ECG abnormalities are seen commonly with TCA toxicity and generally are useful in identifying patients at increased risk for seizures and ventricular dysrhythmias.
The "classic" TCA electrocardiogram is shown in Fig 152-1, consisting of sinus tachycardia, right-axis deviation (RAD), and prolongation of the PR, QRS, and QT
intervals. This "classic" ECG pattern is seen frequently in moderate to severe TCA toxicity, but its absence does not eliminate the possibility of TCA toxicity during the first 6 h after ingestion. Figure 15.2.-2 is an ECG 4 days later with near-complete resolution of all abnormalities. Moderate prolongation of the QT interval is noted frequently, even at therapeutic TCA doses. Nonspecific ST-segment and T-wave abnormalities are commonly observed in TCA overdose. Less common ECG abnormalities include right bundle branch block and high-degree atrioventricular blocks.
FIG. 152-1. "Classic" TCA electrocardiographic abnormalities. Sinus tachycardia and prolonged PR, QRS, and QT intervals. Also, right axis deviation (RAD) of terminal 40 ms.
FIG. 152-2. Repeat ECG 4 days later in the same patient as in Fig 152-1. Only mild QTc prolongation persists.
Life-threatening complications can occur in the absence of significant ECG abnormalities. 9 However, these complications are more likely in the presence of a widened QRS greater than 100 ms and/or RAD of the terminal 40 ms of greater than 120°. The risk of seizures increases as the QRS complex exceeds 100 ms, and ventricular dysrhythmias are more likely if QRS prolongation exceeds 160 ms. RAD is commonly demonstrated as a positive terminal R wave in lead aVR and a negative S wave in lead I (Fig 152:3). Both abnormalities are equally helpful in identifying patients at risk for serious toxicity. 11 They usually occur together but can occur in exclusion of each other. The development of RAD of the terminal 40 ms and/or QRS widening appears to be less predictable of TCA-induced cardiotoxicity in young children. 12 Pediatric ECGs tend to have a wider range of acceptable variant features, and this complicates the ECG identification of TCA toxicity.
FIG. 152-3. A. An example of terminal 40 ms RAD during TCA toxicity. Note the large R wave in aVR and S wave in lead I. B. The same patient after complete resolution of TCA toxicity. Note the decrease in the R wave height in aVR and S wave in lead I.
ECG abnormalities universally develop within 6 h of ingestion and usually resolve over 36 to 48 h. 13 The identification of either QRS widening greater than 100 ms or terminal RAD greater than 120° warrants sodium bicarbonate therapy and admission to a monitored hospital bed. Unfortunately, up to 10 percent of the population will have a prolonged QRS of more than 100 ms or terminal RAD without exposure to sodium channel blocking drugs. Therefore, these ECG abnormalities in isolation are not 100 percent specific for TCA toxicity. Most patients on TCA therapy do not have prior ECGs available for comparison. Thus, any observed ECG abnormalities must be assumed attributable to TCA exposure until proven otherwise.
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