Residency · Residency · Emergency Medicine

Bradydysrhythmias and Pacemaker Emergencies

Classification of Bradycardia

Sinus Node Dysfunction

Sinus bradycardia is defined as a rate below 60 bpm with normal P-wave morphology and regular rhythm. Sinus pause or arrest occurs when the sinus node fails to fire, resulting in a period of absent P-waves. Sinoatrial exit block occurs when the sinus impulse is generated normally but fails to conduct to the atrium. Tachy-brady syndrome, part of sick sinus syndrome, involves alternating episodes of tachycardia (often atrial fibrillation) and bradycardia.

AV Conduction Blocks

First-degree AV block is simply a prolonged PR interval (greater than 200 ms) with every P-wave conducted — it is benign and requires no treatment. Second-degree Type I (Wenckebach) shows progressive PR prolongation until a beat is dropped, creating a grouped beating pattern. The block is usually at the level of the AV node and is typically benign, rarely requiring pacing. Second-degree Type II (Mobitz II) shows a constant PR interval with intermittent non-conducted P-waves. This block is usually infranodal (at the His bundle or below) and carries a high risk of progression to complete heart block — a pacemaker is indicated even in asymptomatic patients. Third-degree (complete) heart block shows complete AV dissociation with no relationship between P-waves and QRS complexes. A junctional escape with narrow QRS at 40 to 60 bpm suggests block at the AV node level, while a ventricular escape with wide QRS at 20 to 40 bpm indicates block below the His bundle with a less reliable escape rhythm. Complete heart block always requires treatment due to the high risk of asystole.

High-Grade AV Block

High-grade AV block involves multiple consecutive non-conducted P-waves, such as 2:1 or 3:1 block. In 2:1 AV block specifically, the block cannot be classified as Type I or Type II from a single rhythm strip because there are no consecutive conducted beats to assess PR interval progression. QRS width is the most useful clue: narrow QRS suggests Type I, while wide QRS suggests Type II.

Clinical Assessment

Symptoms of Hemodynamically Significant Bradycardia

Hemodynamically significant bradycardia manifests as hypotension, syncope or near-syncope, altered mental status, dizziness, signs of shock (cool extremities, diaphoresis, poor perfusion), chest pain or dyspnea from reduced cardiac output, and heart failure symptoms.

Reversible Causes

The most common reversible causes include medications (beta-blockers, calcium channel blockers, digoxin, amiodarone, clonidine, lithium), metabolic derangements (hyperkalemia, hypothyroidism, hypothermia), increased vagal tone (vasovagal responses, inferior MI via the Bezold-Jarisch reflex, increased intracranial pressure via the Cushing response), infections (myocarditis, Lyme disease — which should be considered in young patients with heart block), and post-cardiac surgery or structural heart disease.

Diagnostic Workup

The 12-lead ECG determines the level of block, QRS width, and escape rhythm rate. Continuous telemetry monitoring is essential. Laboratory workup includes electrolytes (especially potassium, calcium, and magnesium), digoxin level if applicable, TSH if hypothyroidism is suspected, and Lyme titers in endemic areas for young patients with unexplained heart block.

Pharmacologic Management

Atropine

Atropine is the first-line agent for symptomatic bradycardia, dosed at 0.5 mg IV every 3 to 5 minutes up to a maximum of 3 mg. It works by blocking vagal tone, increasing sinus rate and AV conduction. It is effective for sinus bradycardia and AV nodal blocks (Type I and some complete heart block with junctional escape). However, atropine is ineffective for infranodal block (Mobitz Type II, complete heart block with wide QRS escape) because these blocks are below the level where vagal tone has influence. An important caution: doses below 0.5 mg may paradoxically worsen bradycardia through central vagal stimulation, so the minimum dose is always 0.5 mg.

Epinephrine

Push-dose epinephrine at 10 to 20 mcg IV every 1 to 2 minutes provides an excellent bridge to pacing. An epinephrine infusion at 2 to 10 mcg/min offers sustained chronotropic support. Epinephrine works on both nodal and infranodal tissue via beta-1 stimulation.

Dopamine

Dopamine infusion at 5 to 20 mcg/kg/min acts as a beta-1 agonist at moderate doses, increasing heart rate and contractility. It is an alternative to epinephrine but is less titratable.

Isoproterenol

Isoproterenol is a pure beta agonist that increases heart rate without alpha-mediated vasoconstriction. Dosed at 2 to 10 mcg/min IV infusion, it is useful for denervated hearts (post-transplant), Torsades de Pointes (providing an overdrive pacing effect), and beta-blocker overdose. Availability has declined, and many EDs no longer stock it. Side effects include hypotension from vasodilation and myocardial ischemia.

Glucagon

For bradycardia induced by beta-blockers or calcium channel blockers, glucagon at 3 to 10 mg IV bolus followed by an infusion of 3 to 5 mg/hr bypasses the beta-receptor to activate adenylate cyclase directly. Nausea and vomiting are common side effects, so pretreatment with ondansetron is advisable.

Calcium

Calcium is indicated for calcium channel blocker-induced bradycardia and hyperkalemia. Calcium chloride 1 g IV (preferably via central line) or calcium gluconate 3 g IV stabilizes cardiac membranes but does not directly increase heart rate.

Transcutaneous Pacing

Indications

Transcutaneous pacing is indicated for symptomatic bradycardia unresponsive to atropine, Mobitz Type II or complete heart block, and as a bridge to transvenous pacing.

Technique

Pads are placed in the anterior-posterior configuration for best capture. The rate is set to 60 to 80 bpm. Output starts low at 20 mA and is increased until electrical capture is achieved — a pacing spike followed by a wide QRS complex and T-wave. Mechanical capture must be confirmed by verifying a palpable pulse with each paced complex, because electrical capture without mechanical capture can occur. The typical capture threshold is 50 to 100 mA. Sedation and analgesia are essential because transcutaneous pacing is painful — ketamine, fentanyl, or midazolam should be administered.

Troubleshooting

If capture fails, the output should be increased, pads repositioned, and good skin contact ensured (shaving chest hair and drying the skin). Chest wall muscle contraction without cardiac capture can mimic a pulse — verification with arterial waveform, ETCO2, or ultrasound is important. If transcutaneous pacing fails, transvenous pacing should be pursued.

Transvenous Pacing

Indications

Transvenous pacing is indicated when transcutaneous pacing fails, when prolonged pacing is needed before permanent pacemaker placement, and when hemodynamic instability requires reliable capture.

Technique Overview

Central venous access (right internal jugular preferred for the most direct route to the right ventricle) is obtained. A balloon-tipped pacing catheter is floated into the right ventricle under fluoroscopy or with ECG guidance. Initial output is set to 5 mA at a rate of 60 to 80 bpm. After confirming capture, the threshold is determined and output is set at 2 to 3 times the threshold. The catheter is secured and a chest X-ray obtained for positioning.

Pacemaker Emergencies

Types of Pacemakers

Single-chamber devices (AAI or VVI) have one lead in either the atrium or ventricle. Dual-chamber devices (DDD) have leads in both chambers, sensing and pacing both. Biventricular devices (CRT) add a left ventricular lead via the coronary sinus for cardiac resynchronization. Implantable cardioverter-defibrillators (ICDs) combine defibrillation capability with pacing.

Pacemaker Malfunction Categories

Failure to pace means no pacing spikes appear on the ECG when they are expected. Causes include lead fracture, battery depletion, oversensing (the device interprets noise as cardiac activity and inhibits pacing), and loose connections. Treatment involves increasing output, applying a magnet (which switches to asynchronous mode and eliminates oversensing), and transcutaneous pacing as a bridge.

Failure to capture means pacing spikes are visible but are not followed by QRS complexes. Causes include lead dislodgment, fibrosis at the lead tip, elevated capture threshold from metabolic derangements or MI, and lead fracture. Treatment involves increasing output, correcting metabolic abnormalities, repositioning the patient, transcutaneous pacing, and cardiology consultation for possible lead revision.

Failure to sense (undersensing) means the device does not detect intrinsic cardiac activity, delivering pacing spikes at inappropriate times. This creates a risk of a pacing stimulus landing on the T-wave (R-on-T phenomenon), which can trigger VT or VF. Causes include lead dislodgment, low intrinsic signal amplitude, and sensitivity set too low. Treatment is to increase sensitivity and consult cardiology.

Oversensing means the device inappropriately senses non-cardiac signals (muscle artifact, electromagnetic interference, T-waves) as cardiac activity, resulting in inappropriate inhibition of pacing and bradycardia. Treatment is magnet application to convert to asynchronous pacing, sensitivity reduction, and cardiology consultation.

Magnet Application

Placing a magnet over a pacemaker generator converts it to asynchronous pacing mode (VOO or DOO), eliminating sensing so the device paces at a fixed rate regardless of intrinsic rhythm. This is useful when oversensing causes inappropriate inhibition. The magnet rate varies by manufacturer and can indicate battery status — a lower magnet rate suggests battery depletion. For ICDs, magnet application disables tachyarrhythmia therapies (shocks) but does not change the pacing mode. A magnet is placed over an ICD when it is delivering inappropriate shocks and must be taped in place rather than briefly applied.

Pacemaker-Mediated Tachycardia (PMT)

PMT occurs in dual-chamber devices when a retrograde P-wave is sensed by the atrial lead, triggering ventricular pacing, which again conducts retrograde — creating a reentrant loop. The rate is usually at the upper tracking limit of the device. Treatment is magnet application to break the loop, followed by reprogramming the upper tracking rate.

Twiddler Syndrome

Twiddler syndrome occurs when a patient manually manipulates the generator in its subcutaneous pocket, causing lead dislodgment. The chest X-ray shows coiled or displaced leads. Surgical revision is required.

Special Scenarios

Bradycardia in Inferior MI

AV block complicates 10 to 20 percent of inferior MIs because the RCA supplies the AV node in 85 percent of patients. The block is usually at the AV nodal level with a junctional escape and narrow QRS. It is often transient, resolving within days. Atropine is frequently effective. Permanent pacing is rarely required.

Lyme Disease and Heart Block

In young patients with unexplained heart block, especially in endemic areas, Lyme disease should be suspected. It can cause any degree of AV block, with third-degree block being the classic association. IV ceftriaxone is the treatment, and the heart block usually resolves with antibiotics. Permanent pacing is rarely needed.

Hyperkalemia-Induced Bradycardia

The ECG progression of hyperkalemia follows a predictable pattern: peaked T-waves, PR prolongation, QRS widening, sine wave pattern, and ultimately asystole. Treatment includes IV calcium (membrane stabilizer), insulin with glucose, bicarbonate, kayexalate or patiromer, and emergent dialysis. Bradycardia is a late and ominous finding in hyperkalemia.

<image>A 12-lead ECG comparison panel showing four types of AV block. Panel A: First-degree AV block with prolonged PR interval (280 ms) with all P-waves conducted. Panel B: Second-degree Type I (Wenckebach) showing progressive PR prolongation with a dropped QRS beat and grouped beating pattern. Panel C: Second-degree Type II (Mobitz II) showing constant PR intervals with sudden non-conducted P-waves and wide QRS complexes. Panel D: Third-degree (complete) heart block showing P-waves and QRS complexes occurring at independent rates with no relationship between them, with a wide QRS ventricular escape rhythm at 35 bpm. Each panel has annotations highlighting the key diagnostic features.</image>

<image>A clinical photograph-style illustration showing the setup for transcutaneous pacing in the ED. The patient is in a resuscitation bay with defibrillator/pacing pads placed in the anterior-posterior configuration. The monitor screen shows pacing spikes followed by wide QRS complexes at a rate of 70 bpm, confirming electrical capture. An inset shows proper pad placement on a torso outline: anterior pad on the left precordium and posterior pad on the left infrascapular region. The defibrillator display shows settings: rate 70 bpm, output 80 mA, mode DEMAND.</image>

<image>An infographic showing the effects of magnet application on pacemakers versus ICDs. The left column shows a pacemaker: magnet converts to asynchronous pacing (VOO/DOO) at a fixed rate, pacing spikes appear regardless of intrinsic rhythm. The right column shows an ICD: magnet disables tachyarrhythmia detection and shock therapy, but pacing mode is NOT changed. Each column includes a rhythm strip demonstrating the effect, clinical indications for magnet use, and key safety considerations.</image>

Clinical Pearls

Atropine is ineffective for infranodal block (Mobitz Type II, complete heart block with wide QRS) — do not waste time with it; go directly to pacing or chronotropic agents. Atropine doses below 0.5 mg can paradoxically worsen bradycardia, so always give at least 0.5 mg. Push-dose epinephrine at 10 to 20 mcg boluses is an excellent bridge to pacing and should be prepared early. Always confirm mechanical capture during transcutaneous pacing — electrical capture alone does not guarantee perfusion. The magnet rule: a magnet on a pacemaker produces asynchronous pacing, while a magnet on an ICD disables shocks only. In 2:1 AV block, Type I versus Type II cannot be determined from a single strip — QRS width is the best clue (narrow favors Type I, wide favors Type II). Always check for reversible causes of bradycardia: medications, hyperkalemia, hypothyroidism, Lyme disease, and inferior MI. Transcutaneous pacing is painful — sedate and provide analgesia, and do not let the urgency of the resuscitation cause you to forget this. Young patients with unexplained heart block in Lyme-endemic areas should receive empiric ceftriaxone and Lyme testing.

References

• Kusumoto FM, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay. Circulation. 2019;140:e273-e326.
• Panchal AR, et al. 2020 AHA Guidelines for CPR and ECC: Adult Bradycardia Algorithm. Circulation. 2020;142(suppl 2).
• Koplan BA, et al. Approach to the patient with bradycardia: diagnosis and management. Circulation. 2009;119:e235-e246.
• Landzberg JS, et al. Temporary cardiac pacing in the emergency department. Ann Emerg Med. 2019;73:638-649.
• Wormser GP, et al. IDSA Guidelines for Lyme Disease. Clin Infect Dis. 2006;43:1089-1134.

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