CHANGES OF THE POWER OF HEART-RATE-VARIABILITY INDUCED BY PROPRANOLOLIN PATIENTS WITH CARDIAC-ARRHYTHMIAS

Citation
Vm. Khayutin et al., CHANGES OF THE POWER OF HEART-RATE-VARIABILITY INDUCED BY PROPRANOLOLIN PATIENTS WITH CARDIAC-ARRHYTHMIAS, Kardiologia, 37(7), 1997, pp. 4-14
Citations number
58
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00229040
Volume
37
Issue
7
Year of publication
1997
Pages
4 - 14
Database
ISI
SICI code
0022-9040(1997)37:7<4:COTPOH>2.0.ZU;2-3
Abstract
Effects of beta-adrenergic receptor blockade on heart rate variability demonstrate 2 phenomena which seem to be paradoxical. First, it has b een claimed that low frequency power significantly rises although beta -blockers are expected to decrease its sympathetic component. Second, high frequency power has also been shown to rise. The nature of this p henomenon is not clear because high frequency heart rate fluctuations reflect parasympathetic influences on the sinus node. Effects of a sho rt course of propranolol an low and high power components were investi gated in 17 patients with different forms of cardiac arrhythmias witho ut organic heart disease. Spectra of variability of heart rate and of amplitudes of QRS complexes were calculated from 5 min ECG recordings obtained in supine and standing positions. Spectra of amplitudes of QR S complexes reflected individual breathing patterns. No relation was f ound between the type of arrhythmia and values of heart rate, low or h igh frequency power neither before nor after propranolol. Propranolol decreased low frequency power in supine position by 50+/-18% in 82% of patients and in standing position by 61+/-17% in 87% of patients. The increase of low frequency power in some patients was determined by ch anges of breathing rate or by short non-periodical ''jumps'' of heart rate which had no relation to regular low frequency changes of heart r ate. High frequency power increased at rest by 145% in 70% of patients . its decrease in other cases was related to slowing of breathing or r eduction of tidal volume. According to the literature, beta-adrenergic blockers penetrating into the brain release norandrenaline from centr al noradrenergic neurons. The latter by activating alpha(1)-adrenorece ptors of medullary cardiomotor parasympathetic neurons increases their excitability and thereby enhances sinus respiratory arrhythmias and h ence law frequency power of heart rate variability.