Lesson 13 Fluid and Electrolytes PDF

- Males have more muscle mass so they have slightly more TBW content than women - ICF -55% of TBW - ECF -- 45% of TBW and subdivided into interstitial and intravascular/plasma - TBW decreases with age e.g. infants have higher, elderly have lower - Intravenous fluids - Cr...

- Males have more muscle mass so they have slightly more TBW content than women - ICF -55% of TBW - ECF -- 45% of TBW and subdivided into interstitial and intravascular/plasma - TBW decreases with age e.g. infants have higher, elderly have lower - Intravenous fluids - Crystalloids increase ECF volume by hydrostatic effect. Fluid does not stay in intravascular space long before diffusing across the semi-permeable membrane - Colloids increase have high oncotic pressure so they increase ECF by osmotic effect by pulling water into the intravascular space - Osmolality is the sum of the positively charged ions in the plasma - Sodium - Key functions = generation of action potentials, volume regulation and osmoregulation - Volume regulation = absolute sodium and water content by controlling extracellular volume - Effectors = RAAS, SNS, ADH, BNP, renal pressure - Osmoregulation = ratio of solutes (i.e. salt) to water to control extracellular osmolality - Effectors = thirst, ADH - Sodium absorption occurs in the distal small bowel and colon - Predominant cation in ECF - Changes to ECF volume are directly related to total body sodium content - Hypernatremia - Loss of water \> sodium - More commonly caused by decrease in circulating blood volume e.g. you lose water so you have a greater proportion of sodium to water - Pts can be hypovolemic, euvolemic, or hypervolemic - Hypovolemic hypernatremia seen in dehydration, diarrhea, osmotic diuresis - Euvolemic hypernatremia seen in DI - Hypervolemia can cause impaired gas exchange - Hypervolemic hypernatremia seen in Cushing syndrome and primary hyperaldosteronism - Diabetes insipidus - Most common cause of hypernatremia with normal total body sodium in conscious pt - Central DI caused by decrease in ADH secretion leading to increased amount of diluted urine - Nephrogenic DI caused by normal ADH secretion but impaired ability of kidney to respond - Congenital or due to kidney disease or the result of medications such as lithium or amphotericin B - Kidney fails to respond to exogenous ADH - Treatment of hypernatremia - Restore plasma osmolality to normal and correct underlying cause - Enteral free water preferred or D5W - Want to correct balance slowly because rapid correction can cause cerebral edema and demyelination syndromes - Do not change Na balance faster than 0.5mEq/L/hr - If decreased total body Na+, restore plasma volume before treatment with a hypotonic solution - If increased total body Na+, give loop diuretic and D5W - Mild hypernatremia is associated with increased perioperative morbidity, mortality, and hospital length of stay - Postpone elective surgeries if pt is hypernatremia \>150 or hyponatremia \ water - Caused by a defect in urinary diluting capacity - Hypoosmolality is nearly always associated with hyponatremia - Exception = pseudohyponatremia - Pseudohyponatremia = a non-sodium solute is holing water in the ECF so that creates a dilutional hyponatremia - Hypoosmolality with decreased total body sodium - Renal cause = diuretics, mineral corticoid deficiency, nephropathy - Extrarenal = vomiting, diarrhea, sweating - Hypoosmolality with normal total body sodium - Causes primary polydipsia, SIADH, hypothyroidism - Hypoosmolality with increased total body sodium - TBW and Na both increase but TBW increases more than Na - Edematous disorders i.e. kidneys can't excrete sodium properly - E.g. CHF, cirrhosis, nephrotic syndrome - Clinical manifestations of hyponatremia are primarily neurological due to increase in intracellular water - Serious manifestations of hyponatremia are seen with plasma concentrations of \3 - Hyperkalemia - Most life-threatening electrolyte abnormality - Rare in pts with normal renal function - Causes = acidosis, hyperkalemic periodic paralysis, succinylcholine administration, beta-blockers, conditions that cause a lot of cell lysis so K+ is released when cells die, ACE inhibitors, blood transfusions - Clinical manifestations = skeletal muscle weakness occurs when K+\>8 - EKG changes happen when K+ is \>7 e.g. peaked T waves, shortened QT, wide QRS, loss of p wave - Treat = diuretics, glucose and insulin, calcium salts to stabilize cardiac membrane, bicarbonate, beta-agonists, avoid LR - May potentiate effects of NMBDs - Correct K+ when its \>6 - Calcium - Role in muscle contraction - Absorption occurs in diet and is dependent on vitamin D - Regulated by PTH, vitamin D, and calcitonin - 50% of calcium is found in free ionized form, 40% bound to albumin, 10% combined with anions and amino acids - Plasma pH affects calcium protein binding. Acidosis = decreased ionized calcium - Hypercalcemia - Causes = hyperparathyroidism and malignancies account for 90% of causes; adrenal insufficiencies, thiazide diuretics, lithium - PTH increases serum Ca++ by increased uptake from bone, increased renal reabsorption, increased renal excretion of phosphate, activation of vitamin D - Calcium levels are indirectly proportional to phosphate - Calcium is magnesium antagonist - Signs and symptoms = weakness, EKG shortened ST and QT - Treat = NS and loop diuretic, bisphosphonates, calcitonin, hemodialysis, avoid acidosis which can worsen hypercalcemia - Hypercalcemia - Should be diagnosed on the basis of ionized calcium - Causes = hypoparathyroidism, pseudohypoparathyroidism, pancreatitis, rhabdomyolysis, fat embolism, chelation of calcium due to mass transfusions or albumin, tumor lysis syndrome, vitamin D deficiency - Symptoms = convulsion, tetany, paresthesias, trousseau's sign, Chvostek sign, prolonged ST and QT, decreased cardiac contractility, hypotension - Symptomatic hypocalcemia is a medical emergency! - Administer calcium with massive transfusions - Phosphorus - Second most abundant mineral in the body after calcium - Needed for maintenance and repair of tissues in cells, nerve conduction, and muscle contraction - PTH promotes phosphorus excretion - Absorption is increased with vitamin D - Hyperphosphatemia - Associated with all cause mortality - Promotes calcification in blood vessels so contributes to LVH, declined renal function, atherosclerosis - Causes = increased intake e.g. laxative abuse, decreased excretion e.g. CKD, hypoparathyroidism - Treatment = phosphate binding antacids - Hypophosphatemia - Associated with all cause mortality - Causes = severe burns, DKA, alcohol withdrawal, alkalosis, CHO ingestion, insulin - Treat = replace phosphate - Avoid hyperglycemia, respiratory alkalosis - IV phosphate with precipitate with calcium - Magnesium - Important cofactor in many of the enzymes in our body - Hypocalcemia, PTH, ECF depletion, metabolic alkalosis increase Mg reabsorption - Hypercalcemia, acute volume expansion, aldosterone, ketoacidosis, diuretics, alcohol ingestion, phosphate depletion increase Mg excretion - Hypermagnesemia - Most commonly seen in pts with CKD - Other causes = excess intake from laxatives or antacids - Symptoms = muscle weakness, vasodilation, bradycardia, myocardial depression, widening of QRS, hyporeflexia - Severe hypermagnesemia can lead to respiratory and cardiac arrest - Treatment = IV calcium, dialysis, diuresis - Reduce doses of NMDAs - Potentiates vasodilation and negative inotropic effects of anesthetics - Hypomagnesemia - Typically due to inadequate intake from diet or malabsorption syndromes, diuretics, hypothyroidism, chronic alcoholism, burns, pancreatitis, ciclosporins, aminoglycosides, long term PPI therapies - Symptoms = atrial fib, weakness, fasciculations, ataxia - Treat = replace magnesium - Consider other electrolyte disturbances e.g. hypokalemia, hypophosphatemia, hypocalcemia