Effects of respiration and vasodilation on venous volume in animals and man, as measured with an impedance catheter

Abstract

Venous return determines cardiac preload and is in turn affected by respiration and vasodilation. The purpose of the present study was to examine the dynamics of venous return and venous volume, using impedance volume measurements in the venous system. In order to develop a methodology for the assessment of venous volume and venous return in man, we first studied 17 endotracheally intubated and ventilated anesthetized closed-chest dogs. We measured central venous and inferior vena cava (IVC) pressure (micromanometer) and volume (impedance catheter). Studies were done above and below the diaphragm with normal ventilation, with positive end-expiratory pressure (PEEP), and with beta-adrenergic blockade and i.v. nitroglycerin. Intrathoracic IVC volume fell and extrathoracic IVC volume rose with lung inflation, while PEEP raised extrathoracic IVC volume and lowered intrathoracic IVC volume. Nitroglycerin lowered intrathoracic IVC volume. Beta blockade did not affect IVC volume, ventilatory variation, or response to PEEP and nitroglycerin. We performed similar studies in 14 human subjects during normal quiet respiration, with measurements above and below the diaphragm, and with interventions including Valsalva maneuver and i.v. nitroglycerin. Intrathoracic IVC volume fell and extrathoracic IVC volume rose with expiration and Valsalva maneuver. Nitroglycerin again lowered intrathoracic IVC volume. We conclude that venous volume and the dynamics of venous return can be assessed in animals and man with an impedance catheter. Specifically, we show the divergent effects of respiration, ventilation, PEEP, and nitroglycerin on IVC volumes above and below the diaphragm. Beta-adrenergic blockage does not appear to play a role in altering any of these effects.(ABSTRACT TRUNCATED AT 250 WORDS)