electrolytes

normal Na range

135-145

hypernatremia causes

usually due to loss of water or hypertonic IV solution, rarely caused by excessive oral intake

hypernatremia pathophys

hypothalamus senses osmolarity → triggers thirst reflec adn secretes ADH to save water

all conditions are hypertonic (over 295 mOsm/kg), must determine if pt is oliguric (under 0.5mL/min) or non-oliguric (over 0.5mL/min)

hypernatremia sx

acute sx due to cell death from shrinkage but chronic Na shifts present w less sx

severe hypernatremia (over 160) = orthostatic hypotension, lethargy, irritability, weakness, hyperthermia, deliruim, seizures, coma, oliguria, rarely osmotic cerebral myelation

oliguric hypernatremia =

urine osmolality over 300

oliguric hypernatremia causes

reduced water = lack access to water, body fluid loss, heat injuries

nonrenal losses = Gi, lungs, sweat

water shift into cells (rare)

osmotic diuresis (mannitol, urea)

non-oliguric hypernatremia=

urine osmolality under 250

non-oliguric hypernatremia causes

central DI = no ADH so kidneys peeing a lot

nephrogenic DI = ADH being produced but renal receptors not accepting it

(both kinds of DI make dilute urine, dx via ADH challenge)

give ADH and they stop peeing = central DI

hypovolemic hypernatremia tx

fluid replacement: if mild give hypotonic fluids (water orally/enterally OR 5% dextrose in water). if severe give NS 0.9% until stable, then give 5%dextrose to fix imbalance

if salt ingestion was the cause give diuretic

how much water do we give to pt w acute hypernatremia (rare)

give 5%dextrose fast until Na drop stop 145, then more slowly to 140

w central DI give DDVAP

extreme cases need dialysis

how much water do we give to pt w chronic hypernatremia

5% dextrose w rate based on weight and Na level, goal is under 140, limit correction of chronic hypernatremia to 12mEq/L in 24hrs

most common intracellular electrolyte, with normal serum levels of 3.5-5

potassium

hypokalemia levels

mild = 3-3.5, moderate = 2.5-3 severe = under 2.5

how are intracellular and extracellular K levels balanced

intracellular = balance w Na/K pump

extracellular = balanced w dietary intake

external eti for hypokalemia (from Gi or kidneys)

hypokadiarrhea (most common in developing countries), meds (diuretics), adrenal tumors (aldosterone secreting), sweat, low magnesium, (no magnesium = no K absorption), inadequate intake

internal eti for hypokalemia (shift from extracellular to intracellular)

from metabolic alkalosis, hyperglycemia/insulin use, beta-2 adrenergic agonists, hypothermia

hypokalemia sx (K is like a spark plug, so when low cell membranes are less reactive to stimulation)

short term = polyuria and polydipsia

long term = tubulointerstitial nephritis

cardiac arrhythmias and arrest, constipation (smooth muscles), weakness/cramps/flaccid paralysis of LE/hyporeflexia (skeletal muscles), respiratory depression, fatigue, hallucinations, delerium, psychosis

hypokalemia dx

EKG is biggest one!!!!! = T wave flattening → ST depressions and T wave inversions → prolonged QT intervals → u waves → torsades

aldosterone, cortisol, renin, TSH, BMP, ABGs

24hr urine K (if under 25 a day kidneys are normal, if over 40 then the kidneys are the problem)

spot K:creatinine ration = under 13 means non renal cause

imaging to find adrenal adenoma, pit tumor, RAAS

hypokalemia tx

tx underlying cause (if metabolic acidosis treat the low K first, then tx acidosis)

mild-mod = oral K

severe (under 3) = IV K

cardiac monitoring

if needed start K sparing diuretic, check magnesium

hyperkalemia levels

over 5.2 = hyper, over 6.5 = severe

hyperkalemia eti caused by release from cells

pseudo-hyperkalemia = articifically inc serum K, seen w clenching fists, tourniquet use, small bore needes (MOST COMMON CAUSE) (seen w drawing blood)

tissue breakdown = rhabdo, tumor lysis syndrome, severe hemolysis,

hyperglycemia (glucose makes K leave cells)

metabolic acidosis = cellular exchange of K for H

hyperkalemia eti from impaired renal excretion

AKI or CKD, hyporeninemic-hypoaldosteronism (less K excretion)

excessive K intake w renal disease or impaired K secretion

hyperkalemia eti from meds

ACE/ARB, BB, K sparing diuretics, aldosterone antagonists, NSAIDS

hyperkalemia sx

mild =asx if develops slowly

severe= too much “electrical noise” on nerves and muscles ESP HEART, interferes how nerves talk to muscles

cardiac cells depolarize adn become more excitable (inc arrhythmia risk, palpitations, SOB, hyperventilation)

weak muscles → flaccid paralysis

worsening metabolic acidosis

what labs do we get for hyperkalemia

CBC, CMP, ABG, aldosterone, renin, cortisol

what do we se on an EKG for hyperkalemia (start seeing if K over 5.5, life threatening K is over 7)

PEAKED T WAVES (heart recharging)

progresses to prolonged PR interval and QRS duration (electrical signal slowing)

loss of P waves → QRS merges w T wave (sine wave pattern) → v-fib or asystole

NORMAL EKG DOES NOT = NORMAL K, gotta check both

emergent hyperkalemia tx (over 6.5 w or w/o EKG changes)

protect heart w IV calcium gluconate (stabilizes cardiac cells and prevents arrhythmias, does NOT lower K)

insulin to shift K into cells (or beta agonist salbuterol)

metabolic acidosis = sodium bicarb

loop diuretics → pee off K

hemodialysis if AKI, CKD, life threatening, or refractory

sodium polystyrene only w life threatening K and dialysis not avalibale or failed (risk for colonic necrosis)

non emergent hyperkalemia tx (under 6.4)

repeat blood tests and get EKG

fix underlying problem (acidosis, renal disease), remove source (supplements, salt substitutes), stop meds (ACE/ARB, K sparing diuretics like spironolactone)

pee it out = loop/thiazide diuretics

poop it out = K binders (patiromer, sodium zirconium cyclosilicate)

filter it out = dialysis

SGLT2 inhibitors to prevent chronic high K