Sudden cardiac death

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]

• Sudden cardiac death (SCD) is a natural, rapid, unexpected death secondary to cardiac causes within an hour of symptom onset in witnessed scenarios, and within a day in unwitnessed cases ^[1].
• The case definitions of sudden cardiac death in clinical registries or epidemiological research vary based on the use of death certificates,^{[2] [3] [4] [5]} reviews of EMS^[5] or hospital records^[6],^{[7] [8][9][10]} or whether the cases met the criteria of epidemiological definitions (eg, World Health Organization),^[11]society definitions (eg, Cardiac Arrest Registry to EnhanceSurvival [CARES]),^[12] outcomes of clinical trials,^[13][14] or the definition required in pathology-based studies.^[15][16][17] Because most individuals who died from sudden cardiac death do not have autopsies to confirm the underlying cause, sudden cardiac death is typically presumed to be of cardiac etiology.^[18]
• Sudden cardiac arrest (SCA) is the unexpected cessation of pumping blood into vital organs due to electrical disturbance in the pathway of sinoatrial node (SA node), atrioventricular node (AV node), His Purkinje fibers or cardiac pumping failure due to cardiogenic shock, massive pulmonary thromboembolism,fulminant myocarditis, and ruptured left ventricular free wall.
• Out-of-hospital cardiac arrests are “events that occur out of the hospital in which an emergency medical services (EMS) rescuer detects no signs of circulation or mechanical cardiac activity.”^[12][19]
• Without any intervention for immediate restoration of the circulation, biologic death will happen minutes to weeks after cardiac arrest. Sudden cardiac death in the United States ranges from 300,000 to 400,000 which is 50% of all causes of deaths. ^[20] In-hospital cardiac arrest happens in 290,000 adults every year in the United States. The most common cause of sudden cardiac death is coronary artery disease and atherosclerosis. The presence of underlying disorders such as malignancy or liver disease at the time of cardiac arrest makes the condition worse. Patients with acute myocardial infarction and in-hospital cardiac arrest with shockable rhythm have a better prognosis. Post cardiopulmonary resuscitation state management should be focused on neurologic complications, hemodynamic stability, and respiratory support.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]

Sudden cardiac arrest (SCA) may be caused by underlying cardiac abnormality including coronary artery abnormality , hypertrophy of myocardium, myocardial disease, valvular heart disease, congenital heart disease, abnormality in conducting system and electrical instability. The type of cardiac disease that is associated with sudden cardiac death (SCD) depends on the age of the individual ^{[1] [2] [3] [4] [5] [6] [7] [8]}.

• Cardiac causes of sudden cardiac death (SCD) depend on the age of the individual ^{[1] [2] [3] [4] [5] [6] [7] [8]}.
• Children/adolescents/young adults (≤35–40 years)In young people: Inhertid cardiomyopathies (HCM, arrhythmogenic, dilated/noncompaction), myocarditis/inflammatory heart disease, primary electrical disease/channelopathies (LQTS,Brugada,CPVT; WPW/conduction disease), congenital/non-atherosclerotic coronary abnormalities (anomalous coronaries, myocardial bridging/spasm), sudden arrhythmic death syndrome/ autopsy-negative sudden unexplained death, and (in some series) early coronary artery disease/ACS. ^{[1] [2] [3] [4] [5] [6] [7] [8]}.
• Autopsy-based studies demonstrate that 55% to 69% of young adults with sudden cardiac death have underlying cardiac causes, including sudden arrhythmic death syndrome (normal heart by autopsy, common in athletes) and structural heart disease such as coronary artery disease. ^[9]
• Combined data from 4 autopsy-based studies worldwide that include 529 presumed sudden cardiac deaths among those aged 14 through 44 years, with autopsy rates ranging from 43% to 100%, demonstrated that cardiac causes accounted for 64% of sudden deaths.
• Young adults—important noncardiac mimics presenting as “cardiac arrest/SCD”: Drug/medication toxicity/overdose, pulmonary embolism, subarachnoid hemorrhage/other acute neurologic catastrophe, seizure, anaphylaxis, and infection/sepsis (including cases with documented VT/VF or heart block but extracardiac cause at autopsy).^[9]
• Over a 3-year study period (2011-2014), autopsies of 32 persons aged 18 through 39 years with presumed sudden cardiac deaths in San Francisco demonstrated that 40% had a noncardiac cause.^[10] Even when a lethal rhythm is documented at the time of sudden death, including VT or VF ^[11]or complete heart block,^[10] be due to underlying noncardiac causes, such as intracranial hemorrhage or drug overdose.
• 4th decade (~30–40s) and older “masters” athletes: coronary artery disease—often presenting as acute coronary syndrome—predominates.^[3],^{[12] [13]}

• Elderly: acquired structural heart disease predominates—coronary heart disease/ischemic scar plus non‑ischemic structural disease (e.g., cardiomyopathy/hypertrophy, valvular disease).^[14][2]

• Coronary artery disease (22% of all presumed suddencardiac deaths)
• Sudden arrhythmic death syndrome (16%)
• Hypertrophic cardiomyopathy (12%)
• Cardiomyopathy (11%)^[10],^[15],^[16],^[17]

• Neurological (9.3%)
• Pulmonary (8.1%)
• Drug overdose (4.7%)
• Infection (4.7%)^[10],^[15],^[16],^[17]

• The distribution of underlying causes of sudden cardiac arrest in resuscitated patients differs from those who were not resuscitated (ie, sudden cardiac death) with significantly more noncardiac causes in the latter.^[18]
• >50% of young adults with presumed sudeen cardiac death had identifiable cardiovascular risk factors such as hypertension and diabetes.^[9]
• 2% to 22% of young adult survivors of outside hospital cardiac arrest had genetic cardiac disease such as long QT syndrome or dilated cardiomyopathy, which is a lower yield than for nonsurvivors (13%-34%) with autopsy-confirmed sudden cardiac death.^[9]

• The number 1 cause of out-of-hospital cardiac arrest in the US among adults between 25 to 35 years is CAD (43%), followed by sudden unexplained death (14%).^[19]
• According to a Canadian study, the most common etiologies of cardiac arrest among 131 individuals aged 25 through 34 years were structural heart disease (including cardiomyopathy and myocarditis) and sudden unexplained death, each accounting for 28%.^[20]
• Among hospitalizations in the US for overdoses, opioid associated out-of-hospital cardiac arrest increased from 1% of hospitalizations in 2000 to 2% in 2013,47,48 although recent CDC data show a decrease in opioid overdose deaths from 84181 in 2022 to 81083 in 2023.^[21]
• Positive drug toxicology was reported in 17.1% of out-of hospital cardiac arrests among persons aged 1 to 50 years(median,42.4years) in an Australian study from April 2019 to April 2021.^[22]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]

• The diagnosis of sudden cardiac arrest (SCA) is made when the following diagnostic criteria are met: the absence of a palpable pulse of the heart due to abrupt cessation of pump function, absent carotid pulse,gasping respiration or no respiration, loss of consciousness due to cerebral hypoperfusion.

• The case definitions of sudden cardiac death vary based on the use of death certificates,^{[1] [2] [3] [4]} reviews of EMS^[4] or hospital records^[5],^{[6] [7][8][9]} or whether the cases met the criteria of epidemiological definitions (eg, World Health Organization),^[10]society definitions (eg, Cardiac Arrest Registry to EnhanceSurvival [CARES]),^[11] outcomes of clinical trials,^[12][13] or the definition required in pathology-based studies.^[14][15][16]
• Sudden cardiac death is typically presumed to be of cardiac etiology because most individuals who died from sudden cardiac death do not have autopsies to confirm the underlying cause.^[17]
• A person resuscitated from an out-of-hospital cardiac arrest to hospitalization is classified as having resuscitated out-of-hospital cardiac arrest,regardless of subsequent in-hospital death or survival to discharge, the latter of whom are sudden cardiac arrest survivors.

• The diagnosis of SCA is made when the following diagnostic criteria are satisfied:

• Absence of a palpable pulse of the heart due to cessation of pumping function whether with prompt intervention will be reversible ^[18]
• Absent carotid pulse^{[19][20][21][22]}
• Gasping respiration or no respiration
• Loss of consciousness due to cerebral hypoperfusion

• Following an initial diagnosis of cardiac arrest, healthcare professionals further categorize the diagnosis based on the ECG rhythm.
• There are 4 rhythms that result in a cardiac arrest. Ventricular fibrillation (VF) and Pulseless Ventricular tachycardia (VTach) are both responsive to a defibrillator and so are colloquially referred to as Shockable rhythms, whereas Asystole and Pulseless Electrical Activity (PEA) are non-shockable.
• The nature of the presenting heart rhythm suggests different causes and treatment and is used to guide the rescuer as to what treatment may be appropriate^[25] (see Advanced Life Support and Advanced Cardiac Life Support, as well as the causes of arrest (below))
• The table below provides information on the differential diagnosis of sudden cardiac death in terms of ECG appearance:

Disease Name	Causes	ECG Characteristics	ECG view
Ventricular tachycardia [26][27][28][29][30]	Ischemic heart disease Illicit drug use such as cocaine and methamphetamine Structural heart diseases Electrolyte disturbances Congestive heart failure Myocarditis Obstructive sleep apnea Pulmonary artery catheter Long QT syndrome	Ventricular tachycardia (VTach originates from a ventricular focus. Lasts more than 30 seconds. Broad QRS complexes: rate of >90 BPM.	[31]
Ventricular fibrillation [32][33][34][35]	Acute coronary ischemia Cardiomyopathies Congenital heart disease Myocardial infarction Heart surgery Electrolyte abnormalities	Poorly identifiable QRS complexes and absent P waves The heart rate is >300 BPM Rhythm is irregular	[36]
Ventricular flutter [37][38][39]	Electrolyte disturbances Medications such as: Disopyramide Quinidine	The ECG shows: A typical sinusoidal pattern Frequency of 300 bpm	[40]
Asystole [41][42]	Hypovolemia Hypoxia Acidosis Hypothermia Hyperkalemia or Hypokalemia Hypoglycemia Cardiac Tamponade Tension pneumothorax Thrombosis Myocardial infarction Thrombosis Pulmonary embolism Cardiogenic shock Degeneration of the sinoatrial or atrioventricular nodes Ischemic stroke	There is no electrical activity in the asystole	[43]
Pulseless electrical activity [44][45]	Hypovolemia Hypoxia Hydrogen ions (Acidosis) Hypothermia Electrolyte disturbances Hypoglycemia Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers Tamponade Tension pneumothorax Thrombosis (Myocardial infarction) Thrombosis (Pulmonary embolism) Trauma (Hypovolemia from blood loss)	Several ppattern are possible including: Normal sinus rhythm Sinus tachycardia, with discernible P waves and QRS complexes Bradycardia, with or without P waves	[46]
Torsade de Pointes [47][48][49]	*Electrolyte disturbances Medications such as: Amiodarone Azithromycin Clozapine Famotidine Flecainide Foscarnet Levofloxacin Lithium Mirtazapine Quetiapine Risperidone Tacrolimus Tamoxifen Ziprasidone	Paroxysms of VTach with irregular RR intervals. A ventricular rate between 200 and 250 beats per minute. Two or more cycles of QRS complexes with alternating polarity. Changing the amplitude of the QRS complexes in each cycle in a sinusoidal fashion. Prolongation of the QT interval. Is often initiated by a PVC with a long coupling interval, R on T phenomenon. There are usually 5 to 20 complexes in each cycle.	[50]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]

Common risk factors related to underlying coronary artery disease (CAD) and inherited causes in the development of sudden cardiac arrest (SCA) are hypertension, male gender ,diabetes mellitus, hyperlipidemia, obesity, smoking, older age, obstructive sleep apnea (OSA) due to hypoxia, early ventricular fibrillation (VF) (within 48 hours of ACS increasing in-hospital mortality five times), early repolarization patten in early phase of myocardial infarction (MI), and family history of sudden death.

• Common risk factors related to underlying coronary artery disease and inherited causes in the development of SCA are:^[1]

• Hypertension
• Male gender
• Diabetes mellitus
• Hyperlipidemia
• Obesity
• Smoking
• Older age
• Obstructive sleep apnea due to hypoxia
• Early VF (within 48 hours of ACS increasing in-hospital mortality five times)
• Early repolarization patten in early phase of MI^[2]
• Family history of premature death (sudden and unexpected) before age 50 attributed to heart disease in > 1 relative, presence of heart disease in close relative less than age 50, presence of ion channelopathies in family members

Generally, athletes are considered healthier than young adults in the general population. In studies of children and young adults, incidence of sudden death in athletes was reported to be low at approximately 1 per 100000 person-years.^[3],^[4] However in a prospective study of 11168 adolescent soccer players (mean age, 16.4 years, 95% male) in the English Football Association cardiac screening program from 1996 through 2016, the incidence of sudden death was 6.8 per 100000 person-years.^[5] Most common cause of cardiac arrests in young athletes are:

1. Sudden arrhythmic death syndrome
2. Coronary anomalies
3. Myocarditis
4. Valvular disease.^[3],^[6]

A meta-analysis evaluating sudden cardiac death etiology in individuals younger than 35 years from 2010 through 2020 demonstrated that the following cardiac conditions were more common among athletes than nonathletes: hypertrophic cardiomyopathy(11.9%vs3.9%;P = .002),dilated cardiomyopathy (3.6% vs 0.8%; P = .047), and anomalous coronary arteries (7.2% vs 1.9%; P = .009).^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]

• Sudden cardiac arrest (SCA) occurs due to sudden disturbance in cardiac electrical propagation or failure of the heart to pumping the blood into vital organs.
• Patients may progress to develop cardiac arrest, sudden collapse, loss of effective circulation, and loss of consciousness.
• Prompt treatment is needed to prevent death which may occur within minutes to weeks, and prevent serious complications.
• Prognosis of in-hospital cardiac arrest is generally better than out-of- hospital cardiac arrest and the 1-year survival rate of patients who survived to hospital discharge was approximately 25% in the GWTG-R registry.
• A retrospective cohort study from the CARES registry reported 101968 out-of-hospital cardiac arrests in the US between 2006 and 2013, approximately 6% of the incidents occurred among individuals between 20 through 39 years; survival rate to hospital discharge ranged from 11%(30-39years) to 16%(20-24years).^[1] Approximately 85% to 95% of out-of-hospital cardiac arrest survivors were discharged with good neurological outcome, as defined by a Cerebral Performance Categories scale of 1 or 2.^{[1] [2]}
• The overall survival rate of young adults experiencing out-of-hospital cardiac arrest was 9% in a US study from 2005 through 2007 involving 665 persons aged 20 through 39 years, and increased to 34.8% for those with bystander-witnessed VT or VF who were more likely to receive prompt initial cardiopulmonary resus citation (CPR) or automated external defibrillator use.^[3]
• In an Australian registry conducted between 2000 and 2009 involving 3912 patients with ages between 16 and 39 years with out-of-hospital cardiac arrest,the survival rate was 8.8%.^[2]

• Sudden cardiac arrest (SCA) in the early clinical stages should be given prompt treatment to prevent progression to sudden cardiac death (SCD.
• Early clinical features include abrupt palpitation, presyncope, syncope, chest pain, dyspnea, hypotension within one hour before terminal event.
• If left untreated or failed resuscitation, death may occur within minutes to weeks.

• Cardiac arrest is the third leading cause of coma.
• Approximately 80% of patients who suffered a cardiac arrest who survived to be admitted to the hospital will be in coma for varying lengths of time.
• Of these patients, approximately 40% will enter into a persistent vegetative state and 80% die within 1 year.
• In contrast, those rare patients who survive until discharge without significant neurological impairment can expect a fair to good quality of life.
• The duration of hypoxia/ischemia determines the extent of neuronal injury
• In patients who suffer hypoxia for less than 5 minutes, are less likely to have permanent neurologic deficits, while with prolonged, global hypoxia, patients may develop myoclonus or a persistent vegetative state.^[4]
• The duration of coma is an important predictor of the recovery of neurologic function. ^[5].
• There was minimal neurologic deficit if coma lasted less than 24 hours.
• The severity of neurological impairment increased with duration of coma.

• Patients who had the initial absence of pupillary light reflexes did not recover independent functioning (52 patients, 25% of patients)^[5].
• In contrast, patients who had the initial presence of pupillary light reflexes, the development of spontaneous eye movements that were roving conjugate or better, and the presence of either extensor, flexor, or withdrawal responses to pain had a 41% chance of regaining independent function (of the 27 patients in this group, 11 (41%) regained independence).^[5].
• In a study by Snyder et al, the absence of corneal or pupillary light reflexes at 3 hours after cardiac arrest was associated with death in all patients ^[6][7]. By 6 hours, all the patients who survived had the presence of three brainstem reflexes: pupillary light reflex, corneal reflex, and reflex eye movements.
• The absence of spontaneous limb movements and the absence of withdrawal to pain in the early hours is a poor prognostic sign.
• The presence of either decorticate or decerebrate posturing is a poor prognostic sign.
• Frequent myoclonic jerking is associated with a poor prognosis.
• The presence of seizures in the initial 24 hours is modestly associated with outcomes: 53% of patients who seize survive compared to 70% of those who do not seize during the first day^[8].

• Most patients who survive become alert by 24-48 hours.
• In one series, of those patients who were in a coma through day 2, only 2 of the 27 (7%) survived.^[9] In a second series, no patient who remained in a coma by the third day survived.^[10]
• Absent motor responses, the presence of posturing (extensor /flexor motor responses) and the lack of spontaneous eye movements that were either orienting or roving conjugate was associated with a lack of independent recovery in 92 of 93 patients. ^[5].
• In contrast, of the 30 patients who showed improvement in their eye-opening responses, obeyed commands or had withdraw to pain, 19 (63%) regained independent function.^[5].
• Seizures that occur after the initial 24 hours are associated with poorer outcomes. In one study only 3 of 15 patients who seized recovered consciousness, and only one patient lived a year^[11]. The presence of status epilepticus at any time following cardiac arrest is associated with a very poor prognosis as all nine patients with status epilepticus died in one series.^[12]
• The absence of spontaneous eye-opening and intermittent visual fixation by the end of the first day is associated with a poor prognosis.
• Although eye-opening is necessary for a good outcome, it alone is not sufficient, as many patients who have spontaneous eye-opening still go on to have a poor prognosis. * Roving eye movements in the absence of visual fixation is often indicative of extensive bilateral cerebral hemispheral damage and portends a poor prognosis.
• If the gaze is sustained in an upward direction, this carries a poor prognosis as well.^[13][14]

• Prognosis of in-hospital cardiac arrest is generally better than out-of-hospital cardiac arrest and the 1-year survival rate of patients who survived to hospital discharge was approximately 25% in the GWTG-R registry.^[15].Survival after out of hospital cardiac arrest and in hospital cardiac arrest has continued to improve over time according to the guideline.
• 60% to 78% of young adults hospitalized after resuscitation from sudden cardiac arrest do not survive to hospital discharge.^[16],^[3],^[17] This in-hospital mortality rate is similar to that of older adults who were resuscitated to hospitalization (≈65%).^[18]
• The 10-year survival rate of sudden cardiac arrest survivors aged 40 years or younger was 90% in an Australian registry.^[19]The rate of recurrent arrest (both out of and in the hospital) or death in survivors aged 18 to 39 years in a Swedish registry was approximately 15% a year after the out-of-hospital cardiac arrest.^[20]

One-year overall mortality of subcutaneous ICD recipients aged 15 to 34 years was 4.3% in one cohort,90 whereas the VT or VF recurrence rate estimated by subcutaneous ICD recording in secondary prevention recipients (age not reported) in a separate study was 9.9% at 1year and15.8% at 3years.^[21]

• Factors associated poor prognosis after in-hospital cardiac arrest include:^[22][23]

• Age > 70 years old
• Concomitant underlying disorders such as pneumonia, hypotension, renal dysfunction, hepatic dysfunction
• Non shockable rhythm such as asystole or pulseless electrical activity

• Factors associated with better prognosis after in-hospital cardiac arrest include:

• Early detection of cardiac arrest or being witnessed during arrest
• Shockable rhythm such as VF, VT
• Women between 15-45 years old^[24]
• Rapid intervention with a defibrillator increases survival rates.^[25][26]

• 58% survival rate was reported by the US Commotio Cordis Registry in 216 persons with sudden cardiac arrest due to commotio cordis (cardiac arrest due to VF triggered by blunt chest trauma) (age range, 0.2-51 years;mean,15years, 95% male) from 2006 through 2012.^[27]
• Prompt resuscitation and participation in organized competitive sports was associated with higher survival rates. Multivariate analysis identified participation in recreational sports with lower survival (odds ratio [OR] compared with organized competitive sports, 0.33; 95%CI,0.16-0.67) and onsite automated external defibrillator with higher survival (OR, 4.61; 95% CI, 1.43-14.88).^[27]
• Individuals aged 18 to 35 years with sports-related sudden cardiac arrest in Germany and France showed improved survival to hospital discharge with public automated external defibrillator use prior to EMS arrival (OR, 6.25; 95% CI, 1.48 43.20); individuals with sudden cardiac arrest who received both immediate bystander CPR and automated external defibrillator had 91%survival.^[28]
• A recent meta-analysis demonstrated that in sports related sudden cardiac arrest, bystander presence (OR, 2.55; 95%CI, 1.48-4.37), bystander CPR (OR, 3.84; 95% CI, 2.36-6.25), and bystander automated external defibrillator use (OR, 5.25; 95%CI,3.58-7.70) were associated with improved survival.^[29]

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Patients with anoxic injury due to cardiac arrest are at risk of death from a variety of causes including recurrent sudden cardiac death, congestive heart failure, pneumonia, sepsis from a variety of sources and pulmonary embolism.

Out-of-hospital cardiac arrest (OHCA) has a worse survival rate (2-8% survival at discharge) than in-hospital cardiac arrest (15% survival at discharge).

A major determining factor in survival is the initially documented electrocardiographic rhythm. Patients with ventricular fibrillation (VF) or ventricular tachycardia (VT) (aka VT/VF) have a 10-15 fold greater chance of survival than patients with pulseless electrical activity (PEA) or asystole. VT and VF are responsive to defibrillation, whereas asystole and PEA are not.

Cardiac arrest is the third leading cause of coma. Approximately 80% of patients who suffered a cardiac arrest who survived to be admitted to the hospital will be in coma for varying lengths of time. Of these patients, approximately 40% will enter into a persistent vegetative state and 80% die within 1 year. In contrast, those rare patients who survive until discharge without significant neurological impairment can expect a fair to good quality of life.

The duration of hypoxia/ischemia determines the extent of neuronal injury i.e. in patients who suffer hypoxia for less than 5 minutes, are less likely to have permanent neurologic deficits, while with prolonged, global hypoxia, patients may develop myoclonus or a persistent vegetative state.^[1]

The duration of coma is an important predictor of the recovery of neurologic function. In a 1979 study of 181 cardiac arrest patients who survived to hospital admission, 84% were comatose for more than 1 hour and 56% were comatose for more than 24 hours^[2]. There was minimal neurologic deficit if coma lasted less than 24 hours. However, among the 85 patients who were comatose for more than 24 hours, only 7 of them were discharged alive. The severity of neurological impairment increased with increased duration of coma. Of the patients who were in coma for more than 7 days, none regained consciousness. It should be noted that 80 patients died in a coma.

A JAMA article in 1985 attempted to identify the multivariate predictors neurologic prognosis in 210 patients with coma due to cerebral hypoxia. A total of 13% of patients regained neurologic function and independent function at some time during the first year.

• Most patients who survive become alert by 24-48 hours. In one series, of those patients who were in a coma through day 2, only 2 of the 27 (7%) survived.^[3] In a second series, no patient who remained in a coma by the third day survived.^[4]
• Absent motor responses, the presence of posturing (extensor /flexor motor responses) and the lack of spontaneous eye movements that were either orienting or roving conjugate was associated with a lack of independent recovery in 92 of 93 patients. ^[2].
• In contrast, of the 30 patients who showed improvement in their eye-opening responses, obeyed commands or had withdraw to pain, 19 (63%) regained independent function.^[2].
• Seizures that occur after the initial 24 hours are associated with a poorer outcomes. In one study only 3 of 15 patients who seized recovered consciousness, and only one patient lived a year^[5]. The presence of status epilepticus at any time following cardiac arrest is associated with a very poor prognosis as all nine patients with status epilepticus died in one series.^[6]
• The absence of spontaneous eye opening and intermittent visual fixation by the end of the first day is associated with a poor prognosis. Although eye opening is necessary for a good outcomes, it alone is not sufficient, as many patients who have spontaneous eye opening still go on to have a poor prognosis. Roving eye movements in the absence of visual fixation is often indicative of extensive bilateral cerebral hemispheral damage and portends a poor prognosis. If the gaze is sustained in an upward direction, this carries a poor prognosis as well.^[7]

In a 1990s study from the UK, resuscitation for cardiac arrest was attempted in 10,081 patients. Of these only 1476 (14.6%) survived to be admitted to the hospital ^[8][9]. Of these small number of patients who survived to admission, 59.3% died during that admission, half of these within the first 24 hours. 46.1% survived to hospital discharge (this is 6.75% of those who had been resuscitated by ambulance staff). Of those who were successfully discharged from hospital, 70% were still alive 4 years after their discharge.

In a review of 68 studies through 1997, the incidence of survival to discharge was higher at 14% with a wide range of 0-28%.^[10]

[[Category:Needs overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]

The mainstay of therapy for patients with cardiac arrest is starting cardiopulmonary resuscitation (CPR) with minimizing interruption in chest compression. The rhythm should be reassessed. If the rhythm is ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), the shock should be delivered immediately. If the rhythm is asystole or pulseless electrical activity (PEA), CPR should be resumed. Advanced life support (ALS) should be kept with minimizing interruption in chest compression including: advanced airway, continuous chest compressions, capnography, intravenous (IV) intraosseous/ (IO) access, vasopressors, and antiarrhythmic therapy. This can address reversible causes such as hypoxia, hypovolemia,hypothermia, hyperkalemia, hypokalemia,acidosis, tension pneumothorax, tamponade, toxins (benzodiazepines, alcohol, opiates, tricyclics, barbiturates, betablockers, calcium channel blockers), thrombosis ST elevation myocardial infarction (STEMI, and massive pulmonary thromboembolism). The following should be considered immediately in post cardiac arrest patients: 12–lead electrocardiogram (ECG) ,perfusion/reperfusion in patients with acute myocardial infarction,(AMI), oxygenation and ventilation, temperature controlling, and treatment of reversible causes. Management of patients in post-cardiac arrest status include treatment of the underlying disorder, hemodynamic stability, respiratory support, and control of neurologic complications.

A critical component of therapy for patients with cardiac arrest is starting cardiopulmonary resuscitation (CPR) with minimizing interruption in chest compression.^[1][2] The 2025 AHA Guidelines reaffirm that high-quality CPR is the single most critical intervention for a patient in cardiac arrest, with a chest compression rate of 100 to 120 compressions per minute and a compression depth of at least 5 cm (2 inches) but not greater than 6 cm (2.4 inches) in adults.^[3]

CPR and use of automated external defibrillators (AED) increase the chances of survival with improved neurological and functional outcomes ^{[4] [5] [6] [7] [8] [9] [10]}. Bystander CPR is provided in approximately 47.7% of adult out-of-hospital cardiac arrests (OHCA), and an AED is applied by a bystander in approximately 7.9% of cases. Survival to hospital discharge for OHCA is approximately 10.5%, with favorable neurological outcome in approximately 8.2%.^[3]

Acute termination of acute coronary syndrome (ACS)-related arrhythmias can be achieved through defibrillation or electrical cardioversion ^{[11] [12]}.

The 2025 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care provide comprehensive, updated recommendations for the resuscitation and management of adults experiencing cardiac arrest, respiratory arrest, and life-threatening cardiovascular emergencies.^[13][14] These guidelines supersede the 2020 AHA Guidelines and the 2023 AHA Focused Update on Adult Advanced Cardiovascular Life Support.^[15]

Key updates regarding vasopressor therapy (2025 AHA):

Epinephrine has been upgraded from Class 2b (2020 AHA) to Class 1 (2025 AHA) based on consistent and compelling evidence from previous RCTs, cohort, and registry studies supporting a potent effect on ROSC, survival to hospital admission, and survival to hospital discharge.^[13]

Earlier administration of epinephrine is associated with improved ROSC. A post-hoc analysis of the PARAMEDIC2 trial found that the effectiveness of epinephrine, compared to placebo, converges at approximately 20 minutes of pulselessness.^[13]

Multiple systematic reviews and meta-analyses have found no difference in survival outcomes when comparing vasopressin alone or vasopressin combined with epinephrine versus epinephrine alone.^[13]

The IVIO trial (2025) compared initial intraosseous versus intravenous vascular access in 1479 adults with out-of-hospital cardiac arrest and found no significant difference in sustained ROSC (30% vs. 29%; risk ratio 1.06; 95% CI, 0.90–1.24; P=0.49), 30-day survival (12% vs. 10%), or 30-day survival with favorable neurologic outcome (9% vs. 8%).^[16]

Key points regarding antiarrhythmic therapy (2025 AHA):

In the ROC-ALPS trial, amiodarone and lidocaine each improved survival to hospital admission over placebo, but there was no difference in survival to hospital discharge. In the subset of patients with witnessed cardiac arrest, survival to hospital discharge was higher with amiodarone or lidocaine compared with placebo.^[17]

Data are insufficient to definitively distinguish between the effectiveness of lidocaine and amiodarone, nor their benefit when given in combination.^[13]

No new evidence emerged from a 2025 ILCOR evidence update regarding the use of other parenteral antiarrhythmic agents in cardiac arrest, including bretylium, sotalol, procainamide, and beta blockers (for which ILCOR found insufficient evidence to recommend for or against use).^[13]

A large multicenter, blinded, placebo-controlled randomized trial of in-hospital cardiac arrest deploying corticosteroids bundled with a vasopressor agent found an improved rate of ROSC but not survival to hospital discharge or neurological outcome.^[13]

Key ECPR trial data:

The ARREST trial (single-center) was stopped early for benefit favoring ECPR.^[18]

The INCEPTION trial (2023) compared ECPR with conventional CPR in patients with refractory OHCA due to ventricular arrhythmia across 10 Dutch centers and did not demonstrate a statistically significant difference in survival with favorable neurologic outcome.^[19]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]

See also Post cardiac arrest syndrome care pathway

Post-cardiac arrest care (PCAC) is a critical component of the chain of survival and demands a comprehensive, structured, multidisciplinary system of care. The following sections are organized according to the 2025 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (Part 11: Post-Cardiac Arrest Care),^[1] the 2025 AHA Executive Summary,^[2] the 2023 AHA Focused Update on Adult Advanced Cardiovascular Life Support,^[3] the 2024 AHA/Neurocritical Care Society Scientific Statement on Critical Care Management of Patients After Cardiac Arrest,^[4] the 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death,^[5] the 2022 ESC Guidelines for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death,^[6] the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes,^[7] and the 2025 ACC/AHA/ASE/HFSA/HRS/SCAI/SCCT/SCMR Appropriate Use Criteria for Implantable Cardioverter-Defibrillators, Cardiac Resynchronization Therapy, and Pacing.^[8]

Hypotension and shock occur in at least two thirds of patients after cardiac arrest.Closing </ref> missing for <ref> tag

Key trial data regarding temperature control:

TTM2 trial (2021): Randomized 1900 patients to 33°C or to normothermia with early treatment of fever (37.8°C) for 28 hours after randomization. There was no difference in the primary outcome of Cerebral Performance Category 1 or 2 at 6 months.^[3][10]

CAPITAL CHILL trial: Randomized 389 patients to moderate (31°C) versus mild (34°C) therapeutic hypothermia for 24 hours. The primary outcome of mortality or poor neurological outcome (Disability Rating Scale score >5) at 6 months did not differ across arms.^[3]

HYPERION trial (2019): Randomized 584 patients with both in- and out-of-hospital cardiac arrest with an initial nonshockable rhythm. Found a higher percentage of participants surviving with a favorable neurologic outcome compared with targeted normothermia, but there was no significant difference in mortality.^[11]

A 2023 updated ILCOR systematic review incorporating 6 additional randomized trials found no difference in survival when applying temperature control at 32°C to 34°C versus 36°C or normothermia; however, the confidence intervals did not exclude a potential beneficial effect of temperature control at colder temperatures. None of the included trials found worse outcomes with lower temperature goals.^[9]

An individual patient data meta-analysis of the TTM2 and HYPERION trials found no difference between hypothermic and normothermic temperature control in patients with nonshockable rhythms.^[11][9]

Seizures and status epilepticus are common acute neurologic complications in the post-cardiac arrest period, occurring in 10% to 35% of patients who do not follow commands after ROSC.Closing </ref> missing for <ref> tag

No MCS device has demonstrated positive results specifically in cardiac arrest patients in randomized trials. MCS use after cardiac arrest should not be routine; in selected patients with cardiogenic shock based on advanced hemodynamic phenotyping, MCS can be considered, balancing the risk of post-arrest severe hypoxic brain injury.^[12]

Hypoxic-ischemic brain injury is the leading cause of morbidity and mortality in patients who achieve ROSC after OHCA.Closing </ref> missing for <ref> tag

Key evidence for secondary prevention ICD:

A meta-analysis using individual patient data from the AVID, CASH, and CIDS trials comparing ICD therapy versus amiodarone demonstrated a significant reduction in death from any cause with the ICD (hazard ratio 0.72; 95% CI: 0.60–0.87; P = 0.006). This 28% reduction in relative risk of death was almost entirely due to a 50% reduction in risk of arrhythmic death. Patients with an LVEF ≤35% derived significantly more benefit from ICD therapy than those with more preserved LV function.^[8]

Although the evidence supporting ICD therapy for secondary prevention is based on randomized trials performed more than 20 years ago, more contemporary registries and observational studies in clinical practice support these findings.^[8]

In patients who present with sustained ventricular arrhythmias and a transient or reversible cause (such as acute myocardial infarction, electrolyte abnormalities, or proarrhythmia due to medication), initial treatment should be directed at the underlying disorder and a thorough evaluation is warranted. However, it is often difficult to exclude primary arrhythmic etiologies. In the AVID trial, patients identified as having “potentially transient or potentially correctable” causes of VT/VF remained at high mortality risk.^[8]

Among persons presenting with VF due to acute myocardial infarction with coronary plaque rupture and/or thrombus (typically <48 hours), risk of a recurrent event is reduced after early revascularization; ICD is generally not indicated for secondary prevention in this setting.^[13]

An alternative to conventional ICD with transvenous leads is a subcutaneous ICD, in which the lead is tunneled subcutaneously instead of passing through the blood vessels. Subcutaneous ICDs have fewer long-term lead-related complications than conventional ICDs and may be reasonable for younger patients with primary arrhythmia syndromes. However, conventional transvenous ICDs are recommended for patients who require pacing for bradyarrhythmias, cardiac resynchronization therapy with coronary sinus lead, or antitachycardia pacing for VT (ESC Class IIa, LOE B).^[13][6]

Catheter ablation is an important therapeutic option for the management of recurrent ventricular tachycardia in cardiac arrest survivors, particularly those with ischemic cardiomyopathy.^[6][5]

Key trial data regarding catheter ablation versus antiarrhythmic drugs:

VANISH2 trial (2025): An international randomized trial of 416 patients with prior myocardial infarction and clinically significant ventricular tachycardia, all with an ICD, compared first-line catheter ablation versus antiarrhythmic drug therapy (sotalol or amiodarone based on prespecified clinical criteria). The primary endpoint was a composite of death from any cause, VT storm, appropriate ICD shock, or sustained VT treated by medical intervention (all >14 days after randomization). Over a median follow-up of 4.3 years, a primary endpoint event occurred in 50.7% of patients assigned to catheter ablation versus 60.6% assigned to drug therapy (hazard ratio 0.75; 95% CI: 0.58–0.97; P = 0.03). Adverse events within 30 days after the procedure included death in 1.0% and nonfatal adverse events in 11.3% of the ablation group, compared with death attributed to drug therapy in 0.5% and nonfatal adverse events in 21.6% of the drug therapy group.^[14]

VANISH2 substudy (2026): A prespecified substudy stratified outcomes by drug eligibility. In the sotalol-eligible stratum (199 patients), catheter ablation resulted in a lower risk of the primary composite endpoint compared with sotalol (46% vs. 59%; HR 0.64; 95% CI: 0.43–0.94; P = 0.02). In the amiodarone-eligible stratum (217 patients with more severe heart disease or VT storm), catheter ablation and amiodarone had comparable efficacy for the primary endpoint (55% vs. 61%; HR 0.86; 95% CI: 0.61–1.22; P = NS). However, patients allocated to amiodarone had approximately 3-fold higher noncardiac death (5.6% vs. 16.5%), 2-fold higher respiratory failure (4.6% vs. 11.0%), and a 4.6% incidence of pulmonary fibrosis/infiltrate (vs. 0%) compared with ablation.^[15]

Despite ICD implantation, cardiac arrest survivors remain at risk of spontaneous VT or VF, with a reported recurrence rate of 37% during a 2-year follow-up. Adjunctive pharmacotherapy (especially amiodarone) or catheter ablation may be used in combination with ICD.^[13]

Survivors of cardiac arrest experience emotional, social, physical, neurological, and cognitive sequelae, which can manifest during or after hospitalization. Survivorship is the journey from stabilization through rehabilitation, recovery, and societal reintegration.Closing </ref> missing for <ref> tag

Key points regarding recovery and survivorship:

Approximately one fourth of cardiac arrest survivors and their caregivers experience emotional distress, including anxiety, depression, and posttraumatic stress. Fatigue is also common and may be related to distress and physical and cognitive symptoms. These symptoms often begin during hospitalization and can persist from months to years.^[9]

Cognitive impairments, particularly in memory, attention, and executive function, are common in cardiac arrest survivors. Physical, neurological, and cardiopulmonary impairments are also prevalent.^[9]

Community reintegration and return to work or other daily activities may be slow and depend on availability of social support and degree of post-arrest sequelae. Survivors and caregivers need direction on managing their post-arrest challenges and returning to daily activities.^[9]

An RCT of semistructured cognitive, medical, and psychosocial support offered to adult OHCA and IHCA survivors for 6 months after discharge demonstrated significant improvement in multiple domains of quality of life at 12 months compared with no intervention, and was found to be potentially cost-effective.^[16]

Clinically significant depression has been reported in 8% to 45%, anxiety in 13% to 42%, and posttraumatic stress disorder (PTSD) in 19% to 27% of cardiac arrest survivors. In the longest follow-up reported (up to 8 years), PTSD was noted in 27% of survivors, with these individuals also reporting lower quality of life, more limited self-care, and more pain and depressed mood.^[17]

Patients with cardiac arrest make up an important pool of potential organ donors because cardiac arrest is common and a substantial proportion of those who cannot recover are still able to donate.Closing </ref> missing for <ref> tag

Extracorporeal perfusion can be initiated after failed CPR specifically to facilitate uncontrolled DCD in patients deemed to have no possibility of recovery. In the United States, the default position is an opt-in approach in which patients are presumed not to be organ donors unless they have specified a wish to do so. Ethical considerations include maintaining public trust, ensuring that decisions for end-of-life care are made independently of organ donation considerations, and equitable distribution of resources.^[18]

Sudden cardiac death is a leading cause of death in patients with heart failure with reduced ejection fraction (HFrEF). ICD therapy for primary prevention is recommended in select patients with reduced LVEF despite guideline-directed medical therapy (GDMT).^[5][6][1]