Accelerated idioventricular rhythm (AIVR) was first described by Thomas Lewis in 1910.  AIVR is currently defined as an enhanced ectopic ventricular rhythm with at least 3 consecutive ventricular beats, which is faster than normal intrinsic ventricular escape rhythm (≤40 bpm), but slo
Posted February 2,2019 in General Medicine.
Accelerated idioventricular rhythm (AIVR) was first described by Thomas Lewis in 1910.AIVR is currently defined as an enhanced ectopic ventricular rhythm with at least 3 consecutive ventricular beats, which is faster than normal intrinsic ventricular escape rhythm (40 bpm), but slower than ventricular tachycardia (at least 100-120 bpm).Importantly, there is potential rate overlap between AIVR and some slow ventricular tachycardia. AIVR should not be diagnosed solely based on ventricular rate; context is important. Other characteristics of AIVR are helpful for its correct diagnosis (see Differentials).
AIVR is generally a transient rhythm, rarely causing hemodynamic instability and rarely requiring treatment. However, misdiagnosis of AIVR as slow ventricular tachycardia or complete heart block can lead to inappropriate therapies with potential complications. AIVR is often a clue to certain underlying conditions, like myocardial ischemia-reperfusion,digoxin toxicity, and cardiomyopathies.[2,3,4]
In most cases, the mechanism of AIVR appears to be related to the enhanced automaticity in His-Purkinje fibers and/or myocardium,sometimes accompanied with vagal excess and decreased sympathetic activity.Ischemia, reperfusion, hypoxia, drugs, and electrolyte abnormalities can all accelerate the phase 4 action potential depolarization rates in His-Purkinje fiber and myocardium, leading to faster spontaneous cell depolarization (enhanced automaticity).When the enhanced automaticity in His-Purkinje fiber or myocardium surpasses that of sinus node, AIVR manifests as the dominant rhythm of the heart. Sinus bradycardia may facilitate the appearance of AIVR.
Under certain conditions such as acute ischemia and digoxin toxicity, triggered activity has been suggested as the mechanism for AIVR.
Most AIVRs originate from a single focus. Occasionally, in patients with acute myocardial ischemia and myocarditis, AIVR can originate from multiple foci.[9,10]The ventricular rate of AIVR is generally between 40 to 100-120 bpm.
Usually, AIVR is hemodynamically well tolerated due to its slow ventricular rate. It is self-limited and resolves as sinus rate surpasses the rate of AIVR. Rarely, AIVR can degenerate into ventricular tachycardia or ventricular fibrillation. In patients with severe myocardial dysfunction, AIVR may lead to hemodynamic instability due to the loss of AV synchrony or relatively rapid ventricular rate.
Clinically, AIVR has been best studied in patients with acute ST-elevation myocardial infarction (STEMI). In the thrombolysis era, AIVR was noted to be a marker of reperfusion.However, not all patients with reopened coronary artery have AIVR. In patients with acutemyocardial infarctiontreated with primarypercutaneous coronary intervention, the reported incidence of AIVR varied significantly, raging from 15-50%, depending on methods of monitoring.[7,12,13]
Recently, studies in patients with STEMI treated with primary percutaneous coronary intervention support that AIVR is a marker of occluded coronary artery reopening, but is not necessarily a marker for complete reperfusion. In fact, AIVR seems to be associated with more extensive myocardial damage and delayed microvascular reperfusion,although the mortality rates are similar in patients with and without AIVR.
The true prevalence of AIVR is unknown.
The true prevalence of AIVR is unknown.
Hingorani et al analyzed drug-free ambulatory ECG recordings from 1273 healthy volunteers (who had normal screening ECGs) from 22 phase 1 studies that were analyzed in a core ECG laboratory. Accelerated idioventricular rhythm was observed in 0.3% of healthy volunteers, and other types of arrhythmias were observed in a higher percentage of healthy volunteers. The results suggest that some cardiac arrhythmias may be due to chance in early-phase studies.
No racial preponderance exists, and men and women are equally affected.
No age predilection exists.
AIVR is a mostly self-limiting rhythm and typically has a benign prognosis when AIVR rather than a slow(ed) VT is the true underlying entity. The prognosis of patients with AIVR largely depends on their underlying conditions.
In general, AIVR does not significantly affect the patients mortality and morbidity. In a very small retrospective observation study, AIVR was found to be associated with a lower 7-day survival rate in postresuscitation patients.
Reassure patients that AIVR per se does not significantly affect their prognosis. Educate patients that some of the underlying etiologies for AIVR should be treated accordingly.
History is helpful for identifying the underlying etiology for AIVR. The presence of the following conditions supports a potential diagnosis of AIVR:
Most patients with AIVR have chest pain or shortness of breath, symptoms related to myocardial ischemia. They often have recent history of myocardial reperfusion with drugs or coronary artery interventions.
Some patients with AIVR have chest discomfort, shortness of breath, peripheral edema, cyanosis, clubbing, symptoms related to cardiomyopathy, myocarditis, and congenital heart diseases.
Occasionally, patients with AIVR have history of using digoxin, some anesthetic agents, or illicit drugs such as cocaine.
Rarely, AIVR can occur in people without apparent heart disease and no identifiable triggers.
There are no specific physical findings for AIVR. The following physical signs may be present:
Slow ( 55 bpm) or fast (100 bpm) pulse rate.
Variable heart sound intensity and cannon A waves related toatrioventricular dissociation.
Some irregularity of heart rate/pulse rate due to competing sinus rhythm and AIVR.
Rarely, hypotension related to either AV asynchrony or relatively rapid ventricular heart rate during AIVR.
The AIVR can occur in people with and without apparent heart diseases.The most common cause of AIVR is myocardial ischemia-reperfusion. Other causes include the following:
Congenital heart disease
Beach et al reported on the case of a boy aged 4 years who appeared to have developed AIVR from the administration of inhaled albuterol to treat his status asthmaticus.
Accelerated idioventricular rhythm (AIVR) is diagnosed based on its characteristic electrocardiography findings. Its main differential diagnosis includes slow ventricular tachycardia, complete heart block, junctional rhythm with aberrancy, supraventricular tachycardia with aberrancy, and slow antidromic atrioventricular reentry tachycardia.
AIVR is a wide QRS ventricular rhythm with rate of 40-120 bpm. However AIVR should not be diagnosed solely by its ventricular rate because of the rate overlap between AIVR and some slow ventricular tachycardia. See the image below.
The following characteristics are important for establishing the diagnosis of AIVR:
AIVR starts gradually as a long-coupled, premature, ventricular beat when the rate of firing in ectopic ventricular focus (with enhanced automaticity) surpasses that of sinus rate. At the onset of AIVR, the rates of AIVR and sinus rhythm are often similar; therefore, it is not uncommon to see ventricular fusion beats at its onset due to partial ventricular capture from both rhythms.
During AIVR, the rate of AIVR is usually slightly faster than or similar to sinus rate, often resulting in nearly isorhythmic AV dissociation (a misnomer, but reflecting that the ventricular rate is similar to or just faster than atrial rate). Due to isorhythmic AV dissociation, ventricular fusion and sinus ventricular capture may be present. Sometimes 1:1 retrograde atrial capture may occur, especially during long AIVR episodes.
AIVR often terminates gradually when sinus rate just surpasses that of AIVR due to either sinus rate acceleration or AIVR rate deceleration, sometimes resulting in ventricular fusion beats.
AIVR can occur inatrial fibrillation(see image below) and other rhythms when the rate of firing in ectopic ventricular focus surpasses that of the underlying dominant ventricular rate.
The characteristic gradual onset and termination of AIVR are helpful in differentiating it from slowventricular tachycardia, which is associated with sudden onset and termination.
The AV dissociation during AIVR is isorhythmicAV dissociationwith ventricular rate similar to or faster than atrial rate. In contrast, in complete heart block, the AV dissociation is not isorhythmic with atrial rate much faster than ventricular rate.
Unlike junctional/acceleratedjunctional rhythm, AIVR has a wide QRS morphology that is different from the narrow QRS morphology in sinus rhythm without aberrancy and the wide QRS morphology with typical bundle branch block patterns.
Obtain levels of troponin, CK and CK-MB for the diagnosis of myocardial infraction.
Obtain BUN and creatinine measurements to assess renal function in patients with suspected digoxin toxicity.
Obtain levels of digoxin and electrolytes.
Obtain echocardiography to evaluate structural heart diseases.
Nuclear perfusion scanning is used to evaluate myocardial ischemia.
Coronary angiography is used to evaluate coronary artery patency.
Electrocardiography is the most important method for the diagnosis of AIVR; AIVR can be distinguished from complete heart block on ECG.Although both show AV dissociation, in complete heart block, P waves are present preceding the QRS complex, but fail to conduct to the ventricle.
Telemetry monitoring, Holter study, event recorder, and loop recorder are often the electrocardiographic modalities from which AIVR diagnosis is established.
Treatment for accelerated idioventricular rhythm (AIVR) does not change the prognosis. The most important therapy for patients with AIVR is to treat the underlying etiology.
AIVR is usually hemodynamically tolerated and self-limited; thus, it rarely requires treatment.
Occasionally, patients may not tolerate AIVR due to (1) loss of atrial-ventricular synchrony, (2) relative rapid ventricular rate, or (3) ventricular tachycardia or ventricular fibrillation degenerated from AIVR (extremely rare). Under these situations, atropine can be used to increase the underlying sinus rate to inhibit AIVR.
Other treatments for AIVR, which include isoproterenol, verapamil, antiarrhythmic drugs such as lidocaine and amiodarone, and atrial overdriving pacing are only occasionally used today.
Patients with AIVR should be treated mainly for its underlying causes, such as digoxin toxicity, myocardial ischemia, and structure heart diseases. Beta-blockers are often used in patients with myocardial ischemia-reperfusion and cardiomyopathy.Transfer to advanced care facility depends on associated conditions.
A cardiology or electrophysiology consult may be helpful in difficult cases.
No particular diet is helpful.
Activity may increase sinus rate and inhibit AIVR in some patients. In others, activity may not be well tolerated during AIVR; therefore, temporary bed rest or atropine therapy is reasonable.
Prevention is usually unnecessary due to the benign nature of most AIVR events. Occasionally for patients with significant symptoms and hemodynamic instability, atropine can be used to reduce AIVR recurrence by increasing sinus rate.
Avoiding drugs that cause AIVR is helpful.
The underlying causes for AIVR should be treated accordingly.
Atropine 0.25-1 mg is sometimes used to accelerate underlying sinus rate to inhibit AIVR.
Isoproterenol, verapamil, and antiarrhythmia drugs such as lidocaine and amiodarone are occasionally used for AIVR.
The goal is to accelerate sinus rate or to improve AV conduction in atrial fibrillation to inhibit AIVR.
Used to increase heart rate through vagolytic effects, causing an increase in cardiac output.