The effects of changes in blood volume on arterial pressure patterns during the Valsalva maneuver are incompletely understood. In the present study we measured beat-to-beat arterial pressure and heart rate responses to supine Valsalva maneuvers during normovolemia, hypovolemia induced with intravenous furosemide, and hypervolemia induced with ingestion of isotonic saline. Valsalva responses were analyzed according to the four phases as previously described (W. F. Hamilton, R. A. Woodbury, and H. T. Harper, Jr. JAMA 107: 853-856, 1936; W. F. Hamilton, R. A. Woodbury, and H. T. Harper, Jr. Am. J. Physiol. 141: 42-50, 1944). Phase I is the initial onset of straining, which elicits a rise in arterial pressure; phase II is the period of straining, during which venous return is impeded and pressure falls (early) and then partially recovers (late); phase III is the initial release of straining; and phase IV consists of a rapid "overshoot" of arterial pressure after the release. During hypervolemia, early phase II arterial pressure decreases were significantly less than those during hypovolemia, thus making the response more "square." Systolic pressure hypervolemic vs. hypovolemic falls were 7.4 ± 2.1 vs. 30.7 ± 7 mmHg (P = 0.005). Diastolic pressure hypervolemic vs. hypovolemic falls were 2.4 ± 1.6 vs. 15.2 ± 2.6 mmHg (P = 0.05). A significant direct correlation was found between plasma volume and phase II systolic pressure falls, and a significant inverse correlation was found between plasma volume and phase III-IV systolic pressure overshoots. Heart rate responses to systolic pressure falls during phase II were significantly less during hypovolemia than during hypervolemia (0.7 ± 0.2 vs. 2.82 ± 0.2 beats · min¹ · mmHg¹; P = 0.05) but were not different during phase III-IV overshoots. We conclude that acute changes in intravascular volume from hypovolemia to hypervolemia affect cardiovascular responses, particularly arterial pressure changes, to the Valsalva maneuver and should be considered in both clinical and research applications of this maneuver.

baroreflex; hypovolemia; hypervolemia

This article has been cited by other articles:

				J. M. Stewart, M. S. Medow, L. D. Montgomery, J. L. Glover, and M. M. Millonas Splanchnic hyperemia and hypervolemia during Valsalva maneuver in postural tachycardia syndrome Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1951 - H1959. [Abstract] [Full Text] [PDF]

				J. M. Stewart and L. D. Montgomery Reciprocal splanchnic-thoracic blood volume changes during the Valsalva maneuver Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H752 - H758. [Abstract] [Full Text] [PDF]

				J. M. Stewart, M. A. Medow, B. Bassett, and L. D. Montgomery Effects of thoracic blood volume on Valsalva maneuver Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H798 - H804. [Abstract] [Full Text] [PDF]

				T. T. Schlegel, T. E. Brown, S. J. Wood, E. W. Benavides, R. L. Bondar, F. Stein, P. Moradshahi, D. L. Harm, J. M. Fritsch-Yelle, and P. A. Low Orthostatic intolerance and motion sickness after parabolic flight J Appl Physiol, January 1, 2001; 90(1): 67 - 82. [Abstract] [Full Text] [PDF]

				D. S. Kimmerly and J. K. Shoemaker Hypovolemia and neurovascular control during orthostatic stress Am J Physiol Heart Circ Physiol, February 1, 2002; 282(2): H645 - H655. [Abstract] [Full Text] [PDF]