ABSTRACT
Supraventricular and ventricular arrhythmias, as well as conduction disturbances are frequently observed in COPD and two major hypotheses for arrhythmogenesis have been proposed: arrhythmias may be a consequence of hypoxaemia, hypercapnia or acid-base dis-turbances since they increase the electrical heterogeneity within the ventricular wall or arrhythmias may be the result of the autonomic neuropathy that characterizes COPD. In this study, we attempted to non-invasively verify these hypotheses in hypoxaemic COPD patients that are not in respiratory failure by examining how PaO2, PaCO2, pH and HCO[3] correlate with QTd in those patients. 25 COPD patients were subjected for Standard 12-lead ECG for arrhythmia detection and the measurement of QT intervals, chest X-ray, two dimensional echocardiogra-phy and myocardial nuclear imaging to exclude IHD. We found negative significant correlation between O2 tension and the occurrence of fatal arrhythmias; the same as between O[2] tension and QTd value [P values were < 0.0005 in both], with QTd as the dependent variable, and age, pulmonary pressure, duration, Mg, Na, K, Hb PH, CO[2] and O[2] tensions as the independent variables in all subjects, it was shown that only PaO[2] was the predictor of QTd with a P value of 0.02. In stable COPD patients enrolled in our study, new cutoff levels for predicting arrhythmic fatality were proposed for the QTc parameter[395 ms with a sensitivity of 92% and a specificity of 83%] and the QTd parameter [58 ms with a sensitivity of 100% and a specificity of 92%]. There is a high positive significant correlation between the age of patients, duration of COPD and Hb level and the occurrence of fatal arrhythmias where P valuesl were 0.009, < 0.0005 and < 0.0005 respectively; the same as with QTd value where the P values were 0.015, 0.001 and 0.039. There is a positive significant correlation between pulmonary pressure and QTc where the P value was 0.041 and pulmonary pressure with QTd where the P value was 0.028. Conclusion: Our results rule out the electropathy hypothesis and underline autonomic neuropathy as the most possible mechanism of arrhythmias in hypoxaemic, non-respiratory failure, and COPD patients