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84 Cards in this Set
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normal serum potassium level
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3.6 - 5.4 mEq/L
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hyperkalemia is a serum potassium level greater than
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5.5 mEq/L
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causes of hyperkalemia
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any conditions which
1. affect aldoseterone system (ACE inhibitors, Addison's disease) 2. cause kidney failure or decreased GFR (NSAIDS - long term use) 3. causes K+ to shift out of cell (trauma, tumors, etc.) or 4. other drugs (K+ sparing diuretics) 5. acidosis |
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conditions that cause a decrease in aldosterone causes
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an increase in potssium
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how does aldosterone affect potassium levels
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aldosterone causes kidney to reabsorb sodium and excrete potassium
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how do ACE inhibitors work
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block conversion from angiotensin I to angiotensin II in the lungs
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what is the angiotensin to aldosterone pathway
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angiotensin I is converted to angiotensin II by ACE in the lungs. Angiotensin II is a potent vasoconstrictor and stimulates release of aldosterone
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how do NSAIDS cause potassium levels to increase
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NSAIDS block the conversion of arachadonic acid to prostaglandins, some of which help renal blood flow. by blocking prostaglandins, renal blood flow is reduced
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what can cause potassium to shift out of the cell
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trauma, crush, burns
rhabdomyolysis hemolytic reactions (red cell infusion reactions) tumors, drugs (beta blockers, succs) |
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a dose of succs increases serum potassium by
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0.5 mEq/l
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symptoms of hyperkalemia are
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associated with disruption of resting membrane potential, so
muscle weakness (muscle in depolarized state) Progressive Arrythmias |
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what is the progression of arrhythmia as hyperkalemia worsens
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peaked T waves
widening QRS prolonged PR Loss of P wave sine wave VF Asystole |
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emergent treatment of hyperkalemia if arrhythmia
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raise depolarization threshold (Ca) - only if see arrhythmias
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what are the doses for calcium to treat hyperkalemic arrythmia
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Calcium gluconate 10% 5 - 10 ml IV
Calcium chloride 10% 3 - 5 ml IV |
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how long does the effect of calcium last when given IV
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15 - 20 minutes (so use it to buy time to reduce K+ levels)
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emergent treatment of hyperkalemia to reduce K+ levels
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calcium
sodium bicarb insulin hyperventilation beta 2 adrenergic agonists diuretics potassium exchange resins (kayexalate) |
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dose of sodium bicarb to treat hyperkalemia
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0.5 - 1 meq/kg
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how fast does sodium bicarb work and how does it work
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it drives K+ into the cell in 5 to 15 minutes
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what is the dosing of insulin for hyperkalemia and time to effect
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10 units regular insulin and 30 - 50 g dextrose - will work in 30 - 60 minutes
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how much does hyperventilation help resole hyperkalemia
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for every 10 mmHg decrease in PaCO2, serum K+ will decrease 0.5 meq/L
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only give calcium to treat hyperkalemia if
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arrhythmias present
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how does sodium bicarb work to reduce serum K+
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adding the base bicarb to the blood causes H+ ions to leave the cell to help buffer the bicarb. K+ then goes into the cell to help keep intracellular neutrality
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how does insulin and beta 2 agonist drugs reduce serum K+ levels
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both increase the Na/K pump activity.
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what electrolyte imbalance do patients receiving continuous albuterol treatments develop
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Hypokalemia - because beta 2 agonists increase the sodium potassium pump and make K go into the cell
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how does hyperventilation lower serum K+
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hyperventilation causes respiratory alkalosis. H+ ions leave the cells to buffer. K+ ions go into the cell in exchange for the H+
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anesthetic considerations of hyperkalemia
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postpone case if possible
avoid succinylcholine avoid K+ containing solutions (LR) avoid metabolic and respiratory acidosis may increase duration of neuromuscular blocking drugs |
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hypokalemia is a potassium level less than
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3.5
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causes of hypokalemia include
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alkalosis, insulin, beta 2 agonists, inadequate intake, urinary loss, vomiting, NG suction, diarrhea, laxatives, diuresis
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symptoms of hypokalemia
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muscle cramping, tetany, weakness, arrhythmias
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arrhythmias seen with hypokalemia
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flattened T waves, U waves, prolonged PR, PVCs
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treatment for hypokalemia, dose, route
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K+ replacement - 10 - 20 mEq/hr, through a central line
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anesthetic considerations for a patient with hypokalemia
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hyperventilation
don't delay surgery unless less than 3 watch for arrhythmias possible increased sensitivity to muscle relaxants |
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what controls calcium levels
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parathyroid hormone, calcitonin, vitamin D
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what form of calcium is unbound
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ionized calcium
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what does calcium bind to
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albumin (primarily)
also other anion complexes |
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normal ionized calcium levels are
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1.15 - 1.30 mmol/L
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functions of calcium are
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action potential in smooth and cardiac muscle
coagulation (factor 4) bone formation muscle contraction membrane excitability (threshold) neurotransmitter release |
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causes of hypocalcemia
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hypoparathyroid
vitamin D deficiency or malabsorption low magnesium, high phosphate radiation therapy chemotherapy large blood transfusions burns pancreatitis respiratory or m,etabolic alkalosis |
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causes of high phosphate levels
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ESRD
nephrotic syndrome |
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one cause of vitamin D deficiency
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anti-seizure drugs
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how do proteins, calcium, and acidosis/alkalosis relate
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proteins are negative so will bind either H+ or Ca++. When H+ ion concentration is reduces (hyperventilation), more Ca++ is bound to the proteins, reducing the ionized Ca++ level
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acidosis makes ionized calcium levels
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go up
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alkalosis makes ionized calcium levels
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go down
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hallmark signs of hypocalcemia
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(neuronal membrane irritability)
-tingling and numbness circumoral, fingers, toes -tetany including carpal spasm, facial nerve, laryngospasm, bronchospasm, respiratory arrest |
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signs and syptoms of hypocalcemia (other than the hallmark signs)
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mental status changes
heart failure hypotension dysrhythmias seizures poor response to beta adrenergics |
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what is trousseaus sign
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carpal spasm when bend hand back sign of hypocalcemia
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what is chvosteks sign
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facial nerve spasm when tapped, sign of hypocalcemia
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causes of hypercalcemia
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(the opposite of hypocalcemia)
hyperparathyroid malignancy granulomatous disease (sarcoidosis, tuberculosis) vitamin D intoxication immobilization (bone demineralization) hypophosphatemis |
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symptoms of hypercalcemia are
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anorexia, nausea, vomiting
dehydration, constipation somnolence, depression kidney stones polyuria hypertension prolonged PR shortened QT |
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calcium level of greater than what is a medical emergency that may require dialysis
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15 mg/dl
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treatments for hypercalcemia
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dialysis
phosphate hydration and diuresis with lasix calcium binding drugs |
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anesthetic considerations for a patient with hypercalcemia
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hydration
assume other electrolyte problems uncertain effect on NDMR careful positioning if osteoporitic digoxin toxicity |
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are hypercalcemic patients dry or wet
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dry
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two main mechanisms for sodium balance
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aldosterone regulates total body sodium
sodium concentrations is effected by body water which is regulated by ADH |
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causes of hyponatremia
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increase in total body water
reduction in sodium secretion (defect in urinary dilution) diuretics (thiazides) aldosterone deficiency renal failure or nephrotic syndrome liver failure CHF excessive free water SIADH free water absorption (TURP) vomiting and diarrhea excessive sweating (so drink gatorade) |
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symptoms of hyponatremia - aka the marathon effect
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confusion, lethargy, seizures, coma, death
arrhythmias muscle cramps nausea, vomiting basically - too much intracellular water |
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treatment for hyponatremia
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treat the cause
infusion of isotonic or hypertonic sodium chloride diuresis water restriction |
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what level is considered hyponatremic
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less than 130 mEq/L should be corrected before surgery
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anesthetic considerations for hyponatremia
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correct if below 130 for elective procedures,
reduction in MAC needed to keep them asleep (less volatiles needed) |
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causes of hypernatremia
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(large free water loss or excessive sodium retention)
patients who are not drinking diabetes insipidus diarrhea sweat hypertonic solutions hyperaldosteronism |
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symptoms of hypernatremia
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restlessness, lethargy
hyperreflexia seizures, coma, death |
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treatment for hypernatremia
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rehydration with hypotonic solution and isotonic solution
vasopressin (DI) |
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anesthetic considerations for hypernatremia
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increased MAC
cancel elective surgery if >150meq/l profound hypotension with induction drugs |
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phosphorus works opposite
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calcium
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all about phosphorus
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absorption dependent on vitamin D
parathyroid hormone inhibits phosphorus reabsorption kidney primary route of excretion primarily intracellular key role in membrane and ATP production |
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normal phosphorus serum levels
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2.5 - 4.5 mg/dl
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causes of hypophosphatemia
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renal loss, vitamin D deficiency, alkalosis
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symptoms of hypophosphatemia
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wide-spread organ dysfunction
encephalopathy, seizures, coma, death coagulopathys, platelet dysfunction, RBC hemolysis, reduced 2,3 DPG production cardiomyopathy, respiratory failure, liver failure |
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anesthetic implications for hypophosphatemia
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post op vent support may be necessary
IV replacement may cause hypocalcemia! |
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causes of hyperphosphatemia
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increased intake,
decreased excretion, decreased bone release |
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symptoms of hyperphosphatemia
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mostly due to associated hypocalcemia - so what are hypocalcemia symptoms
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treatment for hyperphosphatemia
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phosphate binding antacids (ALOH)
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anesthetic considerations for hyperphosphatemia
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same as hypocalcemia
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normal serum magnesium levels
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1.5 - 2.1 meq/L
1.7 - 2.4 mg/dl |
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all about magnesium
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absorbed via bowel
excreted in urine predominantly intracellular component cofactor in enzyme pathways magnesium antagonizes calcium regulates the release of acetylcholine from nerve terminals |
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signs of high magnesium levels
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decreased deep tendon reflexes
paralysis (also of diaphragm) |
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causes of hypomagnesium
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associated with hypokalemia or hypocalcemia
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symptoms of hypomagnesium
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electrical irritability, prolonged PR interval, prolonged QT interval,
increased digoxin toxicity anorexia weakness fasciculation parasthesia seizures |
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treatment of hypomagnesium
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0.4 mmol/kg of 10% solution
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anesthetic considerations for hypomagnesium
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correct other electrolyte abnormalities
watch for arrhythmias correct prior to elective surgery |
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causes of hypermagnesium
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mg based antacids and laxative
decreased renal excretion newborn (if mom on magnesium) increased intake |
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symptoms of hypermagnesium
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hyporeflexia (impairs acetylcholine release),weakness, sedation, vasodilation, bradycardia, heart block, myocardial depression, hypotension
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anesthetic considerations for hypermagnesium
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EKG monitoring, potentiation of hypotension an dnegative inotropic effects with general anesthetic agents, increased NDMR effects
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treatment for hypomagnesium
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calcium, diuresis, hydration
dialysis |
