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Emergency Medicine: Cardiology 213

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  1. Acute Coronary Syndromes: A Focus on STEMI
    10 Topics
    3 Quizzes
  2. Acute decompensated heart failure
    10 Topics
    3 Quizzes
  3. Hypertensive Urgency and Emergency Management
    11 Topics
    3 Quizzes
  4. Acute aortic dissection
    9 Topics
    2 Quizzes
  5. Arrhythmias (Afib, SVT, VTach)
    10 Topics
    2 Quizzes

Participants 220

  • April
  • Alyssa
  • Ashley
  • Amber
  • Sherif
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Atrial Fibrillation

Rate Control


  • 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


  • 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


  • 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


  • 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


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


  • 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


  • 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


  • 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.


Risk Factor                           Points
Congestive heart failure1
Age ≥752
Diabetes mellitus1
Prior stroke or TIA2
 Age 65-741
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
Abnormal renal/liver function 1 each
Labile INRs2
Elderly (Age >65 yea old)1
Drugs (antiplatelets/NSAID) /alcohol  (> 8 drinks)1 each
Score ≥3 indicates high risk for bleeding with anticoagulation

Specific Oral Anticoagulant Agents


  • Target INR 2-3
  • Dose adjusted based on INR monitoring to maintain therapeutic range
  • Lower INR target of 2-2.5 appropriate for low thromboembolic risk settings like post-cardioversion or post-ablation
  • TTR should be >70% for optimal efficacy and safety
  • PK
    • Half life: 40 hr
    • CYP2C9 primary, (CYP3A4, 1A2, 2C19 minor pathways)
    • Elimination: Renal, primarily as metabolites
  • Initiate along with overlapping parenteral anticoagulant (heparin) in high thromboembolic risk patients
  • Food and drug interactions require close monitoring
  • Regular INR testing needed (weekly after initiation, every 4-6 weeks once stable)
  • Reversal agents available (vitamin K, 4-factor PCC)


  • Direct factor Xa inhibitor
  • Dose: 5 mg PO BID
  • PK
    • Half life: 12 hr
    • Renal (27% unchanged drug)
    • Metabolized, primarily by CYP3A4
    • P-gp substrate
  • Dose reduction to 2.5 mg PO BID if ≥2 of: age ≥80, weight ≤60 kg, Cr ≥1.5 mg/dL
  • No dose adjustment if Cr ≥15 mL/min
  • Lower drug interaction potential than other DOACs
  • Lower  bleeding risk compared to warfarin


  • Direct factor Xa inhibitor
  • Dose: 20 mg PO daily with evening meal
  • Reduce dose to 15 mg PO daily if CrCl 15-50 mL/min
  • Avoid if CrCl <15 mL/min
  • PK
    • Half life: 5-9 hr, 11-13 hr in elderly
    • Elimination: Renal (36% unchanged drug)
    • Metabolized, primarily by CYP3A4 and CYP2J2
    • P-gp substrate
  • Lower major bleeding risk compared to warfarin
  • Higher drug interaction potential than other DOACs
  • Once daily dosing may improve compliance over warfarin


  • Direct thrombin inhibitor
  • Dose: 150 mg PO BID
  • Reduce dose to 75 mg PO BID if CrCl 15-30 mL/min
  • Avoid if CrCl <15 mL/min
  • PK
    • Half life:12-17 hr, up to 27 hr in renal failure
    • Over 80% cleared by the kidney
    • P-gp substrate
  • Adverse effect: Dyspepsia
  • Reversal agent available (idarucizumab)
  • Capsules should not be crushed or chewed
  • Higher GI bleeding risk compared to warfarin
  • Lower drug interaction potential than warfarin or rivaroxaban


  • Direct factor Xa inhibitor
  • Dose: 60 mg PO daily
  • Reduce dose to 30 mg PO daily if: CrCl 15-50 mL/min, weight <60 kg, or using P-gp inhibitors
  • Avoid if CrCl >95 mL/min or <15 mL/min
  • PK
    • Half life: 10-14 hr
    • 50% cleared by the kidney
    • Undergoes minimal CYP metabolism
  • Once daily dosing may improve compliance
  • Lower GI bleeding risk than other DOACs
  • Minimal drug interactions

Supraventricular Tachycardia

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

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.

Ventricular Tachycardia

The pharmacologic management of both monomorphic and polymorphic VT aims to restore normal sinus rhythm and prevent recurrence. Here are the key interventions for each:

Monomorphic VT:

Management for Unstable Patients:

  1. Electrical Cardioversion:
    • Administer sedation (etomidate or propofol preferred if conscious).
    • Initial synchronized shock at 100 J or higher; subsequent shocks can increase energy up to a maximum of 200 J if needed for conversion.
    • Consider higher energies if ventricular function is poor.
  2. Amiodarone:
    • First-line for stable monomorphic VT along with procainamide.
    • IV/IO bolus of 150 mg (50 mg/min) over 10 minutes.
    • Follow with infusion of 1 mg/min for the first 6 hours, then 0.5 mg/min.
    • Oral maintenance dosing: 200-400 mg daily.
    • Monitor thyroid function, liver enzymes, and pulmonary toxicity.
    • Avoid in severe sinus node dysfunction due to bradycardia risk.
    • Be cautious about interactions with warfarin, statins, and antitubercular therapy.
  3. Procainamide:
    • IV/IO bolus of 10-15 mg/kg (1,000-1,500 mg) over 30-60 minutes, max 100 mg/min.
    • Stop infusion for hypotension or if VT terminates.
    • Repeat bolus or start infusion at 1-4 mg/min if VT recurs.
    • Monitor ECG for QT prolongation and widening of QRS > 50% baseline.
    • Adjust dose for renal dysfunction; start at 7.5 mg/kg if creatinine clearance <60 mL/min.
    • Avoid in heart block, myocardial depression, and prolonged QT.
  4. Lidocaine:
    • IV bolus 1-1.5 mg/kg (or 100 mg) over 2 minutes.
    • Repeat bolus every 5 minutes until a maximum of 3 mg/kg.
    • If VT recurs, start infusion at 1-4 mg/min.
    • Causes less negative inotropy compared to amiodarone or procainamide.
    • Monitor for CNS toxicity such as seizures and confusion.
    • Reduce dose in hepatic dysfunction.
    • Advantages over amiodarone and procainamide as it does not routinely cause hypotension.

Management for Stable Polymorphic VT:

  1. Magnesium Sulfate:
    • Preferred for torsades de pointes or polymorphic VT associated with a long QT interval.
    • Corrects hypokalemia if present and shortens QT regardless of magnesium level.
    • Dose: 2 g diluted in 10 mL D5W or normal saline IV over 5-20 minutes, repeatable up to 2 additional doses if needed.
    • Monitor for hypotension.
  2. Amiodarone:
    • Can be used first-line if polymorphic VT is not known to be long QT-related.
    • Avoid if the QTc interval is markedly prolonged.
    • Administer a 150 mg IV bolus over 20-60 minutes, followed by an infusion.
    • Monitor QTc interval, hypotension, and AV block; stop amiodarone if QTc prolongs excessively.
  3. Lidocaine:
    • An alternative to amiodarone, especially if QTc prolongation is present.
    • Administer an IV bolus followed by an infusion, titrated to suppress the arrhythmia.
    • Monitor for CNS toxicity symptoms.

Additional Measures:

  • Overdrive Pacing: Temporary transvenous pacing to help suppress recurrent polymorphic VT episodes, targeting a pacing rate of 90-110 bpm. Avoid when QTc is markedly prolonged.
  • Isoproterenol Infusion: Consider for polymorphic VT related to bradycardia or pauses, titrating the infusion to keep the heart rate >70 bpm. Use with caution if long QT is present.

In summary, the pharmacologic management of VT includes electrical cardioversion for unstable monomorphic VT, while stable monomorphic and polymorphic VT are managed with intravenous antiarrhythmics such as amiodarone, procainamide, lidocaine, and magnesium sulfate. The goal is to promptly terminate arrhythmia episodes and prevent deterioration into ventricular fibrillation.