Clinical vignette
A 73-year-old man with a history of hypertension, type II diabetes, and stage III chronic kidney disease who was evaluated in the emergency department due to generalized weakness, dizziness, and syncope at rest. Upon admission, vital signs were recorded, blood pressure of 100/60 mmHg, heart rate 40 bpm, respiratory rate 14 breaths per minute, and pulse oximetry 100% at ambient air. No relevant findings were noted on physical examination. Laboratory tests showed sodium 131 mEq/L, chloride 109 mEq/L, potassium 7.5 mEq/L, bicarbonate 16 mEq/L, BUN 82 mg/dL, and creatinine 2.9 mg/dL. A 12-lead electrocardiogram (ECG) was requested (Figure 1).
Figure 1.
12-Lead Electrocardiogram (ECG).
Questions
Question 1. What is the most likely diagnosis according to the clinical findings and electrocardiographic abnormalities?
Sinoventricular rhythm
Nodal rhythm with atrial premature beats
Complete atrioventricular block
Ventricular escape capture bigemini
Question 2. What is the best physiopathological mechanism that explains this heart rhythm?
Ventricular escape without retroconduction or penetration in the sinus node, followed by an atrial depolarization leading to ventricular capture beats
Automatic activity of the junction with suppression of the sinoatrial node's automaticity
Sinoatrial exit block with nodal escape beats
Ventricular escape beats with wide QRS complexes with a prolonged HV interval
Question 3. What would be the first line of treatment?
Urgently place a temporary transvenous pacemaker
Electrophysiology study
Treat hyperkalemia
Place a permanent bicameral pacemaker
Comments on questions and answers
The 12-lead ECG showed an escape capture bigemini rhythm, with a constant ventricular escape interval of 1400 ms, an RR (RP + PR) interval of 680 ms, and a PP interval of 1880 ms (Supplementary Figure 1). The ventricular escape beats showed a left branch block morphology and the ventricular capture beats were conducted with an ectopic P wave and a narrow QRS complex. (Question 1, Answer 4).
Escape capture bigemini is uncommon and is characterized by a ventricular escape beat followed by a beat conducted by the sinus node or below the sinoatrial tissue with subsequent ventricular capture.1 The ventricular escape beat may originate in the atrioventricular junction or in the ventricle due to intermittent sinus impulse blockage at the sinus node or atrioventricular node, allowing an escape focus below the sinoatrial node to emerge and cause escape capture bigemini.2 The escape beat does not reset the sinus node due to retrograde conduction block or sinus node entry block.1,3 For the capture–escape rhythm to occur, the effective cycle of the primary pacemaker must exceed the escape interval plus the refractory period following the escape complex.1 (Question 2, Answer 1). Furthermore, it cannot be ruled out that it is an escape beat from the junction or ventricular escape with retrograde conduction to the atria and dual AV node properties (atypical Echo beats).
Some drugs such as digoxin, beta-blockers, and calcium channel blockers have been associated with this electrocardiographic abnormality, but they have rarely been associated with hyperkalemia.1,4 After normalization of serum potassium levels, complete resolution of electrocardiographic abnormalities was demonstrated (Supplementary Figure 2). (Question 3, Answer 3).
Escape capture bigemini is an unusual presentation of severe hyperkalemia that may represent a sign of sinoatrial exit block. It can be an early sign of sinus node dysfunction manifested as a sinoatrial exit block. The search for a reversible cause in this type of electrocardiographic abnormalities is essential to avoid delays in correcting the cause and prevent serious complications.
Supplementary Material
Acknowledgments
Special thanks to our cardiology professors at the National Medical Center “November 20”, Institute of Social Security and Services for State Workers, Mexico City, Dr. Julieta D. Morales Portano, Dr. Enrique Gómez Álvarez, Dr. Jorge A. Lara Vargas, and Dr. Juan Francisco Garcia Garcia.
Slide sets: A fully edited slide set detailing these cases and suitable for local presentation is available online as Supplementary data.
Consent: The authors confirm that written consent for submission and publication of this case report including images and associated text has been obtained from the patient’s next-of-kin in line with COPE guidance.
Funding: This ECG challenge case has no fund.
Contributor Information
Elias Noel Andrade-Cuellar, Clinical Cardiology, National Medical Center 20th of November ISSSTE, Ave. Felix Cuevas #540, Col. Del Valle Del. Benito Juarez, C.P. 03100, Mexico, Mexico City.
Aquino-Bruno Heberto, Interventional Cardiology, National Medical Center 20th of November ISSSTE, Av. Felix Cuevas #540, Col. Del Valle Del. Benito Juarez, C.P. 03100, Mexico, Mexico City.
Luis Angel Blancas-Pérez, Clinical Cardiology, National Medical Center 20th of November ISSSTE, Ave. Felix Cuevas #540, Col. Del Valle Del. Benito Juarez, C.P. 03100, Mexico, Mexico City.
Supplementary material
Supplementary material is available at European Heart Journal - Case Reports online.
Data availability
The data underlying this article will be shared on reasonable request to the corresponding author.
References
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The data underlying this article will be shared on reasonable request to the corresponding author.

