Arrhythmias in patients with chronic obstructive pulmonary disease

Abstract Background 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 disturbances since they increase the electrical heterogeneity within the ventricular wall or arrhythmias may be the result of the autonomic neuropathy that characterizes COPD. Aim of the work In this study, we attempted to non-invasively verify these hypotheses in hypoxaemic COPD patients that are not in respiratory failure by examining how PaO 2 , PaCO 2 , pH and HCO 3 correlate with QTd in those patients. Subjects and methods 25 COPD patients were subjected for Standard 12-lead ECG for arrhythmia detection and the measurement of QT intervals, chest X-ray, two dimensional echocardiography and myocardial nuclear imaging to exclude IHD. Results We found negative significant correlation between O 2 tension and the occurrence of fatal arrhythmias; the same as between O 2 tension and QTd value ( P values were 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 values were 0.009, 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.