Drug induced hypertensive emergencies are often short lived, and often aggressive therapy is not needed. Cocaine in particular is noted to be associated with hypertension, ventricular arryhthmias, and acute coronary syndromes. The important key to the treatment of this toxicity is avoiding the use of beta blockers (Class III), especially nonselective agents such as propranolol, as this allows for unopposed alpha adrenergic stimulation and worsening of the hypertension (1). Benzodiazepines (Class IIa) in addition to a short acting, titrateable antihypertensive such as nitrates (Class I) should be the first line of therapy. Should the hypertension be refractory, the use of alpha adrenergic blocking agents (Class IIb) may be considered, keeping in mind that tachycardia and hypotension may result (2).

What should be the response to tricyclic overdose?

Tricyclic antidepressants (TCA) are sodium channel blockers that may result in prolongation of ventricular conduction (increases the PR and QT intervals) and ultimately monomorphic VT (3). The most common clinical features are dry mouth, blurred vision, dilated pupils, sinus tachycardia, pyramidal neurological signs, and drowsiness. In severe poisoning, there may be coma, convulsions, respiratory depression, hypotension, and arrythmias.

Treatment of poisoning due to the TCAs is mainly supportive, however, gastric aspiration and lavage has been recommened by some (4). As these patient are often hypoxemic and acidotic, respiratory alkalosis can be induced as a temporizing measure, until the drug of choice sodium bicarbonate (Class IIa) can be used. Convulsions should be treated with diazepam or chlormethiazole. Hypotension should be treated by fluid replacement and sympathomimetic agents (dopamine or dobutamine) if necessary. Antiarrhythmic drugs, e.g., lidocaine and procainamide (Class indeterminate), should be employed only if there is evidence of circulatory failure which fails to respond to correction of hypotension, as their effects have not been adequately studied. Although physostigmine salicylate can reverse most of the features of TCA poisoning, its effects are short-lived in serious toxicity and it can produce significant side effects. As such, physostigmine should be reserved for those patients who have complications of coma or who have resistant cardiotoxicity or convulsions. Finally, drug screening and quantitative determination of tricyclic antidepressant serum concentrations can be useful in a minority of patients who have severe, unusual or prolonged symptoms.

What should the response be to acute opiate overdose?

If a pulse exists in patients with respiratory insufficiency suspected of an opiate overdose, naloxone should be administered, either intramuscularly, subcutaneously, or intravenously. IM and SC routes may provide less risk of severe withdrawal in patients addicted to IV narcotics. The initial dose of naloxone in 0.4-0.8 mg IV or 0.8 mg IM or SC and should be given to the desired endpoint of adequte airway reflexes and ventilation (2). The goal of complete arousal is not recommended, as the abrupt withdrawal from opiates may increase such complications as pulmonary edema, ventricular arrhythmias, and severe agitation (5).

Author's note: Please see the Question of the Day for March 6, 2001 for the resuscitation drug classification schema.