The effects of vasodilators on right ventricular performance were studied at rest and during exercise in 32 patients with clinically stable chronic respiratory failure.
1) Intravenous isosorbide dinitrate (ISDN) (1γ/kg/min, 11 patients) induced a significant decrease in right atrial pressure (RAP), pulmonary arterial mean pressure (PAMP) and cardiac index (CI), however no change in total pulmonary vascular resistance (TPVR). Right ventricular work index (RVWI) was reduced significantly by ISDN during exercise. CI was reduced by ISDN, however PvO
2, which indicates tissue oxygenation, showed no change.
ISDN reduced the right ventricular preload by means of venodilation and reduced right ventricular work.
2) Sublingual nifedipine (10 mg, 11 patients) induced a significant increase in CI and O
2-transport, but a decrease in PAMP and TPVR. Systemic arterial pressure decreased and heart rate increased significantly after nifedipine administration.
Nifedipine reduced the right ventricular afterload by means of active vasodilation of the pulmonary vascular beds, and increased CI and O
2-transport.
3) Captopril (25mg, 10 patients), an oral angiotensin converting-enzyme inhibitor, acted as a vasodilator, with arterial and venous effects. The hemodynamic response to captopril was similar to the combination administration of intravenous ISDN and sublingual nifedipine. Captopril reduced the increase in CI and O
2-transport, but decreased the PAMP and TPVR, as was ISDN. Heart rates remained unchanged and failed to increase reflexly following reduction in blood pressure, as was observed with other vasodilators. By reducing angiotensin II, a factor in the enhanced systemic vascular resistance, captopril might be useful as adjunctive therapy to counteract vasoconstrictive effects, which was the homeostatic mechanism of chronic vasodilator therapy.
Further long-term studies are necessary to establish therapeutic efficacies of these agents.
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