Adult respiratory distress syndrome following cardiopulmonary bypass: incidence and prediction

Messent, Mark; Sullivan, Katie; Keogh, Brian F; Morgan, C.; Evans, Timothy W.

doi:10.1111/j.1365-2044.1992.tb02134.x

Cited by 148 publications

(84 citation statements)

References 7 publications

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“…4,5 These findings support the theory that accepts the mechanism of postpump syndrome as a neutrophil-mediated destruction of the alveolar-capillary interface. In our model, CPB primes neutrophils, causing them to sequester in the lung, and subsequent exposure to low-dose LPS activates these primed neutrophils, causing degranulation and the release of oxygen radical species, serine proteases, and MMPs.…”

Section: Discussionsupporting

confidence: 78%

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Matrix Metalloproteinase Inhibitor Prevents Acute Lung Injury After Cardiopulmonary Bypass

Carney¹,

Lutz²,

Picone³

et al. 1999

Circulation

120

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Background-Acute lung injury (ALI) after cardiopulmonary bypass (CPB) results from sequential priming and activation of neutrophils. Activated neutrophils release neutral serine, elastase, and matrix metalloproteinases (MMPs) and oxygen radical species, which damage alveolar-capillary basement membranes and the extracellular matrix, resulting in an ALI clinically defined as adult respiratory distress syndrome (ARDS). We hypothesized that treatment with a potent MMP and elastase inhibitor, a chemically modified tetracycline (CMT-3), would prevent ALI in our sequential insult model of ALI after CPB. Methods and Results-Anesthetized Yorkshire pigs were randomized to 1 of 5 groups: control (nϭ3); CPB (nϭ5), femoral-femoral hypothermic bypass for 1 hour; LPS (nϭ7), sham bypass followed by infusion of low-dose Escherichia coli lipopolysaccharide (LPS; 1 g/kg); CPBϩLPS (nϭ6), both insults; and CPBϩLPSϩCMT-3 (nϭ5), both insults plus intravenous CMT-3 dosed to obtain a 25-mol/L blood concentration. CPBϩLPS caused severe lung injury, as demonstrated by a significant fall in PaO 2 and an increase in intrapulmonary shunt compared with all groups (PϽ0.05). These changes were associated with significant pulmonary infiltration of neutrophils and an increase in elastase and MMP-9 activity. Conclusions-All pathological changes typical of ALI after CPB were prevented by CMT-3. Prevention of lung dysfunction followed an attenuation of both elastase and MMP-2 activity. This study suggests that strategies to combat ARDS should target terminal neutrophil effectors. (Circulation. 1999;100:400-406.)

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Section: Discussionsupporting

confidence: 78%

“…1 Despite significant advances in critical care management, mortality from ARDS remains Ͼ40%. [2][3][4] ARDS after cardiopulmonary bypass (CPB) is often called "postperfusion" or "postpump" syndrome, but it is otherwise indistinguishable from acute lung injury associated with trauma, hemorrhage, or sepsis.…”

mentioning

confidence: 99%

Matrix Metalloproteinase Inhibitor Prevents Acute Lung Injury After Cardiopulmonary Bypass

Carney¹,

Lutz²,

Picone³

et al. 1999

Circulation

120

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“…Among the several techniques available to study respiratory mechanics during mechanical ventilation, the single breath method (SBM) (37), the end-inflation occlusion method (EIOM) (11), and the interrupter technique (IT) (38) have been successfully applied to normal humans or patients with acute respiratory failure (1,(21)(22)(23)39). SBM allows a detailed account of respiratory system resistive properties throughout relaxed expiration.…”

Section: Validity and Limitations Of Measurements Of Respiratory Mechmentioning

confidence: 99%

The effects of positive end-expiratory pressure on respiratory system mechanics and hemodynamics in postoperative cardiac surgery patients

Auler

Carmona

Barbas

et al. 2000

Braz J Med Biol Res

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We prospectively evaluated the effects of positive end-expiratory pressure (PEEP) on the respiratory mechanical properties and hemodynamics of 10 postoperative adult cardiac patients undergoing mechanical ventilation while still anesthetized and paralyzed. The respiratory mechanics was evaluated by the inflation inspiratory occlusion method and hemodynamics by conventional methods. Each patient was randomized to a different level of PEEP (5, 10 and 15 cmH 2 O), while zero end-expiratory pressure (ZEEP) was established as control. PEEP of 15-min duration was applied at 20-min intervals. The frequency dependence of resistance and the viscoelastic properties and elastance of the respiratory system were evaluated together with hemodynamic and respiratory indexes. We observed a significant decrease in total airway resistance (13.12 ± 0.79 cmH 2 O l -1 s -1 at ZEEP, 11.94 ± 0.55 cmH 2 O l -1 s -1 (P<0.0197) at 5 cmH 2 O of PEEP, 11.42 ± 0.71 cmH 2 O l -1 s -1 (P<0.0255) at 10 cmH 2 O of PEEP, and 10.32 ± 0.57 cmH 2 O l -1 s -1 (P<0.0002) at 15 cmH 2 O of PEEP). The elastance (E rs ; cmH 2 O/l) was not significantly modified by PEEP from zero (23.49 ± 1.21) to 5 cmH 2 O (21.89 ± 0.70). However, a significant decrease (P<0.0003) at 10 cmH 2 O PEEP (18.86 ± 1.13), as well as (P<0.0001) at 15 cmH 2 O (18.41 ± 0.82) was observed after PEEP application. Volume dependence of viscoelastic properties showed a slight but not significant tendency to increase with PEEP. The significant decreases in cardiac index (l min -1 m -2 ) due to PEEP increments (3.90 ± 0.22 at ZEEP, 3.43 ± 0.17 (P<0.0260) at 5 cmH 2 O of PEEP, 3.31 ± 0.22 (P<0.0260) at 10 cmH 2 O of PEEP, and 3.10 ± 0.22 (P<0.0113) at 15 cmH 2 O of PEEP) were compensated for by an increase in arterial oxygen content owing to shunt fraction reduction (%) from 22.26 ± 2.28 at ZEEP to 11.66 ± 1.24 at PEEP of 15 cmH 2 O (P<0.0007). We conclude that increments in PEEP resulted in a reduction of both airway resistance and respiratory elastance. These results could reflect improvement in respiratory mechanics. However, due to possible hemodynamic instability, PEEP should be carefully applied to postoperative cardiac patients.

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“…Although the incidence of ALI and ARDS as a complication after open heart surgery is not high (ranging from 0.5 to 1.3% in different institutions), the mortality rate can be as high as 53-91%, respectively (Asimakopoulos et al, 1999;Christensen et al, 1996;Messent et al, 1992). Few data are available on the efficacy of surfactant therapy in patients developing ARDS after cardiac surgery (Satoh et al, 1998;Hermon et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Surfactant Therapy for Patients with ARDS After Cardiac Surgery

Баутин

Хубулава

Kozlov

et al. 2006

Journal of Liposome Research

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Adult respiratory distress syndrome following cardiopulmonary bypass: incidence and prediction

Cited by 148 publications

References 7 publications

Matrix Metalloproteinase Inhibitor Prevents Acute Lung Injury After Cardiopulmonary Bypass

Matrix Metalloproteinase Inhibitor Prevents Acute Lung Injury After Cardiopulmonary Bypass

The effects of positive end-expiratory pressure on respiratory system mechanics and hemodynamics in postoperative cardiac surgery patients

Surfactant Therapy for Patients with ARDS After Cardiac Surgery

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