We have investigated pulmonary hemodynamics in 16 patients with COPD with respiratory
insufficiency, exhibiting marked peripheral edema. All the patients had previously
undergone, within the last 6 months (T1), a right heart catheterization, in a stable
state of their disease, when they were free of edema. Patients were subdivided into
two groups according to the level of right ventricular end-diastolic pressure (RVEDP)
during the episode of edema (T2): patients with a markedly elevated RVEDP (> 12 mm
Hg) indicating the presence of right ventricular failure (RVF) = group 1, n = 9; patients
with a normal or slightly elevated RVEDP (< 12 mm Hg) = group 2 (no RVF), n = 7. In
group 1 pulmonary artery mean pressure (PAP) increased very significantly from T1
(27 +/- 5) to T2 (40 +/- 6 mm Hg, p < 0.001) as did RVEDP, from 7.5 +/- 3.9 to 13.4
+/- 1.2 mm Hg (p < 0.001). These hemodynamic changes paralleled a marked worsening
of arterial blood gases, PaO2 falling from 63 +/- 4 to 49 +/- 7 mm Hg (p < 0.01) and
PaCO2 increasing from 46 +/- 7 to 59 +/- 14 mm Hg (p < 0.01). On the other hand, in
group 2, PAP was stable during the episode of edema (from 20 +/- 6 to 21 +/- 5 mm
Hg), as was RVEDP (from 5.5 +/- 2.4 to 5.1 +/- 1.5 mm Hg), and changes in arterial
blood gases from T1 to T2 were small and nonsignificant. It is concluded that RVF
is effectively present in at least some patients with COPD with peripheral edema and
is associated with a significant increase of PAP from baseline, probably accounted
for by hypoxic vasoconstriction. Thus, pressure overload may contribute to the development
of RVF. In other patients there are no hemodynamic signs of RVF, PAP is stable, and
the origin of edema is not well understood.