Pulmonary capillary wedge pressure augments right ventricular pulsatile loading

RJ Tedford, PM Hassoun, SC Mathai, RE Girgis… - Circulation, 2012 - Am Heart Assoc
RJ Tedford, PM Hassoun, SC Mathai, RE Girgis, SD Russell, DR Thiemann, OH Cingolani
Circulation, 2012Am Heart Assoc
Background—Right ventricular failure from increased pulmonary vascular loading is a major
cause of morbidity and mortality, yet its modulation by disease remains poorly understood.
We tested the hypotheses that, unlike the systemic circulation, pulmonary vascular
resistance (RPA) and compliance (CPA) are consistently and inversely related regardless of
age, pulmonary hypertension, or interstitial fibrosis and that this relation may be changed by
elevated pulmonary capillary wedge pressure, augmenting right ventricular pulsatile load …
Background
Right ventricular failure from increased pulmonary vascular loading is a major cause of morbidity and mortality, yet its modulation by disease remains poorly understood. We tested the hypotheses that, unlike the systemic circulation, pulmonary vascular resistance (RPA) and compliance (CPA) are consistently and inversely related regardless of age, pulmonary hypertension, or interstitial fibrosis and that this relation may be changed by elevated pulmonary capillary wedge pressure, augmenting right ventricular pulsatile load.
Methods and Results
Several large clinical databases with right heart/pulmonary catheterization data were analyzed to determine the RPA-CPA relationship with pulmonary hypertension, pulmonary fibrosis, patient age, and varying pulmonary capillary wedge pressure. Patients with suspected or documented pulmonary hypertension (n=1009) and normal pulmonary capillary wedge pressure displayed a consistent RPA-CPA hyperbolic (inverse) dependence, CPA=0.564/(0.047+RPA), with a near-constant resistance-compliance product (0.48±0.17 seconds). In the same patients, the systemic resistance-compliance product was highly variable. Severe pulmonary fibrosis (n=89) did not change the RPA-CPA relation. Increasing patient age led to a very small but statistically significant change in the relation. However, elevation of the pulmonary capillary wedge pressure (n=8142) had a larger impact, significantly lowering CPA for any RPA and negatively correlating with the resistance-compliance product (P<0.0001).
Conclusions
Pulmonary hypertension and pulmonary fibrosis do not significantly change the hyperbolic dependence between RPA and CPA, and patient age has only minimal effects. This fixed relationship helps explain the difficulty of reducing total right ventricular afterload by therapies that have a modest impact on mean RPA. Higher pulmonary capillary wedge pressure appears to enhance net right ventricular afterload by elevating pulsatile, relative to resistive, load and may contribute to right ventricular dysfunction.
Am Heart Assoc