10-12) Shortness of breath and low blood pressure can be symptoms of cardiac dysfunction.13) In this patient, shortness of breath and tachycardia were noted at the time of admission and these symptoms suggesting the presence of cardiac dysfunction.

Electrocardiographic changes are usually nonspecific and may be a misleading index of severity in CO intoxication.1),8) The evaluation of cardiac markers can be of considerable diagnostic value in the presence of chest discomfort or ischemic electrocardiographic changes. Troponin I and Inhibitors,research,lifescience,medical troponin T have been successfully used in the diagnosis of CO-induced cardiotoxicity.5),14) Echocardiography is a good screening tool for detection of CO-induced cardiotoxicity. Diffuse or segmental wall motion abnormality can be observed Inhibitors,research,lifescience,medical in patients with CO exposure. In clinical studies, echocardiography is more sensitive than electrocardiography in detecting CO-induced cardiac damage and more effective for severity assessment.8),15) In one study conducted by Satran et al.14) analyzed total 230 consecutive patients with intentional CO exposure. Of them, 53 patients were underwent echocardiographic examination and 57 percent of patients showed abnormal left ventricular function. Patients with global left ventricular dysfunction were younger (average age 43 years) with few cardiac risk selleck chemical factors and more severe CO poisoning. The proposed mechanism of global left ventricular dysfunction

is Inhibitors,research,lifescience,medical myocardial stunning as a result of CO poisoning. Patients with regional wall motion abnormalities were older (average age 64 years) with a higher frequency of cardiac risk factors. The possible mechanism is unmasking of underlying coronary arterial disease by creating myocardial demand/supply mismatch. Usually, the left ventricular Inhibitors,research,lifescience,medical dysfunction was normalized with conventional

Inhibitors,research,lifescience,medical treatment including high concentration of oxygen. In our case, global left ventricular systolic dysfunction was associated with severe CO poisoning and recovered after conventional therapy. CO exposure may induce reversible or permanent cardiac damage. The conventional diagnostic tools routinely used to evaluate cardiac ischemia (clinical evaluation, and electrocardiography) appear inadequate to correctly assessment of CO induced cardiotoxicity in some cases. Thus more aggressive diagnostic approach with echocardiography tuclazepam should be considered particularly in severe cases and in patients with preexisting heart diseases (coronary arterial diseases and/or heart failure).
A 64-year old woman visited the emergency room due to decreased mentality. She had experienced general weakness since her last delivery. She complained of severe watery diarrhea, more than ten times a day, which had developed 2 days before the visit. On initial presentation, she had a blood pressure of 50/30 mmHg and a pulse rate of 119 beats per minute. Physical examination showed anemic conjunctivae and non-pitting pretibial edema.