REVIEW URRENT C OPINION
Protection strategies during cardiopulmonary bypass: ventilation, anesthetics and oxygen Carlos Ferrando, Marina Soro, and Francisco J. Belda
Purpose of review To provide an update of research findings regarding the protection strategies utilized for patients undergoing cardiopulmonary bypass (CPB), including perioperative ventilatory strategies, different anesthetic regimens, and inspiratory oxygen fraction. The article will review and comment on some of the most important findings in this field to provide a global view of strategies that may improve patient outcomes by reducing inflammation. Recent findings Postoperative complications are directly related to ischemia and inflammation. The application of lungprotective ventilation with lower tidal volumes and higher positive end-expiratory pressure reduces inflammation, thereby reducing postoperative pulmonary complications. Although inhalation anesthesia has clear cardioprotective effects compared with intravenous anesthesia, several factors can interfere to reduce cardioprotection. Hyperoxia up to 0.8 FiO2 may confer benefits without increasing oxidative stress or postoperative pulmonary complications. During the early postoperative period, inhalation anesthesia prior to extubation and the application of preventive noninvasive ventilation may reduce cardiac and pulmonary complications, improving patients’ outcomes. Summary Lung-protective mechanical ventilation, inhalation anesthesia, and high FiO2 have the potential to reduce postoperative complications in patients undergoing CPB; however, larger, well powered, randomized control trials are still needed. Keywords anesthetics, cardiac surgery, mechanical ventilation, oxygen
INTRODUCTION Postoperative complications, such us postoperative pulmonary complications (PPCs) [1 ], cardiac complications [2 ], and infection [3 ], appear in almost all patients who undergo cardiopulmonary bypass (CPB). These complications can range in severity from reversible to fatal, increasing morbidity and mortality. Although many mechanisms are involved, these complications are directly related to the inflammatory response. Inflammation during CPB occurs through a two-insult process: the first insult is caused by the surgical procedure itself, with many different inflammatory triggers such as CPB, ischemia, and surgical trauma [4–7]. The second insult is caused by mechanical ventilation [8]. During CPB, numerous strategies have been oriented to reduce the two-insult inflammation, including lung-protective ventilation, a variety of anesthetic regimens, lung perfusion during CPB, off-pump CPB, and different oxygen inspiratory concentrations. The knowledge and application of &
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these strategies may improve patients’ outcomes. This review is focused on three strategies directly related to anesthesia management: ventilation, choice of anesthetic, and oxygen.
VENTILATION Several scores for predicting PPC have demonstrated that cardiac surgery is an independent risk factor for its development [9 ,10]. The inflammatory response and, consequently, PPC after CPB are aggravated with the use of nonprotective mechanical ventilation &&
Anesthesiology and Critical Care Department, Hospital Clı´nico Universitario, Valencia, Spain Correspodence to Carlos Ferrando, Anesthesiology and Critical Care Department. Hospital Clı´nico Universitario, Av. Blasco Iban˜ez, 17, CP 46010, Valencia, Spain. Tel: +34 609 89 27 32; e-mail: [email protected] Curr Opin Anesthesiol 2015, 28:73–80 DOI:10.1097/ACO.0000000000000143
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KEY POINTS Postoperative complications in patients undergoing CPB are directly related to the inflammatory response. A ventilatory strategy that includes protective tidal volumes, higher PEEP levels, ventilation during CPB, and pre-emptive NIV may reduce inflammatory response, thereby decreasing postoperative complications. Although inhalation anesthesia is currently recommended for cardioprotection during cardiac surgery, interference with other drugs and RIPC should be considered. The use of high FiO2 (up to 0.8) decreases oxidative stress related to IRI and does not increase PPCs.
[11,12]. Mechanical forces such as stress caused by repeatedly opened and closed alveoli (atelectrauma) and strain caused by high transpulmonary pressures (overdistension) cause an inflammatory response known as biotrauma [13–17]. The inflammatory response is favored during CPB by the absence of ventilation or disconnection from the ventilatory circuit [18]. Although larger randomized control trials (RCTs) involving patients undergoing CPB are needed, lung-protective ventilatory strategy, including protective tidal volume, higher positive end-expiratory pressure (PEEP), recruitment maneuvers, continuous positive airway pressure (CPAP), low tidal volume during CPB, and noninvasive ventilation (NIV) during the immediate postextubation period, may help to attenuate inflammation and PPC.
Lung-protective mechanical ventilation Tidal volume of 6–8 ml/kg predicted body weight (PBW) has been considered protective in high-risk postoperative respiratory failure patients [19 ,20 ]. However, the evidence suggests that in cardiac surgery patients with healthy lungs, a tidal volume of 10 ml/kg or less should be considered protective. Chaney et al. [21] demonstrated that a tidal volume of 6 ml/kg improved postoperative lung mechanics and shunt fraction compared with 12 ml/kg. Recently, Lellouche et al. [22] observed during the multivariate analysis of a prospective study, including 3434 patients, that a tidal volume greater than 10 ml/kg is an independent risk factor for prolonged intubation, hemodynamic instability, renal failure, and length of stay in an ICU. However, studies comparing 6 versus 10 ml/kg did not reveal differences in the inflammatory response [23], or revealed minimal differences in response [24]. &&
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Wrigge et al. [24] measured lower plasma tumor necrosis factor (TNF)-a with 6 ml/kg than with 10 ml/kg after 6 h of ventilation, but without differences in the other cytokines measured [interleukin (IL)-2, IL-6, IL-8, IL-10, and interferon (IFN)-g]. Clinically, this is demonstrated as a lack of differences in oxygenation, lung mechanics, and time to extubation [23–25]. All of these studies employed identical PEEP (5 cmH2O) without recruitment maneuver. Atelectasis and atelectrauma during general anesthesia and the positive effects of PEEP have been widely reported in the literature. In cardiac surgery patients, significant differences in the inflammatory response are associated with different PEEP levels. Although Koner et al. [23] did not observe differences in plasma cytokines (IL-6, TNF-a) between 5 and 0 cmH2O after only 2 h of mechanical ventilation, Zunpancich et al. [26] reported a lower inflammatory response (IL-6 and IL-8) with 10 cmH2O than 2–3 cmH2O. Similar results were observed by Reis Miranda et al. [27,28], demonstrating that a strategy of 10 cmH2O PEEP and recruitment maneuver compared with 5 cmH2O PEEP without recruitment maneuver decreased inflammation and improved the functional residual capacity (FRC) and oxygenation, at least during the first 72 h after CPB. Borges et al. [29 ] and Dongelmans et al. [30] observed that 10 cmH2O improved oxygenation and lung mechanics in comparison with 5 and 8 cmH2O during the immediate postoperative period. However, a standardized PEEP level may not be the best strategy; individualized PEEP, which has demonstrated benefits during lung resection [31 ], may be an alternative. Recruitment maneuver to open closed-alveoli increasing transpulmonary pressure has been associated with the benefits of reduced atelectasis and improved oxygenation and respiratory function [28,32,33]. When and how recruitment maneuvers are performed may be important to improve benefits. Reis Miranda et al. [27] showed that an early (postintubation) recruitment maneuver reduces inflammation better than a late (after surgery) recruitment maneuver, probably because the lungs are exposed to mechanical stress for a shorter time. Meanwhile, recruitment maneuver with low transpulmonary pressures or inadequate postrecruitment maneuver PEEP level could render the maneuvers unsuitable, conferring no benefits [34]. &
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Protective strategy during cardiopulmonary bypass The inflammatory response during CPB is mainly related to the contact of blood components with the Volume 28 Number 1 February 2015
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artificial surface of the bypass circuit, ischemia– reperfusion injury (IRI) of the lung, and atelectasis of the nonventilated lung. Schreiber et al. [35] analyzed the effects of different lung-protective ventilatory strategies in a meta-analysis. The use of CPAP [36], recruitment maneuvers [34], or low-tidal volume [37,38] ventilation during CPB decreases inflammation and improves oxygenation, shunt fraction, and lung mechanics; however, these effects last for a limited period, without evidence of a significant impact on the clinical outcome [35]. Because the lungs are only oxygenated through alveolar diffusion and vascular perfusion, these results could be improved with a combined strategy of ventilation and perfusion during CPB. Thus, combining ventilation with lung perfusion may be more helpful for lung protection.
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death [49,50 ,51 ]. From this body of knowledge, many studies have been oriented to develop effective strategies to minimize IRI.
Ischemic preconditioning Ischemic preconditioning is currently performed using remote ischemic preconditioning (RIPC), which consists of applying short episodes of ischemia and reperfusion to noncardiac tissues [52]. The literature is well populated with ‘proof-of-concept’ articles, indicating that RIPC may provide myocardial protection for cardiac surgery patients [53–59]. Three meta-analyses published in 2014 included RCTs that compared RIPC with placebo (no RIPC) in the presence or absence of other myocardialprotective measures: Chai and Liu [60 ] (n ¼ 976 participants), Yang et al. [61 ] (n ¼ 1235 patients), and a report by The Remote Preconditioning Trialists’ Group [62 ] that included 23 trials. These meta-analyses conclude that RIPC may reduce cardiac biomarkers, but concede a lack of evidence that such a change has a significant impact on the clinical outcome [53–59,60 –62 ]. It is interesting to note that groups were anesthetized with either inhaled agents or propofol, and no subanalysis was reported. &&
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Noninvasive ventilation Multiple factors favor atelectasis during the postoperative period. Pre-emptive NIV should be applied in selected patients at high risk of postoperative respiratory failure [39 ]. NIV has not demonstrated clear effectiveness once respiratory failure is established [40 ]. Many studies have reported benefits with the use of pre-emptive CPAP or NIV for oxygenation [41–44], with reported reductions in atelectasis [43,44], PPCs [43–47], reintubation rates, ICU readmissions, and hospital and ICU length of stay [44–47]. &&
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ANESTHETICS Myocardial IRI impairs heart function during the early postoperative period. However, an endogenous protective reaction to IRI is known [48]: repeated episodes of brief myocardial ischemia have a protective effect against a subsequent ischemic insult. The molecular mechanisms underlying ischemic preconditioning (IPC) are not completely known. In summary, preconditioning is triggered by cytokines and chemokines, which are released by myocardial cells in response to ischemia (or I/R). These signals activate several signaling pathways, generating reactive oxygen species (ROS) and other mediators that share common goals: to stabilize the mitochondrial membranes and to inhibit the opening of ATP-sensitive potassium ion channels [mitochondrial permeability transition pores (mPTP)]. The process of reperfusion leads to an abrupt rise in oxidative stress, with acute increases in ROSproducing damage to the cell membrane. This produces severe Ca2þ accumulation, which induces opening of the mPTP, which, in turn, causes damage to the mitochondrial membrane, resulting in cell
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Myocardial conditioning with anesthetics Inhaled agents provide protection when administered before (preconditioning) and after (postconditioning) myocardial ischemia. Several cellular mechanisms have been proposed with similarities to preconditioning. During reperfusion, the cardioprotective mechanism of inhaled agents prevents oxidative stress and attenuates Ca2þ overload by acting on mPTP [63,64 ,65 ]. Propofol has antioxidant properties that may confer a cardioprotective effect by reducing the total amount of ROS [66,67] without interacting with the mPTP. &
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Clinical evidence Two meta-analyses with nearly 3000 patients showed that compared with propofol, inhaled agents significantly decrease postoperative cardiac biomarkers, increase cardiac output, and decrease inotrope use, mechanical ventilation time, and hospital length of stay without beneficial effects on the risk of myocardial infarction (MI) and mortality [68,69]. Two additional meta-analyses [70,71] revealed significant reductions of in-hospital mortality and in-hospital MI. Similar results [72–74] have been observed since then, with some exceptions [75 ,76]. Finally, a recent meta-analysis [77 ]
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that included 3996 patients [41% total intravenous anesthesia (TIVA) and 59% inhaled agents] showed that the use of inhaled agents reduced mortality at the longest follow-up available. Looking at the continuous evidence that inhaled agents provide cardioprotection, the current guidelines of the American College of Cardiology Foundation/American Heart Association recommend a ‘volatile-based anesthesia’ for cardiac surgery procedures (class IIa, level of evidence A) [78]. With a perspective for future assessment, an important study in off-pump coronary artery bypass graft (CABG) surgical patients [79] has demonstrated that sevoflurane and propofol elicit differential genomic responses for cardioprotection. The studied gene expression predicted the effects on postoperative cardiac function. Interference and synergy It seems reasonable that two conditioning stimuli should induce more consistent cell protection overall. Zhou et al. [80 ] have posed a very interesting question, analyzing important factors that affect cardioprotection by RIPC. In an 1155-patient meta-analysis that confirmed the cardioprotective effect of RIPC, a univariate meta-regression analysis and multivariate regression and subgroup analyses showed that cardioprotection may be attenuated when combined with b-blockers or inhaled agents. In addition, propofol interferes with cardioprotective, RIPC-activated signal transduction [81 ]. ROS are necessary to induce ischemia and inhaled agent preconditioning. It is possible that propofol may interfere with preconditioning by eliminating ROS. In this sense, clinical evidence indicating that propofol may abolish the RIPC stimulus has been confirmed in several CABG surgery studies [82,83] in which RIPC during isoflurane, but not during propofol, decreased postoperative myocardial damage (cardiac troponin I levels). In a recent and very well designed clinical trial (n ¼ 329 patients) [84 ] that compared RIPC with a lack of RIPC while intentionally avoiding propofol in most patients, RIPC provided perioperative myocardial protection. As a secondary outcome (underpowered), improvement in all-cause mortality was observed. As complementary evidence, a recent RCT (n ¼ 1280 patients) [85 ] compared RIPC with a lack of RIPC, maintaining anesthesia with propofol and remifentanil. No significant differences were observed between RIPC (pre and postreperfusion) and no RIPC regarding a composite of major adverse outcomes. Similar effects of interference with IPC have been suggested for inhaled agents [86]. A final point is to ascertain whether the propofol-scavenging effect during reperfusion could &&
act synergistically with inhaled agents. This type of synergy has been shown in a study of 120 patients divided into four groups, which concluded that joint isoflurane preconditioning and propofol affect the CPB anesthesia regimen and synergistically attenuate myocardial IRI [87]. Other modes of interference It seems that multiple patient-related factors may influence the extent of myocardial IRI during cardiac surgery, interfering with cardioprotective strategies. These factors have been described previously [49,88], and include genetic susceptibility, age, male sex, and diabetes, diminishing the cardioprotective benefits of anesthesia [89].
Anesthetics during the postoperative period Three RCTs have compared the potential beneficial effects of sedation with sevoflurane versus propofol on markers of myocardial injury (troponin T) in the ICU after CPB [90,91 ,92 ]. All showed that administration of sevoflurane in the ICU is feasible and simple using the AnaConDa device (Sedana Medical, Sweden), and it decreased myocardial injury markers compared with patients who only received sevoflurane intraoperatively; however, administration only during surgery or in the ICU was a better option than TIVA. &
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OXYGEN Today, oxygen (O2) is recognized as a drug with which to treat patients. Dying from hypoxemia is such a clear concept that doctors provide supplemental O2 to any patient at minimal risk of hypoxemia as a matter of course. This has entailed the use of high FiO2 (from 0.5 to 1.0) during cardiac anesthesia since its inception [93], and this practice continues in many operating rooms. In fact, recommended practice is to set FiO2 at 0.8 at the initiation of CPB and to decrease it to 0.6–0.7 during hypothermia [94]. Myocardial IRI was recognized very early, and the use of supplemental O2 in clinical practice was not questioned. At the same time, lung and myocardial injury has been attributed to high FiO2 through impairment of the innate defense response by decreasing receptors in cells, increasing ROS, and many other phenomena that have suggested that perioperative hyperoxia is potentially harmful [95]. Details of the molecular mechanisms that cause such damage are perfectly reviewed in a recent publication on hyperoxia-induced lung injury (HALI) [96 ]. Most hyperoxia experiences that result in HALI are lethal experiences with exposure to 1.0 FiO2 for several &&
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days, although exposure to 1.0 FiO2 for up to 4 days tends to result in sublethal injury. Most of them were realized in animals with normal lungs and spontaneous breathing or injurious mechanical ventilation. In fact, some studies suggest that high tidal volume and hyperoxia have either an additive or a synergistic effect that accentuates alveolar cell death. Furthermore, recent animal studies suggest that lung-protective ventilation may substantially reduce additional risks from hyperoxia. They conclude that in the absence of high-stretch mechanical ventilation, the risk of HALI is minimal with FiO2 0.6 or less; the risk probably begins when FiO2 exceeds 0.7, and likely becomes progressively more problematic when FiO2 exceeds 0.8 for an extended period. PEEP, precise control over FiO2, and protective mechanical ventilation have substantially reduced the risk of HALI for the vast majority of patients who require mechanical ventilation. A second point is that tissue hyperoxia decreases oxidative stress related to I/R with a preconditioning effect related to an increase in the activity of antioxidant enzymes. This has been demonstrated in studies in which hyperoxia (normobaric and hyperbaric oxygen therapy) appears to be an effective therapy for IRI of the heart, brain, small intestine, testes, and liver [97–102]. This effect has been demonstrated in our patient group during colon surgery [103], and the same effect was observed in patients undergoing lobectomy in a current ongoing study [104]. As far as we know, there is only one clinical study of 56 patients undergoing CPB that is evaluating the effect of arterial oxygen tension during reperfusion on cardiac IRI biomarkers [105]. All patients received 0.7 FiO2 during CPB, and FiO2 was lowered to 0.5 (normoxic group) from the last administration of warm cardioplegia to 1 min after aortic unclamping. FiO2 was then raised back to 0.7. This did not affect postoperative myocardial enzyme release or the short-term prognosis. Third, 0.8 FiO2 during anesthesia (and 2–4 h postoperative) has been shown to reduce surgical site infection (SSI) in many surgical procedures [106 ] with an SSI risk reduction of 23% for all surgeries combined [107]. Although it cannot be taken as a definitive review, the effect of perioperative 0.8 FiO2 on SSI has been confirmed recently [108 ,109]. These results may also apply to cardiac surgery, because the rationale for proposing hyperoxia as a factor in SSI prevention is well established [110]. Neutrophils safeguard against infection through nonspecific phagocytosis, and the elimination of bacteria depends on oxygen tension in subcutaneous tissue, which can be doubled with supplemental oxygen. &&
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Fourth, although hyperoxia leads to changes in cardiovascular function, the reduction in cardiac output is not a direct myocardial depressant effect of oxygen; rather, it is a response to increased systemic vascular resistance [111]. This increase was only observed after bypass and entailed reductions in peripheral tissue oxygenation [112]. Although hyperoxemia clearly increases global oxygen delivery and oxygen saturation in mixed venous blood, oxygen consumption declines during CPB. This effect is not associated with improved tissue perfusion [113]. However, the clinical effects of these changes remain unclear. Finally, in spite of the common assertion that supplemental perioperative oxygen increases atelectasis or other pulmonary complications after surgical procedures, several reviews indicate that this is not true [106 ]. However, no study was performed on cardiac surgery patients. The PROXI trial, which included 1382 patients after abdominal surgery, showed that perioperative hyperoxia increased mortality after a median followup of 2.3 years [114]; however, the analysis of noncancer surgical patients revealed no differences in mortality. Similarly, a mortality study of 36 307 consecutive mechanically ventilated ICU patients showed that high arterial oxygen partial pressure during the first 24 h and FiO2 administration were independently associated with in-hospital mortality [115]. However, a new review of 152 680 ventilated ICU patients [116] demonstrated an association between hypoxia (but not hyperoxia) and increased in-hospital mortality during the first 24 h. &&
CONCLUSION In patients undergoing CPB, postoperative complications are mainly related to inflammation. Although lung-protective mechanical ventilation using tidal volume less than 10 ml/kg PBW with higher PEEP levels, ventilation during the CPB procedure, and the use of pre-emptive NIV have been shown to improve patients’ outcomes, larger, well powered RCTs are needed. Inhaled agent is currently recommended by the guidelines because it has a clear cardioprotective effect, and improves relevant outcomes after cardiac surgery compared with TIVA. However, propofol or IPC might interfere significantly with cardioprotection by inhaled agents, which suggests that they should not be used concomitantly during anesthesia. The administration of hyperoxia in the operating room should be approached with the same risk–benefit assessment as any other drug. In general, we think that today it seems wise to continue to administer high FiO2 during cardiac anesthesia because of its
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demonstrated potential benefits and absence of demonstrated clinical drawbacks. However, hyperoxia must be examined further in well designed and well powered RCTs in this setting. Acknowledgements None. Financial support and sponsorship None. Conflicts of interest None.
REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. QJi Q, Mei Y, Wang X, et al. Risk factors for pulmonary complications & following cardiac surgery with cardiopulmonary bypass. Int J Med Sci 2013; 10:1578–1583. This study aims to evaluate perioperative risk factors for PPCs. There were 143 PPCs in 2056 enrolled patients. PPC was not a risk factor for hospital mortality. 2. Luratti Buse GA, Bolliger D, Seeberger E, et al. Troponin T and brain & natriuretic peptide after on-pump cardiac surgery: prognostic impact on 12-month mortality and major cardiac events after adjustment for postoperative complication. Circulation 2014; 130:948–957. [Epub ahead of print] This study describes the incidence of cardiac events in CPB patients. Of the 1559 patients enrolled, 176 (11.3%) suffered a cardiac event. 3. Si D, Rajmokan M, Lakhan M, et al. Surgical site infections following coronary & artery bypass graft procedures: 10 years of surveillance data. BMC Infect Dis 2014; 14:318. This study describes the incidence of cardiac events in CPB patients. There were 1702 surgical site infections following 14 546 CABG procedures performed. 4. Paparella D, Yau TM, Young E. Cardiopulmonary bypass induced inflammation: pathophysiology and treatment. An update. Eur J Cardiothorac Surg 2002; 21:232–244. 5. Ascione R, Lloyd CT, Underwood MJ, et al. Inflammatory response after coronary revascularization with or without cardiopulmonary bypass. Ann Thorac Surg 2000; 69:1198–1204. 6. Gu YJ, Mariani MA, Boonstra PW, et al. Complement activation in coronary artery bypass grafting patients without cardiopulmonary bypass: The role of tissue injury by surgical incision. Chest 1999; 116:892–898. 7. Hirai S. Systemic inflammatory response syndrome after cardiac surgery under cardiopulmonary bypass. Ann Thorac Cardiovasc Surg 2003; 9:365– 370. 8. Reis Miranda D, Gommers D, Peter J, et al. Mechanical ventilation affects pulmonary inflammation in cardiac surgery patients: the role of the open-lung Concept. J Cardiothorac Vasc Anesth 2007; 21:279–284. 9. Mazo V, Sabate´ S, Canet J, et al. Prospective external validation of a && predictive score for postoperative pulmonary complications. Anesthesiology 2014; 121:219–231. This study describes a predictive score for PPC. This prediction may have important consequences to clinical management, at least regarding the use of pre-emptive NIV. 10. Kor DJ, Lingineni RK, Gajic O, et al. Predicting risk of postoperative lung injury in high-risk surgical patients. A multicenter cohort study. Anesthesiology 2014; 120:1168–1181. 11. Dreyfuss D, Saumon G. Ventilatory-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med 1998; 157:294–323. 12. Plataki M, Hubmayr RD. The physical basis of ventilator-induced lung injury. Expert Rev Respir Med 2010; 4:373–385. 13. von Bethmann AN, Brasch F, Nusing R, et al. Hyperventilation induces release of cytokines from perfused mouse lung. Am J Respir Crit Care Med 1998; 157:263–272. 14. Ranieri VM, Suter PM, Tortorella C, et al. Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial. J Am Med Assoc 1999; 282:54–61. 15. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000; 342:1301–1308.
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This meta-analysis demonstrates the importance of protective ventilation (lower tidal volume and higher PEEP) to reduce PPC and emphasizes the need of well powered RCTs to better establish the benefits of intraoperative lung-protective ventilation. 21. Chaney MA, Nikolov MP, Blakeman BP, et al. Protective ventilation attenuates postoperative pulmonary dysfuntion in patients undergoing cardiopulmonary bypass. J Cardiothorac Vasc Anesth 2000; 14:514–518. 22. Lellouche F, Dionne S, Simard S, et al. High tidal volumes in mechanically ventilated patients increase organ dysfunction after cardiac surgery. Anesthesiology 2012; 116:1072–1082. 23. Koner O, Celebi S, Balci H, et al. Effects of protective and conventional mechanical ventilation on pulmonary function and systemic cytokine rele´ase after cardiopulmonary bypass. Intensive Care Med 2004; 30:620–626. 24. Wrigge H, Uhlig U, Baumgarten G, et al. 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This is the first clinical trial to demonstrate the benefits of an individualized PEEP titration trial to oxygenation and lung mechanics, in comparison with a standarized PEEP level. 32. Padovani C, Cavenaghi OM. Alveolar recruitment in patients in the immediate postoperative period of cardiac surgery. Rev Bras Cir Cardiovasc 2011; 26:116–121. 33. Celebi S, Koner O, Menda F, et al. Pulmonary effects of noninvasive ventilation combined with the recruitment maneuver after cardiac surgery. Anesth Analg 2008; 107:614–619. 34. Scherer M, Dettmer S, Meininger D, et al. Alveolar recruitment strategy during cardiopulmonary bypass does not improve postoperative gas exchange and lung function. Cardiovasc Eng 2009; 9:1–5. 35. 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; 26:448–454. 36. 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Protection strategies during cardiopulmonary bypass Ferrando et al. 40. Garcı´a-Delgado M, Navarrete I, Garcia-Palma MJ, et al. Postoperative respiratory failure after cardiac surgery: use of noninvasive ventilation. J Cardiothorac Vasc Anesth 2012; 26:443–447. A retrospective study including 63 postoperative cardiac surgery patients. Authors analyze the use of NIV in respiratory failure after extubation. Reintubation was required in one-half of NIV-treated patients and was associated with increased hospital mortality. 41. Matte P, Jacqet L, Van DM, et al. Effects of conventional physiotherapy, continuous positive airway pressure and noninvasive ventilator support with bilevel positive airway pressure after coronary artery bypass grafting. Acta Anaesthesiol Scand 2000; 44:75–81. 42. Pinilla JC, Oleniuk FH, Tan L. Use of a nasal CPAP mask in the treatment of postoperative atelectasis in aortocoronary bypass surgery. Crit Care Med 1990; 18:836–840. 43. Zarbock A, Mueller E, Netzer S, et al. Prophylactic nasal continuous positive airway pressure following cardiac surgery protects from postoperative pulmonary complications: a prospective, randomized, controlled trial in 500 patients. Chest 2009; 135:1252–1259. 44. Pasquina P, Merlani P, Granier JM. Continuous positive airway pressure versus noninvasive pressure support ventilation to treat atelectasis after cardiac surgery. Anesth Analg 2004; 99:1001–1008. 45. Al Jaaly E, Fiorentino F, Reeves BC, et al. Effect of adding postoperative noninvasive ventilation to usual care to prevent pulmonary complications in patients undergoing coronary artery bypass grafting: a randomized controlled trial. J Thorac Cardiovasc Surg 2013; 146:912–918. 46. Nava S, Gregoretti C, Fanfulla F, et al. Noninvasive ventilation to prevent respiratory failure after extubation in high-risk patients. Crit Care Med 2005; 33:2465–2470. 47. Ferrer M, Valencia M, Nicolas JM, et al. Early noninvasive ventilation averts extubation failure in patients at risk: a randomized trial. Am J Respir Crit Care Med 2006; 173:164–170. 48. Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 1986; 74:1124–1136. 49. Piper HM, Garcia-Dorado D. Reducing the impact of myocardial ischaemia/ reperfusion injury. Cardiovasc Res 2012; 94:165–167. 50. Heusch G. Cardioprotection: chances and challenges of its translation to the && clinic. Lancet 2013; 12:166–175. An excellent review of cardioprotection, including the different pathways of the IRI, the various cardioprotective strategies, and the factors that might affect this cardioprotection. 51. Brooks MJ, Andrews DT. Molecular mechanisms of ischemic conditioning: && translation into patient outcomes. Future Cardiol 2013; 9:549–568. A detailed review that discusses recent advances in the molecular mechanisms involved in IRI and the signaling pathways recruited by ischemic conditioning. It concludes with evidence to support the use of ischemic conditioning in current clinical practice. 52. Przyklenk K. Reduction of myocardial infarct size with ischemic ‘conditioning’: physiologic and technical considerations. Anesth Analg 2013; 117:891– 901. 53. Hausenloy DJ, Yellon DM. The therapeutic potential of ischemic conditioning: an update. Nat Rev Cardiol 2011; 8:619–629. 54. Marczak J, Nowicki R, Kulbacka J, et al. Is remote ischaemic preconditioning of benefit to patients undergoing cardiac surgery? Interact Cardiovasc Thorac Surg 2012; 14:634–639. 55. Sabbagh S, Henry Salzman MM, Kloner RA, et al. Remote ischemic preconditioning for coronary artery bypass graft operations. Ann Thorac Surg 2013; 96:727–736. 56. Pilcher JM, Young P, Weatherall M, et al. A systematic review and metaanalysis of the cardioprotective effects of remote ischaemic preconditioning in open cardiac surgery. J R Soc Med 2012; 105:436–445. 57. Alreja G, Bugano D, Lotfi A. Effect of remote ischemic preconditioning on myocardial and renal injury: meta-analysis of randomized controlled trials. J Invasive Cardiol 2012; 24:42–48. 58. D’Ascenzo F, Cavallero E, Moretti C, et al. Remote ischaemic preconditioning in coronary artery bypass surgery: a meta-analysis. Heart 2012; 98:1267– 1271. 59. Brevoord D, Kranke P, Kuijpers M, et al. Remote ischemic conditioning to protect against ischemia-reperfusion injury: a systematic review and metaanalysis. PLoS One 2012; 7:e42179. 60. Chai Q, Liu J. Early stage effect of ischemic preconditioning for patients && undergoing on-pump coronary artery bypass grafts surgery: Systematic review and meta-analysis. Pak J Med Sci 2014; 30:642–648. This is a meta-analysis of 18 randomized controlled trials. The positive and negative results were equal in all 18 trials. There were no differences between ischemia preconditioning and control groups regarding in-hospital mortality or postoperative MI morbidity. Postoperative differences in cardiac troponin and troponin I were observed. Authors concluded that the meta-analysis results should be interpreted with caution owing to limited effective data. 61. Yang L, Wang G, Du Y, et al. Remoteischemic preconditioning reduces && cardiactroponin I release in cardiac surgery: a meta-analysis. J Cardiothorac Vasc Anesth 2014; 28:682–689. This meta-analysis includes 19 adult and pediatric randomized controlled trials. There were no differences in mortality or morbidity; however, RIPC reduces cardiac troponin I. &&
62. Remote Preconditioning Trialists’ Group, Healy DA, Khan WA, Wong CS, et al. Remote preconditioning and major clinical complications following adult cardiovascular surgery: systematic review and meta-analysis. Int J Cardiol 2014; 176:20–31. This meta-analysis includes 23 randomized controlled trials (2200 patients). RIPC did not have a significant effect on clinical end-points (death, perioperative MI, renal failure, stroke, mesenteric ischemia, length of stay in hospital, or critical care); however, authors concluded that pooled data from pilot trials cannot confirm that RIPC has any significant effect on clinically relevant end-points. 63. Van Allen NR, Krafft PR, Leitzke AS, et al. The role of volatile anesthetics in cardioprotection: a systematic review. Med Gas Res 2012; 28:22. 64. Wu L, Zhao H, Wang T, et al. Cellular signaling pathways and molecular & mechanisms involving inhalational anesthetics-induced organoprotection. J Anesth 2014; 28:740–758. [Epub ahead of print] This review summarizes the signaling pathways and molecular participants in inhaled anesthetic-mediated organ protection published in the current literature. It compares and contrasts the ’preconditioning’ and ’postconditioning’ phenomena, as well as the similarities and differences in mechanisms between organs. 65. Kojima A, Kitagawa H, Omatsu-Kanbe M, et al. Sevoflurane protects & ventricular myocytes against oxidative stress-induced cellular Ca2þ overload and hypercontracture. Anesthesiology 2013; 119:606–620. This experimental study investigated the electrophysiological mechanisms underlying cardioprotective effects of sevoflurane against oxidative stress-induced cellular injury. Oxidative stress is implicated in the pathogenesis of cardiac reperfusion injury, which is characterized by cellular Ca2þ overload and hypercontracture. Volatile anesthetics protect the heart against reperfusion injury primarily by attenuating Ca2þ overload. 66. Ansley DM, Sun J, Visser WA, et al. High dose propofol enhances red cell antioxidant capacity during CPB in humans. Can J Anesth 1999; 46:641– 648. 67. Ansley DM, Xia Z. Propofol preservation of myocardial function in patients undergoing coronary surgery with cardiopulmonary bypass is dose dependent. Anesthesiology 2002; 98:1028–1029. 68. Symons JA, Myles PS. Myocardial protection with volatile anaesthetic agents during coronary artery bypass surgery: a meta-analysis. Br J Anaesth 2006; 97:127–136. 69. Yu CH, Beattie WS. The effects of volatile anesthetics on cardiac ischemic complications and mortality in CABG: a meta-analysis. Can J Anaesth 2006; 53:906–918. 70. Landoni G, Biondi-Zoccai GG, Zangrillo A, et al. Desflurane and sevoflurane in cardiac surgery: a meta-analysis of randomized clinical trials. J Cardiothorac Vasc Anesth 2007; 21:502–511. 71. Landoni G, Fochi O, Tritapepe L, et al. Cardiacprotection by volatile anesthetics: a review. Minerva Anestesiol 2009; 75:269–273. 72. Jakobsen CJ, Berg H, Hindsholm KB, et al. The influence of propofol versus sevoflurane anesthesia on outcome in 10,535 cardiac surgical procedures. J Cardiothorac Vasc Anesth 2007; 21:664–671. 73. Yao YT, Li LH. Sevoflurane versus propofol for myocardial protection in patients undergoing coronary artery bypass grafting surgery: a metaanalysis of randomized controlled trials. Chin Med Sci J 2009; 24:133– 141. 74. Flier S, Post J, Concepcion AN, et al. Influence of propofol-opioid vs. isoflurane-opioid anaesthesia on postoperative troponin release in patients undergoing coronary artery bypass grafting. Br J Anaesth 2010; 105:122– 130. 75. Suryaprakash S, Chakravarthy M, Muniraju G, et al. Myocardial protection & during off pump coronary artery bypass surgery: a comparison of inhalational anesthesia with sevoflurane or desflurane and total intravenous anesthesia. Ann Card Anaesth 2013; 16:4–8. In this prospective study of 139 patients, no differences in cardiac protection (TnT) were observed with either 1–2% sevoflurane or 4–6% desflurane and propofol at doses of 2–4 mg/kg/h. This study was conducted during off-pump surgery, in which myocardial IRI is limited. 76. 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; 64:953–960. 77. Landoni G, Greco T, Biondi-Zoccai G, et al. Anaesthetic drugs and survival: a && Bayesian network meta-analysis of randomized trials in cardiac surgery. Br J Anaesth 2013; 111:886–896. An excellent meta-analysis including 38 RCTs and 3642 patients. This metaanalysis concludes that anesthesia with volatile agents appears to reduce mortality after cardiac surgery compared with TIVA, especially when sevoflurane or desflurane is used. 78. Hillis LD, Smith PK, Anderson JL, et al. 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011; 124:2610– 2642. 79. Lucchinetti E, Hofer C, Bestmann L, et al. Gene regulatory control of myocardial energy metabolism predicts postoperative cardiac function in patients undergoing off-pump coronary artery bypass graft surgery: inhalational versus intravenous anesthetics. Anesthesiology 2007; 106:444– 457. &&
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Cardiovascular anesthesia 80. Zhou C, Liu Y, Yao Y, et al. B-blockers and volatile anesthetics may attenuate cardioprotection by remote preconditioning in adult cardiac surgery: a metaanalysis of 15 randomized trials. J Cardiothorac Vasc Anesth 2013; 27:305– 311. The aim of this meta-analysis was to evaluate the factors affecting cardioprotection by RIPC in adult cardiac surgery. Fifteen trials with a total of 1155 patients were included. This meta-analysis also confirmed the cardioprotection conferred by RIPC, and that the cardioprotective effect may be attenuated when combined with b-blockers or volatile anesthetics. 81. Kottenberg E, Musiolik J, Thielmann M, et al. Interference of propofol with & signal transducer and activator of transcription 5 activation and cardioprotection by remote ischemic preconditioning during coronary artery bypass grafting. J Thorac Cardiovasc Surg 2014; 147:376–382. Prospective trial in 24 nondiabetic patients. Authors showed that propofol interferes with RIPC cardioprotection. 82. Kottenberg E, Thielmann M, Bergmann L, et al. Protection by remote ischemic preconditioning during coronary artery bypass graft surgery with isoflurane but not propofol: a clinical trial. Acta Anaesthesiol Scand 2011; 56:30–38. 83. Kottenberg E, Thielmann M, Bergmann L, et al. Protection by remote ischemic preconditioning during coronary artery bypass graft surgery with isoflurane but not propofol: a clinical trial. Acta Anaesthesiol Scand 2012; 56:30–38. 84. Thielmann M, Kottenberg E, Kleinbongard P, et al. Cardioprotective and && prognostic effects of remote ischaemic preconditioning in patients undergoing coronary artery bypass surgery: a single-centre randomised, doubleblind, controlled trial. Lancet 2013; 382:597–604. Remote ischemic preconditioning provided perioperative myocardial protection and improved the prognosis of patients undergoing elective CABG surgery. 85. Hong DM, Lee EH, Kim HJ, et al. Does remote ischaemic preconditioning & with postconditioning improve clinical outcomes of patients undergoing cardiac surgery? Remote Ischaemic Preconditioning with Postconditioning Outcome Trial. Eur Heart J 2014; 35:176–183. In this single-center RCT including 1280 patients, authors did not observe differences between control and RICP associated with remote ischemic postconditioning. It is important to note that propofol was used to maintain anesthesia. 86. Lucchinetti E, Bestmann L, Feng J, et al. Remote ischemic preconditioning applied during isoflurane inhalation provides no benefit to the myocardium of patients undergoing on-pump coronary artery bypass graft surgery: lack of synergy or evidence of antagonism in cardioprotection? Anesthesiology 2012; 116:296–310. 87. Huang Z, Zhong X, Irwin MG, et al. Synergy of isoflurane preconditioning and propofol postconditioning reduces myocardial reperfusion injury in patients. Clin Sci 2011; 121:57–69. 88. Heusch G. Cardioprotection: chances and challenges of its translation to the clinic. Lancet 2013; 381:166–175. 89. Sharma AK, Khanna D. Diabetes mellitus associated cardiovascular signalling alteration: a need for the revisit. Cell Signal 2013; 25:1149–1155. 90. Soro M, Gallego L, Silva V, et al. Cardioprotective effect of sevoflurane and propofol during anaesthesia and the postoperative period in coronary bypass graft surgery: a double-blind randomised study. Eur J Anaesthesiol 2012; 29:561–569. 91. Guerrero Orriach JL, Gala´n Ortega M, Ramirez Aliaga M, et al. Prolonged & sevoflurane administration in the off-pump coronary artery bypass graft surgery: beneficial effects. J Crit Care 2013; 28:879. (e13-8). This prospective study conducted in 60 patients undergoing OPCABG surgery revealed significant differences in troponin I levels during the first 48 h among three anesthetic regimens (intraoperative–postoperative): propofol– propofol > sevoflurane–propofol > sevoflurane–sevoflurane. The results show that the best option is the use of sevoflurane throughout the perioperative period. 92. Marcos-Vidal JM, Gonza´lez R, Garcia C, et al. Sedation with sevoflurane in & postoperative cardiac surgery: influence on troponin T and creatinine values. Heart Lung Vessel 2014; 6:33–42. In this prospective study of 129 patients undergoing coronary or coronary and valve cardiac surgery, troponin T levels were significantly lower at 12 and 48 h after admission in the sevoflurane group. 93. Hessel II EA. History of cardiac surgery and anesthesia. In Estafanous FG, Barash PG, Reves JG, editors. Cardiac anesthesia: principles and practice. Philadelphia: Lippincott Williams & Wilkins; 2001. (Lippincott’s Interactive Cardiac Anesthesia Library on CD-ROM: www.LWW.com). 94. Karabulut H, Toraman F, Tarcan S, et al. Adjustment of sweep gas flow during cardiopulmonary bypass. Perfusion 2002; 17:353–356. 95. Lumb AB, Walton LJ. Perioperative oxygen toxicity. Anesthesiol Clin 2012; 30:591–605. &&
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96. Kallet RH, Matthay MA. Hyperoxic acute lung injury. Respir Care 2013; 58:123–141. An extensive review of HALI. This review presents evidence that HALI is produced mainly with the use of FiO2 for an extended period of time. Also presents evidence that lung-protective ventilation has greatly reduced the risk of HALI. 97. Brown DM, Holt DW, Edwards JT, et al. Normoxia vs. hyperoxia: impact of oxygen tension strategies on outcomes for patients receiving cardiopulmonary bypass for routine cardiac surgical repair. J Extra Corpor Technol 2006; 38:241–248. 98. Mariero LH, Rutkovskiy A, Stenslokken KO, et al. Hyperoxia during early reperfusion does not increase ischemia/reperfusion injury. Eur J Cardiothorac Surg 2012; 41:149–153. 99. Kang N, Hai Y, Liang F, et al. Preconditioned hyperbaric oxygenation protects skin flap grafts in rats against ischemia/reperfusion injury. Mol Med Rep 2014; 9:2124–2130. 100. Yuan Z, Pan R, Liu W, et al. Extended normobaric hyperoxia therapy yields greater neuroprotection for focal transient ischemia-reperfusion in rats. Med Gas Res 2014; 4:14. 101. Tavafi M, Ahmadvand H, Tamjidipour A, et al. Effect of normobaric hyperoxia on gentamicin-induced nephrotoxicity in rats. Iran J Basic Med Sci 2014; 17:287–293. 102. Caldeira DE, Silveira MR, Margarido MR, et al. Effect of hyperbaric hepatic hyperoxia on the liver of rats submitted to intermittent ischemia/reperfusion injury. Acta Cir Bras 2014; 29 (Suppl 1):24–28. 103. Garcı´a-de-la-Asuncio´n J1, Barber G, Rus D, et al. Hyperoxia during colon surgery is associated with a reduction of xanthine oxidase activity and oxidative stress in colonic mucosa. Redox Rep 2011; 16:121–128. 104. Garcı´a-de-la-Asuncio´ J, Martı´ F, Bruno L, et al. Oxidative stress by lung reexpasion during pulmonary lobectomy: prevention by propofol and FiO2 0.8: 5AP4-5. Eur J Anaesthesiol 2010; 27:100–101. 105. Lee JS, Kim JC, Chung J, et al. Effect of arterial oxygen tension during reperfusion on myocardial recovery in patients undergoing valvular heart surgery. Korean J Anesthesiol 2010; 58:122–128. 106. Hovaguimian F, Lysakowski C, Elia N, et al. Effect of intra-operative high && inspired oxygen fraction on surgical site infection, postoperative nausea and vomiting, and pulmonary function: systematic review and meta-analysis of randomized trials. Anesthesiology 2013; 119:303–316. This meta-analysis of 22 RCTs including7001 patients showed that in comparison with low intraoperative FiO2 (around 0.3), high intraoperative FiO2 (around 0.8) decreases the risks of SSI, has a weak beneficial effect on nausea, and does not increase PPC. 107. Belda FJ, Catala´-Lo´pez F, Greif R, et al. Benefits and risks of intraoperative high inspired oxygen therapy: firm conclusions are still far off. Anesthesiology 2014; 120:1051–1052. 108. Schietroma M, Cecilia EM, Carlei F, et al. Prevention of anastomotic leakage & after total gastrectomy with perioperative supplemental oxygen administration: a prospective randomized, double-blind, controlled, single-center trial. Ann Surg Oncol 2013; 20:1584–1590. This study of 171 patients undergoing elective open anastomosis for gastric cancer showed that 0.8 FiO2 intraoperatively and during the first postoperative 6 h significantly reduced anastomotic leakage. 109. Schietroma M, Cecilia EM, Sista F, et al. High-concentration supplemental perioperative oxygen and surgical site infection following elective colorectal surgery for rectal cancer: a prospective, randomized, double-blind, controlled, single-site trial. Am J Surg 2014; 18:. [Epub ahead of print] 110. Canet J, Belda FJ. Perioperative hyperoxia: the debate is only getting started. Anesthesiology 2011; 114:1271–1273. 111. Anderson KJ, Harten JM, Booth MG, et al. The cardiovascular effects of normobaric hyperoxia in patients with heart rate fixed by permanent pacemaker. Anaesthesia 2010; 65:167–171. 112. Joachimsson PO, Sjoberg F, Forsman M, et al. Adverse effects of hyperoxemia during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1996; 112:812–819. 113. Young RW. Hyperoxia: a review of the risks and benefits in adult cardiac surgery. J Extra Corpor Technol 2012; 44:241–249. 114. Meyhoff CS, Jorgensen LN, Wetterslev J, et al. PROXI Trial Group. Increased long-term mortality after a high perioperative inspiratory oxygen fraction during abdominal surgery: follow-up of a randomized clinical trial. Anesth Analg 2012; 115:849–854. 115. de Jonge E, Peelen L, Keijzers PJ, et al. Association between administered oxygen, arterial partial oxygen pressure and mortality in mechanically ventilated intensive care unit patients. Crit Care 2008; 12:R156. 116. Eastwood G, Bellomo R, Bailey M, et al. Arterial oxygen tension and mortality in mechanically ventilated patients. Intensive Care Med 2012; 38:91–98. &&
Volume 28 Number 1 February 2015
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Protection strategies during cardiopulmonary bypass: ventilation, anesthetics and oxygen Carlos Ferrando, Marina Soro, and Francisco J. Belda
Purpose of review To provide an update of research findings regarding the protection strategies utilized for patients undergoing cardiopulmonary bypass (CPB), including perioperative ventilatory strategies, different anesthetic regimens, and inspiratory oxygen fraction. The article will review and comment on some of the most important findings in this field to provide a global view of strategies that may improve patient outcomes by reducing inflammation. Recent findings Postoperative complications are directly related to ischemia and inflammation. The application of lungprotective ventilation with lower tidal volumes and higher positive end-expiratory pressure reduces inflammation, thereby reducing postoperative pulmonary complications. Although inhalation anesthesia has clear cardioprotective effects compared with intravenous anesthesia, several factors can interfere to reduce cardioprotection. Hyperoxia up to 0.8 FiO2 may confer benefits without increasing oxidative stress or postoperative pulmonary complications. During the early postoperative period, inhalation anesthesia prior to extubation and the application of preventive noninvasive ventilation may reduce cardiac and pulmonary complications, improving patients’ outcomes. Summary Lung-protective mechanical ventilation, inhalation anesthesia, and high FiO2 have the potential to reduce postoperative complications in patients undergoing CPB; however, larger, well powered, randomized control trials are still needed. Keywords anesthetics, cardiac surgery, mechanical ventilation, oxygen
INTRODUCTION Postoperative complications, such us postoperative pulmonary complications (PPCs) [1 ], cardiac complications [2 ], and infection [3 ], appear in almost all patients who undergo cardiopulmonary bypass (CPB). These complications can range in severity from reversible to fatal, increasing morbidity and mortality. Although many mechanisms are involved, these complications are directly related to the inflammatory response. Inflammation during CPB occurs through a two-insult process: the first insult is caused by the surgical procedure itself, with many different inflammatory triggers such as CPB, ischemia, and surgical trauma [4–7]. The second insult is caused by mechanical ventilation [8]. During CPB, numerous strategies have been oriented to reduce the two-insult inflammation, including lung-protective ventilation, a variety of anesthetic regimens, lung perfusion during CPB, off-pump CPB, and different oxygen inspiratory concentrations. The knowledge and application of &
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these strategies may improve patients’ outcomes. This review is focused on three strategies directly related to anesthesia management: ventilation, choice of anesthetic, and oxygen.
VENTILATION Several scores for predicting PPC have demonstrated that cardiac surgery is an independent risk factor for its development [9 ,10]. The inflammatory response and, consequently, PPC after CPB are aggravated with the use of nonprotective mechanical ventilation &&
Anesthesiology and Critical Care Department, Hospital Clı´nico Universitario, Valencia, Spain Correspodence to Carlos Ferrando, Anesthesiology and Critical Care Department. Hospital Clı´nico Universitario, Av. Blasco Iban˜ez, 17, CP 46010, Valencia, Spain. Tel: +34 609 89 27 32; e-mail: [email protected] Curr Opin Anesthesiol 2015, 28:73–80 DOI:10.1097/ACO.0000000000000143
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KEY POINTS Postoperative complications in patients undergoing CPB are directly related to the inflammatory response. A ventilatory strategy that includes protective tidal volumes, higher PEEP levels, ventilation during CPB, and pre-emptive NIV may reduce inflammatory response, thereby decreasing postoperative complications. Although inhalation anesthesia is currently recommended for cardioprotection during cardiac surgery, interference with other drugs and RIPC should be considered. The use of high FiO2 (up to 0.8) decreases oxidative stress related to IRI and does not increase PPCs.
[11,12]. Mechanical forces such as stress caused by repeatedly opened and closed alveoli (atelectrauma) and strain caused by high transpulmonary pressures (overdistension) cause an inflammatory response known as biotrauma [13–17]. The inflammatory response is favored during CPB by the absence of ventilation or disconnection from the ventilatory circuit [18]. Although larger randomized control trials (RCTs) involving patients undergoing CPB are needed, lung-protective ventilatory strategy, including protective tidal volume, higher positive end-expiratory pressure (PEEP), recruitment maneuvers, continuous positive airway pressure (CPAP), low tidal volume during CPB, and noninvasive ventilation (NIV) during the immediate postextubation period, may help to attenuate inflammation and PPC.
Lung-protective mechanical ventilation Tidal volume of 6–8 ml/kg predicted body weight (PBW) has been considered protective in high-risk postoperative respiratory failure patients [19 ,20 ]. However, the evidence suggests that in cardiac surgery patients with healthy lungs, a tidal volume of 10 ml/kg or less should be considered protective. Chaney et al. [21] demonstrated that a tidal volume of 6 ml/kg improved postoperative lung mechanics and shunt fraction compared with 12 ml/kg. Recently, Lellouche et al. [22] observed during the multivariate analysis of a prospective study, including 3434 patients, that a tidal volume greater than 10 ml/kg is an independent risk factor for prolonged intubation, hemodynamic instability, renal failure, and length of stay in an ICU. However, studies comparing 6 versus 10 ml/kg did not reveal differences in the inflammatory response [23], or revealed minimal differences in response [24]. &&
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Wrigge et al. [24] measured lower plasma tumor necrosis factor (TNF)-a with 6 ml/kg than with 10 ml/kg after 6 h of ventilation, but without differences in the other cytokines measured [interleukin (IL)-2, IL-6, IL-8, IL-10, and interferon (IFN)-g]. Clinically, this is demonstrated as a lack of differences in oxygenation, lung mechanics, and time to extubation [23–25]. All of these studies employed identical PEEP (5 cmH2O) without recruitment maneuver. Atelectasis and atelectrauma during general anesthesia and the positive effects of PEEP have been widely reported in the literature. In cardiac surgery patients, significant differences in the inflammatory response are associated with different PEEP levels. Although Koner et al. [23] did not observe differences in plasma cytokines (IL-6, TNF-a) between 5 and 0 cmH2O after only 2 h of mechanical ventilation, Zunpancich et al. [26] reported a lower inflammatory response (IL-6 and IL-8) with 10 cmH2O than 2–3 cmH2O. Similar results were observed by Reis Miranda et al. [27,28], demonstrating that a strategy of 10 cmH2O PEEP and recruitment maneuver compared with 5 cmH2O PEEP without recruitment maneuver decreased inflammation and improved the functional residual capacity (FRC) and oxygenation, at least during the first 72 h after CPB. Borges et al. [29 ] and Dongelmans et al. [30] observed that 10 cmH2O improved oxygenation and lung mechanics in comparison with 5 and 8 cmH2O during the immediate postoperative period. However, a standardized PEEP level may not be the best strategy; individualized PEEP, which has demonstrated benefits during lung resection [31 ], may be an alternative. Recruitment maneuver to open closed-alveoli increasing transpulmonary pressure has been associated with the benefits of reduced atelectasis and improved oxygenation and respiratory function [28,32,33]. When and how recruitment maneuvers are performed may be important to improve benefits. Reis Miranda et al. [27] showed that an early (postintubation) recruitment maneuver reduces inflammation better than a late (after surgery) recruitment maneuver, probably because the lungs are exposed to mechanical stress for a shorter time. Meanwhile, recruitment maneuver with low transpulmonary pressures or inadequate postrecruitment maneuver PEEP level could render the maneuvers unsuitable, conferring no benefits [34]. &
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Protective strategy during cardiopulmonary bypass The inflammatory response during CPB is mainly related to the contact of blood components with the Volume 28 Number 1 February 2015
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Protection strategies during cardiopulmonary bypass Ferrando et al.
artificial surface of the bypass circuit, ischemia– reperfusion injury (IRI) of the lung, and atelectasis of the nonventilated lung. Schreiber et al. [35] analyzed the effects of different lung-protective ventilatory strategies in a meta-analysis. The use of CPAP [36], recruitment maneuvers [34], or low-tidal volume [37,38] ventilation during CPB decreases inflammation and improves oxygenation, shunt fraction, and lung mechanics; however, these effects last for a limited period, without evidence of a significant impact on the clinical outcome [35]. Because the lungs are only oxygenated through alveolar diffusion and vascular perfusion, these results could be improved with a combined strategy of ventilation and perfusion during CPB. Thus, combining ventilation with lung perfusion may be more helpful for lung protection.
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death [49,50 ,51 ]. From this body of knowledge, many studies have been oriented to develop effective strategies to minimize IRI.
Ischemic preconditioning Ischemic preconditioning is currently performed using remote ischemic preconditioning (RIPC), which consists of applying short episodes of ischemia and reperfusion to noncardiac tissues [52]. The literature is well populated with ‘proof-of-concept’ articles, indicating that RIPC may provide myocardial protection for cardiac surgery patients [53–59]. Three meta-analyses published in 2014 included RCTs that compared RIPC with placebo (no RIPC) in the presence or absence of other myocardialprotective measures: Chai and Liu [60 ] (n ¼ 976 participants), Yang et al. [61 ] (n ¼ 1235 patients), and a report by The Remote Preconditioning Trialists’ Group [62 ] that included 23 trials. These meta-analyses conclude that RIPC may reduce cardiac biomarkers, but concede a lack of evidence that such a change has a significant impact on the clinical outcome [53–59,60 –62 ]. It is interesting to note that groups were anesthetized with either inhaled agents or propofol, and no subanalysis was reported. &&
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Noninvasive ventilation Multiple factors favor atelectasis during the postoperative period. Pre-emptive NIV should be applied in selected patients at high risk of postoperative respiratory failure [39 ]. NIV has not demonstrated clear effectiveness once respiratory failure is established [40 ]. Many studies have reported benefits with the use of pre-emptive CPAP or NIV for oxygenation [41–44], with reported reductions in atelectasis [43,44], PPCs [43–47], reintubation rates, ICU readmissions, and hospital and ICU length of stay [44–47]. &&
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ANESTHETICS Myocardial IRI impairs heart function during the early postoperative period. However, an endogenous protective reaction to IRI is known [48]: repeated episodes of brief myocardial ischemia have a protective effect against a subsequent ischemic insult. The molecular mechanisms underlying ischemic preconditioning (IPC) are not completely known. In summary, preconditioning is triggered by cytokines and chemokines, which are released by myocardial cells in response to ischemia (or I/R). These signals activate several signaling pathways, generating reactive oxygen species (ROS) and other mediators that share common goals: to stabilize the mitochondrial membranes and to inhibit the opening of ATP-sensitive potassium ion channels [mitochondrial permeability transition pores (mPTP)]. The process of reperfusion leads to an abrupt rise in oxidative stress, with acute increases in ROSproducing damage to the cell membrane. This produces severe Ca2þ accumulation, which induces opening of the mPTP, which, in turn, causes damage to the mitochondrial membrane, resulting in cell
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Myocardial conditioning with anesthetics Inhaled agents provide protection when administered before (preconditioning) and after (postconditioning) myocardial ischemia. Several cellular mechanisms have been proposed with similarities to preconditioning. During reperfusion, the cardioprotective mechanism of inhaled agents prevents oxidative stress and attenuates Ca2þ overload by acting on mPTP [63,64 ,65 ]. Propofol has antioxidant properties that may confer a cardioprotective effect by reducing the total amount of ROS [66,67] without interacting with the mPTP. &
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Clinical evidence Two meta-analyses with nearly 3000 patients showed that compared with propofol, inhaled agents significantly decrease postoperative cardiac biomarkers, increase cardiac output, and decrease inotrope use, mechanical ventilation time, and hospital length of stay without beneficial effects on the risk of myocardial infarction (MI) and mortality [68,69]. Two additional meta-analyses [70,71] revealed significant reductions of in-hospital mortality and in-hospital MI. Similar results [72–74] have been observed since then, with some exceptions [75 ,76]. Finally, a recent meta-analysis [77 ]
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that included 3996 patients [41% total intravenous anesthesia (TIVA) and 59% inhaled agents] showed that the use of inhaled agents reduced mortality at the longest follow-up available. Looking at the continuous evidence that inhaled agents provide cardioprotection, the current guidelines of the American College of Cardiology Foundation/American Heart Association recommend a ‘volatile-based anesthesia’ for cardiac surgery procedures (class IIa, level of evidence A) [78]. With a perspective for future assessment, an important study in off-pump coronary artery bypass graft (CABG) surgical patients [79] has demonstrated that sevoflurane and propofol elicit differential genomic responses for cardioprotection. The studied gene expression predicted the effects on postoperative cardiac function. Interference and synergy It seems reasonable that two conditioning stimuli should induce more consistent cell protection overall. Zhou et al. [80 ] have posed a very interesting question, analyzing important factors that affect cardioprotection by RIPC. In an 1155-patient meta-analysis that confirmed the cardioprotective effect of RIPC, a univariate meta-regression analysis and multivariate regression and subgroup analyses showed that cardioprotection may be attenuated when combined with b-blockers or inhaled agents. In addition, propofol interferes with cardioprotective, RIPC-activated signal transduction [81 ]. ROS are necessary to induce ischemia and inhaled agent preconditioning. It is possible that propofol may interfere with preconditioning by eliminating ROS. In this sense, clinical evidence indicating that propofol may abolish the RIPC stimulus has been confirmed in several CABG surgery studies [82,83] in which RIPC during isoflurane, but not during propofol, decreased postoperative myocardial damage (cardiac troponin I levels). In a recent and very well designed clinical trial (n ¼ 329 patients) [84 ] that compared RIPC with a lack of RIPC while intentionally avoiding propofol in most patients, RIPC provided perioperative myocardial protection. As a secondary outcome (underpowered), improvement in all-cause mortality was observed. As complementary evidence, a recent RCT (n ¼ 1280 patients) [85 ] compared RIPC with a lack of RIPC, maintaining anesthesia with propofol and remifentanil. No significant differences were observed between RIPC (pre and postreperfusion) and no RIPC regarding a composite of major adverse outcomes. Similar effects of interference with IPC have been suggested for inhaled agents [86]. A final point is to ascertain whether the propofol-scavenging effect during reperfusion could &&
act synergistically with inhaled agents. This type of synergy has been shown in a study of 120 patients divided into four groups, which concluded that joint isoflurane preconditioning and propofol affect the CPB anesthesia regimen and synergistically attenuate myocardial IRI [87]. Other modes of interference It seems that multiple patient-related factors may influence the extent of myocardial IRI during cardiac surgery, interfering with cardioprotective strategies. These factors have been described previously [49,88], and include genetic susceptibility, age, male sex, and diabetes, diminishing the cardioprotective benefits of anesthesia [89].
Anesthetics during the postoperative period Three RCTs have compared the potential beneficial effects of sedation with sevoflurane versus propofol on markers of myocardial injury (troponin T) in the ICU after CPB [90,91 ,92 ]. All showed that administration of sevoflurane in the ICU is feasible and simple using the AnaConDa device (Sedana Medical, Sweden), and it decreased myocardial injury markers compared with patients who only received sevoflurane intraoperatively; however, administration only during surgery or in the ICU was a better option than TIVA. &
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OXYGEN Today, oxygen (O2) is recognized as a drug with which to treat patients. Dying from hypoxemia is such a clear concept that doctors provide supplemental O2 to any patient at minimal risk of hypoxemia as a matter of course. This has entailed the use of high FiO2 (from 0.5 to 1.0) during cardiac anesthesia since its inception [93], and this practice continues in many operating rooms. In fact, recommended practice is to set FiO2 at 0.8 at the initiation of CPB and to decrease it to 0.6–0.7 during hypothermia [94]. Myocardial IRI was recognized very early, and the use of supplemental O2 in clinical practice was not questioned. At the same time, lung and myocardial injury has been attributed to high FiO2 through impairment of the innate defense response by decreasing receptors in cells, increasing ROS, and many other phenomena that have suggested that perioperative hyperoxia is potentially harmful [95]. Details of the molecular mechanisms that cause such damage are perfectly reviewed in a recent publication on hyperoxia-induced lung injury (HALI) [96 ]. Most hyperoxia experiences that result in HALI are lethal experiences with exposure to 1.0 FiO2 for several &&
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Protection strategies during cardiopulmonary bypass Ferrando et al.
days, although exposure to 1.0 FiO2 for up to 4 days tends to result in sublethal injury. Most of them were realized in animals with normal lungs and spontaneous breathing or injurious mechanical ventilation. In fact, some studies suggest that high tidal volume and hyperoxia have either an additive or a synergistic effect that accentuates alveolar cell death. Furthermore, recent animal studies suggest that lung-protective ventilation may substantially reduce additional risks from hyperoxia. They conclude that in the absence of high-stretch mechanical ventilation, the risk of HALI is minimal with FiO2 0.6 or less; the risk probably begins when FiO2 exceeds 0.7, and likely becomes progressively more problematic when FiO2 exceeds 0.8 for an extended period. PEEP, precise control over FiO2, and protective mechanical ventilation have substantially reduced the risk of HALI for the vast majority of patients who require mechanical ventilation. A second point is that tissue hyperoxia decreases oxidative stress related to I/R with a preconditioning effect related to an increase in the activity of antioxidant enzymes. This has been demonstrated in studies in which hyperoxia (normobaric and hyperbaric oxygen therapy) appears to be an effective therapy for IRI of the heart, brain, small intestine, testes, and liver [97–102]. This effect has been demonstrated in our patient group during colon surgery [103], and the same effect was observed in patients undergoing lobectomy in a current ongoing study [104]. As far as we know, there is only one clinical study of 56 patients undergoing CPB that is evaluating the effect of arterial oxygen tension during reperfusion on cardiac IRI biomarkers [105]. All patients received 0.7 FiO2 during CPB, and FiO2 was lowered to 0.5 (normoxic group) from the last administration of warm cardioplegia to 1 min after aortic unclamping. FiO2 was then raised back to 0.7. This did not affect postoperative myocardial enzyme release or the short-term prognosis. Third, 0.8 FiO2 during anesthesia (and 2–4 h postoperative) has been shown to reduce surgical site infection (SSI) in many surgical procedures [106 ] with an SSI risk reduction of 23% for all surgeries combined [107]. Although it cannot be taken as a definitive review, the effect of perioperative 0.8 FiO2 on SSI has been confirmed recently [108 ,109]. These results may also apply to cardiac surgery, because the rationale for proposing hyperoxia as a factor in SSI prevention is well established [110]. Neutrophils safeguard against infection through nonspecific phagocytosis, and the elimination of bacteria depends on oxygen tension in subcutaneous tissue, which can be doubled with supplemental oxygen. &&
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Fourth, although hyperoxia leads to changes in cardiovascular function, the reduction in cardiac output is not a direct myocardial depressant effect of oxygen; rather, it is a response to increased systemic vascular resistance [111]. This increase was only observed after bypass and entailed reductions in peripheral tissue oxygenation [112]. Although hyperoxemia clearly increases global oxygen delivery and oxygen saturation in mixed venous blood, oxygen consumption declines during CPB. This effect is not associated with improved tissue perfusion [113]. However, the clinical effects of these changes remain unclear. Finally, in spite of the common assertion that supplemental perioperative oxygen increases atelectasis or other pulmonary complications after surgical procedures, several reviews indicate that this is not true [106 ]. However, no study was performed on cardiac surgery patients. The PROXI trial, which included 1382 patients after abdominal surgery, showed that perioperative hyperoxia increased mortality after a median followup of 2.3 years [114]; however, the analysis of noncancer surgical patients revealed no differences in mortality. Similarly, a mortality study of 36 307 consecutive mechanically ventilated ICU patients showed that high arterial oxygen partial pressure during the first 24 h and FiO2 administration were independently associated with in-hospital mortality [115]. However, a new review of 152 680 ventilated ICU patients [116] demonstrated an association between hypoxia (but not hyperoxia) and increased in-hospital mortality during the first 24 h. &&
CONCLUSION In patients undergoing CPB, postoperative complications are mainly related to inflammation. Although lung-protective mechanical ventilation using tidal volume less than 10 ml/kg PBW with higher PEEP levels, ventilation during the CPB procedure, and the use of pre-emptive NIV have been shown to improve patients’ outcomes, larger, well powered RCTs are needed. Inhaled agent is currently recommended by the guidelines because it has a clear cardioprotective effect, and improves relevant outcomes after cardiac surgery compared with TIVA. However, propofol or IPC might interfere significantly with cardioprotection by inhaled agents, which suggests that they should not be used concomitantly during anesthesia. The administration of hyperoxia in the operating room should be approached with the same risk–benefit assessment as any other drug. In general, we think that today it seems wise to continue to administer high FiO2 during cardiac anesthesia because of its
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demonstrated potential benefits and absence of demonstrated clinical drawbacks. However, hyperoxia must be examined further in well designed and well powered RCTs in this setting. Acknowledgements None. Financial support and sponsorship None. Conflicts of interest None.
REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. QJi Q, Mei Y, Wang X, et al. Risk factors for pulmonary complications & following cardiac surgery with cardiopulmonary bypass. Int J Med Sci 2013; 10:1578–1583. This study aims to evaluate perioperative risk factors for PPCs. There were 143 PPCs in 2056 enrolled patients. PPC was not a risk factor for hospital mortality. 2. Luratti Buse GA, Bolliger D, Seeberger E, et al. Troponin T and brain & natriuretic peptide after on-pump cardiac surgery: prognostic impact on 12-month mortality and major cardiac events after adjustment for postoperative complication. Circulation 2014; 130:948–957. [Epub ahead of print] This study describes the incidence of cardiac events in CPB patients. Of the 1559 patients enrolled, 176 (11.3%) suffered a cardiac event. 3. Si D, Rajmokan M, Lakhan M, et al. Surgical site infections following coronary & artery bypass graft procedures: 10 years of surveillance data. BMC Infect Dis 2014; 14:318. This study describes the incidence of cardiac events in CPB patients. There were 1702 surgical site infections following 14 546 CABG procedures performed. 4. Paparella D, Yau TM, Young E. Cardiopulmonary bypass induced inflammation: pathophysiology and treatment. An update. Eur J Cardiothorac Surg 2002; 21:232–244. 5. Ascione R, Lloyd CT, Underwood MJ, et al. Inflammatory response after coronary revascularization with or without cardiopulmonary bypass. Ann Thorac Surg 2000; 69:1198–1204. 6. Gu YJ, Mariani MA, Boonstra PW, et al. Complement activation in coronary artery bypass grafting patients without cardiopulmonary bypass: The role of tissue injury by surgical incision. Chest 1999; 116:892–898. 7. Hirai S. Systemic inflammatory response syndrome after cardiac surgery under cardiopulmonary bypass. Ann Thorac Cardiovasc Surg 2003; 9:365– 370. 8. Reis Miranda D, Gommers D, Peter J, et al. Mechanical ventilation affects pulmonary inflammation in cardiac surgery patients: the role of the open-lung Concept. J Cardiothorac Vasc Anesth 2007; 21:279–284. 9. Mazo V, Sabate´ S, Canet J, et al. Prospective external validation of a && predictive score for postoperative pulmonary complications. Anesthesiology 2014; 121:219–231. This study describes a predictive score for PPC. This prediction may have important consequences to clinical management, at least regarding the use of pre-emptive NIV. 10. Kor DJ, Lingineni RK, Gajic O, et al. Predicting risk of postoperative lung injury in high-risk surgical patients. A multicenter cohort study. Anesthesiology 2014; 120:1168–1181. 11. Dreyfuss D, Saumon G. Ventilatory-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med 1998; 157:294–323. 12. Plataki M, Hubmayr RD. The physical basis of ventilator-induced lung injury. Expert Rev Respir Med 2010; 4:373–385. 13. von Bethmann AN, Brasch F, Nusing R, et al. Hyperventilation induces release of cytokines from perfused mouse lung. Am J Respir Crit Care Med 1998; 157:263–272. 14. Ranieri VM, Suter PM, Tortorella C, et al. Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial. J Am Med Assoc 1999; 282:54–61. 15. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000; 342:1301–1308.
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16. Uhlig U, Haitsma JJ, Goldmann T, et al. Ventilation-induced activation of the mitogen-activated protein kinase pathway. Eur Respir J 2000; 20:946–956. 17. Ricard JD, Dreyfuss D, Saumon G. Ventilator-induced lung injury. Curr Opin Crit Care 2002; 8:12–20. 18. Ng C, Arifi A, Wan S, et al. Ventilation during cardiopulmonary bypass: impact on cytokine response and cardiopulmonary function. Ann Thorac Surg 2008; 85:154–162. 19. Garcı´a-Delgado M, Navarrete-Sa´nchez I, Colmenero M. Preventing and && managing perioperative pulmonary complications following cardiac surgery. Curr Opin Anesthesiol 2014; 27:146–152. A concise review focusing in some of the preventive and therapeutic measures that can be implemented to reduce PPC after cardiac surgery. 20. Hemmesa S, Neto A, Schultz M. Intraoperative ventilatory strategies to && prevent postoperative pulmonary complications: a meta-analysis. Curr Opin Anesthesiol 2013; 26:126–133. This meta-analysis demonstrates the importance of protective ventilation (lower tidal volume and higher PEEP) to reduce PPC and emphasizes the need of well powered RCTs to better establish the benefits of intraoperative lung-protective ventilation. 21. Chaney MA, Nikolov MP, Blakeman BP, et al. Protective ventilation attenuates postoperative pulmonary dysfuntion in patients undergoing cardiopulmonary bypass. J Cardiothorac Vasc Anesth 2000; 14:514–518. 22. Lellouche F, Dionne S, Simard S, et al. High tidal volumes in mechanically ventilated patients increase organ dysfunction after cardiac surgery. Anesthesiology 2012; 116:1072–1082. 23. Koner O, Celebi S, Balci H, et al. Effects of protective and conventional mechanical ventilation on pulmonary function and systemic cytokine rele´ase after cardiopulmonary bypass. Intensive Care Med 2004; 30:620–626. 24. Wrigge H, Uhlig U, Baumgarten G, et al. Mechanical ventilation strategies and inflammatory responses to cardiac surgery: a propective randomized clinical trial. Intensive Care Med 2005; 31:1379–1387. 25. Sundar S, Novack V, Jervis K, et al. Influence of low tidal volume on time to extubation in cardiac surgical patients. Anesthesiology 2011; 114:1102– 1110. 26. Zunpancich E, Paparella D, Turani F, et al. Mechanical ventilation affects inflammatory mediators in patients undergoing cardiopulmonary bypass for cardiac surgery. J Thorac Cardiovasc Surg 2005; 130:378–383. 27. Reis Miranda D, Gommers D, Struijs A, et al. Ventilation according to the open lung concept attenuates pulmonary inflammatory response in cardiac surgery. Eur J Cardiothorac Surg 2005; 28:889–895. 28. Reis Miranda D, Struijs A, Koetsier P, et al. Open lung ventilation improves functional residual capacity after extubation in cardiac surgery. Crit Care Med 2005; 33:2253–2258. 29. Borges DL, Nina VJ, Coste Mde A, et al. Effects of different PEEP levels on & respiratory mechanics and oxygenation after coronary artery bypass grafting. Rev Bras Cir Cardiovasc 2013; 28:380–385. Randomized clinical trial in which 136 patients were divided into three groups: 5, 8, and 10 cmH2O. Higher levels of PEEP during the immediate postoperative period improved lung mechanics and oxygenation. 30. Dongelmans DA, Hemmes SN, Kudoga AC, et al. Positive end-expiratory pressure following coronary artery bypass grafting. Minerva Anestesiol 2012; 78:790–800. 31. Ferrando C, Mugarra A, Gutierrez A, et al. Setting individualized positive end&& expiratory pressure level with a positive end-expiratory pressure decrement trial after a recruitment maneuver improves oxygenaiton and lung mechanics during one-lung ventilation. Anesth Analg 2014; 118:657–665. This is the first clinical trial to demonstrate the benefits of an individualized PEEP titration trial to oxygenation and lung mechanics, in comparison with a standarized PEEP level. 32. Padovani C, Cavenaghi OM. Alveolar recruitment in patients in the immediate postoperative period of cardiac surgery. Rev Bras Cir Cardiovasc 2011; 26:116–121. 33. Celebi S, Koner O, Menda F, et al. Pulmonary effects of noninvasive ventilation combined with the recruitment maneuver after cardiac surgery. Anesth Analg 2008; 107:614–619. 34. Scherer M, Dettmer S, Meininger D, et al. Alveolar recruitment strategy during cardiopulmonary bypass does not improve postoperative gas exchange and lung function. Cardiovasc Eng 2009; 9:1–5. 35. 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; 26:448–454. 36. Loeckinger A, Kleinsasser A, Lindner KH, et al. Continuous positive airway pressure at 10 cm H(2)O during cardiopulmonary bypass improves postoperative gas exchange. Anesth Analg 2000; 91:522–527. 37. Gagnon J, Laporta D, Be´¨ıque F, et al. Clinical relevance of ventilation during cardiopulmonary bypass in the prevention of postoperative lung dysfunction. Perfusion 2010; 25:205–210. 38. Davoudi M, Farhanchi A, Moradi A, et al. The effect of low tidal volume ventilation during cardiopulmoanry bypass on postoperative pulmonary function. J Tehran Heart Cent 2010; 5:128–131. 39. Cabrini L, Plumari VP, Nbile L, et al. Noninvasive ventilation in cardiac && surgery: a concise review. Heart Lung Vessel 2013; 5:137–141. In this review, authors concluded that NIV has the potential to be very useful to prevent or treat postoperative respiratory failure, although available data are limited.
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Protection strategies during cardiopulmonary bypass Ferrando et al. 40. Garcı´a-Delgado M, Navarrete I, Garcia-Palma MJ, et al. Postoperative respiratory failure after cardiac surgery: use of noninvasive ventilation. J Cardiothorac Vasc Anesth 2012; 26:443–447. A retrospective study including 63 postoperative cardiac surgery patients. Authors analyze the use of NIV in respiratory failure after extubation. Reintubation was required in one-half of NIV-treated patients and was associated with increased hospital mortality. 41. Matte P, Jacqet L, Van DM, et al. Effects of conventional physiotherapy, continuous positive airway pressure and noninvasive ventilator support with bilevel positive airway pressure after coronary artery bypass grafting. Acta Anaesthesiol Scand 2000; 44:75–81. 42. Pinilla JC, Oleniuk FH, Tan L. Use of a nasal CPAP mask in the treatment of postoperative atelectasis in aortocoronary bypass surgery. Crit Care Med 1990; 18:836–840. 43. Zarbock A, Mueller E, Netzer S, et al. Prophylactic nasal continuous positive airway pressure following cardiac surgery protects from postoperative pulmonary complications: a prospective, randomized, controlled trial in 500 patients. Chest 2009; 135:1252–1259. 44. Pasquina P, Merlani P, Granier JM. Continuous positive airway pressure versus noninvasive pressure support ventilation to treat atelectasis after cardiac surgery. Anesth Analg 2004; 99:1001–1008. 45. Al Jaaly E, Fiorentino F, Reeves BC, et al. Effect of adding postoperative noninvasive ventilation to usual care to prevent pulmonary complications in patients undergoing coronary artery bypass grafting: a randomized controlled trial. J Thorac Cardiovasc Surg 2013; 146:912–918. 46. Nava S, Gregoretti C, Fanfulla F, et al. Noninvasive ventilation to prevent respiratory failure after extubation in high-risk patients. Crit Care Med 2005; 33:2465–2470. 47. Ferrer M, Valencia M, Nicolas JM, et al. Early noninvasive ventilation averts extubation failure in patients at risk: a randomized trial. Am J Respir Crit Care Med 2006; 173:164–170. 48. Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 1986; 74:1124–1136. 49. Piper HM, Garcia-Dorado D. Reducing the impact of myocardial ischaemia/ reperfusion injury. Cardiovasc Res 2012; 94:165–167. 50. Heusch G. Cardioprotection: chances and challenges of its translation to the && clinic. Lancet 2013; 12:166–175. An excellent review of cardioprotection, including the different pathways of the IRI, the various cardioprotective strategies, and the factors that might affect this cardioprotection. 51. Brooks MJ, Andrews DT. Molecular mechanisms of ischemic conditioning: && translation into patient outcomes. Future Cardiol 2013; 9:549–568. A detailed review that discusses recent advances in the molecular mechanisms involved in IRI and the signaling pathways recruited by ischemic conditioning. It concludes with evidence to support the use of ischemic conditioning in current clinical practice. 52. Przyklenk K. Reduction of myocardial infarct size with ischemic ‘conditioning’: physiologic and technical considerations. Anesth Analg 2013; 117:891– 901. 53. Hausenloy DJ, Yellon DM. The therapeutic potential of ischemic conditioning: an update. Nat Rev Cardiol 2011; 8:619–629. 54. Marczak J, Nowicki R, Kulbacka J, et al. Is remote ischaemic preconditioning of benefit to patients undergoing cardiac surgery? Interact Cardiovasc Thorac Surg 2012; 14:634–639. 55. Sabbagh S, Henry Salzman MM, Kloner RA, et al. Remote ischemic preconditioning for coronary artery bypass graft operations. Ann Thorac Surg 2013; 96:727–736. 56. Pilcher JM, Young P, Weatherall M, et al. A systematic review and metaanalysis of the cardioprotective effects of remote ischaemic preconditioning in open cardiac surgery. J R Soc Med 2012; 105:436–445. 57. Alreja G, Bugano D, Lotfi A. Effect of remote ischemic preconditioning on myocardial and renal injury: meta-analysis of randomized controlled trials. J Invasive Cardiol 2012; 24:42–48. 58. D’Ascenzo F, Cavallero E, Moretti C, et al. Remote ischaemic preconditioning in coronary artery bypass surgery: a meta-analysis. Heart 2012; 98:1267– 1271. 59. Brevoord D, Kranke P, Kuijpers M, et al. Remote ischemic conditioning to protect against ischemia-reperfusion injury: a systematic review and metaanalysis. PLoS One 2012; 7:e42179. 60. Chai Q, Liu J. Early stage effect of ischemic preconditioning for patients && undergoing on-pump coronary artery bypass grafts surgery: Systematic review and meta-analysis. Pak J Med Sci 2014; 30:642–648. This is a meta-analysis of 18 randomized controlled trials. The positive and negative results were equal in all 18 trials. There were no differences between ischemia preconditioning and control groups regarding in-hospital mortality or postoperative MI morbidity. Postoperative differences in cardiac troponin and troponin I were observed. Authors concluded that the meta-analysis results should be interpreted with caution owing to limited effective data. 61. Yang L, Wang G, Du Y, et al. Remoteischemic preconditioning reduces && cardiactroponin I release in cardiac surgery: a meta-analysis. J Cardiothorac Vasc Anesth 2014; 28:682–689. This meta-analysis includes 19 adult and pediatric randomized controlled trials. There were no differences in mortality or morbidity; however, RIPC reduces cardiac troponin I. &&
62. Remote Preconditioning Trialists’ Group, Healy DA, Khan WA, Wong CS, et al. Remote preconditioning and major clinical complications following adult cardiovascular surgery: systematic review and meta-analysis. Int J Cardiol 2014; 176:20–31. This meta-analysis includes 23 randomized controlled trials (2200 patients). RIPC did not have a significant effect on clinical end-points (death, perioperative MI, renal failure, stroke, mesenteric ischemia, length of stay in hospital, or critical care); however, authors concluded that pooled data from pilot trials cannot confirm that RIPC has any significant effect on clinically relevant end-points. 63. Van Allen NR, Krafft PR, Leitzke AS, et al. The role of volatile anesthetics in cardioprotection: a systematic review. Med Gas Res 2012; 28:22. 64. Wu L, Zhao H, Wang T, et al. Cellular signaling pathways and molecular & mechanisms involving inhalational anesthetics-induced organoprotection. J Anesth 2014; 28:740–758. [Epub ahead of print] This review summarizes the signaling pathways and molecular participants in inhaled anesthetic-mediated organ protection published in the current literature. It compares and contrasts the ’preconditioning’ and ’postconditioning’ phenomena, as well as the similarities and differences in mechanisms between organs. 65. Kojima A, Kitagawa H, Omatsu-Kanbe M, et al. Sevoflurane protects & ventricular myocytes against oxidative stress-induced cellular Ca2þ overload and hypercontracture. Anesthesiology 2013; 119:606–620. This experimental study investigated the electrophysiological mechanisms underlying cardioprotective effects of sevoflurane against oxidative stress-induced cellular injury. Oxidative stress is implicated in the pathogenesis of cardiac reperfusion injury, which is characterized by cellular Ca2þ overload and hypercontracture. Volatile anesthetics protect the heart against reperfusion injury primarily by attenuating Ca2þ overload. 66. Ansley DM, Sun J, Visser WA, et al. High dose propofol enhances red cell antioxidant capacity during CPB in humans. Can J Anesth 1999; 46:641– 648. 67. Ansley DM, Xia Z. Propofol preservation of myocardial function in patients undergoing coronary surgery with cardiopulmonary bypass is dose dependent. Anesthesiology 2002; 98:1028–1029. 68. Symons JA, Myles PS. Myocardial protection with volatile anaesthetic agents during coronary artery bypass surgery: a meta-analysis. Br J Anaesth 2006; 97:127–136. 69. Yu CH, Beattie WS. The effects of volatile anesthetics on cardiac ischemic complications and mortality in CABG: a meta-analysis. Can J Anaesth 2006; 53:906–918. 70. Landoni G, Biondi-Zoccai GG, Zangrillo A, et al. Desflurane and sevoflurane in cardiac surgery: a meta-analysis of randomized clinical trials. J Cardiothorac Vasc Anesth 2007; 21:502–511. 71. Landoni G, Fochi O, Tritapepe L, et al. Cardiacprotection by volatile anesthetics: a review. Minerva Anestesiol 2009; 75:269–273. 72. Jakobsen CJ, Berg H, Hindsholm KB, et al. The influence of propofol versus sevoflurane anesthesia on outcome in 10,535 cardiac surgical procedures. J Cardiothorac Vasc Anesth 2007; 21:664–671. 73. Yao YT, Li LH. Sevoflurane versus propofol for myocardial protection in patients undergoing coronary artery bypass grafting surgery: a metaanalysis of randomized controlled trials. Chin Med Sci J 2009; 24:133– 141. 74. Flier S, Post J, Concepcion AN, et al. Influence of propofol-opioid vs. isoflurane-opioid anaesthesia on postoperative troponin release in patients undergoing coronary artery bypass grafting. Br J Anaesth 2010; 105:122– 130. 75. Suryaprakash S, Chakravarthy M, Muniraju G, et al. Myocardial protection & during off pump coronary artery bypass surgery: a comparison of inhalational anesthesia with sevoflurane or desflurane and total intravenous anesthesia. Ann Card Anaesth 2013; 16:4–8. In this prospective study of 139 patients, no differences in cardiac protection (TnT) were observed with either 1–2% sevoflurane or 4–6% desflurane and propofol at doses of 2–4 mg/kg/h. This study was conducted during off-pump surgery, in which myocardial IRI is limited. 76. 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; 64:953–960. 77. Landoni G, Greco T, Biondi-Zoccai G, et al. Anaesthetic drugs and survival: a && Bayesian network meta-analysis of randomized trials in cardiac surgery. Br J Anaesth 2013; 111:886–896. An excellent meta-analysis including 38 RCTs and 3642 patients. This metaanalysis concludes that anesthesia with volatile agents appears to reduce mortality after cardiac surgery compared with TIVA, especially when sevoflurane or desflurane is used. 78. Hillis LD, Smith PK, Anderson JL, et al. 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011; 124:2610– 2642. 79. Lucchinetti E, Hofer C, Bestmann L, et al. Gene regulatory control of myocardial energy metabolism predicts postoperative cardiac function in patients undergoing off-pump coronary artery bypass graft surgery: inhalational versus intravenous anesthetics. Anesthesiology 2007; 106:444– 457. &&
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Cardiovascular anesthesia 80. Zhou C, Liu Y, Yao Y, et al. B-blockers and volatile anesthetics may attenuate cardioprotection by remote preconditioning in adult cardiac surgery: a metaanalysis of 15 randomized trials. J Cardiothorac Vasc Anesth 2013; 27:305– 311. The aim of this meta-analysis was to evaluate the factors affecting cardioprotection by RIPC in adult cardiac surgery. Fifteen trials with a total of 1155 patients were included. This meta-analysis also confirmed the cardioprotection conferred by RIPC, and that the cardioprotective effect may be attenuated when combined with b-blockers or volatile anesthetics. 81. Kottenberg E, Musiolik J, Thielmann M, et al. Interference of propofol with & signal transducer and activator of transcription 5 activation and cardioprotection by remote ischemic preconditioning during coronary artery bypass grafting. J Thorac Cardiovasc Surg 2014; 147:376–382. Prospective trial in 24 nondiabetic patients. Authors showed that propofol interferes with RIPC cardioprotection. 82. Kottenberg E, Thielmann M, Bergmann L, et al. Protection by remote ischemic preconditioning during coronary artery bypass graft surgery with isoflurane but not propofol: a clinical trial. Acta Anaesthesiol Scand 2011; 56:30–38. 83. Kottenberg E, Thielmann M, Bergmann L, et al. Protection by remote ischemic preconditioning during coronary artery bypass graft surgery with isoflurane but not propofol: a clinical trial. Acta Anaesthesiol Scand 2012; 56:30–38. 84. Thielmann M, Kottenberg E, Kleinbongard P, et al. Cardioprotective and && prognostic effects of remote ischaemic preconditioning in patients undergoing coronary artery bypass surgery: a single-centre randomised, doubleblind, controlled trial. Lancet 2013; 382:597–604. Remote ischemic preconditioning provided perioperative myocardial protection and improved the prognosis of patients undergoing elective CABG surgery. 85. Hong DM, Lee EH, Kim HJ, et al. Does remote ischaemic preconditioning & with postconditioning improve clinical outcomes of patients undergoing cardiac surgery? Remote Ischaemic Preconditioning with Postconditioning Outcome Trial. Eur Heart J 2014; 35:176–183. In this single-center RCT including 1280 patients, authors did not observe differences between control and RICP associated with remote ischemic postconditioning. It is important to note that propofol was used to maintain anesthesia. 86. Lucchinetti E, Bestmann L, Feng J, et al. Remote ischemic preconditioning applied during isoflurane inhalation provides no benefit to the myocardium of patients undergoing on-pump coronary artery bypass graft surgery: lack of synergy or evidence of antagonism in cardioprotection? Anesthesiology 2012; 116:296–310. 87. Huang Z, Zhong X, Irwin MG, et al. Synergy of isoflurane preconditioning and propofol postconditioning reduces myocardial reperfusion injury in patients. Clin Sci 2011; 121:57–69. 88. Heusch G. Cardioprotection: chances and challenges of its translation to the clinic. Lancet 2013; 381:166–175. 89. Sharma AK, Khanna D. Diabetes mellitus associated cardiovascular signalling alteration: a need for the revisit. Cell Signal 2013; 25:1149–1155. 90. Soro M, Gallego L, Silva V, et al. Cardioprotective effect of sevoflurane and propofol during anaesthesia and the postoperative period in coronary bypass graft surgery: a double-blind randomised study. Eur J Anaesthesiol 2012; 29:561–569. 91. Guerrero Orriach JL, Gala´n Ortega M, Ramirez Aliaga M, et al. Prolonged & sevoflurane administration in the off-pump coronary artery bypass graft surgery: beneficial effects. J Crit Care 2013; 28:879. (e13-8). This prospective study conducted in 60 patients undergoing OPCABG surgery revealed significant differences in troponin I levels during the first 48 h among three anesthetic regimens (intraoperative–postoperative): propofol– propofol > sevoflurane–propofol > sevoflurane–sevoflurane. The results show that the best option is the use of sevoflurane throughout the perioperative period. 92. Marcos-Vidal JM, Gonza´lez R, Garcia C, et al. Sedation with sevoflurane in & postoperative cardiac surgery: influence on troponin T and creatinine values. Heart Lung Vessel 2014; 6:33–42. In this prospective study of 129 patients undergoing coronary or coronary and valve cardiac surgery, troponin T levels were significantly lower at 12 and 48 h after admission in the sevoflurane group. 93. Hessel II EA. History of cardiac surgery and anesthesia. In Estafanous FG, Barash PG, Reves JG, editors. Cardiac anesthesia: principles and practice. Philadelphia: Lippincott Williams & Wilkins; 2001. (Lippincott’s Interactive Cardiac Anesthesia Library on CD-ROM: www.LWW.com). 94. Karabulut H, Toraman F, Tarcan S, et al. Adjustment of sweep gas flow during cardiopulmonary bypass. Perfusion 2002; 17:353–356. 95. Lumb AB, Walton LJ. Perioperative oxygen toxicity. Anesthesiol Clin 2012; 30:591–605. &&
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96. Kallet RH, Matthay MA. Hyperoxic acute lung injury. Respir Care 2013; 58:123–141. An extensive review of HALI. This review presents evidence that HALI is produced mainly with the use of FiO2 for an extended period of time. Also presents evidence that lung-protective ventilation has greatly reduced the risk of HALI. 97. Brown DM, Holt DW, Edwards JT, et al. Normoxia vs. hyperoxia: impact of oxygen tension strategies on outcomes for patients receiving cardiopulmonary bypass for routine cardiac surgical repair. J Extra Corpor Technol 2006; 38:241–248. 98. Mariero LH, Rutkovskiy A, Stenslokken KO, et al. Hyperoxia during early reperfusion does not increase ischemia/reperfusion injury. Eur J Cardiothorac Surg 2012; 41:149–153. 99. Kang N, Hai Y, Liang F, et al. Preconditioned hyperbaric oxygenation protects skin flap grafts in rats against ischemia/reperfusion injury. Mol Med Rep 2014; 9:2124–2130. 100. Yuan Z, Pan R, Liu W, et al. Extended normobaric hyperoxia therapy yields greater neuroprotection for focal transient ischemia-reperfusion in rats. Med Gas Res 2014; 4:14. 101. Tavafi M, Ahmadvand H, Tamjidipour A, et al. Effect of normobaric hyperoxia on gentamicin-induced nephrotoxicity in rats. Iran J Basic Med Sci 2014; 17:287–293. 102. Caldeira DE, Silveira MR, Margarido MR, et al. Effect of hyperbaric hepatic hyperoxia on the liver of rats submitted to intermittent ischemia/reperfusion injury. Acta Cir Bras 2014; 29 (Suppl 1):24–28. 103. Garcı´a-de-la-Asuncio´n J1, Barber G, Rus D, et al. Hyperoxia during colon surgery is associated with a reduction of xanthine oxidase activity and oxidative stress in colonic mucosa. Redox Rep 2011; 16:121–128. 104. Garcı´a-de-la-Asuncio´ J, Martı´ F, Bruno L, et al. Oxidative stress by lung reexpasion during pulmonary lobectomy: prevention by propofol and FiO2 0.8: 5AP4-5. Eur J Anaesthesiol 2010; 27:100–101. 105. Lee JS, Kim JC, Chung J, et al. Effect of arterial oxygen tension during reperfusion on myocardial recovery in patients undergoing valvular heart surgery. Korean J Anesthesiol 2010; 58:122–128. 106. Hovaguimian F, Lysakowski C, Elia N, et al. Effect of intra-operative high && inspired oxygen fraction on surgical site infection, postoperative nausea and vomiting, and pulmonary function: systematic review and meta-analysis of randomized trials. Anesthesiology 2013; 119:303–316. This meta-analysis of 22 RCTs including7001 patients showed that in comparison with low intraoperative FiO2 (around 0.3), high intraoperative FiO2 (around 0.8) decreases the risks of SSI, has a weak beneficial effect on nausea, and does not increase PPC. 107. Belda FJ, Catala´-Lo´pez F, Greif R, et al. Benefits and risks of intraoperative high inspired oxygen therapy: firm conclusions are still far off. Anesthesiology 2014; 120:1051–1052. 108. Schietroma M, Cecilia EM, Carlei F, et al. Prevention of anastomotic leakage & after total gastrectomy with perioperative supplemental oxygen administration: a prospective randomized, double-blind, controlled, single-center trial. Ann Surg Oncol 2013; 20:1584–1590. This study of 171 patients undergoing elective open anastomosis for gastric cancer showed that 0.8 FiO2 intraoperatively and during the first postoperative 6 h significantly reduced anastomotic leakage. 109. Schietroma M, Cecilia EM, Sista F, et al. High-concentration supplemental perioperative oxygen and surgical site infection following elective colorectal surgery for rectal cancer: a prospective, randomized, double-blind, controlled, single-site trial. Am J Surg 2014; 18:. [Epub ahead of print] 110. Canet J, Belda FJ. Perioperative hyperoxia: the debate is only getting started. Anesthesiology 2011; 114:1271–1273. 111. Anderson KJ, Harten JM, Booth MG, et al. The cardiovascular effects of normobaric hyperoxia in patients with heart rate fixed by permanent pacemaker. Anaesthesia 2010; 65:167–171. 112. Joachimsson PO, Sjoberg F, Forsman M, et al. Adverse effects of hyperoxemia during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1996; 112:812–819. 113. Young RW. Hyperoxia: a review of the risks and benefits in adult cardiac surgery. J Extra Corpor Technol 2012; 44:241–249. 114. Meyhoff CS, Jorgensen LN, Wetterslev J, et al. PROXI Trial Group. Increased long-term mortality after a high perioperative inspiratory oxygen fraction during abdominal surgery: follow-up of a randomized clinical trial. Anesth Analg 2012; 115:849–854. 115. de Jonge E, Peelen L, Keijzers PJ, et al. Association between administered oxygen, arterial partial oxygen pressure and mortality in mechanically ventilated intensive care unit patients. Crit Care 2008; 12:R156. 116. Eastwood G, Bellomo R, Bailey M, et al. Arterial oxygen tension and mortality in mechanically ventilated patients. Intensive Care Med 2012; 38:91–98. &&
Volume 28 Number 1 February 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
