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Anaesthesia for patients undergoing ventricular assist-device implantation
Best Practice & Research Clinical Anaesthesiology 26 (2012) 167–177
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Anaesthesia for patients undergoing ventricular assist-device implantation Markus Feussner, MD, Consultant Anesthesilogist a, *, Chirojit Mukherjee, MD, Program director and Consultant Anesthesiologist a, c, Jens Garbade, MD, PhD, Consultant Cardiac Surgeon b, d, Joerg Ender, MD, Chairman a, c a b
Department of Anesthesiology, University Leipzig, Heart Center, Struempellstrasse 39, D-04289 Leipzig, Germany Department of Cardiac Surgery, University Leipzig, Heart Center, Struempellstrasse 39, D-04289 Leipzig, Germany
Keywords: anaesthesia management VAD implantations non-cardiac surgery
In the last 10 years, implantation of ventricular-assist devices has become an interesting option as either bridge-to-transplantation or destination procedure for patients with end-stage congestive heart failure. In the future, the number of ventricular assist device implantations is expected to increase furthermore. In general, this patient cohort is associated with significant co-morbidities, for example, pulmonary hypertension, peripheral vascular disease and renal insufficiency. Anaesthetic management for implantation of ventricular assist devices can be challenging for cardiac anaesthesiologists. Even minor changes in their haemodynamics and physiological parameters can cause significant morbidity and mortality. Experience in haemodynamic monitoring including echocardiography and pharmacological management (use of inotropes, phosphodiesterase inhibitors and vasopressors) is a requirement. Particularly, the diagnosis and therapy of right-sided heart failure after implantation of left-ventricular assist devices should be addressed. Ó 2012 Elsevier Ltd. All rights reserved.
* Corresponding author: Tel.: þ49 3418651060; Fax: þ49 3418651820. E-mail addresses: [email protected] (M. Feussner), [email protected] (C. Mukherjee), [email protected] (J. Garbade), [email protected] (J. Ender). c Tel.: þ49 3418651060; Fax: þ49 3418651820. d Tel.: þ49 3418651060; Fax: þ49 3418651452. 1521-6896/$ – see front matter Ó 2012 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.bpa.2012.06.001
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In Europe and the United States, more than 16 million people live with a diagnosis of congestive heart failure (CHF).1 Furthermore, the incidence of CHF is dramatically increased in people aged over 65 years, and this population is expected to increase twofold within the next 20 years. Heart transplantation is still the gold standard for patients suffering from end-stage CHF refractory to pharmacologic and cardiac resynchronisation therapy.2 The discrepancy between the shortage of appropriate donor organs and the increasing number of people with end-stage CHF has focussed interest on alternative therapies, particularly on mechanical circulatory support. Over the past 50 years, mechanical circulatory support has become established as either bridging or destination therapy in this patient cohort.3 In 1966, DeBakey and Liotta implanted the first left-ventricular assist device (LVAD) in a patient with low cardiac output syndrome, and 10 days later managed to successfully to explant it. From this milestone, the development of technically advanced VAD was initiated and resulted in the REMATCH (Randomised Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure) trial as preliminary climax. The REMATCH trial first observed the survival in long-term mechanical circulatory support.4 This study looked at first-generation VAD, which generated pulsatile flow in patients ineligible for transplantation in a destination-therapy scenario and showed a reduction in long-term mortality in patients with VAD compared with those treated with optimised drug therapy. The evolution of VADs from pulsatile flow-generating systems to continuous flow-generating second- and third-generation VADs provides a further increase in long-term survival compared to first-generation VAD systems5 by reduction of mechanical and thrombotic complications. The demonstration of improved prognosis led to implantation of VADs not only in specialised centres with established transplantation programmes, as a bridge to transplantation, but also as a destination-therapy scenario. Thus, as the indications for VAD therapy broaden, cardiac anaesthesiologists will be more likely to encounter patients requiring anaesthesia and perioperative care for VAD implantations in the future as indeed will non-cardiac anaesthesiologists providing anaesthesia for non-cardiac surgery in patients with VADs.
Patient characteristics, secondary illnesses and medication Patients requiring a VAD usually undergo long-term hospitalisation before surgery and hence a comprehensive preoperative work-up has usually been completed, including diagnostic heart catheter procedures. Extra care should be taken to evaluate pulmonary hypertension if present, and co-morbidities associated with renal, central-nervous and hepatobiliary system, as these are common in this setting. Exceptions include patients requiring emergency support usually admitted following acute myocardial infarction, which may manifest as cardiogenic shock.6 In this group, optimisation of secondary diseases is simply not feasible prior to surgery. Patients suffering from severe CHF are typically treated with b-blockers, intensive diuretic therapy and peripheral resistance reducing angiotensin II-converting enzyme inhibitors (ACE inhibitors) and angiotensin-receptor blockers. There is a general consensus to continue the treatment with b-blockers in the perioperative setting to avoid rebound tachycardia and hypertension. Diuretic treatment should be discontinued on the day of surgery, due to hypovolaemia-induced hypotension after induction of general anaesthesia. Angiotensin-blocking medications are the mainstay of treatment for CHF, and sudden withdrawal could result in an acute exacerbation of heart failure.7 Conversely, a retrospective study in patients undergoing coronary artery bypass graft (CABG) surgery found ACE inhibitors to be an independent risk factor for perioperative mortality and postoperative renal dysfunction.8 A recent study showed a loss of systemic vascular resistance with consequent increased requirements of inotropic support. A low-dose administration of vasopressin prevented post-cardiopulmonary bypass (CPB) hypotension.9 The controversy as to whether angiotensin blockers should be withheld pre-operatively should be decided in consultation with the various team members involved in perioperative management of the patient. Preoperative anxiolytic medication results in a decrease of endogenous sympathetic tone and should therefore be administered judiciously. Furthermore, oversedation could lead to hypoventilation, which in turn results in hypoxia, acidosis and an increase in pulmonary vascular resistance. There is a minimal physiological reserve in this high-risk group and any minor alteration can precipitate major deterioration.
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General anaesthetic setting Standard monitoring (5-lead electrocardiography (ECG), pulse oximetry, capnography and core and peripheral temperature probes) and an invasive arterial blood-pressure monitoring are mandatory. A large-bore peripheral venous access (14 or 16 gauge) as well as a 9-French central venous catheter are also indicated due to the high risk of massive intra- and postoperative haemorrhage.10 A multi-lumen central venous (four or five lumen) catheter is preferred. An ultrasound-guided placement of the central venous catheters is naturally helpful because of the higher incidence (10%) of central venous thrombosis in these long-term hospitalised patients.11–13 In routine cardiac surgery, the internal jugular vein (IJV) is the preferred site for central venous access. In a VAD implantation planned as a ‘bridge-totransplantation’ scenario, puncture of the left IJV is recommended so that the right IJV can be preserved to facilitate endomyocardial biopsy post-transplantation to evaluate for cardiac rejection.14 Typically, a central venous access is present preoperatively having facilitated the administration of inotropes and phosphodiesterase inhibitors. In the operating room, an ultrasound-guided cannulation using local anaesthesia may be preferred before induction of general anaesthesia in unstable patients. Although the use of pulmonary artery catheters (PACs) has not demonstrated a direct improvement in mortality outcomes,15,16 a recent survey of cardiac anaesthesiologists shows that they preferably use a pulmonary catheter during VAD implantation.17 The PAC is the single best measuring device at an anaesthesiologist’s disposal to monitor pulmonary vascular resistance and facilitate goal-directed therapy of pulmonary hypertension, and thereby support adequate right-ventricular function. In addition, mixed central venous oxygen saturation can provide important information about the perfusion status of the patient and also the need for red blood cells.18 The placement of PAC is therefore recommended in this special setting.19 Patients undergoing VAD implantation are typically treated with an automated implantable cardioverter–defibrillator (AICD). To avoid accidental shock delivery during surgery, the AICD is regularly turned off. Arrhythmias, especially ventricular tachycardias, are frequently resistant to drug therapy. Therefore, external shock electrodes should be placed before induction. Before induction, the operating room should be equipped for emergency commencement of CPB and hence, the presence of a surgeon during the induction process is indicated. Placement of guide wires for the CPB cannulas under local anaesthesia is an option in higher-risk patients, but current literature does not support evidence for this procedure. Anaesthetic drugs Etomidate is commonly used for induction of anaesthesia10,20 as it is capable of inducing a state of unawareness without significant myocardial depression or vasodilatation. The risk of relative adrenal insufficiency as a consequence of single induction dose of etomidate is well described, but did not result in a higher demand for vasopressors.21 Propofol as an induction agent has been shown to have a negative inotropic effect and consequently causes decrease in blood pressure.22,23 Conversely, Bendel et al. found that although propofol causes more hypotension than etomidate, there is no difference in cardiac output using either of these drugs.24 Hence, the decrease in blood pressure is caused mainly by a reduction in systemic vascular resistance, which can be counteracted with small doses of a vasoconstrictor, for example, norepinephrine. Propofol does not lead to the induction of myoclonic movements and the inhibition of 11-b-hydroxylase as seen with etomidate. Furthermore, experimental studies suggested that propofol can induce a relaxation of the pulmonary vessels25 with consecutive reduction of pulmonary vascular resistance, which would be beneficial in patients suffering from CHF. The use of propofol as an induction agent in cardiac anaesthesia is well established and the patient haemodynamic remains more stable with controlled induction.26 Therefore, propofol as an induction agent is justified if used in a total dose of 2 mg kg1 of body weight with starting dose of 1 mg kg1 of body weight. Concerning administration of opioids, fentanyl seems to be the standard choice.10,20 The dosage used ranges between 50 and 100 mg kg1 of body weight in these studies. A choice of continuous infusion of fentanyl, sufentanil or remifentanil during the procedure can be institution dependent; however, remifentanil has a major advantage in that it is metabolised
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independent of renal or hepatic function. It acts as a highly potent opioid intra-operatively, and yet facilitates early recovery and extubation when appropriate. For neuromuscular blockade, pancuronium and rocuronium are typically suitable for patients undergoing VAD implantation. Pancuronium was traditionally used by cardiac anaesthesiologists for haemodynamic stability owing to vagolytic27 and indirect sympathomimetic28 properties of this drug, and its longer duration of action. However, a study by Mangar et al. could not confirm these effects on the autonomic nervous system.29 The increase in blood pressure and heart rate could be attributed to inadequate depth of anaesthesia or level of analgesia in their study. As these patients may also have a degree of renal compromise, the use of pancuronium may result in a prolonged neuromuscular blockade, as the excretion of the drug is dependent on kidneys. At our institution, we aim to deliver patients to the intensive care unit (ICU) with closed chest to facilitate fast tracking. Therefore, we use rocuronium to facilitate endotracheal intubation at induction wherever appropriate and maintain anaesthesia with remifentanil infusion (0.2 mg kg1 min1) combined with either propofol infusion or volatile anaesthetic agent. With the use of continuous remifentanil infusion in this manner, we find that the supplemental doses of muscle relaxant after intubation are usually unwarranted. Since the early descriptions of the pre- and post conditioning effects of volatile anaesthetics (VAs),30–32 the use of anaesthetic preconditioning (APC) using VA has evoked enormous scientific and clinical interest. APC mimics ischaemic preconditioning. Sevoflurane and desflurane are proven to reduce mortality and morbidity in cardiac surgery.33 APC depends on the concentration and the timing of exposure to VA.34 Therefore, the maintenance of anaesthesia for VAD implantation in the pre-CPB period is preferably performed with VA in the operating room. Since APC is described for all commonly used VAs (isoflurane, sevoflurane and desflurane), and the differences in haemodynamic effects are minimal, the choice of VA can be institutionally driven. User familiarity may play a role in selection of VA. Maintenance of anaesthesia during CPB in most centres is achieved by continuous administration of propofol; propofol has been shown to result in significant reduction in cerebral metabolic rate, which can contribute to a decreased incidence of cerebrovascular events.35 Maintenance of anaesthesia with VA during CPB is also a valid option, but has not been described so far for VAD implantation. Mechanical ventilation Hypoxic and hypercarbic pulmonary vasoconstriction are known to contribute directly to pulmonary hypertension.36,37 Patients undergoing LVAD implantation are at particular risk for developing right-sided heart failure (RHF). Therefore, mechanical ventilation (MV) must aim to maintain normoxemia and normocarbia. Patients undergoing a VAD implantation procedure may end up requiring medium- or even long-term mechanical ventilation; thus, we advocate adopting a ventilation strategy consistent with that recommended by the acute respiratory distress syndrome (ARDS) network from the outset, to minimise the potential for ventilator-induced lung injury.38 The more invasive open-lung concept was shown in an experimental study to be superior.39 The mean positive end-expiratory pressure (PEEP) levels are higher in this concept than in the ARDS network study.40 PEEP however was not shown to influence right-ventricular function.41 In conclusion, we suggest that tidal volume should be set to a maximum of 6–8 ml per kg ideal body weight. PEEP is best adjusted to maintain lung compliance and RV function (which can be monitored carefully with trans-oesophageal echocardiogram (TEE)) without compromising surgical exposure and operating conditions. Aortic cross-clamping is not required for most LVAD insertions. The ventilation should be maintained during the procedure to avoid atelectasis. Neuromonitoring Continuous measurement of cerebral oxygenation with near infrared spectroscopy is strongly recommended during the perioperative period. There is good evidence to support the use of cerebral oximetry in cardiac surgical patients.42–44 The use of second- or third-generation VADs generating continuous flow may lead to a decrease in pulsatile flow leading to unreliable measurements of peripheral pulse oximetry.45 Therefore, the cerebral oximetry may function as the single continuous noninvasive measure of oxygenation.46
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Dosing of anaesthesia is especially critical in this group, as owing to their predisposition for cardiovascular collapse with even slight anaesthetic overdose, they are traditionally at higher risk of developing intra-operative awareness. To help prevent this, measurement of depth of anaesthesia is recommended.10 The depth of anaesthesia is monitored by electroencephalogram analysis.47,48 Fluid management The aim of the perioperative fluid management is to preserve the intravascular volume so as to facilitate efficient and unimpeded LVAD function without jeopardising right-ventricular (RV) function by causing fluid overload. Patients undergoing a VAD implantation are frequently treated with diuretics culminating in a pre-existing volume deficiency. Although there has been a longstanding debate on this topic, until now randomised multicentre trials have not been able to establish superiority of either these agents.49 One reason for the remaining ambiguity could be the diversity of these two infusion groups. The choice of colloids included dextran, albumin, modified gelatin and hydroxyethyl starch (HES), whereas crystalloids used include saline solution, glucose or balanced electrolyte solution. Intravascular volume optimisation for VAD implantation is a crucial point. Before induction of general anaesthesia, the volume deficiency should be estimated and carefully be substituted. After weaning from CPB, volume management should result in a sufficient VAD performance avoiding a collapse of the left ventricle. The role of TEE in this aspect cannot be over-emphasised. Hypovolaemia must be treated before the introduction of vasopressors.50 Transfusion of RBCs Current consensus is that transfusion of RBCs is an independent risk factor for increased mortality in cardiac surgery.51,52 Multiple factors are involved including increased incidence of renal failure, transfusion-related infections53,54 and vasoplegia.55 There is no haemoglobin level at which there is universal consensus that transfusion of RBC is indicated56,57; the physiological goal is to ensure that circulating blood volume can supply tissue with enough oxygen. Therefore, physiologic transfusion triggers such as mixed venous oxygen saturation or increased lactate combined with low haemoglobin levels should be used.58,59 Characteristically, patients undergoing VAD implantation are usually in a compromised medical condition and tissue hypoxia could become disastrous. Inotropes and vasopressors Patients suffering from CHF are typically managed preoperatively with inotropes (epinephrine or dobutamine) and phosphodiestaerase-III (PDE-III) inhibitors (milrinone or enoximone). Before induction of general anaesthesia, the inotropic drugs in the same dosage should at least be maintained. Vasopressors such as norepinephrine or vasopressin should be available to ensure a sufficient perfusion pressure. Even a slight decrease of the blood pressure could result in acute heart failure and cardiac arrest. Vasoplegia has been described to occur in up to 40% of patients undergoing VAD insertions.60–62 Lack of vasopressin and overwhelming production of nitric oxide by nitric oxide synthases are mainly responsible for the occurrence of vasoplegia.63,64 The continuous infusion of low-dose vasopressin (defined as <0.04 U min1) started before CPB significantly reduced the need for postoperative vasopressors.9,62,65 In severe cases of vasoplegia, it is frequently required to use multiple drugs such as norepinephrine, vasopressin or phenylephrine to maintain adequate systemic vascular resistance.8,63 Methylene blue administration can be considered in catecholamine-resistant vasoplegic shock.60,62,66,67 Inotropes and PDE inhibitors support the right ventricle during weaning from CPB. A small study in patients listed for heart transplantation showed that dobutamine and milrinone are equally effective in the prevention of RHF.68 PDE-III inhibitors were shown to be effective as adjunct or monotherapy in treatment of pulmonary hypertension.69 Milrinone was preferred as the primary inotropic drug due to lack of blood-pressure increase during implantation of continuous flow-generating assist devices
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in one study.70 In common, inotropes are not useful if biventricular assist devices are implanted. Vasoactive agents are required to maintain an adequate perfusion pressure for unsupported right ventricle. For weaning from CPB, the doses of the inotropes and vasoactive agents must be continuously reviewed and titrated. RHF The most crucial parameter for successful weaning from CPB post-LVAD implantation is the performance of the right ventricle. The recurring problem of RHF diminishes the clinical results after LVAD implantation.71 RV dysfunction occurs in 25–50% after LVAD implantation.72–74 The incidence of RHF is largely unpredictable. Risk factors are female gender and non-ischaemic aetiology as well as the haemodynamic parameters such as low pulmonary artery pressure (PAP) and low RV stroke volume index.75 Echocardiographic predictors are an increased RV to LV diastolic diameter,76 tricuspid incompetency and RV geometry, that is, a decrease in long axis to short axis ratio.72 A number of pharmacological approaches have been advocated in attempting to prevent or alleviate to RHF as follows. Inhaled nitric oxide Many institutions use inhaled nitric oxide (iNO) as standard protocol for weaning from CPB after LVAD implantation.77–79 These studies demonstrated a decrease in pulmonary vascular resistance assuming a decrease in right heart failure after implanting an LVAD. A recent randomised multicentre trial showed no difference according to the ‘end’ points mortality, mechanical ventilation, hospital and intensive care stay and the need for right-ventricular assist device (RVAD) implantation.80 Thus, the application of iNO has no clear evidence and must be individually decided. Inhaled iloprost (iIP) The use of the synthetic prostacyclin analogue inhaled iloprost (iIP) in critically ill patients with primary or secondary pulmonary hypertension is well established. The application of iIP is feasible and effective in preventing right heart failure so that an RVAD can be avoided during LVAD implantations. iIP has been shown to be more effective than iNO in reducing pulmonary vascular resistance in patients with primary pulmonary hypertension.81 In comparison with iNO, iIP was superior in facilitating weaning from CPB in patients with pulmonary hypertension in one single-centre study.82 A recent study showed iIP to be an effective agent in reducing the incidence of acute RHF.83 So far, the literature shows only case reports for iIP as a support drug for patients undergoing LVAD implantation.84,85 Since iNO lacks evidence for the prevention of severe RHF in LVAD implantations, iIP may be a better option for the treatment of pulmonary hypertension for these patients. Levosimendan The calcium-sensitising agent levosimendan and its long-lasting active metabolite OR-1896 bind to troponin C. Increased inotropy is not mediated by further increase in intracellular Ca2þ. A second mechanism is the opening of adenosine triphosphate (ATP)-sensitive Kþ channels in vascular smooth muscles.86,87 However, the increased myocardial contractility is not associated with an increase in myocardial oxygen consumption.88,89 The increase in cardiac output after a 24-h infusion is maintained at least for 7 days.90 In cardiac surgery patients with pre-existing low ejection fraction, stroke volume was better preserved with the combination of levosimendan plus dobutamine compared with milrinone and dobutamine.91 A meta-analysis showed levosimendan to reduce troponin release after cardiac surgery.92 Another recent meta-analysis showed that levosimendan provided a mortality benefit after coronary artery surgery.93 Currently, levosimendan non-responders were identified as high-risk candidates for RHF. In this small study, pre-surgery levosimendan treatment non-response was identified by elevated N-terminal pro-hormone brain natriuretic peptide (NT-pro-BNP) levels and predicted post-surgery RHF. Levosimendan however did not prevent RHF.94 Prospective multicentre studies for the use of levosimendan in LVAD implantation are not available.
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Perioperative antibiotic prophylaxis As for many other procedures, the perioperative antibiotic prophylaxis lacks evidence. A recent survey with VAD-implanting institutions revealed differences in perioperative antibiotic prophylaxis ranging from a four-drug regimen including fluconazole down to a one-drug regimen with only vancomycin.95 Crucial for the optimisation of antibiotic prophylaxis are the infection history of the patient and prevalent organism in the hospital, that is, the prevalence of antibiotic-resistant organisms. Optimal perioperative antibiotic prophylaxis is an example of personalised medicine and must be tailored to each individual patient. VAD patients for non-cardiac surgery The increase in the number of VAD implantations will inevitably lead to an increase in noncardiac surgery (NCS) in VAD patients. Several case reports and case series have been published on NCS for VAD patients. Stehlik et al. reported that 24% of their VAD patients (n ¼ 155) required NCS (n ¼ 59) during their study period (1993–2007). Bleeding was the most common complication (10%) and the survival to transplantation was similar to those patients who did not require NCS.96 Brown et al. reported NCS (n ¼ 27) in 142 VAD subjects between years 2000 and 2007. There was no difference in survival between þNCS (44%) and NCS (46%) patients at study conclusion. Bleeding and infection were the most common complications. In their report, þNCS patients were less likely to undergo heart transplantation (12%) compared to NCS patients (35%).97 Chestovich et al. reported NCS (n ¼ 64) in patients receiving mechanical circulatory support (n ¼ 363). Patients on extracorporeal life support and patients who underwent emergent surgery had higher mortality. Fewer VAD patients who required NCS received heart transplantation and NCS also delayed their transplantation.98 Considering the significant impact of NCS in VAD patients, a cardiac anaesthesiologist with TEE skills can be a very useful resource while administering anaesthesia for these patients.99 A VAD engineer should accompany the patient to the operating room and a cardiac surgeon should be available for consultation, if required. Preoperatively, unsupported ventricular function and endorgan function should be evaluated. Since bleeding is described as an important perioperative complication in many studies, the perioperative coagulation management should be discussed with the non-cardiac surgical team and the VAD team. Heartmate II, the most commonly used long-term VAD has less stringent anticoagulation requirements. Anticoagulation can be omitted, decreased or reversed for the perioperative period if the bleeding risk from NCS is significant.100 The cardioverter– defibrillator should be deactivated based on the nature and site of surgery and external defibrillator pads should be applied. Attention should be paid to proper perioperative antibiotic coverage as infection is another common complication in VAD patients. Type of anaesthesia and the anaesthetic drugs administered are less important as long as the haemodynamic management is directed by appropriate monitoring. Choice of monitoring depends on the type of device, the surgical procedure and the function of the unassisted ventricle. In patients with continuous flow VADs, pulse oximetry and osillometric non-invasive blood pressure measurements are not reliable. While auscultation and palpation methods are not reliable, Doppler signals can be used to measure mean blood pressure for simple, less invasive and brief surgical procedures (such as endoscopy under sedation). However, invasive arterial pressure monitoring is advisable for complex procedures of longer duration where haemodynamic fluctuations and blood loss are expected (laparoscopy, thoracoscopy and open abdominal procedures). Ultrasound can be used to guide arterial cannulation. Cerebral oximetry is useful even in patients with non-pulsatile circulation for NCS. Intra-operative haemodynamic management (fluids, inotropes and vasopressors) should be guided by central venous pressure and TEE monitoring. For procedures, which require intensive postoperative care (aortic surgery, major abdominal and thoracic surgery), PA catheters should be used. Aggressive management of hypercarbia, hypoxaemia and acidosis is recommended to prevent increase in pulmonary vascular resistance. The aim is to preserve the function of the unassisted ventricle and avoid the need for rightsided mechanical assistance. This can be very challenging in procedures, which require lung isolation and pneumoperitoneum.
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The Summary Anaesthesia and peri-operative management of patients undergoing implantation of ventricular assist devices are challenging aspects of cardiac anaesthesia. The anaesthesiologist is confronted with a highly compromised and vulnerable patient who frequently presents with difficulties even in otherwise straightforward procedures such as securing central venous access. Sequelae of heart failure such as renal and hepatic insufficiency typically complicate management and may worsen outcome and prognosis. There is special need for teamwork with all involved professional groups. The prediction of right heart failure post LVAD implantation and the optimal treatment options have not yet been fully elucidated. The introduction of minimal invasive VAD systems with transapical approach could be supposed to enable a more widespread use in patients with a higher risk profile. The evolution of VAD into smaller systems with even better flow profiles and less propensity for thromboembolic complications can be anticipated in future, and will hopefully further improve life expectancy and quality of life for this most challenging patient group.
Practice points -
The preoperative identification of co-morbidities is crucial. Before induction, the operating room should be equipped. Diuretic-induced hypovolaemia should be treated with caution. Inotropes and vasopressors must be available. During induction, special attention should be paid to haemodynamic changes. Pre-existing central venous thrombosis is common. Therefore, ultrasound-guided placement of central-venous catheters is helpful. The use of a pulmonary artery catheter is recommended. The use of narcotic drugs is institution dependent. Volatile anaesthetics should be used when possible. Measurement of cerebral oxygenation with near-infrared spectroscopy is recommended. These patients are at risk for developing right-sided heart failure. Mechanical ventilation must achieve normoxaemia and normocarbia. Perioperative antibiotic prophylaxis must be tailored to each individual patient.
Research agenda - The prediction of right-sided heart failure needs to be further investigated. - The therapy of right-sided heart failure lacks evidence. - Newer minimally invasive approaches may bring fresh challenges to anaesthetic management.
Conflict of interest None.
Acknowledgement Special thanks to Maurice Hogan, MD, for his linguistic help.
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Mangar D, Turnage WS, Connell GR et al. Pancuronium, vecuronium, and heart rate during anesthesia for aortocoronary bypass operations. Eur J Cardio Thorac Surg 1993; 7: 524–527. 30. Kersten JR, Schmeling TJ, Pagel PS et al. Isoflurane mimics ischemic preconditioning via activation of K(ATP) channels: reduction of myocardial infarct size with an acute memory phase. Anesthesiology 1997; 87: 361–370. 31. Kersten JR, Lowe D, Hettrick DA et al. Glyburide, a KATP channel antagonist, attenuates the cardioprotective effects of isoflurane in stunned myocardium. Anesth Analg 1996; 83: 27–33. 32. Cason BA, Gamperl AK, Slocum RE et al. Anesthetic-induced preconditioning: previous administration of isoflurane decreases myocardial infarct size in rabbits. Anesthesiology 1997; 87: 1182–1190. 33. 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. 34. Bignami E, Biondi-Zoccai G, Landoni G et al. Volatile anesthetics reduce mortality in cardiac surgery. J Cardiothorac Vasc Anesth 2009; 23: 594–599. 35. Newman MF, Murkin JM, Roach G et al. Cerebral physiologic effects of burst suppression doses of propofol during nonpulsatile cardiopulmonary bypass. CNS subgroup of McSPI. Anesth Analg 1995; 81: 452–457.
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36. Aviado DM, Ling JS & Schmidt CF. Effects of anoxia on pulmonary circulation: reflex pulmonary vasoconstriction. Am J Physiol 1957; 189: 253–262. 37. Barer GR & Shaw JW. Pulmonary vasodilator and vasoconstrictor actions of carbon dioxide. J Physiol 1971; 213: 633–645. 38. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301–1308. 39. Spieth PM, Güldner A, Carvalho AR et al. Open lung approach vs acute respiratory distress syndrome network ventilation in experimental acute lung injury. Br J Anaesth 2011; 107: 388–397. 40. Miranda DR, Gommers D, Papadakos PJ 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. 41. Berglund JE, Halden E, Jakobson S et al. Echocardiographic analysis of cardiac function during high PEEP ventilation. Intensive Care Med 1994; 20: 174–180. 42. de Tournay-Jetté E, Dupuis G, Bherer L et al. The relationship between cerebral oxygen saturation changes and postoperative cognitive dysfunction in elderly patients after coronary artery bypass graft surgery. J Cardiothorac Vasc Anesth 2011; 25: 95–104. 43. Slater JP, Guarino T, Stack J et al. Cerebral oxygen desaturation predicts cognitive decline and longer hospital stay after cardiac surgery. Ann Thorac Surg 2009; 87: 36–45. 44. Heringlake M, Garbers C, Käbler JH et al. Preoperative cerebral oxygen saturation and clinical outcomes in cardiac surgery. Anesthesiology 2011: 114. *45. Ficke DJ, Lee J, Chaney MA et al. Noncardiac surgery in patients with a left ventricular assist device. J Cardiothorac Vasc Anesth 2010; 24: 1002–1009. 46. Oleyar M, Stone M & Neustein SM. Perioperative management of a patient with a nonpulsatile left ventricular assist device presenting for noncardiac surgery. J Cardiothorac Vasc Anesth 2010; 24: 820–823. 47. Laussen PC, Murphy JA, Zurakowski D et al. Bispectral index monitoring in children undergoing mild hypothermic cardiopulmonary bypass. Paediatr Anaesth 2001; 11: 567–573. 48. Glass PS, Bloom M, Kearse L et al. Bispectral analysis measures sedation and memory effects of propofol, midazolam, isoflurane, and alfentanil in healthy volunteers. Anesthesiology 1997; 86: 836–847. 49. Roberts I, Alderson P, Bunn F et al. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2004. CD000567. 50. Mebazaa A, Pitsis AA, Rudiger A et al. Clinical review: practical recommendations on the management of perioperative heart failure in cardiac surgery. Crit Care 2010; 14: 201. 51. Koch CG, Li L, Duncan AI et al. Morbidity and mortality risk associated with red blood cell and blood-component transfusion in isolated coronary artery bypass grafting. Crit Care Med 2006; 34: 1608–1616. 52. Jakobsen CJ, Ryhammer PK, Tang M et al. Transfusion of blood during cardiac surgery is associated with higher longterm mortality in low-risk patients. Eur J Cardiothorac Surg 2012. 53. Leal-Noval S, Rincon-Ferrari M, Garcia-Curiel A et al. Transfusion of blood components and postoperative infection in patients undergoing cardiac surgery. Chest 2001; 119: 1461–1468. 54. Engoren MC, Habib RH, Zacharias A et al. Effect of blood transfusion on long-term survival after cardiac operation. Ann Thorac Surg 2002; 74: 1180–1186. 55. Alfirevic A, Xu M, Johnston D et al. Transfusion increases the risk for vasoplegia after cardiac operations. Ann Thorac Surg 2011; 92: 812–819. 56. Hajjar LA, Vincent JL, Galas FRBG et al. Transfusion requirements after cardiac surgery. JAMA 2010; 304: 1559–1567. 57. Reeves BC & Murphy GJ. Increased mortality, morbidity, and cost associated with red blood cell transfusion after cardiac surgery. Curr Opin Cardiol 2008; 23: 607–612. 58. Vallet B, Robin E & Lebuffe G. Venous oxygen saturation as a physiologic transfusion trigger. Crit Care 2010; 14: 213. 59. Orlov D, O’Farrell R, McCluskey SA et al. The clinical utility of an index of global oxygenation for guiding red blood cell transfusion in cardiac surgery. Transfusion 2009; 49: 682–688. 60. Lavigne D. Vasopressin and methylene blue: alternate therapies in vasodilatory shock. Semin Cardiothorac Vasc Anesth 2010; 14: 186–189. 61. Levin MA, Lin HM, Castillo JG et al. Early on-cardiopulmonary bypass hypotension and other factors associated with vasoplegic syndrome. Circulation 2009; 120: 1664–1671. 62. Riha H & Augoustides JGT. Pro: methylene blue as a rescue therapy for vasoplegia after cardiac surgery. J Cardiothorac Vasc Anesth 2011; 25: 736–738. 63. Fischer Gregory W & Levin Mathew A. Vasoplegia during cardiac surgery: current concepts and management. Semin Thorac Cardiovasc Surg 21-6-2010; 22(2): 140–144. Ref Type: abstract. 64. Levy JH & Tanaka KA. Inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 2003; 75: S715–S720. 65. Papadopoulos G, Sintou E, Siminelakis S et al. Perioperative infusion of low-dose of vasopressin for prevention and management of vasodilatory vasoplegic syndrome in patients undergoing coronary artery bypass grafting-A doubleblind randomized study. J Cardiothorac Surg 2010; 5: 17. 66. Evora PR & Levin RL. Methylene blue as drug of choice for catecholamine-refractory vasoplegia after cardiopulmonary bypass. J Thorac Cardiovasc Surg 2004; 127: 895–896. 67. Leyh RG, Kofidis T, Strüber M et al. Methylene blue: the drug of choice for catecholamine-refractory vasoplegia after cardiopulmonary bypass. J Thorac Cardiovasc Surg 2003; 125: 1426–1431. 68. Aranda Jr. JM, Schofield RS, Pauly DF et al. Comparison of dobutamine versus milrinone therapy in hospitalized patients awaiting cardiac transplantation: a prospective, randomized trial. Am Heart J 2003; 145: 324–329. 69. Haj RM, Cinco JE & Mazer CD. Treatment of pulmonary hypertension with selective pulmonary vasodilators. Curr Opin Anaesthesiol 2006; 19: 88–95. 70. Nussmeier NA, Probert CB, Hirsch D et al. Anesthetic management for implantation of the Jarvik 2000 left ventricular assist system. Anesth Analg 2003; 97: 964–971. 71. Van Meter Jr. CH. Right heart failure: best treated by avoidance. Ann Thorac Surg 2001; 71: S220–S222.
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72. Potapov EV, Stepanenko A, Dandel M et al. Tricuspid incompetence and geometry of the right ventricle as predictors of right ventricular function after implantation of a left ventricular assist device. J Heart Lung Transplant 2008; 27: 1275– 1281. *73. Drakos SG, Janicki L, Horne BD et al. Risk factors predictive of right ventricular failure after left ventricular assist device implantation. Am J Cardiol 2010; 105: 1030–1035. 74. Kavarana MN, Pessin-Minsley MS, Urtecho J et al. Right ventricular dysfunction and organ failure in left ventricular assist device recipients: a continuing problem. Ann Thorac Surg 2002; 73: 745–750. 75. Ochiai Y, McCarthy PM, Smedira NG et al. Predictors of severe right ventricular failure after implantable left ventricular assist device insertion: analysis of 245 patients. Circulation 2002; 106. I-198. 76. Kukucka M, Stepanenko A, Potapov E et al. Right-to-left ventricular end-diastolic diameter ratio and prediction of right ventricular failure with continuous-flow left ventricular assist devices. J Heart Lung Transplant 2011; 30: 64–69. 77. Dang NC, Topkara VK, Mercando M et al. Right heart failure after left ventricular assist device implantation in patients with chronic congestive heart failure. J Heart Lung Transplant 2006; 25: 1–6. 78. Argenziano MDM, Choudhri BSAF, Moazami MDN et al. Randomized, double-blind trial of inhaled nitric oxide in LVAD recipients with pulmonary hypertension. Ann Thorac Surg 1998; 65: 340–345. *79. Furukawa K, Motomura T & Nosé Y. Right ventricular failure after left ventricular assist device implantation: the need for an implantable right ventricular assist device. Artif Organs 2005; 29: 369–377. 80. Potapov E, Meyer D, Swaminathan M et al. Inhaled nitric oxide after left ventricular assist device implantation: a prospective, randomized, double-blind, multicenter, placebo-controlled trial. J Heart Lung Transplant 2011; 30: 870– 878. 81. Hoeper MM, Olschewski H, Ghofrani HA et al. A comparison of the acute hemodynamic effects of inhaled nitric oxide and aerosolized iloprost in primary pulmonary hypertension. J Am Coll Cardiol 2000; 35: 176–182. 82. Winterhalter M, Simon A, Fischer S et al. Comparison of inhaled iloprost and nitric oxide in patients with pulmonary hypertension during weaning from cardiopulmonary bypass in cardiac surgery: a prospective randomized trial. J Cardiothorac Vasc Anesth 2008; 22: 406–413. 83. Martischnig AM, Tichy A, Nikfardjam M et al. Inhaled iloprost for patients with precapillary pulmonary hypertension and right-side heart failure. J Card Fail 2011; 17: 813–818. 84. Winterhalter M, Fischer S, Tessmann R et al. Using inhaled iloprost to wean from cardiopulmonary bypass after implanting a left ventricular assist device. Anesth Analg 2006; 103: 515–516. 85. Meyer AL, Malehsa D, Kuehn C et al. HeartMate II implantation in patients with heparin-induced thrombocytopenia type II. Ann Thorac Surg 2009; 88: 674–675. *86. Papp Z, Csapo K, Pollesello P et al. Pharmacological mechanisms contributing to the clinical efficacy of levosimendan. Cardiovasc Drug Rev 2005; 23: 71–98. 87. Parle NM, Thomas MD, Dembo L et al. Repeated infusions of levosimendan: well tolerated and improves functional capacity in decompensated heart failure – a single-centre experience. Heart Lung Circ 2008; 17: 206–210. 88. Ukkonen H, Saraste M, Akkila J et al. Myocardial efficiency during calcium sensitization with levosimendan: a noninvasive study with positron emission tomography and echocardiography in healthy volunteers. Clin Pharmacol Ther 1997; 61: 596–607. 89. Lilleberg J, Nieminen MS, Akkila J et al. Effects of a new calcium sensitizer, levosimendan, on haemodynamics, coronary blood flow and myocardial substrate utilization early after coronary artery bypass grafting. Eur Heart J 1998; 19: 660–668. 90. Lilleberg J, Laine M, Palkama T et al. Duration of the haemodynamic action of a 24-h infusion of levosimendan in patients with congestive heart failure. Eur J Heart Fail 2007; 9: 75–82. 91. De Hert SG, Lorsomradee S, Cromheecke S et al. The effects of levosimendan in cardiac surgery patients with poor left ventricular function. Anesth Analg 2007; 104: 766–773. 92. Zangrillo A, Biondi-Zoccai G, Mizzi A et al. Levosimendan reduces cardiac troponin release after cardiac surgery: a meta-analysis of randomized controlled studies. J Cardiothorac Vasc Anesth 2009; 23: 474–478. 93. Maharaj R & Metaxa V. Levosimendan and mortality after coronary revascularisation: a meta-analysis of randomised controlled trials. Crit Care 2011; 15. R140. 94. Sponga S, Bertrand OF, Philippon F et al. Reversible circumflex coronary artery occlusion during percutaneous transvenous mitral annuloplasty with the viacor system. J Am Coll Cardiol 2012; 59: 288. 95. Walker PC, DePestel DD, Miles NA et al. Surgical infection prophylaxis for left ventricular assist device implantation. J Card Surg 2011; 26: 440–443. 96. Stehlik J, Nelson DM, Kfoury AG et al. Outcome of noncardiac surgery in patients with ventricular assist devices. Am J Cardiol 2009; 103: 709–712. 97. Brown JB, Hallinan WM, Massey HT et al. Does the need for noncardiac surgery during ventricular assist device therapy impact clinical outcome? Surgery 2009; 146: 627–633. 98. Chestovich PJ, Kwon MH, Cryer HG et al. Surgical procedures for patients receiving mechanical cardiac support. Am Surg 2011; 77: 1314–1317. *99. Stone ME, Soong W, Krol M et al. The anesthetic considerations in patients with ventricular assist devices presenting for noncardiac surgery: a review of eight cases. Anesth Analg 2002; 95: 42–49. *100. Riha H, Netuka I, Kotulak T et al. Anesthesia management of a patient with a ventricular assist device for noncardiac surgery. Semin Cardiothorac Vasc Anesth 2010; 14: 29–31.
Contents lists available at SciVerse ScienceDirect
Best Practice & Research Clinical Anaesthesiology journal homepage: www.elsevier.com/locate/bean
6
Anaesthesia for patients undergoing ventricular assist-device implantation Markus Feussner, MD, Consultant Anesthesilogist a, *, Chirojit Mukherjee, MD, Program director and Consultant Anesthesiologist a, c, Jens Garbade, MD, PhD, Consultant Cardiac Surgeon b, d, Joerg Ender, MD, Chairman a, c a b
Department of Anesthesiology, University Leipzig, Heart Center, Struempellstrasse 39, D-04289 Leipzig, Germany Department of Cardiac Surgery, University Leipzig, Heart Center, Struempellstrasse 39, D-04289 Leipzig, Germany
Keywords: anaesthesia management VAD implantations non-cardiac surgery
In the last 10 years, implantation of ventricular-assist devices has become an interesting option as either bridge-to-transplantation or destination procedure for patients with end-stage congestive heart failure. In the future, the number of ventricular assist device implantations is expected to increase furthermore. In general, this patient cohort is associated with significant co-morbidities, for example, pulmonary hypertension, peripheral vascular disease and renal insufficiency. Anaesthetic management for implantation of ventricular assist devices can be challenging for cardiac anaesthesiologists. Even minor changes in their haemodynamics and physiological parameters can cause significant morbidity and mortality. Experience in haemodynamic monitoring including echocardiography and pharmacological management (use of inotropes, phosphodiesterase inhibitors and vasopressors) is a requirement. Particularly, the diagnosis and therapy of right-sided heart failure after implantation of left-ventricular assist devices should be addressed. Ó 2012 Elsevier Ltd. All rights reserved.
* Corresponding author: Tel.: þ49 3418651060; Fax: þ49 3418651820. E-mail addresses: [email protected] (M. Feussner), [email protected] (C. Mukherjee), [email protected] (J. Garbade), [email protected] (J. Ender). c Tel.: þ49 3418651060; Fax: þ49 3418651820. d Tel.: þ49 3418651060; Fax: þ49 3418651452. 1521-6896/$ – see front matter Ó 2012 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.bpa.2012.06.001
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In Europe and the United States, more than 16 million people live with a diagnosis of congestive heart failure (CHF).1 Furthermore, the incidence of CHF is dramatically increased in people aged over 65 years, and this population is expected to increase twofold within the next 20 years. Heart transplantation is still the gold standard for patients suffering from end-stage CHF refractory to pharmacologic and cardiac resynchronisation therapy.2 The discrepancy between the shortage of appropriate donor organs and the increasing number of people with end-stage CHF has focussed interest on alternative therapies, particularly on mechanical circulatory support. Over the past 50 years, mechanical circulatory support has become established as either bridging or destination therapy in this patient cohort.3 In 1966, DeBakey and Liotta implanted the first left-ventricular assist device (LVAD) in a patient with low cardiac output syndrome, and 10 days later managed to successfully to explant it. From this milestone, the development of technically advanced VAD was initiated and resulted in the REMATCH (Randomised Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure) trial as preliminary climax. The REMATCH trial first observed the survival in long-term mechanical circulatory support.4 This study looked at first-generation VAD, which generated pulsatile flow in patients ineligible for transplantation in a destination-therapy scenario and showed a reduction in long-term mortality in patients with VAD compared with those treated with optimised drug therapy. The evolution of VADs from pulsatile flow-generating systems to continuous flow-generating second- and third-generation VADs provides a further increase in long-term survival compared to first-generation VAD systems5 by reduction of mechanical and thrombotic complications. The demonstration of improved prognosis led to implantation of VADs not only in specialised centres with established transplantation programmes, as a bridge to transplantation, but also as a destination-therapy scenario. Thus, as the indications for VAD therapy broaden, cardiac anaesthesiologists will be more likely to encounter patients requiring anaesthesia and perioperative care for VAD implantations in the future as indeed will non-cardiac anaesthesiologists providing anaesthesia for non-cardiac surgery in patients with VADs.
Patient characteristics, secondary illnesses and medication Patients requiring a VAD usually undergo long-term hospitalisation before surgery and hence a comprehensive preoperative work-up has usually been completed, including diagnostic heart catheter procedures. Extra care should be taken to evaluate pulmonary hypertension if present, and co-morbidities associated with renal, central-nervous and hepatobiliary system, as these are common in this setting. Exceptions include patients requiring emergency support usually admitted following acute myocardial infarction, which may manifest as cardiogenic shock.6 In this group, optimisation of secondary diseases is simply not feasible prior to surgery. Patients suffering from severe CHF are typically treated with b-blockers, intensive diuretic therapy and peripheral resistance reducing angiotensin II-converting enzyme inhibitors (ACE inhibitors) and angiotensin-receptor blockers. There is a general consensus to continue the treatment with b-blockers in the perioperative setting to avoid rebound tachycardia and hypertension. Diuretic treatment should be discontinued on the day of surgery, due to hypovolaemia-induced hypotension after induction of general anaesthesia. Angiotensin-blocking medications are the mainstay of treatment for CHF, and sudden withdrawal could result in an acute exacerbation of heart failure.7 Conversely, a retrospective study in patients undergoing coronary artery bypass graft (CABG) surgery found ACE inhibitors to be an independent risk factor for perioperative mortality and postoperative renal dysfunction.8 A recent study showed a loss of systemic vascular resistance with consequent increased requirements of inotropic support. A low-dose administration of vasopressin prevented post-cardiopulmonary bypass (CPB) hypotension.9 The controversy as to whether angiotensin blockers should be withheld pre-operatively should be decided in consultation with the various team members involved in perioperative management of the patient. Preoperative anxiolytic medication results in a decrease of endogenous sympathetic tone and should therefore be administered judiciously. Furthermore, oversedation could lead to hypoventilation, which in turn results in hypoxia, acidosis and an increase in pulmonary vascular resistance. There is a minimal physiological reserve in this high-risk group and any minor alteration can precipitate major deterioration.
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General anaesthetic setting Standard monitoring (5-lead electrocardiography (ECG), pulse oximetry, capnography and core and peripheral temperature probes) and an invasive arterial blood-pressure monitoring are mandatory. A large-bore peripheral venous access (14 or 16 gauge) as well as a 9-French central venous catheter are also indicated due to the high risk of massive intra- and postoperative haemorrhage.10 A multi-lumen central venous (four or five lumen) catheter is preferred. An ultrasound-guided placement of the central venous catheters is naturally helpful because of the higher incidence (10%) of central venous thrombosis in these long-term hospitalised patients.11–13 In routine cardiac surgery, the internal jugular vein (IJV) is the preferred site for central venous access. In a VAD implantation planned as a ‘bridge-totransplantation’ scenario, puncture of the left IJV is recommended so that the right IJV can be preserved to facilitate endomyocardial biopsy post-transplantation to evaluate for cardiac rejection.14 Typically, a central venous access is present preoperatively having facilitated the administration of inotropes and phosphodiesterase inhibitors. In the operating room, an ultrasound-guided cannulation using local anaesthesia may be preferred before induction of general anaesthesia in unstable patients. Although the use of pulmonary artery catheters (PACs) has not demonstrated a direct improvement in mortality outcomes,15,16 a recent survey of cardiac anaesthesiologists shows that they preferably use a pulmonary catheter during VAD implantation.17 The PAC is the single best measuring device at an anaesthesiologist’s disposal to monitor pulmonary vascular resistance and facilitate goal-directed therapy of pulmonary hypertension, and thereby support adequate right-ventricular function. In addition, mixed central venous oxygen saturation can provide important information about the perfusion status of the patient and also the need for red blood cells.18 The placement of PAC is therefore recommended in this special setting.19 Patients undergoing VAD implantation are typically treated with an automated implantable cardioverter–defibrillator (AICD). To avoid accidental shock delivery during surgery, the AICD is regularly turned off. Arrhythmias, especially ventricular tachycardias, are frequently resistant to drug therapy. Therefore, external shock electrodes should be placed before induction. Before induction, the operating room should be equipped for emergency commencement of CPB and hence, the presence of a surgeon during the induction process is indicated. Placement of guide wires for the CPB cannulas under local anaesthesia is an option in higher-risk patients, but current literature does not support evidence for this procedure. Anaesthetic drugs Etomidate is commonly used for induction of anaesthesia10,20 as it is capable of inducing a state of unawareness without significant myocardial depression or vasodilatation. The risk of relative adrenal insufficiency as a consequence of single induction dose of etomidate is well described, but did not result in a higher demand for vasopressors.21 Propofol as an induction agent has been shown to have a negative inotropic effect and consequently causes decrease in blood pressure.22,23 Conversely, Bendel et al. found that although propofol causes more hypotension than etomidate, there is no difference in cardiac output using either of these drugs.24 Hence, the decrease in blood pressure is caused mainly by a reduction in systemic vascular resistance, which can be counteracted with small doses of a vasoconstrictor, for example, norepinephrine. Propofol does not lead to the induction of myoclonic movements and the inhibition of 11-b-hydroxylase as seen with etomidate. Furthermore, experimental studies suggested that propofol can induce a relaxation of the pulmonary vessels25 with consecutive reduction of pulmonary vascular resistance, which would be beneficial in patients suffering from CHF. The use of propofol as an induction agent in cardiac anaesthesia is well established and the patient haemodynamic remains more stable with controlled induction.26 Therefore, propofol as an induction agent is justified if used in a total dose of 2 mg kg1 of body weight with starting dose of 1 mg kg1 of body weight. Concerning administration of opioids, fentanyl seems to be the standard choice.10,20 The dosage used ranges between 50 and 100 mg kg1 of body weight in these studies. A choice of continuous infusion of fentanyl, sufentanil or remifentanil during the procedure can be institution dependent; however, remifentanil has a major advantage in that it is metabolised
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independent of renal or hepatic function. It acts as a highly potent opioid intra-operatively, and yet facilitates early recovery and extubation when appropriate. For neuromuscular blockade, pancuronium and rocuronium are typically suitable for patients undergoing VAD implantation. Pancuronium was traditionally used by cardiac anaesthesiologists for haemodynamic stability owing to vagolytic27 and indirect sympathomimetic28 properties of this drug, and its longer duration of action. However, a study by Mangar et al. could not confirm these effects on the autonomic nervous system.29 The increase in blood pressure and heart rate could be attributed to inadequate depth of anaesthesia or level of analgesia in their study. As these patients may also have a degree of renal compromise, the use of pancuronium may result in a prolonged neuromuscular blockade, as the excretion of the drug is dependent on kidneys. At our institution, we aim to deliver patients to the intensive care unit (ICU) with closed chest to facilitate fast tracking. Therefore, we use rocuronium to facilitate endotracheal intubation at induction wherever appropriate and maintain anaesthesia with remifentanil infusion (0.2 mg kg1 min1) combined with either propofol infusion or volatile anaesthetic agent. With the use of continuous remifentanil infusion in this manner, we find that the supplemental doses of muscle relaxant after intubation are usually unwarranted. Since the early descriptions of the pre- and post conditioning effects of volatile anaesthetics (VAs),30–32 the use of anaesthetic preconditioning (APC) using VA has evoked enormous scientific and clinical interest. APC mimics ischaemic preconditioning. Sevoflurane and desflurane are proven to reduce mortality and morbidity in cardiac surgery.33 APC depends on the concentration and the timing of exposure to VA.34 Therefore, the maintenance of anaesthesia for VAD implantation in the pre-CPB period is preferably performed with VA in the operating room. Since APC is described for all commonly used VAs (isoflurane, sevoflurane and desflurane), and the differences in haemodynamic effects are minimal, the choice of VA can be institutionally driven. User familiarity may play a role in selection of VA. Maintenance of anaesthesia during CPB in most centres is achieved by continuous administration of propofol; propofol has been shown to result in significant reduction in cerebral metabolic rate, which can contribute to a decreased incidence of cerebrovascular events.35 Maintenance of anaesthesia with VA during CPB is also a valid option, but has not been described so far for VAD implantation. Mechanical ventilation Hypoxic and hypercarbic pulmonary vasoconstriction are known to contribute directly to pulmonary hypertension.36,37 Patients undergoing LVAD implantation are at particular risk for developing right-sided heart failure (RHF). Therefore, mechanical ventilation (MV) must aim to maintain normoxemia and normocarbia. Patients undergoing a VAD implantation procedure may end up requiring medium- or even long-term mechanical ventilation; thus, we advocate adopting a ventilation strategy consistent with that recommended by the acute respiratory distress syndrome (ARDS) network from the outset, to minimise the potential for ventilator-induced lung injury.38 The more invasive open-lung concept was shown in an experimental study to be superior.39 The mean positive end-expiratory pressure (PEEP) levels are higher in this concept than in the ARDS network study.40 PEEP however was not shown to influence right-ventricular function.41 In conclusion, we suggest that tidal volume should be set to a maximum of 6–8 ml per kg ideal body weight. PEEP is best adjusted to maintain lung compliance and RV function (which can be monitored carefully with trans-oesophageal echocardiogram (TEE)) without compromising surgical exposure and operating conditions. Aortic cross-clamping is not required for most LVAD insertions. The ventilation should be maintained during the procedure to avoid atelectasis. Neuromonitoring Continuous measurement of cerebral oxygenation with near infrared spectroscopy is strongly recommended during the perioperative period. There is good evidence to support the use of cerebral oximetry in cardiac surgical patients.42–44 The use of second- or third-generation VADs generating continuous flow may lead to a decrease in pulsatile flow leading to unreliable measurements of peripheral pulse oximetry.45 Therefore, the cerebral oximetry may function as the single continuous noninvasive measure of oxygenation.46
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Dosing of anaesthesia is especially critical in this group, as owing to their predisposition for cardiovascular collapse with even slight anaesthetic overdose, they are traditionally at higher risk of developing intra-operative awareness. To help prevent this, measurement of depth of anaesthesia is recommended.10 The depth of anaesthesia is monitored by electroencephalogram analysis.47,48 Fluid management The aim of the perioperative fluid management is to preserve the intravascular volume so as to facilitate efficient and unimpeded LVAD function without jeopardising right-ventricular (RV) function by causing fluid overload. Patients undergoing a VAD implantation are frequently treated with diuretics culminating in a pre-existing volume deficiency. Although there has been a longstanding debate on this topic, until now randomised multicentre trials have not been able to establish superiority of either these agents.49 One reason for the remaining ambiguity could be the diversity of these two infusion groups. The choice of colloids included dextran, albumin, modified gelatin and hydroxyethyl starch (HES), whereas crystalloids used include saline solution, glucose or balanced electrolyte solution. Intravascular volume optimisation for VAD implantation is a crucial point. Before induction of general anaesthesia, the volume deficiency should be estimated and carefully be substituted. After weaning from CPB, volume management should result in a sufficient VAD performance avoiding a collapse of the left ventricle. The role of TEE in this aspect cannot be over-emphasised. Hypovolaemia must be treated before the introduction of vasopressors.50 Transfusion of RBCs Current consensus is that transfusion of RBCs is an independent risk factor for increased mortality in cardiac surgery.51,52 Multiple factors are involved including increased incidence of renal failure, transfusion-related infections53,54 and vasoplegia.55 There is no haemoglobin level at which there is universal consensus that transfusion of RBC is indicated56,57; the physiological goal is to ensure that circulating blood volume can supply tissue with enough oxygen. Therefore, physiologic transfusion triggers such as mixed venous oxygen saturation or increased lactate combined with low haemoglobin levels should be used.58,59 Characteristically, patients undergoing VAD implantation are usually in a compromised medical condition and tissue hypoxia could become disastrous. Inotropes and vasopressors Patients suffering from CHF are typically managed preoperatively with inotropes (epinephrine or dobutamine) and phosphodiestaerase-III (PDE-III) inhibitors (milrinone or enoximone). Before induction of general anaesthesia, the inotropic drugs in the same dosage should at least be maintained. Vasopressors such as norepinephrine or vasopressin should be available to ensure a sufficient perfusion pressure. Even a slight decrease of the blood pressure could result in acute heart failure and cardiac arrest. Vasoplegia has been described to occur in up to 40% of patients undergoing VAD insertions.60–62 Lack of vasopressin and overwhelming production of nitric oxide by nitric oxide synthases are mainly responsible for the occurrence of vasoplegia.63,64 The continuous infusion of low-dose vasopressin (defined as <0.04 U min1) started before CPB significantly reduced the need for postoperative vasopressors.9,62,65 In severe cases of vasoplegia, it is frequently required to use multiple drugs such as norepinephrine, vasopressin or phenylephrine to maintain adequate systemic vascular resistance.8,63 Methylene blue administration can be considered in catecholamine-resistant vasoplegic shock.60,62,66,67 Inotropes and PDE inhibitors support the right ventricle during weaning from CPB. A small study in patients listed for heart transplantation showed that dobutamine and milrinone are equally effective in the prevention of RHF.68 PDE-III inhibitors were shown to be effective as adjunct or monotherapy in treatment of pulmonary hypertension.69 Milrinone was preferred as the primary inotropic drug due to lack of blood-pressure increase during implantation of continuous flow-generating assist devices
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in one study.70 In common, inotropes are not useful if biventricular assist devices are implanted. Vasoactive agents are required to maintain an adequate perfusion pressure for unsupported right ventricle. For weaning from CPB, the doses of the inotropes and vasoactive agents must be continuously reviewed and titrated. RHF The most crucial parameter for successful weaning from CPB post-LVAD implantation is the performance of the right ventricle. The recurring problem of RHF diminishes the clinical results after LVAD implantation.71 RV dysfunction occurs in 25–50% after LVAD implantation.72–74 The incidence of RHF is largely unpredictable. Risk factors are female gender and non-ischaemic aetiology as well as the haemodynamic parameters such as low pulmonary artery pressure (PAP) and low RV stroke volume index.75 Echocardiographic predictors are an increased RV to LV diastolic diameter,76 tricuspid incompetency and RV geometry, that is, a decrease in long axis to short axis ratio.72 A number of pharmacological approaches have been advocated in attempting to prevent or alleviate to RHF as follows. Inhaled nitric oxide Many institutions use inhaled nitric oxide (iNO) as standard protocol for weaning from CPB after LVAD implantation.77–79 These studies demonstrated a decrease in pulmonary vascular resistance assuming a decrease in right heart failure after implanting an LVAD. A recent randomised multicentre trial showed no difference according to the ‘end’ points mortality, mechanical ventilation, hospital and intensive care stay and the need for right-ventricular assist device (RVAD) implantation.80 Thus, the application of iNO has no clear evidence and must be individually decided. Inhaled iloprost (iIP) The use of the synthetic prostacyclin analogue inhaled iloprost (iIP) in critically ill patients with primary or secondary pulmonary hypertension is well established. The application of iIP is feasible and effective in preventing right heart failure so that an RVAD can be avoided during LVAD implantations. iIP has been shown to be more effective than iNO in reducing pulmonary vascular resistance in patients with primary pulmonary hypertension.81 In comparison with iNO, iIP was superior in facilitating weaning from CPB in patients with pulmonary hypertension in one single-centre study.82 A recent study showed iIP to be an effective agent in reducing the incidence of acute RHF.83 So far, the literature shows only case reports for iIP as a support drug for patients undergoing LVAD implantation.84,85 Since iNO lacks evidence for the prevention of severe RHF in LVAD implantations, iIP may be a better option for the treatment of pulmonary hypertension for these patients. Levosimendan The calcium-sensitising agent levosimendan and its long-lasting active metabolite OR-1896 bind to troponin C. Increased inotropy is not mediated by further increase in intracellular Ca2þ. A second mechanism is the opening of adenosine triphosphate (ATP)-sensitive Kþ channels in vascular smooth muscles.86,87 However, the increased myocardial contractility is not associated with an increase in myocardial oxygen consumption.88,89 The increase in cardiac output after a 24-h infusion is maintained at least for 7 days.90 In cardiac surgery patients with pre-existing low ejection fraction, stroke volume was better preserved with the combination of levosimendan plus dobutamine compared with milrinone and dobutamine.91 A meta-analysis showed levosimendan to reduce troponin release after cardiac surgery.92 Another recent meta-analysis showed that levosimendan provided a mortality benefit after coronary artery surgery.93 Currently, levosimendan non-responders were identified as high-risk candidates for RHF. In this small study, pre-surgery levosimendan treatment non-response was identified by elevated N-terminal pro-hormone brain natriuretic peptide (NT-pro-BNP) levels and predicted post-surgery RHF. Levosimendan however did not prevent RHF.94 Prospective multicentre studies for the use of levosimendan in LVAD implantation are not available.
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Perioperative antibiotic prophylaxis As for many other procedures, the perioperative antibiotic prophylaxis lacks evidence. A recent survey with VAD-implanting institutions revealed differences in perioperative antibiotic prophylaxis ranging from a four-drug regimen including fluconazole down to a one-drug regimen with only vancomycin.95 Crucial for the optimisation of antibiotic prophylaxis are the infection history of the patient and prevalent organism in the hospital, that is, the prevalence of antibiotic-resistant organisms. Optimal perioperative antibiotic prophylaxis is an example of personalised medicine and must be tailored to each individual patient. VAD patients for non-cardiac surgery The increase in the number of VAD implantations will inevitably lead to an increase in noncardiac surgery (NCS) in VAD patients. Several case reports and case series have been published on NCS for VAD patients. Stehlik et al. reported that 24% of their VAD patients (n ¼ 155) required NCS (n ¼ 59) during their study period (1993–2007). Bleeding was the most common complication (10%) and the survival to transplantation was similar to those patients who did not require NCS.96 Brown et al. reported NCS (n ¼ 27) in 142 VAD subjects between years 2000 and 2007. There was no difference in survival between þNCS (44%) and NCS (46%) patients at study conclusion. Bleeding and infection were the most common complications. In their report, þNCS patients were less likely to undergo heart transplantation (12%) compared to NCS patients (35%).97 Chestovich et al. reported NCS (n ¼ 64) in patients receiving mechanical circulatory support (n ¼ 363). Patients on extracorporeal life support and patients who underwent emergent surgery had higher mortality. Fewer VAD patients who required NCS received heart transplantation and NCS also delayed their transplantation.98 Considering the significant impact of NCS in VAD patients, a cardiac anaesthesiologist with TEE skills can be a very useful resource while administering anaesthesia for these patients.99 A VAD engineer should accompany the patient to the operating room and a cardiac surgeon should be available for consultation, if required. Preoperatively, unsupported ventricular function and endorgan function should be evaluated. Since bleeding is described as an important perioperative complication in many studies, the perioperative coagulation management should be discussed with the non-cardiac surgical team and the VAD team. Heartmate II, the most commonly used long-term VAD has less stringent anticoagulation requirements. Anticoagulation can be omitted, decreased or reversed for the perioperative period if the bleeding risk from NCS is significant.100 The cardioverter– defibrillator should be deactivated based on the nature and site of surgery and external defibrillator pads should be applied. Attention should be paid to proper perioperative antibiotic coverage as infection is another common complication in VAD patients. Type of anaesthesia and the anaesthetic drugs administered are less important as long as the haemodynamic management is directed by appropriate monitoring. Choice of monitoring depends on the type of device, the surgical procedure and the function of the unassisted ventricle. In patients with continuous flow VADs, pulse oximetry and osillometric non-invasive blood pressure measurements are not reliable. While auscultation and palpation methods are not reliable, Doppler signals can be used to measure mean blood pressure for simple, less invasive and brief surgical procedures (such as endoscopy under sedation). However, invasive arterial pressure monitoring is advisable for complex procedures of longer duration where haemodynamic fluctuations and blood loss are expected (laparoscopy, thoracoscopy and open abdominal procedures). Ultrasound can be used to guide arterial cannulation. Cerebral oximetry is useful even in patients with non-pulsatile circulation for NCS. Intra-operative haemodynamic management (fluids, inotropes and vasopressors) should be guided by central venous pressure and TEE monitoring. For procedures, which require intensive postoperative care (aortic surgery, major abdominal and thoracic surgery), PA catheters should be used. Aggressive management of hypercarbia, hypoxaemia and acidosis is recommended to prevent increase in pulmonary vascular resistance. The aim is to preserve the function of the unassisted ventricle and avoid the need for rightsided mechanical assistance. This can be very challenging in procedures, which require lung isolation and pneumoperitoneum.
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The Summary Anaesthesia and peri-operative management of patients undergoing implantation of ventricular assist devices are challenging aspects of cardiac anaesthesia. The anaesthesiologist is confronted with a highly compromised and vulnerable patient who frequently presents with difficulties even in otherwise straightforward procedures such as securing central venous access. Sequelae of heart failure such as renal and hepatic insufficiency typically complicate management and may worsen outcome and prognosis. There is special need for teamwork with all involved professional groups. The prediction of right heart failure post LVAD implantation and the optimal treatment options have not yet been fully elucidated. The introduction of minimal invasive VAD systems with transapical approach could be supposed to enable a more widespread use in patients with a higher risk profile. The evolution of VAD into smaller systems with even better flow profiles and less propensity for thromboembolic complications can be anticipated in future, and will hopefully further improve life expectancy and quality of life for this most challenging patient group.
Practice points -
The preoperative identification of co-morbidities is crucial. Before induction, the operating room should be equipped. Diuretic-induced hypovolaemia should be treated with caution. Inotropes and vasopressors must be available. During induction, special attention should be paid to haemodynamic changes. Pre-existing central venous thrombosis is common. Therefore, ultrasound-guided placement of central-venous catheters is helpful. The use of a pulmonary artery catheter is recommended. The use of narcotic drugs is institution dependent. Volatile anaesthetics should be used when possible. Measurement of cerebral oxygenation with near-infrared spectroscopy is recommended. These patients are at risk for developing right-sided heart failure. Mechanical ventilation must achieve normoxaemia and normocarbia. Perioperative antibiotic prophylaxis must be tailored to each individual patient.
Research agenda - The prediction of right-sided heart failure needs to be further investigated. - The therapy of right-sided heart failure lacks evidence. - Newer minimally invasive approaches may bring fresh challenges to anaesthetic management.
Conflict of interest None.
Acknowledgement Special thanks to Maurice Hogan, MD, for his linguistic help.
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