Ventricular Sensing Episode: What is the Rhythm?

Charlotte Mehegan
West Suffolk NHS Foundation Trust, UK

Disclosure: No conflict of interests to declare.



A 74-year-old male was brought in by ambulance following an unwitnessed collapse with no prodromal symptoms. He had a Medtronic Brava CRT-D in situ, which was implanted two years previous for symptomatic ventricular tachycardia (VT) and severe systolic dysfunction (QRSd 172 ms, EF 14.6%).

Decompensation was noted on admission with a systolic blood pressure <90 mmHg, associated with shortness of breath and pre-syncope. His heart rate was fluctuating between 70 bpm and 130 bpm, with frequent variation in QRS morphology noted on telemetry. An inpatient device check was requested to evaluate the patient’s underlying rhythm and assess for an arrhythmic cause of collapse. Since the last device check (one week prior) there had been no monitored or treated ventricular arrhythmias, however two-hundred and fourteen ventricular sensing episodes had been recorded. The EGM in Figure 1 is representative of the most recent ventricular sensing episode and the patient’s presenting rhythm upon device interrogation.

Figure 1: Ventricular sensing episode; channels top to bottom include near-field atrial EGM, near-field ventricular EGM and marker channel.




What is the rhythm shown in the EGM?

A. Atrial Fibrillation with rapid ventricular response.
B. Atrial Tachycardia with 2:1 conduction.
C. Atrial Flutter with 2:1 conduction.
D. Atrial Tachycardia and Slow Ventricular Tachycardia.
E. Sinus rhythm with Far Field R wave over-sensing.



D. Atrial Tachycardia and Slow Ventricular Tachycardia.




Taking a systematic approach to the evaluation of this EGM, we can see a clear tachycardia on the near-field atrial channel. The cycle length of this tachycardia is approximately 300 ms/200 bpm with occasional atrial paced (AP) beats occurring, due to atrial events falling in the refractory period; these appear fused with the native tachycardia, hence the varying atrial morphology. Atrial events measured 0.3 mV, which straddled the programmed sensitivity, culminating in occasional under sensing as noted periodically on the EGM.

On first glance the ventricular EGM shows a short, sharp deflection which is initially positive. The ventricular rate is consistent at 600 ms/100 bpm, which is half the rate of the ongoing atrial tachycardia and below the programmed VT detection zone (125 bpm). In addition to the regular ventricular sensed (VS) rhythm there are three beats where ventricular safety pacing has occurred, due to ventricular events falling within the 110 ms cross-talk window. As the VS events are intrinsic activity and not generated by noise, the resulting QRS complexes appear either entirely paced or fused. These beats likely provide an explanation to the varying QRS morphology seen on telemetry.

On balance it would be entirely reasonable to document this rhythm as atrial tachycardia with 2:1 conduction. However, this particular rhythm does not fit with the decompensation of the patient.

Looking slightly deeper into the EGM, we can see that in fact there are no consistent A-V intervals. This would suggest that the atrial and ventricular rhythms are dissociated. To confirm our thoughts, we compared the rhythm to a true VT recorded in Figure 2, which shows V>A at 540 ms/111 bpm.

Figure 2: Ventricular sensing episode showing true ventricular tachycardia; channels top to bottom include near-field atrial EGM, near-field ventricular EGM and marker channel.


When comparing the two traces, we can see identical ventricular EGM morphologies (initially positive with a terminal negative component), suggesting that these two rhythms originate from a similar focus. In Figure 2 the atrial rhythm is sinus in origin at 75 bpm with no obvious AV association. This further supports the notion that the ventricular rhythm in Figure 1 is not mediated by the atrial tachycardia.

To summarise, this patient has two simultaneous, independent tachycardia circuits; also known as a Dual Tachycardia. The device did not deliver any therapy because the VT cycle length fell beneath the programmed detection interval. Haemodynamic stability and clinical prognosis were compromised as a result of this arrhythmia.



Slow VT has a relatively high incidence (30%) in the cardiac device population.1 The clinical impact of slower VT circuits remains largely variable and notably under-represented in current research.2 Case reports such as this one highlight the deleterious effects of slower ventricular arrhythmias. Similar reports in the literature evidence significant decompensation leading to sudden cardiac death in the worst instances.1

Anti-tachycardia pacing (ATP) has proven safe and effective in cases of slower VTs3 however due to the patient’s haemodynamic instability we decided external cardioversion (DCCV) would be the better option in this case. Cardioversion was successful and biventricular pacing was restored. Pre and Post DCCV ECGs are shown in Figure 3 and Figure 4 respectively.

Figure 3: 12-lead ECG showing atrial tachycardia and slow ventricular tachycardia: Pre-DCCV.


Figure 4 – 12-lead ECG showing bi-ventricular pacing: post-DCCV.


This case teaches us to look beyond the obvious answer. It also illustrates the clinical benefit of VS episode EGMs and the importance of evaluating your device data in the clinical context in which it is found.



1. Leitz, N, Zarqa, K and Been, M. Slow ventricular tachycardia. BMJ 2008;337:a424. PMID: 18599467.

2. Lüsebrink, U, Duncker, D, Hess, M, et al. Clinical relevance of slow ventricular tachycardia in heart failure patients with primary prophylactic implantable cardioverter defibrillator indication. EP Europace 2013;15(6);820–6. PMID: 23325044.

3. Sadoul, N, Mletzko, R, Anselme, F, et al. Incidence and clinical relevance of slow ventricular tachycardia in implantable cardioverter-defibrillator recipients. Circulation 2005;112;946-53. PMID: 16103252.

Co-published with thanks to the British Heart Rhythm Society.

This content is owned by the British Heart Rhythm Society. Permission to reproduce this content must be requested from the rights-holder directly.


ICD Shock Therapy: What Is The Cause?

Jason Collinson
Mid and South Essex NHS Foundation Trust

Disclosure: The author has no conflict of interests to declare.



A remote alert was received from a 65-year-old male with a primary prevention dual chamber implantable cardioverter-defibrillator (ICD) for ‘shock delivered for an episode’. Previous medical history included an ischaemic cardiomyopathy and paroxysmal atrial fibrillation. Figure 1 displays the electrogram (EGM) at the time of the episode. There was a single ventricular fibrillation (VF) therapy zone, programmed with a rate cut off at 200 bpm with 30/40 second intervals to detection.

Figure 1: The recorded EGM at the time of the ICD shock therapy.

Channels top to bottom: near-field atrial EGM, near-field ventricular EGM, marker channel.



What is the diagnosis?

A. Appropriate shock for ventricular fibrillation.
B. Inappropriate shock for electromagnetic interference (EMI).
C. Inappropriate shock for cathode conductor fracture.
D. Inappropriate shock for lead insulation failure.



B. Inappropriate shock for electromagnetic interference (EMI).



The EGM in Figure 1 displays oversensing of the 50 Hz current leak from an external source. The artefact is repetitive, of high frequency and is clearly seen in both the atrial and ventricular channels, with marker intervals recording sensed events at non-physiological intervals.

The episode was discussed with the patient who described no symptoms prior to the shock. He explained that he was cleaning a submersed pond pump of weed, when he had a sudden shock across his chest. His hands were in the water at the time of the episode and it is likely that a current leak from the pump was conducted through the water, passed through the patient’s chest, which was detected by the ICD sensing circuit, resulting in the shock.

The patient was advised to have an electrician check the pond pump circuitry before attempting to clean the pump again and as a further precaution, he was told to unplug the pump from the mains before working on the system again.



Inappropriate shocks from EMI are infrequently seen but are a known risk to patients with ICDs. Case reports have described their occurrence in several settings, including faulty or poorly earthed submerged pond pumps,1,2 alternating-current (AC) leaks from faulty appliances,3 swimming pools4 and jacuzzi’s.5

For physicians involved in ICD follow up, it is important to recognise an EMI artefact on an EGM trace. The artefact is usually repetitive and of a high rate. This is seen as 50 Hz in the UK and 60 Hz in the US.

EMI is often visible simultaneously on all channels, with a greater amplitude on far field EGMs compared to near field EGM’s. However, it may also be seen as only present on the atrial channel, with atrial leads shown to be more susceptible to EMI.6

If EMI is suspected, careful questioning of the patient, their activities and possible electrical items being used at the time of stored episodes or a shock event is required to help determine whether EMI is the likely source of artefact.

When advice is provided to patients with respect to equipment which may or may not interact with their ICD, it may be worth reminding patients that poorly maintained equipment, self-installed electrical systems and water based electrical equipment pose a greater potential risk of interactions, including inappropriate ICD therapies.



1. Knight HM, Cakebread HE, Gajendragadkar PR, et al. Sleeping with the fishes: electromagnetic interference causing an inappropriate implantable cardioverter defibrillator shock. BMJ Case Reports 2014; 2014: bcr2013203462.

2. Vlay S. Fish pond electromagnetic interference resulting in an inappropriate implantable cardioverter defibrillator shock. Journal of Pacing and Clinical Electrophysiology 2002;25(10): 1532.

3. Chan NY, Wai-Ling Ho L. Inappropriate implantable cardioverter – defibrillator shock due to external alternating current leak: Report of two cases. EP Europace 2005;7(2):193-196.

4. Lee SW, Moak JP, Lewis B. Inadvertent detection of 60-Hz alternating current by an implantable cardioverter defibrillator. Pacing and Clinical Electrophysiology 2002;25:518-519.

5. Martin C, Carpenter V. Preventing inappropriate shocks: Integrating ICD programming, drug and interventional treatment and jacuzzi avoidance. BHRS Editorial 2017.

6. Napp A, Joosten S, Studer D, et al. Electromagnetic interference with implantable cardioverter defibrillators at power frequency: an in vivo study. Circulation 2014;129: 441-50.

Co-published with thanks to the British Heart Rhythm Society.

This content is owned by the British Heart Rhythm Society. Permission to reproduce this content must be requested from the rights-holder directly.


A Remote Interrogation Requiring Further Investigation

Dr Farhana Ara, MBBS MSc MRCP(UK), Miss Sandra Silva, BSc CCDS
Royal Papworth NHS Trust, Cambridge, UK

Disclosure: The authors have no conflicts of interest to declare and would like to thank Dr Greg Mellor, Consultant Cardiologist and Electrophysiologist, Royal Papworth NHS Trust, Cambridge, UK.


Case presentation

An 81-year-old male with previous atrial fibrillation underwent a VVI permanent pacemaker (PPM), (Medtronic Vivatron G20A2 SR), implantation for complete heart block. At the post-implant check and six-week in-house device interrogation, the right ventricular (RV) threshold was 0.5 V at 0.4 ms.

The first remote transmission (five months post-implant), showed a gradual increase in threshold from the day of implant.

The RV threshold was 2.5 V at 0.4 ms and the output was automatically set to 5 V at 1.0 ms.


Device settings

Mode: VVIR
Lower rate: 60 ppm
Upper sensor rate: 130 ppm
Pace/sense polarity: Bipolar/bipolar
Output management: Adaptive


Figure 1: RV lead threshold


What would be next step in management?

A: Continue monitoring
C: In-house device interrogation
D: List for lead revision



D: List for lead revision

The patient was listed for a lead revision. Fluoroscopy of the lead and device interrogation on the morning prior to procedure showed no lead noise or displacement, with a stable lead impedance (Figure 2).

Figure 2: RV lead impedance trends

A manual threshold test was then performed (Figure 3), which showed loss of capture at 0.25 V at 0.4 ms, giving a manual threshold of 0.5 V at 0.4 ms.

Figure 3: Manual threshold test

An automated threshold test was also performed (Figure 4).

Figure 4: Automated threshold test



What is the next step in management?

A: Add an atrial lead
B: List for lead revision
C: Monitor
D: Switch off autocapture


D: Switch off autocapture

Autocapture adaptive pacing was switched off. There was a consistently normal RV threshold (0.5 V at 0.4 ms). Inappropriate capture management was noted, and the impression was of inappropriate evoked response due to hyperpolarization.

Lead revision was cancelled, and the patient was well at the three-month follow-up appointment.


Ventricular capture management is an automatic pacing threshold adjustment algorithm, that automatically measures pacing threshold through detection of the evoked response after a pacing stimulus.

This algorithm then automatically updates the pacing output to the optimal value. This function avoids unnecessary high output pacing and is considered to prolong battery longevity.

Pacing threshold search is initiated according to the schedule and frequency programmed by the clinician in pacemakers (nominally set to ‘day-at-rest’).

After implant detection is complete, the device initiates the first pacing threshold search 12 hours after.

If a search cannot be completed, the device retries after 30-minutes.

A ‘high threshold condition’ warning is issued if the amplitude threshold is greater than 2.5 V. The pacemaker responds, by adapting to an amplitude of 5.0 V and a pulse width of 1.0 ms. It will not give you an exact RV threshold measurement (Figure 1).

Figure 5: Ventricular capture management

Figure 5 shows ventricular capture management with a pacing stimulus or ‘test pulse’ being delivered to the right ventricle. When there is no evoked response detected during the pacing search, within a timed interval, back-up pulse is delivered, followed by three further pacing pulses or support events.

Capture verification efficiency relies on the measurement of the evoked response and works by triggering a blanking window (closed), followed by an open window.

If the device detects an evoked response (ER) within this second window, capture is confirmed (Figure 6). Otherwise, it will deliver a 5 V back-up pulse to ensure capture (Figure 7).

Figure 6: Capture verification

Figure 7: Capture verification with back-up pulse

Figure 8: Ventricular capture management in patient

Figure 8 shows that the device is allowing three support cycles as the programmed rate and output followed by a faster test pace. The test pace automatically has a back-up pace at programmed voltage at 1.0 ms, that occurs 110 ms after the test pace. These back-up pulses are not seen on this strip.

This cycle repeats, looking for the 2/3 capture before moving on, or 3/3 capture to confirm measurement. Looking at the timing of the rhythm then, it seems that all test paces capture as the ventricular event does not shift 110 ms later. However, the evoked response signal is not consistently detected by the device and so it sometimes labels this as loss of capture (LOC).

Evoked response detection and limitations: in rare instances, the pacemaker may not detect the electronic waveform created by the contracting myocardium immediately following a pacing pulse. High thresholds may be appropriate due to lead dislodgement, or incomplete connection of the lead in the header block. Acute effects of lead maturation can also cause failure to detect the evoked response. Hyperpolarization of the EGM leading to signal saturation or changes in lead tip and muscle interface (i.e. tissue fibrosis) may be responsible for this.

In our patient, the phenomenon was seen following the lead maturation period (typically within 4 to 12 weeks), when fibrosis between tip to tissue interface is expected. The inflammatory reaction and the resulting fibrous tissue that occurs after implantation may act as an insulating shield around the electrode, effectively raising the threshold for stimulation.Remote transmission has increased during the COVID-19 pandemic. This case highlights the importance of in patient/face-to-face review and interpretation of automated diagnostics.



1. Antretter H, Bonatti J, Cottogni M, et al. A new cardiac pacemaker stimulation technology (autocapture) allows, with unchanged life expectancy, reduction of generator size by half. Acta Med Austriaca 1996;23(5):159-164.

2. Medtronic. Ventricular Capture Management Feature. 2016. (accessed 30th September 2020).

3. Kishihara J, Niwano S, Fukaya H, et al. Pacing failure caused by automatic pacing threshold adjustment system. Journal of Arrhythmia 2017;33: https://10.1016/j.joa.2017.05.005.

4. Hayes D, Pacing system malfunction: Evaluation and management 2019.

5. HRS/EHRA/APHRS/LAHRS/ACC/AHA worldwide practice update for telehealth and arrhythmia monitoring during and after a pandemic (2020).

6. Murgatroyd FD, Helming E, Lemke B, et al. Manual vs. automatic capture management in implantable cardioverter defibrillators and cardiac resynchronization therapy defibrillators. Europace 2010;12:811–816. doi:10.1093/europace/euq053.

Co-published with thanks to the British Heart Rhythm Society.

This content is owned by the British Heart Rhythm Society. Permission to reproduce this content must be requested from the rights-holder directly.


Pre-syncope In An ICD Patient: An Unexpected Aetiology

Charlotte Mehegan
West Suffolk NHS Foundation Trust, UK

Disclosure: The author has no conflicts of interests to declare.



A 65-year-old male was admitted to the coronary care unit following multiple episodes of pre-syncope. He had a history of symptomatic beta-blocker induced sinus bradycardia, a marked first-degree AV block and an idiopathic VF arrest, for which a dual-chamber ICD was implanted in 2016.

Device interrogation was performed to ascertain the cause of his pre-syncope.

There were no monitored or treated ventricular arrhythmias. All battery and lead measurements were within normal limits.

The only stored EGMs since the last follow-up were RYTHMIQ episodes. An EGM which correlated with the patient’s most recent pre-syncopal episode is shown below in Figure 1.

Figure 1: A RYTHMIQ EGM recorded by the device at the time of documented pre-syncope



What was the cause of this RYTHMIQ episode?

A: Atrial loss of capture.
B: Loss of intrinsic conduction.
C: Premature ventricular contraction.
D: AV crosstalk.



C: Premature ventricular contraction.



Figure 2: An annotated RYTHMIQ EGM illustrating the mechanism for device mode switch

This recorded RYTHMIQ episode, illustrates normal device function in the context of a loss of atrioventricular synchrony. The aetiology of this episode demonstrating transition from acute arterial insufficiency (AAI), (VVI backup), to DDD pacemaker was an unfortunately timed premature ventricular contraction (PVC).

In this trace from left to right, we can see atrial demand pacing at a lower rate limit (LRL) of 1000 ms / 60 bpm. Intrinsic conduction appears prolonged, with measured PR intervals ranging from 280 ms to 320 ms.

At beat number eight, (as indicated in the blue box in Figure 2), we can see an uncharacteristically short A-V interval, with the ventricular event falling in the post-atrial ventricular blanking period. It would be notably impossible for this to be a conducted ventricular event, as we know the patient has a marked first-degree AV block at rest. The interval between atrial pace (AP) and VS is non-physiological and therefore can only be as a result of an ectopic beat or non-cardiac signal. We can see that the ventricular-sense (VS) marker in Figure 2 aligns with a QRS complex, with a subtly different morphology noted on both the ventricular and shock EGM channels; suggestive of ectopic ventricular origin.

This is an example of Boston Scientific’s RYTHMIQ algorithm, designed to minimise unnecessary ventricular pacing and prevent deleterious effects in patients with intact AV conduction.1,2 Unlike competitive algorithms, RYTHMIQ provides back-up VVI pacing at 15 bpm below the lower rate limit (LRL); in this case 1333 ms / 45 bpm.

When the device is programmed to RYTHMIQ, it will automatically switch to DDD(R) when three out of 11 ventricular beats are considered as ‘slow’.3

Slow ventricular beats include:4

• ventricular paced event;
• ventricular sensed event (lower rate limit + 150 ms);
• ventricular sensed event (sensor indicated rate + 150 ms).

In this example, the PVC precludes native intrinsic conduction at beat eight, which subsequently allows the ventricular LRL to timeout and deliver back-up asynchronous ventricular pacing (VP). The refractoriness of the ventricle post-VP precludes further AV conduction, leading to three slow asynchronous ventricular beats; thus, triggering DDD(R) mode at beat eleven (as indicated in the red box in Figure 2).

Following the eleventh beat, we can see synchronous atrial and ventricular pacing in the DDD(R) mode.

This case demonstrates normal, yet inappropriate, device behaviour for this patient. Although not well documented within the literature, PVC’s have been found to cause approximately 21% of inappropriate RYTHMIQ mode switches.5 Other causes of inappropriate RYTHMIQ mode transition include ventricular under-sensing, functionally non-conducted atrial events and isorhythmic AV dissociation.



Due to the correlation of pre-syncopal symptoms with RYTHMIQ episodes, we decided that a permanent DDDR mode with search AV+ would prevent future bradycardic events, whilst encouraging native intrinsic conduction in this patient.6 All other device settings were unchanged.

This case teaches us that ventricular tachyarrhythmias are not always the cause of pre-syncope/syncope in ICD patients. It also highlights the importance of appropriate patient selection for specific algorithmic programming.



1. Carsten I. Pacing-induced heart failure: should we avoid right ventricular pacing or not?, EP Europace 2007;19(2):165–168.

2. Sweeney MO, Hellkamp AS, Ellenbogen KA, et al. Adverse effect of ventricular pacing on heart failure and atrial fibrillation among patients with normal baseline QRS duration in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation 2003;107(23):2932-2937.

3. Bastian D and Fessele K. Strategies and pacemaker algorithms for avoidance of unnecessary right ventricular stimulation. In: Roka A. Current issues and recent advances in pacemaker therapy. London: InTech.

4. Pacing Modes Specific For Boston Scientific. 2020. (Accessed 23 August 2020).

5. Strik M, Defaye P, Eschalier R, et al. Performance of a Specific Algorithm to Minimize Right Ventricular Pacing: A Multicenter Study. Heart Rhythm 2016;13(6):1266-1273.

6. The David Trial Investigators. Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator. The dual chamber and VVI implantable defibrillator (DAVID) trial. ACC Current Journal Review 2003;12(2):88.

Co-published with thanks to the the British Heart Rhythm Society.

This content is owned by the British Heart Rhythm Society. Permission to reproduce this content must be requested from the rights-holder directly.

A Common But Not So Common Flutter

Óscar Salvador-Montañés MD1 and Andreu Porta-Sánchez MD PhD2
Hospital University Quirónsalud Madrid, Madrid, Spain


A 69-year-old male with congenital heart disease was admitted to our institution with new onset palpitations. His past medical history was remarkable for an atrial septal defect (ostium primum) that needed surgical correction when he was 10 years old. He had been symptom-free since then and was now an active adult without any health complaints. He was known to be in sinus rhythm with a wide right bundle branch block (RBBB). On admission, the physical exam was remarkable for mild heart failure symptoms and his fast rhythmically arrhythmic heart rate. His baseline ECG at admission (Figure 1).

Figure 1: Basal ECG Flutter 1


Question 1:

What would be the most likely circuit causing the arrhythmia of this patient and how would you approach it?


Answer 1:

The ECG shows a sawtooth pattern at an atrial cycle length of 250 ms with a 2:3 AV conduction and a (known) broad right bundle branch block. This is compatible with a typical counterclockwise atrial flutter, with a circuit turning around the tricuspid ring.

Although a direct current external cardioversion could be a reasonable option, we elected to treat this patient with electrophysiological testing and ablation for a more definitive solution.


Question 2:

Would you use an electroanatomical mapping system in this arrhythmia? If so, why?


Answer 2:

The ECG shows a sawtooth pattern at an atrial cycle length of 250 ms with a 2:3 AV conduction and a (known) broad right bundle branch block. This is compatible with a typical counterclockwise atrial flutter, with a circuit turning around the tricuspid ring.

The typical counterclockwise flutter image of the ECG indicates, with a very high likelihood, for Cavo-Tricuspid Isthmus (CTI) dependent flutter. We elected to perform the procedure as a simple intracardiac electrophysiology study (EPS) with two diagnostic catheters: Inquiry™ decapolar to the coronary sinus (CS) and Livewire™ duodecapolar into the tricuspid ring and an irrigated ablation catheter (FlexAbility™). We placed NavX™ patches in case the circuit was not CTI-dependent, and mapping was needed (Figure 2).

The tracings of activation an entrainment from the CTI are shown in Figure 3.

Figure 2: Fluoroscopic image of catheter location

Figure 3: Post pacing interval tachycardia cycle length at Cavo-Tricuspid Isthmus


Question 3:

Is the diagnosis of CTI-dependent flutter confirmed? Would you perform additional mapping or just ablate in the CTI?

Answer 3:

The findings of concealed entrainment and a post pacing interval tachycardia cycle length (PPI-TCL) of 30 ms during atrial overdrive pacing from the CTI, confirms that the CTI is involved in the circuit.

We decided not to do further mapping at this stage and to perform a CTI ablation line with 35W, 45 degrees and 45 second lesions.

During radiofrequency (RF) close to the inferior vena cava (IVC), the pattern of flutter activation changed to the one seen in the intracardiac recordings (Figure 4), without any motion of the diagnostic catheters.

Figure 4: Flutter change



Question 4:

What does this change in the pattern of activation suggest?


Answer 4:

We interpreted this change in activation pattern as evidence of another flutter that was coexisting with the initial one. In this second flutter, the cycle length (CL) is very similar to flutter 1 and although the pattern of activation suggests that a CTI flutter is present, entrainment from the CTI was not possible due to lack of capture in the area. We then performed entrainment from the CS ostium and had the response depicted in Figure 5 (PPI-TCL with manifest fusion). That response excluded quite certainly the presence of a CTI flutter and we elected to perform mapping of flutter 2.

The propagation map is illustrated in video 1 and the local activation time (LAT) map is illustrated in Figure 6, Panel A. The PPI at the yellow dot showed the response (Figure 7) next to the voltage map obtained during flutter which shows the dense scar of the previous atriotomy and diffuse scar in the lateral wall (Figure 6, Panel B).

Figure 5: FTA 2 post pacing interval tachycardia cycle length at CS Ostium

Video 1: Propagation map

Figure 6: Local activation map


Figure 7: FTA 2 Entrainment


Question 5:

How would you treat this flutter? Would a focal RF terminate the episode? Are there any special safety concerns in this particular region before delivering RF?

Answer 5:

We elected to perform a line of RF after carefully checking the absence of right phrenic nerve capture by pacing at high output in the region. The line joined the heterogeneous scar that acted as anchor point of the flutter with the dense scar of the previous atriotomy. RF at the entrainment spot did not terminate the flutter and it was only after completing the line that flutter 2 slowed and terminated during RF. (Figure 8).

The patient was not inducible for any other flutters and the CTI was still blocked so the procedure was terminated.

Figure 8: FTA #2 Termination



Dealing with atypical atrial flutter can be a very difficult electrophysiological scenario.1,2 The incidence of atrial flutter in congenital heart disease patients is high and it can be poorly tolerated. The circuits involve very frequently the cavo-tricuspid isthmus and that is also the case even for complex anatomies.3 Atrial flutter after surgical repair of an atrial septal defect (ASD) is a well-known long-term complication.4 It is usually recommended for patients with complex anatomies to have available an electroanatomical mapping system when RF is attempted, to ensure that the circuit is well characterized. In our case, we elected a hybrid approach initially without high-density mapping but then switched to activation mapping to delineate a new circuit (flutter 2) that was likely entraining flutter 1.

The approach for macroreentrant flutters such as the one we depicted, is based on anchoring the RF lesions to an unexcitable scar so the circuit is interrupted. The multiple scars present make it unlikely for a focal RF lesion to terminate flutter and achieve non-inducibility and avoid recurrence. High density mapping and new algorithms that depict the circuits with high accuracy are a great addition to the field and may help streamline the process of mapping and ablating in such difficult scenarios.5


1. Roca-Luque I, Rivas-Gandara N, Dos-Subira L et al. Predictors of Acute Failure Ablation of Intra-atrial Re-entrant Tachycardia in Patients With Congenital Heart Disease: Cardiac Disease, Atypical Flutter, and Previous Atrial Fibrillation. J Am Heart Assoc 2018;7(7):e0008063.

2. Yap SC, Harris L, Silversides CK, et al. Outcome of intra-atrial re-entrant tachycardia catheter ablation in adults with congenital heart disease: negative impact of age and complex atrial surgery. J Am Coll Cardiol 2010;56:1589-96. PMid:21029876.

3. Roca-Luque I, Rivas Gandara N, Dos Subira L et al. Intra-atrial re-entrant tachycardia in patients with congenital heart disease: factors associated with disease severity. Europace 2018;20:1343-1351. PMid:29016882.

4. Gatzoulis MA, Freeman MA, Siu SC, et al. Atrial arrhythmia after surgical closure of atrial septal defects in adults. N Engl J Med 1999;340:839-46. PMid:10080846.

5. Deno DC, Bhaskaran A, Morgan DJ et al. High-resolution, live, directional mapping. Heart Rhythm 2020 epub ahead of press. PMid:32438020.

A Ventricular High Rate Episode – What’s the Diagnosis?

Josh Mundy
The Ipswich Hospital NHS Trust, UK


A female patient in her seventies was admitted to the cardiac monitoring unit following an episode of abdominal pain and hyponatraemia. She has a history of paroxysmal atrial fibrillation and recently diagnosed severe left ventricular systolic impairment. A dual-chamber pacemaker was implanted for tachy-brady syndrome in 2017.

An inpatient pacemaker interrogation was requested to assess for arrhythmia. All lead and battery measurements were satisfactory.

One ventricular tachycardia (VT) episode was detected by the device lasting for 13 minutes. The EGM for this episode is seen below (Figure 1):

Figure 1: EGM associated with a ventricular high rate episode recorded by the patient’s device


What is the underlying arrhythmia that has resulted in ventricular high rate detection in this dual-chamber pacemaker?

a. Atrial flutter
b. Dual tachycardia
c. Ventricular tachycardia
d. Pacemaker mediated tachycardia


b. This is a case of dual tachycardia.


Dual tachycardia is defined as an episode of atrial tachycardia or atrial fibrillation which occurs simultaneously with an episode of ventricular tachycardia. This phenomenon is uncommon and is estimated to occur in around 9% of dual-chamber ICD interrogations.1

At the onset of this EGM, the rhythm is sinus tachycardia at a rate of around 120 bpm. An atrial ectopic beat (PAC) occurs on the eighth beat of the strip, resulting in a brief run of atrial tachycardia. This terminates and is followed by a ventricular ectopic beat (PVC).

The next strip shows the presence of an atrial tachycardia, with a cycle length of around 400 ms (150 bpm) and a simultaneous ventricular tachycardia with a cycle length of around 310 ms (194 bpm).

At first glance, it is easy to mistake a 1:1 AV association between the atrial and ventricular EGMs. However, upon closer inspection, it is clear that there is no true AV association due to there being inconsistent A-V intervals. The atrial and ventricular rates are also independent of one another further suggesting the presence of two independent tachycardias.

The final strip shows an ongoing ventricular tachycardia however, the atrial tachycardia appears to have terminated. The small deflections seen on the atrial channel here are likely to be small far-field ventricular signals with a clear, genuine atrial signal occurring towards the end of the strip (AS). This provides further evidence for the presence of a dual tachycardia.


The presence of multiple arrhythmias occurring within the same patient has been demonstrated frequently using electrophysiological studies; with multiple tachycardias demonstrating changing characteristics and emerging within a relatively short time frame in the setting of myocarditis being a specific example. However, the presence of dual atrial and ventricular tachycardias is less commonly documented with many being attributed to Digitalis toxicity.2 However, this is not the only aetiology related to this condition and it is important to identify the arrhythmia substrate to guide the development of a treatment plan.

Studies have aimed to assess the incidence of dual tachycardia in patients receiving dual-chamber ICDs. One particular study found that dual tachycardia is more common than once believed in dual- chamber ICD recipients (8.9% of study participants) who have a history of atrial fibrillation. It was concluded that around 50% of the time, the preceding atrial tachycardia is ≤1 hour in duration and that termination of atrial fibrillation can delay the time to subsequent ventricular tachycardia detection.3

The presence of both atrial and ventricular arrhythmias in patients with cardiomyopathy is well documented and is an important factor when considering the implantation of an ICD for this subset of patients.4 In this case, it was felt likely that the severe left ventricular systolic impairment was a precipitating cause for the sustained episode of ventricular tachycardia, which had never been documented to this degree during the device follow-up of this patient. This patient was discharged with optimised pharmacological therapy for both heart failure and rate control, as well as a cardiology referral for further consideration of upgrading the patient to a dual-chamber ICD system.


1. Li A and Epstein L. Double Trouble: Dual Tachycardia in Patient Presenting with Slow Ventricular Tachycardia, Journal of the American College of Cardiology 2020;75(11).

2. Asirvatham S and Stevenson W. Multiple and Concurrent Arrhythmia, Circulation: Arrhythmia and Electrophysiology 2016;9(7).

3. Stein K, Euler D, Mehra R, et al. Do atrial tachyarrhythmias beget ventricular tachyarrhythmias in defibrillator recipients?”, JACC 2020;40(2).

4. Kassotis J, Haq S and Mongwa M, Multiple Cardiac Arrhythmias Detected by a Dual Chamber Implantable Cardioverter Defibrillator in a Patient with Hypertrophic Obstructive Cardiomyopathy, Hallenic Journal of Cardiology 2004;45:57-60.

Reproduced with thanks from Mr Josh Mundy and the British Heart Rhythm Society

This content is owned by the British Heart Rhythm Society. Permission to reproduce this content must be requested from the rights-holder directly.

Ablation of RV Outflow Tract Ectopic Originating Close to the His Bundle

Dr Chu-Pak Lau, Dr Kathy Lai-Fun Lee & Hung-Fat Tse
The University of Hong Kong and Queen Mary Hospital, Pok Fu Lam, Hong Kong


Catheter ablation of the right ventricular outflow tract (RVOT) premature ventricular depolarizations (VEs) is highly efficacious. However, VEs originating close to the His bundle is an uncommon form of RVOT-VEs, occurring in about 5% of all RVOT-VEs undergoing catheter ablation. Ablation carries a potential risk of damaging the conduction system. We describe a case of RVOT-VE, mapped by high-density electroanatomical mapping and electrocardiographic criteria, with the successful ablation site close to the His bundle. The methods to avoid heart block are discussed.


Ablation of premature ventricular depolarizations (VEs) from the right ventricular outflow tract (RVOT) is associated with a high success and a low complication rate. These VEs share a common feature of inferiorly directed frontal plane QRS axis.1,2 However, due to the proximity of the structures close to the RVOT, such as the left ventricular (LV) outflow and the conduction system, radiofrequency catheter ablation (RFA) may be more difficult and can damage collateral structures. While the origin of the VE site is defined as the site of successful ablation, this reflects the anatomical feasibility, and VEs can also have several exit sites.

Case report

A 62-year-old female complained of palpitations, with symptoms due to frequent VEs (10.9%/day). Her VE exhibited a positive frontal axis in II, III and aVF, with precordial voltage transition at V3, giving a left bundle branch block (LBBB) appearance (Figure 1). An MRI of the heart showed no ischaemia, normal LV function but a borderline RV function of 48.7% (N 51 – 71%).

Figure 1: Right ventricular outflow tract (RVOT) ventricular ectopic (VE) originating just below pulmonary artery (PA). VE showed a +/- aVL suggesting of sub-pulmonary RVOT site. Baseline ECG showed RBBB. ART = Atrial pressure; MAP = CARTO mapping catheter.

Baseline ECG showed RBBB. ART = Atrial pressure; MAP = CARTO mapping catheter.

A CARTO activation map was performed initially in the RV and pulmonary artery (PA), with automatic mapping algorithm of the VEs (Figure 1). There were no early supravalvular PA activation sites. An early RV site -30 ms before QRS was mapped in the RV inflow (Figure 1 and Figure 2). This was designated as VE1. Ablation at this site abolished VE1.

Figure 2: CARTO Mapping of VE1 and VE2 successful ablation sites.

VE1 was below the pulmonary artery (PA), and relatively remote from the His recording. VE2 is 1.2cm from the langs + His recording.

However, another VE with a different morphology emerged after ablation of VE1 that showed a change in the frontal axis with III becoming negative, and the precordial transition now occurred earlier at V2. In addition, it was noticed that aVL had changed from a +/- in VE1 to a fully positive voltage in VE2. A left ventricular outflow tract (LVOT) mapping including the aortic cusps showed no early activation. An early activation site of VE2 was mapped close to the His bundle area (Figure 2 and Figure 3). Pace mapping at this site resulted in a 12/12 matched pace map (Figure 4). The site was about 12 mm from the largest His bundle recording site.

Figure 3: Change in ECG morphology after successful ablation of VE1.

VE2 now showed +ve aVL and decrease positive voltage in lead III suggestive of an inferior and lateral site. At this site, close to the His, the ventricular activation was -50 ms ahead of the surface QRS. ART = Atrial pressure; MAP = CARTO mapping catheter.

Figure 4: Perfect 12/12 pace mapping at site of earliest VE2.

Total RF application 39s, power 20W. ART = Atrial pressure; MAP = CARTO mapping catheter.

Using an SR0 sheath for stability, cautious applications of radiofrequency (RF) starting from 10w were performed, observing junctional rhythm and VE frequency. At the successful site, a short run of junctional rhythm occurred after a total RF application of 39 seconds. This abolished VE2 (Figure 5). Post ablation showed normal PR interval, and 1:1 antegrade conduction identical to that before the ablation. She remained asymptomatic without her clinical VEs on Holter and a normalised RV function on MRI.

Figure 5: Radiofrequency ablation (RF) for VE2 showing a run of slow junctional rhythm before RF termination (arrowed). Total RF application 39s, power 20W. ART = Atrial pressure; MAP = CARTO mapping catheter.


We reported a patient with VEs initially thought to be in the RVOT region. The classical RVOT-VEs originate in anterior and cranial sites due to the anterior and leftward direction of the RVOT and PA. This would give a negative aVL and precordial transition later than V3. The CARTO map and successful ablation site identified VE1 as beneath the PA in the RVOT area. On the other hand, VE2 had a strongly positive aVL axis. As aVL is a superior lead, a positive aVL is highly suggestive of a low-lying focus, especially at the His region.1 The earlier transition at V2 suggests a more posterior site, as the true RV septum is posterior. ECG orientation in the frontal and transverse axis to localise the site of RVOT-VE origin have been described.1,2 An algorithm that may add to such localization has also been reported from our group.3 We have used these criteria, especially the changes in axis, to facilitate RF catheter positioning.

Ventricular arrhythmias occurring in the para-Hisian region has long been recognized.4 An incidence of 5% was reported amongst VEs showing an RVOT morphology and RF was successfully used in these cases without inducing heart block.5,6 We have used electroanatomic mapping to locate the site of largest His electrogram, and titration of RF energy starting with low power. With a sheath stabilized catheter and avoiding the largest His recording, we were able to ablate VE2 successfully without damaging the conduction system.

Induction of heart block is a significant risk. Cryoablation with cryo-mapping has been suggested as an alternative treatment.7 In a registry group of 33 patients with RV VEs, of whom seven were para-Hisian in origin, overall cryoablation success was 55%. However, all para-Hisian cases were successfully ablated. The authors suggested that this energy source may be an alternative to avoid collateral damage to relevant cardiac structures (e.g. conduction system, coronary arteries and phrenic nerves). However, cryo energy has not been extensively utilized. A novel pacing strategy has recently been published to avoid RF damage to the His bundle.8 The authors utilized a strategy with His bundle pacing, similar to that used to exclude the septal accessory pathway. At potential sites, before RF ablation, pacing was performed at different thresholds. The site with the lowest pacing energy for His capture and the largest His recording was considered closest to the His bundle. Ablation was carried out at the earliest VE activation site if His bundle could only be captured at a higher output energy, suggesting the RF site was remote from the His.


We reported a patient with 2 VEs, one below the PA and another para-Hisian. ECG changes that suggest a para-Hisian origin is presented. Using sheath for stabilization, electroanatomic mapping to avoid ablation sites with large His bundle and gradual RF power titration, we were able to achieve ablation success without damaging the atrioventricular node.


1. Asirvatham SJ. Correlative Anatomy for the Invasive Electrophysiologist: Outflow Tract and Supravalvar Arrhythmia. Cardiovasc Electrophysiol 2009;20:955-68. PMid:19490263

2. Hutchinson MD, Garcia FC. An Organized Approach to the Localization, Mapping, and Ablation of Outflow Tract Ventricular Arrhythmias. J Cardiovasc Electrophysiol 2013;24:1189-97. PMid:24015911

3. Zhang F, Chen M, Yang B, et al. Electrocardiographic Algorithm to Identify the Optimal Target Ablation Site for Idiopathic Right Ventricular Outflow Tract Ventricular Premature Contraction. Europace 2009;11:1214-20. PMid:19706640

4. Yamauchi Y, Aonuma K, Takahashi A, et al. Electrocardiographic Characteristics of Repetitive Monomorphic Right Ventricular Tachycardia Originating Near the His-bundle. J Cardiovasc Electrophysiol 2005;16:1041-8. PMid:16191113

5. Wu LP, Li YC, Zhao JL, et al. Catheter Ablation of Idiopathic Premature Ventricular Contractions and Ventricular Tachycardias Originating From Right Ventricular Septum. PLoS One 2013;8:e67038. PMid:23825610

6. Tanaka A, Takemoto M, Masumoto A, et al. Radiofrequency Catheter Ablation of Premature Ventricular Contractions From Near the His-bundle. J Arrhythm 2019;35:252-261. PMid:31007790

7. Di Biase L, Al-Ahamad A, Santangeli P, et al. Safety and Outcomes of Cryoablation for Ventricular Tachyarrhythmias: Results From a Multicenter Experience. Heart Rhythm 2011;8:968-74. PMid:21376835

8. Luo S, Zhan X, Ouyang F, et al. Catheter Ablation of Right-Sided para-Hisian Ventricular Arrhythmias Using a Simple Pacing Strategy. Heart Rhythm 2019;16:380-387. PMid:30248458

Unexplained Syncope & Response to Ajmaline in the Elderly

In this video presentation and discussion, Prof Angelo Auricchio (Cardiocentro Ticino, Switzerland) and Prof Pier Lambiase (Barts Heart Centre, London, UK) meet with Dr Giulio Conte to discuss his recently published case study on Arrhythmia Academy.

They examine and discuss the issues surrounding the unusual presentation in this real-life case as experienced by Dr Conte. They review the effects of ajamaline, the role of the ajamaline test and the mechanisms of ajamaline affecting the ECG pattern.

Unexplained Syncope & Response to Ajmaline in the Elderly

Dr Giulio Conte
Cardiocentro Ticino, Lugano, Switzerland

Case Presentation

A 77-year-old male patient was referred to our institution because of recurrent syncopal events without prodromal symptoms. He had no family history of sudden cardiac death (SCD) and no history of chest pain, dyspnea or fatigue. Cardiological work-up including two-dimensional echocardiography, exercise stress test, tilt-table testing, and coronary angiography did not reveal any significant abnormalities. A 7 day electrocardiogram (ECG) monitoring did not show evidence of cardiac arrhythmias. Neurological evaluation and carotid artery duplex scan were normal. Baseline ECG showed sinus rhythm with 1st degree atrioventricular (AV) block (PR interval 220 ms) and atypical complete right bundle-branch-block (RBBB) with QRS duration of 125 ms and fragmentation in leads aVR, aVL and V1-V4 (Figure 1a). Furthermore, J waves with an amplitude of 1.5 mV were present in leads III and aVF.

Figure 1: Ajmaline challenge and HV measurement during EP study (before and after ajmaline administration).Source: G Conte 2020. Reproduced with permission from the author.  

Based on the clinical history and the presence of an inferior early repolarization pattern, an ajmaline challenge was deemed appropriate to rule out Brugada syndrome (BrS). Unexpectedly, inferior J waves amplitude increased during ajmaline infusion (1 mg/kg IV) and a coved-type Brugada type 1 ECG was unmasked in the inferior leads exclusively as indicated by the arrows in Figure 1a.


Which is the condition underlying these ECG findings and the mechanisms causing the syncopal events: BrS with uncommon phenotypic expression, concealed AV conduction disease or both? Would an electrophysiology study (EPS) be appropriate?


The diagnostic management of elderly patients with recurrent syncope and AV conduction disturbances can be challenging. The ajmaline challenge is an established tool to unmask BrS in patients with recurrent syncope, a structurally normal heart and non-diagnostic baseline ECG. In most cases of BrS, Brugada type 1 ECG is induced in the right precordial leads and very rarely, (up to 5 % of cases), in inferior and/or lateral leads only1, 2. These cases should be considered as having BrS.

Furthermore, European guidelines for the diagnosis and management of syncope3 recommend an EPS in patients with BBB (class IIa, level of evidence B), since abnormal His-ventricular (HV) interval measurement as well as development of intra- or infra-Hisian block on incremental atrial pacing are highly predictive of impending AV block4, 5. Additionally, in elderly patients with recurrent syncope and AV conduction abnormalities on baseline ECG, an ajmaline challenge during an EPS is valuable to rule-out BrS and assess intra- and infra-Hisian conduction6. Prolongation of the HV interval ≥ 100 ms during ajmaline infusion has been considered diagnostic for AV conduction disease7, 8. In these cases, pacemaker implantation is indicated.

In our case, baseline HV interval was normal (38 ms) and no intra or infra-Hisian block occurred during incremental atrial pacing. Corrected sinus node recovery time (400 ms) was also normal, excluding sinus node disease. In order to evaluate the arrhythmic origin of the syncopal episodes, programmed ventricular stimulation (PVS) was performed and no sustained ventricular arrhythmias (VA) were induced.

At the end of EPS, the ajmaline challenge was repeated and HV interval prolonged from 38 to 73 ms during drug administration as indicated by the arrows shown in Figure 1b.

Performing an EPS combined with an ajmaline challenge allowed us to exclude AV conduction disease and hence the necessity of pacemaker implantation. Furthermore, in accordance with the current guidelines,1 the patient did not qualify for ICD implantation, since the diagnosis of Brugada type 1 ECG appeared only after infusion of a class I antiarrhythmic drug and no VAs were induced during PVS. However, as reported by a recent pooled analysis on PVS in BrS, the annual incidence of spontaneous VAs in drug-induced BrS patients with syncope and no VA inducibility during PVS is not negligible (1.3% per year).9 Therefore, indication to ICD implantation was discussed and refused by the patient.

In patients with recurrent syncope, RBBB and signs of AV conduction disturbances, performing an ajmaline challenge during EPS is crucial to confirm BrS diagnosis and exclude AV conduction disease. However, the device-based management of these patients remains controversial.


1. Antzelevitch C, Yan GX, Ackerman MJ, et al. J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge. Heart Rhythm 2016;10:e295-324.

2. Sarkozy A, Chierchia GB, Paparella G, et al. Inferior and lateral electrocardiographic repolarization abnormalities in Brugada syndrome. Circ Arrhythm Electrophysiol 2009 Apr;2(2):154-61.

3. Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope. Eur Heart J 2009;30(21):2631-71.

4. Scheinman MM, Peters RW, Suavé MJ, et al. Value of the H-Q interval in patients with bundle branch block and the role of prophylactic permanent pacing. Am J Cardiol 1982;50:1316–1322.

5. Dhingra RC, Wyndham C, Bauernfeind R, et al. Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block. Circulation 1979;60:1455–1464.

6. Conte G, Levinstein M, Sarkozy A, et al. The clinical impact of ajmaline challenge in elderly patients with suspected atrioventricular conduction disease. Int J Cardiol 2014;172(2):423–7.

7. Click RL, Gersh BJ, Sugrue DD, et al. Role of invasive electrophysiologic testing in patients with symptomatic bundle branch block. Am J Cardiol 1987;59:817–23.

8. Pentimalli F, Bacino L, Ghione M, et al. Ajmaline Challenge To Unmask Infrahisian Disease In Patients With Recurrent And Unexplained Syncope, Preserved Ejection Fraction, With Or Without Conduction Abnormalities On Surface ECG. J Atr Fibrialltion 2016;9(2):1421.

9. Sroubek J, Probst V, Mazzanti A, et al. Programmed Ventricular Stimulation for Risk Stratification in the Brugada Syndrome: A Pooled Analysis. Circulation 2016;133(7):622‐630. doi:10.1161/CIRCULATIONAHA.115.017885.

Bradycardia on Telemetry Following a Pacemaker Implant

Mr Jason Collinson, Chief Cardiac Physiologist
Essex Cardiothoracic Centre, Basildon and Thurrock University Hospital, UK
Twitter: @cardiacjase


A 60-year-old male was implanted with a Sorin/MicroPort™ dual chamber pacemaker, following an emergent admission for syncope associated with intermittent atrioventricular block (AVB).

Three hours post implant, telemetry captured an episode of bradycardia as displayed in Figure 1.

An urgent pacemaker check was requested, with concern that there was device malfunction. The device settings programmed at implant are displayed below:

Mode: AAI-DDD (SafeR)
Lower rate: 60 BPM
Upper rate: 130 BPM
Paced AV delay: 220 ms
Sensed AV delay: 155 ms

Figure 1: Telemetry recording showing an episode of bradycardia a few hours after de-novo pacemaker implant. ECG leads displayed are lead I (top) and V1 (bottom).


Which answer bests explains the telemetry recording?

a. Loss of atrial capture.

b. Ventricular oversensing.

c. Normal pacemaker behaviour.

d. Loss of ventricular capture.


c. Normal pacemaker behaviour.


The telemetry recording displays normal pacemaker behaviour for the programmed settings and shows a mode switch episode, from atrial demand pacing (AAI) to dual chamber pacing (DDD), caused by an episode of AVB.

Figure 2: Telemetry recording showing the mode switch from AAI to DDD pacing with markers annotating events.

In the trace (Figure 2), we can see the first four atrial paced (AP) beats conduct to the ventricle, giving rise to an intrinsic QRS complex with right bundle branch block (rSR pattern in lead V1). There is subtle prolongation of the AV interval with each consecutive AP event: the 5th AP beat captures the atrium but fails to conduct to the ventricle, the 6th AP beat conducts to the ventricle, the 7th and 8th AP beat both fail to conduct to the ventricle, and this triggers a mode switch from AAI to DDD pacing. The rest of the ECG shows atrial paced (AP) and ventricular paced (VP) beats. Note, there is a clear change in QRS morphology with ventricular pacing.

The trace is an ECG example of Sorin/MicroPort’s™ SafeR algorithm in operation. SafeR is one of several manufacturer specific algorithms, designed to reduce unnecessary ventricular pacing, which can help reduce the detrimental effects of RV pacing in patients with sick sinus syndrome and intermittent AVB.

The algorithm works by providing AAI pacing, (this is actually ADI pacing with the ability to sense events in the atrium and ventricle), whilst monitoring AV conduction. If loss of AV conduction is detected by any of the four specific criteria below, the pacing mode switches from ADI pacing to DDD pacing, thus restoring AV synchrony.

The 4 criteria used to detect loss of AV conduction are:

• AVB I criteria – six consecutive long PR intervals;

• AVB II criteria – three non-conducted atrial events out of 12 consecutive cycles;

• AVB III criteria – two consecutive blocked atrial events;

• Pause criteria – V-V interval greater than the programmed pause duration (programmable at 2 or 3 seconds).

In this example, there were two consecutive blocked atrial events. Therefore, mode switch was triggered after AVB III criteria was met.

A device check confirmed normal pacemaker function, consistent with the programmed settings. Stored SafeR event electrograms, confirmed appropriate mode switch to DDD pacing, with AVB III criteria met. The patient was asymptomatic to the episode; however, the SafeR settings were reviewed. A minor change was made to the pause criteria, brought in to 2 seconds from the nominal 3 seconds. This adjustment allowed the device to react quicker to episodes of AVB, triggering mode switch to DDD pacing earlier and thus reducing the potential risk of bradycardia induced symptoms.


Microport™ CRM, Tech Corner: SafeR Pacing Mode: 2018. (accessed 08 June 2020).

Reproduced with thanks from Mr Jason Collinson and the British Heart Rhythm Society