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Sudden Cardiac Death & Arrest: A Complete Guide for the Emergency Resident

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PART 1 - DEFINITIONS AND EPIDEMIOLOGY

• ~341,000-450,000 out-of-hospital cardiac arrests (OHCA) per year in the US
• Estimated overall OHCA survival: 5.4-10.8% (EMS-treated cases only)
• 60% male; peak incidence age >45-50 years
• Only 23% of all cardiac arrests present with VF; the rest are non-shockable
• Survival from VF/pVT is vastly better than from asystole/PEA
• Strong circadian pattern: highest incidence in first hours after awakening (peak sympathetic tone)
• SCD is 30-80% more common in lowest vs highest socioeconomic quartile

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PART 2 - BASIC PHYSIOLOGY OF CARDIAC ARREST

Normal Cardiac Electrophysiology Briefly

• Phase 0: Rapid Na+ influx (fast depolarization) - targeted by Class I antiarrhythmics
• Phase 1: Transient K+ efflux
• Phase 2: Plateau - Ca2+ influx (L-type) balanced by K+ efflux - targeted by Class IV (CCBs)
• Phase 3: Rapid K+ efflux (repolarization) - targeted by Class III antiarrhythmics
• Phase 4: Resting potential; automaticity in pacemaker cells via If (funny current)

Why the Heart Arrests

• Tintinalli's Emergency Medicine, p. 95

Hemodynamics of Cardiac Arrest

• Coronary perfusion pressure (CPP) = Aortic relaxation pressure - Right atrial pressure. CPP must be >15 mmHg for ROSC to occur; epinephrine increases this by peripheral vasoconstriction.
• Cerebral blood flow is critically dependent on uninterrupted CPR; each pause in compressions takes 10-15 seconds to rebuild.
• After 4-6 minutes of no-flow time, cerebral neurons begin irreversible injury.

1. Electrical phase (0-4 min): Immediate defibrillation is most effective
2. Circulatory phase (4-10 min): CPR first to replenish cardiac energy stores, THEN shock
3. Metabolic phase (>10 min): Metabolic derangement limits survival; novel therapies (ECMO) may help

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PART 3 - PATHOLOGY: CAUSES AND STRUCTURAL SUBSTRATES

Etiologies by Frequency

Coronary Artery Disease (CAD) - The Leading Cause

• Coronary atherosclerosis on autopsy in 80% of SCD victims
• Importantly, only 10-20% have acute plaque rupture - most have chronic severe stenosis
• 80-90% of resuscitated SCA patients show NO enzymatic/ECG evidence of acute MI - the arrhythmia precedes necrosis
• Healed remote MIs found in ~40%; subendocardial vacuolization indicating chronic ischemia is common
• Mechanism: chronic ischemia creates areas of fibrosis and electrically unstable periinfarct zones that serve as re-entry substrates

Cardiomyopathies

• Dilated ventricles cause dispersion of depolarization/repolarization
• Creates "islands" firing at different rates - sustains re-entry VT/VF
• EF ≤35% is the single best predictor of SCD risk (primary ICD indication)
• NYHA class II-III carries higher SCD risk; class IV patients more often die from pump failure

• Most common cardiovascular cause of SCD in young athletes (~1/3 of exercise-related SCA)
• Risk ~1% per year
• Mechanism: myocyte disarray, fibrosis, LVOTO creating dynamic outflow obstruction and arrhythmia substrate
• ICD indications: prior VF/VT, family history of SCD, syncope, LV wall thickness ≥30 mm, abnormal BP response to exercise, massive LVH in children

• Hereditary; right-sided failure + VT with LBBB morphology (right ventricular origin)
• ECG: epsilon wave in V1-V3; T-wave inversions in right precordial leads
• Fibrofatty replacement of RV myocardium disrupts conduction

Channelopathies - The "Electrically Silent" Hearts

Myocarditis

• Histologically defined by mononuclear cell infiltrates
• Leading viral causes: Coxsackie B, SARS-CoV-2, parvovirus B19, HHV-6
• Can cause SCA through direct myocyte injury + acute arrhythmia substrate
• Treat underlying cause; arrhythmias managed per standard ACLS

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PART 4 - CARDIAC ARREST RHYTHMS AND THEIR SIGNIFICANCE

The Four Rhythms

• Narrow-complex PEA = mechanical cause (tamponade, PE, tension PTX, hypovolemia, acute MI with rupture) - bedside US shows hyperdynamic LV
• Wide-complex PEA = metabolic cause (hyperkalemia, Na-channel blocker toxicity, severe acidosis, agonal rhythm) - bedside US shows hypokinetic/akinetic LV

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PART 5 - COMPLETE PHARMACOLOGY OF CARDIAC ARREST

Vasopressors

Epinephrine (Adrenaline) - First-Line for All Rhythms

Vasopressin

• Not recommended as substitute or addition to epinephrine (2025 AHA: no advantage)

Antiarrhythmics for Shockable Rhythms (VF/pVT)

Amiodarone - Preferred Agent for Refractory VF/pVT

• Cardiac arrest: 300 mg IV bolus (in 20 mL D5W) → may repeat 150 mg once
• Stable VT: 150 mg IV over 10-15 min, then 1 mg/min x6h, then 0.5 mg/min x18h
• Infusions >2h: use glass or polyolefin containers (precipitates in PVC)

Lidocaine - Acceptable Alternative

Magnesium Sulfate

Drugs for Non-Shockable Rhythms

Atropine

• No longer recommended in cardiac arrest for PEA/asystole (2010 guidelines removed it from the algorithm)
• Still indicated for symptomatic bradycardia with a pulse: 0.5 mg IV every 3-5 min (max 3 mg)
• Mechanism: muscarinic antagonist, blocks vagal slowing of SA/AV nodes

Sodium Bicarbonate

• NOT routine in cardiac arrest
• Use for: severe pre-existing metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose, sodium channel blocker toxicity
• Dose: 1 mEq/kg IV
• Risks: hypernatremia, paradoxical intracellular acidosis, hyperosmolarity; only give if good ventilation is established

Calcium

• Indication: Hyperkalemia, hypocalcemia, calcium channel blocker overdose, hypermagnesemia
• Dose: Calcium chloride 1 g (10 mL of 10% solution) IV - preferred in cardiac arrest; calcium gluconate 3x less potent per mL
• Do NOT mix with sodium bicarbonate (precipitates)

Glucose + Insulin

• For hyperkalemia (drives K+ intracellularly)
• Not part of standard cardiac arrest protocol unless hyperkalemia confirmed

Naloxone

• 2025 AHA Update: Expanded role - administer for suspected opioid-associated respiratory/cardiac arrest
• Dose: 0.4-2 mg IV/IO/IM/IN; may repeat
• BLS and HCP algorithms now include opioid overdose response with naloxone

Specific Antidotes in Special Situations

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PART 6 - HIGH-QUALITY CPR

The Non-Negotiables (2025 AHA)

• Hand and body position optimization improves compression quality
• CPR should be performed on a firm surface whenever possible
• Head-up CPR (Trendelenburg reversal): emerging evidence that 15-30° head elevation during CPR may reduce intracranial pressure and improve cerebral perfusion - 2025 guidelines include this as an option
• Breaths with compressions are now recommended for both HCP and lay rescuers when willing and capable (not compression-only only)

Airway Management During Arrest

• Bag-mask ventilation (BMV) is acceptable and may be preferred over intubation in early arrest
• Supraglottic airways (LMA, i-gel) are reasonable alternatives to ETT in many settings
• ETT remains standard if an experienced provider is available and compressions not interrupted
• Capnography (waveform ETCO2) is MANDATORY for confirming ETT and monitoring resuscitation:
  • ETCO2 <10 mmHg after 20 min = very low ROSC probability
  • ETCO2 ≥20 mmHg = good CPR quality
  • Sudden spike in ETCO2 = first sign of ROSC
  • Do NOT use ETCO2 alone to stop resuscitation

Vascular Access

• IV (peripheral) > IO > central for drug delivery speed in cardiac arrest
• IO is equivalent to IV for drug dosing - same doses
• Central line: longer drug circulation time; reserve for monitoring post-ROSC
• Endotracheal drug delivery is no longer recommended (unreliable absorption in pulmonary edema)
• Flush all IV drugs with 20 mL NS bolus; continue CPR 30-60 seconds before shocking

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PART 7 - RESUSCITATION ALGORITHMS (2025 AHA)

Algorithm 1: VF / Pulseless VT (Shockable)

Unresponsive, no breathing, no pulse
         ↓
Activate emergency response, get AED/defibrillator
         ↓
START HIGH-QUALITY CPR (100-120/min)
         ↓
Rhythm check → VF/pVT confirmed
         ↓
SHOCK (biphasic 200 J or manufacturer-recommended)
Immediately resume CPR x 2 min
         ↓
Rhythm check → Still VF/pVT?
         ↓
SHOCK again (max energy)
Resume CPR x 2 min
Establish IV/IO access
EPINEPHRINE 1 mg IV/IO → repeat q3-5 min
         ↓
Rhythm check → Still VF/pVT?
         ↓
SHOCK
Resume CPR x 2 min
AMIODARONE 300 mg IV/IO bolus
(may repeat 150 mg once)
         ↓
Rhythm check → Still VF/pVT?
         ↓
Continue cycles: shock → CPR x 2 min → epi q3-5 min
Consider LIDOCAINE if amiodarone unavailable or failed
Consider reversible causes (H's and T's)
Consider double sequential defibrillation for refractory VF

Algorithm 2: PEA / Asystole (Non-Shockable)

Unresponsive, no pulse
         ↓
Confirm rhythm (asystole confirmed in ≥2 leads)
START HIGH-QUALITY CPR
         ↓
EPINEPHRINE 1 mg IV/IO (give ASAP)
Repeat q3-5 min
         ↓
Identify and treat H's and T's throughout
         ↓
Rhythm check q2 min
         ↓
If shockable rhythm develops → switch to VF algorithm
If ROSC → post-arrest care

The H's and T's - Reversible Causes

Defibrillation - Technical Points

• Biphasic waveform: start at 120-200 J (device-specific; manufacturer-recommended) or 200 J if unknown
• Resume compressions IMMEDIATELY after shock - do not wait to assess rhythm
• Pre-charge defibrillator while compressions are ongoing to minimize pause

• Double Sequential External Defibrillation (DSED): Two defibrillators placed on different vector axes, both fired within seconds for shock-refractory VF (≥3 failed shocks). The 2022 DOSE VF trial showed superiority over standard defibrillation. 2025 guidelines: may be considered for refractory VF (updated - evidence now supports it), though routine use is not yet established.
• Vector Change Defibrillation: Repositioning pad placement to change the electrical vector for refractory VF. 2025 (New): usefulness not yet established - insufficient evidence to recommend for or against.

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PART 8 - SPECIAL CONSIDERATIONS IN CARDIAC ARREST

Peri-Arrest Conditions (2025 AHA new section)

• Atrial fibrillation/flutter with RVR: Electrical cardioversion (synchronized, 120-200 J biphasic for AF; 50-100 J for flutter). Rate control with diltiazem, metoprolol, or amiodarone if hemodynamically stable.
• New 2025: Updated bradycardia algorithm - transvenous pacing is now explicitly recommended for persistent hemodynamically unstable bradycardia refractory to medications (atropine, dopamine/epinephrine infusion).

ECMO-CPR (eCPR)

• Extracorporeal cardiopulmonary resuscitation - VA-ECMO during cardiac arrest
• Considered for refractory arrest in select patients: witnessed arrest, short no-flow time, reversible etiology (PE, hypothermia, ACS), age <65-75, no DNAR
• Requires institutional capability; emerging evidence supports improved survival in select centers
• 2025 AHA: recommends consideration for refractory arrest at ECMO-capable centers

Hypothermia-Induced Arrest

• "Not dead until warm and dead" - continue resuscitation until core temperature ≥30-32°C
• Use warm IV fluids, forced air warming, ECMO rewarming in severe cases
• Hypothermia protects the brain; excellent neurologic outcomes possible even after prolonged arrest

Pregnancy

• Displace uterus leftward (manual displacement or left lateral tilt ≥15°) to relieve aortocaval compression
• Peri-mortem C-section (PMCD) within 5 minutes of maternal cardiac arrest if no ROSC
• PMCD improves maternal ROSC by relieving aortocaval compression

Opioid Overdose (2025 AHA Update)

• Naloxone 0.4-2 mg IV/IO/IM/IN for respiratory arrest/arrest suspected due to opioids
• Updated BLS algorithm now explicitly includes opioid antagonist step
• If no response to naloxone and no pulse: proceed to standard CPR algorithm
• Public access opioid emergency kits (expanded emphasis in 2025 guidelines)

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PART 9 - POST-CARDIAC ARREST CARE (PCAC)

Immediate Stabilization Post-ROSC

• Intubate if not already done for patients not fully awake
• Titrate FiO2 to SpO2 94-99% - avoid hyperoxia (O2 free radicals worsen reperfusion injury)
• Avoid hypoxia (SpO2 <94%) - equally harmful
• Target PaCO2 35-45 mmHg - avoid hypocapnia (<30 mmHg), which causes cerebral vasoconstriction
• Ventilator rate to maintain normocarbia

• Target MAP 65-100 mmHg (many centers target ≥65-70 mmHg minimum; 90-100 mmHg if needed for cerebral autoregulation)
• Treat hypotension aggressively: IV fluids + vasopressors (norepinephrine is first-line pressor post-ROSC)
• 12-lead ECG immediately to assess for STEMI

• Target glucose 140-180 mg/dL (120-180 mg/dL per some guidelines)
• Avoid both hypoglycemia AND hyperglycemia - both worsen neurological outcome
• Check glucose every 30-60 min

Coronary Angiography Post-ROSC

• STEMI on post-ROSC ECG: Immediate emergent PCI (Class I recommendation - unchanged)
• No STEMI but hemodynamic instability, electrical instability, or evidence of ischemia: Consider emergent angiography
• No STEMI, hemodynamically stable: 2023 TOMAHAWK/COACT trials changed the approach - delayed or selective angiography is now acceptable; emergent angiography does NOT improve outcomes in non-STEMI post-arrest patients
• 2025 AHA: Emergent angiography is reasonable for STEMI; for non-STEMI OHCA, delayed angiography (within 24-72h) is acceptable unless clinical instability dictates earlier intervention

Targeted Temperature Management (TTM) - 2025 Update

• Original 2002 HACA trial and Bernard et al.: hypothermia (32-34°C) improved neurological outcomes in shockable OHCA
• 2013 TTM trial (Nielsen et al.): 33°C vs. 36°C - no difference
• 2021 TTM2 trial (Dankiewicz et al.): Normothermia (37.5°C) with aggressive fever prevention vs. hypothermia (33°C) - no difference in mortality or neurological outcome

• Fever prevention is mandatory: Keep temperature ≤37.5°C for at least 72 hours post-ROSC in comatose patients - aggressive fever treatment even if not actively cooling
• Active cooling to 32-36°C may still be reasonable for select comatose patients, but is no longer universally mandated
• DO NOT use cold saline prehospital boluses (increases pulmonary edema, no benefit)
• Shivering must be treated: analgesia + sedation; NMB if refractory

Neuroprognostication

• Without TTM: ≥72 hours post-ROSC before declaring poor prognosis
• With TTM (32-34°C): ≥72 hours after rewarming (total ~120 hours from arrest)

Seizures Post-Arrest

• Seizures (including non-convulsive status epilepticus - NCSE) occur in 10-30% of post-arrest comatose patients
• NCSE is particularly dangerous and clinically silent
• Continuous EEG monitoring is indicated for all comatose post-arrest patients (at least 24-48h)
• Treat clinical seizures and NCSE promptly: Benzodiazepines → Levetiracetam/Valproate → Keppra → anaesthetic doses
• 2025 Update: Myoclonus definitions and treatment options now explicitly included - differentiate Lance-Adams syndrome (good prognosis) from malignant myoclonus

Mechanical Circulatory Support (MCS)

• Intra-aortic balloon pump (IABP): improves coronary perfusion diastolically; use in cardiogenic shock
• Impella/LVAD: for refractory cardiogenic shock post-arrest
• VA-ECMO: bridge to recovery, transplant, or device; most benefit in reversible causes

Survivorship and Rehabilitation (2025 AHA New Section)

• Structured follow-up for patients, caregivers, and rescuers
• Screen for PTSD, anxiety, cognitive impairment in arrest survivors
• Genetic testing and family screening for all SCA survivors without clear cause (especially for channelopathies, HCM)
• ICD evaluation for all appropriate survivors

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PART 10 - ICD THERAPY AND PREVENTION

Primary Prevention (ICD before first SCA)

• EF ≤35% + symptomatic HF (NYHA II-III) + optimal medical therapy x3 months (MADIT-II, SCD-HeFT trials)
• Prior MI (>40 days) + EF ≤30% + NYHA I symptoms
• HCM with risk factors (wall ≥30 mm, syncope, family SCD, abnormal BP response, prior VT/VF)
• Confirmed channelopathy (Long QT, Brugada, CPVT) with symptoms or high-risk features
• ARVC with VT/VF or high-risk features

Secondary Prevention (ICD after SCA or VT/VF)

• All survivors of SCA without clearly reversible cause (Class I)
• Sustained VT causing hemodynamic compromise or syncope (Class I)

Pharmacologic Prevention

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PART 11 - TERMINATION OF RESUSCITATION (2025 AHA Updated)

Out-of-Hospital Cardiac Arrest (OHCA) - BLS TOR Rule

1. Arrest NOT witnessed by EMS
2. No ROSC at any time
3. No shock delivered (AED)

Advanced Provider TOR Rule

1. Arrest not witnessed by bystander or EMS
2. No bystander CPR provided
3. No ROSC after 3 full ALS rounds (ALS on scene ≥20 min)
4. Not presenting rhythm VF/pVT

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PART 12 - CHAIN OF SURVIVAL (2025 AHA Update)

1. Recognition and activation - Call 911; recognize arrest
2. Immediate high-quality CPR - Bystander CPR with compressions + breaths (when capable)
3. Rapid defibrillation - AED use as soon as available
4. Advanced resuscitation - EMS/ACLS team with drugs, airway, monitoring
5. Post-cardiac arrest care - ICU management, TTM, coronary angio, neuroprognostication
6. Recovery - Survivorship support, rehabilitation, ICD, genetic counseling

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KEY CLINICAL PEARLS FOR THE EMERGENCY RESIDENT

1. The first 4 minutes are everything. Every minute of VF without defibrillation drops survival by ~7-10%. If an AED is present, use it before calling for more help.
2. CPR quality is the intervention that saves lives. Drugs are adjuncts. Maximize compression fraction, rate, and depth. No interruptions.
3. Amiodarone and lidocaine don't improve hospital discharge survival - they help get the patient to the hospital, which is still valuable.
4. PEA demands you think harder, not just push harder. Every PEA patient has a reason. Narrow QRS = mechanical problem; use POCUS. Wide QRS = metabolic/toxic problem; treat with specific antidotes.
5. ETCO2 is your friend. If it's >20 mmHg, your CPR is adequate. If it suddenly jumps 10+ mmHg, ROSC has occurred - check pulse before next cycle.
6. Post-arrest fever kills neurons. Keep temp ≤37.5°C aggressively. That is now the minimum standard regardless of whether you use active cooling.
7. Don't prognosticate too early. Many patients declared to have "poor prognosis" make meaningful recoveries if given 72+ hours. The 2025 guidelines strongly reinforce multimodal, time-appropriate assessment.
8. STEMI + cardiac arrest = cath lab. No debate. For non-STEMI post-arrest patients with hemodynamic stability, it is now acceptable to wait.
9. Think about ICD for every SCA survivor you resuscitate. If they survive to discharge without a clearly reversible cause, they need an ICD - this is a Class I recommendation.
10. The 2025 AHA guidelines are the most current evidence base (published Circulation, October 2025). Read the PMID 41122884 (Adult ALS) and 41122894 (Post-Cardiac Arrest Care) papers directly for full detail.

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