Highlights & Basics
- Cardiac arrest is a sudden state of circulatory failure due to a loss of cardiac systolic function.
- The most common shockable rhythms associated with cardiac arrest are pulseless ventricular tachycardia and ventricular fibrillation.
- The most common underlying causes are ischemic heart disease and myocardial infarction. In some settings, cardiac arrest is the result of respiratory arrest triggered by opioid toxicity.
- Presentation is usually sudden and manifests as loss of consciousness but can be preceded by chest pain or dyspnea.
- Treatment is through implementing the algorithms for basic and advanced cardiac life support, depending on the provider's level of training.
- The overall survival from cardiac arrest, especially unwitnessed, is poor and, among early survivors, is fraught with complications of many organ systems due to ischemic injury (i.e., multisystem organ failure).
Quick Reference
History & Exam
Key Factors
patient unresponsive
absence of normal breathing
absence of circulation
cardiac rhythm disturbance
Other Factors
Diagnostics Tests
1st Tests to Order
continuous cardiac monitoring
CBC
serum electrolytes
ABG
cardiac biomarkers
point of care ultrasound (POCUS)
Other Tests to consider
ECG
coronary angiography
echocardiogram
exercise stress testing
chest x-ray
toxicology screen
cardiac magnetic resonance imaging
coronary computed tomography angiography
signal-averaged ECG (SAECG)
electrophysiologic study
Treatment Options
presumptive
unwitnessed cardiac arrest
CPR
acute
shockable rhythms (pulseless ventricular tachycardia or ventricular fibrillation)
CPR and defibrillation
epinephrine (adrenaline)
anti-arrhythmic
magnesium
Definition
Classifications
Advanced cardiovascular life support pulseless arrest algorithm
- Shockable rhythms (pulseless ventricular tachycardia and ventricular fibrillation), and
- Nonshockable rhythms (pulseless electrical activity and asystole).
Vignette
Common Vignette
Other Presentations
Epidemiology
Etiology
Pathophysiology
Diagnostic Approach
Clinical assessment
- Preceding symptoms: chest pain may indicate myocardial ischemia or pulmonary embolism. Syncopal episodes may indicate structural heart disease or pre-existing arrhythmias. Palpitations may indicate pre-existing arrhythmias. One study found that among individuals with symptomatic OHCA, chest pain and dyspnea in men, and dyspnea in women, were the most common symptoms and had a moderate association with sudden cardiac arrest when compared with a control group of individuals who also called emergency services.[46]
- Past medical history: potential causes include coronary artery disease (CAD) and its associated risk factors (e.g., hypertension, diabetes mellitus, smoking, hypercholesterolemia, obesity), left ventricular dysfunction, hypertrophic cardiomyopathy, long QT syndrome, structural heart disease, use of illicit substances, medications (including those that cause QT prolongation or diuretics that cause electrolyte disturbances), kidney disease (which may lead to hyperkalemia), and history of eating disorders (which may contribute to hypokalemia and/or hypophosphatemia).[40] Risk factors for deep vein thrombosis (DVT) and pulmonary embolism (PE) may increase the suspicion of PE as the etiology; these include prior DVT/PE, unilateral calf swelling, active cancer, recent surgery, recent immobilization, pregnancy, coagulopathy, or oral contraception use.
- Family history of sudden cardiac arrest: may be due to familial QT-interval prolongation syndromes or familial cardiomyopathies. A family history of CAD may also be present.
Investigations
- Patients require continuous cardiac monitoring to assess rhythm.
- A CBC should be performed to look for signs of hemorrhage (e.g., low hematocrit), which may cause hypovolemia. An acute bleed may not show up, however, if hemodilution has not yet occurred.
- Serum electrolytes should be checked for abnormalities, particularly hyper- or hypokalemia; these may occur as either a cause or consequence of cardiac arrest.
- Arterial blood gas (ABG) measurement is essential to assess acid-base status and may reveal respiratory acidosis, metabolic acidosis, respiratory acidosis with renal compensation, metabolic acidosis with respiratory compensation, mixed metabolic and respiratory acidosis, or hyperkalemia. Respiratory and metabolic parameters should be optimized as necessary to normalize acid-base status. Abnormal results may be a result of sudden cardiac arrest itself rather than the underlying cause.
- Cardiac biomarkers may be measured. However, elevations in markers of myocardial infarction (MI) may be a result of sudden cardiac arrest and do not necessarily mean that the underlying cause was an MI.
- Point of care ultrasound (POCUS) may be used as an adjunct for patient evaluation during cardiac arrest, so long as it does not interfere with standard cardiac arrest treatments.[1] [47] International Liaison Committee on Resuscitation guidelines recommend against its routine use, but suggest that if it can be performed by experienced staff without interrupting CPR, it can be used to look for a specific suspected reversible cause.[48] POCUS can be used to identify the presence or absence of cardiac activity, and can also identify features of cardiac tamponade, pneumothorax, hemorrhage, or pulmonary embolism. As these are potentially reversible causes of cardiac arrest, this could alter subsequent management. However, there is evidence that the use of POCUS in cardiac arrest prolongs the length of interruption of CPR during pulse checks.[48] [49] [50]
- An ECG should be performed immediately after ROSC, then subsequently to assess for evolving changes. Abnormalities that may be seen include prolonged QT interval, ST-segment or T-wave changes (indicating ischemia or infarction in the event of ST-segment elevation), conduction abnormalities, ventricular hypertrophy, QRS prolongation in V1 through V3 and/or epsilon waves in cardiomyopathy, and T-wave inversion in V1 through V3 in arrhythmogenic right ventricular dysplasia (ARVD). Ambulatory ECG monitoring can be useful to capture sporadic events, either by continuous monitoring (Holter recording) over 24-48 hours, or using patient-activated ECG recorders (mobile health or smart phone technology) for infrequent events.[6]
- Coronary angiography should be considered after achieving ROSC, as coronary disease is a predisposing factor for sudden cardiac arrest. In patients with ST-elevation MI (STEMI) on ECG, emergency coronary angiography, with or without percutaneous coronary intervention should be performed.[1] [6] [48] Emergency coronary angiography is also reasonable for select patients with suspected acute coronary syndrome without ST elevation, including those with hemodynamic/electrical instability or signs of ongoing ischemia.[1] However, several randomized controlled trials in patients without signs of STEMI have shown no benefit in clinical outcomes for early coronary angiography, compared with delayed angiography.[6] [51] [52] International Liaison Committee on Resuscitation guidelines suggest that in patients without signs of STEMI, either early or delayed coronary angiography is reasonable.[48] PCI should only be performed in patients with culprit lesions on coronary angiography. Unnecessary PCI of stable lesions should be avoided in the early phase after OHCA, given the absence of benefit and increased risk of hemorrhagic complications and stent thrombosis in the setting of sudden cardiac arrest.[53] [54]
- Echocardiography can be used to assess cardiac contractility and check for structural abnormalities, valvular disorders and for evidence of tamponade. Left ventricular function should also be assessed 48 hours after ROSC, after the period of post-arrest myocardial stunning.[55] A normal imaging study in patients with ventricular arrhythmia suggests a primary electrical disorder.[6]
- Exercise stress testing is useful for diagnosing and measuring response to treatment in patients with adrenergic-dependent rhythm disturbances, such as exercise-induced idiopathic monomorphic ventricular tachycardia (VT) or polymorphic VT. The 4-minute recovery QT interval after exercise testing can contribute to the diagnosis of long QT syndrome.[6] [56]
- Chest x-ray may reveal pneumothorax, pulmonary edema, or other disorders of the lungs. The thoracic cage may show causes of, or complications from, cardiac arrest. Endotracheal tube placement should be evaluated if the patient is intubated.
- A toxicology screen may be considered to rule out illicit substances that may predispose to ventricular arrhythmia.
- Cardiac magnetic resonance imaging is used to identify ARVD or other primary cardiomyopathies. It is the preferred test to identify these disorders and should be done if other causes of sudden cardiac arrest are not discovered.
- Coronary computed tomography angiography can be used to rule out coronary artery stenosis in patients who have a low probability of coronary artery disease.[6]
- Signal-averaged ECG: may also be used to identify ARVD if other causes of sudden cardiac arrest are not discovered. Late potentials suggest the diagnosis.[6]
- Electrophysiologic studies: evaluation of primary arrhythmia or conduction abnormalities should be considered if no other cause of sudden cardiac arrest is found, or if there is potential for ablation of an arrhythmogenic source in patients with prior MI. Electrophysiologic studies will delineate the arrhythmogenic focus.[6] [57] [58]
- Screening of family members of patients with suspected or confirmed heritable syndromes, such as Brugada syndrome, long QT syndrome, and dilated or hypertrophic cardiomyopathy.[6]
- Provocative tests can also be considered, such as sodium channel blocker testing for Brugada syndrome and adenosine testing to exclude latent pre-excitation.[6]
Risk Factors
History & Exam
Tests
Criteria
- Ventricular tachycardia (VT): ≥3 consecutive complexes originating in the ventricles at a rate >100 bpm. Sustained VT lasts >30 seconds or results in hemodynamic compromise.
- Monomorphic VT: VT with a stable single QRS morphology from beat to beat.
- Polymorphic VT: VT with a changing QRS morphology from beat to beat.
- Torsades de pointes: VT in setting of a prolonged QT interval, with waxing and waning of QRS amplitude.
- Ventricular fibrillation: rapid, grossly irregular electrical activity with marked variability in waveform; ventricular rate usually >300 bpm (cycle length <200 milliseconds).
Screening
Treatment Approach
Shockable rhythms (pulseless VT and VF)
Nonshockable rhythms (PEA and asystole)
Postresuscitation care
- Simple ice packs with or without wet towels
- Cooling blankets or pads
- Water- or air-circulating blankets
- Water-circulating gel-coated pads
- Transnasal evaporative cooling
- Intravascular heat exchanger
- Extracorporeal circulation.
Termination of resuscitation
- EMS did not witness the arrest
- The patient had no ROSC before transport
- No shock was administered before transport.
- Arrest was not witnessed
- No bystander CPR was provided
- The patient had no ROSC before transport
- No shock was administered before transport.
- Delayed initiation of CPR in unwitnessed cardiac arrest
- Unsuccessful resuscitation after 20 minutes of ACLS guideline-directed therapy
- Conditions that compromise the safety of the emergency care providers.
Treatment Options
unwitnessed cardiac arrest
CPR
Comments
- Circulation of the blood by means of CPR is a demonstrated therapy in patients with sudden cardiac arrest and is thought to work by raising intrathoracic pressure, as well as providing direct cardiac compression.[106]
- Each cycle: 30 compressions (at a rate of 100-120 compressions/minute) and 2 breaths for a total of 5 cycles (2 minutes).[1] The compression depth should be at least 2 inches (5 cm). Full chest wall recoil should be allowed between chest compressions. Interruptions in compressions should be minimized.[1] [48]
- American Heart Association guidelines specify that compressions should be performed as the first priority.[1] Untrained lay-rescuers should perform compression-only CPR.[1] If a rescuer is trained in using compressions and ventilation, it is reasonable to do rescue breaths in addition to chest compressions.[1] [48]
- The patient should be transferred to an emergency care setting as soon as possible.
shockable rhythms (pulseless ventricular tachycardia or ventricular fibrillation)
CPR and defibrillation
Comments
- Circulation of the blood by means of CPR is a demonstrated therapy in patients with sudden cardiac arrest and is thought to work by raising intrathoracic pressure, as well as providing direct cardiac compression.[106]
- Each cycle: 30 compressions (at a rate of 100-120 compressions/minute) and 2 breaths for a total of 5 cycles (2 minutes).[1] The compression depth should be at least 2 inches (5 cm). Full chest wall recoil should be allowed between chest compressions. Interruptions in compressions should be minimized.[1]
- Defibrillation in the setting of pulseless ventricular tachycardia or ventricular fibrillation can restore normal sinus rhythm and should be initiated promptly, as its success diminishes over time.[107]
- For a witnessed arrest, electrical defibrillation should be attempted as soon as possible, not necessarily after 5 cycles (2 minutes) of CPR.[1]
- For unwitnessed out-of-hospital cardiac arrest (OHCA), 5 cycles (2 minutes) of CPR before defibrillation yields more favorable outcomes.[108]
- CPR should be re-started immediately after defibrillation rather than doing an immediate post-shock rhythm check.[1]
- Guideline recommendations are 120-200 J for biphasic defibrillators and 360 J for monophasic defibrillators.[1]
epinephrine (adrenaline)
Primary Options
- epinephrine (adrenaline)
1 mg intravenously/intraosseously every 3-5 minutes; consult specialist for guidance on endotracheal dose
- epinephrine (adrenaline)
Comments
- Given as soon as possible and every 3-5 minutes thereafter.[1]
- Epinephrine is a potent agonist of alpha- and beta-adrenergic receptors.
- The use of epinephrine during cardiac arrest has been shown to increase the rate of achieving return of spontaneous circulation and to increase short-term survival.[67] [68] [69] [70] However, epinephrine use during cardiac arrest has not been shown to lead to significantly improved neurologic outcomes, and may lead to higher rates of severe neurologic impairment among survivors.[67] [68] [69] [70]
- Endotracheal drug administration may be considered when other drug routes are unavailable; however, this leads to unpredictable drug concentrations and is not recommended in the UK.[1]
anti-arrhythmic
Primary Options
- amiodarone
300 mg intravenously/intraosseously as a single dose initially, followed by 150 mg as a single dose if required
- amiodarone
- lidocaine
1 to 1.5 mg/kg intravenously/intraosseously as a single dose initially, followed by 0.5 to 0.75 mg/kg every 5-10 minutes, maximum 3 mg/kg total dose
- lidocaine
Comments
- Amiodarone or lidocaine can be considered for pulseless ventricular tachycardia (VT)/ventricular fibrillation (VF) that is unresponsive to defibrillation.[1] There is evidence that both amiodarone and lidocaine independently increase the rate of return of spontaneous circulation in the setting of pulseless VT/VF refractory to defibrillation, but ultimately lead to no significant difference in the rate of survival to hospital discharge.[109]
- Amiodarone is predominantly a class III anti-arrhythmic agent that also has alpha- and beta-adrenergic blocking properties.
- Use of lidocaine in VT/VF is predominantly based on studies showing its efficacy in suppressing ventricular arrhythmias following acute myocardial infarction.
magnesium
Primary Options
- magnesium sulfate
2 g intravenously as a single dose over 5-10 minutes
- magnesium sulfate
Comments
- In patients with sudden cardiac arrest due to torsades de pointes, giving magnesium may restore a perfusing cardiac rhythm.[82]
nonshockable rhythms (pulseless electrical activity or asystole)
CPR and epinephrine
Primary Options
- epinephrine (adrenaline)
1 mg intravenously/intraosseously every 3-5 minutes; consult specialist for guidance on endotracheal dose
- epinephrine (adrenaline)
Comments
- Circulation of the blood by means of CPR is a demonstrated therapy in patients with sudden cardiac arrest and is thought to work by raising intrathoracic pressure, as well as providing direct cardiac compression.[106]
- Each cycle: 30 compressions (at a rate of 100 compressions/minute) and 2 breaths for a total of 5 cycles (2 minutes).[1]
- Epinephrine is a potent agonist of alpha- and beta-adrenergic receptors. The use of epinephrine during cardiac arrest has been shown to increase the rate of achieving return of spontaneous circulation and to increase short-term survival.[67] [68] [69] [70] However, epinephrine use during cardiac arrest has not been shown to lead to significantly improved neurologic outcomes, and may lead to higher rates of severe neurologic impairment among survivors.[67] [68] [69] [70]
- Endotracheal drug administration may be considered when other drug routes are unavailable; however, this leads to unpredictable drug concentrations and is not recommended in the UK.[1]
return of spontaneous circulation
postresuscitation care
Comments
- Should be instigated immediately and involves continued monitoring, organ support, correction of electrolyte imbalances and acidosis, safe transfer to a critical care environment, and identification and correction of risk factors and underlying causes.
- A 12-lead ECG is recommended immediately after return of spontaneous circulation to determine whether signs of ST-elevation myocardial infarction (STEMI) are present.[1] In patients with STEMI, emergency coronary angiography, with or without percutaneous coronary intervention, should be performed.[1] Emergency coronary angiography is also reasonable for select patients with suspected acute coronary syndrome without ST elevation, including those with hemodynamic/electrical instability or signs of ongoing ischemia.[1]
- Anoxic brain injury is a frequent complication of sudden cardiac arrest. One systematic review of the literature demonstrates that targeted temperature management (TTM) protocols improve survival and neurologic outcome following resuscitation from sudden cardiac arrest, with guidelines continuing to support their use.[1] [88] [89] There remains controversy regarding which target temperature is optimal, with more recent evidence suggesting that maintaining normothermia (i.e., avoidance of fever) may be equivalent to targeting hypothermia. One large randomized controlled trial (TTM2) which studied patients with coma after OHCA found no difference in 6 month survival or neurologic outcome in patients treated with hypothermia (target temperature of 91.4°F [33°C]) compared with normothermia (target temperature ≤99.5°F [≤37.5°C]).[90] An earlier trial (TTM) found that a targeted temperature of 91.4°F (33°C) conferred no benefit compared with 96.8°F (36°C).[91]
- For comatose adult patients with return of spontaneous circulation (ROSC), current American Heart Association (AHA) and European guidelines recommend targeting a temperature between 89.6°F and 96.8°F (32°C and 36°C) for at least 24 hours, and avoiding fever for at least 72 hours after ROSC.[1] [92] In light of the TTM2 trial results, however, the AHA has published an advisory statement recommending that controlling patient temperature to <37.5°C is a reasonable and evidence-based approach for unresponsive post-cardiac arrest patients with characteristics similar to those included in the TTM2 trial (i.e., OHCA of cardiac or unknown cause, excluding those with unwitnessed asystole).[93] This brings US guidelines in line with current International Liaison Committee on Resuscitation guidelines, which recommend actively preventing fever by targeting a temperature of ≤99.5°F (≤37.5°C), commenting that the benefits of targeting hypothermia between 89.6°F and 93.2°F (32°C and 34°C) in selected subpopulations of patients remains uncertain.[48]
- TTM has 3 phases: induction, maintenance, and rewarming. Induction and/or maintenance can be achieved by: simple ice packs with or without wet towels, cooling blankets or pads, water- or air-circulating blankets, water-circulating gel-coated pads, transnasal evaporative cooling, intravascular heat exchanger, extracorporeal circulation.[92]
- Rewarming should be achieved slowly (0.45°F to 0.90°F [0.25°C to 0.50°C] of rewarming per hour) to avoid rebound hyperthermia, which is associated with worse neurologic outcomes.[92]
- There is evidence that patients who receive post-resuscitation care at specialized centers have higher rates of neurologically intact survival, suggesting that post-resuscitative treatment should ideally be performed in this setting.[94] [95] Cardiac arrest centers have been shown to display higher coherence with guidelines compared with noncardiac arrest centers.[96]
- In-patient neurologic rehabilitation may be helpful for survivors who have suffered hypoxic-ischemic brain injury, although specific guidelines and evidence are lacking in this patient population.[92] Many patients will also be eligible for cardiac rehabilitation programs, which have been shown to reduce cardiovascular mortality and hospital admissions, and improve quality of life. They are mostly generic programs, in which patients with different cardiac diseases (e.g., post acute coronary syndrome, heart failure, or post cardiac surgery), can participate. They involve exercise training, risk factor management, lifestyle advice, education, and psychological support.[92]
- Long-term management focuses primarily on prevention of recurrence. Patients should abstain from toxic substances. Use of implantable cardioverter-defibrillators (ICDs) has shown a significant reduction in mortality compared with antiarrhythmic drug therapy in the secondary prevention of sudden cardiac arrest.[6] [97]
no return of spontaneous circulation
continue or consider termination of resuscitation
Comments
- The decision to terminate resuscitation is an ethically challenging issue when treating patients for whom spontaneous circulation does not return in a timely fashion. There is no single factor that can determine when to terminate resuscitative efforts; rather it should be a decision of clinical judgment and respect for human dignity. In prehospital settings where Basic Life Support (BLS) Emergency Medical Services (EMS) are providing care, and Advanced Life Support (ALS) providers are not available or will be significantly delayed, resuscitation may be terminated based on a validated rule if all of the following criteria are met: EMS did not witness the arrest; the patient had no ROSC before transport; and no shock was administered before transport.[1] [98] [99]
- In the prehospital setting where ALS EMS are providing care, resuscitation may be terminated based on a validated rule if all of the following criteria are met: arrest was not witnessed; no bystander CPR was provided; the patient had no ROSC before transport; and no shock was administered before transport.[1]
- Resuscitative measures should be terminated if there is documentation that the patient has a valid "do not resuscitate" order. Termination of resuscitative measures may also be considered on the basis of the following parameters: delayed initiation of CPR in unwitnessed cardiac arrest, unsuccessful resuscitation after 20 minutes of advanced cardiac life support guideline-directed therapy, or conditions that compromise the safety of the emergency care providers.
- After sudden OHCA with unsuccessful resuscitation, organ donation may be considered, but is commonly overlooked. Data from a single-center study in the UK suggest that only 39% of patients who did not recover after OHCA were referred for organ donation. Of those who were referred, consent was obtained in only 68%, and 25% actually went on to donate an average of 1.9 organs per patient.[104] One review by the International Liaison Committee on Resuscitation found that numerous barriers and logistical challenges exist to setting up systems that support organ donation after cardiac arrest; the authors recommend that all health systems should develop, implement, and evaluate protocols designed to optimize organ donation opportunities in this situation.[105]
Emerging Tx
Extracorporeal cardiopulmonary resuscitation
Prevention
Primary Prevention
- Patients with hypertrophic cardiomyopathy (HCM) and two or more of the following risk factors: syncope, left ventricular thickness >3 cm, abnormal blood pressure response to exercise (hypotension), nonsustained ventricular tachycardia (VT), and family history of sudden cardiac death. Patients with only 1 risk factor should be counseled and considered on a case-by-case basis.[27]
- Patients with arrhythmogenic right ventricular dysplasia (ARVD) and extensive disease of the right ventricle, involvement of the left ventricle, history of syncope, or family history of sudden cardiac arrest.
- Patients with congenital long QT syndrome (LQTS) who have a history of cardiac arrest, are symptomatic on beta-blocker therapy and genotype-specific therapies, or who are asymptomatic but have a high-risk profile (based on the 1-2-3 LQTS Risk Calculator).[6]
- Patients with Brugada syndrome and a history of syncope with ST-segment elevations in leads V1 through V3 or documented VT.[37]
Secondary Prevention
Follow-Up Overview
Prognosis
Monitoring
Complications
Citations
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Key Articles
Other Online Resources
Referenced Articles
Guidelines
Diagnostic
Summary
The guidelines provide a methodologic framework for investigating the potential underlying cause of sudden cardiac arrest. This involves extensive laboratory work, imaging studies, coronary angiography, and possibly electrophysiologic studies or genetic testing as appropriate.Published by
American College of Cardiology; American Heart Association; Heart Rhythm Society
Published
2017
Summary
Guidelines for the recognition, treatment, and prevention of cardiac arrest in the perioperative period.Published by
European Society of Anaesthesiology and Intensive Care and the European Society for Trauma and Emergency Surgery
Published
2023
Summary
This guideline is an update to the European Society of Cardiology 2015 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. The update includes new insights into epidemiology, new evidence on genetics, imaging, and risk stratification, and advances in diagnostic and management strategies.Published by
European Society of Cardiology
Published
2022
Treatment
Summary
Overview of the epidemiology, pathophysiology, management, and post-resuscitation care of opioid-associated cardiac arrest.Published by
American Heart Association
Published
2021
Summary
Updated recommendations on adult cardiovascular life support.Published by
American Heart Association
Published
2020
Summary
The guidelines provide a methodologic framework for investigating the potential underlying cause of sudden cardiac arrest. This involves extensive laboratory work, imaging studies, coronary angiography, and possibly electrophysiologic studies or genetic testing as appropriate.Published by
American College of Cardiology; American Heart Association; Heart Rhythm Society
Published
2017
Summary
Guidelines on the management of cardiac arrest due to poisoning by various medications/illicit substances.Published by
American Heart Association
Published
2023
Summary
American Heart Association advice for temperature management in cardiac arrest survivors.Published by
American Heart Association
Published
2023
Summary
A practical guide to enhance in-hospital care of cardiac patients which emphasizes the adoption of a systematic, multimodal approach to neuroprognostication.Published by
Canadian Cardiovascular Society
Published
2023
Summary
Recommendations on management of cardiac arrest, including hot topics within BLS and ACLS.Published by
International Liaison Committee on Resuscitation
Published
2022
Summary
An updated position paper to address questions regarding temperature management in the post-cardiac arrest patient.Published by
Advanced Life Support Task Force of the International Liaison Committee on Resuscitation; American Heart Association Emergency Cardiovascular Care Committee; Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation
Published
2015
Summary
Consensus recommendations for resuscitation suitable for European healthcare professionals trained in resuscitation techniques.Published by
European Resuscitation Council
Published
2021
Summary
Guidelines providing recommendations on the prevention of and advanced life support treatments for in-hospital and out-of-hospital cardiac arrest.Published by
European Resuscitation Council
Published
2021
Summary
Guidelines providing recommendations on the care of patients after cardiac arrest, including the role of coronary angiography, blood pressure targets, targeted temperature management, prognostication, and rehabilitation.Published by
European Resuscitation Council; European Society of Intensive Care Medicine
Published
2021
Summary
This guideline is an update to the European Society of Cardiology 2015 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. The update includes new insights into epidemiology, new evidence on genetics, imaging, and risk stratification, and advances in diagnostic and management strategies.Published by
European Society of Cardiology
Published
2022
Summary
Guidelines providing recommendations for the treatment of cardiac arrest in the operating room environment.Published by
European Society of Anaesthesiology and Intensive Care and the European Society for Trauma and Emergency Surgery
Published
2023