? Serum protein or ? total serum calcium from collagen diseases (i.e., sarcoidosis), myocardial tumors (2) Symptoms: opposite hypocalcemia (heart: spastic/increased contraction) (3) treatment (a) Correct underlying cause (b) Forced diuresis (c) HCO3- bind excess ionized calcium 4. Magnesium imbalances (1.5 2.5 mEq/L) a. ECF has only 1% total body Mg. b. Major roles (1) Acts on the myoneural junction affecting the irritability and contractility (2) Increased Mg decreases neuromuscular irritability (3) Decreased Mg levels increase neuromuscular irritability (4) Required for energy release (the conversion of ATP to ADP) (5) The “forgotten electrolyte,” critical co-factor for the sodium-potassium and the sodium-calcium pumps important for the action potential (6) Coenzyme in the metabolism of CHO and proteins c. Regulation (1) Intestinal absorption and renal excretion (2) Hypomagnesemia results in increased PTH output, but unclear if PTH increased renal reabsorption d. Hypomagnesemia (1.5 mEq/L) (1) Etiology (a) Decreased intake - malnutrition, starvation, prolonged NPO, chronic alcoholism (b) Excessive Mg+ loss R/T diuresis or excessive loss of body fluids (2) Symptoms (a) Skeletal muscles: like hypocalcemia (b) CNS symptoms - confusion, disorientation, coma, seizures, DTs (c) Cardiac: ventricular dysrhythmias, “refractory" V fib, potential for dig. toxicity due to enhanced uptake, EKG similar to hypokalemia (3) Therapy (a) Parenteral MgSO4 * Give slowly, piggyback drip is best * Hypotension and respiratory arrest (b) Tablet form c. Hypermagnesemia (>2.5 mEq/L) (1) Etiology (a) Renal failure (b) Exogenous administration (Mg antacids, MOM) (2) Symptoms relate to inhibited acetylcholine release (a) CNS depression may lead to hypotension, respiratory arrest (b) EKG effects similar to Hyperkalemia (3) Treatmrent (a) Underlying cause (b) CaCl to antagonize resp. and cardiac depression 5. Chloride (95 105 mEq/L) a. Roles Role: Acid base--competes with bicarb for combining with sodium b. Hypochloremia (1) Etiology (a) Loss of gastric secretions (b) Metabolic alkalosis (often diuretics) (c) Dilutional (D5W, CHF, edema) (associated with hyponatremia) (2) Symptoms are due to alkalosis (CNS stimulant) (a) Neuromuscular irritability (b) Weakness (3) Treatment (a) Underlying cause (b) NaCl, KC1 (c) Ammonium chloride c. Hyperchloremia (1) Etiology (a) Excessive administration (b) Dehydration (c) Resp. alkalosis (d) Metabolic acidosis (as HC03-?, Cl-?) (2) Symptoms (related to acidosis) (a) CNS depression (b) Stupor and deep breathing when severe (3) Treat underlying cause and hydrate 6. Phosphate imbalances (2.5 4.9 mEq/L) a. An intracellular anion b. Roles (1) Structural element of bone and cell membranes (2) Important urinary buffer for titratable acids (renal hydrogen buffer) (3) Intracellular energy – ATP formation (4) Component of 2,3DPG in the RBC c. Regulation (1) Intake via GI (2) Fecal & renal secretion (regulated by PTH, and GFR) (3) Regulated with Ca++ but in opposite direction (4) Moves into cells with glycolysis, insulin, epinephrine (5) ? with alkalosis, ? with acidosis d. Hypophosphatemia (1) Etiology (a) Increased cell uptake to form sugar phosphates (insulin therapy, catecholamines as in stress) (b) Decreased bowel absorption * Inadequate intake (chronic ETOH), prolonged NPO under stress * Phosphate binding gels (Amphogel, Alternagel, Phoslo)) (c) Hyperparathyroidism (d) Metabolc alkalosis (2) Symptoms (a) Muscle weakness (decreased ATP production) (b) Hemolytic anemia (decreased 2,3 DPG ? hemolysis) (c) Mental confusion (decreased phosphoproteins and phospholipids loss of cell membrane integrity) (3) Therapy (a) IV or oral potassium (or sodium) phosphate (b) Dietary: milk excellent source e. Hyperphosphatemia (>5.5) (1) Etiology (a) Renal insufficiency/failure (b) Excessive intake * Cathartic abuse, laxatives and enemas * Over administration of IV or p.o. HPO4- (c) Cytolysis (2) Symptoms: similar to that of hypocalcemia (3) Therapy (a) Underlying cause (b) Aluminum hydroxide gels to bind HPO4 (c) Hemodialysis PURPOSE / REGULATION DEFICIT EXCESS K+ (3.8-5.2) IC primary cation IC osmolarity Determines resting membrane potential Vol & smooth muscle, nervous syst. Moves out of cell in acidosis, H+ inward Moves into cell in alkalosis Moves into cell with insulin/glucose Aldosterone control—high K+ ? ? aldosterone ? renal K= loss CAUSES: ? loss: diuretics, GI suction, V&D, intestinal drain, aldosterone release, steroids Alkalosis ? metabolism: Tx DKA or hyperglycemia, insulin and glucose, catecholamines SYMPTOMS: weakness, paralytic ileus, PVCs, ventricular arrhythmias, enhanced dig toxicity TREATMENT: KCl IV no > 20 mEq/hr, oral, KPO4 CAUSES: ? excretion: renal failure, K+ sparing diuretic Overzealous replacement Acidosis Tissue trauma, ICF release SYMPTOMS: Weakness, GI irritability, EKG- peaked t-wave, widened QRS, loss of p-wave, asystole TREATMENT: CaCl to stimulate myocardium, Move K+ back into cells: Na bicarb, glucose & insulin, cation exchange resin (Kayexelate, Sorbital) Ca++ (8.4-10.2) ROLE: bones, conduct electrical impulses, muscle contraction, blood coagulation PROTEIN BOUND physiologic effect is from ionized Ca++ (1.1-1.7 mEq). To correct for hypoalbuminemia: ?serum Ca++ by .8 mEq for each gm ? in albumin (nl is 3.5-5.5 gm) (KNOW) Alkalosis ? ? ionized Ca++ Acidosis ? ? ionized CA++ CONTROL parathyroid, calcitonin, bone formation/reabsorption, activated vit D needed for GI absorption CAUSES: Protein losses, alkalosis, renal failure, blood transfusions (citrate binds Ca++), parathyroidectomy SYMPTOMS: R/T less Ca++ repelling Na+ entry into cell ?repetitive depolarization ? neuromuscular irritability ? motor nerve discharge ? tetany spasm, ? DTRs, tingling/paresthesia of fingers, intestinal cramps Skeletal muscle spasm, carpopedal spasm, bronchospasm, laryngospasm, Chvostek’s sign, Trousseau’s sign CV: depressed myocardial contraction, hypotension if severe TREATMENT: Fix underlying cause, CaCl or Ca-gluconate IV, PO/diet. CAUSES: Bone demineralization: tumor, hyperparathyroid, Vit D intoxication Excessive Mg+ loss, diuresis SYMPTOMS: Lethargy, weakness Smooth muscle depression – constipation, N&V Heart – spastic/increased contraction Calcium deposits, renal calculi Osteoporosis, pathologic fractures TREATMENT: Fix underlying cause, forced diuresis, bicarb to bind excess ionized Ca++ Mg+ 1.7–2.2 mEq ROLE: Facilitates many body enzymes, require for ATP – ADP conversion, role in electrical activity, influences release of PTH which affects serum Ca++ REGULATION: Renal excretion, obtain by oral intake CAUSES: ? intake, starvation, ? GI absorption, chronic ETOH abuse Excessive diuresis SYMPTOMS: confusion, coma, seizures Cardiac: ventricular dysrhythmias, refractory v-fib, enhanced dig toxicity TREATMENT: PO IV: give slowly piggyback, SE are hypotension, cardiac arrest if too fast CAUSES: Renal failure, excessive intake (MOM, Mg antacids) SYMPTOMS: relate to inhibited acetylcholine release CNS depression, ? B/P, respiratory arrest Loss of DTRs, Bradycardia EKG effects like hyperkalemia ? asystole TREATMENT: Fix underlying cause, CaCl to antagonize respiratory and cardiac depression, dialysis PURPOSE / REGULATION DEFICIT EXCESS Cl- 98–107 mEq ROLE: Acid-base, competes with bicarb for combining with Na+, as bicarb ? Cl_ tends to ? and vice versa, thus ? Cl- ? metabolic acidosis CAUSES: gastric secretion loss, metabolic alkalosis (often diuretics), dilutional (D5W, CHF), profuse diaphoresis SYMPTOMS: generally relate to ? Na+, Sx of alkalosis (neuro irritability) and ? Na+ (weakness) TREATMENT: fix underlying cause, NaCl. KCl, NH4Cl CAUSES: NaCl, dehydration, bicarb losses, respiratory alkalosis, hyperparathyroidism (renal phosphate wasting and Cl- sparing) SYMPTOMS: generally relate to ? Na+, Sx of acidosis if present (hyperventilation, stupor) TREATMENT: Hydrate, fix underlying cause PO4- 2.5-4.5 mEq ROLE: Component of ATP – energy Component of proteins and lipids – intracellular molecules, cell membranes Component of 2,3DPG – RBC integrity Acid-base balance – intracellular and renal hydrogen buffer REGULATION: PTH inhibits renal reabsorption Role in calcium regulation, as one ? the other ? CAUSES: During TPN with inadequate replacement or increased glucose uptake, Tx of hyperglycemia with insulin Decreased bowel absorption – inadequate nutrition, NPO when stressed, malabsorption syndrome, phosphate binding drugs Renal phosphate wasting – osteomalacia, rickets, hyperPTH which increases Ca++ and decreases PO4- SYMPTOMS: muscle weakness (? ATP) Hemolytic anemia (? 2,3DPG) Confusion (loss of cell membrane integrity, esp. neurons) TREATMENT: fix underlying cause, replace po or IV (KPO4, or NaPO4), milk excellent source CAUSES: Renal insufficiency/failure Excessive intake – cathartic abuse, laxatives, enemas containing phosphates Cytolysis - - chemo, rhabdomyolysis, malignant hyperthermia, massive trauma, etc. SYMPTOMS: similar to ? Ca++ TREATMENT: fix underlying cause, phosphate binders (Amphogel, Alternagel, etc.), dialysis FLUID AND ELECTROLYTES SELF-ASSESSMENT 1. Percent of body water is influenced by ____________, ____________, _______________. 2. Compared to muscle, fat contains (more, or less) _______________ water. 3. Compared to bone, fate has (more, or less) __________________ water. 4. When calculating water and electrolyte needs, it is best to use_____________ a. Current weight b. Admission weight c. Ideal body weight d. Body build 5. Individuals with high total body fat will be more prone to dehydration. a. true b. false 6. Identify body fluid compartments and state the %or fraction of total body water and which electrolytes predominate in each. Body Fluid Compartment % Total Body Water Electrolyte Content 7. Define: 8. Diffusion 9. Osmosis 10. Active transport 11. Filtration 12. Describe the pathophysiology of peripheral edema in heart failure at the capillary-tissue level in terms of capillary filtration. 13. Serum osmolality is a measure of: a. total body sodium b. volume c. water balance d. all of the above 14. Body water is regulated by: a. the kidneys b. ADH c. Aldosterone d. Thirst e. All of the above f. A, b, c only g. A, b, d only 15. NSl (1 L) 3% NS (1 L) ½ NS (1 L) D5 (1 L) LR (1 L) Albumen (1 gm) PRBC (1 unit) Amount remaining intravascular Tonicity Effect on cellular water 16. The serum sodium also indicates total body sodium. a. True b. False 17. ADH regulates sodium and water. a. True b. False 18. ANF causes renal loss of Na+ and water follows. a. true b. false 19. List 4 symptoms indicating decreased perfusion secondary to hypovolemia. 20. List 4 symptoms of hypervolemia 21. A reliable indication of hypervolemia is: a. hypernatremia b. hyponatremia c. hypo-osmolality d. hyper-osmolality e. none of the above 22. Suzy is admitted into your ICU with the following serum lab values: sodium 130, potassium 5.7, chloride 114, BUN 20, glucose 550. Calculate the serum osmolality. 23. What is her serum osmolality status?____________________ And this is secondary to: _______________________. 24. List four symptoms of hypernatremia. 25. List four symptoms of hyponatremia. 26. List a common cause of hyponatremia in the ICUs. 27. List one electrolyte imbalance that occurs from profuse diaphoresis without water replacement. 28. List at least 4 parameters you monitor for fluid overload when giving fluid challenges. 29. Fill in the fishbone diagram with the electrolytes and their normal ranges in their correct position. 30. Acidosis (? or ? ) ____ serum potassium and alkalosis (? or ? ) __________ serum potassium. 31. The effect of hyperkalemia on cardiac conduction (EKG) is __________________ _____________________________________________________________________ 32. Hypokalemai may cause: a. heart block b. bradycardia c. ventricular arrhythmias as PVCs, ventricular tachycardia d. tetany 33. Steroids are notorious for causing: a. sodium and potassium retention b. sodium retention and potassium loss c. sodium loss and potassium retention d. none of the above 34. Insulin therapy, diuretics, and NGT suction are known to cause: a. hypochloremia b. hyponatremia c. hypokalemia d. hypocalcemia 35. Hyperchloremia is usually associated with a decrease in bicarb. a. true b. false 36. The CO2 on the lab value indicates a. actual amount of carbon dioxide in the blood b. the bicarb in the blood c. carbon dioxide and carbonic acid d. the carbon dioxide, carbonic acid, and the bicarb in the blood 37. The danger of severe hyponatremia is: a. dehydration b. hypervolemia c. cardiac failure d. seizures 38. Electrolyte imbalances that may be caused by prolonged NPO under stress, insulin therapy, loop diuretics and result in muscle weakness are a. Potasium and phosphate b. magnesium and chloride c. phosphate and chloride d. none of the above 39. Hypotension and heart failure may be the result of severe hypocalcemia.