Ventricular Fibrillation

Table of Contents

  1. Overview
  2. Mechanisms and Initiation
  3. Underlying Substrates and Causes
  4. Chain of Survival
  5. CPR Technique
  6. Defibrillation and ACLS
  7. Post-ROSC Care
  8. ICD Therapy and Long-term Management
  9. Prognosis and Neurological Outcomes
  10. Key Research Papers
  11. Connections
  12. Featured Videos

Overview

Ventricular fibrillation (VF) is a disorganized, chaotic electrical rhythm in the ventricles that abolishes coordinated contraction. With no synchronized squeeze of the heart muscle, the ventricles quiver, the heart pumps no blood and the result is cardiac arrest: no pulse and loss of consciousness. A review of sudden cardiac death reports that 95% of patients die after 10 minutes or longer without defibrillation (PubMed PMID: 20142817).

VF is one of the main rhythms found at the start of a sudden cardiac arrest. In a study of confirmed cardiac arrest in which a defibrillator was used within 3 minutes, the first rhythm was VT or VF in 71% of people, asystole in 18% and pulseless electrical activity in 11%; in Seattle, VF was the first rhythm in only 41% of out-of-hospital arrests by the year 2000, after a long decline (PubMed PMID: 20142817). On the electrocardiogram VF appears as an irregular wavy baseline with no recognizable P waves, QRS complexes or T waves.

VF differs from ventricular tachycardia (VT). VT has discrete, organized QRS complexes (even if wide and abnormal) and may maintain some cardiac output; VF has no organized complexes at all. Rapid VT can degenerate into VF, and trials of shock-refractory cardiac arrest have enrolled VF and pulseless VT together (PubMed PMID: 27043165).

VF is often described as primary (arising without detectable structural heart disease, as in idiopathic VF or the inherited channelopathies) or secondary (occurring in a heart with identifiable structural disease such as ischemic or hypertrophic cardiomyopathy).

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Mechanisms and Initiation

VF is usually described as needing two components: a trigger that starts the episode, and a vulnerable substrate in the heart muscle that lets chaotic activity keep going.

A common trigger is a premature ventricular beat that falls in the vulnerable period of repolarization, around the T wave on the ECG (the R-on-T phenomenon). During the T wave, different regions of the heart muscle are at different stages of recovery, so a well-timed stimulus finds some cells ready to fire and others still refractory. The same timing applies to a mechanical trigger: in a swine model, 9 of 10 low-energy chest impacts timed 30 to 15 milliseconds before the peak of the T wave produced VF, and impacts at other times in the cardiac cycle did not (PubMed PMID: 9632447). In people with idiopathic VF, the first beat of each episode often matches isolated premature beats that arise from the Purkinje conducting system (PubMed PMID: 12186801).

Electrical heterogeneity is the substrate concept. When neighboring heart cells have very different refractory periods — because of ischemia, scarring, ion-channel mutations or electrolyte disturbance — a wave of activation can travel through recovered tissue, circle back and re-excite tissue that has just recovered, sustaining a re-entrant loop. Two main models describe how VF keeps itself going once started:

Beyond re-entry, abnormal cell calcium handling can also start ventricular arrhythmias. Early afterdepolarizations arise when repolarization is prolonged, as in long QT syndrome, and can trigger torsades de pointes, which may degenerate into VF. Delayed afterdepolarizations from calcium overload are the mechanism proposed for catecholaminergic polymorphic VT (CPVT), in which mutations in the cardiac ryanodine receptor gene (RyR2) were identified in 4 of 12 affected probands in the first genetic study (PubMed PMID: 11208676).

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Underlying Substrates and Causes

The cause of a VF arrest shapes the long-term risk of recurrence and the treatments studied afterwards.

Ischemic Heart Disease

Coronary heart disease is the most common substrate: autopsy studies of adults with sudden cardiac death find severe coronary disease in about 80% (PubMed PMID: 20142817). Acute ischemia during a heart attack and chronic scar after one both create the electrical heterogeneity described above. The same review notes that the classic teaching that arrhythmias in the first 12–24 hours after a heart attack do not predict later sudden death has been challenged (PubMed PMID: 20142817).

Cardiomyopathies

Dilated, hypertrophic and arrhythmogenic right ventricular cardiomyopathy all raise the risk of VF. In a US registry of 1,866 young competitive athletes who died suddenly or survived cardiac arrest (1980–2006), the most common cardiovascular causes were hypertrophic cardiomyopathy (36%) and congenital coronary artery anomalies (17%) (PubMed PMID: 19221222).

Channelopathies

These inherited disorders of cardiac ion channels can cause VF in hearts that look structurally normal on imaging:

Wolff-Parkinson-White Syndrome

In Wolff-Parkinson-White syndrome, VF can occur during atrial fibrillation when the accessory pathway conducts very rapidly to the ventricles. In a 1979 comparison, patients with WPW who had had VF had a shorter shortest pre-excited R-R interval during atrial fibrillation (mean 180 vs 240 milliseconds), more often had both reciprocating tachycardia and atrial fibrillation, and more often had multiple accessory pathways (PubMed PMID: 492252).

Other Causes

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Chain of Survival

Research on the steps between collapse and hospital care includes:

Overall survival after out-of-hospital cardiac arrest is low. The 79-study meta-analysis pooled survival to hospital discharge at 7.6%, a figure that had not changed significantly in almost three decades (PubMed PMID: 20123673); in the EuReCa ONE registry of 10,682 arrests in 27 European countries in October 2014, 10.3% of those in whom CPR was attempted survived at least 30 days or to discharge (PubMed PMID: 27321577).

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CPR Technique

The American Heart Association published its adult basic and advanced life support guidelines in 2020 (PubMed PMID: 33081529). Research on how CPR is delivered includes:

Compression Rate and Depth

In 10,371 out-of-hospital arrests treated by emergency medical services, after adjustment for compression fraction and depth, compression rates of 100 to 119 per minute were associated with the greatest survival to hospital discharge (PubMed PMID: 25565457). In 9,136 adults from the same consortium, deeper compressions were strongly associated with survival, with the highest survival at a depth of 40.3 to 55.3 mm (peak 45.6 mm); the authors suggested the 2010 guideline target of more than 50 mm might be too high (PubMed PMID: 25252721).

Compression-Only CPR

In the dispatcher trial above, instructions for chest compression alone gave survival similar to compression plus rescue breathing, with a non-significant trend favoring compression alone in arrests of cardiac cause (15.5% vs 12.3%) and shockable rhythms (31.9% vs 25.7%); the authors concluded the results support lay CPR that emphasizes chest compression (PubMed PMID: 20818863).

Mechanical CPR Devices

Two large trials compared mechanical chest-compression devices with manual CPR in out-of-hospital arrest. In LINC (2,589 patients), 4-hour survival was 23.6% with mechanical CPR and 23.7% with manual CPR (PubMed PMID: 24240611). In PARAMEDIC (4,471 patients), 30-day survival was 6% with the device and 7% with manual compressions (adjusted odds ratio 0.86), and the authors concluded that widespread routine use does not improve survival (PubMed PMID: 25467566).

CPR First or Rhythm Analysis First

In a cluster-randomized trial of 9,933 out-of-hospital arrests, 30–60 seconds of emergency-crew CPR before the first rhythm analysis and 180 seconds of CPR before it gave the same rate of survival with good function (5.9% in both groups) (PubMed PMID: 21879896).

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Defibrillation and ACLS

Defibrillation delivers an electrical current through the chest that depolarizes a critical mass of ventricular muscle at once, allowing an organized rhythm to resume. It is the treatment that terminates VF.

AEDs

Automated external defibrillators analyze the rhythm and deliver a shock when they detect VF or pulseless VT. The sudden cardiac death review notes that studies have shown AEDs can be operated by untrained lay people, and that AED programs at airports and casinos have been associated with 50–75% survival when CPR is immediate and defibrillation occurs within 3–5 minutes (PubMed PMID: 20142817). In the Resuscitation Outcomes Consortium study, AEDs applied before emergency services arrived were used by health care workers (32%), lay volunteers (35%) and police (26%) (PubMed PMID: 20394876).

Drug Therapy in Cardiac Arrest

Extracorporeal CPR (ECPR)

In extracorporeal CPR, a heart-lung machine (extracorporeal membrane oxygenation, ECMO) takes over circulation during refractory arrest. In a single-centre phase 2 trial (also named ARREST, 2020) of 30 adults with out-of-hospital arrest and VF that persisted after three shocks, survival to hospital discharge was 43% (6 of 14) with early ECMO-facilitated resuscitation and 7% (1 of 15) with standard advanced life support; the trial was stopped early at its first interim analysis (PubMed PMID: 33197396).

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Post-ROSC Care

Return of spontaneous circulation (ROSC) begins a second phase of illness. An international consensus statement defines the post-cardiac arrest syndrome by four components: brain injury, myocardial dysfunction, a systemic ischemia-reperfusion response, and the persisting condition that caused the arrest (PubMed PMID: 18963350).

Targeted Temperature Management (TTM)

In the 2002 Hypothermia after Cardiac Arrest trial of patients resuscitated from VF, cooling to 32–34°C for 24 hours gave a favorable neurological outcome in 55% compared with 39% at normal temperature, and 6-month mortality of 41% compared with 55% (PubMed PMID: 11856793).

The 2013 TTM trial randomized 950 unconscious adults after out-of-hospital arrest of presumed cardiac cause to a target of 33°C or 36°C, both intended to prevent fever (PubMed PMID: 24237006). Among the 939 patients analyzed, 50% in the 33°C group and 48% in the 36°C group had died by the end of the trial, and death or poor neurological function at 180 days occurred in 54% and 52%; 33°C conferred no benefit over 36°C (PubMed PMID: 24237006). The 2015 American Heart Association update then recommended selecting and maintaining a constant temperature between 32°C and 36°C for at least 24 hours (PubMed PMID: 26472996).

The 2021 TTM2 trial of 1,900 comatose adults compared hypothermia at 33°C with normothermia and early treatment of fever (37.8°C or higher). At 6 months, 50% of the hypothermia group and 48% of the normothermia group had died, and moderately severe disability or worse occurred in 55% of each group; arrhythmia causing hemodynamic compromise was more common with hypothermia (24% vs 17%) (PubMed PMID: 34133859). The 2021 European Resuscitation Council and European Society of Intensive Care Medicine guidelines recommend avoiding fever (above 37.7°C) for at least 72 hours in patients who remain in coma (PubMed PMID: 33765189). The 2015 American Heart Association update notes that observational studies link fever after cardiac arrest to poor outcome and that its fever-avoidance recommendation rests on expert opinion (PubMed PMID: 26472996).

Coronary Angiography

The 2015 American Heart Association update recommends emergent coronary angiography for out-of-hospital arrest of suspected cardiac cause with ST elevation on the ECG; in the series it reviewed, a coronary lesion amenable to emergency treatment was found in 96% of patients with ST elevation and 58% of those without (PubMed PMID: 26472996). For patients without ST elevation, the COACT trial (552 patients) found 90-day survival of 64.5% with immediate angiography and 67.2% with angiography delayed until after neurological recovery — no significant difference (PubMed PMID: 30883057).

Oxygen, Ventilation, Blood Pressure and Glucose

The 2021 European post-resuscitation guidelines (PubMed PMID: 33765189) describe these targets:

Seizures and Neuroprognostication

The 2015 American Heart Association update estimates that seizures, nonconvulsive status epilepticus and other epileptiform activity occur in 12–22% of patients who are comatose after cardiac arrest (PubMed PMID: 26472996). The 2021 European guidelines recommend EEG to diagnose seizures, suggest levetiracetam or sodium valproate as first-line antiepileptic drugs, and suggest against routine seizure prophylaxis (PubMed PMID: 33765189).

On timing, the 2015 American Heart Association update places the earliest prognostication by clinical examination at 72 hours after arrest in patients not treated with TTM, and later when sedation or paralysis may confound the examination (PubMed PMID: 26472996). The 2021 European guidelines describe a multimodal approach: in a comatose patient with a motor score of 3 or less at 72 hours or later, with confounders excluded, a poor outcome is likely when two or more of these are present (PubMed PMID: 33765189):

The same guidelines describe basing decisions on several tests that point in the same direction rather than on any single test (PubMed PMID: 33765189).

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ICD Therapy and Long-term Management

An implantable cardioverter-defibrillator (ICD) monitors the heart rhythm continuously and delivers a shock when it detects VF. The 2021 European post-resuscitation guidelines note that an ICD may be implanted for primary or secondary prevention and that careful patient selection is needed (PubMed PMID: 33765189).

Secondary Prevention ICD

Three randomized trials (AVID, CASH and CIDS) compared ICDs with amiodarone in survivors of VF or sustained VT. A pooled analysis of individual patient data found a 28% reduction in the relative risk of death with the ICD, due almost entirely to a 50% reduction in arrhythmic death; survival was extended by a mean of 4.4 months over 6 years, and patients with an ejection fraction of 35% or less benefited significantly more than those with better-preserved function (PubMed PMID: 11102258).

The subcutaneous ICD places the whole system outside the chest cavity, with no lead inside the heart's veins. In the PRAETORIAN trial of 849 patients who needed an ICD but not pacing, the subcutaneous device was noninferior to a transvenous ICD for the combined rate of device complications and inappropriate shocks (15.1% vs 15.7% at 48 months) (PubMed PMID: 32757521).

Primary Prevention ICD

Randomized trials have tested ICDs in people at high risk who have never had a cardiac arrest:

Drug Therapy in Inherited Arrhythmias

Catheter Ablation

In 27 patients resuscitated from recurrent idiopathic VF, ablating the triggering premature beats left 24 (89%) free of VF recurrence without drugs over 24 ± 28 months (PubMed PMID: 12186801). In 9 men with Brugada syndrome and frequent VF episodes, ablation over abnormal areas of the right ventricular outflow tract epicardium made VT/VF non-inducible in 7 and normalized the Brugada ECG pattern in 89%, with no recurrent VT/VF over 20 ± 6 months (PubMed PMID: 21403098). Both were small, uncontrolled series.

Family Screening

Inherited causes can be found in relatives. In a Dutch study of 43 families with at least one unexplained sudden death at age 40 or younger, cardiological and genetic examination of relatives identified an inherited disease in 17 families (40%) — most often CPVT, long QT syndrome or Brugada syndrome — and found 151 previously unrecognized carriers; the resting and exercise ECG had a high diagnostic yield (PubMed PMID: 15998675).

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Prognosis and Neurological Outcomes

Outcome after VF arrest depends on two largely separate questions: whether the heart recovers, and whether the brain does.

Survival

In the meta-analysis of 79 studies (142,740 patients), pooled survival to hospital discharge after out-of-hospital arrest was 7.6%. Survival was more likely when the arrest was witnessed by a bystander or by emergency crews, when bystander CPR was given, when the first rhythm was VF or VT (14.8% to 23.0%) and when circulation returned (PubMed PMID: 20123673).

Neurological Outcome

Neurological recovery is often graded with the Cerebral Performance Category (CPC) scale, on which CPC 1 or 2 is classed as a good outcome (PubMed PMID: 24240611). In the LINC trial, 99% of 6-month survivors in the mechanical-CPR group and 94% in the manual-CPR group had a CPC score of 1 or 2 (PubMed PMID: 24240611). In the 2002 hypothermia trial, a favorable neurological outcome at 6 months occurred in 55% of patients cooled after VF arrest and 39% of those kept at normal temperature (PubMed PMID: 11856793).

Long-term Outcomes

In Olmsted County, Minnesota, 5-year survival among people who had an out-of-hospital VF arrest and survived to hospital discharge was 79%, equal to that of age-, sex- and disease-matched people without cardiac arrest (PubMed PMID: 20142817). In the PRAETORIAN trial, appropriate shocks occurred in 83 of 426 subcutaneous-ICD patients and 57 of 423 transvenous-ICD patients over a median 49.1 months (PubMed PMID: 32757521).

The 2021 European guidelines report that a lower likelihood of returning to work after cardiac arrest is associated with cognitive problems and fatigue, unwitnessed arrest, absence of bystander CPR, female sex, older age and lower socio-economic status, and they describe functional assessment before discharge and referral to rehabilitation where needed (PubMed PMID: 33765189).

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Key Research Papers

Resuscitation and Post-Cardiac Arrest Care

  1. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346(8):549–556. — PubMed PMID: 11856793 · doi:10.1056/NEJMoa012689
  2. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013;369(23):2197–2206. — PubMed PMID: 24237006 · doi:10.1056/NEJMoa1310519
  3. Dankiewicz J, Cronberg T, Lilja G, et al. Hypothermia versus normothermia after out-of-hospital cardiac arrest (TTM2). N Engl J Med. 2021;384(24):2283–2294. — PubMed PMID: 34133859
  4. Callaway CW, et al. Part 8: Post-Cardiac Arrest Care. 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015;132(18 Suppl 2):S465–S482. — PubMed PMID: 26472996 · doi:10.1161/CIR.0000000000000262
  5. Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine guidelines 2021: post-resuscitation care. Intensive Care Med. 2021;47(4):369–421. — PubMed PMID: 33765189
  6. Nolan JP, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. Resuscitation. 2008;79(3):350–379. — PubMed PMID: 18963350 · doi:10.1016/j.resuscitation.2008.09.017
  7. Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary angiography after cardiac arrest without ST-segment elevation (COACT). N Engl J Med. 2019;380(15):1397–1407. — PubMed PMID: 30883057

CPR, Defibrillation and Drugs

  1. Panchal AR, Bartos JA, Cabañas JG, et al. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142(16 Suppl 2):S366–S468. — PubMed PMID: 33081529
  2. Panchal AR, et al. 2018 American Heart Association focused update on advanced cardiovascular life support use of antiarrhythmic drugs during and immediately after cardiac arrest. Circulation. 2018;138(23):e740–e749. — PubMed PMID: 30571262
  3. Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation (ARREST). N Engl J Med. 1999;341(12):871–878. — PubMed PMID: 10486418
  4. Kudenchuk PJ, Brown SP, Daya M, et al. Amiodarone, lidocaine, or placebo in out-of-hospital cardiac arrest (ALPS). N Engl J Med. 2016;374(18):1711–1722. — PubMed PMID: 27043165
  5. Perkins GD, Ji C, Deakin CD, et al. A randomized trial of epinephrine in out-of-hospital cardiac arrest (PARAMEDIC2). N Engl J Med. 2018;379(8):711–721. — PubMed PMID: 30021076
  6. Yannopoulos D, Bartos J, Raveendran G, et al. Advanced reperfusion strategies for patients with out-of-hospital cardiac arrest and refractory ventricular fibrillation (ARREST): a phase 2, single centre, open-label, randomised controlled trial. Lancet. 2020;396(10265):1807–1816. — PubMed PMID: 33197396
  7. Idris AH, Guffey D, Pepe PE, et al. Chest compression rates and survival following out-of-hospital cardiac arrest. Crit Care Med. 2015;43(4):840–848. — PubMed PMID: 25565457
  8. Stiell IG, Brown SP, Nichol G, et al. What is the optimal chest compression depth during out-of-hospital cardiac arrest resuscitation of adult patients? Circulation. 2014;130(22):1962–1970. — PubMed PMID: 25252721
  9. Rea TD, Fahrenbruch C, Culley L, et al. CPR with chest compression alone or with rescue breathing. N Engl J Med. 2010;363(5):423–433. — PubMed PMID: 20818863
  10. Rubertsson S, Lindgren E, Smekal D, et al. Mechanical chest compressions and simultaneous defibrillation vs conventional cardiopulmonary resuscitation in out-of-hospital cardiac arrest: the LINC randomized trial. JAMA. 2014;311(1):53–61. — PubMed PMID: 24240611
  11. Perkins GD, Lall R, Quinn T, et al. Mechanical versus manual chest compression for out-of-hospital cardiac arrest (PARAMEDIC): a pragmatic, cluster randomised controlled trial. Lancet. 2015;385(9972):947–955. — PubMed PMID: 25467566
  12. Stiell IG, Nichol G, Leroux BG, et al. Early versus later rhythm analysis in patients with out-of-hospital cardiac arrest. N Engl J Med. 2011;365(9):787–797. — PubMed PMID: 21879896

ICD and Prevention

  1. Connolly SJ, Hallstrom AP, Cappato R, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials: AVID, CASH and CIDS studies. Eur Heart J. 2000;21(24):2071–2078. — PubMed PMID: 11102258
  2. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction (MADIT-II). N Engl J Med. 2002;346(12):877–883. — PubMed PMID: 11907286
  3. Bardy GH, et al. Amiodarone or an implantable cardioverter–defibrillator for congestive heart failure (SCD-HeFT). N Engl J Med. 2005;352(3):225–237. — PubMed PMID: 15659722 · doi:10.1056/NEJMoa043399
  4. Køber L, Thune JJ, Nielsen JC, et al. Defibrillator implantation in patients with nonischemic systolic heart failure (DANISH). N Engl J Med. 2016;375(13):1221–1230. — PubMed PMID: 27571011
  5. Knops RE, Olde Nordkamp LRA, Delnoy PHM, et al. Subcutaneous or transvenous defibrillator therapy (PRAETORIAN). N Engl J Med. 2020;383(6):526–536. — PubMed PMID: 32757521
  6. O'Mahony C, Jichi F, Pavlou M, et al. A novel clinical risk prediction model for sudden cardiac death in hypertrophic cardiomyopathy (HCM Risk-SCD). Eur Heart J. 2014;35(30):2010–2020. — PubMed PMID: 24126876
  7. Priori SG, et al. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2015;36(41):2793–2867. — PubMed PMID: 26320108 · doi:10.1093/eurheartj/ehv316

Channelopathies and Ablation

  1. Brugada J, Brugada R, Brugada P. Right bundle-branch block and ST-segment elevation in leads V1 through V3: a marker for sudden death in patients without demonstrable structural heart disease. Circulation. 1998;97(5):457–460. — PubMed PMID: 9490240 · doi:10.1161/01.CIR.97.5.457
  2. Priori SG, et al. Mutations in the cardiac ryanodine receptor gene (hRyR2) underlie catecholaminergic polymorphic ventricular tachycardia. Circulation. 2001;103(2):196–200. — PubMed PMID: 11208676 · doi:10.1161/01.CIR.103.2.196
  3. Schwartz PJ, Priori SG, Spazzolini C, et al. Genotype-phenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias. Circulation. 2001;103(1):89–95. — PubMed PMID: 11136691
  4. Kannankeril PJ, Moore JP, Cerrone M, et al. Efficacy of flecainide in the treatment of catecholaminergic polymorphic ventricular tachycardia: a randomized clinical trial. JAMA Cardiol. 2017;2(7):759–766. — PubMed PMID: 28492868
  5. Haïssaguerre M, Shoda M, Jaïs P, et al. Mapping and ablation of idiopathic ventricular fibrillation. Circulation. 2002;106(8):962–967. — PubMed PMID: 12186801
  6. Nademanee K, Veerakul G, Chandanamattha P, et al. Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium. Circulation. 2011;123(12):1270–1279. — PubMed PMID: 21403098
  7. Tan HL, Hofman N, van Langen IM, et al. Sudden unexplained death: heritability and diagnostic yield of cardiological and genetic examination in surviving relatives. Circulation. 2005;112(2):207–213. — PubMed PMID: 15998675

Epidemiology, Bystander CPR and Special Causes

  1. Adabag AS, Luepker RV, Roger VL, Gersh BJ. Sudden cardiac death: epidemiology and risk factors. Nat Rev Cardiol. 2010;7(4):216–225. — PubMed PMID: 20142817
  2. Sasson C, et al. Predictors of survival from out-of-hospital cardiac arrest: a systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes. 2010;3(1):63–81. — PubMed PMID: 20123673 · doi:10.1161/CIRCOUTCOMES.109.889576
  3. Gräsner JT, et al. EuReCa ONE — 27 Nations, ONE Europe, ONE Registry: A prospective one month analysis of out-of-hospital cardiac arrest outcomes in 27 countries in Europe. Resuscitation. 2016;105:188–195. — PubMed PMID: 27321577 · doi:10.1016/j.resuscitation.2016.06.004
  4. Hasselqvist-Ax I, Riva G, Herlitz J, et al. Early cardiopulmonary resuscitation in out-of-hospital cardiac arrest. N Engl J Med. 2015;372(24):2307–2315. — PubMed PMID: 26061835
  5. Weisfeldt ML, Sitlani CM, Ornato JP, et al. Survival after application of automatic external defibrillators before arrival of the emergency medical system: evaluation in the Resuscitation Outcomes Consortium population of 21 million. J Am Coll Cardiol. 2010;55(16):1713–1720. — PubMed PMID: 20394876
  6. Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980–2006. Circulation. 2009;119(8):1085–1092. — PubMed PMID: 19221222
  7. Klein GJ, Bashore TM, Sellers TD, et al. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med. 1979;301(20):1080–1085. — PubMed PMID: 492252
  8. Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;324(12):781–788. — PubMed PMID: 1900101
  9. Maron BJ, Poliac LC, Kaplan JA, Mueller FO. Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. N Engl J Med. 1995;333(6):337–342. — PubMed PMID: 7609749 · doi:10.1056/NEJM199508103330602
  10. Link MS, Wang PJ, Pandian NG, et al. An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med. 1998;338(25):1805–1811. — PubMed PMID: 9632447 · doi:10.1056/NEJM199806183382504

PubMed Topic Searches

  1. PubMed: Ventricular Fibrillation and Sudden Cardiac Death
  2. PubMed: Post-Resuscitation Care after Cardiac Arrest
  3. PubMed: ICD Primary Prevention Sudden Cardiac Death
  4. PubMed: Channelopathies and Ventricular Fibrillation

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Connections

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