05-07-2008

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ISSN: 1300-0292
İndekslendiği Dizinler: SCIENCE CITATION INDEX EXPANDED
CINAHL, Index Copernicus,
Chemical Abstracts (CA),
Excerpta Medica / EMBASE
Dil: Türkçe, İngilizce
İçerik: Orijinal Araştırma, Derleme, Editöre Mektup, Olgu Sunumu, Tıp Eğitimi, Tıbbi Kitap İncelemeleri

 

REVIEW ARTICLES


Treatment Of Acute Pulmonary Hypertension

Semih BUZ, MD,a Frank WAGNER, MD,a Derya ÖZKAN, MD,a Roland HETZER, MDa

aDepartment of Cardiothoracic and Vascular Surgery, Deutsches Herzzentrum Berlin, GERMANY



A dysfunctional pulmonary vascular endothelium with diminished release of nitric oxide (NO) and increased expression of endothelin-1 is thought to be the main pathophysiological inductive mechanism for acute pulmonary hypertension. New therapeutic approaches are aimed at ameliorating endothelial dysfunction in acute pulmonary hypertension. Whether or not acute pulmonary hypertension has to be treated depends on the degree of functional impairment of the right ventricle resulting from an acute increase in right ventricular afterload. The treatment of acute pulmonary hypertension comprises optimizing right ventricular preload, increasing contractility, lowering right ventricular afterload, improving coronary perfusion and, lastly, mechanical circulatory support. Most importantly, it is essential that pulmonary arterial pressures and right ventricular afterload be lowered in acute pulmonary hypertension. Systemic vasodilators to treat pulmonary hypertension are nonselective and may induce arterial hypotension. Inhaled NO in therapeutic doses selectively dilates the pulmonary vasculature without inducing systemic hypotension. To date, NO inhalation is only approved for the treatment of persistent pulmonary hypertension in newborns. For all other indications, NO therapy is only possible as "off-label use". Inhaled NO has been successfully used for all indications in the treatment of acute pulmonary hypertension following cardio-surgical interventions. It has proved to be especially effective after implantation of left ventricular assist devices and following heart and lung transplantations. As an alternative therapy, inhalation of aerosolized prostanoids similar to inhaled NO selectively decreases pulmonary arterial pressures, but is still awaiting medical approval. In the future, endothelin-receptor antagonists will be available to treat pulmonary hypertension; they are presently being evaluated in extensive clinical trials. Since the advent of the routine use by many centers of inhaled NO following heart transplantations and implantation of left ventricular assist devices, the incidence of right ventricular failure due to pulmonary hypertension is decreasing.

Keywords: Pulmonary hypertension, therapy, endothelin, nitric oxide

Turkiye Klinikleri J Med Sci 2005, 25:295-305

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