ECG Diagnosis: Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm (AIVR) is a ventricular rhythm consisting of three or more consecutive monomorphic beats, with gradual onset and gradual termination.^1,2 AIVR is usually seen during acute myocardial infarction reperfusion (following thrombolytic therapy or percutaneous coronary intervention), and rarely manifests in patients with completely normal hearts or with structural heart disease.² As percutaneous coronary intervention has become a more common treatment for patients presenting with acute myocardial infarction (versus thrombolytic therapy), the observation of AIVR by Emergency Department physicians has become less common than it was during the thrombolytic era.² AIVR has also been associated with several drugs (eg, halothane, aconitine, desflurane, cocaine, and digitalis), electrolyte imbalances (eg, hypo- and hyperkalemia), cardiomyopathies, and during the postresuscitation period following cardiac arrest.^2–5

Electrocardiogram characteristics of AIVR include a regular rhythm, 3 or more ventricular complexes with QRS complex > 120 milliseconds, a ventricular rate between 50 beats/min and 110 beats/min, and occasional fusion or capture beats. This rhythm has two postulated, possibly coexisting causes.⁶ First, the sinoatrial or atrioventricular node may suffer structural damage with depression of nodal automaticity potentiated by enhanced vagal tone. Second, an abnormal ectopic focus within the ventricle may assume the role of dominant pacemaker.⁶ The ventricular ectopic focus manifests when the sinus rate slows down (below the ectopic focus) or when the ectopic focus accelerates above the intrinsic rate by 30 beats/min to 40 beats/min.² When both discharge rates (sinus and ectopic focus) are similar, isorhythmic dissociation, fusion beats, and capture beats can be seen.

AIVR is usually a benign and well-tolerated arrhythmia.² Most cases of AIVR will require no immediate treatment for this dysrhythmia, because AIVR is usually self-limiting and resolves when the sinus rate exceeds that of the ventricular foci.⁶ Administration of antiarrhythmics to patients with AIVR may cause precipitous hemodynamic deterioration and should be avoided.⁶ In cases of AIVR, remember to treat the underlying cause: For example, restore myocardial perfusion (thrombolytics or percutaneous coronary intervention), or correct electrolyte abnormalities. Patients with low cardiac-output states (eg, severe biventricular failure) may benefit from restoration of atrioventricular synchrony to restore atrial kick. In cases of low cardiac output associated with AIVR, atropine may be used in an attempt to increase sinus rate and atrioventricular conduction.⁷

The Law of the Heart

The law of the heart is thus the same as the law of muscular tissue generally, that the energy of contraction, however measured, is a function of the length of the muscle fibre.

— Ernest Henry Starling, 1866–1927, British physiologist

Figure 1.

12-lead electrocardiogram from a 61-year-old man presenting to the Emergency Department with 2 hours of chest pain, demonstrating sinus bradycardia, heart rate of 47 beats/min, minimal (< 1 mm) ST-segment elevation in leads I and aVL, and reciprocal ST-segment depressions in leads III and aVF, which are characteristics consistent with an evolving high lateral-wall myocardial infarction. The electrocardiogram does not meet ST-segment elevation myocardial infarction criteria of ≥ 1 mm ST-segment elevation in 2 or more contiguous leads.

Figure 2.

Repeat 12-lead electrocardiogram from the same patient as in Figure 1, obtained 1 hour after the initial electrocardiogram (after treatment with aspirin and sublingual nitroglycerin, with improvement in chest pain), demonstrating a wide-complex, regular, accelerated junctional rhythm, heart rate of 63 beats/min, which is consistent with an accelerated idioventricular rhythm. In the setting of evolving lateral wall ST-segment elevation myocardial infarction, this finding is suggestive of spontaneous reperfusion of an occluded coronary artery.

Figure 3.

Repeat 12-lead electrocardiogram from the same patient, obtained 1 minute after the electrocardiogram in Figure 2, demonstrating conversion from accelerated idioventricular rhythm back into sinus bradycardia. Subsequent coronary angiography demonstrated 99% stenosis of the first diagonal branch of the left anterior descending coronary artery, which was successfully treated with percutaneous coronary intervention and stenting.