ECG Cardiac Arrest Rhythms

What it looks like on ECG

Ventricular fibrillation (VF) — a chaotic tracing with no discernible P waves, QRS complexes, or T waves. Waves are irregular in shape and amplitude, with a very high and irregular rate. VF is conventionally classified as coarse or fine based on wave amplitude, but there is no uniform standardized threshold (literature cites values from 3 mm to 5 mm); amplitude depends on the lead, signal gain, filters, and electrode contact. The prognostic value of this division is limited and does not alter the indication for immediate defibrillation in confirmed VF.

Pulseless ventricular tachycardia — appears on the monitor as monomorphic or polymorphic VT, typically with a wide QRS ≥120 ms and a rate >100–120/min; in polymorphic VT, measuring QRS and rhythm regularity can be challenging. The patient is pulseless and unresponsive — the rhythm does not provide cardiac output, but this is established clinically rather than by ECG morphology.

Asystole — a practically flat line, occasionally with residual P waves (so-called ventricular asystole with preserved atrial activity) without subsequent QRS complexes. Before confirming asystole, leads, signal gain, and electrode contact must be checked — following the "check cables, check leads, increase gain" protocol, as fine VF can be mistaken for asystole.

Pulseless electrical activity (PEA) — the monitor screen may show virtually any organized rhythm: sinus rhythm, narrow complex, wide QRS, bradycardia — yet no pulse is clinically detectable. This is not a separate morphological pattern, but rather a clinico-electrocardiographic combination.

Mechanism

In VF, multiple chaotic re-entry wavelets circulate simultaneously through the ventricular myocardium, preventing the formation of a single organized front of depolarization — coordinated contraction and effective cardiac output are absent, although chaotic minimal mechanical movements of the myocardium may occur. Pulseless VT is an organized ventricular tachyarrhythmia whose mechanisms may include re-entry, automaticity, or triggered activity; hemodynamic inefficiency is determined by a combination of rate, contraction synchronicity, and myocardial state, rather than excessive rate alone. Asystole is an ECG sign of absent recordable ventricular electrical activity after excluding technical causes; it may result from hypoxia, ischemia, metabolic disorders, hypothermia, drug toxicity, and other reversible causes, rather than serving as an independent pathomorphological diagnosis. PEA is organized electrical activity in the absence of a palpable pulse and effective cardiac output; mechanical activity may be absent or insufficient. Causes include reversible mechanical, hypoxic, hypovolemic, and metabolic states.

Causes

• Coronary artery disease and acute coronary syndrome are among the most frequent causes in adults, especially during sudden arrest
• Cardiomyopathies (dilated, hypertrophic, arrhythmogenic right ventricular cardiomyopathy)
• Electrolyte disturbances: severe hyperkalemia, hypokalemia, hypomagnesemia
• Channelopathies: Brugada syndrome, long QT syndrome, catecholaminergic polymorphic VT
• Hypothermia, hypoxia, severe acidosis
• Tension pneumothorax, cardiac tamponade, massive pulmonary embolism (frequent causes of PEA)
• Overdose of cardiotoxic drugs (tricyclic antidepressants, sodium and calcium channel blockers, digoxin)
• Prolonged asystole as the outcome of untreated VF/VT or the terminal stage of any severe disease

Differential diagnosis

• Fine VF and asystole — when in doubt, increase the gain and check at least two leads; management differs (shock versus CPR without shock), making differentiation more important than any amplitude threshold
• Asystole and electrode disconnection artifact — technical failure can cause a flat line or prominent artifact; check cables, electrodes, gain, and another lead; asystole should not be diagnosed solely based on the appearance of a single line
• Pulseless VT and VT with a pulse — morphology is identical; the only difference is clinical: the presence or absence of a pulse and consciousness
• PEA and profound hypotension with a barely palpable pulse — requires careful clinical evaluation; in doubtful cases, rely on signs of life (breathing, movement, coughing) and available modalities (ultrasound, arterial line)
• Severe hyperkalemia with a sinusoidal pattern may mimic an organized rhythm in PEA — screen for a history of renal failure and wide, merging complexes

Clinical significance and management

Recognition of the cardiac arrest rhythm determines the resuscitation algorithm. If VF or pulseless VT (shockable rhythms) is identified — perform early unsynchronized defibrillation combined with high-quality continuous CPR, with chest compressions resumed without delay before and after the shock. Epinephrine and amiodarone are administered according to the specific CPR protocol (for example, in the ERC algorithm, epinephrine and amiodarone are given after the third ineffective shock, followed by repeated doses per protocol); specific intervals and doses are determined by current national guidelines, and defibrillation and continuous CPR must not be delayed for drug administration. In asystole and PEA (non-shockable rhythms) — a shock is not indicated; the mainstay of treatment is continuous high-quality CPR, early epinephrine (typically 1 mg IV/IO every 3–5 minutes per current protocol), and the search for and treatment of reversible causes (the "4Hs and 4Ts" protocol: hypoxia, hypovolemia, hypo-/hyperkalemia and other metabolic disorders, hypothermia; tamponade, tension pneumothorax, toxins/thromboembolism, coronary thrombosis). The rhythm is assessed every 2 minutes of CPR; interruptions in chest compressions must be as brief as possible, typically not exceeding 10 seconds, with immediate resumption of compressions following rhythm analysis or shock delivery. The transition from one rhythm to another during resuscitation is common and requires reassessing management at each check.

Common interpretation errors

• Confirming asystole without checking leads, gain, and electrode contact
• Confusing fine VF with asystole due to low signal gain
• Delaying defibrillation in VF/VT for the sake of redundant diagnostic maneuvers
• Delivering a shock in asystole or PEA (a shock in these cases is not indicated and does not improve outcomes)
• Prolonged interruption of chest compressions for rhythm analysis or attempts to obtain a "textbook" monitor tracing

Frequently asked questions

Related terms

More in the section "Ventricular Arrhythmias"

Entire section

Sources

• Goldberger's Clinical Electrocardiography, current edition
• Hampton. The ECG in Practice
• Guidelines for Cardiopulmonary Resuscitation (ERC/AHA)
• Orlov V.N. Guide to Electrocardiography

Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.