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Effects of cpb on lungs
- 1. Effects of CPB on Lungs NAHAS N Clinical perfusionist NIMS Medicity
- 2. Introduction
- 3. The lungs receive blood from pulmonary arteries and the bronchial arteries, that supply blood to nourish the lung tissues. Most of the blood from the lungs returns to the heart through the pulmonary veins ( left heart venting necessary). The longer the pump run the more likely there will be pulmonary dysfunction.
- 4. Triggers of lung impairment during CPB Due to, the CPB circuit with the patients’ blood being exposed to a wide range of synthetic materials ( results in SIRS and the ischemia –reperfusion injury). This can lead to Post-op bleeding Infection MODs – ALI or ARDS Alveolar and endothelial damage- resulting in Pulmonary edema, accumulation of alveolar protein, facilitation of inflammatory cell sequestration and brocho-alveolar lavage fluid (thickened alveolar-endothelial barrier). Metabolic acidosis Neutrofilic infiltration in lung tissues.
- 5. Respiratory changes after cardiac surgery Deleterious effect on the muscle pump and chest wall, phrenic nerve damage and/or diaphragm dysfunction ( cold CPG solution) Normal respiratory function may interfere both surgery stress and the presence of chest tube drains. Alveolar edema due to LV distension or elevated pressures. Capillary permeability ( leading to alveolar flooding) may due to either transfusion reactions or allergic reactions to drugs.
- 6. Lung mechanics The mechanical properties of respiratory system is referred as : Compliance – Describes the stiffness of the lungs Change in volume over the changes in pressure Elastance/ elastic recoil – The tendency of the lung to return to its resting state Resistance – Airway resistance
- 7. Effects of CPB on Lung mechanics: - Thoracotomy decreases the lung compliance. - Forced expiratory volume (FEV1) is decreased immediately after CABG. - Changes in flows and volumes both reduces inspiratory strength and reduced on uncoordinated ribcage expansion. - Increases in respiratory rate and a decrease in Tidal volume(TV). - Decrease in respiratory efficiency and increasing the oxygen cost of breathing.
- 8. Respiratory sequelae of CPB Reduced respiratory system compliance Increased respiratory system resistance Reduced lung volumes and gas flows rates Impaired gas exchange Atelectasis Phrenic nerve damage/ dysfunction Reduced pump function (muscle weakness) Cardiogenic pulmonary edema ‘Pump lung’ or ARDS
- 9. Phrenic nerve damage: -Frost-bitten phrenic nerve was originally described in 1963. -Phrenic nerve damage / dysfunction secondary to trauma or extreme cold may result in significant post-op loss of lung volume.
- 10. Surfactant : Special alveolar epithelial cells secrete surfactant leads to fluid that coat inside surface of alveoli lead to 2-10 times decrease surface tension in alveoli which prevents alveolar collapse Alveoli lead to decrease surfactant result in increase surface tension lead to lung collapse (The lack of surfactant function therefore leads to atelectasis). Surfactant changes occur only after significant microvascular damage.
- 12. Gas exchange: Alveolar to arterial oxygen gradient increases immediately after cardiac surgery Decrease in paO2 appears to be due to : -The mechanical changes -Atelectasis -Decrease in lung volume -Increase in pulmonary ventilation -Pleural effusion and/or pleural thickening and greater still if an internal mammary artery graft has been placed.
- 13. CPB induced Hemodilution and post-op lung function Hemodilution during CPB results from, - Non-Haemic prime for the bypass circuitry - Crystalloid CPG infusion - Fluid administration by anesthetists
- 14. Starling equation which relates, capillary permeability factors to hydrostatic and colloid osmotic pressure An increase in capillary hydrostatic pressure or reduction in colloid osmotic pressure should promote fluid transduction from the capillary. Hemodilution alone results in fluid accumulation and reduced plasma oncotic pressure (may responsible for gas exchange abnormalities after CPB). Interstitial and alveolar edema will develop due to trans-capillary fluid transduction (rapid or excessive). The development of lung edema after CPB due to post- op ventricular dysfunction.
- 15. When a decrease in capillary pressure, the Starling Equation suggests that fluid will move from the interstitial space into the vascular space. This, finally, is what leads to anemia. The plasma is "diluted" by fluid shifting from the interstitium.
- 18. oncotic pressure - The osmotic pressure created by colloids (mainly plasma proteins) which are normally retained within the vascular system; oncotic pressure nearly offsets the hydrostatic pressure which acts to drive fluid out of vessels into the extravascular space; the result is that small amounts of fluid cross the vascular barrier, which are then transported back to the blood via the lymphatics; a decrease in oncotic pressure can be a cause of non-inflammatory edema. edema - Any excessive accumulation of serous fluid or interstitial fluid (lymph) in tissue spaces or a body cavity; significant edema will produce obvious swelling of the involved tissues;
- 19. Post perfusion lung syndrome Postperfusion lung syndrome is similar to adult respiratory distress syndrome in clinical features, diagnostic approaches and management strategies. the etiologies and predisposing risk factors may differ between each other. The ARDS that develops early after cardiopulmonary bypass (CPB) is known as post-perfusion or post-pump syndrome, which remains a significant clinical problem on those patients receiving heart operations under CPB. Postperfusion lung syndrome is rare but refractory.
- 20. Both ALI and ARDS were characterized by an acute onset, bilateral pulmonary infiltrations on chest X-ray and pulmonary wedge pressure <18 mmHg. The only differential criterion for both disorders was arterial oxygen tension (PaO2)/fractional inspired oxygen (FiO2) <300 mmHg in ALI, but PaO2/FiO2 <200 mmHg in ARDS. ARDS was classified into 3 levels based on degree of hypoxemia: mild (200 mmHg < PaO2/FiO2 <300 mmHg) moderate (100 mmHg <PaO2/FiO2 <200 mmHg) severe (PaO2/FiO2 <100 mmHg)
- 21. CPB may be of considerable pulmonary pathophysiological consequences in terms of the alveolar-arterial oxygenation gradient [P(A-a)O2], intrapulmonary shunt, degree of pulmonary edema, pulmonary compliance pulmonary vascular resistance, may eventually lead to pulmonary dysfunction. The respiratory dysfunction can be a result of pulmonary ischemia-reperfusion injury, interstitial edema and impaired microcirculation induced by CPB with activated cytokines, enhanced reactive oxygen species and reduced endogenous nitric oxide production
- 23. Pathophysiology Respiratory indicators PaO2/FiO2 - termed as oxygenation index, shows a good correlation with intrapulmonary shunting, and can better reflect anoxia even in the condition of oxygen therapy PaO2 - is easily influenced by mechanical ventilation. As PaO2 decreases in all types of respiratory failure, it cannot reflect the actual respiratory function and may therefore be less reliable, but leading to a delayed diagnosis if taken for an early diagnosis of ARDS Arterial/alveolar oxygen tension ratio [P(A/a)O2] - is an indicator of gas exchange (oxygen intake) impairment. Increase of P(A-a)O2 mean deficiency of gas exchange and is likely to be more sensitive than the decrease of PaO2 Respiratory index (RI) is the ratio of P(A-a)O2 to PaO2. The normal range of RI is 0.1-0.3, ARDS patients with sustained RI elevation may eventually develop multiple organ failure
- 24. Lung compliance Type II cells main function is to produce surfactant. Surfactant plays an essential role in preventing the alveoli from collapsing. type II cell impairment may inevitably result in pulmonary compliance reduction. a marked reduction in lung compliance, the work of breathing and the physiologic dead space increase. Mechanical ventilation may reverse hypoxemia of ALI and prevent from developing into ARDS. With increasing PEEP, PaO2/FiO2 increases and static lung compliance stabilizes.
- 25. Extravascular lung water It is composed of intracellular, intra-alveolar and alveolar interstitial fluid. Increase of extravascular lung water is a prominent feature of ARDS and the actual reason for refractory hypoxemia. Clinically, extravascular lung water index (EVLWI) is an indicator for the description of extravascular lung water. The normal range of EVLWI is 3.0-7.0 mL/kg. An EVLWI >7.0 mL/kg suggests the presence of pulmonary edema. ARDS closely correlated with increase of EVLWI and pulmonary vascular permeability index.
- 26. Intrapulmonary shunting A pulmonary shunt is a condition of ventilation-perfusion mismatch with normal blood perfusion but insufficient ventilation of the lungs. The intrapulmonary shunt is optimal in assessing the severity of hypoxemia. Intrapulmonary shunting has a close relation negative to PaO2/FiO2, but positive to P(A-a)O2, and is also affected by pulmonary artery wedge pressure and cardiac index
- 27. Acid-base imbalances In the early stage of ARDS, respiratory alkalosis is the most common type of acid-base imbalance followed by metabolic acidosis and combined respiratory alkalosis and metabolic alkalosis. while using diuretics and glucocorticoids (for metabolic alkalosis), or in the presence of severe hypoxia, renal dysfunction, or shock (for metabolic acidosis) and electrolyte imbalance (hypokalemia, normal or high blood chloride, and normal or reduced blood sodium) In its late stage, patients may develop respiratory acidosis, respiratory acidosis associated with metabolic acidosis and even triple acid-base imbalance. occur in the condition of reduced ventilation and carbon dioxide retention, often associated with normal or high blood potassium and normal or reduced blood chloride and sodium
- 28. Mechanism of post-perfusion lung syndrome - Remains uncertain - May probably be due to the inflammatory cascade induced by contact between blood and CPB circuit subsequent activations of leukocytes, platelets, coagulation and fibrinolysis system and kallikrein- bradykinin and complement system - After crossclamp removal, joint actions of protease release by leukocytes in the pulmonary vascular beds, production of oxygen free radicals and intestinal endotoxin translocation lead to increased pulmonary microvascular permeability, microthrombus formation in the pulmonary vessels and the quality and quantity changes of pulmonary surfactant predispose to the development of postperfusion lung syndrome
- 29. RISK FACTORS Insufficient perfusion of visceral organs caused by low output syndrome and prolonged hypotension might be responsible. Preoperative cardiac function impairment, bloodstream infection, prolonged crossclamp and operation durations, hypotension episodes hypogammaglobulinemia
- 30. PREVENTION Choices of CPB circuit Apparatus Innovative CPB techniques Modified surgical maneuvers Medicinal agents - corticosteroids and aprotinin Hyperonocotic CPB-prime with hydroxyethyl starch
- 31. MANAGEMENT Ventilatory treatment Pharmaceutical treatment
- 32. Ventilatory treatment Mechanical ventilation - high-frequency oscillatory ventilation Patients with ALI/ARDS, mechanical ventilation with a lower tidal volume (6 mL/kg) than is traditionally used. Adequate PEEP levels avoid alveolar collapse and maintain sufficient pulmonary volume at the end of expiration. Excessive PEEP increases the risk of pneumothorax and airway impairment, causing adverse hemodynamic effects by increasing intra-thoracic pressure and reducing venous return inadequately low PEEP level provokes cyclic alveolar collapse and re-opening, resulting in atelectrauma.
- 33. Pharmaceutical treatment Surfactant therapy Vasodilators - Nitric oxide is a powerful endogenous vasodilator Prostaglandins Glucocorticoids Anti-inflammatory agents Extracorporeal membrane oxygenation (ECMO)
- 34. Extracorporeal membrane oxygenation (ECMO) ECMO is a therapeutic option for patients with severe ARDS. The indications for ECMO use in ARDS patients are failed conventional therapy for 24-96 hours and the conformity of two of the three required slow-entry criteria for ECMO including PaO2/FiO2 <150 mmHg at PEEP >5 cmH2O, semistatic compliance <30 mL/cmH2O and right-left shunt >30%. Only in the patients with life-threatening hypoxemia (PaO2<50 mmHg at FiO2 1.0 and PEEP>5 cmH2O for>2 hours (fast-entry criteria) is immediate ECMO commenced[81]. Mols et al.[82] reported one-quarter of their 245 ARDS patients received ECMO treatment. The survival rate was 55% in ECMO patients and 61% in non-ECMO patients. However, the role of ECMO in the treatment of ARDS is controversial[83]. In neonates treated with ECMO, a survival rate of 80% was achieved. In adult patients with ARDS, two randomized controlled trials revealed the survival rates were 10% and 33%, respectively, in the ECMO groups[84]. Meta-analysis of 9 studies on a total of 1,058 patients with 386 of them treated with ECMO revealed ECMO increased the mortality of ARDS patients. Therefore, it seems that ECMO is not beneficial in adult patients with ARDS as in neonates
Editor's Notes
- PaO2/FiO2 is affected by methods of oxygen supply and oxygen concentration, and hence it is an indicator of impairments of the pulmonary vascular beds and alveoli, irrelevant to extrapulmonary organ failure.
- Increase in capillary endothelial and/or alveolar epithelial permeability and pulmonary surfactant deficiency from type II cell impairment may inevitably result in pulmonary compliance reduction. The inflammatory process and alveolar flooding lead to severe ventilation-perfusion mismatch and intrapulmonary shunt, which are manifested clinically as severe hypoxia with a decrease in the PaO2/FiO2 ratio. However, airway injury and hypokinemia may occur under the treatment of a high positive end-expiratory pressure (PEEP) and positive pressure support. This may in turn worsen the systemic inflammatory reactions and lead to extrapulmonary organ dysfunction or failure[22]. However, a 20-cmH2O PEEP can be a turning point of PaO2/FiO2 and static lung compliance fall
- Extravascular lung water positively correlated with lung injury severity and oxygenation but negatively correlated pulmonary compliance
- Alveolar macrophages are prone to be activated, releasing many inflammatory mediators including TNF-α, interleukin (IL)-6 and IL-8 and superoxide dismutase, etc., and damaging vascular endothelium and alveolar epithelium, thus making the lungs being the first target organ of insult. TNF-α and IL-6 may cause direct lung injury effects by inducing early inflammatory reactions, releasing toxic products and increasing pulmonary permeability[42]. In the lung, TNF-α is generated by activated pulmonary macrophages and accumulates in the bronchoalveolar lavage fluid of ALI patients[43]. The pathogenesis of TNF-α with receptors in neutrophil activation and infiltration of lung injury remain unclear. However, it has been noted that neutrophil accumulation and lung leak were abrogated in mice lacking the p55 TNF-α receptor[44]. TNF-α also stimulates the adhesions of the endothelial cells and neutrophils, and impacts a toxic effect by release of proteases, oxygen free radicals and superoxide dismutase. Productions of ILs including ILs-1, -2, -6 and -8 would be increased by stimulations of mon-macrocytes strengthening the lung injury. Accordingly, an early appearance of TNF-α may herald the development of ARDS and the synthesis and secretion of ILs
- Both direct and indirect lung injuries can be predisposing risk factors leading to ARDS. Surgical trauma and CPB are among indirect risk factors.
- Choices of CPB circuit - use of miniaturized circuits of CPB and circuit with biocompatible surfaces ultrafiltration Apparatus - leukocyte depletion filters and ultrafiltration Innovative CPB techniques (partial restoration of pulmonary artery perfusion during CPB) Modified surgical maneuvers (reducing the use of cardiotomy suction device and reducing the contact-time between free blood and pericardium Medicinal agents - as preventive strategies for ALI during CPB, which were proved to be of satisfactory outcomes on improving the lung function hyperonocotic CPB-prime with hydroxyethyl starch 10% (200:0.5) may improve cardiac function and reduce pulmonary water content in the early postoperative period
- Prone positioning improves gas exchange and has long been used as an adjunct or salvage therapy for severe or refractory ARDS. A strategy employing higher PEEP along with low tidal volume ventilation should be considered for ARDS patients receiving mechanical ventilation. ARDS patients receiving higher PEEP had a strong trend toward improved survival. However, higher PEEP had a strong trend toward harm as higher PEEP can conceivably cause ventilator-induced lung injury by increasing plateau pressures, or cause pneumothorax or decreased cardiac output
- Prostaglandins are endogenous derivatives of arachidonic acid with properties of vasodilation, platelet aggregation inhibition and anti-inflammation. Inhaled prostacyclins cause selective pulmonary vasodilation, thereby enhancing lung function by improving ventilation-perfusion mismatch and oxygenation and by reducing pulmonary vascular resistance Glucocorticoids can reduce inflammation and fibrosis through inhibition of several cytokines including ILs-1, -3, -5, -6 and -8, TNF-α and granulocyte macrophage-colony stimulating factor. High-mobility group box 1 (HMGB1) is a critical mediator in the pathogenesis of many inflammatory diseases. Penehyclidine hydrochloride inhibits the translocation of release of HMGB1 from the nucleus to the cytoplasm and the expression of HMGB1 messenger ribonucleic acid in a dose-dependent manner