Carbon monoxide intoxication is the most prevalent cause of death from carbon monoxide poisoning. We herein report the case of a 56-year-old man who was found unconscious and smelled of smoke after exposure to carbon monoxide from a heater. He scored 5 on the Glasgow Coma Scale, and had respiratory insufficiency and elevated troponin I, creatine kinase-MB fraction and carboxyhaemoglobin levels. He was treated by mechanical ventilation. After regaining consciousness, brain magnetic resonance imaging showed diffusion restriction in the left occipital lobe; there was a loss of vision (right temporal hemianopsia), which improved by the follow-up session. Carbon monoxide intoxication may cause neurologic and cardiac sequelae, and the initial treatment includes oxygen therapy. Acute carbon monoxide poisoning can cause serious injury to the brain, heart and other organs; the most severe damages that could be inflicted to the brain include cerebral ischaemia and hypoxia, oedema, and neural cell degeneration and necrosis.
Brain ; physiopathology ; Brain Ischemia ; physiopathology ; Carbon Monoxide ; chemistry ; Carbon Monoxide Poisoning ; physiopathology ; Carboxyhemoglobin ; chemistry ; Creatine Kinase, MB Form ; blood ; Diffusion ; Glasgow Coma Scale ; Humans ; Hyperbaric Oxygenation ; Hypoxia ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Myocardial Ischemia ; physiopathology ; Stroke ; physiopathology ; Troponin I ; blood

BACKGROUND AND OBJECTIVES: The relationship between QT prolongation and myocardial ischemia is widely known. Due to the limited value of ST depression, we aimed to evaluate, by using four simpler heart rate corrections (Bazett, Framingham, Fridericia and Hodges), the value of maximal exercise-QTc prolongation in the diagnosis of coronary artery disease (CAD) presence and severity. SUBJECTS AND METHODS: We enrolled 234 subjects (mean age 57.3+/-9 years, 143 men) who had undergone exercise testing and coronary angiography due to a suspicion of CAD in the study. Evaluating CAD severity with Gensini scoring, the CAD group (n=122) and controls with non-CAD were compared in terms of corrected QT duration at maximal exercise. RESULTS: Age, gender, hypertension, dyslipidemia, smoking, exercise duration, resting, and peak heart rate were similar between the two groups (all p>0.05). The CAD group had higher raw QT values than the controls {268 (169-438) vs. 240 (168-348), p<0.001}. Although Framingham QTc of > or =350 ms and Fridericia QTc of > or =340 ms were seen to be useful for the diagnosis of CAD, there was no additive diagnostic value of exercise QTc in addition to ST depression. Maximal exercise-QTc Bazett (r=0.163, p=0.01), Framingham (r=0.239, p=0.001), and Fridericia (r=0.206, p=0.001) equations were weakly positively correlated with Gensini scoring. CONCLUSION: The patients with CAD have longer QTc intervals at peak heart rates during exercise. This finding provides insufficient evidence to support routine incorporation of QTc at peak heart rates into exercise test interpretation.
Coronary Angiography ; Coronary Artery Disease* ; Dyslipidemias ; Exercise Test* ; Heart Rate* ; Heart ; Humans ; Hypertension ; Myocardial Ischemia ; Smoking