Hemodynamic effects of changes in lung volume

Lung inflation alters autonomic tone and pulmonary vascular resistance; at high lung volumes, it compresses the heart in the cardiac fossa, limiting absolute cardiac volumes. The associated diaphragmatic dissent increases abdominal pressure and compresses the liver markedly, altering the flow characteristics of venous return. Each of these processes may predominate in determining the final cardiovascular state. Small tidal volumes (<10ml/kg) increase heart rate by vagal withdrawal (respiratory sinus arrhythmia), whereas larger tidal volumes (>15ml/kg) decrease heart rate, arterial tone, and cardiac contractility by sympathetic withdrawal ( Butler 1983). These effects are probably only relevant in the diagnosis of dysautonomia and in the care of neonatal subjects where autonomic tone is high.

The major determinants of the hemodynamic response to increases in lung volume are mechanical in nature ( Butjer .1983). Lung inflation, independent of changes in intrathoracic pressure, primarily affects cardiac function and cardiac output by altering right ventricular preload and afterload and left ventricular preload. First, inspiration induces diaphragmatic dissent which may alter venous return. Venous return is a function of the ratio of the pressure difference between the right atrium and the systemic venous reservoirs to the resistance to venous return. Since a large proportion of the venous blood volume is in the abdomen, increases in intra-abdominal pressure will increase the venous pressure in the vascular spaces, augmenting venous blood flow ( FessleieLal: 1992). However, diaphragmatic descent will also compress the liver, increasing hepatic outflow resistance and decreasing flow from the splanchnic venous reservoirs to the right heart. Complicating this further, inspiration will shift venous flow from high-resistance splanchnic circuits, which must drain through the liver, to low-resistance systemic venous circuits, making flow greater for the same driving pressure. Thus inspiration may increase, decrease, or have no effect on venous return depending on which of these factors is predominant. Inspiration will increase venous return in volume-overloaded states, whereas venous return will decrease in hypovolemic states and hepatic cirrhosis.

Right ventricular output is sensitive to changes in pulmonary outflow resistance. Alveolar collapse often occurs in acute lung injury states and is associated with increases in pulmonary vasomotor tone via hypoxic pulmonary vasoconstriction. Alveolar recruitment by restoring end-expiratory lung volume to functional residual capacity often reverses this process. Increasing lung volume above functional residual capacity also increases right ventricular outflow resistance ( B.utlerJ983.; Pinsky.

eta!, 1985). However, this is due to progressive increases in transpulmonary pressure (airway pressure relative to intrathoracic pressure) associated with increasing lung volume. Since the heart and great vessels are located in the thorax and sense intrathoracic pressure as their surrounding pressure, increases in transpulmonary pressure such that it approaches pulmonary artery pressure will induce pulmonary vascular collapse ( .B.ui!┬žLl9.8.3). Hyperinflation increases pulmonary artery pressure; therefore reversing hyperinflation, by prolonging expiration, reducing levels of positive-end expiratory pressure or tidal volumes, and bronchodilatation, may decrease pulmonary arterial pressure, thus improving right ventricular ejection.

Left ventricular end-diastolic volume (preload) can be altered by ventilation in three ways. First, since the right and left ventricular outputs are in series, changes in right ventricular preload must eventually alter left ventricular preload in the same direction. Second, because of ventricular interdependence, changes in right ventricular end-diastolic volume inversely change left ventricular diastolic compliance ( Taylor..efal 1967). Ventricular interdependence is a major factor in altering left ventricular output during spontaneous ventilation when right ventricular end-diastolic volumes may vary widely from expiration (small) to inspiration (large). Third, increasing lung volume restricts absolute cardiac volume by direct compression of the heart ( ButlerJ983). As the lungs expand, the heart is compressed in the cardiac fossa and absolute biventricular volume is limited in a fashion analogous to cardiac tamponade.

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