MDM Templates

Stable Bradycardia

Patient found to have asymptomatic bradycardia.
They are alert, well-appearing, and hemodynamically stable.

ECG does not show acute ischemic changes or high-degree AV block..
No severe electrolyte abnormality noted.
No overdose, accidental or otherwise.

History and exam lower suspicion for acute coronary syndrome (particularly RCA lesion), high-degree AV block, hyperkalemia, hypothyroidism, toxic ingestion, or sepsis as a cause of bradycardia.

The clinical picture is most consistent with *** (physiologic bradycardia / medication effect / sinus bradycardia of unclear etiology).

Plan: Observation with continuous monitoring. No acute intervention indicated given hemodynamic stability and absence of symptoms.
Disposition: Discharge with prompt outpatient follow-up with for further evaluation including possible Holter monitor. Return precautions given for syncope, presyncope, chest pain, or worsening dyspnea.

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Symptomatic Bradycardia

Patient presents with symptomatic bradycardia with *** (hypotension / altered mental status / signs of shock / acute heart failure / chest pain).

Potential emergent etiologies considered include acute myocardial infarction (RCA lesion), high-degree AV block, hyperkalemia, hypothyroidism, toxic ingestion (beta-blocker, calcium channel blocker, digoxin, clonidine, opioid), sepsis, and increased intracranial pressure.

History and exam raise concern for *** as the most likely etiology.

Hemodynamically unstable — immediate intervention: ***
(Atropine 1 mg IV / Epinephrine infusion 2–10 mcg/min / Transcutaneous pacing / Transvenous pacing)
Consults: Cardiology for *** (temporary pacing / permanent pacemaker evaluation / cath lab activation).
Disposition: Admit to *** (telemetry / ICU) for ongoing monitoring and definitive management of hemodynamically significant bradyarrhythmia.

Admit if: Symptomatic bradycardia, new second-degree Mobitz II or third-degree AV block, hemodynamic instability requiring vasopressors or pacing, suspected acute MI, or new pacemaker-dependent rhythm.

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Pacemaker Malfunction

Patient presents with implanted cardiac pacemaker and concern for device malfunction with *** (symptomatic bradycardia / syncope / presyncope / palpitations / inappropriate shocks).
Device was implanted on *** for indication of ***.
Last interrogation was ***.

ECG demonstrates ***(Failure to capture — pacing spikes without subsequent QRS / Failure to sense — pacing spikes delivered despite native rhythm / Failure to pace — no pacing spikes despite rate below programmed lower limit / Appropriate function).

No evidence of lead migration or pneumothorax on chest x-ray.
Lab workup including BMP (potassium, magnesium) and troponin obtained to evaluate for metabolic and ischemic contributors to device malfunction.
No concern for pocket infection — no erythema, warmth, fluctuance, or drainage at the generator site.

Interventions: ***
If failure to capture: Magnet application to switch to asynchronous pacing mode. Transcutaneous pacing as bridge if hemodynamically unstable.
If oversensing: Magnet application to convert to asynchronous mode.
Consults: Electrophysiology / Cardiology for device interrogation and reprogramming.
Disposition: *** (Admit for device interrogation and reprogramming / Discharge if device interrogated and functioning appropriately with outpatient EP follow-up). Return precautions for syncope, presyncope, palpitations, or chest pain.

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Toxicologic Bradycardia

Patient presents with bradycardia in the setting of suspected *** (beta-blocker / calcium channel blocker / digoxin / clonidine / organophosphate / opioid) exposure.
*** (Intentional ingestion with reported time of ingestion *** / Accidental overdose / Unintentional therapeutic excess).

Patient *** (with / without) concerning signs of hemodynamic instability.

Presentation not consistent with other causes of bradycardia including acute MI, infectious etiology, hypothyroidism, hyperkalemia, or increased intracranial pressure.

ED Interventions: ***
Beta-blocker toxicity: Glucagon 5 mg IV bolus, high-dose insulin 1 U/kg bolus + drip with dextrose, calcium gluconate 3 g IV, IV fluids. Consider intralipid if refractory.
Calcium channel blocker toxicity: Calcium gluconate 3 g IV (30–60 mL of 10% solution), high-dose insulin 1 U/kg bolus + drip with dextrose, IV fluids. Consider intralipid if refractory.
Digoxin toxicity: Digoxin-specific antibody fragments (DigiFab) 10–20 vials.
Organophosphate toxicity: Atropine 2 mg IV q5min titrated to drying of secretions, pralidoxime 1–2 g IV over 15–30 min.
Opioid toxicity: Naloxone 0.4-2mg mg IV, repeat as needed.
Consults: Poison Control, *** (Cardiology / ICU).
Disposition: Admit to ICU for continuous monitoring, serial ECGs, and ongoing antidotal therapy.

Clinical Education

Classification & Etiologies

Bradycardia is defined as heart rate < 60 bpm, but treatment is driven by symptoms and hemodynamic significance — not the number. A heart rate of 45 in a sleeping 25-year-old athlete is physiologic; a heart rate of 58 in a septic 80-year-old on metoprolol may be dangerously inadequate.^[1]

The critical first question: is it sinus or not? Sinus bradycardia has a normal P-wave before every QRS. If P-waves are absent, dissociated, or the PR interval is behaving abnormally, you’re dealing with a conduction problem.

Category	Etiologies
Cardiac	Acute MI (especially RCA / inferior), sick sinus syndrome, conduction disease (AV block), post-cardiac surgery, myocarditis
Toxic / Pharmacologic	Beta-blockers, calcium channel blockers, digoxin, clonidine, opioids, organophosphates, amiodarone, lithium
Metabolic	Hyperkalemia, hypothyroidism, hypothermia, hypoglycemia
Neurologic	Increased ICP (Cushing reflex), spinal cord injury, vasovagal
Physiologic	Athletic heart, sleep, high vagal tone

Workup: CBC, BMP, calcium, magnesium, TSH, troponin, lactate, glucose, ECG. Add UDS, APAP, salicylate, and digoxin level if toxic ingestion suspected. CXR if concern for heart failure or device lead migration.

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ECG Recognition: AV Blocks

First-degree AV block: PR interval > 200 ms, but every P-wave conducts. This is a conduction delay, not a true block. Benign in isolation — reassure and discharge.^[2]

Second-degree Mobitz I (Wenckebach): Progressive PR prolongation until a beat drops. P-waves are regular (constant P-P interval). The grouping pattern and progressive PR lengthening are the hallmarks. Generally a nodal-level block — usually benign, rarely requires pacing unless symptomatic.^[2]

Second-degree Mobitz II: Constant PR interval with intermittently dropped QRS complexes — no progressive prolongation before the dropped beat. P-waves are regular. Often coexists with bundle branch block, so the QRS is frequently wide. This is an infranodal block with structural damage to the conducting system and a significant risk of progression to complete heart block. Admit all Mobitz II — these patients need pacing.^[2]

2:1 AV block: Every other P-wave is blocked. The challenge: you can’t tell Mobitz I from Mobitz II when only one conducted beat separates each dropped beat. A narrow QRS favors Mobitz I (nodal); a wide QRS favors Mobitz II (infranodal). When in doubt, treat as Mobitz II.^[3]

Third-degree (complete) heart block: Complete AV dissociation — P-waves march out at their own rate, QRS complexes occur at a separate regular rate, and the PR interval varies randomly. More P-waves than QRS complexes. The ventricular escape rate and QRS width tell you the level: narrow QRS with rate 40–60 suggests junctional escape; wide QRS with rate < 40 suggests ventricular escape and is more dangerous. All complete heart block requires admission and pacing.^[2]

Key pitfall — blocked PACs mimicking AV block: If P-waves appear irregular and the non-conducted P-waves come early (not on time), think blocked premature atrial complexes rather than true AV block. The P-P interval will be irregular, which distinguishes this from Mobitz I/II where P-waves are regular.^[3]

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ECG Recognition: Junctional & Escape Rhythms

Junctional rhythms arise from the AV junction when supranodal pacemakers fail or are blocked. P-waves are absent, inverted (retrograde conduction), or buried in the QRS. The QRS is narrow unless there is a pre-existing bundle branch block.^[3]

Rhythm	Rate	Significance
Junctional bradycardia	< 40 bpm	Pathologic — evaluate for cause
Junctional escape rhythm	40–60 bpm	Normal AV junction intrinsic rate — protective escape
Accelerated junctional	60–100 bpm	Enhanced automaticity — consider dig toxicity, ischemia, post-surgical
Junctional tachycardia	> 100 bpm	Pathologic — dig toxicity high on differential

Regularized atrial fibrillation = complete heart block. If a patient in atrial fibrillation suddenly develops a regular, slow ventricular rhythm, the irregularly irregular AF impulses are no longer reaching the ventricles — a junctional or ventricular escape rhythm has taken over. This is complete heart block with junctional escape and should be treated as such.^[3]

Regularized AF: fibrillatory baseline with a regular, slow QRS rate — complete heart block with junctional escape.

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ACLS Bradycardia Algorithm

The 2020 AHA guidelines reframe the approach: identify and treat reversible causes first, then escalate pharmacologically, then pace.^[1]

Step 1 — Is the patient symptomatic? Symptoms attributable to bradycardia include hypotension, altered mental status, signs of shock, chest pain, and acute heart failure. If the patient is asymptomatic and hemodynamically stable, monitor and investigate — don’t treat the number.

Step 2 — Atropine first line: 1 mg IV, may repeat every 3–5 minutes, max 3 mg. Works by blocking vagal input at the SA and AV node. Effective for sinus bradycardia and nodal AV blocks. Will not work for infranodal blocks (Mobitz II, complete heart block with wide escape) or denervated transplant hearts.^[1]

Step 3 — If atropine fails: Epinephrine infusion 2–10 mcg/min OR dopamine 2–20 mcg/kg/min OR transcutaneous pacing. The 2020 guidelines place these as equivalent second-line options. In practice, epinephrine drip is the most versatile — it provides chronotropic and inotropic support and works regardless of the level of block.^[1]

Step 4 — Transcutaneous pacing if pharmacologic measures fail or as a bridge to transvenous pacing. Do not delay pacing for medications in the peri-arrest patient.

Step 5 — Transvenous pacing for refractory symptomatic bradycardia or when the cause is not rapidly reversible. Arrange early for any patient with Mobitz II or complete heart block.

Don’t forget aminophylline: For bradycardia in the setting of inferior MI or post-cardiac transplant, aminophylline 250 mg IV over 1–2 minutes can reverse adenosine-mediated bradycardia that won’t respond to atropine.^[4]

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Treatment Ladder

Agent	Dose	Notes
Atropine	1 mg IV q3–5min (max 3 mg)	First line. Anticholinergic — works on vagally mediated and nodal bradycardia. Avoid doses < 0.5 mg (risk of paradoxical bradycardia via central M1 receptor activation).[5] Ineffective in infranodal block, transplant hearts.
Epinephrine infusion	2–10 mcg/min	Most versatile second-line agent. Works across all levels of block. Provides chronotropy + inotropy + vasoconstriction. Push-dose: 10–20 mcg IV bolus as bridge to drip (mix 1 mL of 1:10,000 in 9 mL NS = 10 mcg/mL).[1]
Dopamine infusion	2–20 mcg/kg/min	Alternative to epinephrine. More arrhythmogenic. Less commonly used as first-choice pressor in modern practice.[1]
Isoproterenol	2–10 mcg/min	Pure beta-agonist. Bridge to transvenous pacing. Increases heart rate without vasoconstriction. Risk of hypotension and demand ischemia.[6]
Aminophylline	250 mg IV over 1–2 min	Adenosine antagonist. Useful for inferior MI bradycardia and post-transplant bradycardia refractory to atropine.[4]

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Transcutaneous Pacing Pearls

Transcutaneous pacing is painful — sedate first unless the patient is peri-arrest. Reasonable options include ketamine 10–20 mg IV, etomidate 0.1–0.15 mg/kg IV, or midazolam 2–5 mg IV. Fentanyl 25–50 mcg IV is a good adjunct for analgesia.^[7]

Setup:

Setting	Recommendation
Mode	Fixed/asynchronous — requires pads only. Demand — requires cardiac leads connected to sense native rhythm. Use demand when the patient has some intrinsic rhythm to avoid R-on-T.
Rate	Set to 80 bpm (or at least 30 bpm above the patient’s current rate).
Current	Start at 70 mA. Increase until electrical capture on monitor (typically < 120 mA). Once captured, set 5–10 mA above threshold.

Confirming capture: Electrical capture = wide QRS complex following each pacing spike on the monitor. Mechanical capture = palpable pulse correlating with electrical capture. Always confirm mechanical capture — electrical capture alone does not guarantee perfusion. Check the femoral pulse to avoid confusing pacing-induced muscle contractions with a true pulse.^[7]

Troubleshooting failure to capture: If current exceeds 120 mA without capture, try repositioning pads (anterior-posterior placement often works better than anterior-lateral). Ensure good skin contact — shave chest hair, dry the skin. Correct metabolic derangements (hyperkalemia, acidosis) which raise the capture threshold. In a large body habitus patient, the threshold may simply be higher.

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Transvenous Pacing Pearls

Transvenous pacing is the bridge to definitive permanent pacemaker placement. It is indicated when transcutaneous pacing fails, when sustained pacing is needed beyond the short term, or when the patient cannot tolerate TCP.^[8]

Access: Place a venous introducer sheath — 6 Fr, 10 cm percutaneous sheath introducer via the right IJ (preferred) or left subclavian. The pacer catheter is approximately 5 Fr — do not use an oversized introducer (e.g., 8 Fr) as it will allow blood leak around the catheter.

Generator settings before insertion:

Setting	Initial Value
Rate	Start 20 bpm above current rate (or match TCP rate)
Output	Start maximum (20 mA) — titrate down after capture
Sensitivity	Asynchronous / fixed (simplest during placement)

Technique: Advance catheter 15–20 cm, inflate the balloon, continue advancing. Watch the monitor — once you see capture (paced QRS complexes), deflate the balloon and secure. Slide the plastic sheath over the external portion of the pacing wire to protect it. Post-placement CXR to confirm position and rule out pneumothorax.^[8]

After capture: Slowly decrease the output until capture is lost — that is the threshold. Set the output to 2–3x threshold to ensure a safety margin. Typical threshold is 0.5–1.0 mA.

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Toxicologic Bradycardia & Antidotes

The two most important toxicologic causes of bradycardia in the ED are beta-blocker and calcium channel blocker overdose. They present similarly but have key differentiating features.^[9]

Feature	Beta-Blocker Toxicity	CCB Toxicity
Hallmark	Bradycardia + normoglycemia/hypoglycemia	Bradycardia + hyperglycemia (CCBs block pancreatic insulin release)
Onset	1–4 hours (immediate-release)	1–4 hours (IR); up to 12–16 hours (extended-release)
Progression	Bradycardia → hypotension → AMS	Bradycardia → hypotension → cardiovascular collapse

Unique beta-blocker considerations: Propranolol causes sodium channel blockade (wide QRS, terminal R wave in aVR — consider bicarbonate) and is highly lipophilic so crosses the blood-brain barrier causing AMS even with preserved blood pressures. Sotalol causes potassium efflux channel blockade leading to QT prolongation and increased risk of torsades de pointes.^[9]

Toxin	Antidote & Dose	Mechanism
Beta-blockers	Glucagon 5 mg IV bolus (may repeat), then 2–5 mg/hr drip High-dose insulin 1 U/kg bolus + 1–10 U/kg/hr drip + D10 gtt Calcium gluconate 3 g IV Intralipid 1.5 mL/kg bolus if refractory	Glucagon bypasses beta-receptors → activates adenylate cyclase Insulin improves cardiac myocyte glucose utilization Calcium increases extracellular calcium → improved contractility
CCBs	Calcium gluconate 3 g IV (30–60 mL of 10% soln), may repeat High-dose insulin 1 U/kg bolus + 1–10 U/kg/hr drip + D10 gtt Intralipid if refractory IV fluids	Calcium overwhelms competitive blockade at L-type channels Insulin is the cornerstone of CCB toxicity management
Digoxin	Digoxin-specific antibody fragments (DigiFab) 10–20 vials	Binds free digoxin. Avoid calcium (may worsen toxicity).
Opioids	Naloxone 0.4 mg IV, repeat as needed	Competitive mu-receptor antagonist
Organophosphates	Atropine 2 mg IV q5min (may need >100 mg total — titrate to drying of secretions) Pralidoxime 1–2 g IV over 15–30 min	Atropine blocks muscarinic effects Pralidoxime reactivates acetylcholinesterase (give early — “aging” makes it irreversible)
Clonidine	Supportive care, atropine, IV fluids Consider naloxone 2–10 mg IV (variable response)	Central alpha-2 agonist — decreases sympathetic outflow

Atropine is ineffective in beta-blocker and CCB toxicity — it decreases vagal tone but does not reverse direct myocardial depression. Don’t waste time repeating it.^[9]

Key pearl for all toxic bradycardias: Early Poison Control consultation (1-800-222-1222). If the patient is hypotensive, start vasopressors and high-dose insulin early — do not wait for the patient to decompensate. All significant BB/CCB overdoses should be admitted to the ICU with serial ECGs.^[10]

References

1. Panchal AR, Bartos JA, Cabañas JG, et al. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142(16_suppl_2):S366–S468. PubMed
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. Circulation. 2019;140(8):e382–e482. PubMed
3. Burns E, Buttner R. AV Block — ECG Library. Life in the Fast Lane. 2021. LITFL
4. Bertolet BD, McMurtrie EB, Hill JA, et al. Theophylline for the treatment of atrioventricular block after myocardial infarction. Ann Intern Med. 1995;123(7):509–511. PubMed
5. Bernheim A, Falk RH. Paradoxical bradycardia after intravenous atropine: a report of three cases. Cardiol Rev. 2004;12(1):1–3.
6. Tintinalli JE, Ma OJ, Yealy DM, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill; 2020. Chapter 26: Cardiac Rhythm Disturbances.
7. Nickson C. Transcutaneous Pacing. Life in the Fast Lane. 2020. LITFL
8. Nickson C. Transvenous Pacing. Life in the Fast Lane. 2020. LITFL
9. Graudins A, Lee HM, Druda D. Calcium channel blocker and beta-blocker toxicity. Emerg Med Clin North Am. 2007;25(2):309–331. PubMed
10. St-Onge M, Anseeuw K, Cantrell FL, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med. 2017;45(3):e306–e315. PubMed