Right Ventricular Function in ALI and ARDS View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1998

AUTHORS

F. Brunet , A. T. Dinh-Xuan , J. F. Dhainaut

ABSTRACT

Severity of acute lung injury (ALI) can widely vary amongst patients, ranging from mild-to-moderate to the acute respiratory distress syndrome (ARDS) [1, 2]. An abnormal inflammatory response with acute microvascular lung injury causes permeability edema and pulmonary arterial hypertension (PAH). This acute increase in pulmonary artery pressure is usually progressive and results from several mechanisms including increased vascular tone, extrinsic compression, hypoxic pulmonary vasoconstriction (HPV) and vascular microthrombi [3], Clinical studies have demonstrated elevated pulmonary vascular resistance (PVR) persisting after correction of arterial hypoxemia [4]. The presence of PAH has been identified as a poor prognostic factor in patients with ARDS, but the relationship between PAH and outcome is still not well understood [5, 6]. It is plausible that increased mortality observed in the subset of patients with PAH could be related to the effects of pulmonary hypertension on pulmonary edema formation and right ventricular (RV) performance [3, 7]. We found abnormal RV performance, reflected by an increased right atrial pressure/pulmonary artery occlusive pressure ratio, was an early predictive factor of mortality in a multivariate analysis of patients with severe ARDS [8]. However, RV failure, defined as the in-ability to maintain adequate stroke volume, is rare in ALI/ARDS, in which RV output is usually conserved by the Frank-Starling mechanism [9–13]. RV failure occurs only when PAH is acute and severe, or when associated diseases alter RV contractile state. More... »

PAGES

147-162

Book

TITLE

Acute Lung Injury

ISBN

978-3-642-64532-7
978-3-642-60733-2

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-642-60733-2_10

DOI

http://dx.doi.org/10.1007/978-3-642-60733-2_10

DIMENSIONS

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