Vascular components of ARDS. Clinical pulmonary hemodynamics and morphology.
Mild pulmonary artery hypertension (PAP, 29.6 +/- 10.6 mm Hg, mean +/- SD) due to a 3-fold elevation of pulmonary vascular resistance (PVR, 2.2 +/- 1.1 mm Hg X L/min) is a common finding in severe ARDS. A vasodilator such as nitroprusside (151 micrograms/kg X min) can be administered in early ARDS and will lower PAP and PAOP (capillary wedge pressure) while increasing cardiac output (CO) from 6.9 to 8.75 L/min X M2 and venous admixture from 23% to 31.6%. This suggests diffuse vasoconstriction is present in early ARDS. In 19 patients with severe ARDS, 13 had vascular occlusions on balloon occlusion angiography, and these occlusions correlated with increased post mortem counts of PA thrombi. At autopsy, there was a considerable increase of PA medial thickness and a reduction of lumen diameter. This hemodynamic and morphologic evidence suggests both vasoconstrictor and anatomic changes play major roles elevating the PVR in ARDS.
D000208:Acute Disease; D001808:Blood Vessels / Q000473:pathology / Q000503:physiopathology; D005544:Forecasting; D006439:Hemodynamics; D006493:Heparin / Q000627:therapeutic use; D006494:Heparin Antagonists / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D006976:Hypertension, Pulmonary / Q000139:chemically induced; D011479:Protamines / Q000009:adverse effects / Q000627:therapeutic use; D011652:Pulmonary Circulation; D012128:Respiratory Distress Syndrome / Q000473:pathology / Q000503:physiopathology*
D006494:Heparin Antagonists; D011479:Protamines; D006493:Heparin