46The systolic pressure is less closely related to stroke volume than the pulse pressure because it depends not only on stroke volume 48and arterial compliance but also directly on diastolic pressure (systolic pressure = diastolic pressure + pulse pressure). In this regard, the respiratory variation in left ventricular stroke volume has been shown to be the main determinant of the respiratory variation in pulse pressure. 47Therefore, for a given arterial compliance, the amplitude of pulse pressure is directly related to left ventricular stroke volume. ![]() The arterial pulse pressure (the difference between the systolic and the preceding diastolic pressure) is directly proportional to stroke volume and inversely related to arterial compliance. 41,42(3) Left ventricular afterload decreases during inspiration because positive pleural pressure increases the systolic extracardiac pressure and decreases the systolic intracardiac pressure through a reduction in thoracic blood volume. Thus, the blood is squeezed out of the capillaries toward the left side of the heart. 38–40(2) Left ventricular preload increases during inspiration because the increase in alveolar pressure (surrounding the pulmonary capillaries) is greater than the increase in pleural pressure (surrounding the pulmonary venous bed). In this regard, any increase in transpulmonary pressure (the difference between alveolar and pleural pressure) impedes right ventricular ejection. 3 and 4): (1) Right ventricular afterload increases during inspiration because the increase in alveolar pressure (the pressure surrounding the pulmonary capillaries) is greater than the increase in pleural pressure (the pressure surrounding the pulmonary arterial bed). Three other mechanisms may also participate in the respiratory variation in left ventricular stroke volume ( figs. The reliable analysis of respiratory changes in arterial pressure is possible in most patients undergoing surgery and in critically ill patients who are sedated and mechanically ventilated with conventional tidal volumes. That is, these studies have demonstrated the value of this physical sign in answering one of the most common clinical questions, Can we use fluid to improve hemodynamics?, while static indicators of cardiac preload (cardiac filling pressures but also cardiac dimensions) are frequently unable to correctly answer this crucial question. During the past few years, many studies have demonstrated that arterial pressure variation is neither an indicator of blood volume nor a marker of cardiac preload but a predictor of fluid responsiveness. At the bedside, respiratory changes in aortic blood flow are reflected by "swings" in blood pressure whose magnitude is highly dependent on volume status. Mechanical ventilation induces cyclic changes in vena cava blood flow, pulmonary artery blood flow, and aortic blood flow.
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