[Cardiovascular and hemodynamic changes after artificial pulmonary ventilation]

The cardio-respiratory interactions include mechanical, reflex and humoral mechanisms. However, in the organism they mutually overlap, thus mating their separate investigation is problematic. Mechanical effects of conventional artificial ventilation (AV) and high frequency ventilation (HFV) are elicited by increased intrapulmonary pressure during lung inflation, as well as during application of positive end expiratory pressure (PEEP). The increase in intrapulmonary pressure compresses the pulmonary vessels and increases the pulmonary vascular resistance. These changes deteriorate the right ventricular function. Mechanical factors are responsible for the fall of the left ventricular (LV) filling, stroke volume and alteration of the LV preload and afterload. LV filling is decreased during artificial ventilation (AV) owing to the shifting of blood from the central to the peripheral circulation, and to the rise in pulmonary vascular resistance. Application of positive intrathoracic pressure during ventricular ejection phase can diminish LV afterload and increase the cardiac output. This effect is striking in LV failure. The reflex effects of artificial ventilation are due to the activation of baroreflexes and pulmo-vagally cardiac and vasoactive reflexes. Activation of these reflexes depends on the level and characteristic of the pressure in the airways, lungs, heart and vessels. Humoral effects of AV on the cardiovascular system and hemodynamics are triggered by lung expansion, circulatory changes, and they result in a release of vasoactive substances from lung parenchyma. (Fig. 5, Ref. 45.)