Potassium Disturbances Flashcards
What is the normal extracellular potassium level?
3.5-4.5 mmol/L
Acute vs Chronic potassium disorder
Acute <48hrs
Chronic >48hrs
How does insulin, long-standing alkalemia, hyertonicity, exercise, and cell integrity effect potassium levels?
Insulin: Causes a potassium intracellular influx
Alkalemia: hypokalemia
Hypertonicity: Hyperkalemia
Exercise: Transient potassium shift extracellularly
Cell integrity: Ischemia causes hyperkalemia
External factors that effect potassium levels: Kidney elimination, Metabolic Acidosis, Metabolic alkalosis, Aldosterone, Glucocorticoids, Magnesium deficiency
Kidney Elimination: Eliminates 90% of dietary K+
Metabolic Acidosis: inhibits K+ secretion, hyperkalemia
Metabolic Alkalosis: stimulates K+ secretion, hypokalemia
Aldosterone: increase in K+ stimulates aldosterone, reduces plasma K+, hypokalemia
Glucocorticoid: enhances renal K+ excretion, hypokalemia alkalosis
Mag deficiency: renal potassium wasting.
Five main causes of hyperkalemia with examples
- Excessive potassium intake (typically results from IV administration)
- Abnormal K+ distribution: Tumor lysis syndrome, rhabdo, burns, hemolytic transfusion reactions, mesenteric ischemia
- Pharmaceuticals: Digoxin, Succ
- Acute renal failure
- Pseudohyperkalemia: hemolyzed blood sample
Definition and causes (3) of acute hypokalemia
Hypokalemia developing over hours
DKA: Patients can have a normal K+ level initially, with delivery of insulin K+ shifts back into cells producing hypokalemia
Pharmaceuticals: Albuterol, epinepherine
Therapeutic hypothermia: hypokalemia occurs in cooling phase, careful of replacement due to rebound hyperkalemia.
Cardiovascular, Neuro, and metabolic manifestations of hyperkalemia
Cards: Peaked T-wave, loss of p-wave (Sine wave), prolonged PR, and widened QRS, V-fib, asystole, if K >6.5 regardless of EKG treat emergently
Neuro: parathesias, weakness, paralysis, diaphragm spared, decreased reflexes
Metabolic: decrease renal ammoniagenesis, produces hyperchloremic metabolic acidosis. Prevents kidneys ability to excrete
Cardiovascular, Neuromuscular, and metabolic clinical manifestations of hypokalemia
Cards: ST depression, decreased T wave amplitude, increased U wave amplitude, increase dig toxicity, ventricular ectopy
Neuro: weakness, myalgias, paralysis, rhabdo
Metabolic: glucose intolerance, increased protein catabolism, polydipsea, polyuria, metabolic alkalosis
What is hyperkalemic Periodic paralysis
Rare
Mutation of skeletal muscle Na+ channels
Precipitated by exercise, fasting, cold, and potassium administrations
Prevented with carbs
What is refeeding syndrome?
Glucose initiated hyperinsulinemia, causing K to shift hypokalemia
What is hypokalemic periodic paralysis
Inherited, sporadic, or thyrotoxic
Muscle weakness following acute hypokalemia
Can cause ventilatory failure or cardiac arrhythmia
Can be caused by ingestion of carbs, salt intake, or exercise
Manage with potassium
What is thyrotoxic periodic paralysis
Accompanied by hypophosphatemia
Causes hypokalemia
Manage like hyperthyroidism
What are the labs and questions you want to ask to assess for Hypokalemia or Hyperkalemia
EKG
CMP
GFR and Crt
Aldosterone
Medications
Management of Hyperkalemia
Treat if K >6.5
Insulin R 10 units with D5 amp
Calcium gluconate 1g/10mls for cardiac protection
Albuterol neb 20mg/4mls for temporary decrease
Bicarb (only useful in severe metabolic acidosis)
Diuretics
K Binder (kayexalate)
HD
Management of Hypokalemia
Replete low K+ 10meq corrects by 0.2 mmol K+