Volume 5 Supplement 1
Combined verapamil and atenolol poisoning: resolution of cardiogenic shock with enoximone
© The Author(s) 2001
Received: 15 January 2001
Published: 2 March 2001
A 57-year-old man (b.w. 75 kg), two previous myocardial infarctions and major depressive disorders, was admitted to the emergency room about 1 hour after suicidal ingestion of 2800 mg atenolol and 1600 mg verapamil. The patient was pale, cold, comatose and showed respiratory insufficiency which needed intubation and mechanical ventilation. Hemodynamic monitoring was started, including heart rate (HR), invasive blood pressure (BP) measurement, pulmonary artery pressures and cardiac output (CO). Despite aggressive inotropic therapy with dopamine 30 µg/kg/min, adrenaline 10 µg/kg/min and calcium chloride (4 g total), clinical conditions progressively worsened: BP was 80/60 mmHg, HR was 65 bpm, CO 1.4 l/min, SVR 3371 dyne/s/cm-5, central venous pressure (CVP) 16 mmHg and PCWP 18 cmH2O; urine output dropped to zero.
Four hours after ingestion, a bolus dose of enoximone 1 mg/kg was administered, followed by a continuous infusion at 0.5 mg/kg/h. During the following hours the patient's clinical condition markedly improved: CO increased up to 6 l/min, HR stabilized at 80 bpm, PCWP reduced to 11 mmHg and CVP to 8 mmHg, blood pressure raised to 135/75 mmHg, SVR decreased 1045 dyne/s/cm-5, urine output was stable at 150 ml/h. Adrenaline infusion was progressively reduced and stopped after 24 hours, while enoximone was discontinued on 5th day. Dopamine infusion was maintained at low rates for 10 days after the ingestion. The patient recovered a normal neurological and hemodynamic status, was extubated and dismissed from the ICU on 14th day.
Discussion and conclusions
Most common features of acute beta-blockers poisoning are hypotension, bradycardia and depression of level of consciousness. Calcium channel blockers, particularly verapamil, have an additive effect with beta-blockers and therefore enhance their cardiovascular toxicity, causing severe cardiogenic shock, which can be, as in this case, unresponsive to even high doses of cathecolamines [1,2].
The use of a phosphodiesterase III inhibitor, as enoximone, can bypass the effect of beta-blockers and restore a sufficient cardiac output, without increasing myocardial oxygen consumption, which should be avoided when past history includes angina pectoris or myocardial infarction, as in this case [3,4].
This report strongly supports the use of enoximone in combined beta-blockers and CCBs intoxication and suggests its administration particularly when cathecolamines have been showed ineffective.
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