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Asian Cardiovasc Thorac Ann 2008;16:503-507
© 2008 Asia Publishing EXchange Ltd

REVIEW PAPER

Pulmonary Protection During Cardiac Surgery: Systematic Literature Review

Enisa MF Carvalho, BSc, Edmo A Gabriel, MD, Tomas A Salerno, MD

Division of Cardiothoracic Surgery, University of Miami Miller School of Medicine and Jackson Memorial Hospital Miami, USA

For reprint information contact: Tomas A Salerno, MD Tel: 1 305 585 5271 Fax: 1 305 547 2185 Email: tsalerno{at}med.miami.edu, Cardiothoracic Surgery, 1611 NW 12th Avenue, Miami, Florida 33136, USA.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 FACTORS CONTRIBUTING TO...
 MEASURES TO AVOID LUNG...
 SUMMARY
 REFERENCES
 
Ischemia-reperfusion injury occurs during heart surgery in which cardiopulmonary bypass is used. Current knowledge of the factors contributing to postoperative pulmonary dysfunction and the measures to avoid it are reviewed.


   INTRODUCTION
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 ABSTRACT
 INTRODUCTION
FACTORS CONTRIBUTING TO...
 MEASURES TO AVOID LUNG...
 SUMMARY
 REFERENCES
 
Blood supply to the lungs occurs through extensive connections in the pulmonary and bronchial circulation.1 The bronchial circulation is responsible for approximately 1% of lung irrigation, and its main function is nutrition of the pulmonary structures.2–4 Connections between the pulmonary and bronchial circulation are particularly important when the pulmonary arterial circulation is lacking. In the long-term, the bronchial circulation may dilate and support the functions of the affected areas.5–9

Disturbance of lung function after cardiac surgery remains an important issue because it increases postoperative morbidity and mortality. The disturbance may range from subclinical functional changes that occur in most patients, to full-blown adult respiratory distress syndrome in < 2% after cardiopulmonary bypass (CPB).10,11 The mortality rate associated with adult respiratory distress syndrome is > 50%, and the morbidity leads to delayed postoperative recovery and prolonged hospital stay.10,12 "Post-bypass lung" is characterized by increased intrapulmonary shunting, atelectasis, increased alveolar-arterial oxygen partial pressure difference (PA-aO2), increased extravascular lung water, and decreased compliance.13–17 Major causes of post-bypass lung are reduced or absent blood flow through the lungs during CPB (partial CPB) and entry into the pleural spaces during surgery.9,18 Despite years of research into this phenomenon, understanding of the complex pathophysiology of CPB-induced lung injury remains incomplete. Current knowledge of this subject is reviewed with particular emphasis on some therapeutic modifications.


   FACTORS CONTRIBUTING TO POSTOPERATIVE PULMONARY DYSFUNCTION
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 ABSTRACT
 INTRODUCTION
 FACTORS CONTRIBUTING TO...
MEASURES TO AVOID LUNG...
 SUMMARY
 REFERENCES
 
The etiology of pulmonary dysfunction after cardiac surgery is thought to be multifactorial, occurring as a result of combined effects. These include extra-CPB factors (general anesthesia, sternotomy, and breach of the pleura) and intra-CPB factors (blood contact with artificial material, administration of heparin-protamine, hypothermia, cardiopulmonary ischemia, and lung ventilatory arrest).19,20 A systemic inflammatory response through contact of blood with the artificial material of the CPB circuit, leading to contact-activation of leukocytes and platelets, is regarded as the major contributing factor.9 Similarly, CPB-induced lung injury has been associated with the activation of complement, leukocytes, and endothelial cells and secretion of cytokines and other soluble inflammatory mediators.

GENERAL ANESTHESIA
Using computed tomography, researchers have found that general anesthesia induces atelectasis in nearly all patients.21 However, CPB appears to cause additional lung injury and delays pulmonary recovery compared to other types of major surgery, generally believed to be due to the damaging effects of the systemic inflammatory response associated with CPB.20,22 The best strategy to combat this is use of a membrane oxygenator instead of a bubble oxygenator, with early extubation, leading to fast-track recovery.23

SYSTEMIC TEMPERATURE
Systemic temperature was not found to significantly influence gas exchange (PA-aO2) after coronary artery bypass grafting (CABG).24 However, reduced intrapulmonary shunt function, PA-aO2, and alveolar-arterial CO2 gradient were reported in normothermic patients in another study, indicating that normothermia may preserve lung function after CPB.25

ON-PUMP VS OFF-PUMP CABG
Off-pump CABG is associated with a reduced cytokine response, fewer circulating neutrophils and monocytes, and a significantly lower level of neutrophil elastase compared to on-pump CABG.26–28 In other observational studies and randomized trials however, off-pump CABG was associated with fewer pulmonary complications, less oxygenation impairment, earlier extubation, shorter mechanical ventilation, and a lower incidence of pneumonia than on-pump CABG, but these observations remain largely unexplained.29–37

POLYMORPHONUCLEAR NEUTROPHIL ACTIVATION
Proinflammatory mediators can promote lung injury by augmenting polymorphonuclear neutrophil activation.20,38 Several cytokines including interleukin (IL)-1, IL-2, IL-6, IL-8, and tumor necrosis factor-{alpha} have been shown to promote polymorphonuclear neutrophil activation and recruitment.39–43 The best treatment is corticosteroid administration before CPB, which was found to reduce the release of proinflammatory mediators such as IL-6, IL-8, and tumor necrosis factor-{alpha}, although it had little effect on complement activation.20,44–46 In a porcine model, post-CPB lung function (PA-aO2, pulmonary vascular resistance, and extracellular fluid accumulation) was better preserved after pretreatment with methylprednisolone.47 However, in a randomized clinical trial, patients who received methylprednisolone during sternotomy or at the onset of CPB had similar or higher postoperative PA-aO2 levels and pulmonary shunt function, as well as longer intubation times compared to control subjects.48,49 Aprotinin is known to decrease lung injury by increasing neutrophil deformability and inhibiting the activity of adhesion molecules in neutrophils.50 Aprotinin priming of the CPB circuit may result in reduced postoperative morbidity and shorter intensive care unit stay.20 Leukocyte depletion during CPB may limit the postoperative inflammatory response, as measured by reduced IL-8 production, although its beneficial effects on post-CPB pulmonary function have been inconsistent.51 In some studies, leukocyte depletion did not significantly improve postoperative PaO2 levels and pulmonary hemodynamics.51,52 In other reports, better preserved lung function and less free radical generation was associated with leukocyte-depleted CPB.53–57

FREE RADICALS
Hyperoxic CPB is widely used in cardiac operations, and there is concern about whether oxygenation may induce oxygen-derived free radicals. It has been suggested that hyperoxic CPB increases oxygen free radical damage to the lung, compared to normoxic CPB, which is reflected in lower vital capacity and reduced values of forced expiratory volume in the first second.58


   MEASURES TO AVOID LUNG INJURY
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 ABSTRACT
 INTRODUCTION
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 MEASURES TO AVOID LUNG...
SUMMARY
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MODIFICATION OF CPB CIRCUIT
Heparin-coated circuits are associated with reduced activation of leukocytes and release of cytokines, resulting in less inflammatory reactions following CPB.59–61 Compared with conventional circuits, heparin coating may improve lung compliance and pulmonary vascular resistance, and may reduce intrapulmonary shunting.62,63 However, such benefits can only be transient and might not be clinically significant.64

CONTINUOUS HEMOFILTRATION
High-volume continuous hemofiltration, by removing potentially destructive and inflammatory substances from the circulation during CPB, can significantly reduce systemic edema and pulmonary hypertension, thereby improving lung function.65 The combined use of balanced ultrafiltration and modified ultrafiltration can effectively concentrate the blood, modify the increase of some harmful inflammatory mediators, attenuate lung edema and inflammatory pulmonary injury, and mitigate the impairment of pulmonary function.

MAINTAINING MECHANICAL VENTILATION DURING CPB
Hypoventilation during CPB is associated with the development of micro-atelectasis, hydrostatic pulmonary edema, poor compliance, and a higher incidence of infection.66,67 Hence, some investigators have hypothesized that mechanical ventilation during CPB may limit postoperative lung injury by preventing these complications.66–69 Moreover, the lungs are totally dependent on oxygen supply from the bronchial arteries during the period of cardiac arrest. Atelectasis is more important in postoperative lung gas exchange and ventilatory abnormalities than increased permeability edema.70 The data agree with rapidly developing atelectasis during induction of anesthesia prior to surgery, and may also explain the positive effect on postoperative lung function of continuous airway pressure or ventilation during surgery.36,71,72 One study determined the effect of continuous positive airway pressure at 10 cm H2O during CPB on postoperative pulmonary gas exchange and showed that compared to patients whose lungs had been open to the atmosphere, arterial PO2 was significantly higher and PA-aO2 was significantly lower in the study group 4 hours after CPB completion, and at the time of extubation, gas exchange was significantly better in the study group; thus it was suggested that this treatment may avoid dispersed alveolar collapse throughout the lungs.69

MAINTAINING LUNG PERFUSION DURING CPB
The question remains whether maintaining pulmonary arterial perfusion during CPB could attenuate the deterioration of lung function. In animal models, CPB without pulmonary perfusion resulted in significantly higher pulmonary vascular resistance and PA-aO2, with lower pulmonary compliance.73 Liu and colleagues50 have shown that use of a hypothermic antiinflammatory solution for pulmonary perfusion may help to prevent lung injury, as measured by better post-CPB pulmonary histology and lung function, as well as lower plasma malondialdehyde levels. Richter and colleagues74 reported an attenuated cytokine response (IL-6, IL-8) and better-preserved lung function (less pulmonary shunting, improved PA-aO2 and respiratory indexes, and earlier extubation) in patients undergoing bilateral extracorporeal circulation (Drew-Anderson technique). Another recent study in a canine model demonstrated that biventricular CPB helped to preserve lung function (reduced pulmonary vascular resistance and extravascular lung water, improved lung compliance) compared to conventional heart-lung bypass, which may further support the maintenance of pulmonary artery perfusion during CPB.75 Rahman and colleagues76 reported that malondialdehyde levels in lung tissue increased less in patients receiving aprotinin than in controls after pulmonary artery clamping. This showed that pulmonary artery clamping causes ischemia-reperfusion injury in the lungs. Schlensak and colleagues5 demonstrated in their experimental study that bronchial artery blood flow significantly decreased despite adequate perfusion pressure, and ischemia occurred during total CPB, causing ultrastructural changes. These severe ultrastructural changes highlight the importance of the pulmonary arterial circulation. Continuous pulmonary artery perfusion with oxygenated blood during CPB can decrease lung injury.


   SUMMARY
TOP
 ABSTRACT
 INTRODUCTION
 FACTORS CONTRIBUTING TO...
 MEASURES TO AVOID LUNG...
 SUMMARY
REFERENCES
 
A study reported that in patients with good ventricular function and no preexisting pulmonary disease, CABG with or without the use of CPB caused a similar degree of postoperative lung dysfunction.77 This suggests that the deterioration in pulmonary gas exchange after cardiac surgery is more likely a consequence of the anesthetic and surgical techniques used, rather than an effect of CPB.6,77 When placing an aortic cross clamp during CABG under CPB, if the pulmonary circulation is interrupted, the bronchial circulation becomes insufficient, and ultrastructural injury occurs to the lungs. Perfusion of the lung during these periods may prevent ischemia-reperfusion injury.


   REFERENCES
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 ABSTRACT
 INTRODUCTION
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 MEASURES TO AVOID LUNG...
 SUMMARY
 REFERENCES
 

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