Post–cardiac arrest care is a critical component of advanced life support.
Most deaths that follow return of spontaneous circulation (ROSC) occur during the first 24 hours after cardiac arrest.
There is an association between larger numbers of cardiac arrest cases treated at any one hospital and survival of victims admitted to the hospital following cardiac arrest (see Part 4, Systems of Care).
Because multiple organ systems are affected after cardiac arrest, successful post–cardiac arrest care is improved by the development of system-wide plans for proactive treatment of these patients.
Protocolized hemodynamic optimization and multidisciplinary early goal-directed therapy have been introduced as part of a bundle of care.
It is difficult to distinguish between the benefit of protocols and the beneficial effects of any specific component of care.
Cardiac arrest can result from many different diseases.
Hypoxemia, ischemia, and reperfusion that occur during cardiac arrest and resuscitation may cause damage to multiple organ systems, regardless of cause of the cardiac arrest.
Effective post–cardiac arrest care consists of identification and treatment of the precipitating cause of cardiac arrest combined with the assessment and mitigation of ischemia-reperfusion injury to multiple organ systems (see Figure 1).
Programs should include, as part of structured interventions (see Table 1):
Tailor care to the disease and organ system dysfunctions that affect each patient.
If the patient has ROSC, post–cardiac arrest care should be started. Of particular importance are treatment of hypoxemia and hypotension, early diagnosis and treatment of ST-elevation myocardial infarction (STEMI) (Class I, LOE B) (2010 Part 8) and targeted temperature management. (Class I, LOE B) (2010 Part 8) For additional information, see, also, 2015, Targeted Temperature Management in Part 8, Post-Cardiac Arrest Care, 2015 AHA Guidelines Update. (2015 Part 8)
Acute coronary syndrome is a common cause of cardiac arrest.
Coronary angiography should be performed emergently (rather than later in the hospital stay or not at all) for OHCA patients with suspected cardiac etiology of arrest and ST-elevation on ECG.
(Class I, LOE B-NR) (2015 Part 8)
Emergency coronary angiography is reasonable for select (eg, electrically or hemodynamically unstable) adult patients who are comatose after OHCA of suspected cardiac origin but without ST-elevation on ECG. (Class IIa, LOE B-NR) (2015 Part 8)
Coronary angiography is reasonable in post-cardiac arrest patients for whom coronary angiography is indicated, regardless of whether the patient is comatose or awake. (Class IIa, LOE C-LD) (2015 Part 8)
Early invasive approaches are preferred for patients with ST-segment elevation myocardial infarction.
Early invasive approaches also are suggested for treatment of select post–cardiac arrest patients with acute coronary syndromes without ST-elevation.
These recommendations are consistent with recommendations for the treatment of all patients with ST-elevation and non-ST-elevation MI.
The best care for the patient requires separation of decisions about cardiovascular intervention from assessment of neurologic prognosis.
Post–cardiac arrest patients are often hemodynamically unstable.
Avoiding and immediately correcting hypotension (systolic blood pressure less than 90 mm Hg, mean arterial pressure less than 65 mm Hg) during post-resuscitation care may be reasonable. (Class IIb, LOE C-LD) (2015 Part 8)
Targets for other hemodynamic or perfusion measures (such as cardiac output, mixed /central venous oxygen saturation, and urine output) remain undefined in post-cardiac arrest patients. Systematic reviews have thus far not identified specific targets for other variables.
Vasoactive drugs may be administered after ROSC to support cardiac output and may target:
Specific drug infusion rates cannot be recommended because of variations in pharmacokinetics (relation between drug dose and concentration) and pharmacodynamics (relation between drug concentration and effect) in critically ill patients. Commonly used initial dose ranges are listed in Table 2.
Titrate vasoactive drugs at the bedside to secure the intended effect while limiting side effects in the individual patient.
Be aware of the drug concentrations delivered and compatibilities with previously and concurrently administered drugs.
In general, adrenergic drugs should not be mixed with sodium bicarbonate or other alkaline solutions in the IV catheter or tubing because there is evidence that adrenergic agents are inactivated in alkaline solutions.
Administration of norepinephrine (levarterenol) and other catecholamines through a central venous catheter is preferred whenever possible, because tissue necrosis may result if extravasation occurs.
If extravasation of catecholamine develops, infiltrate 5 to 10 mg of phentolamine diluted in 10 to 15 mL of saline into the site of extravasation as soon as possible to reduce tissue injury and sloughing.
β-blockers can blunt heightened catecholaminergic activity that can contribute to arrhythmias, and can reduce ischemic injury and have membrane-stabilizing effects. Conversely, β-blockers can cause or worsen hemodynamic instability, exacerbate heart failure and cause bradyarrhythmias, making their administration after cardiac arrest potentially hazardous.
There is insufficient evidence to support or refute the routine use of a β-blocker early (within the first hour) after return of spontaneous circulation. (2018 ACLS)
Although lidocaine administration following acute myocardial infarction suppressed premature ventricular complexes and non-sustained VT, several studies after acute myocardial infarction noted an association between lidocaine administration and higher mortality, possibly as the result of higher incidence of asystole and bradyarrhythmias. As a result, the routine practice of administering lidocaine after myocardial infarction has been abandoned. Prophylactic lidocaine administration after VF/pVT cardiac arrest was not associated with improved survival but was associated with decreased incidence of ventricular arrhythmias. There was no data identified regarding the effects of prophylactic lidocaine administration following asystole/pulseless electrical activity arrest.
In the absence of contraindications, the prophylactic use of lidocaine may be considered in specific circumstances (such as during emergency medical services transport) when treatment of recurrent VF/pVT might prove to be challenging. (Class IIb, LOE C-LD) (2018 ACLS)
There is insufficient evidence to recommend for or against the routine initiation or continuation of other antiarrhythmic medications after ROSC following cardiac arrest. (2018 ACLS)
For patients who remained comatose following ROSC after VF/pVT OHCA, combined outcome data from 1 randomized and 1 quasi-randomized clinical trial reported increased survival and increased functional recovery with induced hypothermia 32°C to 34°C. For patients with OHCA and non-shockable rhythms, no randomized data were available regarding the use of induced hypothermia to 32°C to 34°C, and observational data were conflicting. No randomized data were available regarding hypothermia following IHCA.
One well-conducted randomized controlled trial found that neurologic outcomes and survival at 6 months after OHCA were not superior when temperature was controlled at 36°C or 33°C. No direct comparisons were found of different durations of targeted temperature management.
We recommend that comatose (ie, lack of meaningful response to verbal commands) adult patients with ROSC after cardiac arrest have targeted temperature management. (Class I, LOE B-R for VF/pVT OHCA; Class I, LOE C-EO for non-VF/pVT [ie, “nonshockable”] and in-hospital cardiac arrest) (2015 Part 8)
There are no patients for whom temperature control somewhere in the range between 32o C and 36o C is contraindicated; in other words, targeted temperature management is appropriate for all patients following ROSC.
Specific features of the patient may favor selection of one temperature over another for targeted temperature management:
Even if the selected target temperature is not achieved during this 24-hour time frame, clinicians should still try to control temperature for at least 24 hours after cardiac arrest.
After the completion of targeted temperature management for a set duration (such as 24 hours), the optimal approach to subsequent temperature management remains unknown. Two studies documented the association of post-ROSC fever and worse outcome, although other studies did not find this association.
Several randomized controlled trials compared post-ROSC use of cold intravenous fluids to induce hypothermia with no cold intravenous fluids. None demonstrated beneficial effect and one study found an increase in pulmonary edema and re-arrest among patients treated with a goal of prehospital infusion of 2 L of cold fluids.
Brain injury is a common cause of morbidity and mortality in post–cardiac arrest patients. Brain injury is the cause of death in 68% of patients after out-of-hospital cardiac arrest and in 23% of patients after in-hospital cardiac arrest.
Clinical manifestations of post–cardiac arrest brain injury may include coma, seizures, myoclonus, various degrees of neurocognitive dysfunction (ranging from memory deficits to persistent vegetative state), and brain death.
An EEG for the diagnosis of seizure should be promptly performed and interpreted, and then should be monitored frequently or continuously in comatose patients after ROSC. (Class I, LOE C-LD) (2015 Part 8)
Note that when patient temperature is below normal, laboratory values reported for Paco2 might be higher than the actual values in the patient.
To avoid hypoxia in adults with ROSC after cardiac arrest, it is reasonable to use the highest available oxygen concentration until the arterial oxyhemoglobin saturation or the partial pressure of arterial oxygen can be measured. (Class IIa, LOE C-EO) (2015 Part 8)
When resources are available to titrate the Fio2 and to monitor oxyhemoglobin saturation, it is reasonable to decrease the Fio2 when oxyhemoglobin saturation is 100%, provided the oxyhemoglobin saturation can be maintained at 94% or greater. (Class IIa, LOE C-LD) (2015 Part 8)
Shortly after ROSC, patients may have peripheral vasoconstriction that makes measurement of oxyhemoglobin saturation by pulse oximetry difficult or unreliable; arterial blood sampling may be required before titration of Fio2.
It is reasonable to consider the titrated use of sedation and analgesia in critically ill patients who require mechanical ventilation or shivering suppression during induced hypothermia after cardiac arrest.(Class IIb, LOE C) (2010 Part 9)
If patient agitation is life-threatening, neuromuscular blocking agents with adequate sedation can be used for short intervals. Caution should be used in patients at high risk for seizures unless continuous electroencephalographic (EEG) monitoring is available.
If neuromuscular blockers are used at all, the duration of use should be minimized, and the depth of neuromuscular blockade should be monitored with a nerve twitch stimulator.
Caution is needed in the use of neuromuscular blocking agents in patients at high risk of seizures unless continuous electroencephalographic (EEG) monitoring is available.
In general, sedative agents should be administered cautiously with daily interruptions, and the sedatives should be titrated to the desired effect.
Shorter-acting sedative medications that can be used as a single bolus or continuous infusion are usually preferred to longer-acting drugs.
It is not known if the provision of corticosteroids during post–cardiac arrest care improves outcome.
In IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and post- arrest hydrocortisone may be considered; however, further studies are needed before recommending the routine use of this therapeutic strategy.(Class IIb, LOE C-LD) (2015 Part 7)
Hemofiltration has been proposed as a method to modify the humoral response to the ischemic-reperfusion injury that occurs after cardiac arrest. but it is not known whether hemofiltration will improve outcome in post–cardiac arrest patients.
Experienced clinicians should select the proper tests and studies for individual patients:
The earliest time for prognostication using clinical examination in patients treated with targeted temperature management, where sedation or paralysis could be a confounder, may be 72 hours after return to normothermia. (Class IIb, LOE C-EO) (2015 Part 8)
We recommend the earliest time to prognosticate a poor neurologic outcome using clinical examination in patients not treated with targeted temperature management is 72 hours after cardiac arrest. (Class I, LOE B-NR) (2015 Part 8)
The time until prognostication can be even longer than 72 hours after cardiac arrest if the residual effect of sedation or paralysis confounds the clinical examination. (Class IIa, LOE C-LD) (2015 Part 8)
Operationally, the timing for prognostication is typically 4.5 to 5 days after ROSC for patients treated with targeted temperature management. This approach minimizes the possibility of obtaining false-positive results (ie, inaccurately suggesting a poor outcome) because of drug-induced depression of neurologic function.
In some instances, withdrawal of life support may occur appropriately before 72 hours because of underlying terminal disease, brain herniation, or other clearly nonsurvivable situations.
Prediction of outcome based on clinical examination may be challenging.
In comatose patients who are not treated with targeted temperature management, the absence of pupillary reflex to light at 72 hours or more after cardiac arrest is a reasonable exam finding with which to predict poor neurologic outcome (False Positive Rate, 0%; 95% CI: 0%–8%). (Class IIa, LOE B-NR) (2015 Part 8)
In comatose patients who are treated with targeted temperature management, the absence of pupillary reflex to light at 72 hours or more after cardiac arrest is useful to predict poor neurologic outcome (False Positive Rate, 1%; 95% CI: 0%–3%). (Class I, LOE B-NR) (2015 Part 8)
We recommend that, given their unacceptable False Positive Rates, the findings of either absent motor movements or extensor posturing should not be used alone for predicting a poor neurologic outcome (False Positive Rate, 10%; 95% CI: 7%–15% to False Positive Rate, 15%; 95% CI: 5%–31%). (Class III: Harm, LOE B-NR) (2015 Part 8)
We recommend that the presence of myoclonus, which is distinct from status myoclonus, should not be used to predict poor neurologic outcomes because of the high False Positive Rate (False Positive Rate, 5%; 95% CI: 3%–8% to False Positive Rate, 11%; 95% CI: 3%–26%). (Class III: Harm, LOE B-NR) (2015 Part 8)
In combination with other diagnostic tests at 72 or more hours after cardiac arrest, the presence of status myoclonus during the first 72 to 120 hours after cardiac arrest is a reasonable finding to help predict poor neurologic outcomes (False Positive Rate, 0%; 95% CI: 0%–4%). (Class IIa, LOE B-NR) (2015 Part 8)
EEG is a widely used tool to assess brain cortical activity and diagnose seizures.
EEG is the standard tool used to assess brain electrical activity (ie, EEG rhythms) and paroxysmal activity (ie, seizures and bursts).
In comatose post–cardiac arrest patients who are treated with targeted temperature management, it may be reasonable to consider persistent absence of EEG reactivity to external stimuli at 72 hours after cardiac arrest, and persistent burst suppression on EEG after rewarming, to predict a poor outcome (False Positive Rate, 0%; 95% CI: 0%–3%). (Class IIb, LOE B-NR) (2015 Part 8)
In comatose post–cardiac arrest patients who are not treated with TTM, it may be reasonable to consider the presence of burst suppression on EEG at 72 hours or more after cardiac arrest, in combination with other predictors, to predict a poor neurologic outcome (False Positive Rate, 0%; 95% CI: 0%–11%). (Class IIb, LOE B-NR) (2015 Part 8)
In patients who are comatose after resuscitation from cardiac arrest regardless of treatment with targeted temperature management, it is reasonable to consider bilateral absence of the N20 somatosensory evoked potential wave 24 to 72 hours after cardiac arrest or after rewarming a predictor of poor outcome (False Positive Rate, 1%; 95% C:, 0%–3%). (Class IIa, LOE B-NR) (2015 Part 8)
Somatosensory evoked potential recording requires appropriate skill and experience, and utmost care is needed to avoid electrical interference from muscle artifacts or from the intensive care unit environment.
Sedative drugs or temperature manipulation affect somatosensory evoked potentials less than they affect the EEG or clinical examination.
In patients who are comatose after resuscitation from cardiac arrest and not treated with targeted temperature management, it may be reasonable to use the presence of a marked reduction of the grey-white ratio on brain computed tomography obtained within 2 hours after cardiac arrest to predict poor outcome. (Class IIb, LOE B-NR) (2015 Part 8)
It may be reasonable to consider extensive restriction of diffusion on brain magnetic resonance imaging at 2 to 6 days after cardiac arrest in combination with other established predictors to predict a poor neurologic outcome. (Class IIb, LOE B-NR) (2015 Part 8)
Acquisition and interpretation of imaging studies have not been fully standardized and are subject to interobserver variability.
The recommendations for brain imaging studies for prognostication are made with the assumption that images are performed in centers with expertise in this area.
Given the possibility of high False Positive Rates, blood levels of neuron-specific enolase and S-100B should not be used alone to predict a poor neurologic outcome.
(Class III: Harm, LOE C-LD) (2015 Part 8)
When performed with other prognostic tests at 72 hours or more after cardiac arrest, it may be reasonable to consider high serum values of neuron-specific enolase at 48 to 72 hours after cardiac arrest to support the prognosis of a poor neurologic outcome (Class IIb, LOE B-NR), especially if repeated sampling reveals persistently high values. (Class IIb, LOE C-LD) (2015 Part 8)
Multiple studies found no difference in immediate or long-term function of organs from donors who reach brain death after cardiac arrest when compared with organs from donors who reach brain death from other causes.
Clifton W. Callaway, Chair; Michael W. Donnino; Ericka L. Fink; Romergryko G. Geocadin; Eyal Golan; Karl B. Kern; Marion Leary; William J. Meurer; Mary Ann Peberdy; Trevonne M. Thompson; Janice L. Zimmerman
Mary Ann Peberdy, Co-Chair*; Clifton W. Callaway, Co-Chair*; Robert W. Neumar; Romergryko G. Geocadin; Janice L. Zimmerman; Michael Donnino; Andrea Gabrielli; Scott M. Silvers; Arno L. Zaritsky; Raina Merchant; Terry L. Vanden Hoek; Steven L. Kronick
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© Copyright 2015 American Heart Association, Inc.