Why the study?
Alterations of autonomic cardiovascular control are implicated in chronic hypotension, but comprehensive analysis of baroreflex function across cardiac, vascular, and myocardial branches is lacking.
Does baroreflex function and cardiovascular reactivity differ between hypotensive and normotensive individuals at rest and during mental stress?
Does baroreflex function and cardiovascular reactivity differ between hypotensive and normotensive individuals at rest and during mental stress?
Chronic hypotension is associated with altered baroreflex sensitivity and reduced stroke volume, suggesting that hemodynamic deficits are primarily driven by reduced venous return and preload rather than afterload mechanisms.
Baroreflex assessment may aid hypotension evaluation; hypothesis-generating and requires confirmation before clinical use.
PURPOSE: Alterations of autonomic cardiovascular control are implicated in the origin of chronic low blood pressure (BP) (hypotension), but comprehensive analysis of baroreflex function is still lacking. This study explored baroreflex function in its cardiac, vascular and myocardial branches METHODS: Continuous BP was recorded at rest and during a mental arithmetic task in 40 hypotensive and 40 normotensive participants. Assessed cardiovascular variables included stroke volume (SV) (calculated by the Modelflow method), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR) and heart rate variability (HRV). Baroreflex sensitivity (BRS) was calculated using the spontaneous sequence method. RESULTS: Hypotensive participants exhibited greater BRS in the three baroreflex branches, in addition to lower SV, HR and CO and higher HRV and TPR. Reactivity for BP, HRV and CO during the stress task was reduced in hypotensive individuals. The greater cardiac BRS can explain the lower HR and higher HRV observed in hypotension, suggestive of increased vagal cardiac influences. The higher vasomotor BRS may contribute to the greater TPR observed in the hypotensive participants. Abnormal associations between myocardial BRS and SV arose, suggesting aberrant autonomic control of myocardial contractility in hypotension. CONCLUSION: The results indicate that hemodynamic deficits in hypotension are related to preload factors, probably triggered by hypovolemia and reduced unstressed blood reserves, resulting in lower venous return, ventricular preload and SV. In contrast, afterload mechanisms seem to work appropriately.
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Paso et al. (2024) studied this question.
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