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Circulation, Vol 72, 1270-1278, Copyright © 1985 by American Heart Association
JS Janicki, KT Weber, MJ Likoff and AP Fishman
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: the
mean PAP-flow relationship was linear; 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 pulmonary vascular
resistance declined with exercise. Notable exceptions to the third
observation were patients with valvular heart disease or a resting
pulmonary vascular resistance greater than 800 dyne-sec-cm-5.
ARTICLES
The pressure-flow response of the pulmonary circulation in patients with heart failure and pulmonary vascular disease
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