Potassium blood level is dependent on the association between dietary potassium intake, the distribution of potassium between the cells and extracellular fluid, and urinary potassium excretion.1 Potassium secretion is dictated by an increase in the serum potassium concentration, a rise in plasma aldosterone concentration, and enhanced delivery of sodium and water to the distal secretory site.1 All of these factors contribute to potassium homeostasis- a disruption of one property will cause hypokalemia or hyperkalemia.
The normal dietary intake of potassium is 40 to 120 milliequivalents per day; most of this potassium is excreted in the urine. A function of the kidney is to regulate blood levels of potassium to maintain homeostasis. In the event of poor potassium intake, the kidney can lower potassium excretion to about 5 to 25 milliequivalents, thus maintaining a baseline serum potassium level of 3.5 milliequivalents per liter.2-3 Hypokalemia is a clinical sign of depressed potassium levels that is due to poor intake of potassium combined with other causes of hypokalemia. We enumerate the causes:
Symptoms of hypokalemia manifest when serum potassium levels fall below 3.0 milliequivalents per liter and these symptoms resolve once hypokalemia is corrected. These symptoms may include cardiac arrhythmias and electrocardiogram abnormalities such as ventricular tachycardia/ventricular fibrillation, paroxysmal atrial or junctional tachycardia, premature atrial and ventricular beats, sinus bradycardia, and atrioventricular block.4 Characteristic ECG changes in hypokalemia include ST segment depression, a decrease in T wave amplitude, and an increase in U wave amplitude. U waves are usually seen in the precordial leads of V4 to V6 (refer to Figure 1).
Figure 1. Hypokalemia ECG changes.
Other manifestations of hypokalemia include muscle weakness and rhabdomyolysis, as well as renal abnormalities: impaired concentrating ability, increased ammonia production, increased bicarbonate reabsorption, altered sodium reabsorption, hypokalemic nephropathy and elevated blood pressure.5
Hyperkalemia results when there is impaired excretion of potassium due to acute or chronic kidney disease, or disorders or drugs that inhibit the rennin-angiotensin-aldosterone axis. It causes cardiac conduction abnormalities, cardiac arrhythmias, muscle weakness, and paralysis.6 These signs and symptoms manifest when the serum potassium concentration is greater than or equal to 7.0 milliequivalents per liter. Treatments involve inducing potassium loss.6-8
Electrocardiogram changes in hyperkalemia include a tall peaked T wave. As the degree of hyperkalemia becomes more severe, there is slowing of impulse conduction throughout the myocardium; the PR interval and QRS duration increases with a variety of conduction disturbances as follows:9
However, there is no significant correlation between the progression and severity of ECG changes with the serum potassium concentration.
Figure 2. ECG changes in hyperkalemia.
Ascending muscle weakness is a manifestation of hyperkalemia that can progress to flaccid paralysis that is comparable to Guillain-Barre syndrome.10 Hyperkalemic periodic paralysis is an autosomal dominant mutation of sodium channels in skeletal muscles. Myopathic weakness develops in these patients after an increased intake of potassium or resting after vigorous exercise.
Careful monitoring of electrocardiogram changes and muscle weakness in hyperkalemia is important to determine its functional consequences. If these are observed to be severe, immediate correction of hyperkalemia is essential. If serum potassium increases rapidly, cardiotoxicity will ensue.