Anesthesia for emergency surgery after cardiac arrest

INTRODUCTION — Urgent or emergency surgery is sometimes necessary after cardiac arrest, despite an increased risk of perioperative morbidity or mortality. This topic reviews anesthetic considerations for patients who have suffered a recent cardiac arrest with successful resuscitation.

Initial critical nonsurgical interventions for post-cardiac arrest patients are reviewed elsewhere. (See "Initial assessment and management of the adult post-cardiac arrest patient" and "Intensive care unit management of the intubated post-cardiac arrest adult patient".)

Anesthetic management of patients with persistent shock or cardiac arrest caused by traumatic injury is discussed in other topics. (See "Intraoperative management of shock in adults" and "Anesthesia for adult trauma patients".)

GENERAL CONSIDERATIONS — Patients who have experienced a recent cardiac arrest are at risk for cardiovascular collapse for several hours after resuscitation due to the sequelae of ischemic myocardial injury sustained during the arrest, as well as the underlying medical comorbidities that led to the arrest. Post-cardiac arrest syndrome may include myocardial dysfunction, dysrhythmias, brain injury, and systemic ischemia/reperfusion response [1]. Persistent issues related to the precipitating pathology may include the cardiovascular system (eg, acute myocardial infarction, acute coronary syndrome, cardiomyopathy), thromboembolism (eg, pulmonary embolism), central nervous system morbidity (eg, stroke, encephalopathy), sequelae of severe pulmonary disease (eg, acute lung injury, chronic obstructive pulmonary disease, asthma), sepsis, hypovolemia, acute kidney injury, or drug toxicity due to overdose or poisoning [1]. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Major problems and care priorities'.)

While not well studied, urgent surgery should not occur for at least 72 hours after a cardiac arrest to minimize the risk for additional myocardial, cerebral, renal, or pulmonary injury. However, emergency surgery may be necessary in selected patients. Types of surgery in which it might be necessary to proceed would include coronary artery bypass grafting for urgent revascularization, neurosurgery for significantly increased intracranial pressure due to tumor or bleeding, or thrombectomy for acute limb ischemia.

PREOPERATIVE EVALUATION — In addition to performing critical aspects of a standard preanesthesia evaluation as time allows, relevant imaging studies, such as a chest radiograph, computed tomography of the head or chest, or transesophageal or transthoracic echocardiography, should be reviewed prior to induction of anesthesia for an emergency procedure. Laboratory tests, such as hemoglobin, arterial blood gases, renal function, lactate, and tests of coagulation (see "Intraoperative transfusion and administration of clotting factors", section on 'Tests of coagulation function') are also examined once available, as these may be valuable to predict the need for blood component transfusion, guide management of intraoperative fluid administration and selection of anesthetic and neuromuscular blocking agents, as well as monitor the evolution of pathophysiologic processes that often occur after cardiac arrest.

Details regarding the preanesthesia consultation are available in other topics. (See "Preoperative evaluation for anesthesia for noncardiac surgery" and "Preoperative evaluation for anesthesia for cardiac surgery".)

Additional considerations before transport of critically ill patients are discussed in a separate topic (table 1 and table 2). (See "Transport of surgical patients", section on 'Considerations for critically ill patients'.)

ANESTHETIC MANAGEMENT

Intraoperative monitoring

●Hemodynamic monitors – Decisions regarding hemodynamic monitoring after recent cardiac arrest depends on patient-specific considerations (eg, hemodynamic stability, arrhythmia burden, persistent myocardial ischemia or dysfunction), as well as surgery-specific considerations (eg, anticipated blood loss or fluid shifts). An intra-arterial catheter for continuous blood pressure (BP) monitoring is present or inserted in most patients due to the need to control blood pressure, which often involves titration of vasoactive agents. (See 'Blood pressure goals' below and 'Use of vasoactive agents' below.)

Transesophageal echocardiography (TEE) may be employed to diagnose causes of persistent or severe intraoperative hemodynamic instability. (See "Intraoperative rescue transesophageal echocardiography (TEE)".)

Discussion of monitoring considerations for unstable patients is available in another topic. (See "Intraoperative management of shock in adults", section on 'Intraoperative monitoring'.)

Since arrhythmias are common after cardiac arrest, we place transcutaneous pacing/defibrillator pads on the patient prior to induction of anesthesia in case defibrillation, cardioversion, or transcutaneous pacing may become necessary.

●Other monitors

•Temperature – We monitor and manage temperature as noted below. (See 'Temperature management' below and "Perioperative temperature management", section on 'Temperature monitoring'.)

•Electroencephalography – Neuromonitors with raw or processed electroencephalography (EEG) are typically used after cardiac arrest to monitor for seizure activity. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Seizures and myoclonic jerks'.)

Also, burst suppression or EEG silence can be detected. Processed EEG may also be useful to ensure adequate anesthetic depth in patients who received a neuromuscular blocking agent (NMBA) since heart rate and blood pressure (BP) may be poor surrogates of anesthetic depth after cardiac arrest. (See "Accidental awareness during general anesthesia", section on 'Brain monitoring'.)

•Bladder catheter – Urine output (UO) is typically monitored using a bladder catheter. Although traditional targets that attempt to maintain UO >0.5 mL/kg per hour do not predict acute kidney injury in critically ill patients [2], more severe oliguria <0.3 mL/kg per hour is avoided if possible [3]. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)

Induction and maintenance of anesthesia — Anesthetic goals are to produce unconsciousness, analgesia, muscle relaxation, and attenuation of the hemodynamic responses to intubation and surgical stimulation without compromising cerebral or myocardial blood flow.

Most patients arrive in the operating room already intubated and sedated after suffering a cardiac arrest, and may not need an intravenous (IV) induction agent. For conscious patients with potential or actual hypotension, anesthetic induction agents with minimal hemodynamic effects are selected, as described in detail in a separate topic. (See "Intraoperative management of shock in adults", section on 'Induction'.)

Initiating or continuing low doses of opioid, sedative(s), and/or a volatile anesthetic agent will likely be necessary to maintain anesthesia during the procedure. In some cases, an NMBA may also be necessary to facilitate surgery. (See "Maintenance of general anesthesia: Overview".)

After a recent cardiac arrest, many patients have persistent myocardial ischemia or dysfunction which may lead to hypotension. Anesthetic management for these patients is discussed in other topics. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'General anesthesia' and "Intraoperative management for noncardiac surgery in patients with heart failure", section on 'Management of general anesthesia'.)

Fluid management — Fluid management depends on the cause of the recent cardiac arrest, the patient's current hemodynamic stability, and ongoing blood losses or fluid shifts during the surgical procedure. Administration of crystalloid fluid boluses (typically 250 to 500 mL per bolus) for hypovolemic conditions, or administration of blood products to treat anemia, severe or ongoing hemorrhage may be necessary. However, aggressive fluid resuscitation may have been performed during the cardiac arrest. In the post-arrest period, it is important to avoid over-resuscitation and maintain euvolemia. Excess fluid administration will worsen cardiac function in many patients such as those with cardiogenic shock with evidence of pulmonary edema or obstructive shock due to pulmonary embolism. Further discussions of monitoring intravascular volume status and treatment of derangements are available in separate topics. (See "Intraoperative fluid management" and "Intraoperative management of shock in adults".)

Hemodynamic management — Patients presenting for emergency surgery shortly after cardiac arrest may require ongoing treatment to optimize BP and maintain end-organ perfusion (eg, boluses of IV fluid, blood transfusions, or vasopressors and/or inotropic drugs) [4]. Specific interventions depend on the cause of arrest, although etiology may be complex or uncertain in patients presenting to the operating room for emergency surgery (table 3). Such post-arrest interventions may have been initiated in the emergency department or intensive care unit (ICU), in an attempt to prevent secondary injury from hypotension. Evaluation of hypotension occurring in the operating room with transesophageal echocardiography (TEE) is discussed in the algorithm (algorithm 1). (See "Intraoperative rescue transesophageal echocardiography (TEE)".).

Further discussion of hemodynamic instability in these patients is available in other topics:

●(See "Initial assessment and management of the adult post-cardiac arrest patient".)

●(See "Intensive care unit management of the intubated post-cardiac arrest adult patient".)

●(See "Intraoperative management of shock in adults".)

Blood pressure goals — During the perioperative period, we continue to maintain preoperative targeted mean arterial pressure (MAP) values, typically >65 mmHg, in order to achieve optimal end-organ perfusion and reverse the acute shock state after initial resuscitation in patients with shock or cardiopulmonary arrest [5]. However, the optimal BP target for end-organ perfusion is unclear and may vary among individual patients. For example, in patients who have not awakened in a timely manner or do not have an intact neurologic examination after cardiac arrest, the targeted MAP may have been increased to 80 to 100 mmHg to optimize cerebral perfusion since the upper and lower limits of cerebral autoregulation may be shifted upward [6-8]. Episodes of hypotension are avoided, as these can cause secondary brain injury after cardiac arrest [9-11]. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Maintaining end-organ perfusion' and "Intensive care unit management of the intubated post-cardiac arrest adult patient", section on 'Hemodynamic monitoring and goals' and "Intraoperative management of shock in adults".)

Use of vasoactive agents — An intra-arterial catheter for continuous BP monitoring is necessary during titration of vasoactive agents, particularly if surgical interventions are ongoing.

Continuous infusions of vasopressor agents are initiated if administration of IV fluids and reduction of anesthetic agent dosing fail to restore and maintain adequate BP and/or tissue perfusion. We prefer norepinephrine as the first-line vasopressor when hypotension is present in post-cardiac arrest patients (table 4), although there is no evidence demonstrating the superiority of infusion of any one vasopressor/inotropic agent in this setting [12-14]. There is literature that suggests that norepinephrine is preferable to epinephrine or dopamine in similar situations [13-15]. If persistent vasoplegia with low systemic vascular resistance is the likely cause of refractory shock, then a vasopressin infusion is added [16]. In a 2018 meta-analysis of 23 trials (3088 patients) comparing use of catecholamines plus vasopressin versus catecholamines alone to treat patients with distributive shock, vasopressin was associated with lower risk for atrial fibrillation (risk ratio [RR] 0.77, 95% CI 0.67-0.88) and mortality (RR 0.89, 95% CI 0.82-0.97), and possibly lower risk of need for renal replacement therapy (RR 0.74, 95% CI 0.51-1.08) [17]. (See "Intensive care unit management of the intubated post-cardiac arrest adult patient", section on 'Hemodynamic monitoring and goals' and "Intraoperative management of shock in adults".)

Notably, transient global myocardial dysfunction (ie, myocardial stunning) is usually present immediately after cardiac arrest, although this often improves by approximately eight hours after arrest with return of left ventricular function to baseline by about 72 hours after cardiac arrest [18]. The addition of an inotropic agent (eg, milrinone, dobutamine (table 4) ) may be necessary in a patient with significant left or right ventricular failure if hemodynamic goals are not achieved with vasopressors and optimal preload (algorithm 2 and algorithm 3). (See "Intraoperative management for noncardiac surgery in patients with heart failure", section on 'Use of vasoactive and inotropic agents'.)

Myocardial dysfunction typically peaks during the first three days after cardiac arrest, and may be severe enough to cause cardiogenic shock [1,4,18-20]. There may be evidence of global hypokinesis on TEE, or persistently low central venous oxygen saturation (S_cvO₂) in blood drawn from the distal port of a central venous catheter (CVC) or low mixed venous oxygen saturation (S_vO₂) from the pulmonary arterial port of a pulmonary artery catheter (PAC) if a PAC is available [21]. (See "Intraoperative rescue transesophageal echocardiography (TEE)", section on 'Cardiogenic shock' and "Oxygen delivery and consumption", section on 'Oxygen content'.)

Details regarding vasopressor and inotropic agents are available in other topics. (See "Intraoperative management of shock in adults", section on 'Cardiogenic shock management' and "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'.)

Other considerations — Factors that may adversely affect the myocardial oxygen demand/supply balance should be aggressively treated (table 5), including tachycardia, hypotension, intravascular fluid overload, hypoxemia or hypocarbia, severe anemia, and unintentional hypothermia and shivering.

Occasionally, a decision is made to insert a mechanical assist device in a patient with cardiogenic shock (eg, intra-aortic balloon pump, ventricular assist device) if there is inadequate response to inotropic support. (See "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction" and "Short-term mechanical circulatory assist devices".)

Rarely, extracorporeal membrane oxygenation may be used for a patient with refractory hypoxemia and/or severe ventricular dysfunction. (See "Advanced cardiac life support (ACLS) in adults", section on 'Refractory pulseless ventricular tachycardia or ventricular fibrillation'.)

Management of arrhythmias — Arrhythmias are common after cardiac arrest. Acute myocardial infarction, cardiomyopathy, and primary arrhythmias are the most common causes of cardiac arrest. Any underlying causes of arrhythmias are corrected during the perioperative period if possible (eg, acute myocardial ischemia (table 5)), electrolyte imbalances.

Fluctuations in serum potassium may occur during and after cardiac arrest as a result of ischemia, acidosis, and catecholamine administration. Both high and low potassium levels can cause arrhythmias and should be corrected. The most common causes of hyperkalemia are renal insufficiency/failure and drugs that inhibit the renin-angiotensin-aldosterone system. Hypokalemia is often accompanied by hypomagnesemia, which should also be corrected (see "Bicarbonate therapy in lactic acidosis"). Thus, potassium levels and acid-base status, as well as serum levels of magnesium, calcium, and sodium should all be checked in any patient with persistent post-arrest arrhythmias. (See "Intraoperative advanced cardiac life support (ACLS)", section on 'Electrolyte abnormalities' and "Arrhythmias during anesthesia", section on 'Electrolyte abnormalities'.)

No data support the routine or prophylactic use of antiarrhythmic drugs after the return of spontaneous circulation following cardiac arrest, even if such medications were employed during resuscitation. Antiarrhythmic drugs should be reserved for patients with recurrent or ongoing unstable arrhythmias. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Preventing arrhythmia'.)

Management of specific cardiac arrhythmias during anesthesia or in the perioperative period is discussed in detail separately. (See "Arrhythmias during anesthesia" and "Advanced cardiac life support (ACLS) in adults", section on 'Management of specific arrhythmias'.)

Respiratory management — Management of mechanical ventilation balances the need to reverse hypoxemia and acidosis in the post-arrest patient with the potentially deleterious effects of hyperventilation or hyperoxia. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Respiratory considerations'.)

For patients already receiving mechanical ventilation, preoperative mechanical ventilation settings are generally replicated in the operating room. As with all critically ill patients undergoing general anesthesia, we employ a lung-protective ventilation strategy (see "Mechanical ventilation during anesthesia in adults", section on 'Lung protective ventilation during anesthesia' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Low tidal volume ventilation: Initial settings'):

Specific considerations for mechanical ventilation after cardiac arrest include:

●Use low tidal volumes of 6 to 8 mL/kg predicted body weight

●Avoid hyperoxia (defined as partial pressure of oxygen [PaO₂] >300 mmHg), which may be associated with increased in-patient mortality in patients with return of spontaneous circulation following cardiac arrest [22-24]. We adjust the fraction of inspired O₂ (FiO₂) to maintain peripheral oxygen saturation (SpO₂) at approximately 94 percent and/or PaO₂ at approximately 70 to 80 mmHg. Supporting data, limitations, and controversies surrounding this approach are discussed in detail separately. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Respiratory considerations'.)

●Set the respiratory rate to maintain the partial pressure of carbon dioxide (PaCO₂) at 40 to 45 mmHg (with end-tidal CO₂ at 35 to 40 mmHg) to prevent hypocapnia-induced cerebral vasoconstriction. It is unknown whether higher PaCO₂ levels might contribute to vasodilation, hyperemia, or cerebral edema after cardiac arrest. Thus, only mild permissive hypercapnia is allowed (ie, PaCO₂ 40 to 45 mmHg). In patients with metabolic acidosis or known or suspected increased intracranial pressure, a lower target for PaCO₂ may be selected (ie, approximately 35 mmHg). More aggressive hyperventilation is avoided because this increases cerebral vasoconstriction and reduces cardiac output by decreasing preload [25].

●For patients already receiving mechanical ventilation, use the positive end-expiratory pressure (PEEP) that was used in the ICU. For recently intubated patients, use an initial PEEP setting at 0 cm H₂O until adequate resuscitation and hemodynamic stability are ensured. Subsequently, PEEP may be slowly and incrementally increased to 5 cm H₂O if tolerated without provoking hypotension. The goal is to provide an optimal balance between minimizing lung injury and preventing hemodynamic instability. It is particularly important to avoid high levels of PEEP or dynamic hyperinflation with consequent development of auto-PEEP because high PEEP levels increase intrathoracic pressure and decrease venous return, cardiac output, and MAP. Decreasing or discontinuing PEEP and adjusting the ventilator settings to decrease mean airway pressure may improve venous return to the heart and improve these hemodynamic parameters. Furthermore, high PEEP levels may reduce cerebral perfusion pressure and should be modified in patients with suspected or known elevated intracranial pressure (ICP) [26]. (See "Clinical and physiologic complications of mechanical ventilation: Overview", section on 'Hypotension'.)

●For patients receiving inhaled nitric oxide or inhaled epoprostenol for hypoxemia, pulmonary hypertension, or right ventricular failure, avoid interruption of this inhaled therapy throughout the perioperative period. (See "Inhaled nitric oxide in adults: Biology and indications for use".)

Temperature management — Intraoperative normothermia of 36°C is the goal for temperature management in most patients after cardiac arrest. Hyperthermia must be avoided in all patients after cardiac arrest. Fever is associated with worse neurologic outcomes, presumably due to aggravation of secondary brain injury.

Selected patients may have had mild hypothermia (typically with a target of 36°C) induced in the preoperative period, which is usually maintained for approximately 24 hours. Examples include those with moderate coma (not following commands but with some motor response), no evidence of seizure activity on their electroencephalogram, and no evidence of cerebral edema on computed tomography scan. This therapy is discussed in detail in separate topics. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Temperature management' and "Intensive care unit management of the intubated post-cardiac arrest adult patient", section on 'Active temperature control'.)

Perioperative temperature management is described in detail in a separate topic. (See "Perioperative temperature management".)

Glycemic control — Serum glucose should be maintained between 140 and 180 mg/dL (7.8 and 10 mmol/L) during the period following cardiac arrest. Hypoglycemic episodes are carefully avoided. In critically ill patients, there is no benefit and possible harm from intensive control of the serum glucose (70 to 108 mg/dL [3.9 to 6 mmol/L]) compared with more liberal management (108 to 144 mg/dL [6 to 8.1 mmol/L]) [27-30]. However, hyperglycemia is also avoided, as this has been associated with worse outcomes in post-cardiac arrest patients, presumably due to aggravation of secondary brain injury [31-33]. Possible mechanisms include increased tissue acidosis from anaerobic metabolism, free radical generation, and increased blood-brain barrier permeability. (See "Glycemic control in critically ill adult and pediatric patients" and "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Glycemic control'.)

IMMEDIATE POSTOPERATIVE MANAGEMENT — Postoperative intensive care is usually planned for patients who have suffered a recent cardiac arrest and resuscitation. Considerations for transport to the intensive care unit (ICU) (table 1 and table 2), and handoff to ICU personnel (table 6), are discussed in other topics. (See "Transport of surgical patients" and "Handoffs of surgical patients".)

Considerations for further management in the ICU are discussed in a separate topic. (See "Intensive care unit management of the intubated post-cardiac arrest adult patient".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Basic and advanced cardiac life support in adults".)

SUMMARY AND RECOMMENDATIONS

●General considerations – Patients who have experienced a recent cardiac arrest are at risk for cardiovascular collapse for several hours after resuscitation due to the sequelae of ischemic myocardial injury sustained during the arrest, as well as the underlying medical comorbidities that led to the arrest. Ideally, urgent surgery should not occur for at least 72 hours after a cardiac arrest to minimize risk for additional myocardial, cerebral, renal, or pulmonary injury. However, emergency surgery may be necessary in selected patients. Considerations before transport of critically ill patients are noted in the tables (table 1 and table 2). (See "Transport of surgical patients", section on 'Considerations for critically ill patients' and 'General considerations' above.)

●Monitoring – Decisions regarding hemodynamic monitoring after recent cardiac arrest depends on patient-specific considerations (eg, hemodynamic stability, persistent myocardial ischemia or dysfunction), as well as surgery-specific considerations (eg, anticipated blood loss or fluid shifts). Evaluation of intraoperative hypotension with transesophageal echocardiography (TEE) is discussed in the algorithm (algorithm 1). In addition, temperature and urine output are monitored, and raw or processed electroencephalography (EEG) is often employed to monitor for post-arrest seizure activity. (See 'Intraoperative monitoring' above.)

●Management of arrhythmias – Since arrhythmias are common after cardiac arrest, we place transcutaneous pacing/defibrillator pads on the patient prior to induction of anesthesia in case defibrillation, cardioversion, or transcutaneous pacing may become necessary. Any underlying causes of arrhythmias are corrected (eg, acute myocardial ischemia (table 5), electrolyte abnormalities). Antiarrhythmic drugs should be reserved for patients with recurrent or ongoing unstable arrhythmias. (See 'Management of arrhythmias' above.)

●Anesthetic management – Patients who arrive in the operating room already intubated and sedated generally do not need an intravenous (IV) induction agent. For conscious patients who are hypotensive, anesthetic induction and maintenance agents with minimal hemodynamic effects are selected. Initiating or continuing low doses of opioid, sedative(s), and/or a volatile anesthetic agent will likely be necessary to maintain anesthesia during the procedure. In some cases, a neuromuscular blocking agent (NMBA) may also facilitate surgery. (See 'Induction and maintenance of anesthesia' above.)

●Fluid management – Fluid management depends on the cause of the recent cardiac arrest, the patient's current hemodynamic stability, and ongoing blood losses or fluid shifts during the surgical procedure. Administration of crystalloid fluid boluses (typically 250 to 500 mL per bolus) for hypovolemic conditions, or administration of blood products to treat severe or ongoing hemorrhage may be necessary. However, it is important to avoid over-resuscitation and maintain euvolemia. Excess fluid administration worsens cardiac function in many patients (eg, those with cardiogenic shock). (See 'Fluid management' above.)

●Hemodynamic management

•Blood pressure goals – We suggest maintaining preoperative targeted mean arterial pressure (MAP) values, typically >65 mmHg (Grade 2C). This threshold prioritizes achieving optimal end-organ perfusion and reversing the acute shock state after initial resuscitation in patients with shock or cardiopulmonary arrest. However, in patients who have not awakened or do not have an intact neurologic examination, the targeted perioperative MAP may be maintained higher (eg, 80 to 100 mmHg) since the upper and lower limits of cerebral autoregulation may be shifted upward. Episodes of hypotension are avoided, as these can cause secondary injury. (See 'Blood pressure goals' above.)

•Use of vasoactive agents – We suggest norepinephrine as the first-line vasopressor to treat hypotension (table 4) (Grade 2C). For patients with persistent vasoplegia with low systemic vascular resistance is the likely cause of refractory shock, we suggest addition of a vasopressin infusion (Grade 2C). Addition of an inotropic agent (eg, milrinone) may be necessary in patients with significant left or right ventricular failure if hemodynamic goals are not achieved with vasopressors and optimal preload (algorithm 2 and algorithm 3). An intra-arterial catheter for continuous blood pressure (BP) monitoring is necessary during titration of vasoactive agents. (See 'Use of vasoactive agents' above.)

●Management of ventilation – Management of mechanical ventilation balances the need to reverse hypoxemia and acidosis in the post-arrest patient with the potentially deleterious effects of hyperventilation or hyperoxia. As with all critically ill patients undergoing general anesthesia, we employ a lung-protective ventilation strategy, and we usually adjust the fraction of inspired O₂ (FiO₂) to approximately maintain peripheral oxygen saturation (SpO₂) at 94 percent and/or the partial pressure of oxygen (PaO₂) at 100 mmHg, with the respiratory rate set to maintain the partial pressure of carbon dioxide (PaCO₂) at 40 to 45 mmHg. (See 'Respiratory management' above.)

●Temperature management – Intraoperative normothermia is the goal for temperature management in most patients after cardiac arrest. Selected patients may have had mild hypothermia induced in the preoperative period (typically with a target of 36°C), usually to be maintained for approximately 24 hours. Hyperthermia must be avoided in all patients after cardiac arrest (See 'Temperature management' above.)

●Glycemic control – We suggest that serum glucose be monitored and maintained between 140 and 180 mg/dL (7.8 and 10 mmol/L) during the period following cardiac arrest (Grade 2C). Both hyperglycemia and hypoglycemic episodes are carefully avoided. (See 'Glycemic control' above.)

●Transport and handoff to intensive care unit (ICU) personnel – Considerations for postoperative transport to the ICU (table 1 and table 2), and handoff to ICU personnel (table 6), are discussed in other topics. (See "Transport of surgical patients" and "Handoffs of surgical patients".)