ECG Cases 20 – Approach to Bradycardia and the BRADI Mnemonic

In this ECG Cases blog we look at 10 patients’ ECGs who presented with bradycardia, an approach to identify reversible causes with the BRADI mnemonic and use ECG interpretation to guide management.

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman, April 2021

10 patients presented with bradycardia. What’s the diagnosis and management?

Case 1: 85yo with a history of atrial fibrillation on bisoprolol, with weakness/fall. HR 35, BP 160/80

Case 2: 80yo with a history of hypertension on amlodipine, with acute chest pain and vomiting. HR 50, BP 140/70

Case 3: 80yo with a history CAD on metoprolol and diltiazem, with three days of weak/dizzy. HR 50, BP 110/50. Old then new ECG:

Case 4: 90yo with a history hypertension on atenolol, with confusion and weak/dizzy. HR 35, BP 80/50. Old then new ECG:

Case 5: 50yo with VF arrest and ROSC, HR 40, BP 60/40, started on epi infusion. Serial ECGs:

Case 6: 80yo with a history of hypertension on candesartan, with recurring syncope at rest. HR 50, BP 130/70

Case 7: 80yo with a history hypertension on ramipril, with one week fatigue/SOB. HR 70, BP 170/70

Case 8: 60yo with chest pain and lightheadedness. HR 35, BP 140/60

Case 9: 70yo with VF arrest and ROSC, HR 50 BP 90/50

Case 10: 80yo with diarrhea and weakness, HR 30 BP 80/60

Bradycardia and the BRADI mnemonic

Bradycardia/blocks range from normal variants to life threatening emergencies. As the EM Cases main episode podcast explains, the approach includes assessing stability, symptoms, ECG localization, and reversible causes.

According to a retrospective study of nearly 300 patients who presented to the ED with symptomatic bradycardia (with median ventricular rate of 33), the most common chief complaints were: syncope, dizziness, collapse, angina, and dyspnea/heart failure. The basic maneuver of laying the patient flat eliminated symptoms in 40% of bradycardic patients, while the remaining 60% received ACLS intervention(s): atropine in 80%, epinephrine or dopamine in 50%, and transcutaneous pacing in 30%. Regardless of initial management, half of all patients ultimately required a permanent pacemaker, but the other half had a reversible cause. As the article emphasized: “identification of treatable, reversible causes of the bradycardia is the key for successful management.”[1]

The ECG can localize the mechanism of bradycardia/blocks, based on the anatomy of conduction. Normal conduction begins in the SA node and depolarizes the atria (P wave), pauses in the AV node (PR interval) and then travels rapidly through the His bundle and bundle branches to depolarize the ventricles (QRS). Abnormalities can happen at any of these three levels, as outlined by the ACC/AHA guidelines [2]:

1. Sinus node dysfunction
   1. sinus bradycardia (upright P in I/II): can be normal, vagal response, or pathological
   2. escape rhythm: atrial (narrow complex with different P), junctional (narrow complex with absent or retrograde P), ventricular (wide complex)
   3. atrial fibrillation/flutter
2. AV block
   1. nodal: can be normal, usually self-limiting or responds to atropine
      1. First-degree: constant PR>200 without dropped beats
      2. Second-degree type 1 (Wenkebach): PR lengthening before dropped beat
   2. infranodal: requires pacemaker (unless from reversible cause)
      1. Second-dgree type 2: constant PR before dropped beat
      2. Third-degree: variable PR with complete heart block
3. Ventricular conduction disease
   1. wide complex supraventricular
      1. hyperkalemia
      2. fascicular block: RBBB, LAFB, LPFB
   2. wide complex ventricular: idioventricular

The physiology of conduction depends on coronary perfusion and metabolic conditions, and is influenced by the autonomic nervous system and medications. This outlines the list of acute reversible causes of bradycardias/blocks, which can be remembered by the mnemonic BRADI:

BRADI mnemonic for reversible causes of bradycardia

• BRASH/hyperkalemia

  • Isolated hyperkalemia
  • BRASH syndrome (Bradycardia, Renal failure, AV node blockade, Shock and Hyperkalemia)

• Reduced vital signs

  • Hypoxia
  • Hypoglycemia
  • Hypothermia +/- hypothyroid

• Acute coronary occlusion

  • Inferior MI: nodal ischemia and vagal response, self-limiting or responds to atropine
  • Anterior MI: infranodal ischemia, often requires pacing

• Drugs: withdraw if stable, reverse if unstable

  • Beta-blockers
  • Calcium channel blockers
  • Digoxin

• Intracranial pressure, Infection (Lyme, endocarditis): treat underlying

This emphasizes complete vital signs, identifying ECG evidence of hyperkalemia and ischemia, withdrawing or reversing medication toxicity/overdose, and considering other dangerous causes.

Hyperkalemia is the great imitator which can cause a wide variety of ECG manifestations, including bradycardias/blocks. A study of patients with symptomatic bradycardia found that predictors of hyperkalemia included diabetes, treatment with diltiazem, bradycardia, junctional rhythm or atrial fibrillation, and peaked T waves[3]. Another study of patients with hyperkalemia found that predictors of adverse events were bradycardia, junctional rhythm, and wide QRS[4]. This study found that all patients with adverse events had preceding signs on ECG, most patients had adverse events prior to lab confirmation of potassium, but none had adverse events after treatment with calcium. So the ECG can identify hyperkalemic patients at high-risk for adverse events, which can be prevented with empiric calcium. The BRASH syndrome (Bradycardia, Renal failure, AV blockade, Shock, and Hyperkalemia) identifies a synergy of causes that can produce unstable bradycardia, and which requires comprehensive treatment.[5]

Myocardial infarction can also produce a variety of arrhythmias, including different types of bradycardias/blocks. The SA node is perfused by the RCA or circumflex artery, and the AV node is mainly perfused by the RCA: so bradycardia caused by inferior MI is usually from nodal ischemia and vagal response, which is often self-limiting and responds to atropine. Whereas the right bundle and left anterior fascicle is perfused by the LAD: so new RBBB/LAFB from anterior MI is associated with left main or proximal LAD occlusion resulting in ischemia of the conducting system, which has a high mortality rate and often requires a pacemaker. [6]

Back to the bradycardia cases

Case 1: atrial flutter with slow ventricular response, secondary to medications

• Heart rate/rhythm: atrial flutter (best seen in V1) with slow ventricular response
• Electrical conduction: normal ventricular conduction
• Axis: normal axis
• R-wave: normal R wave progression
• Tension: no hypertrophy
• ST/T changes: no ST/T changes

Impression: atrial flutter with slow ventricular response due to beta-blocker, in a symptomatic but stable patient. Normal electrolytes, negative troponin, and acute on chronic renal failure. Admitted for fluids and observation, beta-blocker held and then reintroduced at lower dose. Repeat ECG had atrial fibrillation with normal rate:

Case 2: Sinus bradycardia and Wenkeback block, secondary to infero-posterior Occlusion MI

• H: sinus bradycardia with second-degree AV block type 1 (PR prolongation before dropped beat)
• E: normal ventricular conduction
• A: normal axis
• R: tall R wave in V2, loss of inferior R waves
• T: no hypertrophy
• S: inferior hyperacute T wave (broad and tall relative to QRS) with reciprocal STD/TWI in I/aVL, and anterior STD/TWI

Impression: infero-posterior STEMI(-)OMI(+) and secondary Weckeback block. Cath lab activated: 100% RCA occlusion. First trop I negative and peak 20,000. Transient narrow third degree AV block in cath lab which resolved. Discharge ECG had normal sinus rhythm with resolution of AV block, ongoing loss of inferior R waves and tall anterior R waves, and inferior reperfusion T wave inversion:

Case 3: junctional bradycardia, secondary to medications

• H: junctional bradycardia
• E: normal ventricular conduction
• A: normal axis
• R: normal R wave progression, low voltage (old)
• T: no hypertrophy
• S: no ST/T changes

Impression: junctional bradycardia from combined beta-blockers and calcium-channel blockers, in a symptomatic but stable patient. Normal electrolytes, negative troponin, acute renal failure. Treated with fluids and withholding medications, with normalization of bradycardia:

Case 4: third-degree AV block with junctional escape, secondary to BRASH syndrome

• H: third-degree AV block with junctional escape
• E: LAFB
• A: left axis
• R: normal R wave
• T: no hypertrophy
• S: peaked T waves (narrow and pointy)

Impression: heart block, junctional bradycardia with LAFB and peaked T waves, in hypotensive patient on beta-blockers. Empirically treated with fluids, atropine, epinephrine and calcium. Confirmed BRASH: bradycardia, renal failure, AV nodal blockers, shock and hyperkalemia (K 7.8). Treated with more fluids and insulin/dextrose, with resolution of BRASH. Repeat ECG had return of normal sinus rhythm and resolution of peaked T waves:

Case 5: progression from first to third-degree AV block, secondary to inferior Occlusion MI

• H: first ECG has first-degree AV block, second has third-degree with junctional escape
• E: normal ventricular conduction
• A: normal axis
• R: normal R wave
• T: no hypertrophy
• S: inferior ST elevation with reciprocal STD/TWI in aVL

Impression: progressive AV block from inferior Occlusion MI. Cath lab activated: 100% RCA occlusion. First Trop I = 7,000, peak 25,000. Discharge ECG had normal conduction and inferior Q waves:

Case 6: first-degree AV block and bifascicular block, from primary conduction disease

• H: sinus bradycardia with first-degree AV block
• E: RBBB + LAFB
• A: left axis from LAFB
• R: tall R wave from RBBB
• T: no hypertrophy
• S: no ST/T changes

Impression: first-degree AV block with bifascicular block in stable patient symptomatic with recurring syncope. Normal labs and admitted for pacemaker.

Case 7: infranodal second-degree AV block, from primary conduction disease

• H: sinus bradycardia, second-degree AV block (nonconducted P superimposed on T wave), with 2:1 conduction
• E: RBBB + LAFB
• A: left axis from LAFB
• R: tall R wave from RBBB
• T: no hypertrophy
• S: RBBB repolarization abnormalities, no primary ST/T changes

Impression: second-degree AV block with 2:1 conduction, likely infranodal because of bifascicular block, in symptomatic but stable patient. Normal labs. Admitted for observation, and progressed to third-degree AV block with junctional escape (requiring pacemaker):

Case 8: third-degree AV block with ventricular escape, from primary conduction disease

• H: third-degree AV block with ventricular escape
• E: LBBB morphology escape rhythm
• A: normal axis
• R: delayed R wave progression from LBBB
• T: no hypertrophy
• S: secondary repolarization abnormalities, no Sgarbossa/Smith criteria

Impression: third-degree heart block in symptomatic but stable patient. Had cath lab activated due to chest pain and new LBBB but normal coronaries. No clear cause for heart block, and treated with pacemaker.

Case 9: junctional bradycardia and bifasicular block, secondary to anterior Occlusion MI

• H: junctional bradycardia
• E: RBBB + LAFB
• A: left axis from LAFB
• R: tall R wave from RBBB
• T: no hypertrophy
• S: anterolateral STE with reciprocal inferior STD

Impression: junctional rhythm with bifascicular block and anterolateral STE, concerning for left main or proximal LAD occlusion. Cath lab activated: LAD occlusion, cardiac arrest.

Case 10: junctional bradycardia with wide QRS, secondary to hyperkalemia

• H: junctional bradycardia
• E: wide complex QRS
• A: normal axis
• R: delayed R wave progression
• T: no hypertrophy
• S: peaked T waves

Impression: junctional bradycardia with wide QRS and peaked T waves, in symptomatic unstable patient. Treated empirically with calcium and fluids, then potassium shifting when levels came back at 8. Repeat ECG had return of sinus rhythm with first-degree AV block and narrow QRS:

Take home points for approach to bradycardia and BRADI mnemonic

1. The approach to bradycardia includes assessing stability, symptoms, ECG localization, and reversible causes of BRADI: BRASH/hyperkalemia, Reduced vitals (oxygen, glucose, temp), Acute coronary occlusion, Drugs (eg beta-blockers, calcium blockers, dig), and ICP/Infections (eg Lyme, endocarditis)
2. The ECG can localize the mechanism of bradycardia/blocks and identify two important reversible causes prior to lab confirmation: hyperkalemia and acute coronary occlusion

Episode 154 Approach to Bradycardia and Bradydysrhythmias with Paul Dorian and Tarlan Hedayati

References for approach to bradycardia and BRADI mnemonic

1. Sodeck GH, Domanovits H, Meron G, et al. Compromising bradycardia: management in the emergency department. Resuscitation 2007;73:96-102
2. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 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/Ameriican Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation 2019;140:e382-e482
3. Chon S-B, Kwak YH, Hwang S-S, et al. Severe hyperkalemia can be detected immediately by quantitative electrocardiography and clinical history in patients with sympatomatic or extreme bradycardia: a retrospective cross-sectional study. J of Crit Care 28 (2013):1112.e7-1112.e13
4. Durfey N, Lehnhof B, Bergeson A, et al. Severe hyperkalemia: can the electrocardiogram risk stratify for short-term adverse events? West J Emerg Med 2017 Aug;18(5):963-971
5. Farkas JD, Long B, Koyfman A, et al. BRASH syndrome: Bradycardia, Renal failure, AV blockade, Shock, and Hyperkalemia. J of Emerg Med 2020 Aug 1;59(2): 216-223
6. Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2018;39:119-177