Relation Between Lung Volume and Pulmonary Vascular Resistance

Abstract

Ten experiments were conducted on anesthetized dogs ventilated with a Starling pump and breathing oxygen. While tidal volume, respiratory rate, and arterial pH and pCO 2 were kept constant, lung volume was varied by using either a negative, zero, or positive end-expiratory pressure, leading to average changes in lung volume of -32, 0, and +75 per cent. Pulmonary vascular resistance (PVR) increased with either decreased or increased lung volume, indicating that the relationship between resistance and lung volume is a U-shaped curve. Since the transmural distending pressures of large pulmonary vessels either increased or remained unchanged during these procedures, changes in PVR cannot be ascribed to changes in systemic circulatory dynamics, such as cardiac output. It was noted that cardiac output increased with negative end-expiratory pressure (effectively, negative-pressure breathing) and decreased with positive end-expiratory pressures (effective, positive-pressure breathing), as previously reported. A hypothesis is presented for explaining the U-shaped curve relating resistance and lung volume.

Hemorrhagic Shock in Dogs Without Major Pulmonary Changes

“…A clearly significant rise of PVR might have been prevented by manual lung inflation. Bo and Hognestad [4] have shown that platelet-induced pulmonary hypertension can be reversed by lung inflation, and Simmons et al [20] demonstrated a normalization of elevated PVR values when atelectatic lungs were reexpanded.…”

Atelectasis in the perioperative patient

“…Thus, this notion explained the changes in pulmonary vascular resistance on the basis of physical alteration of the pulmonary blood vessels. Stretching or narrowing of vessels because of increased lung volume, or compression because of decreased lung volume can contribute [45][46][47]. Regional hypoxia develops in atelectatic lungs, however, and it has been shown that the mechanism of increased large vessel pulmonary vascular resistance in the lungs is due to hypoxic pulmonary vascular resistance, due in turn to decreased alveolar and mixed venous oxygen tension [48][49][50].…”

Gradient of bronchial end-tidal CO2 during two-lung ventilation in lateral decubitus position is predictive of oxygenation disorder during subsequent one-lung ventilation

“…The lung volume was reported to be one of the factors in the distribution of pulmonary blood fl ow. Simmons et al [10], in an animal study, showed that the pulmonary vascular resistance increased when the lung was diminished in volume below the functional residual capacity. This fi nding has not been confi rmed in humans.…”