1. Approach to the Patient with Tachyarrhythmia
The management of tachyarrhythmias in the ACLS framework begins with a single critical decision point: Is the patient hemodynamically stable or unstable? This determines whether the provider has time for a pharmacologic approach or must proceed immediately to electrical cardioversion.
1.1 Signs of Hemodynamic Instability
| Sign | Description |
|---|
| Hypotension | Systolic blood pressure <90 mmHg or signs of shock (altered mental status, cool extremities, mottled skin) |
| Altered mental status | Confusion, obtundation, or syncope directly attributable to the tachyarrhythmia |
| Signs of shock | Poor perfusion, diaphoresis, pallor, delayed capillary refill |
| Ischemic chest pain | Ongoing chest pain or acute coronary syndrome attributable to the rapid rate |
| Acute heart failure | New-onset pulmonary edema, severe dyspnea, hypoxia resulting from the tachyarrhythmia |
Critical principle: If any of these signs are present AND are caused by the tachyarrhythmia, immediate synchronized cardioversion is indicated. Do not delay cardioversion to obtain IV access, administer medications, or perform additional diagnostic studies.
1.2 Systematic Classification of Tachyarrhythmias
| QRS Width | Regularity | Most Likely Rhythms |
|---|
| Narrow (≤120 ms) | Regular | Sinus tachycardia, SVT (AVNRT, AVRT), atrial flutter with fixed block, atrial tachycardia |
| Narrow (≤120 ms) | Irregular | Atrial fibrillation, atrial flutter with variable block, multifocal atrial tachycardia (MAT) |
| Wide (>120 ms) | Regular | Ventricular tachycardia (VT), SVT with aberrant conduction (bundle branch block), SVT with accessory pathway (antidromic AVRT), paced rhythm |
| Wide (>120 ms) | Irregular | Polymorphic VT (torsades de pointes if prolonged QT), atrial fibrillation with aberrant conduction, atrial fibrillation with pre-excitation (WPW) |
2. Unstable Tachyarrhythmia: Synchronized Cardioversion
2.1 Synchronized Cardioversion Procedure
| Step | Action |
|---|
| 1 | Sedate the patient if conscious and time permits (midazolam 1–2 mg IV, etomidate 0.15–0.3 mg/kg IV, ketamine 1–2 mg/kg IV, or propofol 0.5–1 mg/kg IV — choose based on hemodynamic status) |
| 2 | Activate sync mode on the defibrillator (verify sync markers are tracking R waves on the monitor) |
| 3 | Select energy level based on rhythm (see table below) |
| 4 | Clear the patient |
| 5 | Deliver synchronized shock — press and hold the shock button (there is a slight delay as the device waits for the next R wave) |
| 6 | Reassess rhythm and clinical status — if tachyarrhythmia persists, increase energy and repeat |
| 7 | Important: After each synchronized cardioversion, verify that sync mode is still activated — many defibrillators default back to unsynchronized (defibrillation) mode after each shock |
2.2 Synchronized Cardioversion Energy Levels
| Rhythm | Biphasic Energy | Monophasic Energy | Notes |
|---|
| Narrow regular (SVT, atrial flutter) | 50–100 J initial; escalate to 200 J if needed | 100 J initial; escalate to 200–300–360 J | Atrial flutter often converts at low energy (50 J) |
| Narrow irregular (atrial fibrillation) | 120–200 J initial; escalate to higher energy | 200 J initial; escalate to 300–360 J | Atrial fibrillation requires higher energy than flutter |
| Wide regular (monomorphic VT) | 100 J initial; escalate to 200–300–360 J | 200 J initial; escalate to 300–360 J | |
| Wide irregular (polymorphic VT/VF) | Unsynchronized shock (defibrillation): maximum energy (biphasic 120–200 J) | 360 J unsynchronized | Do NOT attempt synchronized cardioversion for irregular wide-complex tachycardia — the device cannot reliably track R waves in a chaotic rhythm; treat as VF with defibrillation |
3. Stable Narrow Complex Tachycardia — Regular
3.1 Differential Diagnosis
| Rhythm | ECG Features | Heart Rate | P Waves |
|---|
| Sinus tachycardia | Upright P waves in lead II; one P before every QRS; gradual onset/offset | Usually 100–160 bpm | Normal morphology; 1:1 relationship |
| AVNRT | No visible P waves (buried in QRS) or pseudo-S in lead II / pseudo-R’ in V1; abrupt onset/offset | 150–250 bpm | Absent or retrograde (inverted in inferior leads) |
| AVRT (orthodromic) | Retrograde P waves after QRS (short RP tachycardia); narrow QRS (unless pre-existing BBB) | 150–250 bpm | Retrograde P after QRS |
| Atrial flutter with fixed block | Sawtooth flutter waves (most visible in II, III, aVF, V1); regular ventricular rate | Atrial 250–350; ventricular typically 150 (2:1 block) or 75 (4:1) | Sawtooth pattern |
| Atrial tachycardia | Abnormal P-wave morphology; may have warm-up/cool-down pattern | 100–250 bpm | Present but abnormal |
3.2 Management Algorithm — Stable Regular Narrow Complex Tachycardia
Step 1: Vagal maneuvers
| Maneuver | Technique | Efficacy |
|---|
| Modified Valsalva (preferred) | Patient blows against closed glottis or into a 10-mL syringe for 15 seconds while semi-recumbent, then immediately repositioned supine with passive leg elevation (REVERT technique) | Conversion rate 43% with modified Valsalva vs 17% with standard Valsalva (REVERT trial) |
| Standard Valsalva | Bearing down for 15–20 seconds | Conversion rate ~17% |
| Carotid sinus massage | Firm pressure over carotid sinus for 5–10 seconds; avoid in patients with carotid bruits, known carotid stenosis, or history of TIA/stroke | Conversion rate 14–27% |
| Ice water to face (diving reflex) | Bag of ice water applied to face for 10–15 seconds; more commonly used in pediatric patients | Variable; activates vagal response |
Step 2: Adenosine (if vagal maneuvers fail)
| Parameter | Detail |
|---|
| Mechanism | Transient AV nodal blockade via A1 adenosine receptor activation; terminates re-entrant tachycardias that use the AV node as part of the circuit (AVNRT, AVRT) |
| First dose | 6 mg rapid IV push, followed immediately by a 20 mL normal saline flush |
| Second dose | 12 mg rapid IV push if first dose fails (may be given after 1–2 minutes) |
| Third dose | 12 mg rapid IV push if second dose fails |
| Administration technique | Use the IV site closest to the heart (antecubital or above); use a stopcock or two-syringe technique for rapid flush; warn the patient about brief chest tightness, flushing, and sense of impending doom (very transient, lasting <30 seconds) |
| Diagnostic value | Adenosine will transiently block AV conduction, unmasking atrial flutter waves, atrial tachycardia P waves, or confirming sinus tachycardia — even if it does not terminate the arrhythmia, the brief AV block is diagnostically informative |
| Dose adjustments | Reduce initial dose to 3 mg in patients taking carbamazepine or dipyridamole (potentiate adenosine effect); reduce dose if giving through a central venous catheter (3 mg initial); increase dose in patients consuming heavy caffeine or taking theophylline (adenosine receptor antagonists) |
| Contraindications | Known severe bronchospasm/active asthma (may trigger bronchospasm); second- or third-degree AV block (without pacemaker); sick sinus syndrome (without pacemaker); known hypersensitivity |
| Caution | Do NOT use adenosine for wide-complex tachycardia of uncertain origin unless expert consultation confirms a supraventricular mechanism; adenosine may cause degeneration of pre-excited atrial fibrillation (WPW + AF) to VF |
Step 3: Calcium channel blockers or beta-blockers (if adenosine fails and rhythm is confirmed supraventricular)
| Drug | Dose | Notes |
|---|
| Diltiazem | 0.25 mg/kg IV over 2 minutes (typical adult dose: 15–20 mg); may repeat at 0.35 mg/kg after 15 minutes if needed; infusion: 5–15 mg/hr | Preferred for rate control; avoid in patients with decompensated heart failure or severe hypotension |
| Verapamil | 2.5–5 mg IV over 2 minutes; may repeat at 5–10 mg after 15–30 minutes; max 20–30 mg | Similar efficacy to diltiazem; more negative inotropic effect |
| Metoprolol | 5 mg IV over 2–5 minutes; may repeat every 5 minutes to a total of 15 mg | Preferred in patients with coronary artery disease; avoid in decompensated heart failure, severe bronchospasm |
| Esmolol | 500 mcg/kg IV bolus over 1 minute, then 50–300 mcg/kg/min infusion | Ultra-short acting; useful when the hemodynamic effect of beta-blockade is uncertain; easily titratable |
Critical safety rule: Do NOT combine IV calcium channel blockers with IV beta-blockers — the combination carries a high risk of severe bradycardia, hypotension, and cardiac arrest.
4. Stable Narrow Complex Tachycardia — Irregular
4.1 Atrial Fibrillation (AF)
Atrial fibrillation with rapid ventricular response is the most common irregular narrow complex tachycardia encountered in the emergency setting.
Rate control vs rhythm control in the acute setting:
| Strategy | Indications | Agents |
|---|
| Rate control | Most patients with AF and rapid ventricular response; target heart rate <110 bpm (or <80 bpm if symptomatic) | Diltiazem, metoprolol, esmolol, amiodarone (if heart failure) |
| Rhythm control (cardioversion) | AF duration <48 hours (or adequately anticoagulated for >3 weeks); hemodynamic instability (immediate synchronized cardioversion); patient preference with appropriate anticoagulation assessment | Electrical cardioversion (120–200 J biphasic); pharmacologic: amiodarone 150 mg IV over 10 min then 1 mg/min x 6 hr; procainamide 20–50 mg/min IV until rhythm converts, hypotension occurs, QRS widens >50%, or total 17 mg/kg given; ibutilide 1 mg IV over 10 min (may repeat once) |
Rate control agent selection:
| Clinical Scenario | Preferred Agent | Dose |
|---|
| No heart failure, no pre-excitation | Diltiazem | 0.25 mg/kg IV, then 5–15 mg/hr infusion |
| No heart failure, coronary disease | Metoprolol | 5 mg IV q5min x3, then 25–50 mg PO q6h |
| Heart failure with reduced EF | Amiodarone | 150 mg IV over 10 min, then 1 mg/min x 6 hr, then 0.5 mg/min x 18 hr |
| Heart failure with reduced EF (alternative) | Digoxin | 0.25–0.5 mg IV, then 0.25 mg IV q6h to max 1.5 mg/24h (slow onset — 60–90 min) |
| Pre-excitation (WPW + AF) | Procainamide | 20–50 mg/min IV (max 17 mg/kg); DO NOT use AV nodal blockers (diltiazem, verapamil, beta-blockers, adenosine, digoxin) — these can accelerate conduction through the accessory pathway and precipitate VF |
4.2 Atrial Flutter
- Atrial flutter with variable AV block produces an irregular ventricular response
- Management is similar to AF: rate control with AV nodal blocking agents; cardioversion is highly effective (atrial flutter has a lower defibrillation threshold than AF)
- Synchronized cardioversion energy: start at 50 J biphasic (often converts with low energy)
- Ibutilide is particularly effective for pharmacologic conversion of atrial flutter
4.3 Multifocal Atrial Tachycardia (MAT)
| Feature | Detail |
|---|
| ECG criteria | ≥3 distinct P-wave morphologies; varying P-P intervals; varying PR intervals; rate >100 bpm |
| Typical clinical context | COPD exacerbation, respiratory failure, hypoxia, hypomagnesemia, theophylline use, critical illness |
| Treatment | Treat the underlying condition (improve oxygenation, correct electrolytes); magnesium sulfate 2 g IV; if rate control needed: non-dihydropyridine calcium channel blockers (if no contraindication); cardioversion is NOT effective for MAT |
5. Stable Wide Complex Tachycardia — Regular
5.1 Key Principle
All regular wide complex tachycardias should be treated as ventricular tachycardia (VT) until proven otherwise. This is because VT is the most common cause of regular wide complex tachycardia (approximately 80% of cases), and treating SVT with aberrancy as VT is generally safe, whereas treating VT with AV nodal blockers can be lethal.
5.2 Differentiating VT from SVT with Aberrancy
| Feature | Favors VT | Favors SVT with Aberrancy |
|---|
| AV dissociation | Present (pathognomonic for VT) | Absent |
| Fusion beats | Present (pathognomonic for VT) | Absent |
| Capture beats | Present (pathognomonic for VT) | Absent |
| QRS duration | >160 ms | 120–160 ms |
| QRS morphology | Does not match typical RBBB or LBBB pattern | Matches typical RBBB or LBBB pattern |
| Concordance in precordial leads | All positive or all negative (positive or negative concordance) | Absent |
| Age and cardiac history | Older patient with structural heart disease | Young patient without cardiac history |
| Brugada criteria | Positive (RS interval >100 ms in any precordial lead; no RS complex in precordial leads) | Negative |
| Response to adenosine | No response (typically) | May terminate or slow rate |
5.3 Management Algorithm — Stable Regular Wide Complex Tachycardia
| Priority | Intervention | Details |
|---|
| First-line | Amiodarone | 150 mg IV over 10 minutes; may repeat; then infusion 1 mg/min x 6 hr, 0.5 mg/min x 18 hr. Preferred for VT in patients with structural heart disease or reduced EF |
| Alternative | Procainamide | 20–50 mg/min IV until: arrhythmia terminates, hypotension develops, QRS widens >50% from baseline, or total dose of 17 mg/kg is reached; then infusion 1–4 mg/min. Preferred by some European guidelines as first-line . Do NOT combine procainamide with amiodarone (excessive QT prolongation) |
| Alternative | Sotalol | 1.5 mg/kg IV over 5 minutes; used in some European protocols; avoid in decompensated heart failure |
| If confirmed SVT with aberrancy | Adenosine | 6 mg → 12 mg → 12 mg rapid IV push; diagnostic and potentially therapeutic; safe to give if rhythm is clearly supraventricular in origin |
| If unstable or refractory | Synchronized cardioversion | 100 J biphasic initial; escalate as needed |
| If pulseless at any time | Defibrillation | Unsynchronized shock at maximum energy; full cardiac arrest algorithm |
5.4 Special Consideration: Torsades de Pointes
Torsades de pointes (TdP) is a polymorphic ventricular tachycardia occurring in the setting of a prolonged QT interval. It appears as a “twisting of the points” pattern on the ECG with progressive change in QRS axis.
| Parameter | Detail |
|---|
| Causes of prolonged QT | Drugs (antiarrhythmics [sotalol, procainamide, ibutilide], antibiotics [fluoroquinolones, azithromycin, TMP-SMX], antipsychotics [haloperidol, droperidol], methadone, ondansetron); electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia); congenital long QT syndrome; hypothermia |
| First-line treatment | Magnesium sulfate 1–2 g IV over 1–2 minutes (push dose during arrest; over 5–15 min if perfusing); highly effective; may repeat once |
| If hemodynamically unstable or pulseless | Defibrillation (unsynchronized, maximum energy — treat as VF); do NOT attempt synchronized cardioversion (rhythm is irregular and polymorphic) |
| Overdrive pacing | Temporary transvenous pacing at a rate faster than the intrinsic rate (typically 90–110 bpm) shortens the QT interval and suppresses the arrhythmia; definitive therapy for recurrent TdP |
| Isoproterenol | 2–10 mcg/min IV infusion; increases heart rate and shortens QT interval; bridge to transvenous pacing; use with caution (may exacerbate myocardial ischemia) |
| Correct electrolytes | Target potassium >4.0 mEq/L; magnesium >2.0 mg/dL; correct hypocalcemia |
| Avoid | All QT-prolonging medications; class IA and class III antiarrhythmics (procainamide, amiodarone, sotalol, ibutilide) — these agents will worsen TdP |
6. Stable Wide Complex Tachycardia — Irregular
6.1 Differential Diagnosis
| Rhythm | Features | Management |
|---|
| Polymorphic VT (including torsades de pointes) | Continuously changing QRS morphology and axis; “twisting of the points” if prolonged QT; very rapid rate | If pulseless: defibrillation (unsynchronized maximum energy); if perfusing with prolonged QT: magnesium 1–2 g IV; if perfusing without prolonged QT (ischemic polymorphic VT): treat as VF/pVT if decompensates; amiodarone; beta-blockers; emergent angiography |
| Atrial fibrillation with pre-excitation (WPW + AF) | Irregularly irregular; very rapid rate (often >200 bpm); varying QRS width (some beats narrow, some wide); delta waves in wide beats | Procainamide 20–50 mg/min IV; DO NOT use AV nodal blockers (adenosine, diltiazem, verapamil, beta-blockers, digoxin — these block AV node while allowing uninhibited conduction through accessory pathway → VF); if unstable: synchronized cardioversion |
| Atrial fibrillation with aberrant conduction (BBB) | Irregularly irregular; wide QRS consistent with RBBB or LBBB morphology; rate typically <200 bpm | Rate control with standard AF agents (diltiazem, metoprolol); distinguish from pre-excited AF by absence of delta waves and consistent BBB pattern |
7. Bradyarrhythmia Management
Bradycardia is defined as a heart rate <60 bpm. However, treatment is only indicated when the bradycardia is causing symptoms or hemodynamic compromise. Athletes, well-conditioned individuals, and patients on rate-controlling medications may have bradycardia that is physiologic and requires no intervention.
7.1 Signs and Symptoms of Symptomatic Bradycardia
| Category | Manifestations |
|---|
| Hemodynamic compromise | Hypotension (SBP <90 mmHg), shock, syncope or near-syncope |
| Altered mental status | Confusion, dizziness, lightheadedness |
| Signs of poor perfusion | Diaphoresis, pallor, cool extremities, delayed capillary refill |
| Ischemia | Chest pain, ST-segment changes attributable to the slow rate |
| Heart failure | Dyspnea, pulmonary edema |
7.2 Bradycardia Algorithm — Step by Step
| Step | Action | Details |
|---|
| 1 | Assess ABCs | Maintain airway, assist breathing, monitor vital signs, obtain 12-lead ECG, establish IV access |
| 2 | Identify and treat reversible causes | Hypoxia (provide O2), increased vagal tone (remove stimulus), drugs (review medications: beta-blockers, calcium channel blockers, digoxin, clonidine, amiodarone), hyperkalemia, hypothermia, acute MI (especially inferior STEMI — vagal mediated) |
| 3 | Is bradycardia causing symptoms? | If NO: monitor, observe. If YES: proceed to treatment |
| 4 | Atropine | First-line pharmacotherapy for symptomatic bradycardia |
| 5 | If atropine ineffective | Transcutaneous pacing, dopamine infusion, or epinephrine infusion (may use concurrently) |
| 6 | Prepare for transvenous pacing | If transcutaneous pacing fails or is needed for extended period; consult cardiology |
7.3 Atropine
| Parameter | Detail |
|---|
| Mechanism | Parasympatholytic (anticholinergic); blocks vagal input to the SA node and AV node, increasing heart rate and improving AV conduction |
| Dose | 1 mg IV every 3–5 minutes |
| Maximum dose | 3 mg total (0.04 mg/kg); doses below 0.5 mg may paradoxically worsen bradycardia (central vagal stimulation) |
| Effective for | Sinus bradycardia, junctional bradycardia, symptomatic first-degree AV block, symptomatic second-degree AV block type I (Wenckebach) |
| Ineffective/unreliable for | Second-degree AV block type II (Mobitz II); third-degree (complete) AV block with wide QRS escape; denervated transplanted hearts (no vagal innervation) |
| Key principle | If the bradycardia is due to Mobitz II or third-degree AV block, do NOT rely on atropine — prepare for pacing immediately |
7.4 Transcutaneous Pacing
| Parameter | Detail |
|---|
| Indications | Symptomatic bradycardia unresponsive to atropine; Mobitz type II second-degree AV block; complete (third-degree) AV block; post-cardiac arrest bradycardia |
| Pad placement | Anterior-posterior preferred (anterior pad over left precordium, posterior pad on left posterior chest between spine and scapula); anterior-lateral is acceptable |
| Initial settings | Rate: 60–80 bpm; output (current): start at maximum and decrease until capture is achieved (threshold testing); alternatively, start at minimum and increase until capture |
| Confirming capture | Electrical capture: each pacer spike is followed by a wide QRS complex and T wave on the monitor; mechanical capture: palpable pulse corresponding to each paced beat; do NOT rely solely on electrical capture — verify a pulse |
| Patient comfort | Transcutaneous pacing is painful in conscious patients; provide sedation and analgesia (fentanyl 25–100 mcg IV, midazolam 1–2 mg IV, or procedural sedation with ketamine or propofol if needed) |
| Limitations | May not achieve capture in patients with extensive myocardial infarction, cardiac tamponade, tension pneumothorax, or severe hypothermia; bridge to transvenous pacing — not a long-term solution |
7.5 Dopamine Infusion
| Parameter | Detail |
|---|
| Mechanism | At chronotropic doses (5–20 mcg/kg/min), stimulates beta-1 adrenergic receptors → increased heart rate and contractility |
| Dose | 5–20 mcg/kg/min IV infusion; titrate to heart rate and blood pressure |
| Role | Alternative or bridge when atropine is ineffective and transcutaneous pacing is unavailable or not capturing; may be used concurrently with pacing |
| Cautions | May cause tachyarrhythmias at high doses; increases myocardial oxygen demand; may cause tissue necrosis if extravasation occurs (administer through large-bore IV or central line; phentolamine for extravasation) |
7.6 Epinephrine Infusion
| Parameter | Detail |
|---|
| Mechanism | Beta-1 and beta-2 adrenergic agonist; increases heart rate, contractility, and blood pressure |
| Dose | 2–10 mcg/min IV infusion; titrate to desired heart rate and blood pressure |
| Role | Alternative to dopamine when atropine fails; particularly useful in patients with concurrent hypotension; may be used as bridge to transvenous pacing |
| Preparation | 1 mg epinephrine in 250 mL NS = 4 mcg/mL (or 1 mg in 500 mL NS = 2 mcg/mL); titrate drip rate to desired effect |
7.7 Isoproterenol
| Parameter | Detail |
|---|
| Mechanism | Pure beta-adrenergic agonist (beta-1 and beta-2); potent chronotrope and inotrope |
| Dose | 2–10 mcg/min IV infusion |
| Role | Second-line agent for refractory bradycardia; particularly useful for torsades de pointes (overdrive suppression); also used in beta-blocker overdose-related bradycardia; heart transplant recipients (denervated hearts unresponsive to atropine) |
| Cautions | Potent vasodilator (beta-2 effect) → may cause hypotension; increases myocardial oxygen demand; avoid in ischemic heart disease |
7.8 Transvenous Pacing — Indications
Transvenous pacing is the definitive temporary pacing modality and should be arranged when:
- Transcutaneous pacing fails to achieve capture
- Prolonged pacing is anticipated (transcutaneous pacing is only a temporary bridge)
- Mobitz type II second-degree AV block
- Complete (third-degree) AV block
- Symptomatic bifascicular or trifascicular block
- New bundle branch block in the setting of acute MI
- Bradycardia-dependent tachyarrhythmias (e.g., torsades de pointes requiring overdrive pacing)
- Post-cardiac surgery or post-catheterization bradycardia unresponsive to pharmacotherapy
- Alternating bundle branch block (RBBB alternating with LBBB)
8. Specific Bradycardia Etiologies and Considerations
8.1 AV Block Classification and Management Summary
| AV Block Type | ECG Features | Symptom Likelihood | Atropine Response | Pacing Needed |
|---|
| First-degree | Prolonged PR interval (>200 ms); every P wave followed by QRS | Usually asymptomatic | Yes (if symptomatic) | Rarely |
| Second-degree Type I (Wenckebach) | Progressive PR prolongation → dropped QRS; grouped beating; narrow QRS escape | Sometimes symptomatic | Yes (usually effective) | Sometimes |
| Second-degree Type II (Mobitz II) | Fixed PR interval → sudden dropped QRS; often wide QRS escape | Often symptomatic | Unreliable — may worsen | Yes — high risk of progression to complete block |
| 2:1 AV block | Every other P wave conducted; may be type I or type II depending on QRS width and clinical context | Variable | Variable | Depends on type (wide QRS → likely type II → pacing; narrow QRS → may be type I → trial of atropine) |
| Third-degree (complete) | No relationship between P waves and QRS complexes; ventricular escape rhythm | Usually symptomatic | Unreliable if infranodal (wide QRS escape) | Yes — always |
| High-degree AV block | Multiple consecutive P waves not conducted (3:1, 4:1, or higher ratios) | Usually symptomatic | Unreliable | Yes |
8.2 Bradycardia in Acute Myocardial Infarction
| MI Location | Typical Arrhythmia | Mechanism | Management |
|---|
| Inferior MI | Sinus bradycardia, first-degree AV block, Wenckebach | Increased vagal tone; AV nodal ischemia (RCA supplies AV node) | Usually transient; responds to atropine; pacing rarely needed; treat with reperfusion |
| Anterior MI | Mobitz II, complete heart block with wide QRS escape, bundle branch blocks | Direct His-Purkinje damage (LAD supplies interventricular septum) | High risk; unreliable response to atropine; transcutaneous/transvenous pacing indicated; urgent reperfusion |
| Right ventricular MI | Bradycardia with hypotension | RV failure + vagal tone | Volume resuscitation (avoid nitroglycerin and diuretics); atropine; pacing if needed; avoid agents that reduce preload |
9. Cardioversion and Defibrillation — Quick Reference Summary
9.1 Complete Energy Level Reference
| Rhythm | Synchronized? | Biphasic Energy | Monophasic Energy |
|---|
| Narrow regular SVT / atrial flutter | Yes | 50–100 J → escalate | 100 J → escalate to 200–360 J |
| Atrial fibrillation | Yes | 120–200 J → escalate | 200 J → escalate to 300–360 J |
| Monomorphic VT (with pulse) | Yes | 100 J → escalate to 200–300–360 J | 200 J → escalate to 300–360 J |
| Polymorphic VT / VF / pulseless VT | No (defibrillation) | 120–200 J (device-specific); use maximum energy if uncertain | 360 J |
| Wide irregular tachycardia (uncertain) | No (treat as VF) | Maximum energy | 360 J |
References