Heart rate variability in chronic obstructive pulmonary disease (Doctoral thesis)
Γκολιδάκης, Διαμαντής Μ.
Purpose: Cardiopulmonary disorders coexist with, and contribute to, the morbidity and mortality of Chronic Obstructive Pulmonary Disease (COPD). Various other morbidities have the same or similar causative factors – while exhibiting similar pathophysiological development - as COPD (e.g. heart failure and smoking). Morbidity and mortality examples for COPD that are complicated by comorbidities include congestive heart disease and heart alterations (which are detected in 64% of patients with COPD). Furthermore, it appears that there is a "contribution" (with significant systemic consequences) of COPD in heart disease. Hypoxemia and respiratory acidosis have been implicated as a major cause of cardiac arrhythmias in patients with COPD. Relevant mechanisms include an increase in catecholamines (due to hypercapnia and hypoxemia) that is accompanied by fluid retention and peripheral edema. Thus, given that the cardiac output remains stable and systemic vascular resistance is low (due to the vasodilation caused by hypercapnia), the resulting low blood pressure acts through neurohormonal mechanisms that promote water and electrolyte retention and are responsible for increasing the blood norepinephrine concentration and, potentially, contribute to arrhythmogenesis. Apart from these "systemic" approach, at the level of the heart itself, two important hypotheses have been advanced regarding arrhythmogenesis in COPD: 1) that arrhythmias are the result of hypoxia, hypercapnia or disturbance of acid-base balance, or 2) that arrhythmias they are the result of autonomic neuropathy. The purpose of this study is to investigate the relationship between COPD and cardiac arrhythmias and particularly the impact and relationships between COPD and heart rate variability (HRV) Material and Methods: We studied a total of 68 consecutive patients (30 women and 38 men, mean age 67.37 years (standard deviation 10.24 years) who had given all their consent. Their inclusion was conditional on their being free of hypertension, heart failure, ischemic heart disease, valvular, supraventricular and ventricular arrhythmias, atrial fibrillation or flutter, disturbances of conduction and diabetes. Based on previous studies we excluded patients under medication that prolongs the QT interval, some antibiotics, psychiatric drugs or cholinergic competitors. Finally, patients who under treatment with sympathomimetic drugs and / or aminophylline were also excluded. All patients underwent pulmonary function tests and ECG, while their blood gases were determined. All ECG recordings were performed with patients in a supine position and while in a regular and relaxed breathing pattern. All patients were at rest before the start of measurements Each EEG recording lasted 3 minutes, and each patient completed about 45 respiratory cycles. 1. From the data collected were calculated, two different ECG parameters: The dispersion of the QT interval (QTd), which is associated with ventricular repolarization and 2. The coefficient of variation of the RR interval (CVRR), via the instantaneous heart rate. For the analysis of our results we used a combination of regression methods (single or multiple, where and when appropriate) and methods of heuristic analysis, using the following procedure: 1. Reviewed of the independence of our independent variables. 2. Created the final table of data; we retained only those patients for whom we had complete data set 3. Checked for any and all correlations that may exist between the independent and dependent parameters of our sample 4. Created correlation matrices for each independent parameter and the remaining independent or dependent parameters 5. Created color maps of any relations that became evident (for better visualization) 6. Organized the results for each parameter to allow their analysis with methods of heuristic analysis Results: In our study, we used the CVRR (as the best index of HRV and, therefore, of autonomic neuropathy. We examined all potential correlations of PaO2, PaCO2, pH and HCO3 to the dispersion of the QT interval and CVRR. Based on our results we rejected the electropathy hypothesis (i.e., that arrhythmia is a result of hypoxia, hypercapnia, or acid-base balance disorders) and found that the CVRR correlated with PaO2. We, therefore, conclude that hypoxemia (decreased PaO2) leads to the reduction of CVRR, which, in turn, is linked to autonomic neuropathy. It follows that hypoxemia is the likely mechanism of sudden cardiac death in COPD.
|Institution and School/Department of submitter:||Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής|
|Subject classification:||Χρόνια αποφρακτική πνευμονοπάθεια|
|Keywords:||Χρόνια αποφρακτική πνευμονοπάθεια (ΧΑΠ),Καρδιακή ανεπάρκεια,Μεταβλητότητα του Καρδιακού Ρυθμού (HRV),Υποξαιμία,Υπερκαπνία,Διαταραχές της οξεοβασικής ισορροπίας,Αυτόνομη νευροπάθεια,Chronic obstructive pulmonary disease (COPD),Heart failure,Heart rate variability (HRV),Hypoxia,Hypercapnia,Acid-base balance,Autonomic neuropathy|
|Appears in Collections:||Διδακτορικές Διατριβές|
Files in This Item:
|Δ.Δ. ΓΚΟΛΙΔΑΚΗΣ ΔΙΑΜΑΝΤΗΣ Μ. 2017.pdf||8.63 MB||Adobe PDF||View/Open|
Please use this identifier to cite or link to this item:This item is a favorite for 0 people.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.