Another AV Block?

Electrocardiogram Interpretation, 2022

One of the most difficult decisions for many physicians and advanced practice providers occurs when having to distinguish between simple atrioventricular (AV) dissociation and AV dissociation caused by a third degree AV block. Third degree AV block is only one cause of AV dissociation and it is a very infrequent cause. The majority of simple AV dissociations are caused by variations in the balance of sympathetic and parasympathetic inputs from the autonomic nervous system. All of us probably experience an occasional episode of simple AV dissociation while we are asleep. Treatment for simple AV dissociation may be as simple as having the patient get out of bed and walk around the room a few times, while AV dissociation caused by a third degree AV block is going to require an emergent placement of a permanent pacemaker. In order to make this decision properly and confidently, you must have a very clear understanding of the difference. Here, in this educational paper, we aim to discuss more in this regard.

Pacing and Clinical Electrophysiology, 1983

Journal of Arrhythmia

Clinical Cardiology, 1985

block without associated electrocardiographic (ECG) abnormality is not a well recognized entity. A mother and her daughter had recurrent syncopal episodes, but a normal ECG. The episodes were preceded by nausea and vomiting. ECG during these episodes revealed complete heart block. In the mother, one episode was promptly reversed by atropine. Electrophysiological evaluation of the sinus and AV nodal function and atrial and ventricular effective refractory periods before and after autonomic blockade was normal. Provocative manoeuvres failed to induce AV block. Paroxysmal AV block was vagally mediated in one of the patients, as indicated by prompt response to atropine. In the second case, the vagal dependence could not be proved but appears to be the most likely explanation. It thus appears that paroxysmal, vagally mediated complete AV block should be seriously considered in patients with unexplained syncope.

Circulation: Arrhythmia and Electrophysiology, 2008

AV block after a premature ventricular complex. The sinus rate is unchanged before and after the AV block. Resumption of AV conduction occurs with a narrower QRS and with delayed conduction.

Journal of Cardiovascular Electrophysiology, 2010

This 11-year-old previously healthy female began having syncopal episodes at rest and during exertion. Baseline ECG (PR interval = 155, QRS duration = 85, and QTc = 389 ms) and echocardiogram were normal. During 24-hour ambulatory heart rhythm monitoring, there were several episodes of paroxysmal high grade AV block not associated with symptoms ( ). During block, the maximum RR interval was 2.8 seconds, when the P wave rate was stable at 105 bpm. A diagnostic electrophysiologic study was performed under propofol anesthesia. Standard quadripolar electrode catheters having 2-5-2 interelectrode spacing were placed in the high right atrium, right ventricular apex, and His bundle regions. At baseline, a "split His bundle" electrogram (denoted as H-H') was always present during sinus rhythm and atrial pacing, with a constant H'V interval of 35-38 ms. During atrial extrastimulus testing and incremental atrial pacing, the AH and AH' intervals increased similarly with a nearly constant H-H' and without classic criteria for dual AV nodal physiology. What do you think is the mechanism of block?

Pacing and Clinical Electrophysiology, 2011

A 65-year-old woman underwent dualchamber permanent pacemaker implantation for degenerative complete atrioventricular (AV) block. The measured P/R waves, pacing threshold, and impedance obtained through the analyzer were 4 mV, 0.5 V at 0.4 ms and 620 and 16 mV, 0.3 V at 0.4 ms and 580 , respectively, in the implanted passive-fixation bipolar atrial and ventricular leads. The leads were connected to the pulse generator (Sensia SEDR01, Medtronic Inc., Minneapolis, MN, USA) with nominal parameters (except the mode that was changed to DDD, others being lower rate 60/min, upper tracking rate 130/min, AV delay sensed and paced 120 and 150 ms, rate-adaptive AV delay off, and mode switch on at detect rate of 175/min), and the device was placed in the subcutaneous pocket created earlier. Intermittent loss of tracking of single P waves was noted immediately on the electrocardiogram monitor . The leads were verified to be in optimal position on fluoroscopy and the device was then interrogated. The electrogram obtained from the programmer during the loss of atrial tracking is shown in . The sensing and pacing parameters obtained through the programmer were as follows: atrial-P wave 3.5 mV, threshold 0.5 V at 0.4 ms, impedance 625 and ventricular-R wave 15.68 mV, threshold 0.5 V at 0.4 ms, and impedance 560 . The problem persisted despite turning off search AV+, noncompetitive atrial pacing and premature ventricular contraction response, and changing the postven-Conflicts of Interest: None.

The American Journal of Cardiology, 1992

Pacing and Clinical Electrophysiology, 2010

narrow complex tachycardia, accessory pathway, spontaneous automaticity Case Presentation A 42-year-old man was referred to our laboratory because of recurrent episodes of palpitations in spite of treatment with oral flecainide (200 mg per day). A narrow complex tachycardia had been documented during one of the episodes with a heart rate of 165 beats per minute. Basal 12-lead electrocardiogram (ECG) showed normal sinus rhythm with no conduction disturbances and without any evidence of preexcitation. Standard catheters were inserted through the right femoral vein and placed in the high right atrium (HRA), atrioventricular (AV) junction, and right ventricular apex (RVA). A decapolar catheter was placed in the coronary sinus (CS) through the left antecubital vein with the proximal pair of electrodes placed in the CS ostium (CS 9-10) and the distal pair of electrodes in the lateral mitral annulus (CS 1-2). Baseline intervals during sinus rhythm included an atrial-His (AH) of 86 ms and a Hisventricular (HV) of 40 ms. During incremental atrial pacing progressive lengthening of the AH interval without modifications in the HV interval was registered. No jump in the AH interval was assessed and no arrhythmias could be induced by programmed atrial stimulation. Incremental right ventricular pacing evidenced the presence of eccentric and decremental retrograde conduction with the earliest retrograde atrial activation registered at the distal pole of the CS catheter (Fig. 1). Programmed ventricular stimulation with introduction of a single extrastimulus was able to reproducibly induce the clinical tachycardia (Fig. 2). What is the mechanism of the tachycardia? What is the mechanism of induction? Disclosures: None.

The American Journal of Cardiology, 1974

Repeated episodes of paroxysmal atrioventricuiar (A-V) block were recorded from a 78 year old woman with Stokes-Adams seizures. After a single or occasionally two consecutive and conducted atrial extrasystoles, all the succeeding P waves were blocked. Normal A-V conduction was resumed only when a P wave fell within a certain time interval after a ventricular escape beat. Three A-V conduction phases were identified: an early phase of A-V block, a late phase of A-V block and an intermediate phase during which A-V conduction was preserved. Within the phase of preserved A-V conduction, three intraventricular conduction subphases were found: an early phase of incomplete left bundle branch block, an intermediate phase of normal intraventricular conduction (mixed with incomplete right bundle branch block) and a late phase of high grade right bundle branch block. Thus, conduction was initially impaired more or only in the left bundle and, as the R-P intervals increased, conduction deteriorated progressively in both bundle branches but at a higher rate in the right bundle, until conduction failed totally in both bundle branches. This case, a complex variant of paroxysmal A-V block, seems to be the first reported instance of enhanced diastolic depolarization occurring in both bundle branches simultaneously and giving rise to phase 4 bilateral bundle branch block. From the Services of Cardiology of "Hospital ltaliano" and "Hospital Balaberry," Buenos Aires, Argentina. Manuscript accepted June 20, 1973.