Pharmacotherapy: Supraventricular Arrhythmias

Atrial Fibrillation

Rate Control

Beta-blockers

• Mechanism: Reduce conduction through the AV node by inhibiting beta-1 adrenergic receptors. Also provide cardioprotective benefits.
• Metoprolol:
  • Dose: 2.5-5 mg IV bolus over 2-5 minutes, repeat every 5 minutes for a total of 3 doses
  • Onset: 5-10 minutes, duration 6-8 hours
  • Adverse effects: Hypotension, bronchospasm, worsened heart failure

• Esmolol:
  • Dose: 500 mcg/kg IV bolus over 1 minute followed by 50-200 mcg/kg/min infusion
  • Onset: 2 minutes, duration 10-20 minutes
  • Adverse effects: Hypotension, bronchospasm

Calcium channel blockers

• Mechanism: Inhibit AV nodal conduction by blocking L-type calcium channels
• Diltiazem
  • Dose: 0.25 mg/kg IV bolus over 2 minutes, may repeat with 0.35 mg/kg after 15 minutes up to total dose of 1 mg/kg
  • Onset: 2-7 minutes, duration up to 4 hours
  • Adverse effects: Hypotension, worsened heart failure

• Verapamil
  • Dose: 2.5-5 mg IV over 2 minutes, may repeat with 5-10 mg after 15 minutes up to total dose of 20 mg
  • Onset: 3-5 minutes, duration 1-6 hours
  • Adverse effects: Hypotension, high-degree AV block

Digoxin

• Mechanism: Vagal mediated reduction in SA and AV nodal conduction
• Dose: 0.25 mg IV, may repeat 0.25 mg every 6 hours up to 1.5 mg daily
• Onset: 30-120 minutes, duration 6-8 hours
• Adverse effects: AV block, digoxin toxicity
• May be less effective in high adrenergic states
• Useful in heart failure patients

Amiodarone

• Mechanism: Potassium channel blockade prolongs repolarization. Also exerts beta blockade and mild calcium channel inhibition.
• Dose: 150 mg IV over 10 minutes, then 1 mg/min infusion for 6 hours
• Onset: 5-15 minutes when given IV
• Adverse effects: Hypotension, bradycardia, phlebitis with IV infusion

Rhythm Control

Electrical Cardioversion

• Delivers synchronized direct current shock using paddles or patches
• Recommended starting dose: 100 J biphasic
• Success rate around 90%
• Sedation recommended prior to procedure
• Resume anticoagulation immediately after procedure

Antiarrhythmic Medications

Flecainide

• Dose: Single oral dose 200-300 mg
• Mechanism: Sodium channel blockade slowing conduction velocity
• Efficacy around 60-80% in recent-onset AF
• Contraindicated in structural heart disease

Propafenone

• Dose: Single oral dose 450-600 mg
• Mechanism: Sodium channel blockade slowing conduction velocity
• Efficacy similar to flecainide
• Contraindicated in structural heart disease

Amiodarone

• Dose: 600 mg daily oral loading for 4 weeks, then 200 mg daily maintenance
• Mechanism: Multichannel (sodium, potassium, calcium channel) blocker
• Useful when structural heart disease present
• Slow onset limits utility for acute conversion

Ibutilide

• Dose: 1-2 mg IV over 10 minutes
• Mechanism: Potassium channel blockade prolonging repolarization
• Efficacy around 50% for acute conversion
• QT prolongation and torsades de pointes are primary risks
• Requires inpatient monitoring during administration

Procainamide: 15-18 mg/kg IV over 30-60 minutes

• Class Ia antiarrhythmic, sodium channel blocker
• Hypotension is primary adverse effect
• Avoid in structural heart disease

Anticoagulation

• Before cardioversion, patients with AF of 48 hours duration or longer should be anticoagulated for at least 3 weeks prior with warfarin (INR 2-3) or DOACs.
• After successful cardioversion back to normal sinus rhythm, anticoagulation should be continued for at least 4 more weeks regardless of stroke risk. This allows time for atrial mechanical function to recover.
• For patients undergoing cardioversion of AF less than 48 hours duration, anticoagulation is started as soon as possible but 3 weeks of pretreatment is not needed.
• If a thrombus is seen on transesophageal echocardiogram (TEE) prior to planned cardioversion, the procedure should be postponed and anticoagulation continued for several more weeks until resolution.

Long Term Anticoagulation
Decisions about long-term anticoagulation after cardioversion are based on the patient’s stroke risk (CHA2DS2-VASc score), not on whether they are in sinus rhythm. Anticoagulation is recommended for most patients with atrial fibrillation to reduce the risk of ischemic stroke and other thromboembolic events. The decision to initiate anticoagulation is based on the patient’s stroke risk, which can be assessed using the CHA2DS2-VASc score. Patients with a score ≥2 in males or ≥3 in females should receive oral anticoagulation.

The benefits of anticoagulation typically outweigh the increased bleeding risk. However, the bleeding risk should also be evaluated using the HAS-BLED score. While a high HAS-BLED score identifies patients at elevated bleeding risk, it should not be used alone to exclude patients from anticoagulation. Additional risk factors like frequent falls, comorbidities, and patient preferences should be considered.

CHA₂DS₂VASc

Risk Factor	Points
Congestive heart failure	1
Hypertension	1
Age ≥75	2
Diabetes mellitus	1
Prior stroke or TIA	2
Age 65-74	1
Vascular disease*	1
Sex category (female)	1

*Prior MI, PAD, or aortic plaque

Recommend anticoagulation if score ≥2 for males, ≥3 for females

HAS-BLED Risk Score

Risk Factor	Points
Hypertension	1
Abnormal renal/liver function	1 each
Stroke	2
Bleeding	1
Labile INRs	2
Elderly (Age >65 yea old)	1
Drugs (antiplatelets/NSAID) /alcohol  (> 8 drinks)	1 each

Specific Oral Anticoagulant Agents

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Supraventricular Tachycardia

Vagal maneuvers: These are techniques that stimulate the vagus nerve and can often slow down the heart rate. They include the Valsalva maneuver (bearing down as if having a bowel movement) or carotid sinus massage. Various antiarrhythmic drugs can be used to help control AVNRT episodes, either for acute termination or chronic prevention. They work by modifying conduction or refractoriness in the reentrant circuit pathways.

Acute Treatment

Vagal maneuvers: These are techniques that stimulate the vagus nerve and can often slow down the heart rate. They include the Valsalva maneuver (bearing down as if having a bowel movement) or carotid sinus massage.

Adenosine is the preferred agent for acute pharmacologic termination of AVNRT. It works by hyperpolarizing cells in the AV node, suppressing conduction through slow pathway cells. This interrupts the reentrant circuit and restores normal conduction. Adenosine is given as a rapid IV bolus, with onset of action within seconds and a very short half-life. It terminates AVNRT episodes in up to 90% of cases. Side effects are transient and include chest pain, flushing, dyspnea, and AV block.

• Adenosine
  • Dose: Dose: 6 mg rapid IV bolus followed by 12 mg x 2 if not successful
  • May need higher dose in patients ingesting signficant amount of caffeine
  • Caution in patients with heart transplant
  • Adenosine is often considered contraindicated in heart transplant patients due to parasympathetic denervation.

• Administration
  • Stopcock method
  • Diluted method by McDowell et al
    • Rapid push of mixture of adenosine and 20-30 mL normal saline given as a rapid IV push      

• Side effects
  • Flushing
  • Feeling of doom
  • Temporary Asystole
  • Can cause severe bronchospasm in asthma patients.

Calcium Channel Blockers

• DIltiazem IV
  • 0.25 mg/kg IV bolusover 2 mins, may repeat with 0.35 mg/kg IV; follow with 5—15 mg/hour infusion
  • Side effects
    • Hypotension
  • Caution
    • Avoid in hypotension, heart failure, cardiomyopathy, and acute coronary syndromes
  • Convert SVT to normal sinus rhythm in 64% to 98% of patients
  • A Cochrane systematic review of 7 RCTs (622 patients) found similar rates of conversion to sinus rhythm with adenosine or calcium channel blockers (90% versus 93%) and no significant difference in hypotension.

• Verapamil
  • 2.5—5 mg IV; may repeat up to total 20 mg
  • Side effects
    • Hypotension
  • Convert SVT to normal sinus rhythm in 64% to 98% of patients

β-Adrenergic Blockers

• Metoprolol
  • 2.5–5 mg over 2 min, up to 3 doses
  • Avoid in decompensated heart failure

• Esmolol
  • 500 μg/kg IV over 1 min bolus then 50–300 μg/kg per min
  • Short duration of action; avoid in decompensated heart failure

Choice of agent depends on factors like presence of structural heart disease, kidney function, and side effect profile. Most patients require combination therapy with two medications from different classes to adequately control recurrences. Frequent monitoring is recommended to assess efficacy and minimize potential toxicity.

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