16.20 and 16.21 present examples of a distinctive arrhythmia called accelerated idioventricular rhythm (AIVR), sometime referred to as slow VT. Recall that with typical VT the heart rate is more than 100 beats/min. Warren Smith, Margaret Hood, in Cardiothoracic Critical Care, 2007. The ventricular rate is generally between 70 and 100 bpm (near the sinus rate) but should not be considered to be “slow VT.” AIVR is distinguished from VT by its slower rate (< 100 bpm). These VTs are sensitive to autonomic tone and frequently display chronotropic properties. There is AV dissociation, with the atrial and ventricular rates typically being relatively similar. These arrhythmias originate within the reperfusion zone and likely reflect myocellular reperfusion injury. AIVR is often short lived and has no hemodynamic consequences. AIVR may also terminate abruptly. From: Goldberger's Clinical Electrocardiography (Ninth Edition), 2018, Dina M. Sparano, Judith A. Mackall, in Cardiac Intensive Care (Third Edition), 2019. More rarely (see Fig. The rate of AIVR is less than 100 bpm. Similarly, AIVR may terminate abruptly because the sinus rate increases or because the ventricular escape rate slows. Reperfusion injury produces a second peak of myocardial necrosis, which depends on the duration of the preceding ischemia. AIVR is defined by its rate, under 100 beats/min. The law of the heart states that the fastest pacemaker is the one that governs the heart. AIVR is classically seen in the reperfusion phase of an acute ST-segment-elevation myocardial infarction (STEMI; post thrombolytic therapy or primary percutaneous coronary intervention). Figs. The ECG diagnosis of AIVR consists of establishing the ventricular origin of the rhythm. It is a benign rhythm and does not progress to VT or VF. None is indicated unless symptomatic (rare) (Table 3.7). This is typically an escape rhythm that should not be suppressed with antiarrhythmic agents such as lidocaine. In conjunction with thrombolytic therapy, reperfusion ventricular arrhythmias were considered as a noninvasive marker of successful infarct artery recanalization; however, current evidence suggests that those arrhythmias are neither specific nor sensitive. It can also occur in normal athletic hearts and during return of spontaneous circulation (ROSC) following cardiac arrest. When AIVR is sustained and hypotension is observed, an agent such as atropine may be useful in overdriving the AIVR by accelerating the sinus node. Also known as “accelerated ventricular rhythm” Tachyarrhythmia caused by increased automaticity in pacemaking cells of bundle branches and their fascicles Results when the rate of an ectopic ventricular pacemaker exceeds that of the sinus node Often associated with increased vagal tone and decreased sympathetic tone In contrast to AIVR, a ventricular escape rhythm can have a similar morphology, but its rates are 20 to 40 bpm. AIVR is a regular rhythm with a wide QRS complex (> 0.12 seconds).