The pressure-flow response of the pulmonary circulation in patients with heart failure and pulmonary vascular disease.

Abstract

Although it is well known that the pulmonary circulation is altered in patients with pulmonary arterial or venous hypertension, the resultant hemodynamic behavior has not been systematically studied. We undertook to do so in a group of patients with pulmonary hypertension of diverse etiology. We measured pulmonary arterial (PAP) and occlusive wedge pressures and cardiac output at rest (i.e., standing) and during progressive upright treadmill exercise in 51 patients. Forty-two had chronic, stable, cardiac failure secondary to ischemic, myopathic or valvular heart disease and were grouped according to whether their mean PAP was less than (normotensive) or greater than (hypertensive) 19 mm Hg, and nine had pulmonary vascular disease of diverse etiology and were considered separately. In the majority of patients, we found that irrespective of whether the hypertension was arterial or venous in origin or etiology: (1) the mean PAP-flow relationship was linear; (2) pulmonary capillary wedge pressure was greater than or equal to the average closure pressure of the pulmonary vascular bed and could therefore be used as the downstream pressure in calculating pulmonary vascular resistance; and (3) pulmonary vascular resistance declined with exercise. Notable exceptions to the third observation were patients with valvular heart disease or a resting pulmonary vascular resistance -5 greater than 800 dyne-sec-cm Circulation 72, No. 6, 1270No. 6, -1278No. 6, , 1985 THE HEMODYNAMIC behavior of a vascular bed can be characterized by the relationship between blood flow and the pressure gradient. In the absence of external forces, the pressure gradient is simply the difference between the upstream or arterial and the downstream or venous pressure. However, because most of the pulmonary vasculature is contained within the parenchyma of the lung, it is subjected to extravascular pressures that result in a critical closure pressure. 1 2 It is not certain whether this pressure normally exceeds the venous pressure and therefore the calculation of the true pressure gradient of the pulmonary circulation remains uncertain. In the isolated lung preparation, in

Haemodynamic evaluation of pulmonary hypertension

“…3). Recent studies have confirmed a predominant increase in arterial resistance in thrombo-embolic disease, a significant increase in arterial but also in venous resistance in primary PH, and the expected major increase in venous resistance in pulmonary venoocclusive hypertension [38,53].…”

“…The fall in PVRI reflects passive distension of compliant small vessels and/or recruitment of additional vessels in the superior portions of the lung [10][11][12][13]38].…”

Pulmonary artery pressure measurement during exercise testing in patients with suspected pulmonary hypertension

“…Pulmonary artery occlusion pressure was not remeasured after exercise if the resting measurement was normal for the reasons previously discussed. It is likely that wedge pressure would have risen on exercise [20,21].…”

The Role of Exercise Testing in the Modern Management of Pulmonary Arterial Hypertension

“…The data for PVR and PAOP in PAH are very limited. In the study by Janicki et al [24] which included a mixture of subjects with PAH and pulmonary hypertension (PH) related to lung disease, PAOP rose from 8 mmHg at rest to 18 mmHg on exercise with PVR unchanged. As discussed earlier, there has been controversy over the S v O2 values achieved at maximal exercise in PAH.…”