7.3.11 Pulmonary function and ventilation on bypass

Ventilation and ECC

Although ventilation is not required for gas exchange during bypass surgery, lungs left alone collapse as well as lymphatic drainage, atelectasis sets in. When the aorta is clamped, pulmonary artery flow stops and bronchial artery flow falls by 50% [12]. The ventilatory mode during bypass surgery is an unresolved issue. No study has so far clearly demonstrated the superiority of one technique over another.

A routine is to leave a continuous low flow of O2 and air (1 L/min, FiO2 0.3-0.5) without PEEP. CPAP (continuous positive airway pressure) at 5-10 cm H2 O, low tidal volume (3-4 mL/kg) and low frequency (6 cycles/min) mechanical ventilation, or vital capacity manoeuvres during bypass surgery, do improve oxygenation parameters at the moment of weaning off pump, but this effect is not sustained and has no impact on patient outcome [3,7,8,17]. A recent meta-analysis confirms the momentary improvement of the alveolar-arterial gradient by CPAP but the absence of impact of ventilation on pulmonary complications and on the duration of postoperative respiratory assistance [22]. There is therefore nothing in the literature to recommend any form of ventilation other than a passive flow of O2 /air mixture, especially as ventilation clutters the operating field and brings blood back into the LA, which will bring huge hindrance to the operator [4,19]. The incidence of postoperative atelectasis also does not seem to be related to the ventilatory mode during bypass surgery (continuous mechanical ventilation, CPAP in apnoea, or no ventilation), provided that the lungs are correctly re-expanded when ventilation is resumed [13,21]. In contrast, vital capacity manoeuvres (30-40 cm H2 O for 20-30 seconds) are essential when ventilation is resumed before weaning off pump. As lung expansion is disruptive to the surgeon and may place undue strain on a mammery graft, the surgical field should be carefully monitored during these manoeuvres.

Mechanical ventilation is clearly beneficial as soon as the heart is ejecting blood, before or after aortic clamping. When the heart is beating in bypass surgery (aorta unclamped), the blood that perfuses the coronaries is largely blood propelled by the LV, thus returning from the lungs via the pulmonary veins; its O2 content increases if the lungs are ventilated. The same applies to partial bypass surgery (e.g. femoral-femoral). In these conditions, reduced ventilation is recommended: TV 3-4 mL/kg, rate 6-8 cycles/min, FiO2 0.3-0.5, no PEEP. If the perfusionist administers a halogen in the oxygenator while the patient is ventilated, it is important to add the same fraction of the halogen inspired on the ventilator, otherwise the halogen is eliminated from the lungs simultaneously with its administration in the bypass circuit.

Halogens have been shown to reduce the impact of ischaemia and reperfusion injury, particularly in coronary artery surgery, through their preconditioning effect; compared with intravenous anaesthesia, they reduce markers of myocardial injury, improve immediate functional recovery and marginally reduce mortality [5,8,11]. However, some problems arise with incorporating a vaporiser on the bypass circuit [16].

  • Isoflurane, sevoflurane and desflurane in their liquid form cause cracking in the polypropylene used for the structure of oxygenators and connectors, so the vaporiser should always be below the ECC circuit.
  • The outlet of the oxygenator is open to the air; without an adequate exhaust system, halogen can pollute the operating room (maximum tolerated amount: 2 ppm).
  • Polymethylpentene membranes (used mainly in ECMO) are poorly permeable to halogens, so the fraction dissolved in the blood is much lower than that assumed from the inspired fraction. Gas transfer is not affected by other membrane types.
  • Several manufacturers do not mention the possibility of including a vaporiser in their ECC circuit, which raises doubts about the legality of this setup (not authorised in France and Germany).

At the moment of re-ventilation at the end of bypass, a maximum vital capacity insufflation manoeuvre is necessary to reduce the risk of subsequent atelectasis [13]. Lung compliance is usually lowered and ventilation pressures are higher than their initial values; the lungs easily air-trap. Normoventilation or even hyperventilation must be maintained despite this phenomenon. As this overpressure is gradually relieved, it is important to reventilate early enough before weaning off pump, so that the lung problem is solved by the time the normal circulation is restored. Activation of kinins, cytokines and complement by contact with foreign surfaces in the bypass circuit is responsible for these changes, which also come along with pulmonary vasoconstriction. The situation may be worsened by protamine injection, which is a potent pulmonary vasoconstrictor and bronchoconstrictor. In the case of tracheobronchial congestion, suctioning is carried out with care because the patient is anticoagulated: exchanging secretions for haemoptysis is of no benefit! Forgetting to ventilate the patient before weaning off pump is a possible but catastrophic event; the best prevention of this accident lies in the strict application of a protocol including starting the ventilator as soon as the aorta is unclamped or the heart beats spontaneously. For safety, it is advisable for the perfusionist to check with the anaesthetist that the patient is ventilated before lowering the pump output.

Pulmonary complications

Cardiac surgery is not a benign procedure for the lung, and almost all operated heart patients suffer from impaired gas exchange [9]. With an incidence of 5-15% of cases, pulmonary complications are the second most common source of postoperative morbidity after cardiac complications [10]. It is common to see a deterioration in gas exchange at the end of the bypass procedure, which is disrupted for a few hours or even a few days. Several phenomena are involved (see Chapter 21, Pulmonary Complications) [1,10,18].

  • Ischaemia-reperfusion lung injury related to pulmonary exclusion during bypass surgery. These are manifested by cytokine and free radical release, exaggerated capillary permeability, increased PAR and oedema.
  • Release of inflammatory mediators: Activation of the complement cascade (C3a and C5a) by foreign surfaces is supplemented by circulating leukocyte activators, interleukins, TNF, histamine, kinins (kallikrein, bradykinin) and the protamine response; these lead to systemic vasodilation, pulmonary vasoconstriction (PAH), bronchospasm and systemic inflammatory response (SIRS). The peak effect occurs 2-6 hours after bypass surgery. The lungs are particularly sensitive to SIRS as it affects endothelial cells and activates leukocytes secondarily sequestered in the lung parenchyma [1].
  • High pulmonary capillary hydrostatic pressure: transient left ventricular failure and decreased cardiac compliance increase filling pressures. This postoperative left ventricular failure remains the major component of pulmonary dysfunction and is the main determinant of postoperative morbidity and mortality.
  • Non-cardiogenic pulmonary oedema ("pump-lung"): due to increased capillary permeability, systemic inflammatory syndrome, fluid accumulation and capillary stasis, ARDS occurs in 1-2% of ECC patients [14]. When associated with haemodynamic failure, this factor is associated with a mortality of 15-40% [15].
  • TRALI (Transfusion-Related Acute Lung Injury) is a major complication of transfusion and is considered the leading cause of death after haemolysis and sepsis [20]. Its incidence is proportional to the amount of plasma administered with the transfusion.
  • Interstitial fluid accumulation: bypass surgery and infusions result in excess crystalloid weight gain up to 3-5 kg, which is proportional to the duration of bypass surgery. However, the effect of this accumulation is modest in the absence of left dysfunction and pulmonary venous stasis.
  • Decrease in lung volumes: the change is most striking during the first 24 hours, but remains measurable for up to 2-3 weeks [2]; the major reasons are atelectasis, a 15-50% decrease in FRC, and a 50% decrease in FEV1.
  • Decreased lung compliance and increased air resistance: together with tachypnoea, these increase the cost of ventilation; up to 20% of overall O2 consumption is devoted to this effect.
  • Phrenic nerve injury: Direct trauma or cold cardioplegia damages the left phrenic nerve and is responsible for left diaphragmatic hemiparesis in 15% of cases [6].
  • Sternotomy, pain (drains) and postoperative muscle weakness deteriorate the mechanical respiratory performance of the rib cage.

These alterations, which are of little clinical significance in normal individuals, are particularly important in patients with pre-existing lung diseases: COPD, restrictive syndrome, asthma, etc. (see Chapter 21 Lung diseases). They are sufficient to precipitate severe ventilatory failure requiring prolonged respiratory therapy in intensive care. Mechanical ventilation with reduced tidal volume (6-8 mL/kg) and PEEP (10 cm H2 O) improves postoperative functional recovery compared to high tidal volume (10-12 mL/kg) [18]. In cardiac surgery, right ventricular failure is often the major complication in patients with chronic lung disease.

Prevention of complications

As pulmonary complications are multifactorial in origin, their prevention is therefore based on several measures [10].

  • The reduction of bypass tubes lenght reduces the contact of blood with foreign surfaces and with the air in the tank, thus reducing the intensity of the inflammatory reaction. Biocompatible materials function the same way.
  • Ultrafiltration removes free water and thereby increases oncotic pressure; it lowers inflammatory cytokines.
  • Retrograde priming at the beginning of ECC decreases the amount of crystalloid
  • The duration of CPB and non-pulmonary ventilation should be as short as possible.
  • Unfortunately, ventilation on bypass is only useful for the prevention of atelectasis; it has no effect on long-term gas exchange. In contrast, vital capacity manoeuvres are effective in improving postoperative ventilatory indices.
  • The preconditioning effect of halogens also affects the lung and promotes gas exchange after bypass surgery.

 

 Lung function
There is no specific protection for the lungs apart from judicious management of ventilation:
            - Low tidal volume ventilation (6-8 mL/kg) with PEEP (5-10 cm H2 O) and FiO2 0.3-0.6
            - O flow2 /pulsed air during ECC
            - Lung expansion by vital capacity manoeuvres during bypass surgery and in the post-ECC period

 

© CHASSOT PG, GRONCHI F, April 2008, last update, December 2019

 

References

 

  1. APOSTOLAKIS  E, FILOS KS, KOLETSIS E, et al. Lung dysfunction following cardiopulmonary bypass. J Cardiac Surg 2010; 25:47-55
  2. BERRIZBEITA LD, TESSLER S, JACOBOWITZ IJ, et al. Effect of sternotomy and coronary artery bypass surgery on postoperative pulmonary mechanics. Chest 1989; 96:873-6
  3. BIGNAMI    E, GUARNIERI M, SAGLIETTI F, et al. Mechanical ventilation during cardiopulmonary bypass. J Cardiothorac Vasc Anesth 2016; 30:1668-75
  4. BOLDT J, KING D, SHELD HH, et al. Lung management during cardiopulmonary bypass: Influence on extravascular lung water. J Cardiothorac Vasc Anesth 1990; 4:73-8
  5. DE HERT S, VLASSELAERS D, BARBE R, et al. A comparison of volatile and non-volatile agents for cardioprotection during on-pump coronary surgery. Anaesthesia 2009; 64:953-60
  6. FEDULLO AJ, LERNER RM, GIBSON J, et al. Sonographic measurement of diaphragmatic motion after coronary artery bypass surgery. Chest 1992; 102:1683-6
  7. FERGUSON BD, MANECKE GR. Goal-directed therapy in cardiac surgery: are we there yet? J Cardiothorac Vasc Anesth 2013;27:1075-8
  8. FERRANDO C, SORO M, BELDA FJ. Protection strategies during cardiopulmonary bypass: ventilation, anesthetics and oxygen. Curr Opin Anesthesiol 2015; 28:73-80
  9. GARCIA-DELGADO M, NAVARETTE-SÀNCHEZ I, COLMENERO M. Preventing and managing perioperative pulmonary complications following cardiac surgery. Curr Opin Anesthesiol 2014; 27:146-52
  10. HUFFMYER JL, GROVES DS. Pulmonary complications of cardiopulmonary bypass. Best Pract Res Clin Anaesthesiol 2015; 29:163-75
  11. LANDONI  G, GRECO T, BIODI-ZOCCAI G, et al. Anaesthetic drugs and survival: a Bayesian network meta-analysis of randomized trials in cardiac surgery. Br J Anaesth 2013; 111:886-96
  12. LELLOUCHE   F, DELORME M, BUSSIÈRES J, OUATTARA A. Perioperative ventilatory strategies in cardiac surgery. Best Pract Res Clin Anaesthesiol 2015; 29:381-95
  13. MAGNUSSON L, ZEMGULIS V, RENLING A, et al. Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass. Anesthesiology 1998; 88:134-42
  14. MESSENT M, SULLIVAN K, KEOGH BF, et al. Adult respiratory distress syndrome following cardiopulmonary bypass: incidence and prediction. Anaesthesia 1992; 47: 267-8
  15. MILOT J, PERRON J, LACASSE Y, et al. Incidence and predictors of ARDS after cardiac surgery. Chest 2001; 119:884-8
  16. NETO CN, LANDONI G, VASSARA L, et al. Use of volatile anesthetics during cardiopulmonary bypass: a systematic review of adverse events. J Cardiothorac Vasc Anesth 2014; 28:84-9
  17. SCHREIBER J, LANCE M, DE KORTE M, et al. The effect of different lung-protective strategies in patients during cardiopulmonary bypass: a meta-analysis and semiquantitative review of randomized trials. J Cardiothorac Vasc Anesth 2012; 26:448-54
  18. SLINGER  P. Perioperative lung injury. Best Pract Res Clin Anaesthesiol 2008; 22: 177-91
  19. SVENNEVIG JL, LINDBERG H, GEIRAN O, et al. Should the lungs be ventilated during cardiopulmonary bypass? Clinical, hemodynamic, and metabolic changes in patients undergoing elective coronary artery surgery. Ann Thorac Surg 1984; 37:295
  20. TRIULZI DJ. Transfusion-related acute lung injury: Current concepts for the clinician. Anesth Analg 2009; 108:70-6
  21. WALL MH, ROYSTER RL. Pulmonary dysfunction after cardiopulmonary bypass: should we ventilate the lungs on pump? Crit Care Med 2000; 28:1658-60
  22. WANG YC, HUANG CH, TU YT. Effects of positive airway pressure and mechanical ventilation of the lungs during cardiopulmonary bypass on pulmonary adverse events after cardiac surgery: a systematic review and meta-analysis. J Cardiothorac Vasc Anesth 2018; 32:748-59