Electrolyte homeostasis is the foundation of physiology. Even slight abnormalities in the concentration of any electrolyte can have significant effects on cardiovascular function. The management of electrolyte abnormalities is directed to prevent and treat life-threatening complications, to diagnose and treat the underlying cause, and if needed, to correct the electrolyte imbalance by repletion or removal of the unbalanced electrolyte. The severity of the electrolyte derangement should dictate the urgency of therapy but one should also remember that rapid correction of electrolytes might be detrimental.
Potassium, the major intracellular cation, exists in greater concentrations inside the cell as compared to the extracellular space. It is this difference in concentration that plays a crucial role in membrane potentials. In addition to its role in membrane potential, potassium also plays a role in neuromuscular excitability and cardiac rhythmicity. The normal range for serum potassium concentration is 3.5–5.5 mEq/L. The degree and duration of deviation in serum potassium concentration from this range is proportional to the severity of the clinical manifestations of hypo- or hyperkalemia.
Hypokalemia, simply defined as a serum potassium level less than 3.5 mEq/L, can be due to three main processes: (1) inadequate potassium intake, (2) altered potassium distribution between the intracellular compartment and the extracellular space, and (3) loss of potassium from the body. This loss can occur from the skin, gastrointestinal tract, or kidneys.
In most cases, mild hypokalemia (levels between 3.0 and 3.5 mEq/L) is asymptomatic. Clinically significant hypokalemia is generally defined as a serum potassium level less than 3.0 mEq/L. This increases the resting membrane and increases both the duration of the refractory period and the duration of the action potential, the former to a greater degree. This impairs the ability of the myocardial cell to depolarize and contract appropriately, potentially leading to arrhythmias. In addition, hypokalemia increases the resting membrane potential (hyperpolarization), which also leads to arrhythmias. The presence of other factors such as ischemic heart disease, preexisting arrhythmias, concurrent use of digitalis, increased beta adrenergic activity and hypomagnesemia can exacerbate hypokalemia and further the development of arrhythmias.
A wide range of arrhythmias may be seen in patients with hypokalemia, including premature atrial and ventricular contractions, atrial fibrillation, junctional tachycardia, ventricular tachycardia, and ventricular fibrillation.
Hypokalemia also produces characteristic electrocardiogram changes: ST segment depression, T wave depression, and prominent U waves, which are most often seen in the lateral precordial leads V4 to V6 (Figure 179-1). In addition, hypokalemia prolongs the QT interval. This is particularly significant in those patients with a pre-existing genetic predisposition to long QT syndrome or those patients who are concomitantly ingesting medications that prolong the QT interval as this can potentially trigger torsades de pointes.
Prominent U waves seen in hypokalemia. (Reproduced with permission from Knoop ...