LAUSR

A 52-year-old male with no previous history of heart disease was referred to our emergency room for impaired consciousness due to intentional exposure to carbon monoxide (CO). His Japan Coma Scale was 100 and his blood pressure was 111/45 mmHg. Sinus tachycardia (heart rate of 120 beats/ min) was revealed. Laboratory tests showed elevation of carboxyhemoglobin (CO-Hb) (42.5%), creatine kinase (3365 U/L) and troponin I (179 pg/mL) levels. Although, CO-Hb (6.4%) was improved after intubation and ventilation with FiO2 of 100%, hypotension (90/60 mmHg) persisted. Initial transthoracic echocardiography (TTE) performed 7 h after hospitalization revealed general severe hypokinesis of both the left ventricle (LV) and right ventricle (RV) with severe systolic dysfunction (Fig. 1a–d). CO-induced myocardial damage of both ventricles was suspected, and hyperbaric oxygen therapy (HBOT) was performed at 8 h (100%-oxygen at 2.8 atmospheres absolute (ATA) for 60 min and 2.0 ATA for 60 min) and 25 h (100%-oxygen at 2.0 ATA for 120 min) after hospitalization. Intravenous inotropic agents (dopamine 5 μg/kg/min and noradrenaline 0.3 μg/kg/min) were required for maintaining his hemodynamic status until successful treatment with HBOT. Second TTE performed 30 h after hospitalization showed normalized wall motion of both ventricles and notable improvement of both LV and RV systolic function (Fig. 1d–g). LV diastolic dysfunction found in the first TTE (E/A 0.6 and septal e′ 8.0 cm/s) was also significantly improved in the second TTE (E/A 1.2 and septal e′ 12.1 cm/s). Further improvement of LV systolic function (ejection fraction 63%) was observed in the third TTE performed 8 days after admission. CO-induced myocardial dysfunction might occur when CO-Hb is greater than 25% [1], and the proposed mechanism of global LV dysfunction after CO poisoning is myocardial stunning due to a catecholamine surge [2]. CO-induced myocardial dysfunction was found in 22–57% of patients who underwent TTE after CO poisoning [2, 3]. Approximately one-third to half of these patients showed global LV wall motion abnormality, as was seen in present case. Most prior studies [2, 3] focused on LV dysfunction after CO poisoning. RV dysfunction after CO poisoning was shown in only a few studies [3, 4]. RV dysfunction after CO poisoning was confirmed in our case, and there was rapid improvement of RV function after HBOT, as has been shown for LV function after HBOT [5]. The findings in our case indicate that TTE is useful for detection of biventricular CO-induced myocardial dysfunction and for evaluation of improvement in biventricular function after HBOT. Furthermore, not only LV function, but also RV function should be evaluated by TTE in patients with CO poisoning.