Abstract
The pulmonary circulation is a high-flow/low-pressure system, coupled with a flow generator chamber–the right ventricle–, which is relatively unable to tolerate increases in afterload. A right heart catheterization, using a fluid-filled, balloon-tipped Swan-Ganz catheter allows the measurement of all hemodynamic parameters characterizing the pulmonary circulation: the inflow pressure, an acceptable estimate the outflow pressure, and the pulmonary blood flow. However, the study of the pulmonary circulation as a continuous flow system is an oversimplification and a thorough evaluation of the pulmonary circulation requires a correct understanding of the load that the pulmonary vascular bed imposes on the right ventricle, which includes static and dynamic components. This is critical to assess the prognosis of patients with pulmonary hypertension or with heart failure.Pulmonary compliance is a measure of arterial distensibility and, either alone or in combination with pulmonary vascular resistance, gives clinicians the possibility of a good prognostic stratification of patients with heart failure or with pulmonary hypertension. The measurement of pulmonary arterial compliance should be included in the routine clinical evaluation of such patients.
Highlights
Pulmonary compliance is a measure of arterial distensibility and, either alone or in combination with pulmonary vascular resistance, gives clinicians the possibility of a good prognostic stratification of patients with heart failure or with pulmonary hypertension
The inflow pressure is the pulmonary arterial pressure (PAP); the outflow pressure is the left atrial pressure (Pla), an acceptable estimate of which is provided by the pulmonary capillary wedge pressure (PCWP), obtained by inflating the balloon at the tip of the catheter; and the pulmonary blood flow is assessed by a number of clinical methods, such as thermodilution or the Fick principle.[3]
In a population of heart failure due to left ventricular systolic dysfunction, PCa significantly outperformed all hemodynamic parameters and emerged as the strongest predictor of cardiovascular death or hard events, regardless of the presence or absence of pulmonary hypertension.[31]. This finding is highly relevant from a clinical perspective, since it suggests that structural changes of large vessels might precede the increase in pulmonary vascular resistance (PVR) in patients with heart failure; this is in agreement with the hypothesis formulated in pulmonary arterial hypertension patients that the early phase of pulmonary vascular disease cannot be detected by right heart catheterization with elevation of PVR but only with a reduction in PCa (Figure 6).[10]
Summary
The pulmonary circulation can be defined as a high-flow/low-pressure system in which the right ventricle represents a thin wall flow generator; meaning the right ventricle can accommodate large changes in volume loading (as it may happen in congenital, systemic-to-pulmonary shunts), but has a limited contractile reserve to match rapid increases in afterload (as may happen in acute pulmonary embolism).[1,2]. The fact that the radius in the equation is raised to the fourth power explains why PVR is extremely sensitive to even the smallest changes in diameter of the resistive pulmonary arterioles, which is the site of most pulmonary vascular diseases. For this reason PVR is a good hemodynamic marker of the state of constriction or dilation of the small pulmonary vessels, useful to detect alterations of the calibre of the arteries due to changes in their tone and/or structure. Unlike the PVR, which represents the static component of the right ventricular afterload, the pulmonary impedance (PVZ) and compliance (PCa) include both static and dynamic pulsatile components
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