Shock, cardiogenic; disulfiram/poisoning, adverse effects.Drug intoxication with disulfiram is a rare condition that may lead to severe and potentially fatal cardiovascular manifestations such as cardiogenic shock. We report the case of a female patient with refractory shock after deliberate self-poisoning with disulfiram. Clinical, biochemical and echocardiographic assessment, as well as invasive monitoring confirmed cardiogenic shock associated with this drug. The known mechanisms of action of disulfiram are discussed, and the major collateral effects, especially cardiovascular effects, are described. We underscore the importance of suspecting this diagnosis and of adopting prompt and the most adequate therapeutic approach in this context. Cardiogenic Shock Caused by Disulfiram Case ReportA 49-year-old female patient with major depression and chronic alcoholism was admitted to the emergency room four hours after deliberate ingestion of 60 disulfiram tablets (15g), 16 clonazepam tablets (8mg) and six maprotiline tablets (450mg), in association with alcohol.Her clinical examination was notable for sleeplessness, tachypnea, and poor peripheral perfusion. Blood pressure: 68 x 35mmHg; heart rate: 105 bpm. Pulmonary auscultation revealed diffuse coarse crackles.Laboratory studies were significant for increased C-reactive protein (CRP) -31 mg/dL. Her blood gas showed severe hypoxemia (PaO 2 66 mmHg, with FiO 2 85%).Markers of myocardial ischemia resulted negative. Electrocardiography showed sinus tachycardia, with no changes consistent with acute ischemia. Chest radiography showed alveolar opacities bilaterally (Figure 1).Volume resuscitation measures were introduced immediately, followed by dopamine. Blood cultures were collected and broad-spectrum antibiotic therapy was started. Despite these measures, the patient remained in refractory shock and progressed with worsening of the respiratory distress and increasing desaturation. Orotracheal intubation was required and mechanical ventilation was started. The patient was transferred to the ICU.The clinical picture was initially interpreted as mixed -cardiogenic and septic -shock. Sepsis was assumed as the major component, having possibly originated from aspiration pneumonia due to prostration. The cardiogenic component could result from the collateral effects of the medications taken.

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