Key result
Heart rate variability produces cardiac output variations, but cardiac output variations do not efficiently buffer mean arterial pressure variations during supine rest and mild orthostasis.
Why the study?
Do oscillations in heart rate and cardiac output buffer fluctuations at approximately 0.1 Hz in arterial blood pressure in healthy humans?
Do oscillations in heart rate and cardiac output buffer fluctuations at approximately 0.1 Hz in arterial blood pressure in healthy humans?
Heart rate variability produces cardiac output variations, but these do not efficiently buffer mean arterial pressure variations during supine rest and mild orthostasis.
Challenges assumption of efficient pressure buffering by cardiac output oscillations; leaves open baroreflex roles in hypertension or orthostasis.
OBJECTIVE: Cardiovascular variability is a complex physiological phenomenon associated with the outcome of cardiovascular diseases. Blood pressure oscillations may cause cardiovascular complications, which, however, are also claimed to have antihypertensive effects. The physiological understanding is limited. This study evaluates whether oscillations in heart rate (HR) and cardiac output (CO) buffer fluctuations at approximately 0.1 Hz in arterial blood pressure (Mayer waves). METHOD: We recorded mean arterial pressure (MAP), left cardiac stroke volume (SV), and HR in 10 healthy humans during autonomic blockade in supine and tilted (30 degrees) position. Variability in the cardiovascular variables at 0.04-0.15 Hz and phase angles (time lags) between the variables were calculated by spectral analysis. RESULTS: Fluctuations in cardiovascular variables at 0.1 Hz decreased after removal of HR variability (HRV) by propranolol and atropine in the supine position. Tilting from supine did not change fluctuations in MAP or total peripheral resistance (TPR), whereas variations in CO decreased. Variations in CO remained decreased in tilt after atropine compared to supine control, whereas variations in MAP and in TPR were unchanged. HRV were in phase with oscillations in CO. Variations in CO were in inverse phase with variations in TPR. CONCLUSION: TPR oscillations produce fluctuations in MAP at 0.1 Hz. HRV produces CO variations, but CO variations do not efficiently buffer MAP variations during supine rest and mild ortostasis. Both feedback and feedforward mechanisms are responsible for the interaction between HR and MAP.
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Elstad et al. (2011) studied Healthy (n=10). Autonomic blockade (propranolol and atropine) and tilting vs. Supine control was evaluated on Fluctuations in cardiovascular variables at 0.1 Hz and phase angles. Heart rate variability produces cardiac output variations, but cardiac output variations do not efficiently buffer mean arterial pressure variations during supine rest and mild orthostasis.
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