Lungs & CPB

Lungs & CPB

The most common pulmonary complication associated with cardiopulmonary bypass is postoperative atelectasis of the lungs.

Preoperative conditions that predispose the patient to developing partial or total collapse of the lung are, surfactant depletion and mucus cell hyperplasia associated with chronic bronchitis developed from smoking, decreased FRC encountered with obesity, and cardiogenic pulmonary edema.  Passive ventilation of a paralyzed diaphragm and lack of changing ventilatory pattern consistent with mechanical breathing are intraoperative factors that lead to preferential gas distribution to non-dependent areas of the lung.  This leads to a ventilation-perfusion mismatch and results in hypoventilation of the dependent lung sections

Postoperative atelectasis manifests due to compression of the immobile left lobe by the heart, lung compression resulting from pleural drainage and bleeding, and alterations of surfactant levels during the operation.  Various approaches to prevent atelectasis have been studied.  These include delivery of positive pressure ventilation, intermittent sighs, or static inflation, none of which demonstrate definitive or reliable effect.

Acute lung injury may occur in association with cardiopulmonary bypass.  Morphologic changes to lung tissue include diffuse congestion, edema in the alveolar and interstitial regions, and hemorrhagic atelectasis.

This type of injury has been termed pump lung  and may result from a range of causes during the operation.  Microembolism of: protein aggregates; disintegrated platelets; damaged fibrin; and fat particles; represents one theory on the development of this condition.  Complement activation, inflammatory response, hemodilution, lung hypoxia, and elevated pulmonary artery pressures, are other factors inviting acute lung injury.

Prevention

Reduction of microemboli proliferation via blood filtration, prevention of pulmonary vascular distension, and hemodilution, are methods that when augmented with the administration of steroids and vasodilator prostaglandins, may preclude the onset of this process.

Key Points:

• The lung is a target organ for injury induced by CPB.
  • Atelectasis
  • Smoking, chronic bronchitis, chronic obstructive pulmonary disease, and obesity all predispose patients to atelectasis.
  • Atelectasis decreases oxygenation and C_L.
• Acute lung injury
  • Lung injury related to CPB and microemboli is decreased by blood filtration.
  • Complement activation correlates with lung dysfunction after CPB.
  • Inflammatory response produced by “contact activation” of blood (activation of neutrophils and endothelium, generation of complement and cytokines) contributes to lung injury after CPB.
• Noncardiogenic pulmonary edema is rare but has a high mortality rate, is most commonly associated with complement activation and protamine, and is treated by volume expansion, mechanical ventilation, and cardiac support.
• Acute bronchospasm
  • Acute bronchospasm is related to complement activation.
  • Cold urticaria can be treated with H₁ and H₂ blockade.
  • Inaccuracy of EtCO₂
• Prevention of lung injury is by:
  • Blood filtration
  • Membrane oxygenators
  • Hemodilution
  • Pharmacology, such as steroids (controversial), prostaglandins (i.e., leukocyte and platelet inhibition), and aprotinin (inhibits plasmin, kallikrein, bradykinin).
• Exclusion of lung circulation during CPB impairs normal metabolic functions, such as clearance of prostaglandins, serotonin, bradykinin, and norepinephrine and generation of prostaglandins and angiotensin.

References:

Cardiopulmonary Bypass: Principles and Practice

To View Cited Work- Click Here

Ross AF, Gomez MN, Tinker JH.  Anesthesia for adult cardiac procedures. In:  Rogers MC, Tinker JH, Covino BG, Longnecker DE, eds. Principles and Practice     of Anesthesiology. St. Louis, MO. Mosby Year Book; 1993;2:1649-1679.

Sladen RN, Berkowitz DE. Cardiopulmonary bypass and the lung. In Gravlee GP,     Davis RF, Utley JR, eds. Cardiopulmonary Bypass: Principles and Practice. Baltimore, MD. Williams & Wilkens; 1993:468-487.