Electrolytes Flashcards
What is the principle extracellular cation, essential for the generation of action potentials in neuro and cardiac tissue?
Sodium
The most common electrolyte disturbance in hospitalized patients; typically an excess of TBW (not decreased Na)
Hyponatremia
S/Sx are dependent on the rate and severity of decrease.
Arterial HTN, increased CVP, pulm edema, decreased cardiac function, arrhythmias, malaise, headache, lethargy, seizure/coma
Hyponatremia
Why do rapid decreases in plasma Na cause an increase in brain swelling?
Blood-Brain barrier is not really permeable to sodium, but is freely permeable to water
Plasma Na > ____ is safe for general anesthesia
130
TURP surgeries use hypotonic irrigation fluids during the resection. What are the anesthesia plans for a patient undergoing a TURP?
1) Use neuraxial block with an awake patient to monitor neuro status
2) Use isotonic solutions to replace fluid/blood loss
How to calculate the Na deficit?
0.6 x wt in kg x (desired Na - actual Na) → amt mEq to give
-½ deficit replaced in first 8 hours, remainder over 24-72 hours if S&S resolved → 0.9% NS with loop diuretic
Raise serum Na slowly to about 120-125 meq/L to avoid ____?
CNS complications (Pontine demyelination)
Absolute or relative TBW deficit related to Na; Plasma Na > 145 causes water loss from cells/crenation; loss of ability to concentrate urine & decreased thirst in geriatric patients
Hypernatremia
Tremors, weakness, irritability, confusion, seizures/coma, hypovolemia, renal insufficiency, diabetes insipidus
Hypernatremia
Due to water loss exceeding Na loss: diarrhea, vomiting, osmotic diuresis, inadequate intake, fever, burns, exposed surgical areas, prolonged positive pressure ventilation w/o humidity
-Hypotension, dec CVP, dec UOP, dec skin turgor, inc HR
-Tx: replace with 0.45 or 0.9 NS and then remaining free water deficit with D5W
Hypovolemia with Hypernatremia
Due to Na overload: dialysis with hypertonic solutions, treatment with hypertonic saline, Na bicarb administration
-Inc weight, inc BP, edema, CHF, rales
-Tx: dialysis, diuretics, replace water deficit with D5W
Hypervolemia with hypernatremia
The principle intracellular cation; essential for maintaining resting membrane potentials and in generating action potentials in neuro & cardiac tissue
Potassium
Causes:
-redistribution from ECV to ICV due to inc activity of Na/K pump (alkalemia, insulin, beta2 agonists, hypercalcemia, hypomagnesemia)
-total body K deficit (vomiting, diarrhea, NG suction, diuresis, hyperaldosteronism, surgical trauma, excess cortisol)
-decreased intake
Hypokalemia
Why does hypomagnesemia precipitate hypokalemia?
Hypomagnesemia impairs retention of K+ in the kidneys, resulting in increased excretion in the urine.
Weakness, augmentation of NMB, decreased cardiac contractility, ECG changes due to hyperpolarization of the cardiac cell (flattened T/U, increased PR/QT, ST depression, arrhythmias)
Hypokalemia S/Sx
Anesthesia Considerations:
avoid glucose fluids (bc carbs increase insulin), avoid hyperventilation, rapid correction of acidosis may lead to fatal hypokalemia, consider replacing Mg
Hypokalemia
No need to correct chronic hypoK unless digitalis therapy, IV replacement → < 10meq/hr. Slow PO correction is safest
Hypokalemia treatment
Causes:
-Decreased excretion
-ICF to ECF shift
-inability to excrete K (caution w/ penicillin, NSAID, ACEI, CSA in renal failure patients)
-hypoaldosteronism (potassium sparing diuretics act as aldosterone antagonists & interferes with renal elimination of potassium)
-acidosis (0.1 pH decrease increases K conc by 0.5 meq/L)
-upregulation of receptors following burns, stroke, paraplegia, prolonged bed rest (be careful giving succinylcholine because all the receptors open at once!)
Hyperkalemia
Muscle weakness (esp legs/resp system), paresthesia, cardiac conduction changes (prolonged PR, loss of P, wide QRS, peaked T, eventually asystole)
Most detrimental effects are on the cardiac conduction system!!
Hyperkalemia S/Sx
Anesthesia Considerations:
-Patient history (renal issues? Meds that retain K+?)
-consider canceling elective surgery if K > 5.5, always treat >6
-Avoid hypoventilation
-avoid succhinycholcine use
-remove K from IV fluids
-Meds: emergency drugs ready, muscle relaxant responses unclear.
-Consider using smaller doses of NMB and frequent neuromuscular monitoring with nerve stimulator
Hyperkalemia
Tx:
-1 amp CaCl -> Stabilize myocardium to prevent vfib
-Shift K into cell: Administer 10 units Insulin and 25g D50 - monitor glucose or
administer a beta agonist (Albuterol)
-Enhance K+ elimination -> Loop diuretic
-Hemodialysis
Hyperkalemia
Intracellular ion, NMDA receptor antagonist, essential for many enzyme rxns (DNA/Protein synthesis, energy metabolism, glucose utilization, FFA synthesis/breakdown), controls K reabsorption in renal tubules, stabilizes cell membranes, influences release of neurotransmitters (endogenous Ca antagonist- inhibits entry of Ca into presynaptic nerve terminals)
Magnesium
Why do you frequently see hypokalemia with hypomagnesemia?
The Na/K pump is Mg dependent
