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This Article Full Text Full Text (PDF) All Versions of this Article: 287/2/H798    most recent 01174.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Stewart, J. M. Articles by Montgomery, L. D. Search for Related Content PubMed PubMed Citation Articles by Stewart, J. M. Articles by Montgomery, L. D.

Effects of thoracic blood volume on Valsalva maneuver

Departments of ¹Pediatrics and ²Physiology, New York Medical College, Valhalla, New York 10595; and ³LDM Associates, San Jose, California 95126

Submitted 15 December 2003 ; accepted in final form 26 February 2004

The Valsalva maneuver (VM) is frequently used to test autonomic function. However, the VM is also affected by changes in blood volume and blood volume redistribution. We hypothesized that even a standardized VM may produce a wide range of thoracic blood volume shifts. Larger blood volume shifts in some normovolemic individuals may be sufficient to induce decreases in blood pressure (BP) that preclude autonomic restoration of BP in phase II of the VM. To test this hypothesis, we studied 17 healthy volunteers aged 15–22 yr. All had similar vasoconstrictor responses when supine and upright and normal blood volume measurements. We assessed changes in thoracic blood volume by impedance plethysmography before and during the VM performed while subjects were supine. In some subjects, large decreases in BP were produced by thoracic hypovolemia. The maximum fractional decrease in BP correlated well (r² = 0.64; P < 0.001) with thoracic hypovolemia and with systolic BP at the end of phase II of the VM (r² = 0.67; P < 0.001). The BP overshoot in phase IV of the VM was uncorrelated to phase II changes, which suggests intact autonomic vasoconstriction. We conclude that the BP decrease during the VM is related to a variable decrease in thoracic blood volume that may be sufficient to preclude pressure recovery during phase II even with normal resting peripheral vasoconstriction. The VM depends on vascular as well as autonomic activation, which broadens its utility but complicates its analysis.

vasoconstriction; veins; thoracic; supine; upright; pleural; cardiac

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