Author: Nivedita Poola

Peer Editors: Alec Feuerbach and Nicole Anthony

Faculty Editor: Mark Silverberg

 

 

Case  

A 72-year-old female with a past medical history of hypertension, hyperlipidemia, asthma, CVA with residual right sided weakness and aphasia was admitted to the hospital from subacute rehabilitation after a recent subacute infarct. During the inpatient admission, the patient developed new-onset atrial fibrillation (Afib) with rapid ventricular response (RVR) (ECG below). Initially, rate control was attempted with metoprolol via nasogastric tube. However, over the course of one week, her Afib with RVR recurred and persisted with rates 130s-160s, not responding to nasogastric or IV medication.

 

 

The patient was transferred to the CCU and started on an esmolol drip and metoprolol. The Afib with RVR remained uncontrolled despite high doses of esmolol and metoprolol. Cardioversion was contraindicated as TEE demonstrated evidence of thrombosis in the left atrial appendage. 

Ultimately, the patient underwent AV node ablation and dual chamber permanent pacemaker placement. By ablating the AV node and blocking impulse conduction through it, the misfiring atrium is ignored. Doing so, however, necessitates a pacemaker to generate a heart rate to provide appropriate cardiac output. According to American College of Cardiology/American Heart Association/Heart Rhythm Society guidelines, this is a reasonable approach when pharmacological therapy is inadequate and rhythm control cannot be achieved.[1] The European Society of Cardiology guidelines are similar but suggest first considering direct catheter-based or surgical ablation to eliminate the abnormally firing impulses in the atrium.[2] One meta-analysis comparing AV-nodal ablation with pacemaker to pharmacologic therapy alone for refractory afib found that AV-nodal ablation/pacemaker led to a significant improvement in quality of life and symptoms with minimal morbidity. For patients with refractory Afib and reduced systolic function, the nodal ablation and pacemaker approach showed small but statistically significant improvement in echocardiographic parameters as well.[3]

Following placement of the pacemaker, the following ECG was obtained.

 

 

How do we interpret this ECG? What are the significant findings that can discern information about the type of pacemaker placed?

 

Interpreting Paced ECGs  

 

Before discussing the ECG above, it is important to understand the basics of interpreting the ECG of a patient with a pacemaker. 

I) Type of Pacemaker  

The North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group (NASPE/BPEG) Pacemaker code is a five-letter series that describes the settings of a patient’s pacemaker. For patients in the ED, it is important to focus on the first three letters: 

Letter 1 – Chamber paced: chamber where pacemakers leads are located

Letter 2 – Chamber sensed: chamber where intrinsic depolarization is detected

Letter 3 – Sensing response: sensing response can be triggered, in which a depolarization results in a pacemaker discharging; inhibited, in which depolarization inhibits pacemaker discharging; dual, in which both inhibition or triggering can occur; and none, in which neither triggering nor inhibition occurs 

 

NASPE/BPEG Pacemaker Code [5]

 

For example, a common setting, DDD, signifies that both intrinsic atrial and ventricular activity are sensed and both atrial and ventricle are paced accordingly. If there is any intrinsic depolarization in either chamber, pacing will be inhibited in that chamber.[4,5,6,7]

 

II) Interpreting normal, paced ECGs 

 

Paced ECGs should be assessed systematically, similar to other ECGs, paying special attention to the location of the pacer spikes in relation to the P waves and the morphology of the QRS complex.

In an atrial paced ECG, pacer spikes will appear before a normal morphology P wave (see below).

 

figure from [7]

If the pacer spike is seen after an intrinstic P wave and before a wide QRS complex with left bundle branch pattern, the pacer is likely to be a single right ventricular pacing device (see below).  If the pacer spike appears after the P wave but before a narrow QRS then biventricular pacing is likely. One can also see two pacer spikes before a narrow QRS in a biventricular pacemaker.  

 

figure from [7]

In the case of active dual chamber pacing, one would see pacer spikes before both the P wave and the QRS complex.[4,5,6,7]

 

III) Paced Rhythm Pathology:

 

Failure to capture: Pacer spikes without following P waves or QRS complexes is termed failure to capture. This means that the pacer stimulation does not result in the expected myocardial depolarization. Causes can include lead displacement, lead fracture, exit block, myocardial infarction, and electrolyte abnormalities.[5,6,7,8]

figure from [5]

Failure to sense: Failure to sense occurs when a pacemaker is not detecting or understanding intrinsic cardiac activity, resulting in asynchronous pacing (i.e pacer spikes within the cardiac cycle as shown below). Causes can include a new bundle branch block, electrolyte abnormalities (most commonly hyperkalemia), class IC antiarrhythmics, and lead insulation break.[5,6,7,8]  

figure from [5]

Failure to pace: Failure to pace occurs when the stimulus is not generated, resulting in decreased pacemaker function (i.e. decreased or absent pacer spikes). Causes include oversensing and lead displacement.[5,6,7,8]

figure from [5]

IV) Assessment for acute myocardial ischemia 

The chamber of pacing is critical to assessing ischemia in a patient with a pacemaker. Since atrial pacing alone does not affect the QRS complex or ST interval, it does not change how ischemia is determined on an ECG. 

Identifying acute myocardial ischemia in patients with ventricular pacing is more complicated because the QRS complexes appear similar to the LBBB pattern. In this case, one can compare the current ECG with previous paced ECGs if available to identify any acute changes or one can utilize the modified Sgarbossa’s criteria. Previous studies have shown that the modified Sgarbossa’s criteria are more sensitive than the original criteria for ventricular paced rhythms.[10,11] Finally, the pacemaker can be temporarily inactivated to examine intrinsic cardiac rhythms.[8,9,10,11] 

 

Interpreting Our Patient’s ECG

This ECG shows a rate of about 90 per minute. P waves are seen clearly in lead V1 at times preceding the QRS and at times in various portions of the QRS complex (see below). The axis is normal. 

Pacer spikes are seen before every QRS which has Left Bundle Branch morphology suggesting that this is a single right ventricular pacing device. There is no concordant ST-elevation or depression nor excessively discordant ST-elevation to suggest myocardial infarction. 

 

Take away points

1) Understanding pacer settings can help to interpret paced ECGs and recognize abnormalities

2) The approach to paced ECGs is similar to other ECGs, but keep in mind the common malfunctions

3) In patients with paced rhythms, utilize modified Sgarbossa’s criteria to help rule in acute myocardial ischemia

 

References

1) January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2014;64:e1–e76.

2) Camm AJ, Kirchhof P, Lip GY, et al. Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC) Eur Heart J. 2010;31:2369–2429.

3) Chatterjee NA, Upadhyay GA, Ellenbogen KA, McAlister FA, Choudhry NK, Singh JP. Atrioventricular nodal ablation in atrial fibrillation: a meta-analysis and systematic review. Circ Arrhythm Electrophysiol. 2012;5(1):68-76. doi:10.1161/CIRCEP.111.967810

4) Burns, E. Buttner, R. “Pacemaker Rhythms-Normal Patterns.” LITFL. June 2021. 

5) Jerrard, G. Berberlan, J. Zeserson, E. “Pacemaker Basics for the Emergency Physician.” EMResident. February 2019. 

6) Swaminathan, A. “Pacemaker Basics.” RebelEM. Aug 2017 

7) “Pacemaker & CRT: ECG, Function, Troubleshooting, and Management.” ECG & Echo Learning.

8) Burns, E. Buttner, R. “Pacemaker Malfunction.” LITFL. June 2021. 

9) Costello, L. “Pacemaker Essentials: How to Interpret a Pacemaker ECG.” Canadiem. May 2016. 

10) Dodd KW, Zvosec DL, Hart MA, et al. Electrocardiographic Diagnosis of Acute Coronary Occlusion Myocardial Infarction in Ventricular Paced Rhythm Using the Modified Sgarbossa Criteria. Ann Emerg Med. 2021;78(4):517-529. 

11) DeSouza, I. Mattu, A. Marill, K. “Improving the ECG Diagnosis of the Elusive, Acute Coronary Occlusion in Patients with Ventricular Paced Rhythm.” Annals of Emergency Medicine. October 2021. 

 

The following two tabs change content below.

feuerbacham


0 Comments

Leave a Reply

Avatar placeholder

Your email address will not be published. Required fields are marked *