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The post–cardiac arrest syndrome is a highly inflammatory state characterized by organ dysfunction, ischemia and reperfusion injury, and persistent precipitating pathology.
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Patients with ST-elevation myocardial infarction or high suspicion for cardiac etiology should undergo early coronary angiography.
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Multiple trials have shown that active temperature management after cardiac arrest, regardless of rhythm, results in improved outcome.
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After cardiac arrest, arterial oxygen and carbon dioxide
Critical Care of the Post–Cardiac Arrest Patient
Section snippets
Key points
The post–cardiac arrest syndrome
Following ROSC after cardiac arrest, many patients suffer from the post–cardiac arrest syndrome (PCAS), which includes 4 components: (1) brain injury, (2) myocardial dysfunction, (3) systemic ischemia and reperfusion injury, and (4) persistent precipitating pathology.1
Brain injury after cardiac arrest is complex, with underlying pathophysiology that involves excitotoxicity, abnormal calcium homeostasis, free radical formation, pathologic protease cascades, and activation of apoptotic pathways.1
Identifying and addressing etiology
Identifying the etiology of cardiac arrest allows for tailored medical therapy and interventions targeting the underlying condition. All patients should receive an ECG immediately after ROSC to assess for ST-segment elevation myocardial infarction (STEMI).
Temperature management
After multiple preclinical studies, 2 landmark clinical trials demonstrated that treatment with induced mild therapeutic hypothermia improved neurologic outcome after OHCA18, 19 (Table 1). Bernard and colleagues18 randomized patients with ventricular fibrillation (VF) or ventricular tachycardia (VT) OHCA to receive therapeutic hypothermia at 33°C or normothermia for 12 hours. They demonstrated an improvement from 26% to 49% in neurologically intact survival to hospital discharge among the 43
Oxygenation
Preclinical studies found that reducing the fraction of inspired oxygen (Fio2) after cardiac arrest decreases neuronal injury and oxidative stress.34, 35, 36 Clinical studies have demonstrated mixed results. A retrospective analysis of more than 6000 patients in a large critical care database found that Pao2 greater than or equal to 300 mm Hg was associated with an 18% absolute increase in hospital mortality compared with patients who were maintained within the normal range.37 Hypoxemia was
Hemodynamics
Given the propensity for hemodynamic lability and the sensitivity of the brain to additional ischemia after cardiac arrest, careful hemodynamic monitoring is essential. The authors recommend invasive arterial blood pressure monitoring and central venous access for comatose cardiac arrest survivors with evidence of hemodynamic compromise. Pulmonary artery catheters and cardiac output monitoring may be considered but have not been shown to improve outcome.2 The authors also recommend early
Prognostication
Withdrawal of life-sustaining therapy (WLST) is the most common cause of death for patients admitted after OHCA.76 Accurate prognostication is, therefore, imperative. Most prognostication tools offer insight into which patients are likely to have poor neurologic recovery, whereas few tools help clinicians predict who will awaken (Table 3).
Summary
Critical care after cardiac arrest should focus on restoring normal physiology, limiting further injury, and optimizing neurologic outcome. Key aspects include identifying and addressing etiology, restoring adequate hemodynamics and organ perfusion, TTM, maintenance of normal oxygen and carbon dioxide tensions and prevention of lung injury, and multimodal prognostication (see Fig. 1).
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Cited by (17)
Electroacupuncture attenuates brain injury through α7 nicotinic acetylcholine receptor-mediated suppression of neuroinflammation in a rat model of asphyxial cardiac arrest
2022, Journal of NeuroimmunologyCitation Excerpt :Asphyxial cardiac arrest (CA), although with a low incidence, is associated with a high mortality rate and a poor neurological prognosis. Despite advances in cardiopulmonary resuscitation (CPR) methods, the neurological recovery after CA is still unsatisfactory (Geocadin et al., 2017; Stoecklein and Youngquist, 2018; Walker and Johnson, 2018). It is necessary to reduce neurological complications and promote functional recovery after CPR.
Management of temperature control in post-cardiac arrest care: an expert report
2021, Medicina IntensivaThe optimal peripheral oxygen saturation may be 95–97% for post-cardiac arrest patients: A retrospective observational study
2021, American Journal of Emergency MedicineCitation Excerpt :The optimal SpO2 during the first 24 h for patients admitted to the intensive care unit with ROSC after CA may be 95–97%. Optimal oxygenation is paramount important for PCA care [6]. Hypoxemia is one of the causes of CA, so avoiding hypoxemia after ROSC is strongly recommended by guidelines [31].
Post-cardiac arrest syndrome
2020, AACN Advanced Critical CareCitation Excerpt :The goal MAP should be guided by the patient’s underlying physiology and cause of the cardiac arrest. Hypotension should be avoided because it worsens ischemia-reperfusion injury and ROS.3 Blood pressure support can be managed with fluids, blood administration if needed, vasopressors, and mechanical hemodynamic support (namely, intra-aortic balloon pump or extracorporeal life support) if needed.
Disclosure: N.J. Johnson receives funding from the National Institutes of Health (U01HL123008-02) and Medic One Foundation. A.C. Walker has nothing to disclose.