INTRODUCTION — An estimated 350,000 people present with out-of-hospital cardiac arrest in the United States each year [1]. Survival rates for out-of-hospital cardiac arrest are extremely poor but have improved with resuscitation measures and aggressive supportive care in the intensive care unit (ICU).
The management of patients in the ICU following cardiac arrest will be reviewed here. Our approach is in keeping with the European Resuscitation Council and European Society of Intensive Care Medicine [2,3]. Cardiopulmonary resuscitation, post-cardiac arrest management in the emergency department, and cardiac evaluation in survivors of cardiac arrest are discussed separately. (See "Adult basic life support (BLS) for health care providers" and "Advanced cardiac life support (ACLS) in adults" and "Initial assessment and management of the adult post-cardiac arrest patient" and "Cardiac evaluation of the survivor of sudden cardiac arrest".)
INITIAL ASSESSMENT IN THE INTENSIVE CARE UNIT — For patients who arrive to the ICU with return of spontaneous circulation (ROSC) following sudden cardiac arrest (SCA), initial assessment is focused on assessing the etiology and complications of SCA (table 1 and table 2) and providing care that ensures continued hemodynamic stability. We encourage a multidisciplinary approach to management.
Immediate post-cardiac arrest assessment and testing
●Brief physical assessment – On arrival to the ICU, vital signs are recorded. We briefly examine for an elevated jugular venous pressure, abnormal heart and lung sounds, and burns and wounds. We also assess airway devices, intravascular catheters, and other support devices (eg, pacemaker, intra-aortic balloon pump [IABP]) that may have been placed during the arrest. We examine the abdomen for bowel sounds, masses, and tenderness, and lower extremities are examined for pulses and for signs of deep venous thrombosis and venipuncture sites. We perform a brief neurologic assessment of mental status, response to verbal commands, presence or absence of purposeful motor movements, and pupillary reaction to light.
●Fluid status assessment – In general, many patients are already receiving post-resuscitation fluids and vasopressors, which should be continued or stopped depending on the evaluation of their volume status. Hemodynamic goals are discussed below. (See 'Hemodynamic monitoring and goals' below.)
●Device assessment – Most patients already have intravenous and/or intraosseous access and we assess the need for peripheral or central venous catheter placement. Occasionally, patients have an IABP in place, are on extracorporeal membrane oxygenation (ECMO), or have a pericardial drain or temporary pacemaker in place; we make note of the settings and ensure proper function of such devices. If not already in place, we plan for targeted temperature management, if indicated. (See 'Active temperaturte control' below and "Intraaortic balloon pump counterpulsation" and "Emergency pericardiocentesis" and "Extracorporeal membrane oxygenation (ECMO) in adults".)
●Testing – If not already obtained in the emergency department (ED), we obtain an electrocardiogram (ECG), a chest radiograph, complete blood count, troponin I or T, brain natriuretic peptide (BNP; or N-terminal BNP), routine chemistries including phosphate, magnesium, calcium, coagulation studies, liver function tests, and arterial blood gases. Bedside echocardiography or point of care ultrasound may also be performed.
Other tests that may be obtained depend upon the suspicion for select etiologies and include blood cultures and urinalysis (when infection is suspected), urine and serum toxicology screen (when drug overdose is suspected), and computed tomography of the brain, chest, and/or abdomen (if trauma is suspected).
●Subspecialty consultations – Evaluation and management of SCA is multidisciplinary. We consult appropriate subspecialty clinicians early in the course of patients who present with SCA so that the approach involves a well-balanced team (eg, pulmonary, cardiology, neurology, intensivist). This is particularly important for implementing early intervention and for prognostication for both cardiac and non-cardiac reasons for SCA.
Further details regarding the immediate post-cardiac arrest assessment in the ED and the assessment by cardiologists for cardiac etiologies associated with SCA are discussed separately. (See "Cardiac evaluation of the survivor of sudden cardiac arrest", section on 'Initial evaluation' and "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Identifying and treating reversible causes of cardiac arrest'.)
Reassessment of cardiac arrest etiology — Following admission to the ICU, a key first step is the re-evaluation of the etiology of SCA. The majority of sudden death cases are cardiac in etiology; however, approximately 15 to 25 percent of cases are not (table 1 and table 2) [4-7]. At the time of initial presentation, collateral information is often not available; however, there is usually more time to gather this information while the patient is in the ICU. Re-evaluation involves retaking the history from witnesses (if available) and family or friends and re-reviewing the records of the first responders and emergency department as well as re-reviewing electrocardiographic, radiographic, and laboratory studies. The evaluation of patients for the etiology is discussed in detail separately. (See "Pathophysiology and etiology of sudden cardiac arrest", section on 'Etiology of SCD' and "Initial management of trauma in adults" and "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock" and "Cardiac evaluation of the survivor of sudden cardiac arrest".)
Hemodynamic monitoring and goals — Patients after cardiac arrest often have vasodilatory hypotension, necessitating vasopressors and fluid management. We suggest maintaining a systolic blood pressure of 90 mmHg and a mean arterial pressure (MAP) goal of 65 mmHg during the post-arrest period. Use of vasopressors may be needed to achieve these goals but higher spontaneous values do not necessarily need to be lowered to these targets.
This approach is based upon observational studies that suggest that a systolic blood pressure of less than 90 mmHg was associated with worse mortality [8-10]. Several studies that have evaluated bundles of care that included a MAP goal of 65 to 80 mmHg have also demonstrated an improvement in survival [11,12]. Targeting a MAP >65 mmHg may not have any added benefit. This was evidenced by a randomized trial of 789 cardiac arrest survivors that demonstrated the composite outcome of death and severe disability or coma at discharge was no different among patients in whom a MAP of 63 mmHg was targeted compared with MAP of 77 mmHg [13]. These results may be impacted by the lower-than-expected difference in blood pressure between the groups and loss to follow up.
We prefer norepinephrine as the first-line vasopressor when hypotension is present. While there are limited data in patients with cardiogenic shock that suggest there is no difference in mortality when norepinephrine is used as compared to dopamine [14], other studies have suggested that dopamine may be associated with harm due to an increased risk of arrhythmia and possible increased risk of death when compared with norepinephrine [15]. When cardiogenic shock is present, we assess the need for mechanical support (eg, intra-aortic balloon pump, ventricular assist device) or inotropic support (eg, dobutamine 2 to 15 mcg/kg/minute or milrinone 0.125 to 0.5 mcg/kg/minute). (See "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)
Aggressive fluid resuscitation is generally performed during the cardiac arrest. In the post-cardiac arrest period, we prefer to avoid over-resuscitation and maintain euvolemia. In some cases, diuresis may be needed with loop diuretics to achieve this goal.
Hypotension should resolve within 48 to 72 hours. For those with persistent hypotension, we assess patients for possible sepsis or cardiomyopathy. (See "Evaluation and management of suspected sepsis and septic shock in adults" and "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction" and "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock".)
A pulmonary artery catheter is rarely necessary but may be indicated when patients remain hypotensive and fluid status is uncertain. The value of other novel dynamic hemodynamic monitoring tools in this population is unknown. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults" and "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults" and "Novel tools for hemodynamic monitoring in critically ill patients with shock".)
Assessing the need for immediate coronary revascularization — The approach varies depending upon the etiology for SCA.
●Patients with non-cardiac etiology for SCA – For patients who have a clear non-cardiac cause for SCA (eg, acute pulmonary embolism or drug overdose), angiography is not typically necessary.
●Patients with likely cardiac etiology for SCA – In patients with a cardiac etiology for SCA, ECG, bedside echocardiography, and consultation with a cardiologist are typically performed to facilitate the need for coronary revascularization.
•Patients with ST segment elevation myocardial infarction (STEMI) or new left bundle branch block (LBBB) – For patients with ECG findings consistent with STEMI or new LBBB who are without contraindications, we perform emergency coronary angiography with intent to revascularize. We prefer percutaneous coronary intervention, if feasible, but medical reperfusion therapy is acceptable if catheterization is not available and no contraindications are present. (See "Cardiac evaluation of the survivor of sudden cardiac arrest", section on 'Coronary angiography' and "Acute ST-elevation myocardial infarction: The use of fibrinolytic therapy".)
•Patients with potential cardiac etiology for SCA but without STEMI – In patients with cardiac arrest but without STEMI on their ECG, practice and opinion vary in regard to whether coronary angiography should be performed early (immediately) or be delayed (within days, or following discharge). We believe that coronary angiography can safely be delayed in many patients without STEMI on ECG. However, there may be a role for early angiography in select patients. (See 'Ongoing assessment of the need for revascularization' below.)
We have a low threshold to perform early angiography in patients with the following:
-Known pre-existing coronary artery disease
-Evidence of recurrent ischemia
-Electrical or hemodynamic instability
-Witness-reported chest pain prior to SCA
If coronary angiography was not performed early after cardiac arrest, we consider proceeding with delayed coronary angiography in patients with the following:
-Unexplained cardiac arrest
-Left ventricular dysfunction
-Recurrent symptoms after recovery from cardiac arrest
-Inducible ischemia on a stress test
-Planned placement of an intracardiac defibrillator
Data describing outcomes when early angiography is performed in patients with SCA without ST elevation on ECG have been conflicting, although newer evidence does not generally support early angiography. Further investigation in this area is ongoing.
-Evidence in favor of early catheterization was derived from older observational studies that report the identification of significant coronary lesions in up to a third of patients with SCA without ST elevation on ECG [16-18] and a potential survival benefit from intervention [19,20].
-However, newer evidence does not support early angiography in this population. In the only randomized trial of 552 patients without STEMI on initial ECG post-cardiac arrest, there was no significant difference in survival at 90 days [21] or at one year [22] between an immediate angiography strategy (median time 2.3 hours) and delayed angiography strategy (median time 121.9 hours). In a meta-analysis of 11 studies that included this randomized trial, there was no difference in 30-day mortality or neurologic outcomes between early or late angiography [23].
Assess need for other immediate interventions — For patients who do not need coronary revascularization, we assess whether other immediate interventions or therapies are needed, such as the following:
●A pericardial drain (for cardiac tamponade) (see "Diagnosis and treatment of pericardial effusion", section on 'Pericardial fluid drainage')
●A temporary pacemaker (for heart block or bradycardia) (see "Temporary cardiac pacing")
●Bronchodilators (for bronchospasm due to exacerbation of chronic obstructive pulmonary disease [COPD] or asthma) (see "COPD exacerbations: Management", section on 'Initial pharmacologic therapy')
●Chest tube (for pneumothorax) (see "Thoracostomy tubes and catheters: Placement techniques and complications")
●Intravenous (IV) fluids and antibiotics (for sepsis) (see "Evaluation and management of suspected sepsis and septic shock in adults")
●Thrombolytic therapy and/or anticoagulation (for pulmonary embolism) (see "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults")
●Electrolyte replacement (for electrolyte disturbances)
GENERAL CRITICAL CARE MANAGEMENT — Most patients who survive sudden cardiac arrest (SCA) are intubated and require mechanical ventilation.
General supportive care — Supportive care for patients in the ICU is typically bundled. Bundled care is associated with improved outcomes and involves the following [24-26]:
●Ventilator-associated pneumonia precautions (eg, elevating the head of the bed to 30 degrees, mouth care). (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Position' and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Preventing aspiration'.)
●Stress ulcer prophylaxis. (See "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention".)
●Venous thromboembolism (VTE) prophylaxis. (See "Prevention of venous thromboembolic disease in acutely ill hospitalized medical adults".)
●Early physical and occupational therapy. (See "Post-intensive care syndrome (PICS)", section on 'Prevention and treatment'.)
●Early nutrition (not initiated during therapeutic hypothermia [TH] due to reduced bowel motility). (See "Nutrition support in critically ill patients: An overview".)
●Glycemic control. (See "Glycemic control in critically ill adult and pediatric patients".)
The target blood glucose is similar to that in critically ill patients without SCA (ie, 140 and 180 mg/dL [7.8 and 10 mmol/L]). Data to support this approach are based upon studies in patients with SCA that demonstrate worse outcomes in this population with hyperglycemia [27-29] as well as data that report no benefit and possible harm from hypoglycemia when strict glucose targets (70 to 108 mg/dL; 3.9 to 6 mmol/L) are compared with more liberal strategies (108 to 144 mg/dL; 6 to 8.1 mmol/L) [30-33].
●Infection prevention measures to prevent skin (eg, frequent turning) and urinary tract infections (eg, early urinary catheter removal).
Airway, ventilation, and oxygen targets — If a temporizing rescue airway device (eg, laryngeal mask) was used during the initial resuscitation, we switch to a more definitive airway (eg, endotracheal tube). Intubation and airway management are discussed separately. (See "Approach to advanced emergency airway management in adults" and "Basic airway management in adults" and "Rapid sequence intubation for adults outside the operating room".)
There is no optimal mode of ventilation for this population. We typically use a volume-limited assist control mode using initial settings outlined in the table (table 3). (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit".)
We obtain arterial blood gas measurements after the body temperature has dropped significantly during TH (eg, 33°C) since hypothermia decreases the minute ventilation and also affects blood gas interpretation. In post-cardiac arrest patients (including those receiving hypothermia), we typically use the following target ventilation and oxygenation strategies:
●We target an arterial carbon dioxide tension (PaCO2) of approximately 40 mmHg (or end-tidal CO2 of approximately 35 mmHg). Maintaining a PaCO2 in a normal range (35 to 45 mmHg) is associated with improved outcomes in patients with SCA [34,35]. The exception is patients with chronic hypercapnia (eg, chronic obstructive pulmonary disease) who require ventilator adjustments to achieve prehospitalization PaCO2 values. Hyperventilation should also be avoided since a low PaCO2 can lead to cerebral vasoconstriction [36,37] as well as a reduction in preload and a decrease in cardiac output and coronary perfusion pressure [38].
When a patient's core temperature is 33°C, the patient's actual PaCO2 may be 6 to 7 mmHg lower than the value reported by the blood gas machine [39]. We suggest targeting slightly higher PaCO2 values in order to avoid unintended hyperventilation and the resulting cerebral vasoconstriction.
●We target a peripheral oxygen saturation (SpO2) between 94 and 96 percent and an arterial oxygen tension (PaO2) between 65 and 100 mmHg. Hyperoxia (eg, PaO2 >100 mmHg) and hypoxemia (eg, PaO2 <65 mmHg) should both be avoided. Hypoxemia may aggravate cerebral edema and hyperoxia has been shown to be associated with an increased mortality [40]. The lower end of this range is supported by an open-label randomized trial of 789 cardiac arrest survivors that demonstrated the composite outcome of death and severe disability or coma at discharge was no different among patients in whom a liberal oxygen level (PaO2 98 to 105 mmHg [13 to 14 kPa]) was targeted compared with a restrictive oxygen target (PaO2 68 to 75 mmHg [9 to 10 kPa ]) [41]. These results may have been impacted by loss to follow up and higher-than-expected spontaneous oxygenation in the restrictive strategy group.
At a core temperature of 33°C, the PaO2 reported by the laboratory may be higher than the patient's actual PaO2. Thus, in this clinical setting, maintaining a laboratory PaO2 between 70 and 120 mmHg is reasonable.
Oxygen targets prior to ICU admission are discussed separately. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Respiratory considerations'.)
Transfusions — We do not routinely calculate oxygen delivery and do not advocate red blood cell transfusion to a normal hematocrit given the prothrombotic state seen in patients with SCA. Failure of the serum lactate to clear over time suggests inadequate perfusion and prompts us to re-evaluate all aspects of oxygen delivery:
●Cardiac output
●Intravascular volume
●Hemoglobin concentration
●Blood pressure
Transfusion parameters in critically ill patients including those with cardiac ischemia are discussed separately. (See "Use of blood products in the critically ill", section on 'RBC indications' and "Indications and hemoglobin thresholds for red blood cell transfusion in the adult", section on 'ACS (including MI)'.)
Antibiotic therapy and prophylaxis — Despite the development of pneumonia in many patients following SCA, we suggest not administering prophylactic antibiotic therapy routinely in this patient population. We typically limit administration of antibiotics to patients with evidence of infection (eg, sepsis).
While early retrospective studies have suggested a possible reduction in pneumonia in patients with SCA treated with antibiotics [42], a meta-analysis of 11 studies (three randomized trials and eight observational studies) reported that antibiotic prophylaxis in this population was not associated with a reduction in the incidence of pneumonia, survival, or ICU length of stay [43]. (See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)
Early discussion of the patient's wishes — We advise that the patient's wishes and goals of care be established early. Many patients with SCA are intubated and sedated and/or have hypoxic encephalopathy and are, therefore, unable to participate in a goal-of-care discussion. Thus, we hold family meetings early and frequently (eg, daily) to obtain an appropriate plan of care that is consistent with the patient's wishes. Involving the palliative care team on day one of ICU admission is prudent given the poor outcome for most of these patients. Key components of holding a successful family meeting are provided separately. (See "Communication in the ICU: Holding a meeting with families and caregivers" and "Palliative care: Issues in the intensive care unit in adults".)
ACTIVE TEMPERATURTE CONTROL — For patients who achieve return of spontaneous circulation and do not initially have purposeful neurologic activity on examination (eg, responding appropriately to verbal commands, withdrawing to painful stimuli), we perform active temperature control (ATC) regardless of initial rhythm or location of arrest. In most patients, ATC is begun in the emergency department and continued in the ICU. However, for patents who are quickly admitted to the ICU from the emergency department or who experience sudden cardiac arrest (SCA) on the floor or other parts of the hospital, ATC is often begun and maintained in the ICU. The rationale for ATC following SCA is based upon the observation that fever is harmful [44-48] and that ATC improves survival and neurologic outcome in this population. The optimal temperature is unknown and ranges from 32 to 37.5°C, the details of which are discussed below. (See 'Setting the target temperature' below.)
Further details regarding the indications and contraindications for the initiation of ATC after cardiac arrest are reviewed separately. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Indications and contraindications'.)
Phases — ATC consists of three phases:
●An initiation phase, which should be started as soon as possible after return of spontaneous circulation (ROSC) and often begun in the emergency department (ED) (see 'Initiation' below)
●A maintenance phase, which lasts for a minimum of 24 hours (see 'Maintenance' below)
●A rewarming phase (see 'Rewarming' below)
In general, central venous or arterial access is warranted since multiple laboratory draws are needed during TTM to monitor for adverse effects.
Initiation — Establishing ATC involves selecting a method for temperature control, setting a target temperature, and applying it as soon as possible.
Devices — A cooling device with an automated feedback mechanism is necessary to actively control patient temperature. There are several commercially available devices. Each institution typically selects their own device so it is prudent that clinicians and healthcare staff be educated regarding its use. Institutions should utilize a cooling technique that is feasible to consistently deploy based on resources and equipment availability.
Techniques for ATC include the following:
●Surface methods such as water and/or air-circulating blankets and water-circulating gel-coated pads.
●Intravascular methods such as an intravascular cooling catheter.
●Rapid infusion of cold saline and ice packs may be used in an emergency setting when automated cooling devices are not available and the patient needs transport to a facility that has ATC capability.
There is insufficient evidence to recommend one cooling modality over another [49-51], although some data suggest that intravascular and surface cooling methods are no different in terms of neurological outcomes and survival. Surface cooling methods (eg, cooling blankets) are more commonly used in ICUs than intravascular cooling methods. We typically use a surface cooling device. In general, surface cooling methods can often achieve desired temperatures quickly and effectively since many patients are already mildly hypothermic (35 to 35.5°C) from the mixing of cooler peripheral blood with core blood during resuscitation.
Setting the target temperature — For most patients managed with ATC following cardiac arrest, we suggest, for the first 24 hours, controlling the core body temperature to either a target between 33 and 36°C (also known as therapeutic hypothermia [TH]) or between 36.5 and 37.5°C (ie, targeted normothermia); both approaches should be coupled with proactive avoidance of fever (eg, ≥37.5°C) for an additional 48 hours after discontinuation of ATC (see 'Rewarming' below). While there is no universal optimal target temperature, patient-specific factors may influence whether the lower or upper end of the target range between 33 and 37.5°C is selected. For example:
●A target temperature on the higher end of this range (eg, 36.0 to 37.5°C; ie, maintenance of normothermia) may be appropriate for patients with mild brain injury, higher bleeding risk, trauma, recent surgery, septic shock, or patients with severe underlying comorbid medical conditions since the risks of bleeding, arrhythmias, and electrolyte disturbances are lower at this temperature compared with TH.
●Patients who may benefit from a temperature target on the lower end of this range (eg, 33 to 36°C; ie, TH) include patients with stroke [52,53], severe brain injury (eg, loss of motor response or brainstem reflexes, malignant EEG patterns [54], or early CT scan changes suggesting the development of cerebral edema) [54-56], subarachnoid hemorrhage [57], or hepatic encephalopathy [58,59]. In these patients, a greater degree of hypothermia may help reduce cerebral edema and seizure activity.
Data that describe the impact of different ATC strategies include the following:
●TH versus no ATC – Early trials used a target temperature of 32 to 34°C (ie, TH) and demonstrated benefit with ATC in this range compared with standard care without ATC [44,60]. These data are discussed below. (See 'Efficacy' below.)
●TH versus normothermia – By contrast, subsequent trials comparing TH (32 to 33°C) with targeted normothermia (36 to 37.8°C) found similar outcomes between these strategies [61-64].
•In one trial (TTM trial), 939 patients with out-of-hospital cardiac arrest (ventricular fibrillation [VF] or pulseless ventricular tachycardia [VT] in 78 percent) were randomized to ATC targeting a temperature of 33 or 36°C [61]. At six months, the number of patients who had died or had poor neurologic outcome was similar in both groups (54 percent in the 33°C group versus 52 percent in the 36°C group; risk ratio [RR] 1.02, 95% CI 0.88-1.16). The findings were consistent irrespective of age, initial cardiac rhythm, time to return of spontaneous circulation, or scale used for neurologic assessment.
•Similarly, a subsequent trial (TTM 2) of 1850 adults with out-of-hospital cardiac arrest also showed no six-month mortality benefit when targeted hypothermia (33°C) was compared with targeted normothermia (≤37.8°C) (50 percent [TH] versus 48 percent [normothermia]) [63]. In addition, the proportion of patients with moderate to severe disability following SCA, as measured by a modified Rankin score ≥4, was also no different (55 percent each). The lack of benefit was consistent across subgroups including sex, age, initial cardiac rhythm, time to return of spontaneous circulation, and presence or absence of shock on admission. Arrhythmia and hemodynamic compromise were more common with patients treated with TH (24 versus 17 percent). The baseline severity of brain injury of included patients appeared to be mild in this study. Whether targeted normothermia is as effective in subgroups with more severe injury is unknown. A metanalysis of TTM and TTM 2 data showed a similar lack of six-month mortality benefit [64].
•One network meta-analysis of 10 randomized trials (4218 patients) examined the efficacy and safety of deep hypothermia (31 to 32°C), moderate hypothermia (33 to 34°C), mild hypothermia (35 to 36 C), and normothermia (37 to 37.8°C) during ATC [65]. No difference in survival was reported when hypothermic strategies were compared with maintenance of normothermia (low certainty of the effect): deep hypothermia (odds ratio [OR] 1.30, 95% CI 0.73-2.30), moderate hypothermia (OR 1.34, 95% CI 0.92-1.94), mild hypothermia (OR 1.44, 95% CI 0.74-2.80). However, compared with normothermia, the incidence of arrhythmia was higher with moderate and deep hypothermia (OR 1.45, 95% CI 1.08-1.94 and OR 3.58, 95% CI 1.77-7.26), respectively. Other meta-analyses have shown similar results [64].
●Two levels of TH – Another randomized trial found no difference in outcomes when two target levels of TH (CAPITAL CHILL) were compared [66]. In that study, 733 comatose patients were randomly assigned to receive TH with a target of 31 or 34°C for 24 hours after cardiac arrest. No difference was reported in either mortality or neurologic outcomes, although ICU length of stay was longer in those who received 31°C. The study may have been underpowered to detect a difference.
Timing — We initiate ATC within minutes to hours of ROSC. It is likely that the earlier TTM is started, the greater the potential benefit.
In observational studies, delays in initiation of ATC were associated with worse neurologic outcomes in post-cardiac arrest survivors [67-69]. However, there is no proven advantage to starting ATC while resuscitation is ongoing compared with early initiation following ROSC [70]. In a trial in which patients were randomized to prehospital cooling initiated by paramedics or cooling started after hospital admission, prehospital cooling resulted in earlier achievement of target temperature, but mortality and neurologic outcomes were similar in both group [71].
Exceptions to early timing of ATC include the following:
●Patients with resuscitated cardiac arrest who have evidence of ST segment elevation myocardial infarction (STEMI) on electrocardiogram (ECG). In such patients, urgent revascularization takes priority. ATC is generally initiated once revascularization has occurred, although it may also be initiated earlier if it does not result in delay of revascularization. (See "Overview of the acute management of ST-elevation myocardial infarction", section on 'Choosing and initiating reperfusion with PCI or fibrinolysis'.)
●In patients who have documented intracranial hemorrhage, ATC should not delay neurology and neurosurgery evaluation. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".)
Maintenance
●Monitoring core temperature – We monitor core body temperature (which closely approximates brain temperature) continuously [72]. Axillary and tympanic membrane measurements should not be used since they do not adequately measure core temperature.
Although the gold standard for core temperature measurement is the measurement of central venous temperature, other less invasive options are typically used. These include esophageal, bladder, and rectal temperature probes [73]. Data suggest that esophageal temperature monitoring is the most accurate method to approximate core body temperature [74]. Bladder monitoring may be inaccurate as urine output rates fluctuate post-arrest. Rectal measurements may also be inaccurate, as the rectal temperature may lag behind the core temperature [73]. Selecting one of these three options is at the discretion of the institution and their policy regarding ATC. Importantly, the clinician should be aware of the accuracy of whatever modality they choose to use.
●Sedation – We administer sedation during ATC. Common approaches to sedation in post-cardiac arrest patients include the following [75]:
•Continuous infusions of propofol (20 mcg/kg/minute to a maximum dose of 50 mcg/kg/minute) and fentanyl (25 mcg/hour to 100 mcg/hour); alternatively, a propofol infusion with intermittent fentanyl boluses may be used if sufficient sedation and shivering suppression can be achieved with propofol alone.
•As an alternative to propofol in hypotensive patients, a continuous infusion of midazolam (2 to 10 mg/hour) can be considered. However, we prefer to avoid benzodiazepines, if feasible, since they may have a longer half-life and interfere with neurologic evaluation post-cooling.
Sedation should be titrated according to standard sedation scales and to suppress shivering. (See "Sedative-analgesic medications in critically ill adults: Selection, initiation, maintenance, and withdrawal" and "Sedative-analgesic medications in critically ill adults: Properties, dose regimens, and adverse effects" and 'Adverse effects' below.)
●Monitoring for adverse effects – We monitor patients routinely during maintenance with hourly blood pressure measurement and continuous telemetry. We monitor for adverse effects including shivering, bleeding, arrhythmias, and electrolyte disturbances. The QT interval may be followed on telemetry and confirmed with an ECG when prolongation is suspected. (See 'Adverse effects' below.)
We obtain the following laboratory tests every four hours:
•Complete blood count with differential
•Chemistries including potassium, magnesium, and calcium levels
•Activated partial thromboplastin time and International Normalized Ratio (INR)
•Lactic acid
•Cardiac enzymes (eg, troponin-I or -T)
●Duration – For most patients managed with ATC following cardiac arrest, we suggest a duration of at least 24 hours. This is consistent with the 2015 American Heart Association guidelines [34]. However, the optimal duration of ATC is uncertain. In the available clinical trials of ATC, the duration of cooling ranged from 8 to 28 hours (see 'Efficacy' below). Whether extending ATC for longer than 24 hours is of additional benefit is not clear. A randomized trial comparing ATC for 24 versus 48 hours is ongoing (NCT01689077).
Rewarming — We suggest a slow rewarming phase, targeting a rise in temperature at a rate of 0.25 to 0.5°C per hour until normothermic. Slow rewarming avoids rapid fluxes in metabolic rates and plasma electrolyte concentrations, thereby avoiding hyperkalemia, seizures, and cerebral edema. In addition, we suggest the avoidance of fever during the rewarming phase and for 48 hours thereafter, to decrease the risk of deleterious neurologic effects related to hyperthermia [34]. Our approach is consistent with guidelines from the European Resuscitation Council [76].
To control the rewarming process carefully, we advocate for the use of active automated devices rather than passive rewarming. Automated devices are often part of systems used for cooling and utilize surface or intravascular methods to slowly raise core body temperature back to normal [77,78]. However, they may not be universally available. In such cases, the patient may be manually rewarmed by increasing the set point for the temperature by 0.5°C every two to three hours until a normal temperature is reached. For those receiving ATC at 36°C, passive rewarming by switching the device off is appropriate; however core temperature should still be measured for an additional 48 hours to ensure normothermia and avoidance of fever.
If needed, the rate of rewarming can also be increased by raising the room temperature, applying a convective heating device, using heating lamps, or warming the inspired air via the ventilator heating circuit on the humidifier. These measures may be necessary when achieving the desired temperature increase per hour is not occurring with either active or passive rewarming techniques. While there are no data to determine the optimal timing for adding each of these rewarming interventions, it is reasonable to add them one at a time to avoid the adverse effects from overly rapid rewarming.
Adverse effects — The main adverse effects associated with TH are shivering and coagulopathy (and consequently bleeding). Others include arrhythmias, fluid and electrolyte imbalances, hyperglycemia, and an increased risk of infection.
●Shivering – Shivering is a natural response to cooling that raises the core body temperature and interferes with achieving the target temperature [79-82].
We typically titrate patient sedation to suppress shivering (eg, increased rates of propofol and/or fentanyl infusions). In patients who are refractory to escalated sedation, dexmedetomidine, neuromuscular blocking agents (NMBAs), and meperidine are options. Dexmedetomidine can suppress shivering [83], but has side effects of hypotension and bradycardia that may limit its use in patients with SCA. NMBAs are also effective but may mask seizure activity, and if used continuous EEG monitoring is prudent. Meperidine can also be used but has proconvulsant side effects and is not recommended in patients with renal failure, which is often present in patients with SCA.
●Coagulopathy and bleeding – As the core body temperature decreases, platelet function diminishes and clotting enzymes are impaired [84-88]. As a result, bleeding may be seen in up to 20 percent of patients being treated with ATC [89].
In general, major bleeding that requires red blood cell transfusion is rare. If bleeding cannot be controlled (eg, noncompressible site, intracranial hemorrhage, etc), then ATC should be stopped and the patient should be rewarmed. Additional interventions for bleeding are discussed separately. (See "Use of blood products in the critically ill", section on 'Other approaches to treat or prevent bleeding'.)
●Arrhythmias – Abnormal cardiac conduction and arrhythmias may be seen during TTM because cardiac electrical conduction is slowed by hypothermia, thereby precipitating arrhythmias [90].
Bradycardia is the most common arrhythmia and acceptable heart rates as low as 40 beats per minute may be tolerated provided the blood pressure is appropriate.
Hypothermia-induced prolongation of the QT interval may also induce arrhythmias especially when the patient is receiving other medications that prolong the QT interval (eg, fluoroquinolones).
Depressed myocardial function can also occur during hypothermia, a phenomenon which should be kept in mind when assessing cardiac function following cardiac arrest.
Other non-ATC-related cardiovascular issues that arise in this population are discussed below. (See 'Cardiovascular considerations' below.)
●Fluid and electrolyte imbalances – Hypothermia induces a "cold diuresis," which results in hypovolemia and electrolyte disturbances including hypokalemia, hypomagnesemia, and hypophosphatemia [91]. When indicated, we administer fluid boluses (eg, 250 to 500 cc of crystalloid) and replace electrolytes.
●Hyperglycemia – Hyperglycemia due to insulin resistance has been noted during hypothermia and should be managed similar to that in any critically ill patient [90,92]. (See "Glycemic control in critically ill adult and pediatric patients".)
●Increased risk of infection – The increased risk of infection related to ATC is thought to be due to impaired leukocyte function at lower temperatures [44,93]. However, data from a large randomized trial that compared patients cooled to 33°C with patients maintained at 36°C, suggest no significant difference in infection rates between the groups [61]. In addition, the increased risk of infection does not appear to be associated with an increase in mortality.
Efficacy — The efficacy of ATC in patients with SCA is supported by randomized trials, meta-analyses, and observational studies demonstrating lower mortality and better neurologic outcomes in patients managed with TTM compared with those managed without ATC [44,60-63,93-97]. Most patients enrolled in randomized trials evaluating ATC that demonstrated benefit had shockable rhythms (ie, VF and pulseless VT). The evidence supporting ATC in patients with nonshockable rhythms (eg, pulseless electrical activity [PEA] or asystole) is largely observational and remains conflicting.
●Studies comparing ATC versus no ATC – In a meta-analysis of three trials in which 366 survivors of cardiac arrest (VF or VT in 87 percent) were randomized to ATC or standard care without AQTC, patients in the ATC group had lower mortality (43 versus 56 percent; RR 0.79, 95% CI 0.66-0.95) and were more likely to have good neurologic outcome at hospital discharge (48 versus 39 percent; RR 1.41, 95% CI 1.09-1.82) [62]. Similar findings were noted in another meta-analysis that included the same three trials plus eight observational studies [97]. In a meta-analysis of a 2016 systematic review of six trials in which 437 patients were randomized to TH (target temperature 32 to 34°C) or no cooling, more patients in the TH group had favorable neurologic outcome (53 versus 33 percent; RR 1.94, 95% CI 1.18-3.21) and survival (RR 1.35, 95% CI 1.10 to 1.65) [94].
●Studies comparing TH versus normothermia – These data are discussed above. (See 'Setting the target temperature' above.)
●Impact of cardiac rhythm – Evidence in support of ATC is more robust in patients with VF and pulseless VT than those with nonshockable rhythms (eg, PEA or asystole):
•VF and pulseless VT – The randomized trials and meta-analyses discussed in the previous sections have demonstrated that ATC reduces mortality and improves neurologic outcomes in patients who have out-of-hospital cardiac arrest with an initial rhythm of VF or pulseless VT [44,60]. The benefit is assumed to extend to patients with in-hospital cardiac arrest from VF and pulseless VT.
•Nonshockable rhythms – The evidence supporting ATC in patients with SCA who have initial rhythms other than VF or pulseless VT is less robust than that in patients with shockable rhythms [98-111].
-In one small randomized trial, 30 patients with PEA or asystole were randomized to TH (target temperature 34°C) or normothermia [110]. The study did not detect a difference in mortality, which was similarly high in both groups (81 and 93 percent); however, the trial was not adequately powered to detect a true difference.
-Similarly, in another randomized trial of 584 patients, mortality was no different among patients who underwent TH (target temperature 33°C) compared with those in whom normothermia was targeted, although there was a higher percentage of patients with improved neurologic outcomes in the TH group [111]. In contrast, a post-hoc analysis of this trial reported that TH was associated with better neurologic outcomes on day 90 in patients with a nonshockable rhythm compared with normothermic patients [112]. However, the sample size was limited, resulting in wide confidence intervals, thereby limiting the interpretation of this finding.
-Observational data are conflicting, with some studies suggesting lower mortality in patients with nonshockable cardiac arrest who received ATC compared with those who did not receive ATC [98-101,109]. In contrast, other studies have not found significant improvement in survival or neurologic outcome in this population [102-108]. A systematic review of 10 nonrandomized studies of patients with cardiac arrest due to nonshockable rhythms demonstrated a lower in-hospital mortality in patients treated with ATC (RR 0.86, 95% CI 0.76-0.99), and a nonsignificant trend towards lower risk of poor neurologic outcome at discharge (RR 0.96, 95% CI 0.90-1.02); however, the quality of evidence was low [109].
NEUROLOGIC CONSIDERATIONS — Hypoxic encephalopathy, cerebral edema, seizure activity, and myoclonic jerks, are common after sudden cardiac arrest (SCA) and often indicate severe brain injury. We perform daily examination that also includes assessment of brainstem function. In addition, we typically obtain electroencephalography (EEG) and computed tomography of the brain to assist in this evaluation, since collectively these data can support clinical findings and inform prognosis [113].
Hypoxic brain injury and cerebral edema — The most common cause of death and morbidity in patients after resuscitated cardiac arrest is hypoxic encephalopathy [114]. Further details regarding the evaluation of patients with hypoxic brain injury are provided separately. (See "Hypoxic-ischemic brain injury in adults: Evaluation and prognosis".)
Active temperature control (ATC) is focused on reducing death and improving neurologic recovery from hypoxic brain injury. ATC is discussed separately. (See 'Active temperaturte control' above.)
Positioning patients with the head of the bed at 30 degrees is typical in mechanically ventilated patients and helps lower the intracranial pressure by improving outflow from the brain.
Seizures — In patients who are treated with ATC post-cardiac arrest, the incidence of seizures may be as high as 33 percent [115]. Many seizures in patients with hypoxic encephalopathy from SCA are nonconvulsive, clinically subtle, and often require EEG for detection (table 4). A smaller proportion are convulsive.
Electroencephalography — Whether continuous EEG monitoring should be routinely performed following cardiac arrest is unclear, in part because of uncertainty as to whether aggressive treatment of nonconvulsive or convulsive epileptiform activity improves neurologic outcomes [116,117]. Nonetheless, in patients with SCA undergoing ATC (ie, comatose patients), we perform continuous EEG monitoring in order to detect subclinical seizure activity. We advocate that continuous EEG monitoring begin as early as feasible, generally within 6 to 12 hours of ATC initiation. We continue EEG monitoring through the ATC period and for at least 24 hours after rewarming.
However, continuous EEG monitoring is not universally available. In such circumstances, a strategy of intermittent EEG monitoring may be utilized in the 6 to 12 hour range after ATC initiation and then again at least 24 hours after rewarming. One small prospective study suggested that standard intermittent EEG had comparable performance with continuous EEG monitoring for evaluation, although data were flawed [118].
Interpretation of EEG patterns in comatose patients after hypoxic brain injury may be difficult due to the effect of sedation. In addition, muscle movements occurring during the rewarming phase of ATC may cause artifact that can complicate interpretation. We prefer direct discussion with a consulting neurologist or epileptologist to integrate clinical and EEG data in order to facilitate management of EEG findings. (See "Nonconvulsive status epilepticus: Classification, clinical features, and diagnosis", section on 'Electroencephalography'.)
In patients with SCA, EEG patterns that are generally associated with a poor prognosis and reduced hospital survival (0 to 12 percent) are termed "malignant" EEG patterns. These include [119-122]:
●Nonconvulsive status epilepticus
●Convulsive status epilepticus
●Myoclonic status epilepticus
●Rhythmic and periodic epileptiform discharges
Malignant epileptiform patterns are less common in patients with early, diffuse cerebral edema; these patients tend to have suppression burst or complete suppression as their primary EEG pattern, and also have a poor prognosis [123]. (See "Electroencephalography (EEG) in the diagnosis of seizures and epilepsy".)
Treatment — In patients with SCA who have epileptiform discharges that progress to outright seizures (either convulsive or nonconvulsive), we treat with anti-epileptiform agents. While the identification of those with convulsive seizures may be obvious, identifying an outright seizure in those with suspected nonconvulsive seizures may be more challenging. Identifying intermittent eye blinking, nystagmus, or facial twitching can often be clues to progression to seizure, and these should trigger consultation with a neurologist or epileptologist.
Among the options, there is no single agent that is superior. Thus, we prefer a therapeutic approach similar to that described in patients with seizures due to non-SCA etiologies (table 5 and algorithm 1). This includes benzodiazepines for acute seizure treatment followed by a preventative agent, such as valproic acid, levetiracetam, lacosamide, or phenytoin (may be associated with hypotension). However, treatment of seizures in this setting is challenging because many are refractory to single agent therapy. For refractory cases, double or triple agent oral therapy as well as propofol or midazolam infusions, or phenobarbital may be appropriate. (See "Nonconvulsive status epilepticus: Treatment and prognosis" and "Convulsive status epilepticus in adults: Management", section on 'Emergency antiseizure treatment'.)
Data to support the optimal approach in this population are limited to single center case series. As an example, in one series, anticonvulsive treatment improved EEG status epilepticus patterns temporarily (ie, <6 hours) [124]. However, there was no difference in neurological recovery between patients treated with or without anti-epileptic agents and neurologic outcomes in general were poor.
Prophylaxis — We do not routinely administer seizure prophylaxis since there is no high-quality evidence that clearly demonstrates benefit from seizure prophylaxis in the post-cardiac arrest patient.
In support of this practice, one open-label trial of 172 survivors of cardiac arrest who had rhythmic and periodic EEG patterns compared prophylactic antiseizure medication for at least 48 hours plus standard care with standard care alone [125]. Despite effective suppression of EEG activity in 56 percent of patients in the antiseizure medication group, there was no difference between the groups in the rate of poor neurologic outcome (90 versus 92 percent) or mortality (80 versus 82 percent).
Myoclonic jerks — Myoclonic jerks and other movements are common after cardiac arrest. Myoclonus can be epileptic (ie, driven by an epileptic focus in the brain) or nonepileptic (also known as "isolated" myoclonus). EEG is used to distinguish these from one another. Consultation with a neurologist is critical to interpret EEG patterns associated with myoclonus. The classification and evaluation of myoclonus is discussed separately. (See "Classification and evaluation of myoclonus".)
Our treatment strategies are similar to those in non-SCA-related myoclonus. In general, for patients with mild or intermittent nonepileptiform myoclonus, we either treat with an intermittent benzodiazepine (eg, midazolam or clonazepam) or elect not to treat it. For patients who have severe myoclonus (eg, myoclonus causing dyssynchrony or rhabdomyolysis, myoclonus that prevents adequate care or reduces safety for interventions) or epileptiform myoclonus, we prefer treatment using scheduled levetiracetam with or without scheduled midazolam or clonazepam and/or a propofol infusion. Additional details regarding treatment of myoclonus is provided separately. (See "Treatment of myoclonus".)
Nonepileptic myoclonic jerks in patients following cardiac arrest are generally benign and do not have prognostic significance. Conversely, status myoclonus, defined as repetitive myoclonic jerks lasting more than 30 minutes, is generally a poor prognostic sign. For example, in one study of 401 patients with myoclonus following SCA, three quarters were found to have early postanoxic multifocal myoclonus (PAMM) that was associated with suppression-burst background and high-amplitude polyspikes [126]; no patients with this pattern survived.
CARDIOVASCULAR CONSIDERATIONS — Most patients with sudden cardiac arrest (SCA) are managed collaboratively by intensivists and cardiologists. The cardiologist assessment is important for evaluation and management of cardiac ischemia and other potential cardiac etiologies associated with SCA. Discussion in this section is limited to ICU-specific measures while a detailed approach to cardiac evaluation of the survivor of SCA is provided separately. (See "Cardiac evaluation of the survivor of sudden cardiac arrest".)
Electrocardiography and echocardiography — We typically follow patients for three days with daily electrocardiography (ECG) and as needed ECG for suspected ischemic or arrhythmic events.
Follow-up echocardiography may also be performed, generally 48 hours or more after cardiac arrest to assess myocardial and valvular function. Low ejection fractions noted during or immediately following arrest often improve by this time but lack of resolution may suggest an underlying pathology. A significant proportion of patients with SCA have myocardial dysfunction, ranging from 33 to 44 percent [127,128]. In one study, myocardial dysfunction was associated with male gender, a history of congestive heart failure, longer duration of resuscitation, and therapeutic hypothermia [128]. Further details regarding echocardiography in the evaluation of patients with SCA are provided separately. (See "Cardiac evaluation of the survivor of sudden cardiac arrest", section on 'Echocardiography'.)
Ongoing assessment of the need for revascularization — For patients who did not have revascularization performed immediately following cardiac arrest, a low threshold should be maintained for performing coronary angiography in those at risk. The value of diagnostic angiography in patients with SCA is discussed separately. (See 'Assessing the need for immediate coronary revascularization' above and "Cardiac evaluation of the survivor of sudden cardiac arrest", section on 'Coronary angiography' and "Cardiac evaluation of the survivor of sudden cardiac arrest".)
OTHER COMPLICATIONS — Following sudden cardiac arrest patients may suffer from ischemic injury to other vital organs, the management of which is largely supportive (eg, acute kidney injury, shock liver, ischemic bowel). (See "Overview of the management of acute kidney injury (AKI) in adults" and "Ischemic hepatitis, hepatic infarction, and ischemic cholangiopathy" and "Nonocclusive mesenteric ischemia".)
SPECIAL POPULATIONS — Details regarding management of special populations are found in the following links:
●(See "Evaluation of sudden cardiac arrest and sudden cardiac death in dialysis patients".)
●(See "Sudden cardiac arrest and death in pregnancy", section on 'Postarrest care'.)
●(See "Anesthesia for emergency surgery after cardiac arrest".)
PROGNOSIS — The overall prognosis of patients following cardiac arrest remains poor, with approximately 50 percent of patients surviving to discharge [61,129]. Prognosis is determined mostly by the extent of hypoxic brain injury but also by several other factors including the reversibility of the underlying etiology for sudden cardia arrest (SCA), comorbidities, and complications associated with critical illness (eg, acute respiratory distress syndrome, acute kidney injury). Poor prognostic factors are listed in the table (table 6).
Early prognostication in patients with SCA can be difficult. Serial neurologic assessment together with electroencephalographic data and computed tomography of the brain are key components that help determine the overall neurologic prognosis [113]. Generally, the earliest time interval for neurologic prognostication should be at least 72 hours after rewarming [34]. This time point allows for sedative and/or paralytic medications to be cleared from the system, but longer periods of time may be necessary.
Post-cardiac arrest scores have been developed, but generally these include cardiac arrest-specific data that are not always reliably recorded [130-132].
Further details regarding the prognosis of patients with SCA and prognosis of patients with hypoxic brain injury are provided separately. (See "Prognosis and outcomes following sudden cardiac arrest in adults" and "Hypoxic-ischemic brain injury in adults: Evaluation and prognosis".)
We set realistic expectations with families and loved-ones early during the course in the ICU. We pursue active and engaged interaction with families in the hours and days post-arrest to help determine the patient's wishes. (See "Communication in the ICU: Holding a meeting with families and caregivers" and "Palliative care: Issues in the intensive care unit in adults" and "Withholding and withdrawing ventilatory support in adults in the intensive care unit" and "Ethics in the intensive care unit: Responding to requests for potentially inappropriate therapies in adults".)
REFERRAL TO SPECIALIZED CENTER FOR POSTRESUSCITATION CARE — The American Heart Association has proposed that following successful resuscitation for cardiac arrest, patients may benefit from referral to regionalized centers for post-cardiac arrest care [133]. However, this is not yet routine. Further discussion on this matter is provided separately. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Patient disposition'.)
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".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Sudden cardiac arrest (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Assessment – For patients who arrive to the intensive care unit (ICU) with return of spontaneous circulation (ROSC) following sudden cardiac arrest (SCA), initial assessment is focused on assessing the etiology and complications of SCA (table 1 and table 2). We encourage a multidisciplinary approach to management.
•We review records of the event, obtain an expanded history from close contacts and witnesses, and perform a brief physical, neurologic, hemodynamic, and device assessment (eg, pacemaker, venous access). Repeat testing includes electrocardiogram (ECG), a chest radiograph, complete blood count, troponin I or T, brain natriuretic peptide, (BNP; or N-terminal BNP), chemistries, coagulation studies, liver function tests, and arterial blood gases. (See 'Immediate post-cardiac arrest assessment and testing' above and 'Reassessment of cardiac arrest etiology' above.)
•We also typically assess (or reassess) the need for coronary revascularization (immediate or delayed) as well as the need for other interventions (eg, pericardial drain, permanent pacemaker, and central venous and arterial access). (See 'Assessing the need for immediate coronary revascularization' above and 'Assess need for other immediate interventions' above.)
●General critical care management – General critical care management is aimed at ensuring continued hemodynamic stability. This includes the following (see 'General critical care management' above):
•Mechanical ventilation – Most patients who survive SCA are intubated and mechanically ventilated. We suggest targeting normal CO2 and oxygen levels rather than other strategies (eg, permissive hypercapnia) during the initial post-arrest period (Grade 2C). Typical targets are arterial CO2 tension (PaCO2) 35 to 45 mmHg, peripheral oxygen saturation (SpO2) between 94 and 96 percent, and arterial oxygen tension (PaO2) between 65 and 100 mmHg, understanding that therapeutic hypothermia may falsely lower the PaCO2 and raise the PaO2. (See 'Airway, ventilation, and oxygen targets' above.)
•Hemodynamic support – Fluid therapy and vasopressor support should be adjusted to maintain euvolemia and adequate perfusion during the post-arrest period. Typical targets are a systolic blood pressure of 90 mmHg and mean arterial pressure of 65 mmHg. For most patients who require vasopressor therapy, we suggest norepinephrine as the first-line vasopressor (Grade 2C). (See 'Hemodynamic monitoring and goals' above.)
•Bundled care – Patients should receive bundled care including (see 'General supportive care' above):
-Ventilator-associated pneumonia prevention measures. We suggest careful vigilance and monitoring and reserving antibiotics for patients with clinical concern for pneumonia rather than administering prophylactic antibiotics for the prevention of pneumonia (Grade 2C). (See 'Antibiotic therapy and prophylaxis' above and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Prevention'.)
-Stress ulcer prophylaxis. (See "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention".)
-Venous thromboembolism prophylaxis. (See "Prevention of venous thromboembolic disease in acutely ill hospitalized medical adults".)
-Physical therapy. (See "Post-intensive care syndrome (PICS)".)
-Nutrition. (See "Nutrition support in critically ill patients: An overview".)
-Glycemic control measures. (See "Glycemic control in critically ill adult and pediatric patients".)
-Transfusions if indicated. (See "Use of blood products in the critically ill", section on 'RBC indications'.)
•It is important to discuss the patient's wishes with the family/health care proxy and establish goals of care early. (See 'Antibiotic therapy and prophylaxis' above and 'Early discussion of the patient's wishes' above.)
●Active temperature control – The purpose of active temperature control (ATC) is the avoidance of harm associated with fever based upon data that suggest a mortality and neurologic benefit.
•Indications – For patients who achieve ROSC following arrest due to ventricular fibrillation and pulseless ventricular tachycardia but do not initially have purposeful neurologic activity on examination, we recommend ATC rather than no ATC (Grade 1B). In randomized trials in this population, ATC reduced mortality and improved neurologic outcomes. For patients with ROSC following nonshockable rhythms (eg, pulseless electrical activity and asystole), we suggest ATC (Grade 2C). The efficacy of ATC in this setting is less certain, but observational data suggest a possible benefit. (See 'Active temperaturte control' above and 'Efficacy' above.)
•Setting the target temperature – We suggest a target temperature between 33 and 37.5°C rather than higher or lower targets (Grade 2C). Patient-specific factors may influence whether the lower or upper end of the target range is selected. For example, targeted normothermia (eg, 36.4 to 37.5°C) may be preferred in patients with mild brain injury or higher bleeding risk, while targeted hypothermia (eg, 33 to 36°C) may be preferred in those who are not actively bleeding or those with severe brain injury, stroke, subarachnoid hemorrhage, or hepatic encephalopathy. The target temperature typically is maintained using an automated cooling device with a feedback mechanism to achieve rapid cooling. (See 'Initiation' above.)
•Timing – Following ROSC, we typically start ATC as soon as is feasible (ie, within minutes to hours; the earlier the better) but should not delay coronary angiography if needed in the setting of ST segment elevation myocardial infarction. We suggest that ATC be continued for 24 to 48 hours rather than shorter or longer hours (Grade 2C) and be followed by gradual rewarming (0.25 to 0.5°C per hour). Fever should be avoided for an additional 48 hours after ATC is discontinued (See 'Maintenance' above and 'Rewarming' above.)
•Adverse effects – Adverse effects including shivering, bleeding from coagulopathy, arrhythmias, fluid and electrolyte imbalances, and hyperglycemia are managed supportively. (See 'Adverse effects' above.)
●Neurologic considerations – In patients with SCA, hypoxic encephalopathy, cerebral edema, seizure activity, and myoclonic jerks are common and often indicate severe brain injury and a poor prognosis.
•We perform daily examination that also includes assessment of brainstem function. In addition, we typically obtain electroencephalography (EEG) and computed tomography of the brain to assist in this evaluation; collectively, these data can support clinical findings and inform prognosis. Seizures are typically nonconvulsive, clinically subtle, and often require continuous EEG for detection (table 4). (See 'Neurologic considerations' above.)
•Treatment of hypoxic brain injury and cerebral edema are largely supportive. (See "Hypoxic-ischemic brain injury in adults: Evaluation and prognosis" and "Evaluation and management of elevated intracranial pressure in adults", section on 'General management'.)
•Patients with SCA who have clinically apparent seizures require anticonvulsant therapy (table 5 and algorithm 1). Patients are often refractory and need combination therapy to control seizure activity. (See 'Seizures' above and "Nonconvulsive status epilepticus: Treatment and prognosis" and "Convulsive status epilepticus in adults: Management", section on 'Emergency antiseizure treatment'.)
•For patients with myoclonus following SCA, treatment strategies are similar to those in non-SCA-related myoclonus (eg, benzodiazepine for non-epileptiform myoclonus or levetiracetam for epileptiform myoclonus). (See 'Myoclonic jerks' above and "Treatment of myoclonus".)
●Cardiovascular considerations – A cardiologist assessment is important for evaluation and management of cardiac ischemia and other potential cardiac etiologies associated with SCA.
•Electrocardiographs may be followed serially for three days or as needed for suspected ischemic or arrhythmic events. Follow-up echocardiography may also be performed, generally 48 or more hours after cardiac arrest to assess myocardial and valvular function. (See 'Cardiovascular considerations' above and 'Electrocardiography and echocardiography' above.)
•A low threshold should be maintained for performing coronary angiography in those at risk (eg, patients with known pre-existing coronary artery disease, evidence of recurrent ischemia, electrical or hemodynamic instability, or witnessed chest pain prior to SCA). (See 'Cardiovascular considerations' above and 'Assessing the need for immediate coronary revascularization' above and "Cardiac evaluation of the survivor of sudden cardiac arrest" and "Cardiac evaluation of the survivor of sudden cardiac arrest", section on 'Echocardiography'.)
●Prognosis – In patients with SCA, prognosis is generally poor. Prognosis is determined mostly by the extent of hypoxic brain injury but also by several other factors including the reversibility of the underlying etiology for SCA, comorbidities, and complications associated with critical illness (eg, acute respiratory distress syndrome, acute kidney injury). Poor prognostic factors are listed in the table (table 6). (See 'Prognosis' above.)
