Sudden Cardiac Death

Meet the patient

A 58-year-old smoker collapses at the bus stop minutes after clutching his chest. A bystander starts CPR; the paramedics find coarse VF and shock him once at the scene. He rolls through the door with a pulse, intubated, cooling already begun.[1][3]

The consultant's first question on the phone is not "what is it?" — it is "is the cause reversible?" because that single answer decides whether he leaves hospital with an ICD. The rest of this page exists to answer two questions every arrest throws at you: can I restart the heart and protect the brain? and whose job is it to stop it happening again?[1]

What counts as "sudden" — the 1-hour rule

SCD is natural death from a cardiac cause, within one hour of symptom onset when witnessed, or within 24 hours of last being seen alive when unwitnessed — and the time and mode of death are unexpected. That last word is what separates SCD from the terminal arrhythmia of advanced heart failure or septic shock.[1]

The split between sudden cardiac arrest (SCA) and sudden cardiac death (SCD) is operational, not biological. SCA is the event; if the patient walks out of hospital it becomes aborted SCD. Only about 8 to 10 percent of out-of-hospital arrests survive to discharge, so SCA far outnumbers SCD.[1]

The cruel epidemiology is that SCD is the first manifestation of cardiac disease in roughly half of all victims, and the first manifestation of coronary disease in a quarter. Risk tools catch only a minority of those who will die — which is why population-level coronary prevention and family screening of the young do more work than any individual test.[2][3]

The numbers you own before the viva:[1]

[1]

Why the heart stops — substrate, trigger, modulator

Three things must converge for the heart to arrest: a substrate, a trigger, and a modulator. A patient can carry a scarred myocardium for decades without event, then arrest during an adrenergic surge, an electrolyte shift, or an episode of acute ischaemia. The triplet explains every case.[1][2]

The substrate is the fixed abnormality. In ischaemic disease it is a post-infarct scar with surviving myocyte channels embedded in fibrous tissue — slow conduction and unidirectional block, the anatomy of re-entry. In cardiomyopathy it is disorganised architecture, fibrosis, and disarray. In channelopathies there is no scar at all — only a mutated membrane (potassium loss-of-function in LQT1/2, sodium gain-of-function in LQT3, sodium loss-of-function in Brugada, ryanodine-receptor leak in CPVT).[1]

The trigger is the spark. It is usually a short-coupled premature ventricular complex landing on the vulnerable repolarisation window — the downslope of the T wave, roughly 10 to 30 ms before its peak, when dispersion of repolarisation is maximal. In acute ischaemia the trigger is more chaotic: heterogeneous depolarisation across the border zone organises fast into polymorphic VT and then VF.[1]

The modulator shifts the threshold. A sympathetic surge (exercise, emotion, the morning cortisol rise) lowers the VF threshold; hypokalaemia and hypomagnesaemia prolong repolarisation; QT-prolonging drugs (macrolides, fluoroquinolones, antipsychotics, methadone) do the same; and acute ischaemia on top of a chronic scar is the classic double-hit that produces monomorphic VT.[1]

Why VF degrades — and why bradyasystole is worse

VF produces no effective output; coronary perfusion collapses; the myocardium becomes ischaemic and acidotic; the rhythm becomes harder to terminate with each passing minute. After 8 to 10 minutes the myocardium enters an unresponsive phase and VF often degrades to asystole. Bradyasystolic arrest (asystole and PEA) is different in kind — usually the terminal manifestation of severe myocardial failure, hypoxia, or a mechanical catastrophe (tamponade, massive PE, tension pneumothorax, hypovolaemia) — and carries the worse prognosis because it signals end-stage disease, not a treatable electrical event.[1]

Etymology for viva gold: fibrillation describes a wormlike, uncoordinated quiver of muscle fibres, from the Latin fibrilla, "small fibre". The fibrillating ventricle looks like a bag of worms, produces no stroke volume, and dies within minutes unless you shock it.[1]

Three quarters ischaemic — read the substrate by age

In adults over 35, coronary artery disease is the substrate in 75 to 80 percent of SCD. Under 35, inherited cardiomyopathies, channelopathies, and congenital coronary anomalies dominate. That single age cut is the question examiners use to sort the differential.[1]

[1]

Read the rhythm — shockable or not

The monitor decides the first move, not the history. Shockable rhythms (VF, pulseless VT) get a shock; non-shockable rhythms (asystole, PEA) get adrenaline and a hunt for a cause. The split is examinable, and it has shifted over the decades.[1]

[1]

The discriminator examiners love is the rhythm at arrest. VF or pulseless VT in a middle-aged adult is ischaemic until proven otherwise and mandates urgent coronary angiography. PEA with a narrow complex and a history of immobility or malignity points to pulmonary embolism. PEA with electrical alternans and a history of malignity or trauma suggests tamponade. Asystole in the unwitnessed, prolonged down-time arrest is usually medical futility unless a reversible cause is found.[2]

Chain of survival — the four earlies

Outcome is set by four things, all beginning with the word early: recognition, CPR, defibrillation, and ALS. Survival in VF falls by roughly 10 percent for every minute without defibrillation; good bystander CPR halves that slope. No hospital intervention has ever matched what a bystander with two hands and an AED does in the first five minutes.[1][2]

[1]

High-quality CPR — 100 to 120, 5 to 6 cm, full recoil

High-quality compressions are the foundation, and most arrests do them badly. The four non-negotiables: rate 100 to 120 per minute, depth 5 to 6 cm, full chest recoil between compressions, and minimal interruption (chest-compression fraction above 0.6, ideally above 0.8).[1]

Ventilate at 30 compressions to 2 breaths with a bag-valve-mask until an advanced airway is in, then compressions become continuous at 100 to 120 per minute with one breath every 6 seconds. Avoid excessive ventilation — it raises intrathoracic pressure and steals coronary perfusion.[1]

Shockable rhythms — shock, CPR, adrenaline, amiodarone

VF and pulseless VT are the rhythms you can save, and the first action is a shock, not a drug. Deliver a biphasic shock at 150 to 200 J (or the manufacturer-recommended energy), escalating to maximum (typically 360 J biphasic) for later shocks. Resume CPR immediately for 2 minutes before reassessing rhythm — pausing to check a pulse post-shock wastes the recovering-perfusion window.[1]

The drug ladder, in order: adrenaline 1 mg IV every 3 to 5 minutes, started after the second shock, to raise coronary and cerebral perfusion pressure; amiodarone 300 mg IV bolus after the third shock, then 150 mg after the fifth shock if VF or VT persists; lidocaine 1 to 1.5 mg/kg IV is the alternative. Hunt the 4 Hs and 4 Ts alongside.[1]

[1]

Non-shockable rhythms — adrenaline and hunt the cause

In asystole and PEA there is no role for defibrillation. The algorithm centres on adrenaline 1 mg IV immediately, then every 3 to 5 minutes, 2-minute cycles of CPR with rhythm and pulse checks, and an aggressive hunt for the reversible cause — because in PEA the rhythm is a symptom of a mechanical catastrophe, and the patient dies unless the catastrophe is reversed.[1]

The 4 Hs and 4 Ts — the eight reversible causes

Memorise them as two clusters of four, and treat each as you find it. Every PEA arrest hides one of these until proven otherwise — and the patient who survives is the one whose cause you found and fixed.[1]

[1] [1]

Targeted temperature management — the only neuroprotective therapy

Of everything done after ROSC, only targeted temperature management has been proven to improve neurological outcome. Cool comatose survivors of cardiac arrest (any rhythm) to 32 to 36 degrees C for at least 24 hours.[11][12]

The Bernard HACA trial (2002) established that induced hypothermia after out-of-hospital VF arrest improved both survival and neurological outcome. The TTM trial (Nielsen 2013) then showed no difference between 33 and 36 degrees C — shifting practice toward 36 degrees C with strict fever avoidance, though both targets remain acceptable.[11][12]

Bundle TTM with normoxia (SpO2 94 to 98 percent, avoiding hyperoxia), normocapnia (PaCO2 35 to 45 mmHg), mean arterial pressure above 65 mmHg, glucose 8 to 10 mmol/L, and seizure control with continuous EEG to catch non-convulsive status.[3]

Urgent angiography — presume ischaemic until proven otherwise

VF or pulseless VT in a middle-aged adult is ischaemic until proven otherwise. Survivors with ST elevation or haemodynamic instability go to the catheter lab immediately (within 2 hours); those without ST elevation but a suspected cardiac cause get early angiography within 2 to 24 hours, because occult plaque rupture is common. An out-of-hospital arrest with no obvious non-cardiac cause is presumed ischaemic.[1]

The ICD decision — secondary first, primary second

Once ROSC is achieved and the cause identified, the prevention question has two doors: has the patient already arrested (secondary prevention), or are we trying to stop a first arrest (primary prevention)? Each door has its own evidence and its own waiting periods.[1]

Secondary prevention — any survivor gets an ICD

Any survivor of cardiac arrest due to VF or haemodynamically unstable VT, in whom the cause is not fully reversible, gets an ICD before discharge. This is a class I indication. The three classic RCTs — AVID (NEJM 1997), CIDS, and CASH — together showed roughly a 25 to 30 percent relative reduction in mortality with ICD versus antiarrhythmic drugs, predominantly amiodarone.[4]

[4]

The classic trap: early VF within the first 48 hours of a STEMI is ischaemia-driven and treated by reperfusion — it does not by itself mandate an ICD. But VF occurring after 48 hours reflects a scar substrate and is a secondary-prevention indication.[1]

Primary prevention — LVEF 35 percent or less, after the waiting period

Primary prevention rests on a scaffold of landmark trials, each defining a high-risk subgroup. The shared entry ticket: LVEF 35 percent or less on at least 3 months of optimal medical therapy, with expected survival of more than 1 year with a meaningful functional status — and for ischaemic patients, more than 40 days after MI and 3 months after revascularisation.[1]

The trials, and what each one bought:[1]

[5] [6] [7]

The synthesis, encoded in the 2015 ESC and 2017 AHA/ACC/HRS guidelines, sorts patients into three bands:[1][3]

[1]

The 40-day rule — do NOT implant an ICD early after MI

This is the most-tested SCD trap. Two RCTs — DINAMIT (2004) and IRIS (2009) — showed that implanting an ICD 6 to 40 days after MI reduced arrhythmic death but increased non-arrhythmic death, with no overall mortality benefit. The guidelines therefore require a 40-day wait after MI and a 3-month wait after revascularisation before a primary-prevention ICD.[8]

The reason the rule works: roughly one third of patients with LVEF 35 percent or less at the time of MI recover above that threshold by 40 days on modern therapy — so waiting avoids futile implants. A wearable cardioverter-defibrillator can bridge the gap in high-risk patients (the VEST trial, 2018, showed a non-significant trend toward reduced sudden death but a significant reduction in arrhythmic mortality).[8][3]

Why did DINAMIT and IRIS show no mortality benefit?

DINAMIT randomised patients 6 to 40 days post-MI with LVEF 35 percent or less and impaired heart rate variability to ICD versus no ICD. The ICD reduced arrhythmic death by 58 percent but increased non-arrhythmic death by 88 percent — net zero. IRIS reached the same conclusion. The leading explanation is that in the early post-MI window, the patients who would have died arrhythmically are sicker overall, and the ICD simply re-labels the mode of death. MADIT-II required MI at least 1 month prior; SCD-HeFT's average time from MI was years.[8]

The non-ischaemic caveat — DANISH and the CRT-D option

DANISH (2016) questioned whether a primary-prevention ICD still adds benefit in non-ischaemic DCM in the modern drug era. It found no significant reduction in all-cause mortality — tempering enthusiasm, especially in younger patients and those with a CRT indication. ICDs are still implanted in non-ischaemic DCM meeting criteria, but the decision is now more considered than it was.[10]

For patients with NYHA III to IV symptoms, QRS over 120 ms, and LVEF 35 percent or less, CRT-D (cardiac resynchronisation therapy with a defibrillator) reduced all-cause mortality by 36 percent versus medical therapy in COMPANION (2004) — and is the preferred device when the QRS is wide.[9]

[9] [10]

Electrical storm and recurrent VT — when the ICD fires and fires

Electrical storm is three or more sustained VT or VF episodes in 24 hours — a cardiac emergency in its own right. Treat with beta-blockade, amiodarone, deep sedation, catheter ablation (the VTACH and SMASH-VT trials support ablation as an adjunct to the ICD in scar-based VT), and autonomic modulation such as stellate ganglion block in refractory cases. Recurrent appropriate ICD shocks destroy quality of life; recurrent inappropriate shocks (sinus tachycardia, AF, T-wave oversensing) are a separate and fixable problem.[1]

Pharmacological adjuncts — beta-blocker first

Beta-blockers are the single drug class that reduces SCD across heart-failure and post-MI populations (metoprolol succinate, bisoprolol, carvedilol). Amiodarone controls recurrent VT or VF but does not improve mortality in primary prevention — SCD-HeFT showed no benefit and possible harm in NYHA III — and carries cumulative pulmonary, thyroid, hepatic, and cutaneous toxicity. Statins reduce coronary events and SCD indirectly.[7]

Specific substrates that bite — the viva favourites

Each high-risk substrate has its own prevention logic, and examiners test the distinctions. The one-liners below carry the marks.[2]

[2]

Family screening — the preventable next death

After any SCD under 40 (and selected older cases), all first-degree relatives must be screened. The bundle is a 12-lead ECG, transthoracic echo, and an exercise test (plus a 24-hour Holter in selected cases). If a pathogenic variant is found in the proband — by molecular autopsy if the victim died — cascade targeted genetic testing replaces clinical screening: carriers enter surveillance, non-carriers are discharged.[2]

Cardiac MRI is added when the phenotype suggests ARVC, sarcoid, or infiltrative disease. This is the single most effective secondary-prevention strategy for inherited SCD syndromes — and it is the question examiners love, because the answer (screen the family) is also the public-health intervention.[2][3]

Investigations — hunt the cause, because the cause sets the device

In a survivor, every test serves one question: what caused this, and is it reversible? The answer decides ICD, revascularisation, ablation, medical therapy, or reassurance.[1]

The layered work-up, by clock:[1]

[1]

A 12-lead ECG is the single most important immediate test. Look for ST elevation (STEMI — straight to angiography), Brugada type 1 (coved ST in V1 to V3), long QT (over 470 ms in men, 480 ms in women), epsilon waves and T-wave inversion in V1 to V3 (ARVC), a delta wave (WPW), or low voltage (infiltrative disease, tamponade). Cardiac MRI is the gold standard for tissue — late gadolinium enhancement distinguishes ischaemic scar (subendocardial) from DCM, myocarditis, and sarcoid (mid-wall).[1][2]

Genetic testing and the molecular autopsy

In survivors under 40, those with a phenotype suggesting an inherited syndrome (HCM, ARVC, long QT, Brugada, CPVT), and all young SCD victims post-mortem, a cardiomyopathy and channelopathy gene panel is indicated. A molecular autopsy — post-mortem genetic testing on blood or tissue — is recommended when a young person dies suddenly and autopsy is negative, because up to 25 percent of such cases carry a pathogenic channelopathy variant. A pathogenic variant in the proband unlocks cascade testing of relatives.[2][3]

Special populations — where the algorithm bends

Athletes. Pre-participation screening — a 14-element personal and family history, a focused examination, and a 12-lead ECG read with the Seattle criteria — detects HCM, long QT, Brugada, ARVC, WPW, and coronary anomaly in many cases. Competitive sport is contraindicated in symptomatic HCM, ARVC, symptomatic long QT, CPVT, and anomalous coronary.[2]

Pregnancy. SCD rises in the last trimester and peripartum, driven by peripartum cardiomyopathy (sharing genetic predisposition with DCM, particularly titin variants), pre-existing cardiomyopathy, and aortic dissection in connective tissue disease. In third-trimester arrest use manual left uterine displacement, and perimortem caesarean section within 4 minutes, by 5 minutes, when the uterus is above the umbilicus — for the fetus and for maternal venous return.[1]

The elderly. Ischaemic disease dominates; the ICD decision balances benefit against comorbidity, frailty, and the burden of end-of-life shocks. A fit 80-year-old with LVEF 28 percent and NYHA II is a reasonable candidate; an 80-year-old with NYHA IV, dialysis, or metastatic cancer is not. Make the decision shared, and plan for shock deactivation when goals shift to comfort.[3]

Paediatric SCD. The substrate is different — congenital heart disease (post-repair tetralogy, transposition), cardiomyopathies (HCM, DCM, LV non-compaction), channelopathies, myocarditis, anomalous coronary. The algorithm is age-adjusted: two-thumb encircling technique in infants, 15:2 ratio with two rescuers, weight-based drug dosing. Family screening is essential after a paediatric SCD.[1]

Prognosis — one number, hidden variation

Overall survival to discharge after out-of-hospital arrest is 8 to 10 percent — but the range is enormous. Witnessed VF with bystander CPR and early defibrillation can exceed 50 percent; unwitnessed asystole is under 2 percent. The Utstein template stratifies outcomes by rhythm and circumstance. Of those who survive, 50 to 80 percent have a good neurological outcome (CPC 1 or 2).[2]

After a secondary-prevention ICD, survival is 80 to 90 percent at 5 years and 70 to 80 percent at 10 years — most late deaths are non-arrhythmic (heart failure, recurrent MI). Driving restrictions apply: in the UK, no driving for 6 months after a secondary-prevention ICD and for 1 month after a primary-prevention ICD; restrictions differ by region after an arrhythmic event.[4]

How SCD patients come to harm — the preventable list

• Agonal breathing mistaken for normal breathing — bystanders and dispatchers withhold CPR. Public education is the only fix.[1]
• Pausing compressions to check a pulse or rhythm — every second off the chest lowers coronary perfusion. Resume within 5 seconds.[1]
• Premature prognostication within 72 hours of ROSC — declaring futility before TTM is complete and rewarming is finished leads to inappropriate withdrawal of life-sustaining therapy.[11]
• Missing the reversible cause in PEA — the patient dies of a tamponade or tension pneumothorax you could have decompressed.[1]
• Implanting an ICD within 40 days of MI — no mortality benefit, exposed to surgical and shock risk for nothing.[8]
• Failing to screen the family of a young SCD victim — the preventable next death.[2]
• Misdiagnosing myoclonic jerks as a seizure — a small but real fraction of "first seizure in an adult" presentations are aborted cardiac arrests, particularly in long QT syndrome.[1]

Regional deltas — one algorithm, local translation

[1] [1] [1] [1]

The mantra, and the mnemonic

[1]

The mantra: defibrillate the shockable, adrenaline and hunt the cause in the rest, cool the brain, and give the survivor an ICD.[1][11]

Ward-round test — four stems, thirty seconds each

Stem 1 — coarse VF on the monitor (answer)

A 58-year-old smoker is in VF. The defibrillator is charged. What is the sequence for the next five minutes? Model: Confirm VF, deliver a biphasic shock at 150 to 200 J, and resume CPR immediately for 2 minutes before reassessing rhythm — do not pause to check a pulse post-shock. Continue the loop, escalating energy toward 360 J. Give adrenaline 1 mg IV after the second shock, then every 3 to 5 minutes, and amiodarone 300 mg IV after the third shock (150 mg after the fifth). Throughout, hunt the 4 Hs and 4 Ts and prepare for post-ROSC targeted temperature management and coronary angiography.[1]

Stem 2 — asystole on the monitor (answer)

The rhythm strip is flat. What is the first drug, and what do you NOT give? Model: This is a non-shockable rhythm — no defibrillation. Give adrenaline 1 mg IV immediately, then every 3 to 5 minutes, with 2-minute CPR cycles and rhythm checks. Do not give atropine — it is no longer recommended for asystole or PEA. The outcome hinges on finding and reversing a 4 H or 4 T cause, so run that hunt in parallel from the first cycle.[1]

Stem 3 — the survivor and the 40-day rule (answer)

A 52-year-old is resuscitated from VF on day 10 of a large anterior MI. LVEF is 28 percent. The registrar wants to implant a primary-prevention ICD before discharge. What is the right call? Model: Do not implant a primary-prevention ICD now. DINAMIT and IRIS showed no overall mortality benefit from ICD implantation 6 to 40 days post-MI — arrhythmic deaths fell but non-arrhythmic deaths rose. Wait until at least 40 days after the MI and 3 months after revascularisation, then reassess LVEF — about a third of such patients recover above 35 percent. A wearable cardioverter-defibrillator can bridge the gap in high-risk patients. Note: this VF was within the peri-infarct window, so if it was clearly ischaemia-driven it does not by itself mandate an ICD either.[8]

Stem 4 — the family of a young victim (answer)

A previously well 19-year-old dies suddenly while playing football; autopsy is negative. What do you do for the family? Model: Arrange a molecular autopsy (post-mortem genetic testing) on blood or tissue — up to 25 percent of such negative-autopsy young deaths carry a pathogenic channelopathy variant. Meanwhile, refer all first-degree relatives for cascade clinical screening with a 12-lead ECG, transthoracic echo, and an exercise test (plus Holter in selected cases). If the molecular autopsy finds a pathogenic variant, switch the relatives to targeted cascade genetic testing — carriers enter surveillance, non-carriers are discharged. This is the single most effective secondary prevention strategy for inherited SCD syndromes.[2]

References

1. [1]Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Circulation, 2006.PMID 16935995
2. [2]Priori SG, Blomström-Lundqvist C, Mazzanti A, et al. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC) Eur Heart J, 2015.PMID 26320108
3. [3]Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society J Am Coll Cardiol, 2018.PMID 29097296
4. [4]Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias N Engl J Med, 1997.PMID 9411221
5. [5]Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators N Engl J Med, 1996.PMID 8960472
6. [6]Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction N Engl J Med, 2002.PMID 11907286
7. [7]Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure N Engl J Med, 2005.PMID 15659722
8. [8]Hohnloser SH, Kuck KH, Dorian P, et al. Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction N Engl J Med, 2004.PMID 15590950
9. [9]Bristow MR, Saxon LA, Boehmer J, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure N Engl J Med, 2004.PMID 15152059
10. [10]Køber L, Thune JJ, Nielsen JC, et al. Defibrillator Implantation in Patients with Nonischemic Systolic Heart Failure N Engl J Med, 2016.PMID 27571011
11. [11]Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia N Engl J Med, 2002.PMID 11856794
12. [12]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.PMID 24237006