Cardiac Arrest Rhythms Caused by Heart Attacks
Acute myocardial infarction primarily causes ventricular fibrillation (VF) and ventricular tachycardia (VT) as cardiac arrest rhythms, with VF being the most common shockable rhythm, while bradyarrhythmias and heart block can also precipitate arrest, particularly in inferior wall infarctions. 1
Primary Arrhythmias in Acute MI
Ventricular Fibrillation (VF)
- VF is the predominant cardiac arrest rhythm in acute MI, occurring in approximately 3-5% of patients, with highest incidence in the first 4 hours after infarction 1
- Primary VF (occurring without heart failure or hypotension) accounts for a substantial portion of early arrests and characteristically occurs within the first 72 hours of MI 2
- Among cardiac arrest patients during MI hospitalization, sustained VT/VF was present in 34.7% of cases and was associated with significantly better survival to discharge (47.5%) compared to arrests without ventricular tachyarrhythmias (19.8%) 3
Ventricular Tachycardia (VT)
- Both monomorphic and polymorphic VT can precipitate cardiac arrest during acute MI 1
- Sustained monomorphic VT lasting >30 seconds or causing hemodynamic compromise requires immediate intervention 1
- Polymorphic VT should be treated similarly to VF with unsynchronized electrical shock 1
- The vast majority of post-MI VT and VF occur within the first 48 hours of infarction 1
Bradyarrhythmias and Conduction Blocks
Heart Block
- Heart block develops in approximately 6-14% of patients with acute MI and predicts increased in-hospital mortality 1
- Sinus bradycardia occurs in 30-40% of patients, especially with inferior MI and right coronary artery reperfusion (Bezold-Jarisch reflex) due to increased vagal tone 1
- Complete AV block, particularly when infranodal, can lead to cardiac arrest and is often refractory to atropine 4
- Bundle branch block was present on admission in 4% of acute MI patients in thrombolysis trials and predicted substantially increased in-hospital mortality 1
Temporal Patterns and Risk Stratification
Timing of Arrhythmias
- All cases of primary VF occur within the first 72 hours of admission 2
- VT/VF occurring more than 72 hours after admission carries a significantly higher in-hospital mortality rate (57%) compared to early occurrence within 72 hours (20%) 2
- Over a 20-year period, the incidence of VF declined while VT rates remained stable 5
Secondary vs. Primary Arrest
- Secondary VT/VF (occurring with hypotension or heart failure) has dramatically worse prognosis with 51% in-hospital mortality versus 8% for primary VT/VF 2
- Cardiac arrest occurred in 4.8% of hospitalized AMI patients overall, with 29.4% survival to discharge 3
Pathophysiologic Mechanisms
The arrhythmogenic substrate in acute MI involves:
- Micro-reentry is the primary electrophysiological mechanism for early-phase arrhythmias 1
- Heightened adrenergic nervous system tone, hypokalemia, hypomagnesemia, and intracellular calcium overload contribute to arrhythmogenesis 1, 6
- Sympathetic activation and parasympathetic dysfunction create a particularly arrhythmogenic cardiac environment 6
Clinical Predictors of Cardiac Arrest
High-risk features include:
- Hypotension (systolic BP <90 mmHg), Q-wave MI, advanced age, heart failure, and initial heart rate abnormalities (bradycardia or tachycardia) 3
- Higher Killip class, ST elevation, and atrial fibrillation 5
- Women experience cardiac arrest more frequently than men (6.0% vs 4.4%) 3
- Inferior wall infarction has lower cardiac arrest prevalence compared to other ST-elevation infarction types 3
Important Caveats
- Electrolyte abnormalities should not be assumed to be the sole cause of cardiac arrest except in drug-induced long QT syndrome 1
- Patients with non-Q-wave infarction (biomarker elevation only) have significantly higher risk of late cardiac arrest compared to Q-wave infarction survivors 1
- Ventricular arrhythmias after MI are associated with a 6-fold increase in 30-day mortality 5