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Cardiogenic Shock, Sudden Cardiac Death & CPR/AED Algorithms

Independent Work — Emergency Cardiology

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PART 1: CARDIOGENIC SHOCK

1.1 Definition

• Persistent systolic BP < 90 mmHg, or mean arterial pressure (MAP) < 60–65 mmHg, unresponsive to volume replacement
• Requirement of vasopressors to maintain adequate BP
• Clinical features of peripheral hypoperfusion: cold clammy extremities, oliguria, altered mental status
• Elevated arterial lactate > 2 mmol/L as an objective marker of hypoperfusion

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1.2 Etiology and Incidence

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1.3 Pathophysiology

1. Myocardial ischemia/necrosis → profound depression of myocardial contractility
2. Reduced cardiac output (CO) → decreased systemic BP
3. Decreased coronary perfusion pressure → worsening myocardial ischemia
4. Further reduction of contractility → further reduction of CO (the "vicious cycle")

• Ischemic injury triggers release of cytokines (TNF-α, interleukins) and activation of inducible nitric oxide synthase (iNOS)
• Excessive nitric oxide (NO) and peroxynitrite cause myocardial depression and vasodilation — paradoxically, systemic vascular resistance (SVR) may be inappropriately low rather than elevated
• This creates a mixed picture: pump failure combined with a distributive component (SIRS)

• ↓ Stroke volume → ↓ Cardiac Index (CI < 2.2 L/min/m²)
• Compensatory neurohormonal activation → tachycardia, vasoconstriction, fluid retention
• ↑ LV end-diastolic pressure (LVEDP) → pulmonary congestion / pulmonary edema
• ↑ Pulmonary capillary wedge pressure (PCWP > 18 mmHg)
• ↓ Mixed venous O₂ saturation (SvO₂) reflecting increased O₂ extraction

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1.4 SCAI Classification (Severity Staging)

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1.5 Clinical Signs

• Dyspnea, orthopnea
• Chest pain (if underlying MI)
• Profound weakness, fatigue
• Anxiety, confusion, altered consciousness

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1.6 Diagnostics

• ST-elevation or depression (ischemia/infarction)
• New LBBB, Q waves
• Arrhythmias (VT, AF, complete heart block)

• Cardiomegaly
• Pulmonary vascular congestion / pulmonary edema (butterfly pattern)
• Pleural effusions

• First-line imaging tool — identifies cause, severity, and type of CS
• Assesses: LV/RV function and size; wall motion abnormalities; pericardial effusion/tamponade; valvular pathology (MR, AI); VSR
• Distinguishes LV, RV, or biventricular failure

• Cardiac Index (CI): < 2.2 L/min/m² (< 1.8 L/min/m² in severe CS)
• PCWP: > 18 mmHg (elevated in LV failure)
• SVR: typically elevated (occasionally low due to SIRS)
• SvO₂: decreased

• Immediately indicated in all CS complicating MI for reperfusion assessment
• Also consider in resuscitated cardiac arrest survivors without ST-elevation (~70% have significant CAD)

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PART 2: SUDDEN CARDIAC DEATH

2.1 Definition

• Within 1 hour of symptom onset, or
• Within 24 hours of being last seen well (if unwitnessed)

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2.2 Epidemiology

• SCD is most prevalent in individuals > 45–50 years old; 60% occur in males
• Circadian pattern: highest incidence in the first few hours after awakening from sleep (increased sympathetic activity)
• Most events occur in the home (~70%), though public cardiac arrests have better survival rates (higher likelihood of shockable rhythm, bystander CPR, and AED access)
• Socioeconomic gradient: SCD is 30–80% higher in the lowest vs. highest socioeconomic quartile

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2.3 Etiology

• Coronary artery disease (CAD): 65–80% of cases — the leading cause; SCD may be the first manifestation of IHD
• Cardiomyopathy (dilated, hypertrophic): 10–15%
• Other structural/electrical causes: 5–10%

• Chronic severe atherosclerotic stenosis is found in most; acute plaque rupture in only 10–20% of cases
• 80–90% of resuscitated SCA victims show no enzymatic or ECG evidence of myocardial necrosis
• Healed remote MIs present in ~40%
• Subendocardial myocyte vacuolization (chronic severe ischemia) is common

• Hereditary channelopathies (Long QT syndrome, Brugada syndrome, CPVT)
• Hypertrophic cardiomyopathy (HCM) — most common cause of SCD in young athletes
• Dilated cardiomyopathy
• Congenital coronary artery abnormalities
• Myocarditis / sarcoidosis
• Mitral valve prolapse
• Pulmonary hypertension
• Pericardial tamponade, pulmonary embolism
• Drug-induced (cocaine, methamphetamine)

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2.4 Mechanisms and Pathophysiology

Primary Mechanisms:

• Most common terminal arrhythmia in witnessed SCD (~70–80% of initial rhythms in public arrests)
• Triggered by electrical irritability of the myocardium (usually ischemia-mediated)
• Multiple re-entry circuits generated within the ventricular myocardium → ventricular tachycardia (VT) → degenerates to VF
• VF is present in only 23% of all cardiac arrests overall (many are unwitnessed and have degenerated to asystole by first EMS contact)
• Shockable rhythm: responds to defibrillation

• Organized ventricular rhythm at high rate without effective cardiac output
• Degenerates rapidly to VF
• Shockable rhythm

• Complete cessation of electrical activity
• Common in unwitnessed or prolonged arrests
• Non-shockable; prognosis very poor if unwitnessed
• Primary vs. secondary: primary = failure of conduction system; secondary = external factors (hypoxia, drugs)

• Organized electrical rhythm without detectable pulse
• Caused by profound reduction of CO due to myocardial depression or mechanical obstruction (tamponade, tension pneumothorax, PE, hypovolemia)
• Non-shockable; treatment targets reversible causes (the "Hs and Ts")

• Ischemic injury causes heterogeneity of conduction and refractory periods → substrate for re-entry
• Healed infarct scar provides anatomical substrate for re-entrant circuits
• Acute ischemia, catecholamine surges, electrolyte disturbances, and autonomic imbalance act as triggers
• In structurally normal hearts (channelopathies): mutations in ion channels (Na⁺, K⁺, Ca²⁺) cause aberrant depolarization/repolarization → spontaneous VF

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2.5 Risk Factors / Predictors

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2.6 Clinical Signs (Cardiac Arrest Presentation)

• Sudden loss of consciousness (collapse)
• No pulse / no detectable blood pressure
• Apnea or agonal gasping
• Cyanosis developing rapidly
• Fixed, dilated pupils (if prolonged)
• ECG: VF, pVT, asystole, or PEA

• Chest pain, palpitations, dizziness, syncope
• However, in >50% of cases, SCD occurs without prior warning

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2.7 Diagnostics

• Identify rhythm: VF, pVT, asystole, PEA
• Post-ROSC: look for ST elevation (STEMI → emergent cath), QTc prolongation, Brugada pattern, delta waves (WPW)

• Identifies tamponade, massive PE, severe wall motion abnormality, hypovolemia
• Differentiates true asystole from pseudo-PEA

• Troponin, CK-MB (myocardial necrosis)
• ABG (acidosis, hypoxia, hypercarbia)
• Electrolytes (K⁺, Mg²⁺, Ca²⁺ — reversible causes)
• Lactate (degree of hypoperfusion)
• Toxicology screen (drug-induced arrest)
• TSH (hypothyroidism)

• Immediately for post-arrest STEMI
• Considered in hemodynamically unstable post-arrest patients without ST-elevation

• For risk stratification in survivors; identifies inducible arrhythmias

• For unexplained syncope or suspected channelopathy

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PART 3: CPR AND AED ALGORITHMS

3.1 Overview and the "Chain of Survival"

1. Early recognition and activation of emergency medical services (EMS)
2. Early high-quality CPR
3. Rapid defibrillation (AED or manual defibrillator)
4. Advanced cardiac life support (ACLS)
5. Post-cardiac arrest care (integrated care system)

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3.2 Basic Life Support (BLS) — Adult CPR Algorithm

• No normal breathing (absent or only gasping) AND no pulse → begin CPR

• Compressions first (C before A-B per current AHA guidelines)
• Start 30 chest compressions before giving 2 breaths

• Ratio: 30:2 (30 compressions : 2 breaths)
• Each breath: 1 second; visible chest rise
• Tilt head – lift chin (jaw thrust if trauma suspected)

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3.3 AED Algorithm

1. Power ON the AED (open lid or press power button)
2. Apply pads as directed (right clavicle/upper sternum; left lateral chest/apex)
3. Analyze rhythm — ensure no one is touching the patient ("CLEAR!")
4. If shock advised: deliver shock → immediately resume CPR (do not check pulse first)
5. If no shock advised (PEA/asystole): resume CPR immediately; reanalyze every 2 minutes
6. Continue until:
   • Signs of life return (ROSC)
   • ACLS providers take over
   • Victim is declared deceased

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3.4 ACLS Algorithms

Shockable Rhythms: VF / Pulseless VT

VF / pVT identified
        ↓
Shock (biphasic: 120–200 J; monophasic: 360 J)
        ↓
Immediately resume CPR × 2 minutes (no pulse check)
        ↓
Rhythm check
    ├── VF/pVT → 2nd Shock → CPR × 2 min
    │           → IV/IO access → Epinephrine 1 mg IV q3–5 min
    │           → 3rd Shock → CPR × 2 min
    │           → Amiodarone 300 mg IV bolus (or Lidocaine 1–1.5 mg/kg)
    │           → Continue: Shock → CPR × 2 min → Epinephrine → Amiodarone...
    └── ROSC → Post-cardiac arrest care

• Epinephrine 1 mg IV/IO every 3–5 minutes (given after 2nd shock, then every other cycle) — improves coronary perfusion pressure; evidence for neurologically intact survival is limited but remains standard
• Amiodarone 300 mg IV bolus as first antiarrhythmic; second dose 150 mg if persistent VF/VT
• Lidocaine 1–1.5 mg/kg IV — alternative if amiodarone unavailable

Non-Shockable Rhythms: Asystole / PEA

Asystole / PEA identified
        ↓
CPR × 2 minutes (high-quality, continuous)
        ↓
IV/IO access → Epinephrine 1 mg IV q3–5 min (as soon as possible)
        ↓
Identify and treat REVERSIBLE CAUSES ("5 Hs and 5 Ts")
        ↓
Rhythm check every 2 minutes
    ├── Remains asystole/PEA → Continue CPR + Epi → Treat reversible causes
    └── Shockable → Switch to VF/pVT algorithm
    └── ROSC → Post-cardiac arrest care

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3.5 Post-Cardiac Arrest Care (Post-ROSC)

1. Airway: Secure advanced airway (endotracheal intubation); confirm placement
2. Ventilation: Target SpO₂ 92–98%; avoid hyperoxia; target PaCO₂ 35–45 mmHg (avoid hyperventilation)
3. Hemodynamics: Target MAP ≥ 65 mmHg; vasopressors (norepinephrine preferred) if hypotensive
4. 12-lead ECG: Identify STEMI → emergent PCI
5. Targeted Temperature Management (TTM): Maintain temperature 32–36°C for 24 hours in comatose survivors (neuroprotection)
6. Coronary angiography: Emergent if STEMI; consider in unstable patients without ST elevation
7. Treat precipitating cause: ACS, electrolyte disturbance, toxin, PE, etc.
8. Neurological assessment: Glasgow Coma Scale, pupillary reflexes, CT brain if trauma/hemorrhage suspected

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3.6 Special Considerations

• Primary prevention: EF ≤ 35%, NYHA Class II–III on optimal medical therapy ≥ 3 months
• Secondary prevention: survivors of VF/VT arrest not from reversible cause
• ICDs "sense and electrically counteract episodes of ventricular fibrillation" — markedly improve prognosis in at-risk patients. — Robbins & Kumar Basic Pathology, p. 362

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Summary Table

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• Harrison's Principles of Internal Medicine, 22nd Edition (2025) — Ch. 316
• Tintinalli's Emergency Medicine: A Comprehensive Study — Ch. 11, 12
• Robbins & Kumar Basic Pathology (10th Ed.) — Ch. 9
• Robbins, Cotran & Kumar Pathologic Basis of Disease — Ch. 9