Cardiac Arrest and ACLS

Ischemic (most common adult mechanism)

• Acute coronary syndrome: ischemic myocardium becomes electrically heterogeneous, favoring reentry and degeneration into VF/pulseless VT. Coronary disease underlies the majority of sudden cardiac death in adults per the AHA/ACC/HRS 2017 ventricular arrhythmia and sudden cardiac death guideline.
• Prior MI with scar: fixed reentrant circuits around the border zone; the strongest predictor is reduced LVEF, the basis for prophylactic ICD referral.

Structural non-ischemic

• Cardiomyopathies: dilated, hypertrophic (leading cause in young athletes), and arrhythmogenic right ventricular cardiomyopathy; also infiltrative disease (sarcoid, amyloid) and severe aortic stenosis.

Primary electrical (structurally normal heart)

• Channelopathies: congenital long QT, Brugada (coved ST elevation V1–V2, arrest during sleep/fever), catecholaminergic polymorphic VT (arrest with exertion or emotion), and WPW with atrial fibrillation degenerating to VF.
• Commotio cordis: blunt precordial blow during the vulnerable T-wave upstroke.

Non-cardiac / reversible (the Hs and Ts already listed)

• Respiratory: hypoxia is the dominant pathway in children and drowning — arrest follows respiratory failure rather than preceding it.
• Toxicologic: QT-prolonging drugs, cocaine, tricyclics (Na-channel blockade, wide QRS), digoxin, opioids (hypoventilation).
• Metabolic/mechanical: hyperkalemia, massive PE, tension pneumothorax, tamponade, exsanguination.

Non-modifiable risk factors examiners plant

• Male sex, older age, family history of sudden death or drowning under age 40, known channelopathy mutation, prior MI or reduced LVEF, prior sustained VT, CKD/dialysis.

Modifiable risk factors

• Smoking, hypertension, dyslipidemia, diabetes, obesity, physical inactivity — targeted by the ACC/AHA 2019 primary prevention guideline; also electrolyte derangement, QT-prolonging polypharmacy, stimulant use, and nonadherence to guideline-directed HFrEF therapy (ARNI or ACEI/ARB, beta blocker, MRA, and SGLT2 inhibitor), which itself lowers arrhythmic death.

Primary mechanisms of cardiac arrest and cellular injury

• Ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT) — Loss of organized electrical activity leads to ineffective myocardial contractions; these "shockable" rhythms are associated with the best prognosis if treated rapidly with defibrillation. Underlying mechanism typically involves acute coronary syndrome or primary arrhythmia.

• Asystole and pulseless electrical activity (PEA) — "Non-shockable" rhythms reflect either complete cessation of electrical activity (asystole) or electrical activity without mechanical contraction (PEA), usually secondary to profound shock, myocardial infarction, tension pneumothorax, massive hemorrhage, or severe metabolic derangement.

• Cerebral and myocardial ischemia — Cessation of perfusion causes rapid transition from aerobic to anaerobic metabolism within seconds. Lactate accumulates, causing intracellular acidosis. ATP depletion occurs, disrupting Na-K ATPase function, leading to cellular edema and calcium influx, activating destructive proteases and endonucleases.

• Reperfusion injury — Restoration of blood flow paradoxically generates reactive oxygen species (ROS) and inflammatory mediators that cause additional cellular damage; this manifests as post-cardiac arrest syndrome with myocardial dysfunction, cerebral injury, and systemic inflammation.

• Metabolic derangement — Lactic acidosis, hyperkalemia (from cellular breakdown), hypoxia, and hypercapnia occur rapidly; prolonged arrest leads to irreversible organ damage despite restoration of perfusion.

• Immediate collapse with unresponsiveness — Patient suddenly loses consciousness; family or bystanders may report sudden loss of awareness or describe "weird behavior" preceding arrest; witnessed arrests have better outcomes than unwitnessed.

• Absence of pulse and respirations — Check for central pulse (carotid or femoral) for no more than 10 seconds; if absent or uncertain, assume cardiac arrest and begin CPR immediately. Agonal gasping (irregular, ineffective breathing attempts) may occur and should not be mistaken for normal breathing; this is a sign of severe hypoxia.

• Loss of blood pressure and perfusion — Complete absence of blood pressure; patient becomes cyanotic and loses all responsiveness to stimuli within seconds.

• Seizure-like activity — Myoclonic jerking may occur due to severe cerebral hypoxia and should not be confused with primary seizure disorder; this is a sign of profound anoxia.

• Important clinical pearl: Time to first intervention is critical; "time is brain" — every minute without CPR and defibrillation decreases survival by approximately 7-10%; the "golden period" for resuscitation is within the first 4-6 minutes.

• Clinical diagnosis based on unresponsiveness and absent pulse — No laboratory tests are required to initiate resuscitation; diagnosis is made clinically by checking for responsiveness and absence of pulse. Do not delay CPR for diagnostic confirmation.

• Electrocardiography (ECG) classification of arrest rhythms:
• Shockable rhythms (VF/pVT): Require immediate defibrillation; associated with primary cardiac causes (acute MI, primary arrhythmia). Better prognosis if defibrillated within first few minutes.
• Non-shockable rhythms (asystole/PEA): Do not respond to defibrillation; indicate profound shock or secondary cardiac arrest from medical/surgical cause. Prognosis is significantly worse.

• Rapid assessment during resuscitation:
• Check rhythm every 2 minutes during CPR
• Identify reversible causes using the "Hs and Ts" mnemonic:
• H's: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypokalemia/Hyperkalemia, Hypothermia
• T's: Tension pneumothorax, Tamponade (pericardial), Thrombosis (coronary or pulmonary), Toxins

• Point-of-care ultrasound (POCUS) — May be used to assess for presence of cardiac activity and identify reversible causes (pericardial effusion, pneumothorax) but should not delay CPR initiation; organized contractility on ultrasound during arrest is associated with better prognosis.

Immediate management (universal approach for all cardiac arrest)

• High-quality CPR as foundation — Begin CPR immediately without delay; perform chest compressions at 100-120 compressions per minute with adequate depth (2-2.4 inches in adults) and allow full recoil. Minimize interruptions in compressions; rotate CPR providers every 2 minutes to prevent fatigue and ensure quality. Compression-to-ventilation ratio is 30:2 for single rescuer, continuous chest compressions (hands-only CPR) without rescue breaths is acceptable for adults and equally effective in first few minutes.

• Defibrillation for shockable rhythms (VF/pVT):
• Apply automated external defibrillator (AED) or manual defibrillator as soon as available; do not delay CPR to apply AED.
• Defibrillate with 200 J biphasic (or 360 J monophasic) initial shock, then continue CPR for 2 minutes before checking rhythm again.
• Repeat defibrillation every 2 minutes if VF/pVT persists; this is the only truly reversible initial rhythm if treated promptly.

Pharmacologic management (during continuous CPR)

• Epinephrine (adrenaline):
• Dosing: 1 mg IV/IO push every 3-5 minutes (repeat every other CPR cycle)
• Mechanism: Alpha-1 adrenergic agonism increases coronary and cerebral perfusion pressure
• May be given via intraosseous (IO) route if IV access unavailable
• Note: High-dose epinephrine (3-5 mg) is no longer recommended and does not improve outcomes

• Amiodarone (preferred antiarrhythmic for shockable rhythms):
• Dosing: First dose 300 mg IV/IO during resuscitation (for VF/pVT after failed defibrillation attempts), then 150 mg after 3-5 minutes if still in VF/pVT
• Mechanism: Class III antiarrhythmic (potassium channel blocker) with additional beta-blocking and calcium channel blocking properties; increases defibrillation success rate
• Preferred over lidocaine (which may be used as alternative at 1-1.5 mg/kg IV/IO initially, then 0.5-0.75 mg/kg every 5-10 minutes, max 3 mg/kg)

• Sodium bicarbonate:
• Consider for tricyclic antidepressant toxicity or severe metabolic acidosis
• Dosing: 1 mEq/kg IV push during resuscitation

Airway and breathing management

• Establish airway:
• Bag-valve-mask (BVM) ventilation is adequate initially and provides immediate oxygenation without intubation delay
• Place supraglottic airway (i-gel, laryngeal mask airway) or endotracheal intubation once IV/IO access obtained; intubation should not delay CPR initiation
• Target SpO2 ≥94% and ETCO2 35-40 mmHg as goals

• Post-resuscitation ventilation:
• Use 10 mL/kg/minute minute ventilation (approximately 10-12

Complications of the arrest itself

• Hypoxic-ischemic brain injury: the dominant cause of death after ROSC in out-of-hospital arrest. Signaled by persistent coma, absent pupillary/corneal reflexes, or status myoclonus. Neuroprognostication should be multimodal and deferred at least 72 hours after return to normothermia (AHA 2020) — early withdrawal of care is a real-world error.
• Post-cardiac arrest myocardial stunning: global hypokinesis from reperfusion injury causing cardiogenic shock hours after ROSC; signaled by falling MAP, rising lactate, low ScvO2. Emergency — needs vasopressor/inotrope support and evaluation for mechanical support.
• Re-arrest / recurrent VF: most common in the first minutes after ROSC. Emergency; keep pads on the patient.
• Post-arrest seizures: often nonconvulsive; low threshold for EEG in the comatose patient.
• AKI (ATN), ischemic hepatitis, bowel ischemia, DIC: downstream of shock; transaminases in the thousands with normal bilirubin suggests shock liver.

Complications of resuscitation

• Chest wall injury: rib and sternal fractures are expected with adequate-depth compressions; occasionally hemothorax, pneumothorax, liver or splenic laceration — suspect with unexplained post-ROSC hypotension or falling hematocrit. Tension pneumothorax is an emergency.
• Over-ventilation: raises intrathoracic pressure, decreases venous return and coronary perfusion pressure, and causes gastric insufflation with aspiration. A classic exam-tested harm of "bagging too fast."
• Hyperoxia and hypocapnia after ROSC: both worsen neurologic outcome; titrate FiO2 to normoxia and avoid hyperventilating to a low PaCO2.
• Drug effects: epinephrine causes post-ROSC tachyarrhythmia and hypertension; amiodarone causes hypotension and bradycardia; sodium bicarbonate causes hypernatremia, hyperosmolarity, and paradoxical intracellular acidosis.
• Targeted temperature management: shivering, bradycardia, hypokalemia during cooling with rebound hyperkalemia on rewarming, coagulopathy, and infection.

• The shockable pair is VF and pulseless VT — nothing else. Asystole and PEA are never shocked; "defibrillate the asystole" is the most common wrong answer on the exam. For a witnessed arrest with a defibrillator at hand, the single best next step is immediate defibrillation; otherwise compressions first.
• Epinephrine timing differs by rhythm. Give it as early as feasible in asystole/PEA; in VF/pVT give it after the initial defibrillation attempts have failed, since the shock is the definitive therapy (AHA 2020).
• End-tidal CO2 is the CPR quality monitor. A persistently low ETCO2 (roughly under 10 mmHg) means inadequate compressions or futile physiology; an abrupt jump toward normal during compressions is the earliest sign of ROSC — check a pulse, do not stop for a drug.
• Match the antidote to the H or T. Calcium for hyperkalemia or calcium-channel-blocker toxicity, sodium bicarbonate for tricyclic overdose with wide QRS, magnesium for torsades de pointes, thrombolysis for suspected massive PE, needle/finger thoracostomy for tension pneumothorax, pericardiocentesis for tamponade.
• "Not dead until warm and dead." Hypothermic arrest and local-anesthetic or drug-toxicity arrest warrant prolonged resuscitation and consideration of extracorporeal rewarming/ECPR.
• Pregnancy after roughly 20 weeks: continuous manual left uterine displacement to relieve aortocaval compression, and resuscitative hysterotomy considered if there is no ROSC within about 4 minutes (AHA 2020, consistent with ACOG).
• Post-ROSC ECG drives the cath lab decision. STEMI mandates emergent angiography. A new LBBB alone is not a STEMI equivalent — apply Sgarbossa criteria.
• Post-arrest care is a package: normoxia (avoid hyperoxia), normocapnia, MAP support, targeted temperature management with active fever prevention, and delayed multimodal neuroprognostication.