Frequent non-cardiac causes seen in the intensive care unit include severe electrolyte disturbances. These can be reflected in the ECG, as can the response to therapy. Hyperkalemia is common and can be fatal. It is often due to severe renal failure and can also result from potassium salts of penicillin, digitalis toxicity, or acidosis. The action potential across the cell membrane depends upon the concentration of ions across the membrane. Hyperkalemia shortens the action potential duration and slows conduction. Severe hyperkalemia can have negative inotropic effects and can increase the threshold for capture of artificial pacemakers. Hyperkalemia can lead to non-conducted atrial beats, asystole, ventricular tachycardia, ventricular fibrillation, and conduction disturbances including both type I and type II second-degree atrioventricular block, accelerated idioventricular ventricular rhythm, and ventricular escape rhythms. ECG changes progress from a flattened PR interval to peaked T waves, prolonged QRS, and prolonged QT intervals ( Fig 5). Severe arrhythmias including ventricular fibrillation can occur without warning.
Fig. 5 Manifestations of hyperkalemia: (a) 12-lead ECG for a patient with potassium level of 7.2 mg/dl shows sinus rhythm with left bundle branch block, slurring of the QRS and ST segments, increased QT interval, and symmetrically peaked T waves; (b) with decrease in potassium to 5.2 mg/dl following treatment with calcium gluconate, bicarbonate, glucose, and insulin, there is narrowing of the QRS, resolution of ST segment shifts, decrease in QT interval, and resolution of T-wave changes.
Hypokalemia can also cause severe arrhythmias, for example paroxysmal atrial tachycardia with block, atrioventricular block, atrioventricular dissociation, and ventricular fibrillation. It may increase the chance of digoxin toxicity and drug-induced long QT interval. ECG changes include a long QT interval, ST depression, decreased T waves, prominent U waves, and prolonged QRS duration. Hypokalemia can be worsened by coexisting hypocalcemia, which rarely causes rhythm abnormalities by itself but can lead to ST segment prolongation. Hypermagnesemia can prolong PR and QRS durations and lead to sinoatrial and atrioventricular blocks. Hypomagnesemia can worsen digoxin toxicity and facilitate ventricular arrhythmias.
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