32 - Electrolyte Disorders Flashcards
Describe what happens to potassium in the body
- Total body stores = 3000-4000 mmol
- 98% intracellular, 2% extracellular
- Na+/K+/ATPase pump results in 3:2 ratio of Na+ out to K+ in
- Normal serum level = 3.5-5 mmol/L, intracellular = 150 mmol/L
- Intracellular & extracellular levels are in dynamic flux
- Many important roles including protein synthesis, cell metabolism, action potential across cell membrane, & BP
Describe potassium homeostasis
- Intake through diet
- Elimination usually 90% renally (secretion from distal tubules) & 10% GI
- Homeostasis affected by – hormones, acid-base status, hyperosmolality
Which hormones affect potassium hormones and how?
- Insulin, catecholamines, & aldosterone affect homeostasis
- Insulin stimulates Na+/K+/ATPase pump to transport K+ intracellularly
- Catecholamines (ex: epinephrine) = beta-receptor stimulation, which:
- Activates Na+/K+/ATPase pump -> drives potassium intracellularly
- Causes glycogenolysis -> increases glucose -> releases insulin, drives potassium intracellularly
- Aldosterone – acts at distal tubule, increased urinary potassium excretion
Describe how acid-base and osmolality affect potassium homeostasis
- Acid-base status affects K+ shifting; in simple terms:
- Decreased blood pH – body responds by moving H+ into cells & K+ out (0.1 unit decrease in pH = ~0.6-0.8 mmol/L increase in serum K+ = false hyperkalemia b/c not actually changing amount in body, just shifting)
- Increased blood pH – body responds by moving H+ out of cells & K+ in (0.1 unit increase in pH = ~0.6 mmol/L decrease in serum K+ = false hypokalemia)
- Hyperosmolality – K+ shifts to extracellular fluid
Hypokalemia definition
- Definition = serum K+ < 3.5 mmol/L
- Mild = 3.1-3.5 mmol/L
- Moderate = 2.5-3 mmol/L
- Severe < 2.5 mmol/L
Causes of hypokalemia
- Due to total body K+ deficit or intracellular shift
- Most common cause = medications
- Other causes = excessive GI loss (diarrhea, vomiting, metabolic alkalosis can develop & decrease serum K+ further); hypomagnesemia (increases renal excretion of potassium; **important – need to correct underlying magnesium deficiency to correct potassium)
Why is hypokalemia a problem?
- Moderately low = cramps, weakness, myalgias
- Severely low = EKG changes, arrhythmias, increased digoxin toxicity
Hypokalemia tx
- Non-pharms = adequate dietary intake of K+, potassium salt substitutes
- Pharm = oral supplementation when mild & N/V not a concern; IV replacement for severe and/or vomiting; replacement of magnesium first if hypomagnesemia (oral or IV)
- General rule of thumb = 100 mmol of oral replacement increases serum K+ by ~1 mmol/L
Hypokalemia monitoring
- Acute inpatient setting correcting severe hypokalemia = can monitor serum levels numerous times/day, EKG w/ high rate infusions
- Inpatient setting w/ mild to moderate acute deficiency = replace & check serum levels daily to q3days
- Remember to check Mg2+ levels if K+ replacement isn’t correcting serum levels
- Ambulatory setting (ex: K+ supplementation w/ diuretic) = check serum level, renal function q1-2 months if levels have been stable
Hyperkalemia definition
- Definition = serum K+ > 5 mmol/L
- Mild = 5.1-5.9 mmol/L
- Moderate = 6-7 mmol/L
- Severe > 7 mmol/L
Why is hyperkalemia a problem?
- Mildly elevated = usually asymptomatic
- Moderately to severely elevated = EKG changes, arrhythmias, mortality
Main causes of hyperkalemia
- Increased K+ intake
- Decreased K+ excretion
- Decreased effect of aldosterone
- Extracellular movement of total body K+ (pseudohyperkalemia)
How can increased K+ intake cause hyperkalemia?
- Increased intake usually only a problem in severe renal impairment or dialysis
- Non-compliance w/ diet restriction (ex: products w/ high K+ content like potato, sweet potato, prunes, carrots, plain yogurt, orange juice)
- Unwittingly using KCl salt substitutes (200 mmol K+ pet 5 mL)
- OTC/alternative products containing potassium
How can decreased K+ excretion cause hyperkalemia?
- Impaired excretion in renal failure alone or in conjunction w/ medications (ex: ACEis, ARBs, K+ sparing diuretics, NSAIDs; less common = digoxin, TMP-SMX, heparin)
- Caution w/ additive effects of > 1 medications (ex: TMP-SMX added short term to pt already receiving ACEi + NSAID
What is important to note about K+ lab tests?
- Blood sample hemolysis = falsely elevated serum K+
- Intracellular K+ can spill from RBCs
- Lab will usually note if sample appear hemolyzed
- Consider false elevation if other labs (blood CO2, renal function) normal
- Redraw sample before making tx decision
Hyperkalemia tx
- Mild = may self-correct w/ monitoring, may or may not op to treat
- Hyperkalemia w/ EKG changes = emergency, immediate tx needed
- Available therapies aim to either reduce total body stores of K+ or correct extracellular (serum) levels by temporarily driving K+ intracellularly
Severe hyperkalemia tx
- First, stabilize cardiac membrane (reverse EKG changes) w/ IV calcium gluconate
- Acts w/in 5 minutes, lasts 30-60 mins
- Doesn’t change serum K+ level
- Next, drive serum potassium intracellularly w/ regular insulin 10 U IV x1 (if not already hyperglycemic, give dextrose 25 g IV x1 concurrently to avoid hypoglycemia) +/or beta-2 agonists (salbutamol 10 mg nebule inhaled x1)
- Don’t use subcut insulin b/c duration is too long for what its being used for (will cause hypoglycemia)
- For metabolic acidosis (decreased extracellular pH), can also give sodium bicarbonate 50-100 meq IV x1
- Raises pH, potassium moves into cells
- Not tx of choice outside of metabolic acidosis px
- Doesn’t work as well in px w/ ESRD
Mild hyperkalemia tx
- Sodium polystyrene sulfonate (commonly known by brand name Kayexalate)
- Cation exchange resin
- Exchanges sodium for potassium 1:1 in intestine
- Takes many hours to see full effect
- Can give PO or PR, typically 15-45 g per dose
- CI in bowel dysfunction or constipation
- Risk of colonic necrosis
- May bind other medications
- Furosemide (ex: 40 mg IV x1) to increase urinary K+ loss – onset w/in minutes, duration 4-6 h
Describe what happens to sodium in the body
- Human body requires ~1.5 g per day
- Predominant extracellular cation
- normal serum concentration 135-147 mmol/L
- Kidneys normally function to excrete excess sodium or conserve it in a deficit situation, keeping concentration tightly controlled
What is hyponatremia?
- Serum sodium < 135 mmol/L
- Most common electrolyte abnormality
- Associated w/ significant morbidity & mortality, especially w/ rapid swings in sodium levels
Categories of hyponatremia
- Hypovolemic hypotonic hyponatremia (common w/ thiazide diuretics)
- Euvolemic hyponatremia (associated w/ SIADH, syndrome of inappropriate ADH secretion)
- Hypervolemic hyponatremia (associated w/ cirrhosis, HF, nephrotic syndrome
Hyponatremia – clinical presentation
- Mild (> 125 mmol/L) = usually asymptomatic; impairment of attention & gait & increased fall risk
- Moderate (115-124 mmol/L) = headache, lethargy, restlessness, disorientation
- Severe (< 115 mmol/L) = seizures, coma, respiratory arrest, brain damage, death
Hyponatremia tx
- Treat underlying cause to correct level
- Hypovolemic hyponatremia – treat w/ IV NaCl (0.9% or sometimes 3% if severe)
- Euvolemic or hypervolemic = try fluid restriction first
- Rapid swings in sodium levels (normally caused by correcting deficiency too rapidly) can cause osmotic demyelination syndrome (damage to myelin sheath of brainstem) -> can result in paralysis or death in minutes
- Rule of thumb – never increase serum Na+ level more than 12 mmol/L/24 h
Describe the options for K+ replacement
- Oral – consider tablet vs. liquid, tolerance can be an issue (split doses to minimize GI irritation) – potassium chloride = 8 meq per tablet (avoid giving more than 24 meg per dose to minimize GI irritation and wait at least 2 h before giving additional doses; chronic deficiency may often give ~8-16 meq oral replacement daily)
- IV – severe hypokalemia, inpatient setting, high replacement rates need EKG monitoring; ex: 1 L bags of 40 meq KCl in 0.9% NaCl (not in D5W b/c dextrose will increase blood glucose and cause insulin release, which will decrease K+)