Pulmonary Vascular Tone Improves Pulmonary Gas Exchange in the Adult Respiratory Distress Syndrome

Mélot, Christian; Naeije, Robert; Mols, Pierre; Hallemans, Roger; Lejeune, Philippe; Jaspar, Nadine

doi:10.1164/ajrccm/136.5.1232

Cited by 48 publications

(28 citation statements)

References 16 publications

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“…Elliot et al (6) reported persistent abnormalities of DLco as in our cases 1, 2, and 4. They also observed persistent abnormalities of oxygen transfer across the lung during exercise, a condition associated with pulmonary fibrosis.…”

Section: Discussionsupporting

confidence: 66%

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Acute Respiratory Distress Sy n d rome (ARDS): HRCT Findings in Survivors

Jung

Park

Lee

et al. 1999

J Korean Radiol Soc

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Acute lung injury, the most severe form of which is ARDS is defined as rapid alteration of the alveoli that results in impairment of gas exchange. Despite improvement in supportive care for patients with acute lung injury, the mortality rate for ARDS has hovered around the 50 % for the past decade (1). Recent studies have suggested that once a patient has survived initial injury, subsequent gas exchange problems may arise in part from an inadequately regulated healing response (2).Although the plain radiographic and CT findings of ARDS are well known, HRCT findings in survivors of ARDS have not been fully evaluated. We recently encountered four patients who survived from ARDS who were diagnosed according to the definition of Murray et al. (3). We describe the chest radiographic and HRCT findings in these cases, and believe they may explain the pathogenesis of fibrotic lung. Case 1A 30-year-old pregnant woman at gestational week 35

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Section: Discussionsupporting

confidence: 66%

“…Interstitial emphysema, bullae, and pneumothorax are frequently found during the ARDS support, possibly due to barotrauma (6).…”

Section: Discussionmentioning

confidence: 99%

Acute Respiratory Distress Sy n d rome (ARDS): HRCT Findings in Survivors

Jung

Park

Lee

et al. 1999

J Korean Radiol Soc

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“…Moreover, preventing this redistribution can increase the deterioration in oxygenation [13]. Similarly, in patients with ARDS, the characteristic refractory hypoxaemia is primarily the result of intrapulmonary shunting and increased ventilation/perfusion (V9/Q9) mismatch [14], which is further exacerbated by the administration of intravenous vasodilators [15]. Thus, while the increase in Ppa attributable to HPV increases right ventricular afterload, it is a consequence of a physiological reflex designed to preserve V9/Q9 mismatch and attenuate arterial hypoxaemia.…”

Section: Discussionmentioning

confidence: 99%

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

Moloney

Evans²

2003

Eur Respir J

112

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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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“…Not surprisingly, several older clinical trials designed to evaluate the effects of intravenous vasodilators [e. g., nitroglycerin [17], nitroprusside [15], diltiazem [16]] found that pulmonary arterial pressure and pulmonary vascular resistance fall and PaO 2 and systemic O 2 delivery decreased as a result of increased shunt and V A /Q heterogeneity. These deleterious effects were presumed to occur secondary to the inhibition of hypoxic vasocon-943 Fig.…”

Section: Vasodilatorsmentioning

confidence: 99%

“…In humans, it has been difficult to separate vasoconstriction from the effects of PEEP although both seemingly contribute as the degree of pulmonary hypertension changes with titration of PEEP, and intravenous vasodilators reduce pulmonary vascular pressures and improve cardiac output [14,15,27,28]. Unfortunately, this beneficial hemodynamic effect is associated with worsening axygen delivery and increasing shunt (14)(15)(16) attributable to attenuation of hypoxic vasoconstriction. However, inhaled agents can circumvent this problem to some extent (see below).…”

Section: Introductionmentioning

confidence: 99%

Altering ventilation-perfusion relationships in ventilated patients with acute lung injury

Sinclair

Albert

1997

Intensive Care Med

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IntroductionSince its description by Ashbaugh and Petty in 1967, the acute respiratory distress syndrome (ARDS) has been a major research focus in pulmonary and critical care medicine. However, despite rigorous investigation, it remains a common and vexing problem with a high (albeit possibly decreasing) mortality and no specific therapy. The cornerstone of managing patients with ARDS continues to be meticulous supportive care. Severe hypoxemia is a defining characteristic and is usually treated by high fractional inspired oxygen concentrations and the application of positive end expiratory pressure (PEEP). Recently, in response to a better understanding of the mechanisms of hypoxemia, the regional distribution of pulmonary blood flow and ventilation, several additional approaches to improving gas exchange in ARDS have been described. Although studies have not yet been reported to allow comment on whether these new approaches alter measures of clinical outcome, they have the potential to markedly improve our ability to manage these patients.In this review, the regional ventilation-perfusion (V A / Q ) relationships seen in ARDS are described as well as a number of new interventions designed to alter these in a favorable fashion.Ventilation-perfusion relationships in ARDS: mechanisms of hypoxemia ARDS results from a variety of predisposing factors which lead to injury of the pulmonary endothelium and alveolar epithelial membrane [1,2]. This is manifest clinically in diffuse pulmonary infiltrates and marked hypoxemia with increased venous admixture as calculated from arterial blood gases [1, 3]. The hypoxemia is usually relatively refractory to increasing F I O 2 but frequently responds in part, to the application of PEEP [4,5].Early investigators [3], using the multiple inert gas elimination technique, found that hypoxemia in ARDS is due primarily to intrapulmonary shunt, with an additional contribution from regions of very low V A /Q in some patients. These findings are consistent with those seen in experimental models of ARDS [6][7][8]. A subsequent study [9] confirmed these findings and demonstrated that the application of PEEP reduced shunt and redistributed blood flow to regions of low or normal V A /Q . Pulmonary hypertension is described in patients with ARDS and in animal models of the syndrome. The duration in pulmonary arterial pressure is usually modest but is associated with an increased mortality [10,11]. In animal models the degree of pulmonary hypertension is considerably greater [12] and in the early stages of injury has been attributed to neurohormonal mediators constricting the pulmonary circulation [13]. In humans, it has been difficult to separate vasoconstriction from the effects of PEEP although both seemingly contribute as the degree of pulmonary hypertension changes with titration of PEEP, and intravenous vasodilators reduce pulmonary vascular pressures and improve cardiac output [14,15, 27, 28]. Unfortunately, this beneficial hemodynamic effect is associated with worsening axygen delivery ...

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Pulmonary Vascular Tone Improves Pulmonary Gas Exchange in the Adult Respiratory Distress Syndrome

Cited by 48 publications

References 16 publications

Acute Respiratory Distress Sy n d rome (ARDS): HRCT Findings in Survivors

Acute Respiratory Distress Sy n d rome (ARDS): HRCT Findings in Survivors

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

Altering ventilation-perfusion relationships in ventilated patients with acute lung injury

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