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Bradycardia

Season 3 Episode 7

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Welcome back to AudioBoards. Today we're tackling a topic that shows up everywhere—from the emergency department and ICU to telemetry floors, board exams, ACLS scenarios, and cardiology consults: bradycardia management.

Bradycardia is more than just a slow heart rate—it’s a clinical problem that requires careful assessment of symptoms, hemodynamic stability, and the underlying rhythm. In this AudioBoards episode, we review the 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Bradycardia and Cardiac Conduction Delay, focusing on a practical, board-relevant approach to diagnosis and treatment.

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Welcome back to AudioBoards. Today we're tackling a topic that shows up everywhere—from the emergency department and ICU to telemetry floors, board exams, ACLS scenarios, and cardiology consults: bradycardia management.

One of the biggest mistakes clinicians make is treating the number instead of the patient. A heart rate of 40 beats per minute can be completely normal in one patient and life-threatening in another.

The central principle of bradycardia management is simple:

Treat symptoms and hemodynamic consequences, not just the heart rate.

So not every patient with a heart rate under 60 needs intervention?

Exactly. Many healthy athletes, sleeping patients, and older adults can have resting bradycardia without requiring any treatment at all. The key question is whether bradycardia is causing symptoms or instability. 

Bradycardia is generally defined as a heart rate below 60 beats per minute.

However, the guideline emphasizes that there is no specific heart rate threshold that automatically requires treatment.

Instead, management is driven by:

  • Symptoms
  • Hemodynamic status
  • Presence of conduction disease
  • Underlying cause
  • Risk of progression to more serious block 

Whenever you encounter bradycardia, your first question should be:

"Is the patient unstable?"

Look for signs of poor perfusion:

  • Hypotension
  • Altered mental status
  • Syncope
  • Presyncope
  • Ischemic chest pain
  • Acute heart failure
  • Shock
  • Severe dyspnea

If any of these are present, you're dealing with symptomatic bradycardia and immediate intervention may be necessary.

If none are present, you have time to determine the cause. 

Next, determine exactly what rhythm you're dealing with.

The major categories include:


Sinus Bradycardia which Normal sinus rhythm with a slow rate.


Sinus Node Dysfunction Previously called sick sinus syndrome.


First-Degree AV Block where there is Delayed conduction through the AV node.


Second-Degree AV Block Mobitz type I and II.


Third-Degree AV Block which is Complete heart block.


Bundle Branch and Fascicular Disease where there is Evidence of conduction system disease below the AV node. 

WHat is SINUS NODE DYSFUNCTION

It is the most common cause of chronic bradycardia is sinus node dysfunction.

This is usually caused by progressive fibrosis and degeneration of the sinus node and surrounding atrial tissue.

Patients may present with:

  • Fatigue
  • Exercise intolerance
  • Dizziness
  • Presyncope
  • Syncope
  • Tachy-brady syndrome

A critical guideline pearl is that there is no minimum heart rate or pause duration that mandates pacing.

The decision to intervene depends on establishing a clear relationship between symptoms and bradycardia. 

So even profound sinus bradycardia doesn't automatically mean pacemaker?

Correct. Symptoms drive therapy.

Before implanting devices or escalating therapy, always search for reversible causes.

Common causes include:


Medications like Beta blockers, Calcium channel blockers, Digoxin, Amiodarone and Antiarrhythmics


Metabolic Disorders like Hyperkalemia, Hypothyroidism and Hypothermia


Ischemia: Especially inferior wall myocardial infarction.


Increased Vagal Tone see in Athletes, during Sleep and Vasovagal episodes


Also Sleep Apnea is One of the most commonly overlooked causes of nocturnal bradycardia.

The guideline specifically highlights treatment of sleep apnea because nocturnal bradycardia alone is not an indication for permanent pacing. 

What is the workup for BRADYCARDIA 

Every evaluation begins with:

  • Detailed history
  • Physical examination
  • Medication review
  • 12-lead ECG

The ECG is essential because it helps determine:

  • Sinus node disease
  • AV block
  • Bundle branch block
  • Ischemia
  • Electrolyte abnormalities

When symptoms are intermittent, ambulatory monitoring becomes critical, and the Options include: Holter monitor, Event monitor, External loop recorder or the Implantable loop recorder

The goal is always symptom-rhythm correlation. 

Now let's talk about the scenario everybody gets tested on.

The patient is hypotensive, diaphoretic, confused, and has a heart rate of 30.

What do you do?

First: Check if Oxygen if needed, hook patient on to a Cardiac monitor, establish IV access, get an 12-lead ECG and then work on identifying reversible causes

If symptoms are severe, treatment should begin immediately.

Atropine is usually the first medication used for symptomatic bradycardia.

It works by blocking parasympathetic activity and increasing sinus node firing and AV nodal conduction.

However, atropine tends to work best in: Sinus bradycardia and AV nodal block

It is often less effective in: Mobitz II AV block, Infranodal disease and Complete heart block

Those patients frequently require pacing. 

If atropine fails—or if the patient is critically unstable—transcutaneous pacing should be initiated.

This is especially important in: High-grade AV block, Mobitz II AV block, Third-degree AV block and Severe symptomatic bradycardia

Pacing provides immediate electrical support while more definitive therapy is arranged.

This is why we always place pacing pads early on in unstable patients?

Exactly. Don't wait for deterioration before preparing for pacing.

When pacing isn't immediately available or is ineffective, vasoactive infusions can be used.

Options include: Dopamine infusion or Epinephrine infusion

These agents increase heart rate and support blood pressure while definitive treatment is arranged.

They are often used as bridges to transvenous pacing or permanent pacing.

Okay no Let's review the AV blocks.


Yes firstly, FIRST-DEGREE AV BLOCK where Every P wave conducts. The PR interval is simply prolonged. Most patients require no treatment.

Permanent pacing is rarely indicated unless symptoms are clearly attributable to the conduction delay. 

Then we have MOBITZ I (WENCKEBACH) where there is Progressive PR prolongation followed by a dropped beat. Usually occurs within the AV node. Often benign. Many patients simply require observation.


What about MOBITZ II?


Yes, Now this is where things become more serious. This usually reflects disease below the AV node in the His-Purkinje system. Here PR intervals remain constant and there are sudden dropped QRS complexes. This rhythm has a substantial risk of progression to complete heart block.

The guideline recommends permanent pacing in most patients with Mobitz II that is not due to a reversible cause. 


What about THIRD-DEGREE AV BLOCK?

Complete heart block occurs when atrial impulses fail to conduct to the ventricles.

The atria and ventricles beat independently. Patients may present with: Syncope, Severe hypotension, Heart failure and Sudden cardiac death

Unless a reversible cause exists, permanent pacemaker implantation is recommended. 

Now WHO NEEDS A PERMANENT PACEMAKER?

Permanent pacing is generally indicated for:


Symptomatic Sinus Node Dysfunction —> meaning Symptoms must correlate with bradycardia.


Acquired Mobitz II AV Block, Without reversible causes.


High-Grade AV Block and Third-Degree AV Block Without reversible causes. 

What about patients with sleep apnea causing bradycardia?

Many sleep apneic patients develop significant nocturnal bradycardia. The answer is usually not a pacemaker. The answer is identifying and treating sleep apnea. Always consider sleep-disordered breathing when unexplained nighttime bradycardia is present. 

SPECIAL PEARL: BUNDLE BRANCH BLOCK

Speaker 1:

Bundle branch block may be the first clue to significant conduction system disease.

Patients with:

  • Bifascicular block
  • Alternating bundle branch block
  • Progressive conduction abnormalities

Require careful evaluation because they may eventually develop advanced AV block. 

Can we finish with some rapid board pearls?

Absolutely. Scenario 1

Heart rate 38. Marathon runner. No symptoms.

No treatment.



Right! Scenario 2

Heart rate 42. Taking metoprolol. Dizzy and hypotensive.

Evaluate medication effect and treat symptomatic bradycardia.


Perfect! Scenario 3

Mobitz II AV block.

Think of a permanent pacemaker.

Great! Scenario 4 Third-degree AV block.

Temporary stabilization followed by permanent pacing.


Correct! Scenario 5

Nocturnal pauses in a patient with obesity and daytime sleepiness.

Evaluate for obstructive sleep apnea before considering pacing. 

So the major takeaway is that bradycardia management isn't about chasing a specific heart rate—it's about identifying symptoms, determining the underlying rhythm, correcting reversible causes, and recognizing when pacing is necessary.

Exactly! Thanks for listening to AudioBoards. Stay tuned for more educational content in our next episode! The views and opinions expressed on the AudioBoards Podcast do not necessarily reflect those of our employers. This podcast is for educational purposes only and should not be used to diagnose or treat any medical conditions. It is not a substitute for professional medical advice. Always consult a qualified, board-certified healthcare provider for any medical concern.