Prostaglandin E1 and intrapulmonary shunt in cardiac surgical patients with pulmonary hypertension Academic Article Article uri icon

Overview

MeSH Major

  • Cysteine
  • Isoquinolines
  • Neuromuscular Blockade
  • Neuromuscular Nondepolarizing Agents

abstract

  • Unlike many other vasodilators, prostaglandin E1 may reduce pulmonary vascular resistance without changing intrapulmonary shunt in patients with adult respiratory distress syndrome. Whether the same is true for surgical patients with cardiogenic pulmonary hypertension but normal gas exchange remains unclear. Data from the intraoperative records of 8 patients with pulmonary hypertension and elevated pulmonary vascular resistance were used for the study. Hemodynamic variables had been monitored through radial arterial cannulas and pulmonary arterial catheters. Arterial and mixed venous oxygen tension, carbon dioxide tension, oxygen saturation, and hemoglobin level, as well as cardiac output and pulmonary capillary wedge pressure, had been determined in each patient before prostaglandin E1 infusion was started and again when the desired pulmonary vascular response had been achieved. Pulmonary and systemic vascular resistances and intrapulmonary shunt were calculated from standard formulas. Infusion rates of prostaglandin E1 ranged from 7 to 135 ng/kg/min. Prostaglandin E1 reduced mean pulmonary arterial pressure, pulmonary vascular resistance, and pulmonary capillary wedge pressure but did not change intrapulmonary shunt. Heart rate and mean arterial and right atrial pressures were not changed, whereas systemic vascular resistance decreased and cardiac output increased. The present study shows that prostaglandin E1 reduces pulmonary arterial pressure and pulmonary vascular resistance without dramatic changes in intrapulmonary shunt in patients with pulmonary hypertension secondary to cardiac disease.

publication date

  • January 1990

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1016/0003-4975(90)90257-7

PubMed ID

  • 2106846

Additional Document Info

start page

  • 463

end page

  • 5

volume

  • 49

number

  • 3