A 64yr old male in no acute distress. History includes ischemic cardiomyopathy w/ EF~10%, multiple MIs, multiple stents, sustained VT, hypertension, CHF, hyperlipidemia, and past tobacco use.
Anti-tachycardia pacing (ATP) via ICD device can effectively terminate >90% of reentrant VT, avoiding the high energy expenditure and pt. discomfort associated with synchronized cardioversion.
This pt. presented to EMS complaining of left subclavicular tenderness and purulent discharge from the incision site through which he had received a biventricular ICD one month prior. Although there is some possibility of infection-induced myocardial irritability, these ECGs most likely represent incidental findings consistent only with the pt’s ongoing state of arrhythmogenic advanced ischemic heart disease.
Two different electrophysiologic approaches can be used to model the mechanism of reentrant VT. Under the first approach, islands of anatomic or functional conduction block arising due to structural or ischemic disease present electrical “forks in the road” at which a depolarizing wavefront can split into two or more signal pathways. Reentrant tachycardia occurs when one of the pathways around the island is unidirectional and sufficiently longer than the other, allowing the ventricle to depolarize via the short path (1), and then repolarize in time to be reactivated by the delayed signal from the long path (4). By the time the ventricle has finished depolarizing via the long path, the short path has had time to recover excitability, and the cycle repeats itself.
Fig. 1: Propagation of normal action potential (left) and conditions for reentrant excitation (right).
An alternative viewpoint holds that the post-ischemic islands of damaged myocardium do not present obstacles of non-conductive terrain, but instead zones of slow conduction. These slow-conduction zones can entrap or waylay a portion of an electrical wavefront long enough for it to emerge on the other side into already repolarized ventricular tissue. By the time the waylaid electrical signal escapes from the slow conduction zone, the initial wavefront has passed, and the healthy myocardium has had time to repolarize. The newly liberated signal then reactivates the ventricle, circles back around, and reenters the damaged hypoconductive region.
Under both models, the physiologic substrate of reentrant VT is damaged, fibrotic myocardial scar tissue. The arrhymogenic cycle can be terminated by overriding the reentrant circuit; anti-tachycardia pacing supercedes the rate of the pt’s VT, seizing control of the wavefront’s path of depolarization. When pacing is withdrawn, the resulting refractory period enables normative conduction pathways to reestablish dominance.
Anti-tachycardia pacing can be categorized into burst and ramp modalities, as distinguished by the graphic below.
Fig. 2: Burst vs. Ramp ATP.
Examination of the second case study ECG presented above reveals a demand pacemaker rhythm overtaken by RBBB pattern monomorphic VT of 265ms cycle length. Burst-type ATP can be seen interceding for ~7 beats at 240ms CL followed by termination and a compensatory pause before the pt’s normative rhythm resumes in the third ECG.
Interrogation of this pt’s pacemaker indicated 56 incidents of ATP-terminated VT within the past two weeks. On the seventh hospital day, a surgical excision and debridement of the pacemaker pocket was undertaken with the placement of a temporary transvenous device and initiation of temporizing amiodarone therapy. An electrocardiogram from this period is seen below.
Six days later Infections Disease Services cleared the pt. for a replacement ICD which was subsequently implanted in the right chest. The pt. was discharged back into his normal state of health 48hrs later.
Fig. 1: Reentrant VT. S. Sinha: Spatiotemporal Dynamics Of Reentry Termination by Pacing.
Fig. 2: Burst vs. Ramp ATP. Michael O. Sweeney: Antitachycardia Pacing for Ventricular Tachycardia Using Implantable Cardioverter Defibrillators. (Medscape, 2004)
Philip J Podrid: Reentry and the Development of Cardiac Arrhythmias (UpToDate, 2006)
Steven J Compton: Ventricular Tachycardia. (EMedicine, 2010)
An 84yr old white female, s/p VT/PEA arrest.
This ECG demonstrates AV dual sequenced pacing with loss of atrial capture. Note the high left axis in the x-y plane, consistent with typical pacer findings, but an atypical rightward shift of electrical forces across the precordial z-axis (inverse R-wave progression). Traditionally ventricular pacing electrodes are deployed in the right heart and result in a LBBB ECG morphology as the myocardial tissue depolarizes from right to left. Yet in this case we see a dramatic RBBB pattern, raising concerns about displacement or septal perforation, particularly given that the pt. has received CPR. The etiology of RBBB pacer morphology is not exclusively pathological, however, and receives a good discussion on Dr. S. Venkatesan’s Cardiology Blog. Note that the QRS in this case is elongated above 160ms, and necessarily reflects slow and poorly coordinated ventricular contraction, perhaps betraying a newly aberrant interventricular conduction pathway, even for this 100% paced patient.
Another interesting example of a similar RBBB effect can be seen at Dr. M. Rosengarten’s electrocardiography site, and there is a thorough case report and research analysis of the phenomenon in The Journal of Electrocardiography Vol.6 No. 1, 2003.
Shortly after this 12-lead was captured, the pt. again deteriorated into PEA and was lost to resuscitative efforts.