Cardiac arrest due to myocardial ischemia

Article written and reviewed by Dr Luca Moretti

Cardiac arrest due to myocardial ischemia is the sudden cessation of effective circulation caused by acute coronary disease or the electrical substrate of ischemic heart disease. The initial rhythm is frequently ventricular fibrillation or pulseless ventricular tachycardia, but progression to pulseless electrical activity or asystole becomes more likely with the passage of time, shock, hypoxia, and extensive myocardial injury.
Etiological diagnosis follows recognition of the arrest: unresponsiveness and absence of normal breathing require immediate activation of emergency services, high-quality chest compressions, and early defibrillator use. Every minute without CPR and defibrillation reduces the probability of neurologically intact survival.

Acute ischemia alters ATP, pH, extracellular potassium, conduction, and refractoriness, creating electrical dispersion and reentry. After myocardial infarction, channels of viable myocardium within scar sustain monomorphic tachycardias that may degenerate. Cardiac arrest may also result from mechanical rupture, shock, bradyarrhythmia, or atrioventricular block.
The pathway continues after return of spontaneous circulation with control of oxygenation, ventilation, blood pressure, and temperature, serial ECGs, echocardiography, and investigation of the cause. Persistent ST-segment elevation or a strong suspicion of occlusion with instability points to urgent coronary angiography. In stable patients without ST elevation, an indiscriminate immediate invasive strategy has not demonstrated benefit.

Etiology, risk factors, pathogenesis, and pathophysiology

Acute ischemia rapidly reduces ATP production and alters the function of membrane ion pumps. Extracellular potassium accumulation, acidosis, reduced membrane potential, changes in sodium and calcium currents, and nonuniform shortening of the action potential produce heterogeneity of conduction and refractoriness. Adjacent regions may therefore recover excitability at different times and conduct the impulse at different velocities, conditions that favor unidirectional block and reentry circuit formation.
In the early phases of coronary occlusion, electrical instability may manifest as premature ventricular beats, polymorphic ventricular tachycardia, or ventricular fibrillation. Increased sympathetic activity, pain, hypoxemia, and electrolyte abnormalities may amplify the risk. Ventricular fibrillation does not necessarily require a preexisting scar: it can be generated by the marked electrical nonuniformity of acutely ischemic myocardium and is one of the principal mechanisms of cardiac arrest in the early phases of infarction.

Reperfusion again alters the electrophysiological milieu. Rapid restoration of flow may be associated with premature beats, accelerated idioventricular rhythm, nonsustained ventricular tachycardia, and, more rarely, sustained arrhythmias. Accelerated idioventricular rhythm is classically observed after reperfusion and, in the absence of hemodynamic compromise, does not itself require aggressive antiarrhythmic therapy. Sustained ventricular arrhythmias instead require the same severity assessment used in other settings.
As the infarction heals, necrotic tissue is replaced by fibrosis. The scar is not electrically uniform: bundles of viable cardiomyocytes may persist between areas of collagen and create slow-conduction channels. If conduction time allows previously refractory tissue to recover excitability, a reentry circuit capable of sustaining monomorphic ventricular tachycardia is created. QRS morphology during tachycardia reflects the circuit exit site, whereas the critical circuit may lie deep within the scar or at its margins.

The ischemic substrate may also promote atrial arrhythmias and bradyarrhythmias, but the causal relationship is less specific than for ventricular arrhythmias. Ischemia and heart failure increase atrial pressure and neurohormonal activation, promoting atrial fibrillation; an inferior infarction may involve the blood supply to the atrioventricular node and cause often transient nodal block, whereas a large anterior infarction may damage the His-Purkinje system and produce more distal conduction disorders with a less favorable prognosis.

Clinical manifestations

Premature ventricular beats are common during ischemia and after infarction, but their significance depends on the context. Pharmacological suppression of ectopy alone is not a prognostic goal. The Cardiac Arrhythmia Suppression Trial demonstrated that eliminating premature beats with encainide or flecainide in infarction survivors increased mortality, establishing a fundamental principle: improving an electrocardiographic endpoint is not equivalent to reducing sudden death, and class Ic drugs must not be used for this purpose in structural ischemic heart disease.
Nonsustained ventricular tachycardia may reflect acute electrical irritability or a scar substrate. In a patient with previous infarction, its presence requires assessment of ventricular function, residual ischemia, therapy, and the overall clinical picture. It is not by itself an automatic indication for chronic antiarrhythmic therapy or an ICD, but may contribute to risk stratification in specific algorithms, especially when associated with ventricular dysfunction.

Late sustained monomorphic ventricular tachycardia after infarction is the phenotype most typical of scar-related reentry. It may be hemodynamically tolerated, cause syncope, or degenerate into ventricular fibrillation. Apparent stability must not be interpreted as benignity because recurrence is frequent and risk depends on ventricular function, scar burden, and the possibility of treating the substrate.
Polymorphic ventricular tachycardia and ventricular fibrillation should prompt rapid investigation for ongoing ischemia, electrolyte abnormalities, hypoxia, QT prolongation, and proarrhythmic drugs. During an acute coronary syndrome, treatment of the ischemic cause is an integral part of arrhythmia control. Repeated recurrence of ventricular arrhythmias within a short period constitutes an electrical storm and requires multidisciplinary intensive management, reduction of adrenergic activation, appropriate drugs, correction of triggers, and, when indicated, urgent ablation or neuromodulation strategies.

Ischemic bradyarrhythmias have different characteristics. In inferior infarction, atrioventricular block is often nodal, associated with a relatively stable escape rhythm, and may regress after reperfusion. In anterior infarction, an infranodal block indicates more extensive damage to the conduction system and may be associated with hemodynamic instability. Atropine, transcutaneous or transvenous pacing, and treatment of the cause are selected according to the level of block, heart rate, perfusion, and clinical response.

The presentation of ischemic cardiac arrest varies with location, speed of rescue, and disease phase. Acute occlusion may be preceded by chest pain, pressure, dyspnea, nausea, or sweating, but sudden death may be the first recognized manifestation of coronary artery disease. Intermittent prodromal symptoms may occur in the preceding hours or days without being interpreted as cardiac. Retrospective identification helps reconstruct the cause but must not foster the false belief that every arrest is predictable. Sudden syncope during exertion or without prodromes, especially with known heart disease, requires urgent assessment for ventricular arrhythmia.
In patients with post-infarction scar, rapid palpitations, presyncope, ICD shocks, or episodes of tolerated tachycardia may precede hemodynamic deterioration. Arrest due to monomorphic tachycardia is more likely with a chronic substrate, whereas fibrillation and polymorphic tachycardia point toward acute ischemia, QT abnormalities, or metabolic factors. These associations guide investigation but are not absolute.

The probability of a coronary origin increases with age, male sex, atherosclerotic factors, previous myocardial infarction, ischemic abnormalities, and regional dysfunction, but diagnosis cannot be inferred from epidemiology. Intracranial hemorrhage, pulmonary embolism, aortic dissection, hypoxia, poisoning, myocarditis, cardiomyopathies, and channelopathies may cause the same event. Moreover, coexisting coronary artery disease is common and may be a noncausal finding. Absence of ST elevation reduces but does not eliminate the probability of acute coronary occlusion.
The rhythm documented by the defibrillator, shock sequence, and tracings preceding collapse provide information that may be lost during transfer. Preserving AED data, interrogating implanted devices, and collecting witness accounts of symptoms, activity, medication, and no-flow time are part of medical assessment, not merely administrative documentation.

Cardiac arrest during myocardial infarction is not always purely electrical. Free-wall rupture may cause tamponade and pulseless electrical activity; papillary-muscle or septal rupture rapidly causes pulmonary edema, shock, and arrest; massive right ventricular infarction impairs left-sided filling, whereas severe ischemia of the conduction system may cause extreme bradycardia. Identifying the hemodynamic mechanism changes treatment: defibrillation is decisive in fibrillation but does not correct tamponade or a post-infarction shunt.
For this reason, after return of circulation or during prolonged resuscitation by expert teams, ultrasound assesses effusion, biventricular function, and gross signs of complications. A new murmur may be absent when output is minimal; absence of an auscultatory finding does not exclude rupture, and deterioration after initial recovery must immediately reopen the investigation.

Systemic injury results from a no-flow phase followed by global reperfusion. Cerebral ischemia, inflammatory activation, endothelial dysfunction, vasoplegia, coagulation abnormalities, and myocardial depression constitute the post-cardiac arrest syndrome. Severity depends on time without CPR, quality of generated flow, time to return of circulation, and cause. Two patients with the same rhythm may therefore follow completely different trajectories. Post-arrest stunning may be severe yet recover, whereas neurological injury evolves over subsequent hours through edema, excitotoxicity, and microcirculatory abnormalities.
This pathophysiology justifies continuity of care: obtaining a pulse does not end resuscitation but opens a phase in which ventilation, perfusion, temperature, glycemia, seizures, and coronary reperfusion can change outcomes. The quality of the entire system, from the witness’s call to rehabilitation, matters more than any isolated procedure.

Investigations and diagnosis

Diagnosis begins with a 12-lead ECG obtained during symptoms whenever possible. Morphology, rate, regularity, and the relationship between atrial and ventricular activity make it possible to distinguish ventricular tachycardias, supraventricular tachycardias with aberrancy, and conduction disorders. In a patient with structural heart disease and wide-QRS tachycardia, ventricular tachycardia must be considered the leading diagnosis until proved otherwise.
Continuous monitoring is essential in acute infarction and unstable patients. In the outpatient phase, Holter monitoring and prolonged monitoring systems are selected according to symptom frequency. Rare syncopal episodes may require long-term monitoring; the temporal correlation between symptoms and rhythm is especially important when premature beats or nonsustained tachycardia are nonspecific findings.

Echocardiography assesses ejection fraction, volumes, aneurysms, ischemic mitral regurgitation, and other conditions that modify risk. Cardiac magnetic resonance with late gadolinium enhancement can define scar distribution and transmurality and identify heterogeneous tissue at the margins of the infarction. The amount and architecture of fibrosis add information about the arrhythmic substrate, although device indications remain anchored to validated clinical criteria and not to the presence of enhancement alone.
When an arrhythmia occurs together with chest pain, ST-segment changes, increased troponin, or hemodynamic instability, active ischemia must be assessed. CCTA, coronary angiography, and functional tests are used according to the acute or chronic context. Revascularization may eliminate the ischemic trigger, but not necessarily the scar substrate of late monomorphic tachycardia.

The electrophysiological study retains a selective role. It may be used to define the mechanism, plan ablation, and, in specific populations with coronary artery disease, ventricular dysfunction, and nonsustained ventricular tachycardia, contribute to stratification through inducibility of sustained ventricular tachycardia. It is not a universal post-infarction screening test.

Acute treatment and prevention of recurrence

Ventricular tachycardia or a wide-QRS arrhythmia with hemodynamic instability requires synchronized cardioversion; ventricular fibrillation and pulseless ventricular tachycardia require defibrillation and cardiopulmonary resuscitation according to advanced algorithms. In the ischemic setting, electrical therapy must proceed in parallel with correction of the cause, with particular attention to reperfusion, oxygenation when necessary, acid-base balance, and electrolytes.
Amiodarone or lidocaine may be used in specific acute ventricular arrhythmias, including refractory ventricular fibrillation or pulseless ventricular tachycardia according to resuscitation algorithms. Magnesium is not a universal antiarrhythmic drug for ischemia: it is specifically indicated for torsades de pointes and documented hypomagnesemia. Indiscriminate antiarrhythmic prophylaxis after infarction is not recommended.

Beta-blockers, when not contraindicated by shock, severe bradycardia, advanced block, or other conditions, reduce adrenergic activation and are fundamental in the management of many patients with ischemic heart disease and ventricular dysfunction. Sympathetic control is particularly important in electrical storm. The choice and route of administration must, however, be adapted to hemodynamic stability and ventricular function.
Secondary prevention of sudden death with an implantable cardioverter-defibrillator is indicated in many patients who survive ventricular fibrillation or sustained ventricular tachycardia not attributable to a completely reversible cause. An arrhythmia confined to the very early phase of an acute infarction, eliminated by reperfusion without a residual high-risk substrate, requires a different assessment from late scar-related tachycardia. The decision must therefore integrate timing, reversibility, coronary anatomy, ventricular function, and life expectancy.

For primary prevention, ejection fraction remains the most validated clinical parameter. Guidelines recommend an ICD in selected patients with ischemic heart disease at least 40 days after infarction, persistently reduced ejection fraction despite optimized medical therapy, and a reasonable expectation of survival with good functional status. Implantation very early after infarction has not demonstrated a reduction in total mortality because fewer arrhythmic deaths may be offset by nonarrhythmic deaths during the phase of greatest clinical instability.
CRT is not a therapy for ischemic arrhythmia itself. It is indicated in patients with heart failure, reduced ejection fraction, and specific features of electrical dyssynchrony, particularly left bundle branch block with a wide QRS, despite optimal therapy. In patients who also meet criteria for prevention of sudden death, a device with defibrillation capability is often used.

Catheter ablation is central to the treatment of recurrent scar-related monomorphic ventricular tachycardia. Mapping identifies slow-conduction channels, late potentials, and critical isthmuses; ablation aims to interrupt the circuit and modify the substrate. In patients with coronary artery disease and symptomatic recurrences or ICD shocks despite amiodarone, ESC guidelines favor ablation over simply escalating antiarrhythmic therapy.
Optimal treatment ultimately includes therapy for ischemic heart disease: control of atherogenic lipoproteins, antiplatelet therapy when indicated, management of blood pressure and diabetes, smoking cessation, treatment of heart failure, and revascularization of lesions causing ischemia. Reducing ischemic risk decreases future triggers, while heart failure therapy and reverse remodeling may modify arrhythmic risk over time.

Resuscitation, post-cardiac arrest care, and determination of ischemic etiology

Recognition of cardiac arrest is clinical and does not require a prolonged pulse check by a lay rescuer. An unresponsive patient who is not breathing normally, including agonal breathing, must be considered in cardiac arrest. Immediate activation of emergency services, cardiopulmonary resuscitation, and retrieval of a defibrillator form a single sequence. Compressions maintain minimal coronary and cerebral flow until defibrillation or correction of the cause. Their effectiveness depends on appropriate rate and depth, complete recoil, a firm surface, and minimal pauses.
Ventilation must avoid both hypoventilation and excessive intrathoracic pressure from breaths that are too rapid or large, which reduces venous return and coronary perfusion. After placement of an advanced airway, compressions and ventilations proceed without synchronized pauses according to the algorithm. Capnography confirms tube position, indirectly measures generated output, and may signal return of circulation through a sudden rise in exhaled CO2, but is not by itself a criterion for terminating efforts.

In shockable rhythms, an early shock terminates chaotic electrical activity but does not directly restart effective contraction. Compressions must therefore resume immediately after the shock without a prolonged pulse check. Two-minute cycles allow energy and drugs to be delivered and the rhythm reassessed while limiting pauses. Correct pad position, energy escalation according to the device, and, in refractory cases, verification of contacts and vector are components of technically sound defibrillation.
Epinephrine is administered according to the specified sequence, with different timing in shockable and nonshockable rhythms, whereas amiodarone or lidocaine may be used in refractory ventricular fibrillation or pulseless ventricular tachycardia. These drugs do not replace shocks and compressions, and their effect on neurologically intact survival is more limited than that of early resuscitation. Bicarbonate, calcium, and magnesium are not given routinely, but only for specific indications such as hyperkalemia, selected poisonings, or torsades de pointes.

Nonshockable rhythms require systematic investigation of reversible causes: hypoxia, hypovolemia, potassium and metabolic abnormalities, hypothermia, tamponade, tension pneumothorax, toxins, and coronary or pulmonary thrombosis. In ischemic arrest, pulseless electrical activity may represent massive infarction with pump failure, free-wall rupture with tamponade, a mechanical complication, or late progression of untreated fibrillation. Point-of-care ultrasound may identify tamponade, severe right ventricular dilatation, or absence of activity, but must be performed during planned pauses and must not prolong interruption of compressions.
Thrombolysis during resuscitation is not used indiscriminately merely because myocardial infarction is possible; it may be considered when pulmonary embolism is suspected and circumstances support it. PCI during refractory arrest is feasible only in highly organized systems, sometimes with extracorporeal support. Selection must consider witnessed arrest, initial rhythm, no-flow time, CPR quality, biological age, and a correctable cause, because complex technology cannot compensate for irreversible anoxic injury.

After return of spontaneous circulation, priority shifts from generating flow to preventing secondary injury. Oxygen saturation is measured reliably and oxygen is titrated to avoid hypoxemia and prolonged hyperoxia. Ventilation targets normocapnia because hypocapnia reduces cerebral blood flow, whereas marked hypercapnia may worsen acidosis and intracranial pressure. Blood-gas analysis, capnography, and chest radiography or ultrasound assess gas exchange, device position, and associated pulmonary causes.
Hypotension and hypoperfusion are treated with an individualized combination of fluids, vasopressors, and inotropes guided by echocardiography and organ-perfusion signs. Right ventricular infarction may require cautious preload, whereas severe congestive left ventricular dysfunction worsens with indiscriminate fluid expansion. The pressure target is not identical for everyone: a history of hypertension, cerebral perfusion, lactate, urine output, and response to drugs determine whether the achieved value is sufficient.

A post-resuscitation ECG is obtained early and repeated because global ischemia, electrolyte abnormalities, and catecholamines may produce transient changes. Persistent ST-segment elevation consistent with occlusion indicates immediate coronary angiography and revascularization. The same urgency may be appropriate without ST elevation when cardiogenic shock, recurrent electrical instability, or strong clinical evidence suggests a treatable coronary lesion. The decision is made together with the initial neurological assessment, without automatically excluding comatose patients when the circumstances of arrest are favorable.
In hemodynamically and electrically stable patients without ST elevation, the COACT and TOMAHAWK trials did not demonstrate an advantage of immediate coronary angiography over a delayed or selective strategy. This does not mean that coronary anatomy is irrelevant, but that automatically transferring every survivor to the catheterization laboratory may delay alternative diagnoses and intensive care. History, initial rhythm, echocardiography, troponin, instability, and probability of a noncoronary cause guide the timing of testing.

Troponin is frequently elevated after cardiac arrest because of global ischemia, defibrillation, catecholamines, and resuscitation-related injury; the value alone does not prove acute thrombosis. Early echocardiography assesses global or regional dysfunction, right ventricular infarction, tamponade, pulmonary embolism, valvular disease, and hypovolemia, while accounting for post-arrest stunning that may transiently reduce function. Recovery over subsequent hours or days distinguishes some reversible dysfunction from preexisting scar, and serial examinations change treatment and prognosis.
When coronary angiography does not identify a sufficient cause, CMR may detect myocardial infarction, myocarditis, cardiomyopathy, or Takotsubo syndrome. Chest and brain CT are selected for embolism, dissection, intracranial hemorrhage, or other causes. Toxicology, electrolytes, and medication history complete the pathway. An apparently ischemic arrest may be caused by a channelopathy, and incidental coronary plaque must not prematurely end the investigation.

In patients who do not regain consciousness, temperature control prevents fever and maintains a defined target through a protocol, sedation, and monitoring. After TTM2, hypothermia at 33 °C is not considered universally superior to normothermia with early fever treatment, but this finding does not justify passive thermal care: hyperthermia and uncontrolled fluctuations remain harmful. The strategy must include shivering prevention and attention to electrolytes, infection, rhythm, and drug metabolism.
Clinical or electrographic seizures are diagnosed with EEG and treated, whereas routine prophylactic antiseizure medication without seizures is not recommended. Glycemia, sodium, blood pressure, and ventilation are maintained while avoiding extremes; nutrition, infection prevention, and mobilization are integrated into intensive care. Brain and heart are managed simultaneously rather than sequentially because hypotension, hypoxia, fever, and recurrent arrhythmia worsen both.

Neurological prognostication must be multimodal and sufficiently delayed. Sedatives, neuromuscular blockers, kidney or liver failure, hypothermia, and metabolic abnormalities may suppress responses and produce falsely pessimistic predictions. After confounders are excluded, neurological examination, brainstem reflexes, EEG, somatosensory evoked potentials, biomarkers, and CT or MRI are integrated. No single uncertain finding should determine withdrawal of care.
The decision must also consider the risk of a self-fulfilling prophecy: if treatment is withdrawn because of an early test, the outcome can no longer validate the prediction. Timing, results, and confounders must be documented and communicated to the family while distinguishing uncertainty, probability, and certainty. Recovery of consciousness may be delayed, especially after prolonged sedation or organ failure.

Preventing recurrence requires determining whether the arrest occurred during a reversible ischemic phase or on a persistent substrate. Ventricular fibrillation during the early phase of myocardial infarction, clearly related in time to occlusion and without residual dysfunction, is not equivalent to late scar-related tachycardia. However, a cause must not be declared “reversible” merely because PCI was performed. Completeness of revascularization, ventricular function, scar, residual ischemia, electrolytes, and medication are reassessed before ICD protection is excluded.
In survivors of ventricular tachycardia or fibrillation not attributable to an eliminated cause, the ICD reduces arrhythmic death and is the cornerstone of secondary prevention. The device does not prevent every arrhythmia, and shocks may impair quality of life. Programming with appropriate thresholds and detection times, antitachycardia pacing, beta-blockade, and ablation in patients with recurrences reduce unnecessary therapies and electrical storm.

Ejection fraction is reassessed after recovery and optimized therapy. In primary prevention, waiting after myocardial infarction and revascularization avoids implanting a device in patients whose stunning and reverse remodeling allow substantial recovery. During this phase, risk, monitoring, and a possible wearable defibrillator are considered case by case because routine effectiveness of the latter has not been demonstrated across the entire post-infarction population.
Late-enhancement CMR may show the extent and border zone of scar and helps characterize the substrate but does not replace validated clinical criteria. Electrophysiological study has selective indications, and ablation does not eliminate the need for an ICD when the risk of fibrillation persists. The different techniques are complementary, not universal alternatives.

Discharge requires post-cardiac arrest rehabilitation addressing the heart, brain, and psychological health. Deficits of memory, attention, and executive function may be subtle and interfere with adherence, work, and driving. Anxiety, depression, and post-traumatic stress affect survivors and family members. Neurocognitive screening, device education, cardiac rehabilitation, and social support must be arranged rather than treating return of circulation as the end of the pathway.
Physical activity is resumed gradually after ischemia, ventricular function, and arrhythmia control have been defined. Driving and high-risk occupations follow specific regulations and waiting periods. Genetic counseling is reserved for cases in which age, family history, phenotype, or absence of a sufficient coronary cause suggests cardiomyopathy or channelopathy. Even when ischemia is plausible, an incomplete investigation may leave relatives with an inherited disease unprotected.

Complications

Prognosis is heterogeneous and does not follow an obligatory progression from premature beats to tachycardia and then ventricular fibrillation. Many acute-phase arrhythmias disappear after reperfusion; others identify extensive myocardial damage; late scar-related tachycardias may instead recur for years. The risk of sudden death is greatest when severe ventricular dysfunction, heart failure, residual ischemia, or previous sustained ventricular arrhythmias coexist with the scar substrate.
The modern strategy therefore does not consist of suppressing every ectopic beat, but of distinguishing reversible triggers, structural substrate, and prognostic risk. Prompt defibrillation during the acute event, reperfusion when necessary, prognostic medical therapy, an ICD in appropriate patients, and ablation of recurrent tachycardias have transformed the management of ischemic arrhythmias, reducing mortality without exposing patients to indiscriminate and potentially proarrhythmic antiarrhythmic therapy.

Adult CPR prioritizes chest compressions of adequate depth with complete recoil, minimal interruptions, effective ventilation, and defibrillation as soon as available for shockable rhythms. Epinephrine and amiodarone or lidocaine are used according to the algorithm, while hypoxia, hypovolemia, potassium abnormalities, tamponade, pneumothorax, coronary or pulmonary thrombosis, and toxins are investigated as reversible causes.
After return of circulation, hyperoxia and hyperventilation are avoided. Hypotension and shock require echocardiography, selective fluids, vasopressors, inotropes, and mechanical support in selected cases. Temperature control aims to prevent fever and secondary injury, whereas neurological prognosis must be multimodal and delayed, avoiding conclusions during sedation, hypothermia, or metabolic instability.

Revascularization treats the culprit occlusion but does not replace comprehensive management. A completely reversible cause limits an automatic ICD indication. Conversely, survival after ventricular fibrillation or tachycardia unexplained by a transient cause, ischemic scar, and persistent dysfunction requires assessment for secondary prevention. Beta-blockade, heart-failure therapy, correction of ischemia, and ventricular tachycardia ablation reduce recurrences in appropriate settings.
Rehabilitation integrates cardiac, neurological, and psychological recovery. Survivors and relatives may develop cognitive deficits, anxiety, depression, and fear of recurrence, which are part of the clinical outcomes of cardiac arrest.