Nitroprusside infusion does not improve biventricular performance in patients with acute hypoxemic respiratory failure

Sibbald, William J.; Driedger, Albert A.; McCallum, Duncan; Cunningham, David; Cheung, H.

doi:10.1016/s0883-9441(86)80001-6

Cited by 19 publications

(6 citation statements)

References 23 publications

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“…2) two distinct groups of patients can be identified: In the patients who exhibited pathologically low RVEF values in the control period (RVEF < 45%) [5] the raean increase in RVEF was 6.8%. This number exceeds the limit which is considered to be a significant response to RVEF to a therapeutic intervention for both the thermodilution [18] and radionuclide techniques [7]. In contrast the response in the four patients with normal baseline RVEF values was a mean change of RVEF of 1.6%.…”

Section: Discussionmentioning

confidence: 74%

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Prostacyclin and right ventricular function in patients with pulmonary hypertension associated with ARDS

et al. 1990

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Eight patients who developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2, 12.5-35.0 ng.kg-1.min-1) for 45 min. We examined whether reducing the right ventricular (RV) outflow pressures by PGI2 infusion would increase the right ventricular ejection fraction (RVEF) measured by thermodilution. PGI2 reduced the pulmonary artery pressure (PAP) from 35.6 to 29.1 mmHg (p less than 0.01). The cardiac index (CI) increased from 4.2 to 5.81.min-1.m-2 (p less than 0.01) partly due to an increased stroke volume. The decreased PAP together with the increased CI resulted in a fall of the calculated pulmonary vascular resistance index (PVRI, from 5.1 to 2.5 mmHg.min.m2.1-1, p less than 0.01). In the patients with subnormal baseline RVEF the increased stroke volume was associated with an increased RVEF (from 47.6% to 51.8%, p less than 0.05) suggesting improved RV function. This result was underscored by a significant relationship between the changes in PVRI and RVEF (r = 0.789, delta % RVEF = 2.11.delta PVRI-1.45). Despite an increased venous admixture from 27.8% to 36.9% (p less than 0.05) the arterial PO2 remained constant resulting in an increased oxygen delivery from 657 to 894 ml.min-1.m-2 (p less than 0.01). We conclude that short term infusions of PGI2 increased CI concomitant to improved RV function parameters when baseline RVEF was depressed. Since improved oxygen availability should be a major goal in the management of patients with ARDS PGI2 may be useful to lower pulmonary artery pressure in ARDS.

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Section: Discussionmentioning

confidence: 74%

“…As unloading the right ventricle might improve RV function [5] vasodilator treatment of PH has been advocated. Infusing prostaglandin E 1 [6] or conventional vasodilators such as sodium nitroprusside [7], however, has failed to improve global RV function in patients with ARDS.…”

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confidence: 99%

Prostacyclin and right ventricular function in patients with pulmonary hypertension associated with ARDS

et al. 1990

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“…They should also be selective for well-ventilated alveoli as opposed to poorly ventilated alveoli, thereby avoiding increased right-to-left shunt, venous admixture and worsening oxygenation. Several trials of intravenously infused agents (including agents infused directly into the pulmonary artery) have demonstrated that reductions in PAP can only be gained at the expense of systemic hypotension, with the concomitant risks of RV ischaemia and heart failure [69][70][71][72][73][74][75] . Furthermore, increased flow to the areas of poor ventilation induced by systemic vasodilators worsens .…”

Section: Vasodilator Therapymentioning

confidence: 99%

Pulmonary Hypertension and Selective Pulmonary Vasodilators in Acute Lung Injury

Blythe

Heerden

Power

1998

Anaesth Intensive Care

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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 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 and increasing shunt (14)(15)(16) attributable to attenuation of hypoxic vasoconstriction.…”

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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Nitroprusside infusion does not improve biventricular performance in patients with acute hypoxemic respiratory failure

Cited by 19 publications

References 23 publications

Prostacyclin and right ventricular function in patients with pulmonary hypertension associated with ARDS

Prostacyclin and right ventricular function in patients with pulmonary hypertension associated with ARDS

Pulmonary Hypertension and Selective Pulmonary Vasodilators in Acute Lung Injury

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

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