Intraoperative advanced cardiac life support (ACLS)

INTRODUCTION — This topic addresses advanced cardiac life support (ACLS) guidelines specific for management of intraoperative cardiac arrest. In this setting, patient comorbidities are known, and precipitating cause(s) are typically witnessed just before the event. Thus, focused and tailored clinician responses are possible, with generally better outcomes compared with out-of-hospital or unwitnessed in-hospital cardiac arrests [1,2].

Separate topics address basic life support (BLS) and ACLS guidelines developed by the American Heart Association for other settings:

●(See "Adult basic life support (BLS) for health care providers".)

●(See "Advanced cardiac life support (ACLS) in adults".)

General and perioperative management after initial resuscitation from cardiac arrest is presented separately:

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

●(See "Anesthesia for emergency surgery after cardiac arrest".)

INCIDENCE AND OUTCOMES OF INTRAOPERATIVE CARDIAC ARREST — Intraoperative cardiopulmonary arrest is rare, occurring in approximately five to six of every 10,000 anesthetic cases [3-5]. One study noted that only 0.74 per 10,000 anesthetics were thought to be associated with anesthesia-related causes [4]. However, hypoxemia, acidosis, and hypovolemia due to fluid shifts or blood loss are often contributory factors.

The etiology of cardiac arrest is often readily apparent during a surgical procedure because arrest is almost always witnessed by clinician(s) familiar with the patient's medical history, and the precipitating cause may be known and rapidly reversible. Thus, initiation of treatment is usually timely and focused, resulting in better outcomes in terms of survival or residual neurologic deficits compared with arrest in other settings [1,6]. In one retrospective registry study of patients suffering a perioperative cardiac arrest, one-third survived to hospital discharge, with good neurologic outcomes seen in two-thirds of the survivors [7].

CONSIDERATIONS FOR PATIENTS AT RISK FOR CARDIAC ARREST

Identification of high-risk patients — Cardiac arrest occurs most frequently in patients undergoing cardiac, thoracic, or vascular surgery [3]. Patients often have congestive heart failure, pulmonary circulation disorders, peripheral vascular disease, end-stage renal disease, or fluid and electrolyte abnormalities. Patients in shock and those who have suffered major trauma are also at risk. In one study, intraoperative calls for help in the intraoperative setting were most frequently for airway, cardiac, or hemorrhagic emergencies [8]. (See "Intraoperative management of shock in adults" and "Anesthesia for adult trauma patients".)

Formal documentation of an advanced direction refusing life-sustaining medical treatment (LSMT) is now commonly documented in a patient’s electronic medical record [9,10]. Preoperative discussion with the patient and/or family should define the role of the patient’s goals and wishes regarding the specific LSMT options that would be acceptable in the event of cardiac arrest during the perioperative period.

Intraoperative monitoring decisions — In some cases, a patient has known or impending shock before entering the operating room for urgent or emergency surgery. Such patients are continuously monitored with noninvasive and invasive monitors to avoid or immediately treat cardiac arrest, as described separately. (See "Intraoperative management of shock in adults", section on 'Intraoperative monitoring'.)

Monitoring decisions include:

●Electrocardiogram – Standard intraoperative electrocardiography (ECG) is necessary in all patients for immediate recognition and treatment of arrhythmias. A five-lead ECG and computerized ST-segment trending may also be useful for diagnosis of abnormalities suggestive of ischemia or pericarditis (ST segment changes), pericardial effusion (low voltage of the QRS complex or electrical alternans), or pulmonary embolism (S1Q3T3 pattern, new right bundle branch block, or anterior T-wave inversion). (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Monitoring for myocardial ischemia'.)

●Defibrillator-pacemaker pads – For patients at risk for development of arrhythmias leading to cardiac arrest, transcutaneous pacing/defibrillator pads should be placed before induction of anesthesia since defibrillation, cardioversion, or transcutaneous pacing may become necessary [1,2]. An external defibrillator with pacing capability should be immediately available. During cardiac arrest, delay in defibrillation for more than two minutes is associated with lower chance of survival in the perioperative setting [11].

●Intra-arterial catheter – An intra-arterial catheter is inserted for patients who would benefit from continuous monitoring of blood pressure (BP; eg, critical illness, low cardiac output state, preoperative infusion of vasoactive agents), for evaluation of respirophasic variations in the arterial pressure waveform to predict fluid responsiveness, and for frequent blood sampling. Of all the non-standard monitoring techniques, arterial catheterization for continuous monitoring of blood pressure is probably the most critically important additional monitoring method and should be frequently utilized. (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation", section on 'Uses'.)

●Central venous catheter or pulmonary artery catheter – A central venous catheter (CVC) is inserted for patients who need central venous access for infusion of vasoactive drugs, fluid or blood administration, measurement of central venous pressure (CVP), or measurement of central mixed venous oxygen saturation (S_cvO₂).

A pulmonary artery catheter (PAC) is inserted less frequently, but is often appropriate if the patient would benefit from hemodynamic measurements of cardiac output, systemic vascular resistance, pulmonary artery pressure (PAP), and pulmonary vascular resistance.

●Transesophageal echocardiography or point-of-care ultrasonography – Transesophageal echocardiography (TEE) monitoring may be useful for continuous monitoring of cardiac function and intravascular volume status in high-risk patients. (See "Intraoperative transesophageal echocardiography for noncardiac surgery".)

Even if a TEE probe is not inserted initially, "rescue" TEE can be performed urgently to diagnose the cause of cardiac arrest or refractory hypotension. (See "Intraoperative rescue transesophageal echocardiography (TEE)".)

Point-of-care ultrasonography (POCUS) is an alternative modality for diagnosis or confirmation of the cause of shock or cardiac arrest. (See "Intraoperative management of shock in adults", section on 'Point-of-care ultrasonography'.)

While invasive cardiovascular monitors may be helpful for recognition and management of the cause of cardiopulmonary arrest and may also provide useful information as subsequent interventions are performed, attempts to insert an intra-arterial catheter, CVC, or TEE probe should not delay treatment. (See 'Initial resuscitation' below.)

Recognition of cardiopulmonary arrest — Recognition of impending or actual cardiopulmonary arrest may be challenging in the operating room compared with other settings. The patient is typically either sedated or under general anesthesia with controlled ventilation. Thus, loss of consciousness, physical collapse, and cessation of breathing cannot be observed. Patients with a pacemaker continue to have spikes on the ECG monitor. Furthermore, patients under general anesthesia cannot respond to queries about their status. In addition, patient positioning for the surgical procedure and the presence of drapes covering most of the body typically make assessment difficult [1,2]. For example, it may not be possible to access and check the femoral (or the carotid) pulse.

Notably, the pulse oximeter may be unreliable or nonfunctioning in a patient with shock. In some patients, body habitus (eg, obesity) or pathology (eg, burns, hypothermia, anasarca, and vasculopathy) impedes noninvasive monitor function. The overall positive predictive value for alarms built into anesthesia machines and clinical monitors is very poor, and the vast majority of these alarms are false [12].

In the intraoperative setting, the most commonly recognized indicators of cardiopulmonary arrest are:

●A nonperfusing rhythm evident on the ECG (eg, pulseless rhythms including ventricular fibrillation, ventricular tachycardia, severe bradycardia, or asystole). It is critically important to check for a carotid (or other accessible) pulse as soon as an abnormal rhythm is detected. Loss of pulse for >10 seconds is an indicator of cardiopulmonary arrest [1].

●"Loss" of the intra-arterial pressure waveform tracing. It should be noted, however, that even with a pulseless rhythm such as ventricular fibrillation or asystole, arterial pressure pulsations will cease, but the digital value of the BP will not be zero, but rather will fall toward mean systemic pressure (also called mean circulatory filling pressure), which is typically approximately 10 mmHg [13].

●Loss of pulse oximetry plethysmography. (See "Basic patient monitoring during anesthesia", section on 'Pulse oximetry'.)

●Loss of the end-tidal carbon dioxide (EtCO₂) tracing or low EtCO₂ values. An attenuated trace may be optimized by more effective CPR [14]. However, evaluation of EtCO₂ should be performed in the context of an individual patient's clinical status since other causes for low readings may exist [1]. Clinical applications and limitations of EtCO₂ monitoring are discussed separately. (See "Basic patient monitoring during anesthesia", section on 'Capnography' and "Carbon dioxide monitoring (capnography)".)

Considerations in COVID-19 patients — Critically ill patients with novel coronavirus disease 2019 (COVID-19) may require a surgical intervention (eg, for thrombotic/ischemic complications). To minimize the risk for viral aerosolization during resuscitation of an intubated mechanically ventilated COVID-19 patient, the closed anesthesia ventilator circuit containing a high efficiency particulate air (HEPA) filter should not be disconnected. Overall perioperative management of COVID-19 patients is discussed separately. (See "Overview of infection control during anesthetic care", section on 'Infectious agents transmitted by aerosol (eg, COVID-19)' and "Overview of infection control during anesthetic care", section on 'Considerations with COVID-19 or other agents spread by aerosol'.)

The prone position is used in certain surgical procedures and to improve oxygenation in mechanically ventilated patients with acute respiratory distress syndrome (ARDS). CPR should be commenced immediately after intraoperative cardiac arrest, but decisions to start CPR in the prone position depend on procedure- and patient-related factors. The patient is rolled into the supine position when this is feasible without incurring a prolonged interruption in CPR [15-17]. Other aspects of performance of ACLS in COVID-19 patients are discussed in a separate topic. (See "Advanced cardiac life support (ACLS) in adults", section on 'Resuscitation of patients with COVID-19 or similar illness'.)

INITIAL RESUSCITATION — We employ the Anesthesia ACLS (A-ACLS) Comprehensive Algorithm to guide treatment of cardiopulmonary arrest in the operating room (algorithm 1).

Initiate chest compressions, defibrillation, epinephrine — As in any other setting, cardiopulmonary resuscitation (CPR) and ACLS are initiated as soon as cardiac arrest is recognized [1,2]. This includes performance of excellent chest compressions, ensuring ventilation, and defibrillation as rapidly as possible if ventricular fibrillation or pulseless ventricular tachycardia is present. Once pulselessness has been detected, delays greater than two minutes in initiation of CPR with chest compressions, defibrillation if warranted, and administration of epinephrine have each been associated with lower survival after witnessed in-hospital cardiac arrest [18].

However, starting chest compressions without delay in the operating room is challenging if the patient is positioned in prone, lateral, steep Trendelenburg, or beach chair position to facilitate the surgical procedure. Ideally, the patient can be rapidly repositioned to be supine. Also, the patient's back must be against a hard surface to provide uniform force and sternal counterpressure during chest compressions. However, CPR in the prone position is a reasonable alternative to supine CPR when the airway is already secured; defibrillation in the prone position is also possible [16].

Case reports, simulation-based studies, and cadaver feasibility studies have described return of spontaneous circulation (ROSC) or other successful outcomes after CPR performed in unusual positions [19-23]. For example, during CPR in the prone position, attempts are made to deliver effective compressions on the thoracic spine by using the same rate and force that would be delivered in a supine position [19-21]. Also, case reports have described successful intraoperative CPR with apparently adequate chest compressions performed on patients in the lateral position by placing a hard surface positioned behind the patient during CPR or having a second rescuer provide back support [20,22-24].

For cardiopulmonary arrest in the pregnant patient, left lateral uterine displacement is necessary if fundal height is at or above the umbilicus, to minimize aortocaval compression, optimize venous return (preload), and generate adequate stroke volume during CPR. Manual uterine displacement is preferred so that supine positioning of the upper torso is preserved to facilitate optimal chest compression vector forces. A hand is used to apply maximal leftward push to the right upper border of the uterus to achieve uterine displacement that is approximately 1.5 inches from the midline [25]. Other aspects of management are similar to cardiac arrests in nonpregnant adults [26], as discussed separately. (See "Sudden cardiac arrest and death in pregnancy".)

Regardless of patient position, the nadir pressure occurring during release of each chest compression (ie, diastolic relaxation pressure) can be measured if an intra-arterial catheter is in place during CPR. Compressions that result in a diastolic blood pressure (BP) between 30 to 40 mmHg have a higher chance of successful ROSC [27]. Effectiveness of chest compressions can also be gauged by measuring end-tidal carbon dioxide (EtCO₂) levels; a sudden increase in EtCO₂ to 35 to 40 mmHg indicates ROSC. However, this must be confirmed by noting the presence of an arterial waveform, palpable carotid or femoral pulse, and/or by obtaining a noninvasive BP cuff measurement. EtCO₂ readings >20 mmHg during CPR are associated with better outcome and survival, while EtCO₂ readings <10 mmHg for 20 minutes are associated with failure of ROSC [27].

Treat the etiology of the cardiac arrest — General causes of intraoperative cardiac arrest are sought and treated immediately. These include the 8 H's (ie, hypoxia, hypovolemia, hydrogen ions [acidosis], hyperkalemia/hypokalemia, hypothermia, hypoglycemia, and malignant hyperthermia) and 8 T’s (ie, tension pneumothorax, tamponade [cardiac], toxins, thrombosis [embolus], thrombosis [coronary], trauma, qT prolongation, pulmonary hyperTension). However, during sedation or general anesthesia, the depth of sedation or noxious stimulation during a surgical procedure may affect the patient's responses and clinician recognition of these etiologies [1,2]. (See "Pathophysiology and etiology of sudden cardiac arrest".)

Specific causes of cardiac arrest that are more common in the operating room than in other settings include arrhythmias, anaphylaxis, local anesthetic systemic toxicity (LAST), adverse effects of neuraxial anesthesia, excessive doses of intravenous (IV) or inhalation anesthetic agents, or traumatic injuries requiring surgery. (See 'Causes of intraoperative cardiopulmonary arrest' below.)

Nontechnical skills (eg, use of cognitive aids for emergencies, structured communication, team training, simulation practice) are critically important for optimal management of cardiac arrest. Detailed discussions of development and maintenance of such nontechnical skills is available in a separate topic. (See "Cognitive aids for perioperative emergencies" and "Patient safety in the operating room", section on 'Communication-based errors' and "Patient safety in the operating room", section on 'Team and simulation training'.)

Recognition of futility — The finding of very low EtCO₂ (<10 mmHg) following prolonged resuscitation (>20 minutes) is a sign of absent circulation and a strong predictor of acute mortality [27]. Also, absent cardiac contractility using point-of-care ultrasound (POCUS) or transesophageal echocardiography (TEE) following a reasonable period of CPR indicates limited probability for ROSC [28]. (See "Advanced cardiac life support (ACLS) in adults", section on 'Termination of resuscitative efforts'.)

Limited data suggest that extracorporeal membrane oxygenation (ECMO) may be beneficial in selected patients after ROSC (those with a likely reversible cause of cardiopulmonary arrest and potential for neurologically intact survival) [29-31]. (See "Extracorporeal life support in adults in the intensive care unit: Overview".)

INTRAOPERATIVE MANAGEMENT AFTER RESUSCITATION

Management of ventilation — Management of ventilation during and after cardiopulmonary arrest balances the need to reverse hypoxemia and acidosis with the potentially deleterious effects of hyperoxia and hyperventilation. We employ a lung-protective ventilation strategy with either a volume- or pressure-limited ventilation mode that includes low tidal volumes (6 to 8 mL/kg) and mild permissive hypercapnia (partial pressure of carbon dioxide [PaCO₂] 40 to 45 mmHg). Higher PaCO₂ levels might contribute to vasodilation, hyperemia, or cerebral edema after cardiac arrest [32,33]. We titrate oxygen (O₂) concentration to a peripheral arterial oxygen saturation (SpO₂) of approximately 94 percent [32-37]. Prolonged hyperoxia after return of spontaneous circulation (ROSC) is deleterious to survival [32,33,35,36,38].

In patients who have metabolic acidosis or increased intracranial pressure, a lower target for PaCO₂ may be selected (approximately 35 mmHg). However, more aggressive hyperventilation is avoided as this may decrease cerebral blood flow, causing cerebral vasoconstriction and exacerbating any cerebral ischemic injury [32,33,35,36,39]. Notably, ventilation at 20 breaths per minutes is associated with lower survival than 10 breaths per minute [35]. Hyperventilation with larger tidal volumes may lead to auto-positive end-expiratory pressure (auto-PEEP) with further exacerbation of hypotension after cardiac arrest [40]. Also, hyperventilation can lead to less effective chest compressions and poor coronary and cerebral artery perfusion [35]. Furthermore, excessive ventilation may cause rapid changes in pH and consequent shifts in potassium that can exacerbate metabolic abnormalities due to other causes. (See 'Acid-base disturbances' below and 'Electrolyte abnormalities' below.)

Further discussion of ventilation management in post-arrest anesthetized patients is available in other topics. (See "Anesthesia for emergency surgery after cardiac arrest", section on 'Respiratory management' and "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Respiratory considerations'.)

Hemodynamic management — During initial resuscitation in patients with shock or cardiopulmonary arrest, we target a mean arterial pressure (MAP) of approximately 65 to 70 mmHg, although the optimal blood pressure (BP) target for end-organ perfusion is unclear, and may depend on baseline values [41-47]. Several studies have noted that a low systolic BP of <90 mmHg is associated with higher mortality and diminished functional recovery after cardiac arrest [41-43,47].

After initial resuscitation, MAP is maintained at ≥65 mmHg, and sometimes increased to 80 to 100 mmHg to optimize cerebral perfusion since the upper and lower limits of cerebral autoregulation may be shifted upward after cardiac arrest [45,46,48]. Episodes of hypotension can cause secondary injury, in addition to any initial insult incurred during the arrest by the brain and other organs. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Maintaining end-organ perfusion'.)

If administration of intravenous (IV) fluids fails to restore and maintain adequate BP and/or tissue perfusion (see 'Fluid management' below), we initiate continuous infusion of vasopressor agent(s) to maintain the target MAP (table 1). Norepinephrine is typically the first-line vasopressor in most post-arrest patients, since epinephrine or dopamine have greater potential to increase myocardial O₂ consumption and induce arrhythmias, while phenylephrine may decrease ventricular performance and cardiac output, and dobutamine may cause tachycardia or exacerbate hypotension due to decreased systemic vascular resistance [49-53].

If persistent vasoplegia with low systemic vascular resistance is the likely cause of refractory shock, then a vasopressin infusion is initiated. Studies indicate that vasopressin may decrease serum creatinine, risk of renal failure, use of renal replacement therapy, and mortality risk in these circumstances [54,55].

The addition of an inotropic agent may be necessary to mitigate preexisting low cardiac output in a patient with left ventricular (LV) or right ventricular (RV) failure (algorithm 2 and algorithm 3), or the myocardial dysfunction that often occurs in the first 24 to 48 hours after cardiac arrest, particularly if hemodynamic goals are not achieved with vasopressors and optimal preload (table 1). While post-arrest myocardial dysfunction is generally reversible and responsive to inotropes, the severity and duration of dysfunction may result in cardiogenic shock that impacts survival in some patients [56].

Details regarding selection of vasopressor and inotropic agents are available in other topics:

●(See "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'.)

●(See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Vasopressors'.)

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

In all patients suffering cardiopulmonary arrest, hemodynamic status is continually assessed via changes in BP, heart rate, and end-tidal carbon dioxide (EtCO₂) values. An intra-arterial catheter for continuous BP monitoring is recommended to guide titration of vasopressors and inotropic agents, particularly if surgical interventions create a dynamic environment due to ongoing noxious stimuli, fluid shifts, and/or blood loss.

Insertion of a transesophageal echocardiography (TEE) probe is helpful to recognize and treat underlying ventricular dysfunction, as well as other causes of hypotension (eg, hypovolemia, LV outflow tract obstruction). (See "Intraoperative rescue transesophageal echocardiography (TEE)".)

Other indicators of cardiogenic shock may include low cardiac index measured with a pulmonary artery catheter (PAC), or persistently low mixed venous O₂ saturation (S_vO₂) or S_cvO₂ measured in the superior vena cava. Novel techniques for hemodynamic monitoring have been employed in some centers. However, there are no data showing improved outcomes after cardiac arrest due to use of a PAC or noninvasive cardiac output monitoring [56]. (See 'Intraoperative monitoring decisions' above and "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Cardiac output'.)

Fluid management — Intravascular volume status can be assessed using traditional hemodynamic parameters (eg, BP, heart rate, urine output, and central venous pressure [CVP]). However, sole use of these parameters to guide fluid therapy may result in either hypovolemia or hypervolemia, and significant intraoperative reduction in tissue perfusion may not be recognized. We measure dynamic hemodynamic indices of responses to fluid challenges when possible, as these provide superior guidance for goal-directed fluid therapy in patients with persistent hemodynamic instability during ongoing significant fluid shifts or blood loss after cardiac arrest. For example, variations in the arterial pressure waveform that occur during respiration (eg, pulse pressure variation [PPV], stroke volume variation [SVV], systolic pressure variation [SPV]) (figure 1). (See "Intraoperative fluid management", section on 'Monitoring intravascular volume status'.)

Correction of metabolic abnormalities — Electrolyte and acid-base disturbances require rapid recognition and correction since persistent abnormalities worsen post-arrest outcomes [57]. However, diagnosis of electrolyte abnormalities may be delayed during surgery and anesthesia because the clinical manifestations are typically nonspecific and may not present in orderly fashion. (See "Arrhythmias during anesthesia", section on 'Electrolyte abnormalities'.)

Electrolyte abnormalities — Rapid fluctuations in serum potassium may occur as a result of ischemia, acidosis, and catecholamine administration. Both high and low potassium levels can cause arrhythmias and should be corrected [57].

●Hyperkalemia – The most common causes of hyperkalemia are renal insufficiency/failure and drugs that inhibit the renin-angiotensin-aldosterone system. Prevention of hyperkalemic cardiac arrest is key. If patient risk factors for hyperkalemia were identified in the preoperative assessment and/or baseline blood levels were abnormal, then repeated post-arrest potassium levels should be obtained [1,2]. (See "Causes and evaluation of hyperkalemia in adults".)

Empiric treatment of a hyperkalemic emergency is appropriate in the operating room. This includes (algorithm 4 and table 2) (see "Treatment and prevention of hyperkalemia in adults"):

•IV calcium (eg, calcium chloride 500 to 1000 mg) to directly antagonize the cell membrane actions of hyperkalemia. Since hypocalcemia exacerbates potassium-induced cardiotoxicity, ionized calcium levels are monitored, and hypocalcemia is treated. (See "Treatment and prevention of hyperkalemia in adults", section on 'Calcium'.)

•IV insulin (typically given with IV glucose) to drive extracellular potassium into cells. (See "Treatment and prevention of hyperkalemia in adults", section on 'Insulin with glucose'.)

•In rare circumstances, bicarbonate therapy 1 to 2 mEq/kg may be administered over two to five minutes to raise pH and drive extracellular potassium into cells (eg, if severe acute metabolic acidosis [ie, pH <7.1 to 7.2] coexists with severe hyperkalemia). The bicarbonate dose may be repeated if pH remains <7.1 after 30 minutes. Further details are available elsewhere:

-(See "Potassium balance in acid-base disorders", section on 'Metabolic acidosis'.)

-(See "Approach to the adult with metabolic acidosis", section on 'Overview of therapy'.)

-(See "Bicarbonate therapy in lactic acidosis".)

●Hypokalemia – Hypokalemia is associated with a variety of arrhythmias including premature atrial or ventricular ectopic beats, ventricular tachycardia, and ventricular fibrillation. Clinical manifestations and treatment are discussed separately. (See "Clinical manifestations and treatment of hypokalemia in adults".)

●Hypomagnesemia – Hypokalemia is often accompanied by hypomagnesemia; thus, serum levels of magnesium should also be checked in any patient with arrhythmias suspected to be due to hypokalemia. (See "Hypomagnesemia: Evaluation and treatment".)

Acid-base disturbances — Although some patients have significant metabolic acidosis after cardiac arrest, this generally improves once adequate perfusion is restored. Mild hyperventilation is often used to provide some respiratory compensation for the metabolic acidosis; however, excessive hyperventilation is avoided due to adverse effects. (See 'Management of ventilation' above and "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Respiratory considerations'.)

Sodium bicarbonate therapy is generally avoided during or after cardiac arrest (unless severe hyperkalemia is also present) (see 'Electrolyte abnormalities' above). Administration is associated with hypernatremia, worsening acidosis, and worse survival rate and neurological outcomes [58]. (See "Bicarbonate therapy in lactic acidosis".)

Hyperglycemia or hypoglycemia — Serum glucose should be maintained between 140 and 180 mg/dL after cardiopulmonary arrest [59]. Both hypoglycemia and hyperglycemia are avoided. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Glycemic control'.)

Temperature management — Normothermia is the goal for temperature management immediately after intraoperative cardiopulmonary arrest. Hyperthermia must be avoided in all patients after cardiac arrest since fever is associated with worse neurologic outcomes, presumably due to aggravation of secondary brain injury [60-62].

Details regarding perioperative temperature management are available in a separate topic. (See "Perioperative temperature management".)

After transport to the intensive care unit (ICU), mild hypothermia at 36°C may be targeted for 24 hours in selected patients, as described elsewhere [63]. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Temperature management'.)

Steroid administration — Stress-induced adrenal insufficiency leading to severe hypotension or cardiac arrest can occur in patients with chronic steroid use, in trauma patients with adrenal hemorrhage, or septic patients with adrenal infarcts. An IV bolus of hydrocortisone 100 mg or dexamethasone 4 mg is administered if adrenal shock is suspected, particularly if the patient is not responding to initial resuscitation efforts. In such cases, failure to administer a therapeutic dose of glucocorticoid may result in unsuccessful resuscitation and death. (See "Intraoperative management of shock in adults", section on 'Endocrine shock'.)

Although we do not routinely administer steroids to every patient suffering cardiac arrest, retrospective studies have noted that administration of hydrocortisone or other glucocorticoids during or after cardiopulmonary resuscitation (CPR) may improve survival [64,65]. One randomized trial in 268 consecutive patients with cardiac arrest reported improved survival with good neurologic status in those treated with the combination of methylprednisolone, vasopressin, and epinephrine during CPR and stress-dose hydrocortisone in post-resuscitation shock, compared with those treated with epinephrine/saline placebo [66]. (See "Therapies of uncertain benefit in basic and advanced cardiac life support", section on 'Vasopressin, glucocorticoid, and epinephrine'.)

CAUSES OF INTRAOPERATIVE CARDIOPULMONARY ARREST

General considerations — Causes of cardiopulmonary arrest in the operating room are often associated with the procedure, anesthetic technique, or known patient comorbidities, and are usually different from causes in other inpatient hospital areas or outside the hospital [1-3]. Arrest occurs most frequently in patients undergoing cardiac, thoracic, or vascular surgery, and patients often have congestive heart failure, pulmonary circulation disorders, peripheral vascular disease, end-stage renal disease, or fluid and electrolyte abnormalities [3]. The etiology is usually more readily apparent than in other settings because the arrest is witnessed by clinician(s) familiar with the patient's medical history, and the precipitating cause may be known and rapidly reversible. Examples of intraoperative causes of cardiac arrest that are rarely seen outside the operating room include asystole due to vagal reflexes, sympathectomy caused by neuraxial anesthesia resulting in unopposed parasympathetic tone, excessive dosing of intravenous (IV) or inhalation anesthetics, anaphylaxis, local anesthetic toxicity, malignant hyperthermia, auto-positive end-expiratory pressure (auto-PEEP), bronchospasm, pulmonary embolism (air, fat, thrombus), or tension pneumothorax [1,2,67-70].

In contrast, ischemic heart disease is the most common cause of out-of-hospital cardiac arrest, accounting for 70 to 80 percent of events [71]. (See "Overview of sudden cardiac arrest and sudden cardiac death", section on 'Etiology'.)

Arrhythmias — Arrhythmias are a primary cause of cardiac arrest in the operating room as in other settings. Post-arrest arrhythmias are also common. Treatment of the underlying cause of an arrhythmia is critical (eg, electrolyte disturbances, acute myocardial ischemia, adverse effect of an inotrope).

Antiarrhythmic drugs are reserved for patients with recurrent or ongoing unstable arrhythmias [72]. For example, amiodarone boluses and/or infusion may be employed to ensure rhythm stability after defibrillation for ventricular fibrillation, or for unstable ventricular tachycardia or atrial fibrillation. No data support routine or prophylactic use of antiarrhythmic drugs after return of spontaneous circulation (ROSC) following cardiac arrest, even if such medications were employed during resuscitation [56]. Details regarding management of specific cardiac arrhythmias is discussed separately. (See "Advanced cardiac life support (ACLS) in adults", section on 'Management of specific arrhythmias' and "Arrhythmias during anesthesia".)

Notably, sinus bradycardia occurs frequently in the operating room as a result of vagal reflexes due to surgical manipulations, neuraxial anesthesia with a high T1 to T4 anesthetic level, or administered medications such as negative chronotropic agents, anticholinesterase agents, opioids, or vasoconstrictors. Bradycardia does not usually require pharmacologic treatment unless it is severe (heart rate <40 beats per minute) and associated with signs of inadequate perfusion (table 3). (See "Arrhythmias during anesthesia", section on 'Sinus bradycardia'.)

Continuous electrocardiogram (ECG) monitoring and vigilance are necessary to detect recurrence of arrhythmias. Survivors of cardiac arrest with uncontrolled dysrhythmias should be evaluated by a consultant cardiologist as soon as feasible for possible placement of a permanent pacemaker, antiarrhythmic drug therapy, or other antitachycardia therapies, such as wearable or implantable cardioverter-defibrillator [56]. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Preventing arrhythmia'.)

Anaphylaxis — Agents commonly used in the operating room may cause anaphylaxis (eg, antibiotics, neuromuscular blocking agents, latex (table 4)). Also, immunologic anaphylactic reactions may occur due to transfusion of a blood product. Treatment is based upon prompt administration of intravenous (IV) epinephrine and fluid resuscitation (table 5). Further details regarding the prevalence, etiologies, clinical manifestations, acute diagnosis, and management of perioperative anaphylaxis are available in a separate topic. (See "Perioperative anaphylaxis: Clinical manifestations, etiology, and management".)

Local anesthetic systemic toxicity — Local anesthetic systemic toxicity (LAST) is a life-threatening adverse event that can occur during or after the administration of local anesthetic drugs through a variety of routes. Cardiac arrest may occur due to ventricular arrhythmias and/or asystole, typically preceded by prolonged PR intervals and widened QRS complexes as well as a variety of neurologic symptoms. (See "Local anesthetic systemic toxicity", section on 'Clinical presentation of toxicity'.)

Management of LAST is summarized in the table (table 6) [73]. Notably, smaller doses of epinephrine are employed in management of cardiac arrest due to LAST rather than other causes, since use of vasopressors worsens acidosis and arrhythmias [74]. Also, lipid emulsion rescue therapy is typically employed, with an initial bolus of 1.5 mL/kg of 20 percent lipid emulsion, followed immediately by infusion at 0.25 mL/kg/minute, and repeat bolus if necessary for persistent or recurrent cardiovascular instability. (See "Local anesthetic systemic toxicity", section on 'Management of LAST' and "Local anesthetic systemic toxicity", section on 'Lipid rescue'.)

Neuraxial anesthesia — Cardiac arrest occurs during a neuraxial (ie, spinal or epidural) anesthetic is approximately 7 out of every 10,000 spinal anesthetics [5]. Severity of injury (eg, brain damage or death) is high in this circumstance [75]. Of note, the onset of cardiac arrest may be delayed and occur several minutes after the spinal anesthetic dermatomal level is achieved [76,77].

Neuraxial anesthetic administration results in blockade of sympathetic, motor, and sensory nerves as well as compensatory reflexes to these effects, and also results in unopposed parasympathetic tone. The magnitude of these physiologic effects depends in part on the extent and speed of onset of the block, as well as patient factors. Vagal responses are likely triggered by decreases in preload due to vasodilation during and after administration of a neuraxial anesthetic [78,79]. Preload decreases are mitigated by prophylactic fluid boluses and worsened by hemorrhage and third-space losses. (See "Overview of neuraxial anesthesia", section on 'Cardiovascular'.)

Pre-arrest hypotension can be treated with IV fluid and vasopressor administration (eg, ephedrine 5 to 10 mg boluses and/or phenylephrine 40 to 160 mcg boluses or infusion of 20 to 200 mcg/minute). Bradycardia should be treated promptly with atropine 0.4 to 0.6 mg IV, with use of ephedrine 5 to 10 mg IV (repeated as necessary up to 25 to 50 mg) as second-line therapy; if necessary, small doses of epinephrine 5 to 10 mcg are administered. For severe bradycardia or cardiac arrest, full resuscitation doses of epinephrine (ie, 1 mg IV) should be promptly administered and ACLS protocols are initiated [80]. (See "Spinal anesthesia: Technique", section on 'Hemodynamic management'.)

Excessive dosing of anesthetic agents — Excessive doses of IV or inhalation anesthetic agents may induce cardiac arrest.

Most IV anesthetic agents have dose-dependent adverse effects that include hypotension due to venous and arterial dilation as well as decreased myocardial contractility, and respiratory depression. (See "General anesthesia: Intravenous induction agents", section on 'Dosing considerations'.)

Similarly, excessively high concentrations of sevoflurane, desflurane, and isoflurane cause progressive vasodilation, bradycardia, and decreased contractility, as well as profound respiratory depression, and can eventually induce cardiovascular collapse. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Cardiovascular effects' and "Inhalation anesthetic agents: Clinical effects and uses", section on 'Respiratory effects'.)

Malignant hyperthermia — Although rare, acute malignant hyperthermia can rapidly progress to cardiac arrest, and is nearly always fatal without timely recognition and treatment. Clinical physical signs include hypercapnia, tachycardia, muscle rigidity, rhabdomyolysis, hyperthermia, and arrhythmia; these are associated with laboratory abnormalities that include respiratory and possibly metabolic acidosis, hyperkalemia, elevated creatine kinase, and serum and urine myoglobin. Details regarding treatment are present in the table and in a separate topic (table 7). (See "Malignant hyperthermia: Diagnosis and management of acute crisis".)

Traumatic cardiac arrest — The most common etiology of traumatic cardiac arrest is hemorrhage (48 percent) [81]. Other causes include tension pneumothorax, cardiac tamponade, and hypoxemia. Although traumatic cardiac arrest has a high mortality rate, neurologic outcome is better in those who survive compared with other types of cardiac arrest [82].

Resuscitative efforts in the operating room focus simultaneously on assessment, airway management, and surgical control of hemorrhage. Notably, upper airway management and chest compressions may not be effective if tension pneumothorax or cardiac tamponade is present [2]. Checklists are often used as cognitive aids to ensure optimal preparation and intraoperative resuscitation of trauma patients (table 8) [2,83,84]. (See "Anesthesia for adult trauma patients".)

Hemorrhage — Hemorrhagic shock leads to lost pulses and eventual pulseless electrical activity or asystole. Prodromal symptoms typically include tachycardia, tachypnea, and decreased pulse pressure. However, hypotension may not be present until just before cardiopulmonary arrest [2].

Tension pneumothorax or hemothorax — Intraoperative tension pneumothorax manifests as hypotension and worsening oxygenation leading to cardiopulmonary arrest, and should be suspected after blunt thoracic trauma, attempted insertion of a central venous catheter (CVC), or surgical procedures that may unintentionally violate the pleural space and lung. Emergency needle decompression is followed by chest tube placement by the surgeon, as described elsewhere. (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children", section on 'Tension pneumothorax'.)

Cardiac tamponade — Cardiac tamponade is the underlying cause of cardiac arrest in approximately 10 percent of trauma patients [81]. Survival is approximately four times higher after a cardiac stab wound compared with injury from a gunshot [85]. Management of impending or actual cardiac arrest due to cardiac tamponade is discussed separately. (See "Anesthesia for thoracic trauma in adults", section on 'Cardiac tamponade' and "Anesthesia for thoracic trauma in adults", section on 'Surgical drainage of cardiac tamponade'.)

Pulmonary embolism — Venous embolism of thrombus, air, fat, or amniotic fluid may lead to pulmonary embolism and cardiopulmonary arrest during various types of surgical procedures. Diagnosis often occurs with transesophageal echocardiography (TEE). (See "Intraoperative rescue transesophageal echocardiography (TEE)", section on 'Pulmonary embolus'.)

Right ventricular (RV) dysfunction is typically present; thus, anesthetic management is similar to that for right-sided cardiogenic shock (algorithm 3 and table 9). (See "Intraoperative management of shock in adults", section on 'Cardiomyopathic shock'.)

Immediate treatments for different types of embolic material to the pulmonary arterial tree are discussed separately:

●(See "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults", section on 'Initial approach and resuscitation'.)

●(See "Air embolism", section on 'Treatment'.)

●(See "Fat embolism syndrome", section on 'Treatment'.)

●(See "Amniotic fluid embolism", section on 'Initial emergency management for unstable patients'.)

PATIENT TRANSPORT AND HANDOFF IN THE INTENSIVE CARE UNIT — Once hemodynamic stability is achieved after intraoperative cardiopulmonary arrest, consultation with the intensive care unit (ICU) staff is obtained to arrange postoperative care [1,2]. (See "Initial assessment and management of the adult post-cardiac arrest patient".)

Some patients may need to undergo another intervention in the immediate postoperative period, depending on cause of the arrest. Examples include insertion of a mechanical circulatory support device (eg, extracorporeal membrane oxygenation [ECMO], intra-aortic balloon pump [IABP]) or insertion of a coronary stent. If such an intervention requires transportation to another location (eg, cardiac catheterization laboratory, interventional radiology suite), this should be completed before admission to the ICU [1,2,86]. Patients are at high risk for hemodynamic and/or respiratory compromise during transport from the operating room to another interventional location or to the ICU. Perioperative transport of critically ill surgical patients is discussed in a separate topic. (See "Transport of surgical patients".)

Upon arrival, patient information is communicated to the ICU team using a formal process termed a "handoff" or "handover" (table 10) [87-90]. In all cases, the anesthesiologist should remain with the patient until hemodynamic and overall stability are ensured. (See "Handoffs of surgical patients".)

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

●Incidence and outcomes – Intraoperative cardiopulmonary arrest is rare, occurring between five and six of every 10,000 anesthetic cases. The etiology is usually more readily apparent than in other settings because the arrest is witnessed by clinician(s) familiar with the patient's medical history, and the precipitating cause may be known and rapidly reversible. Initiation of treatment is usually timely and focused, resulting in better outcomes (eg, survival, neurologic function) compared with other settings. (See 'Incidence and outcomes of intraoperative cardiac arrest' above.)

●Common causes – Common intraoperative causes include (see 'Causes of intraoperative cardiopulmonary arrest' above):

•Arrhythmias – (See 'Arrhythmias' above.)

•Anaphylaxis – (See 'Anaphylaxis' above.)

•Local anesthetic systemic toxicity (LAST) – (See 'Local anesthetic systemic toxicity' above.)

•Adverse effects of neuraxial agents – (See 'Neuraxial anesthesia' above.)

•Excessive dosing of intravenous (IV) or inhalation agents – (See 'Excessive dosing of anesthetic agents' above.)

•Malignant hyperthermia – (See 'Malignant hyperthermia' above.)

•Traumatic cardiac arrest – (See 'Traumatic cardiac arrest' above.)

•Tension pneumothorax or hemothorax – (See 'Tension pneumothorax or hemothorax' above.)

•Pericardial tamponade – (See 'Cardiac tamponade' above.)

•Pulmonary embolism – (See 'Pulmonary embolism' above.)

Hypoxemia, acidosis, and hypovolemia due to fluid shifts or blood loss are often contributory factors.

●Recognition – Recognition of impending cardiopulmonary arrest in the operating room can be challenging in patients under general anesthesia with controlled ventilation. Typical signs are nonperfusing rhythm evident on the electrocardiogram (ECG) and/or loss of the intra-arterial pressure waveform, pulse oximetry plethysmography, and/or the end-tidal carbon dioxide (EtCO₂) tracing. (See 'Recognition of cardiopulmonary arrest' above.)

●Positioning for initial resuscitation – Cardiopulmonary resuscitation (CPR) and advanced cardiac life support (ACLS) are initiated as soon as cardiac arrest is recognized (algorithm 1). Repositioning to the supine position is optimal (rather than prone, lateral, steep Trendelenburg, or beach chair position). Also, the patient's back must be against a hard surface during chest compressions to provide uniform force and sternal counterpressure. (See 'Initial resuscitation' above.)

●Management of ventilation – During and after cardiopulmonary arrest, management of ventilation balances the need to reverse hypoxemia and acidosis with the potentially deleterious effects of hyperventilation and/or hyperoxia. We employ a lung-protective ventilation strategy with low tidal volumes (6 to 8 mL/kg), mild permissive hypercapnia (partial pressure of carbon dioxide [PaCO₂] 40 to 45 mmHg), and titration of oxygen (O₂) concentration to maintain O₂ saturation >90 percent. (See 'Management of ventilation' above.)

●Hemodynamic management – During initial resuscitation, we target a mean arterial pressure (MAP) of approximately 65 to 70 mmHg. If administration of IV fluids fails to restore and maintain adequate blood pressure (BP) and/or tissue perfusion, we initiate a continuous infusion of vasopressor agent(s). Addition of an inotropic agent may be necessary in patients with preexisting low cardiac output or post-arrest myocardial dysfunction (table 1). (See 'Hemodynamic management' above.)

●Fluid management – We measure dynamic parameters to assess response to a fluid challenge (ie, volume responsiveness) when possible (eg, variations in the arterial pressure waveform that occur during respiration) (figure 1). Visual assessment of left ventricular (LV) cavity size on transesophageal echocardiography (TEE) imaging and changes in superior vena cava or inferior vena cava diameter on point-of-care ultrasound (POCUS) are also useful. Traditional static parameters (eg, BP, heart rate, urine output, central venous pressure) provide supplemental information. (See 'Fluid management' above.)

●Electrolyte management – Metabolic abnormalities (eg, hyperkalemia, hypokalemia, hypomagnesemia, hypoglycemia, hyperglycemia) are rapidly corrected. Although some patients have significant metabolic acidosis after cardiac arrest, reversal generally occurs once adequate perfusion is restored. Mild hyperventilation is often used to normalize metabolic acidosis; however, excessive hyperventilation is avoided. Sodium bicarbonate therapy is also avoided in most cases since administration may result in hypernatremia and worsening acidosis. (See 'Correction of metabolic abnormalities' above.)

●Temperature management – Intraoperative normothermia is maintained after arrest. Hyperthermia is carefully avoided. (See 'Temperature management' above.)

●Postoperative transport to intensive care unit (ICU) – Patients are at high risk for hemodynamic and/or respiratory compromise during transport from the operating room to another interventional location or to the ICU. Upon arrival, patient information is communicated to the ICU team using a formal process termed a "handoff" or "handover" (table 10). (See 'Patient transport and handoff in the intensive care unit' above.)