No therapy has been proved to be effective for patients with severe chloroquine poisoning, which is usually fatal. In a retrospective study of 51 cases, we found that ingestion of more than 5 g of chloroquine was an accurate predictor of a fatal outcome, and therefore chose this dose as the criterion for severe chloroquine poisoning. We selected as a control group 11 consecutive patients who had ingested more than 5 g of chloroquine between July 1983 and December 1985. We then undertook a prospective study to determine whether a better outcome could be obtained with immediate mechanical ventilation and the administration of diazepam and epinephrine. Eleven consecutive patients who ingested more than 5 g of chloroquine in 1986 received this combination therapy. Ten of these patients survived, whereas only one control had survived (P = 0.0003). There was no significant difference between the combination-therapy and control groups in age (29 +/- 3 vs. 27 +/- 2 years), amount of chloroquine ingested (7.5 +/- 0.5 vs. 8.5 +/- 0.8 g), systolic arterial pressure (74 +/- 2 vs. 74 +/- 3 mm Hg), or QRS duration (0.14 +/- 0.01 vs. 0.14 +/- 0.01 second). In our combination-therapy group, blood chloroquine levels ranged from 40 to 80 mumol per liter, whereas a literature search showed that no patient in whom blood levels were more than 25 mumol per liter had survived. These preliminary data suggest that combining early mechanical ventilation with the administration of diazepam and epinephrine may be effective in the treatment of severe chloroquine poisoning.

In conclusion, HECVs appear to be antigenically distinct from viruses of the Berne-Breda group and antigenically related to HCV OC43. The preliminary characterization of HECV polypeptides appears promising and suggests that more-extensive studies on HECV should be done to obtain futher data on its biology and to further define its epidemiology and its pathological role.

SUMMARYIn eight mechanically ventilated patients in cardiogenic shock, we assessed the hemodynamic effects of an infusion of dopamine and dobutamine and evaluated its role in preventing the deleterious effects of administering each amine alone. Each patient received three infusions in a randomly assigned order: dopamine, 15 ,.tg/kg/min; dobutamine, 15 ,tg/kg/min; and a combination of dopamine, 7.S ,g/kg/min, and dobutamine, 7.5 ,ug/kg/min. Stroke volume index increased similarly with the three infusions, but dopamine alone increased oxygen consumption (p < 0.05 vs dobutamine alone and dopamine-dobutamine combined). The dopamine-dobutamine combination increased mean arterial pressure (p < 0.05 vs dobutamine), maintained pulmonary capillary wedge pressure within normal limits (p < 0.05 vs dopamine), and prevented the worsening of hypoxemia induced by dopamine (p < 0.05). The dopamine-dobutamine combination appears to be useful in the management of mechanically ventilated patients in cardiogenic shock.THE HEMODYNAMIC PICTURE of heart failure is characterized by a decrease in stroke volume and an increase in ventricular filling pressures. When acute pump failure is so severe that an adequate cardiac output cannot be maintained, hypotension supervenes despite the elevated peripheral resistance, and cardiogenic shock ensues. In this setting, diuretics and vasodilators cannot be used alone, and the therapeutic use of sympathomimetic amines such as dopamine and dobutamine is required.Dopamine, a precursor in the endogenous synthesis of norepinephrine, is a potent inotropic agent.I-1 It increases stroke volume both by a direct action and through the release of norepinephrine stores.4 When dopamine is used at a dose of 10-15 ig/kg/min, vasopressor effects appear. These effects are of particular value in patients with hypotension.5 However, an important side effect limits its use in cardiogenic shock: At a dose of 10 to 15 ,ug/kg/min, it may induce an increase in pulmonary capillary wedge pressure (PCWP). As a result, its use may be associated with pulmonary vascular congestion, arterial desaturation and increase in venous admixture.6 Dobutamine is also a potent inotropic agent that acts directly on adrenergic myocardial receptors without any release of norepinephrine from nerve endings.' In the treatment of severe heart failure, dobutamine induces an increase in cardiac output and stroke volume with a reduction of PCWP.6 In contrast to dopamine, dobutamine probably has minimal direct vascular activity even when it is used at higher dosages. However, a reduction in systemic arterial resistance (SAR), frequently accompanied by a slight fall in mean arterial pressure (MAP), generally occurs during dobutamine infusion in patients with chronic, low-output cardiac failure.8 This decrease in SAR may be due to a reduc- tion in compensatory vasoconstriction secondary to an improvement in stroke volume index (SVI). The aim of this study was to assess the efficacy of a combined dopamine-dobutamine infusion, 7.5 Ag/kgl min each, in t...