Venous return and pulmonary hemodynamics under the positive end-expiratory pressure mechanical ventilation

Author:

Evlakhov Vadim I.,Poyassov Ilya Z.

Abstract

In the review we have discussed the mechanisms of the changes of the venous return and pulmonary hemodynamics which take place in clinical cases of the mechanical lung ventilation with positive end-expiratory pressure. In these conditions the elevating of right atrial pressure does not cause the decreasing of the venous return, because the mean circulatory filling pressure also increases. Thus, the gradient for venous return remains relatively constant. In case of the mechanical lung ventilation with positive end-expiratory pressure the decreasing of the venous return is the result of the elevation of the venous resistance as consequence of the direct increasing of the intrathoracic and transdiaphragmatic pressures and activation of the reflectory neurogenic mechanisms. In the conditions, indicated above, the increased alveolar pressure leads to the improvement of the diffused lung capacity for oxygen, which decreases the manifestations of the hypoxic pulmonary vasoconstriction and thus diminishes pulmonary vascular resistance. The character of changes of the last one is determined by the reactions of the two types (alveolar and extraalveolar) intraparenchimal pulmonary vessels. This leads to the changes of the resistive and capacitive functions of the pulmonary vessels. In case of the high levels of the positive end-expiratory pressure (more than 30 cm of water column) the value of alveolar pressure is comparable or even more excessive than pulmonary artery pressure (1216 mm Hg), which can be the reason of the decreasing of the right ventricular contractility and the venous return. The increasing of the capillary filtration coefficient of pulmonary vessels in the conditions of the mechanical lung ventilation with positive end-expiratory pressure can be the result of the activation of the mechanosensitive transient receptor potential vanilloid-4 (TRPV4) channels and the increasing endothelial calcium entry.

Publisher

ECO-Vector LLC

Subject

General Medicine

Reference1 articles.

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