Steven H. Mitchell1, Christopher P. Holstege2, and William J. Brady3 1 Department of Emergency Medicine, University of Washington School of Medicine, Seattle, WA, USA 2 Division of Medical Toxicology, Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA, USA 3 Departments of Emergency Medicine and Medicine, University of Virginia School of Medicine, Charlottesville, VA, USA The proliferation and wide spread usage of medications that result in cardiotoxicity in overdose is a reality of prehospital medicine today. Toxicity can result in a variety of electrocardiographic changes that pose life‐threatening risks to the patient. Clinicians managing the overdose patient should be aware of the various electrocardiographic changes that can potentially occur in the acutely poisoned patient. ECG abnormalities including the PR interval prolongation, widening of the QRS complex, alterations in the T wave and the ST segment, and lengthening of the QT interval can all be seen (Figure 15.1). Potential toxins can be placed into broad classes based on their cardiac effects (Box 15.1). Recognizing changes consistent with each class will assist the clinician in determining the severity of toxicity and its associated risks; also, recognizing these changes can suggest the most appropriate therapy in overdose situations (Box 15.2). The primary medication toxicity classes are discussed in detail below. Myocardial repolarization, which is represented electrocardiographically by the T wave, is predominantly created by potassium moving out of cardiac cells. Blockade of the outward potassium movement prolongs the action potential and subsequently prolongs the QT interval of the ECG (Figure 15.1). In these situations, patients can experience ventricular dysrhythmias, including torsades de pointes. Commonly encountered medication classes include antibiotics, antiemetics, and antihistamines (Table 15.1). A prolonged QT interval (Figure 15.2a) is the hallmark of potassium efflux blocking agents and may result in vulnerability to reentry rhythms such as polymorphic ventricular tachycardia, most often in the form of torsades de pointes (Figure 15.2b). The QT interval is measured from the beginning of the QRS complex to the end of the T wave and is influenced by the patient’s heart rate. Several formulas have been developed to correct the QT interval for the effect of heart rate using the RR interval. When evaluating a rhythm strip for a patient in sinus rhythm, a QT interval that is greater than half the RR interval may indicate QT interval prolongation (Figure 15.2c). Computerized ECG interpretations report the corrected interval as the QTc, using the formula QTc = QT/√RR. In general, the QTc is considered prolonged when it exceeds 450 ms; specifically, the QT interval is considered long when the QTc interval is greater than 440 ms in men and is greater than 460 ms in women. Arrhythmias are most common with values greater than 500 ms. The cardiac sodium channels are located in the cell membrane and open rapidly in response to an action potential. This rapid opening of sodium channels leads to cell depolarization, which in turn propagates the action potential throughout the ventricles. The QRS complex represents depolarization of cardiac myocytes located in the right and left ventricles. Blockade of sodium influx causes a widening of the QRS complex (Figure 15.1). Common medications that are sodium channel blocking agents include antidepressants, antiarrythmics, and diphenhydramine (Table 15.2). Figure 15.1 Impact of sodium channel and potassium efflux blocking drugs on the ECG with QRS complex widening and QT interval prolongation. Electrocardiographic manifestations of the sodium channel blocking agents: Sodium channel blockage manifests electrocardiographically as a widened QRS complex, usually greater than 120 ms. Early stages of toxicity affect the first phase of depolarization (phase 0) and as a result, the upslope of depolarization is slowed. As toxicity increases and fewer sodium channels are available for depolarization, the QRS complex continues to widen (Figure 15.3
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The Electrocardiogram in the Poisoned Patient
Potassium Efflux Blocking Agents
Electrocardiographic Manifestations of the Potassium Efflux Blocking Agents
Sodium Channel Blocking Agents
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