Spectral patterns and frequency response characteristics of arterial pressure in heart paced dogs
- 1 July 1995
- journal article
- Published by Institute of Electrical and Electronics Engineers (IEEE) in IEEE Transactions on Biomedical Engineering
- Vol. 42 (7), 708-717
- https://doi.org/10.1109/10.391170
Abstract
The role of heart rate in buffering and/or generating aortic pressure (AP) oscillations that occur at rest and in response to oscillatory blood volume shifts was studied. Six supine dogs with chronic AV blockade were used to examine: 1) resting HR and AP spectra when the ventricular rate was controlled by atrial depolarization (natural sinus rhythm); 2) resting AP and stroke volume (SV) spectra when the heart was AV sequentially paced at 60, 120, and 180 bpm before and after ganglionic blockade; and 3) the frequency response characteristics of AP and SV to whole-body sinusoidal acceleration (+/- 2gz, 0.008-0.23 Hz) at each heart rate before and after ganglionic blockade. During atrial regulation of HR, the spectra of both AP and HR had dominant peaks located at the breathing frequency (0.2-0.4 Hz) and relatively smaller peaks centered at approximately 0.05 Hz. During constant heart rate pacing, the spectra of AP had a dominant component at approximately 0.05 Hz. The power of this component was: 1) larger than during atrial regulation, 2) increased with increasing pacing rate, and 3) abolished by ganglionic blockade. There was no effect of pacing rate or ganglionic blockade on SV spectra. During oscillatory acceleration, AP regulation in the heart paced dogs was frequency dependent. Regions of good regulation occurred below 0.016 Hz and above 0.1 Hz, and poor regulation between 0.035 and 0.075 Hz centered at approximately 0.05 Hz. The oscillations in the poor regulation region were enhanced by increased pacing rate. After ganglionic blockade, the frequency response of AP was primarily hydraulic (low-pass). The frequency response of SV had a neural component. We conclude that: 1) resting AP fluctuations at respiratory frequencies resulted from respiration-linked HR variation; 2) the 0.05-Hz fluctuations in AP during rest and the poor regulation of AP at 0.05 Hz during acceleration resulted from a peripheral vascular response that lagged disturbances by approximately 10 s; 3) HR regulation was important in minimizing AP variation in the 0.05-Hz region both at rest and during oscillatory acceleration; and 4) inotropic control of SV was an important component of AP regulation during low-frequency acceleration.Keywords
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