Hemodynamic effects of changes in intrathoracic pressure

The heart within the thorax is a pressure chamber within a pressure chamber. Therefore changes in intrathoracic pressure will affect the pressure gradients for both systemic venous return to the right ventricle and systemic outflow from the left ventricle, independent of the heart itself. Decreases in intrathoracic pressure by increasing venous return and impeding left ventricular ejection will increase intrathoracic blood. Spontaneous inspiratory efforts, by decreasing intrathoracic pressure, both increase lung volume and decrease right atrial pressure (Pra). The fall in Pra accelerates blood flow into the right ventricle (Pinsky 1984). This increased venous return is transmitted to the pulmonary artery on the subsequent beat. Thus normal respiration-associated hemodynamic changes maximize ventilation-perfusion temporal matching because the spontaneous inspiration matches an increase in alveolar oxygen flux with an increase in pulmonary capillary flow. However, the maximum increase in venous blood flow is limited because, as Pra becomes negative with respect to atmospheric pressure, the veins collapse as they enter the chest, limiting blood flow. Accordingly, maximum venous return is rapidly reached during spontaneous inspiration and further decreases in intrathoracic pressure do not produce any additional increase in venous return. Thus markedly negative swings in intrathoracic pressure, as may occur with spontaneous inspiratory efforts with upper airway obstruction, bronchospasm, or pulmonary edema, do not induce a massive increase in venous return which, potentially, could impair right ventricle function. Furthermore, since venous return is limited, the hemodynamic consequences of marked negative swings in intrathoracic pressure are not primarily due to increased venous return. However, decreases in intrathoracic pressure at a constant arterial pressure will increase left ventricular transmural pressure and thus increase left ventricular afterload, impeding left ventricular ejection ( Budaefa/: 1979). Spontaneous inspiration, by decreasing intrathoracic pressure, increases left ventricular afterload. This afterload effect will progressively increase as the swings in intrathoracic pressure become more negative until the ejection pressure is so high that no left ventricular ejection can occur.

To put both the venous return and left ventricular afterload processes together, loaded spontaneous ventilatory efforts decrease left ventricular stroke volume via a complex mechanism collectively called pulsus paradoxus. Transient intraventricular septal shift into the left ventricular lumen from right ventricular dilation plus pericardial volume restraint decrease absolute left ventricular end-diastolic volume. Increases in left ventricular afterload impede left ventricular ejection, increasing left ventricular end-systolic volume. Although the increase in left ventricular afterload can be explained by increases in left ventricular transmural pressure alone, increases in aortic input impedance and altered series contraction of the left ventricular myocardium have also been described during loaded spontaneous inspiration. However, these two additional effects appear to be mild.

Accordingly, weaning patients from positive-pressure ventilation, by allowing the return of decreases in intrathoracic pressure, may precipitate acute left ventricular failure and pulmonary edema in patients with borderline left ventricular function ( Lemaire..et al 1988). In this regard, weaning can be seen as a form of cardiac stress testing because left ventricular loading invariably occurs in the transition from positive-pressure to spontaneous ventilation. Furthermore, this line of reasoning forms the basis for the assertion made above that cardiovascular impairment must play an important role in subjects who fail to wean from mechanical ventilatory support.

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