Sudden Cardiac Arrest and Resuscitation

Immediate Arrest Mechanisms

• VF/pulseless VT: Disorganized electrical activity or rapid, ineffective contractions prevent meaningful perfusion; electrical instability results from acute myocardial ischemia, electrolyte derangements, or direct cardiac injury
• Asystole and pulseless electrical activity (PEA): Represent end-stage hypoxia, severe acidosis, or profound circulatory collapse; asystole reflects absence of electrical activity, while PEA shows organized electrical complexes without mechanical output ("dissociation")
• Ischemic cascade: Within seconds of arrest, cerebral and coronary perfusion ceases; anaerobic metabolism begins, producing lactate and causing cellular acidosis; ATP depletion leads to loss of ion pump function and cellular edema

Myocardial Effects

• Stunned myocardium: Even brief arrests cause transient contractile dysfunction due to calcium overload, oxidative stress, and mitochondrial dysfunction; stunned myocardium recovers over hours to days if reperfusion occurs
• Reperfusion injury: Following resuscitation, restoration of oxygen delivery generates reactive oxygen species (ROS) and inflammatory cytokines, paradoxically worsening cellular damage; particularly relevant in post-arrest myocardial dysfunction and global ischemia-reperfusion injury

Cerebral Hypoperfusion Sequelae

• Brain ischemia develops within seconds; selective neuronal necrosis affects hippocampus, cerebellum, and watershed zones preferentially
• Post-anoxic encephalopathy: Results from combined hypoxia-ischemia, reperfusion injury, seizures, and cerebral edema; manifests as decreased consciousness, myoclonic jerks, and potential permanent neurological injury
• Metabolic derangements (severe acidosis, hyperkalemia, hypoxemia) during arrest worsen all organ systems

Cardiac Causes (85% of arrests)

• Acute coronary syndrome (ACS): Most common cause in adults; ST-elevation MI (STEMI), non-STEMI, and unstable angina can precipitate VF
• Cardiomyopathies: Dilated cardiomyopathy (ischemic or nonischemic), hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, peripartum cardiomyopathy
• Valvular disease: Acute aortic regurgitation, prosthetic valve thrombosis, endocarditis
• Channelopathies and genetic conditions: Long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), Wolff-Parkinson-White syndrome
• Structural heart disease: Aortic stenosis, hypertrophic obstructive cardiomyopathy (HOCM), pulmonary hypertension, left ventricular thrombus
• Myocarditis and pericarditis: Viral, bacterial, or autoimmune etiologies

Non-Cardiac Causes (15% of arrests)

• Pulmonary embolism (PE): Acute right ventricular failure and severe hypoxemia; classically presents with PEA
• Severe hypoxemia: Pneumonia, ARDS, asphyxiation, drowning, choking
• Tension pneumothorax: Mechanical compression of heart and decreased venous return
• Acute stroke or intracranial hemorrhage: Sudden massive increase in intracranial pressure
• Septic shock: Severe infection with profound vasodilatation and myocardial depression
• Electrolyte abnormalities: Severe hyperkalemia, hypokalemia, severe hypomagnesemia

Toxicological and Metabolic Causes

• Drug overdose (cocaine, sympathomimetics, antiarrhythmics), anticholinergic toxicity
• Severe hypothermia, severe acidosis, severe hyperglycemia

Risk Factors for SCA

• Prior myocardial infarction or reduced ejection fraction (EF ≤35%)
• Family history of sudden cardiac death or arrhythmogenic syndromes
• Smoking, hypertension, diabetes, hyperlipidemia
• Structural heart disease, prior arrhythmias
• Electrolyte abnormalities, QT-prolonging medications

Cardinal Presentation

• Sudden loss of consciousness: Patient collapses without prodrome or with minimal warning (seconds)
• Absent pulses (carotid or femoral preferred) and unresponsiveness
• Apnea or gasping: Brief agonal breathing common in first minutes; should not be mistaken for normal respiration
• Skin pallor, cyanosis, or ashen appearance within seconds

Rhythm-Specific Presentations

• VF/pulseless VT: Sudden collapse during activity; witnessed arrests often show VF on monitor within seconds
• Asystole: "Flatline" appearance on monitor; associated with prolonged untreated arrest or severe hypoxia
• PEA: Organized rhythm on monitor but no pulse; associated with cardiac tamponade, tension pneumothorax, severe hypovolemia, pulmonary embolism, or end-stage illness

Physical Examination Findings (During Arrest)

• Unresponsiveness to verbal and tactile stimulation
• Absent carotid or femoral pulse
• Fixed, dilated pupils (develops within minutes; nonspecific for outcome)
• Mottled, cool skin (peripheral vasoconstriction)
• No heart sounds or very faint/irregular sounds
• Absent breath sounds or only occasional agonal gasps

Post-Resuscitation Presentations (if return of spontaneous circulation achieved)

• Variable mental status (comatose to alert depending on cerebral perfusion time)
• Myoclonic jerks or seizures (anoxic seizures)
• Hemodynamic instability requiring vasopressors
• Signs of underlying etiology (chest pain from MI, dyspnea from PE, focal neurologic deficits)

Immediate Rhythm Recognition

• 12-lead ECG and continuous cardiac monitoring: Essential for identifying rhythm type (VF, pulseless VT, asystole, PEA); VF appears as fine or coarse disorganized waves; pulseless VT shows rapid, organized wide complexes; asystole shows straight line; PEA shows organized complexes
• Clinical confirmation: Check for carotid pulse for no more than 10 seconds; absence of pulse in unresponsive, apneic patient confirms arrest

Laboratory Investigations (During/After Resuscitation)

• Arterial or venous blood gas: Reveals severe metabolic acidosis (pH often <7.0), hypercarbia, and hypoxemia during arrest; used to guide ventilation and medication dosing
• Electrolytes: Identify critical abnormalities (hyperkalemia, severe hypokalemia, severe hypomagnesemia, severe hypocalcemia) causing arrest
• Troponin and myoglobin: Elevated troponin supports ACS diagnosis; myoglobin elevation suggests rhabdomyolysis
• Complete blood count: Anemia or thrombocytopenia noted
• Coagulation studies and D-dimer: D-dimer elevation raises suspicion for PE
• Lactate: Severe elevation during arrest; clearance monitored post-resuscitation as prognostic indicator

Imaging and Diagnostic Studies

• Chest X-ray: Evaluates for pneumothorax, pulmonary edema, aspiration, underlying pneumonia
• 12-lead ECG post-ROSC: Identifies STEMI, other acute ischemic changes, prolonged QT, Brugada pattern, or other channelopathy features
• Echocardiography: Assesses cardiac function, wall motion abnormalities (acute MI), ventricular thrombus, pericardial effusion/tamponade, prosthetic valve function
• Coronary angiography: Emergent cath lab activation for suspected ACS (especially STEMI); improves outcomes if performed in selected post-arrest patients
• CT pulmonary angiography (CTPA): If PE suspected; may be deferred until after stabilization
• Head CT: If seizures, focal neurologic deficits, or trauma suspected; not routine screening

Diagnostic Criteria

• Arrest confirmation: Unresponsiveness + absent pulse + apnea (or only agonal gasps)
• Rhythm classification: Shockable (VF/pulseless VT) vs. non-shockable (asystole/PEA)
• Resuscitation endpoints: Termination of resuscitation typically considered after ≥30 minutes of continuous ACLS without return of spontaneous circulation (ROSC) in witnessed arrest with unfavorable initial rhythm, or after ≥20 minutes in unwitnessed arrest or asystole as initial rhythm (variable by protocol)

Immediate Management (First Minutes)—High-Quality CPR

Chest Compressions (Cornerstone of Resuscitation)

• Compression rate: 100–120 compressions per minute (firm and fast)
• Compression depth: 5–6 cm in adults (approximately one-third anterior-posterior chest diameter)
• Hand position: Lower half of sternum with heels of both hands; allow full recoil between compressions to restore coronary perfusion pressure
• Minimize interruptions: Target <10 seconds of compression interruption during initial rhythm check
• Perform continuous compressions; do not wait for airway placement to begin

Airway Management

• Initial approach: Head-tilt chin-lift or jaw thrust if trauma suspected; provide rescue breathing (2 breaths per cycle if 2-person CPR) or allow passive oxygenation if trained rescuer unable to perform
• Rapid sequence intubation (RSI): Once ALS team arrives, secure airway with endotracheal intubation or supraglottic airway; minimize interruption of chest compressions (≤10 seconds)
• Ventilation rate post-intubation: 10–12 breaths/minute (avoid hyperventilation, which increases intrathoracic pressure and reduces coronary perfusion)
• Waveform capnography: Target end-tidal CO2 (ETCO2) 35–40 mmHg as marker of perfusion adequacy; ETCO2 <10 mmHg suggests poor perfusion or inadequate resuscitation

Defibrillation (if VF or Pulseless VT)

• Automated external defibrillator (AED) or manual defibrillation: Apply as soon as available; initial shock energy 200 J (or manufacturer default) for biphasic defibrillators, or 360 J for monophasic
• Timing: If VF/pulseless VT confirmed, deliver shock after 2 minutes of CPR or within 3 minutes of collapse if AED immediately available
• Post-shock management: Immediately resume CPR for 2 minutes before reassessing rhythm; do not delay compressions to check pulse

Pharmacological Management (Advanced Cardiac Life Support)

Vasopressors for All Arrest Rhythms

• Epinephrine (adrenaline): 1 mg IV/IO push every 3–5 minutes during CPR (2–10 mcg/min infusion post-ROSC); increases coronary and cerebral perfusion pressure via α-adrenergic effect; standard agent
• Amiodarone (preferred antiarrhythmic for VF/pulseless VT): 300 mg IV/IO first dose, then 150 mg second dose if VF persists; loading dose 150 mg over 10 minutes post-ROSC; slows conduction, prolongs refractoriness, non-competitive β-blocker and calcium channel blocker effects
• Lidocaine (alternative antiarrhythmic): 1–1.5 mg/kg IV/IO initial dose (75–100 mg), repeat 0.5–0.75 mg/kg every 5–10 minutes to max 3 mg/kg; less favorable evidence than amiodarone but acceptable alternative
• Vasopressin: No longer routinely recommended but may be considered in refractory VF (single 40 IU IV/IO dose)

Medications for Specific Arrest Scenarios

• Sodium bicarbonate: Indicated for severe metabolic acidosis (pH <7.0), tricyclic antidepressant overdose, or hyperkalemia (causes alkalinization); dose 50–100 mEq IV/IO
• Calcium: For hyperkalemia or calcium channel blocker overdose; 10 mL of 10% calcium chloride IV/IO (calcium gluconate if peripheral line only)
• Magnesium: 1–2 grams IV/IO for torsades de pointes (polymorphic VT with prolonged QT)
• Atropine: No longer recommended for asystole or PEA (removed from 2015 ACLS guidelines)

Post-ROSC Medications

• Beta-blockers (e.g., metoprolol 25–100 mg IV): Reduce reinfarction risk and sudden death, especially post-MI
• ACE inhibitors or ARBs: Indicated for reduced EF or anterior MI; started after stabilization
• Statins: Initiated post-ACS for plaque stabilization
• Dual antiplatelet therapy: Aspirin + P2Y12 inhibitor (clopidogrel, ticagrelor, prasugrel) if ACS-related arrest

Non-Pharmacological Measures

Therapeutic Hypothermia / Targeted Temperature Management (TTM)

• Indication: All comatose patients with ROSC regardless of initial rhythm (Class IIa recommendation)
• Target temperature: 32–36°C maintained for 12–24 hours, then passive rewarming; reduces cerebral metabolism and limits reperfusion injury
• Methods: Cold IV saline, ice packs, intravascular cooling catheters, extracorporeal rewarming (ECMO) in severe hypothermia
• Monitoring: Continuous EEG if available to detect seizures; frequent neuroexamination

Extracorporeal Membrane Oxygenation (ECMO) or Extracorporeal CPR (ECPR)

• Indication: Refractory VF/pulseless VT after conventional ACLS failure; select cases of acute PE with cardiac arrest
• Benefit: Provides complete cardiac and pulmonary support while correcting underlying pathology (e.g., coronary intervention, PE thrombolysis); improves survival in carefully selected young patients with reversible causes
• Timing: Ideally initiated within 15 minutes of arrest; requires interventional capability on-site

Percutaneous Coronary Intervention (PCI) and Thrombolysis

• Emergent cardiac catheterization: Indicated if ACS-related arrest; can be performed during ongoing CPR
• Fibrinolytic therapy: May be considered for PE-related arrest if ECPR unavailable and no contraindications

Ongoing Supportive Care

Hemodynamic Support

• Vasopressors (norepinephrine, dopamine, epinephrine infusions): Maintain mean arterial pressure >65 mmHg to preserve organ perfusion
• Inotropic agents (dobutamine, milrinone): Support myocardial contractility in post-arrest cardiogenic shock
• Fluid management: Cautious IV fluids; avoid overload given post-arrest pulmonary edema risk; balance perfusion vs. cerebral edema prevention

Mechanical complications of CPR

• Rib and sternal fractures: the most common injury from guideline-depth compressions; crepitus or a palpable "give" mid-resuscitation. Do not reduce depth — inadequate compression depth kills more patients than fractures do.
• Tension pneumothorax or hemothorax: from fractured rib fragments or barotrauma with over-aggressive bag-mask ventilation; signaled by rising peak pressures, absent unilateral breath sounds, and re-arrest into PEA. Emergency — needle decompression before further diagnostics.
• Hepatic or splenic laceration: from low hand position over the xiphoid; suspected with post-ROSC hypotension, falling hematocrit, and abdominal distension. Emergency.
• Gastric insufflation and aspiration pneumonitis: from ventilating against a closed glottis; regurgitant material in the oropharynx and later hypoxemia with infiltrates.

Complications of the arrest state (post-cardiac arrest syndrome)

• Hypoxic-ischemic brain injury: the leading cause of death after ROSC; selective necrosis of hippocampus and cerebellum produces persistent coma, absent brainstem reflexes, or status myoclonus. The AHA advises multimodal prognostication delayed at least 72 hours after normothermia, since sedation and hypothermia confound the exam.
• Post-arrest myocardial stunning: calcium overload and reperfusion injury produce a low-output state with vasopressor-dependent hypotension and a globally depressed EF on echo that typically recovers over days.
• Re-arrest / recurrent VF: ongoing ischemia or electrolyte derangement; emergency requiring immediate defibrillation and correction of K+ and Mg2+.
• Acute kidney injury and rhabdomyolysis: ischemic ATN plus myoglobin load; oliguria with rising creatinine and CK.

Treatment-related complications

• Hyperoxia and hyperventilation: excess oxygen amplifies reactive oxygen species and hypocapnia causes cerebral vasoconstriction; AHA post-arrest care recommends titrating FiO2 to a normal SpO2 and targeting normocapnia.
• Targeted temperature management: shivering, bradycardia, coagulopathy, and cold diuresis with hypokalemia — with rebound hyperkalemia during rewarming, a classic arrhythmia trigger.
• Drug effects: amiodarone-induced hypotension and bradycardia; sodium bicarbonate causing hypernatremia, alkalosis, and paradoxical intracellular acidosis when given reflexively rather than for a defined indication.

• The shockable pair is VF and pulseless VT: for a witnessed arrest with a defibrillator at hand, the single best next step is immediate defibrillation — not epinephrine, not intubation, not IV access. For asystole and PEA the answer is CPR plus epinephrine; shocking asystole is the classic distractor.
• After a shock, resume compressions immediately for 2 minutes: per the AHA 2020 ECC guidelines, do not check a pulse or rhythm right after the shock. Stems that offer "reassess pulse" as the next step after defibrillation are testing this.
• Epinephrine 1 mg IV/IO every 3–5 minutes in any arrest rhythm; give it early in non-shockable arrest, but defibrillate first in shockable rhythms. High-dose epinephrine has been abandoned.
• PEA means hunt for a cause: run the Hs and Ts. Board favorites are hyperkalemia (peaked T waves in a dialysis patient → calcium first), tension pneumothorax, tamponade, and massive PE. Bedside echo during a rhythm check is the fastest discriminator.
• Polymorphic VT with a long QT is torsades: give magnesium sulfate IV, not amiodarone — amiodarone prolongs QT further.
• ETCO2 is the resuscitation vital sign: an abrupt spike toward normal signals ROSC; a persistently low value after prolonged high-quality CPR predicts failure and reflects inadequate cardiac output, not inadequate ventilation.
• The one association examiners love: a survivor of VF/pulseless VT arrest not attributable to a reversible or transient cause earns a secondary-prevention ICD (ACC/AHA/HRS 2017 ventricular arrhythmia/SCD guideline). Arrest occurring within the first 48 hours of an acute MI, or from a correctable electrolyte or drug cause, is the exception — revascularize and correct instead.
• Post-ROSC ECG pitfalls: a new LBBB alone is not a STEMI equivalent — apply Sgarbossa criteria. In hypothermic arrest, continue resuscitation during rewarming: "not dead until warm and dead."