Chest
Volume 121, Issue 4, April 2002, Pages 1269-1277
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Reviews
Pulmonary Dysfunction After Cardiac Surgery

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Postoperative lung injury is one of the most frequent complications of cardiac surgery that impacts significantly on health-care expenditures and largely has been believed to result from the use of cardiopulmonary bypass (CPB). However, recent comparative studies between conventional and off-pump coronary artery bypass grafting have indicated that CPB itself may not be the major contributor to the development of postoperative pulmonary dysfunction. In our study, we review the associated physiologic, biochemical, and histologic changes, with particular reference to the current understanding of underlying mechanisms. Intraoperative modifications aiming at limiting lung injury are discussed. The potential benefits of maintaining ventilation and pulmonary artery perfusion during CPB warrant further investigation.

Section snippets

The Phenomenon

Lung injury after CPB is evident by the presence of postoperative pulmonary functional, physiologic, biochemical, and histologic changes.

How Much of the Lung Injury Is CPB-Related?

Few would argue about the presence of lung injury following CPB. However, pulmonary dysfunction after CPB may be the result of multiple insults from various aspects of CPB surgery.25,26 These include extra-CPB factors (ie, general anesthesia, sternotomy, and breach of the pleura) and intra-CPB factors (ie, blood contact with artificial material, administration of heparin-protamine, hypothermia, cardiopulmonary ischemia, and lung ventilatory arrest).26 Thus, it is questionable whether lung

PMN Activation

It is well-known that CPB primes and activates polymorphonuclear cells (PMNs) through mechanical shear stress38,39 and contact with the artificial surfaces of the CPB circuit. Proinflammatory mediators can subsequently promote lung injury by augmenting PMN activation.26,40 For instance, several cytokines such as interleukin (IL)-1,41 IL-2,42 IL-6, IL-8,43 and tumor necrosis factor (TNF)-α,41,42 have been shown to promote PMN activation and recruitment. In addition, platelet-activating factor,

Pharmaceuticals

The commonly scrutinized pharmacologic agents with which to treat pulmonary dysfunction are corticosteroids and aprotinin. Corticosteroid administration before CPB has been shown to reduce the release of proinflammatory mediators such as IL-6, IL-8, and TNF-α,26 although there was little effect on complement activation.65,66,67 In addition, methylprednisolone therapy can inhibit neutrophil CD11b expression51 and neutrophil complement-induced chemotaxis,67 thereby decreasing neutrophil

Summary

Although severe lung injury after CPB is uncommon, it remains a significant cause of morbidity and mortality with a major impact on health-care expenditures. There is little doubt that CPB is associated with pulmonary dysfunction, as supported by the ample experimental and clinical evidence of chemical, cellular, and pulmonary functional disturbances after CPB. However, whether CPB itself is directly responsible for postoperative lung dysfunction is still controversial. Some studies have shown

References (99)

  • JM Pearl et al.

    Acute hypoxia and reoxygenation impairs exhaled nitric oxide release and pulmonary mechanics

    Thorac Cardiovasc Surg

    (2000)
  • AL Picone et al.

    Multiple sequential insults cause post-pump syndrome

    Ann Thorac Surg

    (1999)
  • S Wan et al.

    Inflammatory response to cardiopulmonary bypass: mechanisms involved and possible therapeutic strategies

    Chest

    (1997)
  • I Birdi et al.

    Effects of cardiopulmonary bypass temperature on pulmonary gas exchange after coronary artery operations

    Ann Thorac Surg

    (1996)
  • R Ascione et al.

    Inflammatory response after coronary revascularization with or without cardiopulmonary bypass

    Ann Thorac Surg

    (2000)
  • BM Matata et al.

    Off-pump bypass graft operation significantly reduces oxidative stress and inflammation

    Ann Thorac Surg

    (2000)
  • CM Cox et al.

    Effect of cardiopulmonary bypass on pulmonary gas exchange: a prospective randomised study

    Ann Thorac Surg

    (2000)
  • SC Stamou et al.

    Beating heart versus conventional single-vessel reoperative coronary artery bypass

    Ann Thorac Surg

    (2000)
  • T Yokoyama et al.

    Off-pump versus on-pump coronary bypass in high-risk subgroups

    Ann Thorac Surg

    (2000)
  • F Abdullah et al.

    The novel chemokine mob-1: involvement in adult respiratory distress syndrome

    Surgery

    (1997)
  • DE Carney et al.

    Soluble tumor necrosis factor receptor prevents post-pump syndrome

    J Surg Res

    (1999)
  • ME Faymonville et al.

    Myeloperoxidase and elastase as markers of leukocyte activation during cardiopulmonary bypass in humans

    Thorac Cardiovasc Surg

    (1991)
  • GE Hill et al.

    Aprotinin and methylpredisolone equally blunt cardiopulmonary bypass-induced inflammation in humans

    Thorac Cardiovasc Surg

    (1995)
  • WJ Dreyer et al.

    Intercellular adhesion molecule-1 regulation in the canine lung after cardiopulmonary bypass

    Thorac Cardiovasc Surg

    (1998)
  • AM Gillinov et al.

    Complement and neutrophil activation during cardiopulmonary bypass: a study in the complement-deficient dog

    Ann Thorac Surg

    (1994)
  • J Butler et al.

    Systemic inflammatory responses to cardiopulmonary bypass: a pilot study of the effects of pentoxifylline

    Respir Med

    (1993)
  • JL Johnson et al.

    Interleukin-6 augments neutrophil cytotoxic potential via selective enhancement of elastase release

    J Surg Res

    (1998)
  • G Ferry et al.

    Activation of MMP-9 by neutrophil elastase in an in vivo model of acute lung injury

    FEBS Lett

    (1997)
  • K Ihnken et al.

    Normoxic cardiopulmonary bypass reduces oxidative myocardial damage and nitric oxide during cardiac operations in the adult

    Thorac Cardiovasc Surg

    (1998)
  • K Sato et al.

    Increase pulmonary vascular contraction to serotonin after cardiopulmonary bypass: role of cyclooxygenase

    J Surg Res

    (2000)
  • AJ Lodge et al.

    Methylprednisolone reduces the inflammatory response to cardiopulmonary bypass in neonatal piglets: timing of dose is important

    Thorac Cardiovasc Surg

    (1999)
  • MA Chaney et al.

    Methylprednisolone does not benefit patients undergoing coronary artery bypass grafting and early tracheal extubation

    Thorac Cardiovasc Surg

    (2001)
  • YJ Gu et al.

    Leukocyte depletion during cardiac operation: A new approach through the venous bypass circuit

    Ann Thorac Surg

    (1999)
  • T Mihaljevic et al.

    The influence of leukocyte filtration during cardiopulmonary bypass on post-operative lung function: a clinical study

    Thorac Cardiovasc Surg

    (1995)
  • D Johnson et al.

    Depletion of neutrophils by filter during aortocoronary bypass surgery transiently improves postoperative cardiorespiratory status

    Chest

    (1995)
  • D Johnson et al.

    Neutrophil-mediated acute lung injury after extracorporeal perfusion

    Thorac Cardiovasc Surg

    (1994)
  • K Morioka et al.

    Leukocyte and platelet depletion with a blood cell separator: effects on lung injury after cardiac surgery with cardiopulmonary bypass

    Thorac Cardiovasc Surg

    (1996)
  • K Bando et al.

    Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass

    Thorac Cardiovasc Surg

    (1990)
  • YJ Gu et al.

    Heparin-coated circuits reduce the inflammatory response to cardiopulmonary bypass

    Ann Thorac Surg

    (1993)
  • H Te Velthuis et al.

    Heparin coating of extracorporeal circuits inhibits contact activation during cardiac operations

    Thorac Cardiovasc Surg

    (1997)
  • S Wan et al.

    Heparin-coated circuits reduce myocardial injury in heart or heart-lung transplantation: a prospective, randomised study

    Ann Thorac Surg

    (1999)
  • M Ranucci et al.

    Beneficial effects of Duraflo II heparin-coated circuits on postperfusion lung dysfunction

    Ann Thorac Surg

    (1996)
  • L Magnusson et al.

    Repeated vital capacity maneuvers after cardiopulmonary bypass effects on lung function in a pig model

    Br J Anaes

    (1998)
  • A Serraf et al.

    Alteration of the neonatal pulmonary physiology after total cardiopulmonary bypass

    Thorac Cardiovasc Surg

    (1997)
  • S Wan et al.

    Myocardium is a major source of proinflammatory cytokines in patients undergoing cardiopulmonary bypass

    Thorac Cardiovasc Surg

    (1996)
  • PJ Chai et al.

    Effects of ischemia on pulmonary dysfunction after cardiopulmonary bypass

    Ann Thorac Surg

    (1999)
  • T Suzuki et al.

    Continuous pulmonary perfusion during cardiopulmonary bypass prevents lung injury in infants

    Ann Thorac Surg

    (2000)
  • Y Liu et al.

    Pulmonary artery perfusion with protective solution reduces lung injury after cardiopulmonary bypass

    Ann Thorac Surg

    (2000)
  • AA Fowler et al.

    Adult respiratory distress syndrome: risk with common predispositions

    Ann Intern Med

    (1983)
  • Cited by (0)

    This study was supported in part by the Direct Grant for Research (Chinese University of Hong Kong No. CRE-2001–021) and the Research Grant Council Earmarked Grant (Chinese University of Hong Kong No. 4310/99M), Hong Kong SAR.

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