The Daily Differential — Thursday, May 21, 2026

2 of 4

Bradydysrhythmias

Bradycardia ranges from benign athletic sinus bradycardia to unstable high-grade AV block. Board-relevant management depends less on the heart rate number...

At the Bedside

Define instability
Hypotension.
Altered mental status.
Ischemic chest discomfort.
Acute heart failure/pulmonary edema.
Syncope or shock.

Initial ED actions
Monitor, IV access, oxygen if hypoxemic, pads on patient.
12-lead ECG.
Check glucose if altered.
Review meds: beta-blockers, calcium channel blockers, digoxin, clonidine, opioids, antiarrhythmics.
Consider toxicologic causes early.

Key ECG patterns
Sinus bradycardia: each P before QRS, slow sinus rate.
1st-degree AV block: PR >200 ms, all P waves conducted.
Mobitz I/Wenckebach: progressive PR prolongation then dropped QRS; usually AV nodal.
Mobitz II: fixed PR with intermittent dropped QRS; infranodal, high risk.
3rd-degree AV block: AV dissociation; atria and ventricles independent.
Junctional escape: narrow QRS, absent/inverted P waves, rate 40–60.
Ventricular escape: wide QRS, rate 20–40.

Workup
ECG and rhythm strip.
BMP, Mg, Ca.
Troponin if ACS concern.
TSH if unexplained/subacute.
Digoxin level if relevant.
Drug levels/tox workup when indicated.
Consider Lyme testing in endemic exposure with AV block.
CXR/echo if heart failure or structural disease suspected.

Reversible causes
Hypoxia.
Hyperkalemia.
Hypothermia.
Increased vagal tone.
Inferior MI.
Medication/toxin effect.
Increased intracranial pressure.
Myocarditis.
Lyme carditis.

Management
Stable and asymptomatic: observe, identify cause, avoid unnecessary treatment.
Symptomatic/unstable bradycardia:

1. Atropine. 2. If ineffective: transcutaneous pacing and/or epinephrine/dopamine infusion. 3. Treat cause in parallel.

High-grade AV block/Mobitz II/complete heart block:
Place pads early.
Atropine may fail, especially infranodal block with wide QRS.
Prepare for pacing and cardiology consultation.
Hyperkalemic bradycardia: calcium first, then insulin/dextrose, albuterol, bicarbonate if acidemic, dialysis when indicated.
Beta-blocker/CCB toxicity: fluids, calcium, glucagon, high-dose insulin euglycemia therapy, vasopressors, toxicology.
Digoxin toxicity: digoxin immune Fab for life-threatening dysrhythmia, hyperkalemia, shock.

Disposition
Discharge may be appropriate for asymptomatic sinus bradycardia with clear benign cause.
Admit/telemetry for symptomatic bradycardia, medication adjustment, new conduction disease, electrolyte abnormalities.
ICU for unstable bradycardia, pacing, high-grade AV block, toxicologic bradycardia, or recurrent syncope.

A Classic Presentation

A 72-year-old woman presents with syncope and dizziness. HR is 32, BP 78/44, and ECG shows complete heart block with a wide ventricular escape rhythm. Pads are placed, atropine is given but ineffective, transcutaneous pacing is initiated with sedation, and cardiology is called for transvenous pacing and permanent pacemaker evaluation.

Study Directive

Memorize the ACLS unstable bradycardia algorithm from memory.
Practice identifying Mobitz I, Mobitz II, and complete heart block on rhythm strips.
Make a one-page toxicologic bradycardia differential: beta-blockers, CCBs, digoxin, clonidine, opioids.
Rehearse hyperkalemia treatment dosing without looking.
On shift, locate transcutaneous pacing settings on your ED defibrillator.

Key Medications

Atropine: 1 mg IV q3–5 min; max 3 mg.
Epinephrine infusion: 2–10 mcg/min IV, titrate to perfusion.
Dopamine infusion: 5–20 mcg/kg/min IV.
Calcium chloride for hyperkalemia/CCB toxicity: 1 g IV via central line preferred; may use peripheral cautiously in emergencies.
Calcium gluconate: 3 g IV for hyperkalemia; commonly 1–3 g IV for CCB toxicity depending protocol. Dosing varies — check institutional/toxicology guidance.
Regular insulin for hyperkalemia: 5–10 units IV with dextrose depending glucose/institutional protocol.
Glucagon for beta-blocker toxicity: 3–5 mg IV bolus; may repeat, then infusion if response. Dose varies — check toxicology reference.
High-dose insulin euglycemia therapy: typically 1 unit/kg IV bolus then 0.5–1 unit/kg/hr infusion with dextrose/potassium monitoring; consult toxicology/poison center.

High-Yield Pearls

Treat the patient, not the number: HR 38 with normal perfusion may need observation; HR 50 with shock needs action.
Atropine works best for AV nodal/vagal bradycardia and often fails in Mobitz II or complete heart block with wide QRS.
Hyperkalemia can mimic almost any bradydysrhythmia — give calcium immediately if suspected.

Board Question

A patient has hypotension and complete heart block with a wide QRS escape rhythm. Atropine is given without improvement. What is the next best step?

AObserve because complete heart block is usually benign
BStart oral metoprolol
CInitiate transcutaneous pacing
DGive adenosine

Reveal answer

Correct: C

Unstable high-grade AV block requires immediate pacing when atropine fails or is unlikely to work. Wide QRS escape rhythms suggest infranodal disease, where atropine is often ineffective.

Recent Literature

Review or guideline Bradydysrhythmias and atrioventricular conduction blocks
Emerg Med Clin North Am, 2006 · cited 20×
Recent clinical Pearls and Pitfalls: Severe Bradycardia
J Emerg Med, 2026

3 of 4

Cardiac Pacing

Pacing is a lifesaving bridge for unstable bradycardia and high-grade conduction disease. EM residents must be able to initiate transcutaneous pacing...

At the Bedside

Indications for emergent pacing
Unstable bradycardia refractory to atropine.
Mobitz II AV block with symptoms.
Complete heart block with symptoms or wide escape rhythm.
Symptomatic bradycardia after cardiac transplant.
Overdrive pacing for recurrent torsades due to bradycardia/pauses, usually with cardiology support.
Bradycardic peri-arrest where meds are failing.

Transcutaneous pacing: practical steps

1. Place anterior-posterior pads if possible. 2. Set mode to pacing. 3. Choose rate, usually 60–80 bpm. 4. Increase current from low setting until electrical capture. 5. Increase 5–10 mA above capture threshold. 6. Confirm mechanical capture with pulse/BP/arterial waveform/POCUS. 7. Provide analgesia/sedation if patient awake. 8. Treat underlying cause and arrange definitive pacing.

Electrical vs mechanical capture
Electrical capture: pacing spike followed by wide QRS and T wave.
Mechanical capture: palpable pulse, improved BP, arterial waveform, or cardiac contraction on ultrasound.
Muscle twitching alone is not capture.

Transvenous pacing
Indications:
TCP ineffective or not tolerated.
Prolonged need for pacing.
High-grade AV block awaiting permanent pacemaker.
Severe bradycardia with unreliable escape rhythm.
Usually placed via right internal jugular, subclavian, or femoral vein.
ED should stabilize with TCP/pressors while cardiology/critical care prepares TVP unless local scope requires ED placement.

Permanent pacemaker considerations
Symptomatic sinus node dysfunction.
Mobitz II.
Advanced/complete AV block not due to reversible cause.
Certain post-MI conduction disease.
Recurrent syncope due to conduction system disease.

Pacemaker malfunction in ED
Failure to pace: no pacer spikes when expected.
Causes: battery depletion, lead fracture/dislodgement, oversensing.
Failure to capture: pacer spike without QRS.
Causes: lead dislodgement, high threshold, ischemia, acidosis, hyperkalemia.
Failure to sense: pacer fires inappropriately despite intrinsic beats.
Risk: R-on-T phenomenon.
Workup: ECG, CXR for lead position, electrolytes especially K/Mg, device interrogation.

Special scenarios
Hypothermia: pacing may be less effective; rewarming is definitive.
Hyperkalemia: pacing may not capture until calcium and potassium-shifting therapies are given.
Inferior MI with bradycardia: atropine often works; pacing if unstable.
Anterior MI with AV block: high risk infranodal disease; pacing often required.

A Classic Presentation

A 61-year-old man with chest pain becomes pale and confused. ECG shows Mobitz II with HR 28 and BP 70 systolic. Atropine is given while pads are placed, but his pressure remains low. TCP is started at 70 bpm, capture occurs at 60 mA, output is set to 70 mA, mechanical capture is confirmed by pulse and BP improvement, fentanyl is given, and cardiology is called for transvenous pacing.

Study Directive

Hands-on task: use a defibrillator trainer and practice setting TCP rate/current until capture.
Write out the difference between failure to pace, failure to capture, and failure to sense.
Review 5 ECGs of pacemaker malfunction.
Practice verbalizing: “electrical capture confirmed, now checking mechanical capture.”
Learn your ED’s pathway for emergent transvenous pacing: who places it, where supplies are, and how EP/cardiology is contacted.

Key Medications

Atropine: 1 mg IV q3–5 min; max 3 mg.
Epinephrine infusion: 2–10 mcg/min IV.
Dopamine infusion: 5–20 mcg/kg/min IV.
Fentanyl for pacing discomfort: 0.5–1 mcg/kg IV; repeat small doses as needed.
Midazolam: 1–2 mg IV titrated; use caution in hypotension.
Ketamine for analgesia/sedation: 0.5–1 mg/kg IV for dissociative/procedural sedation; lower analgesic doses 0.1–0.3 mg/kg IV may be used. Institutional practice varies.
Etomidate: 0.1–0.2 mg/kg IV for brief sedation in unstable patients; less analgesia, so pair with analgesic when possible.

High-Yield Pearls

TCP is a bridge, not definitive therapy for most high-grade conduction disease.
Always set pacing output above the capture threshold, not exactly at threshold.
Hyperkalemia and severe acidosis raise capture thresholds — correct physiology while pacing.

Board Question

During transcutaneous pacing, the monitor shows pacing spikes followed by wide QRS complexes. The patient still has no palpable pulse and no arterial waveform. What should you do next?

AAssume capture is adequate because QRS complexes are present
BConfirm and optimize mechanical capture, including increasing output if needed
CTurn off pacing and give adenosine
DRemove the pads and place them laterally

Reveal answer

Correct: B

Electrical capture is not enough; mechanical capture must be confirmed by pulse, BP, waveform, or ultrasound. If there is no mechanical capture, increase current, optimize pad position, and continue resuscitation.

Recent Literature

Review or guideline 2023 HRS/APHRS/LAHRS guideline on cardiac physiologic pacing for the avoidance and mitigation of heart failure
Heart Rhythm, 2023 · cited 472×

Full text · open access
Recent clinical Cost-effectiveness of leadless versus transvenous single-chamber ventricular pacing: a propensity-weighted real-world study in France
Ann Med, 2026

Full text · open access

4 of 4

Congenital Long QT

Congenital long QT syndrome predisposes young, often otherwise healthy patients to torsades de pointes, syncope, seizures, and sudden death. The ED must...

At the Bedside

Core concept
Congenital long QT = abnormal cardiac ion channel repolarization.
Prolonged repolarization allows early afterdepolarizations, which can trigger torsades.

Typical presentations
Syncope during exercise, swimming, emotional stress, startle, or sleep.
“Seizure” with rapid recovery and no postictal state.
Family history of sudden unexplained death, drowning, single-car crash, or known long QT.
Palpitations or cardiac arrest in young patient.

ECG findings
QTc prolonged:
Generally concerning if QTc >450 ms in men or >470 ms in women.
QTc ≥500 ms is high risk.
T-wave abnormalities may suggest subtype:
LQT1: broad-based T waves, exercise/swimming triggers.
LQT2: low-amplitude/notched T waves, auditory/emotional triggers.
LQT3: late-appearing T waves, events during sleep/rest.
Measure QT carefully; automated QTc can be wrong.

ED workup
12-lead ECG with QTc calculation.
Electrolytes: K, Mg, Ca.
Medication review for QT-prolonging drugs.
Troponin if ischemia/myocarditis concern.
Pregnancy test when relevant.
Consider tox screen if overdose possible.
Ask specifically about family sudden death and exertional syncope.

Management
If torsades/polymorphic VT with pulse:
If unstable: immediate unsynchronized defibrillation if polymorphic/irregular and cannot sync reliably.
Magnesium sulfate.
Correct K/Mg/Ca.
Stop QT-prolonging drugs.
If pulseless torsades/VF:
Defibrillate, CPR, ACLS.
Magnesium sulfate.
If recurrent torsades due to pauses/bradycardia:
Increase heart rate with temporary pacing.
Isoproterenol is used for acquired pause-dependent torsades but is generally avoided in congenital LQTS unless specialist-directed because adrenergic stimulation can worsen some congenital forms.
Stable prolonged QT without torsades:
Remove offending meds.
Replete electrolytes.
Cardiology consultation.
Start/continue beta-blocker if known/suspected congenital LQTS and no contraindication, usually with cardiology guidance.
Long-term definitive therapy
Beta-blockers, especially nadolol or propranolol.
ICD for survivors of cardiac arrest or high-risk recurrent events despite therapy.
Left cardiac sympathetic denervation in select refractory cases.
Family screening/genetic counseling.

Avoid QT-prolonging ED meds when possible
Ondansetron, droperidol, haloperidol.
Macrolides, fluoroquinolones.
Methadone.
Many antipsychotics.
Class IA/III antiarrhythmics: procainamide, quinidine, sotalol, dofetilide, ibutilide, often amiodarone.
Use a QT medication checker or institutional resource when uncertain.

Disposition
Admit/telemetry for QTc ≥500 ms with symptoms, syncope, torsades, significant electrolyte abnormality, or concerning family history.
ICU for torsades, cardiac arrest, recurrent syncope, need for pacing/infusion.
Discharge only if asymptomatic, mild QTc prolongation, reversible cause corrected, no concerning history, and follow-up is secure.

A Classic Presentation

A 16-year-old girl collapses while swimming and has brief shaking movements but wakes quickly. Her brother died suddenly at age 18. ECG shows QTc 530 ms with broad T waves. Electrolytes are checked and optimized, QT-prolonging medications are avoided, she is admitted on telemetry, and cardiology is consulted for congenital long QT treatment and family screening.

Study Directive

Practice manually calculating QTc using Bazett formula: QTc = QT / √RR.
Make a “do-not-give” list of common ED QT-prolonging medications.
Memorize the triggers: LQT1 exercise/swimming, LQT2 auditory/emotion, LQT3 sleep/rest.
Review torsades management: defibrillation if unstable/pulseless, magnesium, K/Mg/Ca correction, stop QT drugs.
Read one ECG tutorial on distinguishing torsades from monomorphic VT and artifact.

---

Mechanism Pearl of the Day: Today’s topics all revolve around controlling myocardial electrical timing: ICDs terminate malignant depolarization circuits, pacing restores an adequate depolarization rate, bradycardia algorithms support failed impulse generation/conduction, and congenital long QT reflects delayed repolarization that permits early afterdepolarizations and torsades.

Key Medications

Magnesium sulfate for torsades with pulse: 2 g IV over 10–15 min.
Magnesium sulfate in pulseless torsades/VF: 1–2 g IV/IO.
Potassium repletion: target K 4.5–5.0 mEq/L in torsades risk if renal function allows; dosing varies by route/level — check institutional protocol.
Nadolol: common chronic therapy 1–1.5 mg/kg/day PO, often once daily; initiation/titration should be coordinated with cardiology.
Propranolol: chronic therapy often 2–3 mg/kg/day PO divided; dosing varies by patient and formulation — check cardiology/reference.
Avoid amiodarone/procainamide/sotalol/ibutilide for congenital long QT-associated polymorphic VT because they can worsen QT prolongation.
Pediatrics: congenital LQTS often presents in children/adolescents; beta-blocker dosing is weight-based and should be coordinated with pediatric cardiology.

High-Yield Pearls

“Seizure” during exertion or swimming may be torsades until proven otherwise.
QTc ≥500 ms is a major danger threshold for torsades risk.
In congenital LQTS, beta-blockers reduce adrenergic triggers; in acquired pause-dependent torsades, increasing heart rate is often key.

Board Question

A young patient with known congenital long QT develops recurrent torsades de pointes. Which medication should be avoided because it may worsen QT prolongation?

AMagnesium sulfate
BPotassium supplementation
CAmiodarone
DNadolol

Reveal answer

Correct: C

Amiodarone can prolong QT and is generally avoided in congenital long QT-associated polymorphic VT. Magnesium and electrolyte correction are acute therapies; beta-blockers such as nadolol are core chronic treatment.

Recent Literature

Review or guideline CONGENITAL LONG QT SYNDROME: A SYSTEMATIC REVIEW
Acta Clin Croat, 2021 · cited 22×

Full text · open access
Recent clinical Right Stellate Ganglion Blockade as a Bridging Therapy Prior to Sympathectomy in a Hemodynamically Unstable Adolescent With Ventricular Storm Secondary to Congenital Long QT Syndrome
Case Rep Anesthesiol, 2026

Full text · open access

TheDaily Differential

Automated Internal Cardioverter-Defibrillators

At the Bedside

Study Directive

Recent Literature

More in Today's Issue

Bradydysrhythmias

Cardiac Pacing

Congenital Long QT

Journal Watch

Deadline Approaching: Get Your ED Pediatric Ready

Podcast Picks

Wide Complex Tachycardia

EMA 2026 May

Pharmacology Corner

Piperacillin-Tazobactam

Succinylcholine

ECG of the Day

Case of the Day