Cause of the Raised Wedge Pressure on Exercise in Chronic Obstructive Pulmonary Disease

Abstract

Patients with chronic obstructive pulmonary disease (COPD) markedly increase their pulmonary artery wedge pressure on mild exercise even though they have no overt left heart disease and no increase in the esophageal pressure (as a reflection of mean intrathoracic pressure). We wondered if lung distension due to gas trapping during the hyperpnea of exercise might cause the wedge pressure to rise by increasing juxtacardiac pressures above esophageal pressures. If this were so, then (1) tachypnea alone, without exercise, should cause the FRC and intracardiac pressures to increase in patients with COPD, (2) there should be an increase in FRC associated with the rise in wedge pressure on exercise, and (3) these changes should not occur in patients without COPD. We studied 39 patients with COPD (Ppa = 21 +/- 6 mm Hg [mean +/- SD], FEV1 [% predicted] = 39 +/- 16) and 13 control patients with similar pulmonary artery pressures but no airflow obstruction (Ppa = 22 +/- 20 mm Hg, FEV1 [% predicted] = 110 +/- 24). In those with COPD, light exercise raised the FRC by 0.5 +/- 0.5 L. Tachypnea alone, at the rate present during exercise, raised the FRC by 0.6 +/- 0.4 L and there was a 10% increase in left lower lobe area on lateral chest X-ray. Wedge, right atrial, and pulmonary artery pressures rose together during tachypnea with and without exercise. By contrast, in the control patients without COPD, the right atrial pressure change on exercise did not reflect that of the left atrium in extent or direction.(ABSTRACT TRUNCATED AT 250 WORDS)

Systemic manifestations and comorbidities of COPD

“…These findings are best explained by an incapacity of the heart to normally raise the cardiac output with exercise as its function is impaired by the pressure that surround it. Indeed, right heart catheterisation shows that patients with severe COPD who hyperinflate either during exercise or by voluntary hyperventilation develop high negative intra-thoracic pressures resulting in increased pulmonary and capillary wedge pressures, suggestive of left ventricular dysfunction [106]. Taken together these studies suggest that the function of the heart is mechanically constrained by the dynamic hyperinflation that is associated with exercise or increased ventilatory demand in patients with COPD whose resting hyperinflation is already a limiting problem.…”

Pulmonary hypertension at exercise in COPD: does it matter?

“…In the study of HILDE et al [6], PCWP was on average normal at rest, but increased markedly at exercise, in patients with, as well as without, pulmonary hypertension. It has been previously shown that in patients with COPD, PCWP and PAP increase at rest and more so at exercise, along with oesophageal pressures, in relation to dynamic hyperinflation and expiratory muscle contraction [14][15][16]. Therefore, pulmonary vascular pressures may actually increase with intrathoracic pressure becoming higher than reference atmospheric pressure, although a direct compression of the heart may also occur, thereby further increasing left ventricular end-diastolic pressure [14][15][16].…”

“…It has been previously shown that in patients with COPD, PCWP and PAP increase at rest and more so at exercise, along with oesophageal pressures, in relation to dynamic hyperinflation and expiratory muscle contraction [14][15][16]. Therefore, pulmonary vascular pressures may actually increase with intrathoracic pressure becoming higher than reference atmospheric pressure, although a direct compression of the heart may also occur, thereby further increasing left ventricular end-diastolic pressure [14][15][16]. As illustrated in figure 1, intrathoracic pressure swings in patients with COPD may be huge, but are more positive than negative.…”

“…Pulmonary vascular pressures used to be averaged over two to three respiratory cycles, rather than measured only at endexpiration as currently recommended [14][15][16]. In the study by HILDE et al [6], pulmonary vascular pressures were measured at end-expiration and the authors even added a temporary breath-hold.…”

“…However, the question remains as to whether it makes ''physiological'' sense to read PAP and PCWP exclusively at the moment when intrathoracic pressure is highest. It may be more sensible to subtract oesophageal pressures from pulmonary vascular pressures for a realistic evaluation of the pulmonary circulation in the presence of marked variations in intrathoracic pressures [14][15][16].…”