Hemodynamic effects of positive-pressure inflation.

In 14 anesthetized mongrel dogs, we studied the factors that influenced aortic systolic pressure (PaO) and peak aortic systolic flow (Qao) during positive-pressure inflations at three respiratory rates: 8, 14, and 24 breaths/min. At all three respiratory rates, pulmonary arterial flow fell by 15% of the preinspiratory value by end inhalation. Qao also fell at all three respiratory rates, reaching a nadir close to end exhalation (EE). Qao fell less (7% of the base line) at the fast respiratory rate than at the medium and slow respiratory rates (15% of the base line). Pao rose more during the early part of inflation at the medium and fast rates (5 +/- 0.9 Torr) than at the slow rate (3 +/- 0.7 Torr); then Pao fell to a nadir near EE at the slow (-5.6 +/- 1.6 Torr) and at the medium (-2.3 +/- 1 Torr) respiratory rates. At the fast rate it fell to a value not different from control (0.1 +/- 0.5 Torr). The ratio of peak arterial pressure to peak arterial flow increased throughout inflation reaching a peak at EE. A model was developed that predicted the major qualitative features of the changes in Qao seen in these studies. Changes in Pao resulted from the interaction between decreases in Qao and transmitted increases in pleural pressure, and are modified by changes in systemic impedance.