K+ 3.5 – 5.0 mEq/L Total K+ = 50 mEq/kg
- 98% intracellular (75% is in muscle)
- Disorders of potassium
- Problems with K+ intake
- Normally kidneys protect against hyperkalemia by extreting excess K+
- Problems with distribution between IC and EC spaces
- Transcellular shift – integrity of cell membrane, Na-K-ATPase activity, internal state of body ([K+], acid-base status, serum tonicity); rhabdomyolysis; insulin and beta 2-adrenergic catecholamines (increase Na-K-ATPase activity, drive K+ intracellularly); acidosis (H+ into cell and K+ out); alkalemia and hypertonicity i.e. hyperglycemia (K+ moves into cells)
- 0.1 ∆ in pH = 0.6 ∆ in K+ (correct for pH)
- Problems with K+ excretion
- Amount of K+ excreted depends on
- Plasma [K+] (if increased, stimulates nephron Na-K-ATPase – K+ moves into tubular lumen and excretion
- Plasma aldosterone (K+ excretion)
- Delivery of Na+ and H2O to DCT (if increased, stimulates Na-K-ATPase and increased tubular flow – K+ washout and elimination)
- Amount of K+ excreted depends on
- Problems with K+ intake
Hypokalemia
- Symptoms
- ↓↓↓ in extracellular K+ and ↓ in intracellular K+ → hyperpolarization of cell membrane and prolongation of AP and refractory periods (increased automaticity and excitability)
- Cardiac: dysrhythmias, conduction defects
- Skeletal muscle: weakness (LE affected more than UE, cranial muscles spared), paralysis, rhabdomyolysis, fasiculations and tetany
- GI: ileus
- Renal: nephrogenic DI, and metabolic alkalosis
- EKG changes:
- Increased P-wave amplitude
- Prolonged PR interval
- U waves
- ST depression
- Flat T-wav
- Etiology
- Inadequate intake (rare) – eating clay which binds K+
- Transcellular shif
- Medication induced:
- Beta2 sympathomimetic agonists (increase Na+ into cells in exchange for H+ which stimulates Na-K-ATPase to drive Na+ out and K+ in) i.e. ventolin
- Phosphodiesterase inhibitors (theophylline, caffeine)
- Insulin
- Barium poisoning
- Verapamil overdose
- Digoxin
- Non-medication induced:
- Metabolic and respiratory alkalosis (exchange EC K+ for IC H+)
- Hypothermia
- Medication induced:
- Excessive loss
- Extra-renal (vomit, diarrhea, NG tube)
- Renal – do a urine K+ (will be ↑)
- Diuretics (thiazide and loop – ↑ Na+ and Cl– to DCT)
- Osmotic diuresis
- Aldosterone (↑ open Na+ pores, ↑ Na-K-ATPase in nephron) – 10 or 20 hyperaldosteronism, Cushing’s, high dose steroids or ↑ renin
- Cyclosporin
- Treatment:
- Determine cause and treat cause
- Oral KCl – 20-80meq/d (safest)
- Liquid KCl – 40-60meq/dose (rapid elevation – urgent, not emergent)
- IV KCl – 20-40 meq/hr (severe symptoms)
- Watch out for rebound hyperkalemia due to transcellular shift
Hyperkalemia
- Symptoms
- Cardiac – impaired conduction with risk of asystole or V fib.
- Neuromuscular – cramps, weakness, paralysis, paresthesias, ↓DTR
- GI
- EKG changes
- Tall peaked T-waves
- Flat P-waves
- Wide QRS comple
- Etiologies
- Pseudohyperkalemia (K+ released from cells at time of phlebotomy or after collection)
- ↓ K+ excretion (↓ Na+ and H2O to DCT – RF or real/effective circulating volume depletion; ↓ effectiveness or concentration of aldosterone) – K+ sparing diuretic plus an ACEi (decreased aldosterone)
- Increased K+ load
- Transcellular shifting (insulin deficiency, rhabdomyolysis, tumor lysis syndrome, hemolysis, acidosis, hypertonicity, exercise, Drugs)
- Treatment
- Cardiac membrane stabilization (significant EKG abN)
- Calcium gluconate 10mL of 10% soln, repeat once in 5-10min.
- Reduce plasma K+ by transcelular shift
- Insulin and glucose (10 units IV with 50 mL of 50% soln or 10 units in 500mL of D10W over 1 hour) – give the glucose first
- Beta-2 agonists like albuterol – 10-20mg in 4 mL saline nebulized over 20min
- Remove K+ from body
- Kayexalate or sodium polystyrene sulfonate – exchange resin working across GI mucosa; 30g PO, 50g PR – takes ~1hour to work
- Lasix or furosemide 20-40mg IV
- Dialysis
- Determine cause / prevent recurrence
- Cardiac membrane stabilization (significant EKG abN)
Mild 5.0-6.5
Worry if >6.5
But also assess symptoms and ECG changes!!!!