Bradycardias and AV blocks: ECG Case Conference

Table of Contents

Table of Contents

July 2022

Jack Stacy, MD1, Michael Rosenberge, MD2
Executive Editor: Brandon Fainstad, MD3

1. Resident, Internal Medicine Residency, University of Colorado, 2. Assistant Professor, Cardiac Electrophysiology, University of Colorado, 3. Assistant Professor, Medicine, University of Colorado


  1. Identify sinus bradycardia by calculating a bradycardic heart rate and confirming the atrial depolarization originates from the sinus node.
  2. Identify a junctional rhythm by the absence of a narrow complex and preceding P wave.
  3. Describe the electrophysiologic process that leads to atrial bigeminy. 
  4. Identify first-degree AV block and determine the significance based on the context of the atrial rate and other signs of conduction abnormalities. 
  5. Identify second degree AV block and differentiate between Mobitz Type 1 and type 2 based on evidence of PR prolongation or response to sympathetic stimuli.
  6. Determine the need, urgency, and best options for pacing high-grade second-degree AV blocks.
  7. Identify complete heart block and determine the urgency and best options for short and long-term pacing.  

Teaching Instructions

Preparation: Plan to spend 45-60 minutes familiarizing yourself with the background information below, key findings on the electrocardiographs and the progressions of animations on the PowerPoint. This conference is intended as an introduction to our six-part ECG conference series.  Each case builds on foundational concepts of the cardiac conduction pathway and appropriate management.

How to present: Present the PowerPoint either by expanding the window (bottom right icon on the viewer below) in a browser or downloading the PowerPoint file to use on a desktop app (downloading is recommended).  Have the image pulled up in presenter mode before learners look at the screen to avoid revealing the diagnosis. Each case progresses through three or more questions, beginning with an overall interpretation, identification of a generalizable rule, and a clinical integration question.  We recommend a pair-share structure with a junior and senior trainee.  For each successive question, the presenter can elect to have pairs discuss their thoughts and then ask for a volunteer to share or, to expedite the conference, simply ask for audience response.   Ask a leaner to provide an overall interpretation.  Advance using the keyboard arrows or mouse click to reveal subsequent questions and then answers with their accompanying graphics.  You can go back to prior graphics and questions by using the back arrow or scrolling back on the mouse wheel.

Case 1: Sinus Bradycardia

Official ECG interpretation: Sinus bradycardia at a rate of 35-40bpm with non-specific T-wave changes, likely “U” waves which are often rate-dependent and more prominent in bradycardia

DiagnosisSinus bradycardia in the setting of hypoglycemia.


Confirming a sinus rhythm:

      • Is every P followed by a QRS complex?
      • Does every QRS follow a P wave?
        • This confirms that the pacemaker is in the atria and the atria is communicating to the ventricle.  There is no AV block or ectopic ventricular rhythm.
      • Is the P wave originating from the sinus node?
        • A sinus P should be positive in I and II, negative in aVR
        • The sinus node is in the posterior, superior aspect of the RA, so depolarization should travel inferiorly, and laterally corresponding to an axis of 0 to +75 degrees.

Next step in management: If asymptomatic and normotensive, ok to observe, stop negative ionotropic agents, and treat the underlying condition.

Case 2: Juncional bradycardia

Official ECG interpretation: Junctional escape with sinus bigeminy at a combined rate of ~40-45 bpm

Diagnosis: Severe sinus bradycardia due to nodal blockade from propranolol resulting in junctional escape and sinus bigeminy.

Identifying and defining junctional rhythm:

    1. Junctional rhythm is defined by a regular, narrow complex not preceded by a P wave.  This indicates that the pacemaker is originating from the AV node or high up in the Purkinje fibers rather than from the atria. This is most commonly due to a diseased or suppressed SA node.
    2. Bigeminy occurs when there are two concurrent rhythms that organize into couplets. The most common scenario is a sinus rhythm followed shortly by a premature atrial (PAC) or ventricular (PVC) beat that is followed by a prolonged refractory period. This case differs in that the first beat is a non-sinus escape rhythm followed by a sinus or atrial rhythm.

Next step in management: Given hypotension -> symptomatic bradycardia ACLS algorithm

  1. Trascutaneous pacer pads in place firstBe prepared to pace in case pharmaceutical interventions make things worse.  Atropine or positive ionotropes can worsen second degree type 2 block.
  2. Atropine 0.5-1 mg every 5 minutes up to 3 mgAtropine is short acting. So, in a case like this where the underlying cause is unlikely to be quickly reversible, it may be wiser to start IV ionotropes like isoproterenol or epinephrine
  3. No response? -> transcutaneous pacing -> transvenous pacing
 Case 3: First-degree AVB

Official ECG interpretation: Borderline sinus tachycardia with first-degree AVB. Along with RBBB and left axis deviation (likely due to left anterior fascicular block), suggesting “bifascicular block.”

Diagnosis: First-degree AV block.


    1. Consistent PR intervals > 200 ms = first degree atrioventricular block. A first-degree atrioventricular block is a misnomer since all P’s are conducted to the ventricles. It would be more accurately described as AV delay.
    2. Development of first-degree AVB in high vagal tone states with bradycardic rhythms is common and normal. Prolonged PR intervals in tachycardia, as in this example, are more likely pathologic.
    3. While there are no indications for intervention in first-degree AVB it may represent a harbinger of developing conduction disease.
Case 4:  Mobitz 1

Official ECG interpretation: Sinus rhythm with second-degree type 1 AVB (Mobitz type 1)

Diagnosis: Mobitz type 1 (“Wenckebach”)


    1. Mobitz 1 is defined by progressive prolongation of the PR interval until, finally, a P wave fails to be conducted to the ventricles leading to a dropped QRS. As a result you will see “grouped beats.” In this instance you see a pattern of 4 P’s conducted to a QRS followed by one non-conducted P wave.
    2. Mobitz 1 involves AV nodal pathology with a healthy SA node, so the atrial rate will be regular and consistent.
    3. It can be difficult to see beat-to-beat prolongation of the PR interval. A trick is to compare the intervals preceding and succeeding the dropped QRS. The PR interval preceding the dropped QRS should be longer than that succeeding the dropped beat.
    4. Conduction disease in Mobitz 1 involves intra-AV nodal pathology, as such, it is less unlikely to progress to complete heart block, it is rarely symptomatic, and is not an indication for a permanent pacemaker.  An exception is “high-grade AVB” with more than one consecutive non-conducted P waves. 
Case 5: Mobitz 2

Official ECG interpretation: Sinus rhythm with second-degree type 2 AVB (Mobitz type 2) and right bundle branch block. 

Diagnosis: Mobitz tpe 2


    1. Mobitz 2 is defined by a constant A rate with a consistent PR interval and intermittent non-conducted P waves. 
    2. Mobitz 2 involves intranodal disease and often progresses to complete heart block. Furthermore, second-degree type 2 rarely has a dependable escape rhythm and as such may be more symptomatic or hemodynamically significant than CHB with a stable escape. Therefore, second-degree type 2 is an indication for permanent pacemaker placement
Case 6: Second-degree 2:1

Official ECG interpretation: Sinus rhythm with 2:1 second degree AV block.

Clinical Diagnosis: Symptomatic second-degree heart block, unknown Mobitz type. 

Teaching: With 2:1 AVB, it is not possible to evaluate for progressive PR prolongation to differentiate between Mobitz 1 and Mobitz 2?

    • Mobitz 1 = Nodal pathology
      • AV node is innervated by ANS and regulated by sympathetic/parasympathetic input.
        • Mobitz 1 improves with increased sympathetic (e.g., exercise and ionotropes) or decreased vagal tone (e.g., atropine) 
        • Mobitz 1 worsens with increasing vagal tone (e.g., beta-blockers or vagal maneuvers) 
    • Mobitz 2 = Infranodal pathology
      • His-Purkinje system is less dependent on ANS, so increasing vagal tone has no effect on block
        • Increasing atrial rate with exercise or atropine may increase the frequency of blocks. 
Case 7: Complete Heart Block

Official ECG interpretation: Sinus atrial rhythm at a rate of 125 bpm without A to V conduction.   Ventricular escape rhythm at 40 bpm.  Complete heart block.

Clinical Diagnosis: Complete heart block.


    1. Complete heart block will have a regular and consistent atrial rate that is not equal to a regular and consistent ventricular escape rhythm and no evidence of atrial to ventricular conduction.
    2. You can identify the origin of the escape rhythm based on the morphology of the QRS complexes.  A narrow QRS complex indicates a more superior origin of the escape rhythm, either junctional or high within the His-Purkinje system. A wide QRS indicates a ventricular origin of the escape rhythm.
    3. More superior escape rhythms tend to be quicker while inferior escape rhythms tend to be slower. Therefore, more superior escape rhythms also tend to be more stable.

Next step in management:

  • Regardless of stability, CHB is an indication for PPM placement (if reversible causes have been identified and treated). Stability should guide the urgency of your management
  • If unstable,  transcutanesous pace until a transveous wire can be placed for transvenous pacing. 
  • If stable, a permanant PM is still indicated, but is not emergent
    • Syncope or inconsistent escape rhythms should prompt more urgent PPM placement and higher level of care in the meantime.

Presentation Board

Take Home Point

  1. Bradycardia is defined by a ventricular rate <60 bpm.
  2. A P wave that is up in I and II suggests it originates from the SA node.
  3. A junctional escape rhythm will have a narrow complex (assuming no aberrancy) without a preceding P  wave.  
  4. First-degree AV block (PR >200ms) is a misnomer as there is no dropped QRS and is rarely of clinical significance.  
  5. Second-degree AV blocks are defined by an intermittently dropped QRS complex and Mobitz 1 is differentiated from Mobitz 2 by a progressive PR prolongation.
  6. In the case of 2:1 block, Mobitz 2 is suggested over Mobitz 1 by the presence of infranodal disease (e.g., bundle branch blocks) and a lack of response to increased sympathetic tone.  
  7. Mobitz 2 and complete heart block without reversible causes are always indications for permanent pacemaker (PPM) placement and should have pacer pads in place as a precaution and transcutaneous pacing initiated if the patient is unstable. 


  1. Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R. 2018 ACC/AHA/HRS guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology. 2019 Aug 20;74(7):e51-156.
  2. Oken K, Schoenfeld MH, Kusumoto F. Evaluation and Treatment of Patients With Bradycardia and Cardiac Conduction Delay. JAMA cardiology. 2019 Jul 1;4(7):708-9.
  3. Grigg WS, Nagalli S. Ashman Phenomenon.
Brandon Fainstad


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