A Practical Step-by-Step Guide
Based on RECAPEM Article by Dr. Shahriar Lahouti

Treat the perfusion problem

A slow heart rate becomes an emergency when cardiac output is inadequate. Stroke volume may compensate for a lower rate until ischemia, ventricular dysfunction or loss of AV synchrony limits that reserve. Judge the patient by mentation, blood pressure and peripheral perfusion, not the monitor number alone.

Adults with a pulse only. If pulseless, start CPR; pacing must not delay resuscitation. AHA.

Assess and stabilize together

Assess hypotension with poor perfusion, altered consciousness, ischemic chest discomfort and acute heart failure. Is bradycardia causing deterioration?

Call for help; attach ECG monitoring and pacing/defibrillation pads, obtain IV access, support oxygenation/ventilation. Obtain 12-lead ECG without delaying treatment; reassess. AHA.

Read the rhythm without delaying support

Identify P waves, their relationship to QRS complexes, dropped beats, pauses and the escape rhythm. A narrow QRS can accompany nodal disease but does not exclude disease below the AV node. A wide QRS raises concern for distal conduction disease, while also prompting a search for hyperkalemia, drug effects or pre-existing bundle-branch block. ACC/AHA/HRS conduction guidance.

Mobitz II block, complete block with a broad escape complex, recent asystole or ventricular pauses longer than 3 seconds warrant urgent expert assessment even after initial improvement. ERC 2025 ALS.

Use ultrasound to answer a focused question

POCUS may reveal severe ventricular dysfunction, a pericardial effusion with tamponade physiology, or pulmonary congestion. Integrate several views with the examination: isolated IVC size or collapsibility is not a fluid prescription, and a limited scan cannot exclude a dangerous cause of shock. Do not postpone rate support for imaging.

Absent lung sliding alone does not diagnose pneumothorax. If tension pneumothorax is clinically suspected in a deteriorating patient, treatment cannot wait for a technically reassuring scan. International lung-ultrasound recommendations.

Look for a cause you can reverse now

Check oxygenation, temperature, bedside glucose, potassium, renal function and acid–base status. Review beta-blockers, verapamil/diltiazem, digoxin and other relevant exposures, including recent dose changes. Consider ischemia, hypothermia, severe hypothyroidism and intrinsic conduction disease; investigate according to the clinical context.

Think BRASH when renal dysfunction, AV-nodal blockade, hyperkalemia and shock coexist. Potassium and nodal-blocking drugs can reinforce one another, producing marked bradycardia without a massive overdose or classic hyperkalemic ECG. Stop contributing drugs, treat hyperkalemia, restore perfusion and assess volume carefully. Atropine alone may not break this cycle. Evidence for BRASH-specific treatment is largely case-based. Published BRASH case report.

Avoid the shortcuts that miss the cause

Treat causes alongside rate support; bradycardia is not automatically benign.

With suspected inferior infarction, assess leads II, III and aVF and obtain right-sided leads V3R–V4R for RV involvement. Standard V1 is not a replacement. Activate the appropriate reperfusion pathway when indicated. ESC acute coronary syndrome guideline.

Choose rate support and cause-specific treatment

Atropine IV: 1 mg (AHA) or 500 micrograms (ERC/RCUK). Repeat every 3–5 minutes, maximum 3 mg. Follow the locally adopted pathway.

Atropine removes vagal inhibition; it cannot reliably restore a failing distal conduction system. Prepare pacing early. ERC advises against atropine in high-degree AV block with a wide QRS and in heart-transplant recipients. Do not wait through repeated ineffective doses while perfusion deteriorates.

After ineffective atropine: transcutaneous pacing and/or IV infusion of epinephrine 2–10 micrograms/min or dopamine 5–20 micrograms/kg/min, titrated to perfusion (AHA). Infusions, not boluses. ERC additionally lists isoprenaline IV, initially 5 micrograms/min; vasodilation may worsen hypotension.

Hyperkalemic ECG toxicity: give calcium while arranging potassium shifting and removal. UKKA specifies 10 mL of 10% calcium chloride IV over 5 minutes or 30 mL of 10% calcium gluconate IV over 10 minutes; chloride is preferred in resuscitation/peri-arrest settings; use gluconate for other patients with hyperkalemic ECG changes. Check the preparation and IV site, particularly with chloride because extravasation can injure tissue. Reassess the ECG and repeat calcium if toxicity persists according to the protocol. Calcium stabilizes the myocardium; it does not lower potassium. The salts are not interchangeable gram for gram. UKKA July 2026 guidance.

Poisoning: involve the poison centre early. For life-threatening beta-blocker poisoning, vasopressors and, if hypotension persists, high-dose insulin are recommended; glucagon is a reasonable adjunct. For life-threatening calcium-channel blocker poisoning, use vasopressors and high-dose insulin, with calcium as an adjunct; glucagon benefit is uncertain. Insulin requires a full glucose, potassium and dextrose-monitoring protocol. Digoxin-associated life-threatening toxicity calls for digoxin-specific antibody fragments. A generic bradycardia drug list is not an antidote prescription. AHA 2025 toxicology recommendations.

Sustained polymorphic VT needs immediate unsynchronized shock. Magnesium may help recurrent long-QT torsades, not routine bradycardia. Seek expert help for pause-dependent recurrence. AHA.

Prepare pacing early and verify that it works

Transcutaneous pacing is a bridge. Arrange expert support and transvenous pacing when needed. AHA.

Follow the device protocol for pad placement, sensing, rate and output. Increase current until each pacing stimulus produces a ventricular complex. Electrical capture means ventricular depolarization, usually a new broad QRS followed by a T wave. A pacing spike or monitor-derived heart rate alone is insufficient.

Mechanical capture requires a corresponding pulse and evidence of forward flow. Correlate the paced rhythm with palpable pulses, measured blood pressure and perfusion; use a reliable arterial waveform if available. Muscle twitching can mimic a pulse. Recheck capture after movement and whenever the patient worsens. If capture is absent, check connections and pads, adjust output and correct hypoxia or metabolic disturbance while escalating support. Manufacturer guidance on pacing capture.

Titrate analgesia and necessary sedation cautiously with airway/hemodynamic support ready; never delay lifesaving pacing. Sedation can worsen hypotension. Persistent shock requires reassessing capture and causes.

When an implanted pacemaker may be failing

Absent spikes are concerning only when pacing should be occurring; programmed settings and an adequate intrinsic rhythm can explain them. Ventricular spikes without subsequent QRS complexes suggest loss of capture. Spikes at unexpected times may reflect sensing problems, programmed asynchronous pacing or artifact. Obtain urgent interrogation while supporting the patient.

Identify the device before using a magnet. Pacemaker responses vary with model, programming and battery state. A magnet over an ICD generally inhibits tachyarrhythmia therapy without changing bradycardia pacing; it does not reliably fix loss of capture. Maintain external pacing/defibrillation capability and obtain device expertise. AHA device-management statement.

Before leaving the bedside

Confirm a sustained perfusing rhythm, document the response and keep monitoring. Recheck electrolytes and the treatment of reversible causes. Patients with ongoing infusion or pacing needs, recurrent symptoms or high-risk conduction disease need monitored care and a clear escalation plan. A transiently improved heart rate is not the endpoint.

Original educational source: Dr. Shahriar Lahouti’s RECAPEM review.