Seizures, ventricular tachycardia, and rhabdomyolysis as a result of ingestion of venlafaxine and lamotrigine.

Few cases of overdoses have been described involving venlafaxine, lamotrigine, or a combination of the two agents. We describe a combined venlafaxine and lamotrigine ingestion in a patient presenting with a seizure, ventricular tachycardia, and rhabdomyolysis. We conclude that patients with overdoses that involve venlafaxine can exhibit severe cardiac effects in addition to seizures, especially if venlafaxine is combined with other agents.

A unique left-to-right shunt characterized by multimodality cardiac imaging.

We describe the first reported patient with a persistent left superior vena cava that communicates directly with the left atrium as an isolated congenital defect. She developed mitral stenosis and physiologic conditions that favored left-to-right shunting--a modified Lutembacher's syndrome. Noninvasive cardiac imaging completely elucidated her cardiac anatomy and physiology.

Tricyclic antidepressants in red cells and plasma: correlation with impaired intraventricular conduction in acute overdose.

OBJECTIVE: Tricyclic antidepressant levels in red blood cells and plasma in acute overdose and their association with cardiotoxicity were studied. METHODS: This was a prospective study in 15 patients with acute tricyclic antidepressant overdose. Tricyclic antidepressant parent compounds and metabolites were measured in red blood cells and plasma, and tricyclic antidepressant levels were correlated with ECG indexes of toxicity. RESULTS: Plasma levels of the parent compounds were higher than their red blood cell levels on admission (mean +/- SD, 691 +/- 409 and 337 +/- 220 ng/ml, respectively). Admission metabolite levels were higher in red blood cells than in plasma (264 +/- 180 and 190 +/- 164 ng/ml, respectively). QRS duration and the red blood cell levels of the metabolites were significantly correlated at the time of admission (r = 0.77, p < 0.01), as well as at 6 to 10 hours (r = 0.74, p < 0.01). CONCLUSIONS: In acute overdose, a shift of tricyclic antidepressants from plasma to red blood cells and increased levels of red blood cell metabolites reflect tissue redistribution of the drug. Tricyclic antidepressant red blood cell metabolites are the best markers for impaired intraventricular conduction.

Hyperventilation. Benign symptom or harbinger of catastrophe?

Hyperventilation is a common feature of many acute clinical conditions that can be benign or potentially catastrophic. The symptoms accompanying hyperventilation are diverse and non-specific, reflecting a physiologic state of hypocapnia secondary to alveolar overventilation. Results of arterial blood gas analysis confirm hypocapnia and may lead to identification of the clinical cause, with pH or PaO2 measurements indicating acid-base abnormalities or hypoxemia. Treatment should be directed at correcting the underlying clinical condition. In patients whose hyperventilation is caused by anxiety states, anxiolytic drug therapy in the acute phase should be followed by education, reassurance, retraining to change breathing patterns, and psychotherapy.

Cardiopulmonary resuscitation. A current perspective.

Cardiopulmonary resuscitation is effective if established early and coupled with specific therapeutic interventions. Most cardiopulmonary arrest is due to ventricular fibrillation and early defibrillation offers the highest probability of success. External cardiac compression alone is inadequate to provide adequate perfusion to vital organs and, therefore, cannot sustain life unless coupled with advanced therapeutic interventions. Many new techniques for increasing flow have been developed, but have not been established clinically. The American Heart Association guidelines for CPR are still valid and are the basis for our current CPR. A practical perspective is presented whereby the therapeutic interventions are pursued systematically in an expeditious and coordinated fashion so that the key interventions are made within the first 10 to 15 minutes of the arrest.

Reversal of tricyclic-antidepressant-induced cardiac conduction abnormalities by phenytoin.

Ten patients with cardiac conduction defects due to severe tricyclic antidepressant poisoning were successfully treated with intravenous phenytoin. Eight patients had combined first degree AV block and intraventricular conduction delay; one patient had first degree AV block alone; and one patient had intraventricular conduction delay alone. Phenytoin was injected at a rate of 50 mg/min in amounts not exceeding 500 mg (approximately 5 mg/kg to 7 mg/kg). Five patients had complete normalization within 46 min. The remaining five patients showed improvement in their conduction defects shortly after phenytoin treatment, with complete normalization occurring within 14 hr. This investigation demonstrated the effectiveness of phenytoin in reversing tricyclic-antidepressant-induced cardiac conduction abnormalities. Phenytoin is a logical drug for the treatment of severe tricyclic antidepressant poisoning signalled by first degree AV block and/or intraventricular conduction delay.