Pulmonary and Cardiovascular Alterations in ARDS: Morphology, Hemodynamics and Therapy

  • W. M. Zapol
Conference paper
Part of the Update in Intensive Care and Emergency Medicine book series (UICM, volume 1)

Abstract

We have reported that the pulmonary artery pressure (\(\overline {PAP} \)) and vascular resistance (PVR) are always elevated in moderate and severe ARDS of diverse etiology [1, 2]. This occurs despite a normal PaO2 and can occur within a few hours after acute lung injury. We are uncertain as to the precise cause of the increased PVR but its effect, pulmonary hypertension, places a severe load on the lung which is exchanging fluid in the face of both an increased microvascular permeability and an increased hydrostatic pressure. Late in ARDS the PVR is not reduced by infusing vasodilators (nitroprusside, phentolamine, ibuprofen). However, early in ARDS, Snider et al. have reported that infusing nitroprusside reduced the PAP and pulmonary capillary wedge pressure (PCWP), while increasing cardiac output, thus vasodilation or vascular recruitment occurred [2, 3]. There was no effect on the elevated PVR of altering PvO2 or pHv over a wide range of partial bypass flow rates using ECMO.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1986

Authors and Affiliations

  • W. M. Zapol

There are no affiliations available

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