Phasic changes in lung blood volume (LBV) during the respiratory cycle may play an important role in the genesis of the respiratory wave in arterial pressure, or pulsus paradoxus. To better understand the effects of lung inflation on LBV, we studied the effect of changes in transpulmonary pressure (delta Ptp) on pulmonary venous flow (Qv) in eight isolated canine lungs with constant inflow. Inflation when the zone 2 condition was predominant resulted in transient decreases in Qv associated with increases in LBV. In contrast, inflation when the zone 3 condition was predominant resulted in transient increases in Qv associated with decreases in LBV. These findings are consistent with a model of the pulmonary vasculature that consists of alveolar and extra-alveolar vessels. Blood may be expelled from alveolar vessels but is retained in extra-alveolar vessels with each inflation. The net effect on LBV and thus on Qv is dependent on the zone conditions that predominate during inflation, with alveolar or extra-alveolar effects being greater when the zone 3 or zone 2 conditions predominate, respectively. Lung inflation may therefore result in either transiently augmented or diminished Qv. Phasic changes in left ventricular preload may therefore depend on the zone conditions of the lungs during the respiratory cycle. This may be an important modulator of respiratory variations in cardiac output and blood pressure.

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Using an isolated, fibrillated canine heart-lung preparation, we studied the effects of simultaneous lung inflation and chest compression on blood flow in a model of cardiopulmonary resuscitation. The heart and lungs were placed in an artificial thorax with the great vessels and trachea exteriorized and attached to an artificial perfusion circuit and respirator, respectively. The blood volume of the system was adjusted to obtain various levels of static equilibrium pressure. Blood flow was obtained by cyclically raising and lowering the pressure in the artificial thorax, simulating the changes in pleural pressure that occur during cardiopulmonary resuscitation. Lung inflation during the compression phase caused an increase in cardiopulmonary resuscitation blood flow when the change in pleural pressure was small and when static equilibrium pressure was high. In contrast, lung inflation caused a decrease in blood flow when changes in pleural pressure were high and when blood volume was low. These results suggest that the driving pressure for blood flow during chest compression may be increased by lung inflation when the pulmonary blood vessels are filled with blood. However, blood may become trapped in the right heart and unavailable for transfer to the periphery during chest compression if lung inflation causes the alveolar blood vessels to collapse.