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Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome

Imperial College School of Medicine, Royal Brompton Hospital, London, UK

CORRESPONDENCE: T.W. Evans, Adult Intensive Care Unit, Royal Brompton Hospital, Sydney Street, London, SW3 6NP, UK. Fax: 44 207 351 8524. E-mail: t.evans@rbh.nthames.nhs.uk

Keywords: acute respiratory distress syndrome, pulmonary hypertension

Received: December 23, 2002
Accepted January 3, 2003

E. Moloney is supported by a European Respiratory Society Fellowship.

Abstract

Pulmonary hypertension (PH) is a characteristic feature of the acute respiratory distress syndrome (ARDS). The magnitude of PH has been shown to correlate with the severity of lung injury in patients with ARDS independently of the severity of associated hypoxaemia and has an adverse prognostic significance.

Early in the histopathological evolution of ARDS, pulmonary vasoconstriction, thromboembolism and interstitial oedema contribute to the development of PH, although pulmonary vascular remodelling probably occurs eventually. Intravenous vasodilator agents lead to an increase in intrapulmonary shunting and systemic hypotension, which can limit their therapeutic use, and have not been shown to improve survival. By contrast, rapidly metabolised vasodilators administered by inhalation induce selective pulmonary vasodilatation and decrease shunting, but again do not appear to confer a survival benefit.

Research aimed at further understanding the mechanisms that underlie pulmonary hypertension, a characteristic feature of the acute respiratory distress syndrome, are expected to provide improvements in pharmacological interventions for the treatment of pulmonary hypertension in the acute respiratory distress syndrome.

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