Prostaglandin E1 and Nitroglycerin Reduce Pulmonary Capillary Pressure but Worsen Ventilation—Perfusion Distributions in Patients with Adult Respiratory Distress Syndrome

Radermacher, Peter; Šantak, B.; Becker, Heinz; Falke, K. J.

doi:10.1097/00000542-198904000-00008

Cited by 165 publications

(38 citation statements)

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“…Some have reported that a reduction in pulmonary water or endothelial permeability could be connected to a decrease in capillary filtration pressure [16]. However, most of the clinical studies in ARDS patients have only shown modest effects by these drugs on pulmonary capillary pressure [22][23][24], and the most recent large studies have not reported prognostic benefit with the systematic use of inhaled NO in cases of acute lung injury or ARDS [25]. Fluid restriction that is more or less associated with a diuretic treatment makes it possible to reduce both pulmonary capillary pressure and central venous pressure.…”

Section: Fluid Restriction and Diuretics: Clinical Studies And Practimentioning

confidence: 99%

Fluid Management in Acute Lung Injury and ARDS

Roch

Guervilly

Papazian

2010

Yearbook of Intensive Care and Emergency Medicine

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Section: Fluid Restriction and Diuretics: Clinical Studies And Practimentioning

confidence: 99%

Fluid Management in Acute Lung Injury and ARDS

Roch

Guervilly

Papazian

2010

Yearbook of Intensive Care and Emergency Medicine

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“…Vasodilators such as nitroglycerin reduce PaO2 by increasing ventilation-perfusion mismatching and shunt fraction. 19 An intravenous injection of vasodilators was used to control systolic blood pressure in the majority of the patients in this study, but both groups were similar in terms of the use of an intravenous injection of vasodilators. Also, the use of vasodilators was not a predictor of oxygenation impairment in the present study.…”

Section: Discussionmentioning

confidence: 95%

Reduction of the PaO2/FiO2 Ratio in Acute Aortic Dissection - Relationship Between the Extent of Dissection and Inflammation -

Kurabayashi

Okishige

Azegami

et al. 2010

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp cute aortic dissection (AAD) is frequently accompanied by acute respiratory failure. This respiratory failure has been hypothesized by some investigators to be due to activation of systemic inflammatory reactions in AAD, 1-3 given that acute respiratory distress syndrome (ARDS) and its less severe form, acute lung injury (ALI), can have etiology that is systemic, rather than pulmonary, such as in disseminated intravascular coagulation. The systemic inflammatory reaction in AAD is provoked by acute aortic injury and is reflected in an increment in serum C-reactive protein (CRP), 1-4 white blood cell (WBC) count 2 and proinflammatory cytokine levels. 1 We hypothesized that some measure of the extent of aortic dissection, such as its volume, might correlate with the severity of the inflammatory response, and in turn, with respiratory function. To our knowledge, these relationships have never been studied, with the exception of one study in which inflammatory markers were shown to be higher in DeBakey type IIIb AAD than in type IIIa AAD. 2 The specific aims of our study were to identify predictors of oxygenation impairment and to assess the relationship between the incidence of respiratory failure and the extent of aortic dissection. Because proximal type AAD (DeBakey type I or II 5 ) often requires surgical intervention, which could also lead to pulmonary complications, we chose to limit our study to patients with distal type AAD (DeBakey type III 5 ). Background: Acute aortic dissection (AAD) often accompanies acute respiratory failure. The aim of this study was to clarify the relationship between the incidence of oxygenation impairment and the extent of distal type AAD. Methods Study Population

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“…Similar effects of L-NAME on arterial oxygenation were described by Sprague et al 34 using a model of unilateral alveolar hypoxia in anesthetized rabbits. Furthermore, in a study by Radermacher et al, 35 it was found that the increase in CO by systemic administration of nitrovasodilators worsened ventilation-perfusion mismatching and gas exchange in patients with ARDS. The combined use of NO inhalation with systemic inhibition of NO synthesis may prove to be effective therapy in the future.…”

Section: Discussionmentioning

confidence: 97%