Special Feature - Hyperkalemia: Electrocardiographic Recognition and Initial Therapeutic Considerations
Hyperkalemia: Electrocardiographic Recognition and Initial Therapeutic Considerations
By William J. Brady, MD
Hyperkalemia is an electrolyte disorder with life-threatening potential. The spectrum of clinical presentation is wide, ranging from asymptomatic laboratory discovery to cardiac arrest. The most common cause is red blood cell hemolysis, which occurs after the patient’s blood sample has been obtained. Hyperkalemia also frequently is encountered in patients with renal failure (both acute and chronic); diabetic ketoacidosis and other acidotic states; digoxin toxicity; type IV renal tubular acidosis; and medication-related issues (agents that affect kidney function or the renal reclamation of potassium).
The electrocardiographic manifestations of hyperkalemia may involve all phases of the cardiac impulse. The expected progression of electrocardiographic changes associated with hyperkalemia is well described.1 (See Table 1.) Significant variation may be found among patients at any particular serum potassium level, however. Furthermore, the electrocardiogram (ECG) may not demonstrate classic abnormality in all patients;2-5 in fact, the ECG may appear normal, non-specifically abnormal, or may reveal unusual abnormalities such as a heart block and bundle branch block.
|
Characteristic Changes in the ECG
Peaked or prominent T waves in the precordial leads are among the earliest and most common findings on the ECG. Modest increases in the serum potassium enhance or accentuate repolarization of the myocyte, which are manifested electrocardiographically by alterations in the T wave.2 (See Figure 1.) The T wave becomes prominent and is described as tall and narrow with a symmetric structure. The polarity of the T wave also may change, particularly in patients with left ventricular hypertrophy, with the normally inverted lateral T waves becoming upright or "pseudonormalized."4
|
Continued increase in the serum potassium will produce a slowing or prolongation of cardiac conduction. All cardiac myocytes are sensitive to elevated potassium levels, but atrial tissue is significantly more sensitive. The P wave will lessen in amplitude early in the process, with complete disappearance as the potassium rises. Despite the electrocardiographic loss of the P wave, sinus rhythm continues with maintained sinus node activity.6 In fact, sinus impulses (bypassing the atria) are conducted along internodal tracts directly to the atrioventricular node, creating the "sinoventricular" rhythm of hyperkalemia.2,6 At progressively higher serum levels, the QRS complex widens (See Figure 2), at times resembling a bundle branch block. Eventually, the QRS complex blends with the T wave, forming a "sine-wave" appearance on the ECG. Progressive increases in the potassium level eventually result in ventricular fibrillation and asystole.4
|
Treatment of Hyperkalemia
The resuscitative management of hyperkalemia (see Table 2) is guided in large part by the patient’s clinical situation, including the electrocardiographic findings; in fact, the ECG should guide both the urgency as well as the magnitude of therapy. The goals of therapy are a reduction of the serum potassium level coupled with a stabilization of the myocardial cell membrane. The serum potassium temporarily is reduced with a transient shift of the electrolyte intracellularly, and permanently lowered with potassium removal from the body.
Stabilizing the Cardiac Membrane. Response to therapy is often prompt with real-time changes noted on the electrocardiographic monitor. (See Figure 3.) The most appropriate initial medication is calcium, which works by restoring a more appropriate electrical gradient across the cell membrane. In essence, calcium "fools" the cell into thinking that a more "normal" electrical difference exists between the intracellular and extracellular compartments. Intravenous administration of calcium will result in a transient narrowing (lasting no longer than 30 minutes) of the QRS complex, and thus is most appropriately given to the patient with a widened QRS complex. Note that calcium does not cause intracellular shift of potassium. Calcium chloride (13.6 mEq/10 mL) contains roughly three times the elemental calcium of that in the gluconate preparation (4.6 mEq/10 mL); calcium chloride should be administered through a large peripheral vein, if possible, in that it is highly sclerosing. The dose is 10 mL IV over one minute in the patient with spontaneous circulation; with cardiac arrest, a similar dose is given via rapid IV push. The maximum dose is 20 mL within any given 30-minute period; repeat administrations may be required. Extreme caution is advised in the setting of hyperkalemia related to digoxin toxicity; anecdotal reports suggest an increased tendency towards asystole in this clinical setting.
|
Transcellular Potassium Shift. Several agents are capable of transiently moving potassium from the extracellular to intracellular space. (See Table 2.) This intracellular shift is short-lived, yet temporarily will reduce cardiac irritability and stabilize the patient while more definitive therapies are arranged. These medications include glucose/insulin, beta-adrenergic agonists, magnesium, sodium bicarbonate, and intravenous saline. Note that the potassium-lowering effect of these various therapies is transient, with repeat administration necessary if hemodialysis has not been initiated.
Potassium Removal. Complete and permanent removal of potassium from the body is accomplished via furosemide-hastened saline diuresis, binding resins, and dialysis. (See Table 2.) Hemodialysis is the treatment of choice in such situations and should be employed in the vast majority of patients who presented with a sine-wave QRS complex or who have experienced cardiac arrest related to hyperkalemia. Peritoneal dialysis may be used, yet it removes less potassium over a much longer period of time compared with hemodialysis.
References
1. Mattu A, et al. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000;18:721-729.
2. Martinez-Lopez JI. ECG of the month. Harbinger of evil. Hyperkalemia. J La State Med Soc 1997;149:103-104.
3. Pick A. Arrhythmias and potassium in man. Am Heart J 1966;72:295-306.
4. Martinez-Vea A, et al. Severe hyperkalemia with minimal electrocardiographic manifestations: A report of seven cases. J Electrocardiol 1999;32:45-49.
5. Yu AS. Atypical electrocardiographic changes in severe hyperkalemia. Am J Cardiol 1996;77:906-908.
6. Dittrich KL, et al. Hyperkalemia: ECG manifestations and clinical considerations. J Emerg Med 1986;4:449-455.
Dr. Brady, Associate Professor of Emergency Medicine and Internal Medicine, Vice Chair, Emergency Medicine, University of Virginia, Charlottesville, is on the Editorial Board of Emergency Medicine Alert.
Hyperkalemia is an electrolyte disorder with life-threatening potential. The spectrum of clinical presentation is wide, ranging from asymptomatic laboratory discovery to cardiac arrest.
Subscribe Now for Access
You have reached your article limit for the month. We hope you found our articles both enjoyable and insightful. For information on new subscriptions, product trials, alternative billing arrangements or group and site discounts please call 800-688-2421. We look forward to having you as a long-term member of the Relias Media community.