QRS interval prolongation

A. Assessment. Examples of drugs and toxins causing QRS interval prolongation are listed in Table 1-5. 

QRS interval prolongation of greater than 0.12 seconds in the limb leads (Figure 1-4) strongly indicates serious poisoning by tricyclic antidepressants (see p 90) or other membrane-depressant drugs (eg, quinidine [p 324], fleoainide [p 78], ohioroquine [p 165], and propranolol [p 131]). 

QRS interval prolongation may also result from a ventricular escape rhythm in a patient with complete heart block (eg, from digitalis, calcium antagonist poisoning, or intrinsic cardiac disease). 

B. Complications. QRS interval prolongation in patients with tricyclic antidepressant or similar drug poisonings is often accompanied by hypotension, AV block, and seizures. 

Sinus tachycardia and supraventricular tachycardia accompanied by QRS interval prolongation (eg, with tricyclic antidepressant poisoning) may have the appearance of ventricular tachycardia (see Figure 1-4). 

B. Specific drugs and antidotes. There are no specific antidotes. Sodium bicarbonate (see p 419) has not been studied, but it has been recommended for lamotrigine-induced QRS interval prolongation. 

Diagnosis. A noncyclic antidepressant overdose should be suspected in patients with a history of depression who develop lethargy, coma, or seizures. These agents do not generally affeot cardiac conduction, and QRS interval prolongation should suggest a tricyclic antidepressant overdose (see p 90). 

Sinus tachycardia accompanied by QRS interval prolongation may resemble ventricular tachycardia (see Figure 1-4, p 12). True ventricular tachycardia and fibrillation may also occur. Atypical or polymorphous ventricular tachycardia (torsade de pointes see Figure 1-7, p 15) associated with QT interval prolongation may occur with therapeutic dosing, but is actually uncommon in overdose. Development of bradyanhythmias usually indicates a severely poisoned heart and carries a poor prognosis. 

In patients with QRS interval prolongation or hypotension, administer sodium bicarbonate (see p 419), 1-2 mEq/kg IV, and repeat as needed to maintain the arterial pH between 7.45 and 7.55. Sodium bicarbonate may reverse membrane-depressant effects by increasing extracellular sodium concentrations and by a direct effect of pH on the fast sodium channel. 

IV. Diagnosis. The findings of hypotension and bradycardia, particularly with sinus arrest or AV block, in the absence of QRS interval prolongation should suggest calcium antagonist intoxication. The differential diagnosis should include beta blockers and other sympatholytic drugs. 

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