Introduction: We tested the hypotheses that hypovolemia would result in attenuated elevation in blood pressure, greater baroreflex-mediated tachycardia, and reduced capacity for vasoconstriction during a Valsalva maneuver (VM).
Methods: Heart rate (HR) and mean arterial pressure (MAP) were measured beat-by-beat before strain, during a 15-s VM strain at 30 mmHg expiratory pressure, and post-strain. Eight subjects performed three VM trials in each of three postures (supine, sitting, and standing) under two experimental conditions (normovolemic and hypovolemic). Hypovolemia was acutely induced by a bolus injection of 30 mg furosemide. Each experimental condition was conducted on a different day, separated by one week. delta MAP was used in analyses of phase I, late phase II (an indicator of vasoconstriction) and phase III of VM. The ratio delta HR/delta MAP, an index of nonspecific baroreflex control of HR, was used in analysis of early phase II and phase IV of the VM.
Results: Compared to normovolemia, hypovolemia resulted in 12% lower plasma volume (p = 0.0001). delta MAP for both phase I and phase III of the VM differed between postures (p = 0.0132 and p = 0.0003, respectively) and was lower in the hypovolemic condition than in the normovolemic condition for phase I in the standing posture (-5 mmHg, p = 0.0385).
Conclusions: HR and blood pressure responses to alterations in intrathoracic pressure are affected by fluid redistribution (posture change), but not by circulating blood volume. Therefore, our results did not support our hypothesis that hypovolemia would result in attenuated elevation in blood pressure, greater baroreflex-mediated tachycardia, and reduced capacity for vasoconstriction during a Valsalva maneuver. However, moderate hypovolemia can be specifically predicted by the phase I response to a VM performed in the standing posture.