Treatment of patients with cocaine-induced arrhythmias: bringing the bench to the bedside

Abstract

Widespread use of cocaine and its attendant toxicity has produced a wealth of benchwork studies and small animal investigations that evaluated the effects of cocaine on the cardiovascular system. Despite this wealth of knowledge, very little is known about the frequency or types of arrhythmias in patients with significant cocaine toxicity. The likely aetiologies; catecholamine excess, sodium channel blockade, potassium channel blockade, calcium channel effects, or ischaemia may act alone or in concert to produce a vast array of clinical findings that are modulated by hyperthermia, acidosis, hypoxia and electrolyte abnormalities. The initial paper in the series by Wood & Dargan providing the epidemiological framework of cocaine use and abuse is followed by a detailed review of the electrophysiological effects of cocaine by O'Leary & Hancox. This review is designed to complement the previous papers and focuses on the diagnosis and treatment of patients with cocaine-associated arrhythmias.

Figure 2

Figure 2 shows a wide-complex tachycardia most likely resulting from sodium channel blockade in a patient with clinical signs and symptoms of acute cocaine toxicity. Note again the prominent R wave in lead aVR. This patient was treated simultaneously with oxygen, diazepam, hypertonic sodium bicarbonate and intravenous fluids, and the ECG normalized

Figure 1

Figure 1A demonstrates the early sodium channel blocking effects of cocaine. Specifically demonstrated are the presence of an S wave in leads I and aVL and an R wave in lead aVR. The QRS duration is slightly prolonged at approximately 120 ms. Figure 1B shows the the ECG on the same patient from Figure 1A immediately following the infusion of 44 mEq of hypertonic sodium bicarbonate. Note that the QRS duration has narrowed significantly and that the changes in leads I, aVL and aVR have essentially normalized

Figure 3

Rabbits were intubated endotracheally and sedated with xylazine. Figure 3A demonstrates the heart rate (and corresponding blood pressure following an LD₁₀ dose of cocaine. The heart rate increases from baseline (120 beats min⁻¹) to nearly 200 beats min⁻¹. In Figure 3B a larger (LD₉₀) dose of cocaine is given. The heart rate slows, the QRS prolongs, the T waves become large and peaked (as in hyperkalaemia), the blood pressure falls and heart block develops. In Figure 3C, the rabbit from Figure 3B has been given 100% oxygen and 1 mEq kg⁻¹ of hypertonic sodium bicarbonate. A regular rhythm returns at a rate of nearly 300 beats min⁻¹ (note the speed of the chart recorder was changed to capture more information) with a narrow QRS complex and restoration of blood pressure