7. Arrhythmias (Tachyarrhythmias, Bradyarrhythmias, Cardioversion/Defibrillation)

Quick Recap

Cardiovascular System, Protocol 8/12. Covers tachyarrhythmias, bradyarrhythmias, and defibrillation/cardioversion technique. Post-cardiac-arrest management has its own dedicated protocol under Neurology.

1. Definition & Initial Framework

Arrhythmias disrupt cardiac output (CO = HR x SV) by impairing rate and/or stroke volume. Presentation spans: asymptomatic ECG/telemetry finding -> symptoms without hemodynamic instability (palpitations, dyspnea, syncope, chest pain) -> hemodynamic instability in a conscious patient -> cardiac arrest.

Universal first steps regardless of rhythm: airway/breathing support, continuous rhythm/BP/SpO2 monitoring, adequate IV access, adequate support personnel. Use 12-lead ECG when possible, but initial treatment can be based on the bedside monitor/defibrillator rhythm if the patient is unstable — do not delay life-saving therapy for a formal 12-lead.

Core triage question: is the patient hemodynamically stable? Unstable (hypotension, altered mentation, ischemic chest pain, acute heart failure signs) -> electrical therapy first, regardless of rhythm mechanism. Stable -> time for pharmacologic therapy and specific rhythm diagnosis.

2. Cardioversion vs Defibrillation

Defibrillation: unsynchronized shock delivered at any point in the cardiac cycle; terminates VF and pulseless/unstable VT by globally depolarizing and "stunning" the heart, allowing the native pacemaker to resume.

Cardioversion: shock SYNCHRONIZED to the QRS complex, avoiding delivery during the vulnerable period (~60-80ms before to 20-30ms after the T wave peak) to prevent inducing VF. Terminates reentrant arrhythmias with an organized rhythm (AF, atrial flutter, AVNRT, AVRT, stable monomorphic VT).

Energy levels (biphasic preferred where available):

Rhythms responsive to electrical therapy: SVT types (AVNRT, AVRT, sinoatrial nodal reentry), AF, atrial flutter (cardioversion); pulseless VT, VF, unstable polymorphic VT, monomorphic VT with pulse (defibrillation).

Rhythms NOT responsive to electrical therapy (automaticity/triggered activity, not reentry): sinus tachycardia, focal atrial tachycardia, junctional tachycardia, idiopathic monomorphic VT, accelerated idioventricular rhythm — shocking these is ineffective and potentially harmful; treat the underlying cause or use pharmacologic/rate-control therapy instead.

Procedure essentials: confirm synchronized mode is engaged for cardioversion (most defibrillators default to unsynchronized — must be reset before EACH shock); pad placement anterolateral (most common) or anteroposterior (may be more successful for AF with monophasic shock); sedation for elective/stable cardioversion (propofol preferred for rapid recovery, or midazolam for conscious sedation) — NOT required for unstable VT/VF with impending arrest.

Anticoagulation for AF/flutter cardioversion: required if arrhythmia duration >48-72h or unknown duration — either 3-4 weeks of anticoagulation pre-cardioversion (elective) or TEE to exclude LA thrombus, and anticoagulation continued >=4 weeks post-cardioversion regardless of approach, given the risk of thromboembolism from restored atrial mechanical contraction.

Caution/relative contraindications: digitalis toxicity, significant electrolyte imbalance (increased VF/VT risk post-shock), inadequately anticoagulated chronic AF/flutter >48h.

3. Supraventricular Tachycardias (SVT)

AVNRT (most common PSVT in adults): reentrant loop within the AV node, rate 120-250, narrow QRS (absent aberrancy), P waves often not visible (buried in QRS) or appear as "pseudo-R" in V1 / "pseudo-S" in lead II. Not disease-specific, more common in women.

Accessory pathway-mediated (WPW): delta wave + short PR interval on baseline ECG = manifest pathway; orthodromic reentrant tachycardia (antegrade via AV node, retrograde via pathway) = narrow QRS; antidromic (reverse direction) = wide QRS. Preexcited atrial fibrillation via an accessory pathway is dangerous — the pathway's short refractory period allows very rapid ventricular rates (up to 300/min), risking hemodynamic collapse or degeneration to VF.

Treatment of typical PSVT:

1. Vagal maneuvers (Valsalva, carotid massage, cold water face immersion)
2. Adenosine 6mg rapid IV push (half-life ~10 sec, always flush immediately) -> if ineffective, 12mg after 1-2 min -> third dose 12-18mg if needed. Side effects: flushing, headache, transient AV block, brief asystole (expected/self-limited)
3. If adenosine fails: AV nodal blocking agents — metoprolol 2.5-5mg IV q5min (max 15mg/15min), diltiazem 0.25mg/kg IV over 2min (repeat 0.35mg/kg after 15min if needed), or digoxin 0.25-0.5mg IV (reduce 50% in renal failure)

CRITICAL: preexcited AF/flutter with WPW must NOT be treated with AV nodal blockers (adenosine, beta-blockers, CCBs, digoxin) — blocking the AV node while leaving the accessory pathway unblocked can paradoxically increase conduction through the pathway and precipitate VF. Treat with synchronized cardioversion (if unstable) or Class IA/IC/III drugs (procainamide, flecainide, amiodarone) which slow conduction through the accessory pathway itself.

4. Atrial Fibrillation and Atrial Flutter

Atrial flutter: macro-reentrant circuit typically dependent on the cavotricuspid isthmus, atrial rate ~300/min, classic "sawtooth" flutter waves (narrow, negative in inferior leads II/III/aVF); ventricular rate usually 150/min (2:1 block) or ~100/min (3:1 block); can be regular or irregular with variable block. Untreated flutter may degenerate to AF.

Initial management (both AF and flutter): identify and treat precipitating factors (electrolyte derangement, hyperthyroidism, infection, ischemia, post-surgical, pulmonary disease); preoperative beta-blockade reduces postoperative AF/flutter incidence.

Rate vs rhythm control, thromboembolic risk assessment (Table):

Score >=2 (>=3 if female): anticoagulation benefit for stroke risk reduction.

Each point increases major bleeding risk — used alongside CHA2DS2-VASc to individualize anticoagulation decisions, not as an automatic exclusion.

Anticoagulation approach: acute thromboembolic risk management typically starts with IV heparin; long-term with a NOAC (apixaban, rivaroxaban, edoxaban, dabigatran) UNLESS mechanical valve or moderate-severe mitral stenosis, in which case warfarin (goal INR >2) with heparin bridge is required instead.

Refractory to cardioversion/pharmacotherapy: consider electrophysiology consultation for ablation.

5. Ventricular Arrhythmias

Wide-complex tachycardia of uncertain origin: ALWAYS assume VT and treat accordingly until proven otherwise — treating presumed SVT-with-aberrancy as SVT when it is actually VT can be harmful (e.g., verapamil in true VT can cause hemodynamic collapse).

Non-sustained VT (NSVT): may be idiopathic or occur with acute ischemia/HF. Do NOT give direct pharmacologic antiarrhythmic treatment (lidocaine/amiodarone) for NSVT in the setting of active ischemia/infarct — treat the underlying ischemia instead. In the absence of ischemia/structural heart disease, NSVT is often asymptomatic with limited prognostic significance; symptomatic NSVT can be treated with beta-blockers for symptom relief.

Sustained VT:

• With pulse, hemodynamically stable: synchronized cardioversion (with sedation) OR antiarrhythmic drug (amiodarone or lidocaine) if well-tolerated
• With pulse, hemodynamically unstable, OR pulseless (monomorphic or polymorphic): immediate asynchronous defibrillation, followed by antiarrhythmic drugs as needed
• Once stabilized, consider VT ablation for long-term management/prevention of recurrence and further defibrillation therapy
• VT/VF storm: defined as >=3 episodes of sustained VT/VF or appropriate ICD shocks in a short period — a distinct, refractory electrical emergency requiring escalating antiarrhythmic therapy, sedation, possible sympathetic blockade (e.g., stellate ganglion block), and urgent EP involvement

Torsades de pointes: polymorphic VT associated with QT prolongation.

• Sustained with hemodynamic collapse: asynchronous cardioversion/defibrillation
• Core treatment: correct underlying electrolyte abnormalities (magnesium, potassium) and STOP all QT-prolonging drugs — recurrence is likely if the precipitant is not eliminated
• Magnesium sulfate 1-2g IV push over 5-20 min is first-line pharmacotherapy even with normal serum magnesium
• Lidocaine or phenytoin may be suppressive adjuncts (do NOT use other QT-prolonging antiarrhythmics like amiodarone/procainamide/sotalol, which can worsen torsades)

6. ACLS Pharmacotherapy Reference Table

7. Bradyarrhythmias

Assess for hemodynamic significance (hypotension, altered mentation, ischemic symptoms, acute HF signs) before treating asymptomatic bradycardia. Atropine 0.5-1mg IV q3-5min (up to 0.04mg/kg/24h) for symptomatic bradycardia; if refractory, transcutaneous pacing, dopamine, or epinephrine infusion as a bridge to transvenous pacing. Identify reversible causes: hyperkalemia, hypothyroidism, beta-blocker/CCB/digoxin toxicity, high vagal tone, inferior MI (AV nodal ischemia), Lyme disease.

8. Consultation Matrix

9. Monitoring Framework

Continuous telemetry, serial ECG for QT monitoring if on QT-prolonging drugs, electrolyte trend (K+, Mg2+, Ca2+) especially with diuretics/renal impairment, post-cardioversion rhythm and hemodynamic reassessment.

10. Complications

Thromboembolism/stroke (AF/flutter cardioversion without adequate anticoagulation), VF induction from unsynchronized shock delivered during vulnerable period (avoided by correct sync mode use), torsades recurrence if QT-prolonging drug not stopped, hemodynamic collapse from AV nodal blockade in preexcited AF. Prevention: correct device mode selection, anticoagulation protocol adherence, avoiding AV nodal blockers in WPW-associated preexcited AF, electrolyte correction before/during antiarrhythmic therapy. Rescue: repeat cardioversion/defibrillation, escalating antiarrhythmic therapy, mechanical support/ECPR for refractory arrest.

11. Documentation & Medicolegal Checklist

12. Key Guidelines

2017 AHA/ACC/HRS Guideline for Management of Patients with Ventricular Arrhythmias and Prevention of Sudden Cardiac Death (Al-Khatib et al., Circulation 2018); AHA ACLS Guidelines (pharmacotherapy dosing reference).

13. Controversies

Optimal timing of anticoagulation relative to cardioversion (3-4 week pre-treatment vs TEE-guided early cardioversion) involves a genuine tradeoff between bleeding exposure duration and time-to-rhythm-control, without a single universally preferred strategy. Rate vs rhythm control strategy for AF in critically ill patients specifically is less well-studied than in the outpatient AFFIRM/RACE-trial population this evidence is extrapolated from. Anteroposterior vs anterolateral pad placement superiority for AF cardioversion specifically remains only modestly supported by monophasic-shock-era data, with less clarity for modern biphasic devices.

14. References

1. Wiener PC, Sodhi SS, Cooper DH. Cardiac Arrhythmias and Conduction Abnormalities. Washington Manual of Critical Care, 4th ed, 2025 (Ch. 21).
2. Chawla R, Bali RK, Jain P. Defibrillation and Cardioversion. ICU Protocols: A Step-wise Approach, 2nd ed. Springer; 2020 (Ch. 42).
3. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Circulation. 2018;138:e272-e391.