Tachycardia treat r
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Here is a comprehensive overview of tachycardia treatment, organized by rhythm type and patient stability.
Tachycardia Treatment
Step 1 - Assess Hemodynamic Stability
The first and most important question in any tachycardia is: Is the patient stable or unstable?
Signs of instability (any one warrants immediate action):
- Hypotension / shock
- Altered mental status
- Chest pain / myocardial ischemia
- Acute heart failure / pulmonary edema
If unstable → Immediate synchronized electrical cardioversion (for all sustained tachycardias except sinus tachycardia). Use procedural sedation/analgesia if the clinical situation allows.
Step 2 - Classify the Rhythm: Narrow vs. Wide Complex
NARROW-COMPLEX TACHYCARDIA (QRS < 120 ms)
| Rhythm | First-line Treatment | Notes |
|---|---|---|
| Sinus tachycardia | Treat underlying cause | Never cardiovert; it is compensatory |
| Multifocal atrial tachycardia (MAT) | Treat underlying cause (usually COPD, hypomagnesemia) | Verapamil or metoprolol for rate control if needed |
| AVNRT / AVRT (Paroxysmal SVT) | Vagal maneuvers → Adenosine → CCB or beta-blocker | See below for details |
| Atrial fibrillation / flutter | Rate control (beta-blocker, diltiazem) or rhythm control + anticoagulation | Depends on duration and clinical context |
Paroxysmal SVT (AVNRT / AVRT) - Stable Management
Step-up approach:
-
Vagal maneuvers (first line, no drug risk):
- Modified Valsalva: Blow into 10-mL syringe for 15 s, then lie flat with legs elevated 45° for 15 s - more effective than standard Valsalva
- Carotid sinus massage: 20 s, only one side at a time, listen for bruit first
- Ice-water diving reflex (more effective in infants)
-
Adenosine (blocks AV node; drug of choice when vagal maneuvers fail):
- First dose: 6 mg IV rapid push (central or antecubital vein)
- If no response: 12 mg IV, can repeat once
- Very short half-life (~10 s); transient chest pain, dyspnea, and anxiety are common
- Contraindicated in cardiac transplant patients (hypersensitivity risk)
- Use cautiously in WPW - can precipitate AF
- May unmask underlying atrial flutter or AF
-
IV Beta-blockers (esmolol, metoprolol) or calcium channel blockers (verapamil, diltiazem):
- Slow AV nodal conduction; effective for conversion and rate control
- Risk of hypotension; longer duration of action than adenosine
- Contraindicated in preexcited AF (WPW + AF) - may dangerously accelerate conduction over accessory pathway
-
Synchronized cardioversion if drugs fail or patient becomes unstable
WPW / Preexcited AF (wide, irregular): Avoid ALL AV nodal blockers (adenosine, verapamil, diltiazem, beta-blockers, amiodarone IV). Use electrical cardioversion, IV procainamide, or ibutilide instead.
WIDE-COMPLEX TACHYCARDIA (QRS ≥ 120 ms)
Treat as ventricular tachycardia (VT) until proven otherwise.
If unstable → Immediate synchronized cardioversion
If stable, pharmacologic options (in order of preference):
| Drug | Dose | Notes |
|---|---|---|
| Procainamide | 20-50 mg/min IV infusion (max 17 mg/kg); slow infusion to avoid hypotension | Drug of choice for stable VT and WPW; superior to amiodarone and lidocaine for conversion |
| Amiodarone | 150 mg IV over 10 min, then 1 mg/min infusion | Broad-spectrum; used in refractory VT or when procainamide is unavailable |
| Lidocaine | 1-1.5 mg/kg IV bolus; repeat 0.5-0.75 mg/kg q5-10 min | Alternative to amiodarone; also used in pulseless VT/VF if amiodarone unavailable |
| Magnesium | 2 g IV over 10-20 min | Specifically for torsades de pointes or VT with QT prolongation |
VENTRICULAR FIBRILLATION / Pulseless VT
This is a cardiac arrest rhythm - not tachycardia management per se:
- Immediate defibrillation (unsynchronized shock)
- CPR between shocks
- Epinephrine 1 mg IV q3-5 min
- Amiodarone 300 mg IV after 3rd shock (then 150 mg); lidocaine if amiodarone unavailable
TORSADES DE POINTES (Polymorphic VT + prolonged QTc)
- Remove offending drug (QT-prolonging medications)
- Correct electrolytes (K⁺, Mg²⁺)
- IV Magnesium sulfate 2 g (even if Mg²⁺ is normal)
- Definitive treatment: Ventricular pacing to overdrive the arrhythmia and shorten QT
- Consider isoproterenol to increase heart rate and shorten QT until pacing is available
Summary: Drug Quick Reference
| Drug | Class | Main Use |
|---|---|---|
| Adenosine | AV nodal blocker | SVT (AVNRT, AVRT) |
| Verapamil / Diltiazem | Calcium channel blocker | SVT, AF/flutter rate control |
| Metoprolol / Esmolol | Beta-blocker | SVT, AF/flutter rate control |
| Procainamide | Class IA | Stable VT, WPW + AF |
| Amiodarone | Class III | VT/VF, refractory SVT |
| Lidocaine | Class IB | VT alternative |
| Magnesium | Electrolyte | Torsades de pointes |
| Ibutilide | Class III | AF/flutter cardioversion, WPW + AF |
Long-term / Definitive Management
- Catheter ablation is now the preferred definitive therapy for recurrent AVNRT, AVRT, atrial flutter, and many forms of VT
- Antiarrhythmic drugs (oral flecainide, propafenone, sotalol, amiodarone) for recurrence prevention when ablation is declined or not feasible
- ICD (implantable cardioverter-defibrillator) for high-risk VT/VF (structural heart disease, reduced EF, prior cardiac arrest)
Sources: Tintinalli's Emergency Medicine, Harrison's Principles of Internal Medicine 22E (2025), Fuster and Hurst's The Heart 15th Edition, Lippincott Illustrated Reviews: Pharmacology
Afib
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Here is a thorough breakdown of atrial fibrillation (AF) - from classification through management.
Atrial Fibrillation (AF)
Definition & ECG Features
- Disorganized atrial electrical activity - no distinct P waves; replaced by irregular fibrillatory waves
- Irregularly irregular ventricular response (hallmark)
- Narrow QRS (unless aberrant conduction or WPW)
- Ventricular rate typically 100-160 bpm if uncontrolled
Classification
| Type | Definition |
|---|---|
| Paroxysmal | Self-terminating within 7 days (often within 24-48 h) |
| Persistent | Continuous >7 days, requires intervention to terminate |
| Long-standing persistent | Continuous >1 year |
| Permanent | Patient and clinician have accepted ongoing AF; no further rhythm control attempts |
Up to 70% of otherwise healthy ED patients with acute-onset AF spontaneously convert within 48-72 hours.
Common Causes / Risk Factors
- Hypertension (most common)
- Valvular heart disease (esp. mitral stenosis)
- Heart failure
- Coronary artery disease / acute MI
- Hyperthyroidism
- Alcohol ("holiday heart"), obesity, sleep apnea
- Pulmonary embolism, pneumonia (secondary AF)
- Increasing age
Complications
- Stroke/thromboembolism - ~5% annual risk on average; up to 13%/yr with prior stroke/TIA
- Heart failure - loss of atrial kick; particularly problematic in diastolic dysfunction
- Tachycardia-induced cardiomyopathy (with prolonged uncontrolled rate)
Step 1 - Is the Patient Stable?
Unstable (hypotension, ischemia, severe HF) → Immediate synchronized DC cardioversion
Stable → Proceed to rate vs. rhythm control decision + anticoagulation
Step 2 - Rate Control vs. Rhythm Control
Key Principle
Studies (AFFIRM, RACE trials) showed rate control and rhythm control have similar mortality and stroke outcomes in most patients. Stroke risk persists even in rhythm control; anticoagulation decisions are based on risk factors regardless of strategy.
Rate Control (preferred for most patients, especially minimally symptomatic)
Goal: Resting heart rate < 100-110 bpm
| Drug | Notes |
|---|---|
| Diltiazem IV/PO | First-line for acute rate control; more effective than metoprolol acutely |
| Metoprolol / Esmolol | Good option; esmolol useful when titration needed (short-acting) |
| Verapamil | Effective; avoid combination with beta-blockers (risk of bradycardia/HF) |
| Digoxin | Second-line; poor rate control during activity/exercise; useful in HFrEF |
| Amiodarone | Last resort for rate control when others fail |
| AV node ablation + pacemaker | When pharmacologic rate control fails or is not tolerated |
Avoid beta-blockers and non-DHP calcium channel blockers in decompensated heart failure.
Rhythm Control (for symptomatic patients, first episode, exercise intolerance, or younger patients)
Cardioversion options:
| Method | Notes |
|---|---|
| DC cardioversion | 150-200 J biphasic; highly effective; more likely to succeed if AF <48 h and atria not dilated |
| Ibutilide IV | Highest pharmacologic conversion rate; avoid with hypokalemia, prolonged QT, or history of HF (torsades risk for 4-6 h) |
| Flecainide / Propafenone | "Pill in the pocket" for paroxysmal AF; avoid in structural heart disease |
| Procainamide, Amiodarone | Broader use; amiodarone also for rate control |
| Dofetilide | Requires inpatient initiation due to QT monitoring |
"Pill in the pocket" (flecainide or propafenone taken at AF onset by the patient at home) is an option in selected outpatients with paroxysmal AF and no structural heart disease.
Step 3 - Anticoagulation for Cardioversion
The main risk is that AF >48 h causes atrial thrombus (usually in left atrial appendage). Cardioversion can dislodge this clot.
| Scenario | Approach |
|---|---|
| Unstable - immediate cardioversion | Don't delay; start IV heparin as soon as possible; anticoagulate ≥4 weeks post-cardioversion |
| Stable, AF <48 h | Cardioversion with concurrent anticoagulation (UFH, LMWH, or DOAC); then 4 weeks anticoagulation |
| Stable, AF ≥48 h or unknown duration | Option A: Anticoagulate for 3 weeks before cardioversion, then 4 weeks after. Option B: TEE to exclude LAA thrombus → if no thrombus, cardiovert with heparin → 4 weeks anticoagulation |
Step 4 - Long-Term Stroke Prevention (Anticoagulation)
CHA₂DS₂-VASc Score
| Risk Factor | Points |
|---|---|
| C - Congestive heart failure | 1 |
| H - Hypertension | 1 |
| A₂ - Age ≥75 | 2 |
| D - Diabetes mellitus | 1 |
| S₂ - Stroke / TIA / thromboembolism | 2 |
| V - Vascular disease (MI, PAD, aortic plaque) | 1 |
| A - Age 65-74 | 1 |
| Sc - Sex category (female) | 1 |
| Max | 9 |
Annual stroke risk by score:
- Score 0: 0.2% (no anticoagulation)
- Score 1: 0.6% (anticoagulation optional in males; not in females where 1 point = female sex only)
- Score ≥2: >2.2% → anticoagulation recommended
Anticoagulation decisions apply to both rate control and rhythm control strategies - achieving sinus rhythm does NOT eliminate stroke risk.
Anticoagulation Options
| Drug | Type | Notes |
|---|---|---|
| Apixaban | DOAC (factor Xa inhibitor) | Preferred in most; reduced dosing if ≥2 of: age ≥80, weight ≤60 kg, creatinine ≥1.5 |
| Rivaroxaban | DOAC (factor Xa inhibitor) | Once daily with evening meal |
| Dabigatran | DOAC (direct thrombin inhibitor) | Avoid if CrCl <15 mL/min |
| Edoxaban | DOAC (factor Xa inhibitor) | |
| Warfarin | VKA | Target INR 2.0-3.0; required for mechanical valves and rheumatic mitral stenosis (INR 2.5-3.5) |
DOACs are first-line for nonvalvular AF - easier dosing, no INR monitoring, fewer drug/food interactions. Reversal of DOAC bleeding requires specific monoclonal antibodies (idarucizumab for dabigatran; andexanet alfa for factor Xa inhibitors). Vitamin K, FFP, and PCC are generally ineffective for DOACs.
HASBLED Score (Bleeding Risk)
| Factor | Points |
|---|---|
| Hypertension (SBP >160) | 1 |
| Abnormal renal function | 1 |
| Abnormal liver function | 1 |
| Stroke history | 1 |
| Bleeding history or predisposition | 1 |
| Labile INR | 1 |
| Elderly (age >65) | 1 |
| Drugs (antiplatelets/NSAIDs) or alcohol | 1-2 |
Score ≥3 = high bleeding risk; use to identify modifiable bleeding risk factors, not to withhold anticoagulation in high-stroke-risk patients.
Long-Term Rhythm Control / Procedural Options
- Catheter ablation (pulmonary vein isolation, PVI): preferred for paroxysmal AF refractory to drugs; increasingly used for persistent AF; reduces recurrences significantly
- Surgical ablation (Cox-Maze procedure): for patients undergoing cardiac surgery
- Left atrial appendage (LAA) occlusion (Watchman device): for patients who cannot tolerate long-term anticoagulation
Atrial Flutter (brief comparison)
Managed the same as AF for rate/rhythm control and anticoagulation. Atrial flutter responds to cardioversion with very low energy (25-50 J). Hemodynamically better tolerated than AF due to organized atrial contraction. Catheter ablation (cavotricuspid isthmus ablation) is highly effective and often preferred over long-term drug therapy.
Sources: Tintinalli's Emergency Medicine (comprehensive study), Symptom to Diagnosis 4th Ed., Braunwald's Heart Disease, Harrison's Principles of Internal Medicine 22E (2025)
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