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Atrial Fibrillation and Ventricular Arrhythmias. Ibrahim Sales, Pharm.D . Assistant Professor of Clinical Pharmacy King Saud University Supraventricular Arrhythmias. Supraventricular arrhythmia Sinus Bradycardia AV Nodal Block Atrial fibrillation

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atrial fibrillation and ventricular arrhythmias

Atrial Fibrillation and Ventricular Arrhythmias

Ibrahim Sales, Pharm.D.

Assistant Professor of Clinical Pharmacy

King Saud University

supraventricular arrhythmias
Supraventricular Arrhythmias
  • Supraventricular arrhythmia
    • Sinus Bradycardia
    • AV Nodal Block
    • Atrial fibrillation
    • Paroxysmal Supraventricular Tachycardia (PSVT)
  • Ventricular arrhythmia
    • Ventricular Premature depolarization
    • Ventricular tachycardia
    • Ventricular fibrillation
    • Torsades de Pointes
atrial fibrillation
Atrial Fibrillation
  • The most common sustained arrhythmia encountered in clinical practice
  • Rapid & disorganized conduction in atria leading to loss of mechanical contraction
  • "irregularly irregular" appearance on ECG
  • HR of 120–180 usually observed because AV node unable to block all atrial impulses
classification of af
Classification of AF
  • Paroxysmal (self-terminating) :
    • episodes terminate spontaneously in less than seven days,
    • usually less than 48 hours.
  • Persistent AF :
    • fails to self-terminate within 7 days.
    • Episodes may eventually terminate spontaneously, or they can be terminated by cardioversion.

ACC/AHA/European Society of Cardiology

classification of af1
Classification of AF
  • Permanent AF
    • arrhythmia lasts for more than one year and cardioversion either has not been attempted or has failed.
  • "Lone" AF:
    • describes paroxysmal, persistent, or permanent AF in individuals withoutstructural heart disease (usually young patients, <60 yrs)
classification of af2
Classification of AF
  • Nonvalvular AF:
    • Not caused by valvular disease, prosthetic heart valves, or valve repair
  • Recurrent atrial fibrillation:
    • ≥ 2 episodes of atrial fibrillation
causes of af
Causes of AF
  • Hypertensive heart disease 
  • Coronary disease 
  • Valvular heart disease 
  • Heart failure
  • Hypertrophic cardiomyopathy
  • Congenital heart disease
  • pulmonary embolism
  • COPD
  • Obstructive sleep apnea
  • Hyperthyroidism 
  • Alcoholism (Holiday Heart Syndrome)
  • Surgery: CABG 30-40%
  • Inflammation and infection
  • Medications: theophylline, bisphosphonate
c linical implications of af
Clinical implications of AF

Am Fam Physician.

2011 Jan 1;83(1):61-68

goals of therapy
Goals of Therapy
  • Disease specific goals of therapy
    • Control ventricular rate
    • Preventing thromboembolic events
    • Restore sinus rhythm
    • Maintain sinus rhythm
  • Global goals:
    • Reduce mortality
    • Improve QOL
    • Decrease hospitalization and ER visits
    • Optimize the cost effectiveness of treatment
approach to therapy of afib
Approach to therapy of AFib
  • Evaluate the need for acute treatment
      • By starting a rate control drug
  • Contemplate restoration of SR taking into consideration the risks
      • restoring and maintaining SR may not be a desirable goal for all patients
  • Consider thromboembolic prophylaxis with appropriate antithrombotic drug based on stroke risk
rate control vs rhythm control
Rate control vs. rhythm Control
  • Overall Conclusion:
    • No significant difference in overall mortality between rate-control and rhythm-control strategies
    • Anticoaugulant (AC) need is similar in both groups
rate control strategy
Rate control Strategy
  • At least as effective as rhythm control strategy for preventing stroke and death in atrial fibrillation
  • Fewer adverse events than rhythm control strategy
    • Rhythm control with AAD maybe considered if patient remained symptomatic despite adequate ventricular rate control
  • Target HR:
    • Lenient resting HR< 110 bpm vs. strict rate control, resting HR< 80 BPM, have similar cardiovascular outcomes
      • Therefore, target a resting heart rate of < 110 bpm

AAD: anti-Arrhythmic Drugs

rate control strategy1
Rate control Strategy
  • Drugs for long-term rate control
    • Beta blocker (oral)
      • metoprolol50-200 mg/day, propranolol 80-240 mg/day)
    • Non-dihydropyridine(oral)
      • diltiazem120-360 mg/day, verapamil 120-360 mg/day)
    • Digoxin (oral)
      • AF with HF, LVD (LVEF < 40%) or for sedentary individuals
      • not recommended as monotherapy to control ventricular rate in patients with paroxysmal atrial fibrillation
rate control strategy2
Rate control Strategy
    • Amiodarone (oral)
      • when other medical therapy has failed to control heart rate adequately
    • AF with pre-excitation
      • preferred drugs for rate control are oral propafenone or amiodarone
  • combination therapy with any of digoxin, beta blocker, or non-DHP-CCB may be used to control heart rate at rest and with exercise
rhythm control strategy
Rhythm control strategy
  • Recommended in patients with symptomatic AF despite rate control
  • Pharmacologic rhythm control strategy associated with more hospitalizations and adverse events without apparent benefit compared to rate control strategy in AF
  • Rate control should be continued throughout rhythm control approach
rhythm control strategy1
Rhythm control strategy
  • Cardioversion with DCC
    • DCC is useful to start rhythm control strategy for atrial fibrillation
    • Pretreatment with amiodarone, flecainide, ibutilide, propafenone or sotalol before DC cardioversion may increase success rate and prevent recurrent atrial fibrillation
  • Pharmacological cardioversion:
    • Success rate lower than DC
    • Selection of agent:
      • If the AF is ≤7 days duration:
        • Dofetilide, flecainide, ibutilide, propafenone or, to a lesser degree, amiodarone (preferred if structural heart dz)
      • If the AF is >7 days duration
        • dofetilide or, to a lesser degree, amiodarone or ibutilide
rhythm control strategy2
Rhythm control strategy
  • Thromboembolic prophylaxis during cardioversion:
    • for AF of known duration < 48 hours
      • immediate cardioversion indicated without delay for anticoagulation if hemodynamic instability
      • starting anticoagulation (with LMWH or IV UFH at full venous thromboembolism treatment doses) before cardioversion suggested if possible
rhythm control strategy3
Rhythm control strategy
  • for atrial fibrillation of ≥ 48 hours or of unknown duration
    • initial therapeutic anticoagulation recommended with either:
      • Option 1: Therapeutic anticoagulation (adjusted-dose vitamin K antagonist [VKA] therapy to target INR range 2-3, LMWH at full venous thromboembolism treatment doses, or dabigatran) for at least 3 weeks before cardioversion
rhythm control strategy4
Rhythm control strategy
    • Option 2: Transesophagealechocardiography (TEE)-guided approach with initial anticoagulation (LMWH or IV heparin) then cardioversion within 24 hours of confirmation of no thrombus
        • less hemorrhagic complications, but trend toward increased mortality
  • Post-cardioversionanticoagulation recommended for ≥ 4 weeks
rhythm control strategy5
Rhythm control strategy
  • Maintenance of NSR
    • Intermittent antiarrhythmic drug therapy
      • “Pill in the Pocket”
    • AAD:
      • Also increase the risk of arrhythmia
        • torsades de pointes (TdP): a potential adverse effect with dofetilide and sotalol
        • ventricular tachycardia or conversion to atrial flutter with tachyarrhythmia is a potential adverse effect with flecainide and propafenone
      • The AAD associated with increased mortality include sotalol, quinidine, and possibly disopyramide
rhythm control strategy6
Rhythm control strategy
      • “Pill in the Pocket”
    • A transient outpatient therapy for reversion of NSR in paroxysmal AF
    • single oral high dose taken only when an episode of AF is recognized by the patient
  • Agents: propafenone600 mg, or flecainide 300 mg
  • Very strict patient criteria
    • Absence of: structural heart disease,sinus and AV node dysfunction, QT interval prolongation, Brugada syndrome
    • Presence of AV nodal blockade with a BB or CCB to prevent rapid AV conduction if atrial flutter occurs.
Recommended Antiarrhythmic Therapy in Patients with Recurrent Paroxysmal or Persistent Atrial Fibrillation:
ablation therapy
Ablation Therapy
  • ablation of AV node or accessory pathway (and pacemaker implantation)
    • indicated when medical therapy fails to control heart rate or produces intolerable side effects
  • Catheter ablation, or surgical ablation in patients having cardiac surgery for other reasons
    • recommended for patients with symptomatic paroxysmal atrial fibrillation after failure of antiarrhythmic drugs
  • may improve quality of life and reduce hospital readmission rates
thromboembolic prophylaxis
Thromboembolic Prophylaxis
  • Guidelines consistently agree that most patients with AF should receive antithrombotic therapy.
  • AT is recommended to patients with permanent, persistent, or paroxysmal atrial fibrillation, atrial flutter, and patients managed with rate or rhythm control strategy
antithrombotic in atrial fibrillation
Antithrombotic in Atrial Fibrillation
  • Return of SR restores effective contraction in the atria >> dislodge poorly adherent thrombi
  • Selection of the antithrombotic agent depend on the level of risk:
  • CHADS2 or CHA2DS2-VASc score for risk stratification
stroke risk stratification
Stroke Risk Stratification
  • Have ONE of the following factors:
  • Prior ischemic stroke, TIA
  • Mitral valve stenosis
  • Prosthetic heart valve
  • Have ONLY one of the following factors:
    • Age > 75 y Or HTN Or DM Or moderately or severely impaired LV systolic function and/or HF
  • Age > 75 y With none of the conditions listed above in the high- or intermediate-risk categories

High Risk Patients:

  • Have > 2 of the
  • Age > 75 y
  • HTN
  • DM
  • Moderately or severely impaired LVSD and/or HF


Intermediate Risk Patients:

Low-Risk Patients:

stroke risk stratification1
Stroke Risk Stratification
  • CHADS2 risk score predicts stroke risk
  • Helps predict stroke risk in AF patients and determine which antithrombotic (AT) is appropriate

ACCP 9th edition, 2012 Guidelines for the Management of Patients With AF

recommendation for at in af
Recommendation for AT in AF

AC: Anticoagulation

ACCP 9th edition, 2012 Guidelines for the Management of Patients With AF

cha 2 ds2 vasc

ACCP 9th edition, 2012 Guidelines for the Management of Patients With AF

vitamin k antagonist warfarin
Vitamin K antagonist: Warfarin
  • The most commonly used AC
  • Target INR of 2-3 in patients without mechanical heart valves
  • lower target INR of 2 (range 1.6-2.5) may be considered for patients ≥ 75 y/o or if at  risk of bleeding but without contraindications to oral anticoagulant therapy
vitamin k antagonist warfarin1
Vitamin K antagonist: Warfarin
  • Starting dose 5-10 mg adjusted based on INR
  • No need to bridge patient with heparin when initiating warfarin in AF patients
  • Determine INR at least weekly during initiation and monthly when INR is stable.
    • suggests monitoring INR at least every 12 weeks rather than every 4 weeks when INR consistently stable
vitamin k antagonist warfarin2
Vitamin K antagonist: Warfarin
  • Limitation:
    • Narrow therapeutic index
    • Require frequent dose adjustments and monitoring
    • Significant drug-drug and drug-food interaction
    • time required to achieve its pharmacologic effect is dependant on the T½ of the coagulation proteins.
    • full antithrombotic effect achieved in 5 to 7 days after
    • Pregnancy Category X
dabigatran pradaxa
Dabigatran (Pradaxa®)
  • Dabigatranetexilateis a selective, competitive, reversible direct thrombin inhibitor
  • Approved by FDA in 2010 for stroke prevention in atrial fibrillation
  • Approved in Canada & Europe for VTE prevention after hip and knee replacement surgery
dabigatran pradaxa1
Dabigatran (Pradaxa®)
  • Oral capsule
  • Rapid onset of action
  • Half-life 12-17 hours, dosed TWICE Daily
  • No routine monitoring required
  • No reversal antidote
    • dialyzable
  • No dietary/food interactions
  • SE: Bleeding, Dyspepsia (common, likely due to tartaric acid)
  • Cost: $$$ compared to warfarin
dabigatran pradaxa2
Dabigatran (Pradaxa®)
  • Renal elimination
    • CrCl>30 ml/min:
      • 150 mg orally twice daily
        • Outside US: 110 mg twice daily for age >75 or propensity for GI bleeding
    • CrCl 15-30 ml/min:
      • 75 mg orally, twice daily*
  • Metabolism: P-gp substrate
    • use with caution when administered concomitantly with P-gp inhibitors or inducers
converting to and from dabigatran
Converting to and from Dabigatran
  • Warfarin to Dabiatran
    • D/c warfarin and start dabigatranwhen INR <2.0
  • Dabigatran to Warfarin
    • CrCl >50 ml/min: start warfarin 3 days before d/c DabiCrCl31-50 ml/min: start warfarin 2 days before D/c dabigatran
    • CrCl15-30 ml/min: start warfarin 1 day before stopping dabigatran
    • CrCl<15 ml/min: no recommendation
dabigatran pradaxa5
Dabigatran (Pradaxa®)
  • Product Stability:
    • Once bottle is opened, manufacturer recommends that drug be used within 30 days. Keep bottle tightly closed
    • Manufacturer package insert indicates potency is maintained for 120 days after first opening bottle.
dabigatran pradaxa6
Dabigatran (Pradaxa®)
  • Contraindications:
    • Active pathologic bleeding
    • History of serious hypersensitivity reaction to dabigatran (e.g., anaphylaxis, anaphylactic shock)
    • Patients with mechanical prosthetic heart valves
  • Pregnancy Category C
rivaroxaban xarelto
Rivaroxaban (Xarelto®)
  • Direct factor Xa inhibitor
  • Approved by FDA in 2011 for prevention of stroke in non-valvular AF.
    • Also in treatment and prophylactic in DVT/PE and following knee- or hip-replacement surgery
  • No laboratory monitoring required
  • No dosage adjustment for gender, age, extreme body weight
  • No reversal
    • Half life 5-9 hours
rivaroxaban xarelto1
Rivaroxaban (Xarelto®)
  • Dosing:
  • Oral tablet, once daily (cost $231.60 USA)
  • Primarily renal elimination
    • If CrCl> 50 ml/min: give 20 mg once daily with evening meal
    • If Crcl15-50 ml/min give 15 mg once daily with evening meal
    • Contraindicated for creatinine clearance < 15 mL/minute
rivaroxaban xarelto2
Rivaroxaban (Xarelto®)
  • Contraindications:
    • Active pathologic bleeding
    • Severe hypersensitivity reaction to rivaroxaban
  • Pregnancy Category C
  • Lactation: Discontinue nursing or the drug
  • DI: Drugs Affecting and/or P-glycoprotein and CYP3A4
    • Avoid using with itraconazole, ketoconazole, Antiretrovirals, HIV protease inhibitors, Carbamezapine, rifampin, phenytoin, St. John's wort
apixaban eliquis
Apixaban (Eliquis®)
  • Direct factor Xa inhibitor
  • Approved by FDA in 2012 for risk reduction of stroke and systemic embolism in nonvalvular AF
  • No routine lab testing
  • No reversal
    • Half life 8-15 hours
  • Metabolized in liver via CYP3A4 and CYP independent mechanisms
  • Eliminated via multiple pathways
apixaban eliquis1
Apixaban (Eliquis®)
  • Dose: 5 mg tablet Twice daily
  • To switch from warfarin, stop warfarin, then start apixaban when INR <2
  • Cost: (5 mg BID): $250.37 (USA)
  • Pregnancy Category B
  • Lactation: Discontinue nursing or the drug
  • May prolong PTT and INR in a concentration-dependent fashion
stopping pradaxa dabigatran xarelto rivaroxaban or eliquis apixaban in af patients
Stopping Pradaxa (dabigatran), Xarelto (rivaroxaban), or Eliquis (apixaban) in AF patients
  • Discontinuing new oral AC places patients at an increased risk of thrombotic events. An increased rate of stroke was observed following discontinuation in clinical trials in patients with nonvalvular atrial fibrillation.
  • If anticoagulation must be discontinued for a reason other than pathological bleeding, coverage with another anticoagulant should be strongly considered.
limitations of novel ac
Limitations of Novel AC
  • Irreversibility
  • Cost
  • Renal function
    • Not studied where CrCL<30mL/min
  • Lack of monitoring
    • No readily available test
    • No therapeutic interval
  • Long term safety not known
  • No data on use in pediatric population
types of ventricular arrhythmias
Types of Ventricular Arrhythmias
  • Premature Ventricular Contractions (PVCs)
    • Ectopic ventricular beat
    • non-life-threatening and usually asymptomatic.
    • Sx: palpitations or uncomfortable heartbeats.
  • Ventricular Tachycardia (VT)
    • a life-threatening situation associated with hemodynamic collapse or may be totally asymptomatic.
    • >3 consecutive PVCs occurring at a rate >100 beats/min
    • Could be monomorphic or polymorphic
  • Ventricular Fibrillation (VF)
    • results in hemodynamic collapse, syncope, and cardiac arrest. Cardiac output and blood pressure are not recordable.
pvcs treatment
PVCs Treatment
  • No drug therapy indicated for asymptomatic patients without structural heart disease
  • BB is drug of choice for symptomatic patients
  • after myocardial infarction BB improve survival
  • no evidence that prolonged suppression with drugs AAD improves survival
    • CAST I and II studies demonstrated higher mortality in the AAD group

Treat Guidel Med Lett 2007 Jun;5(58):51 

ventricular tachycardia vt
Ventricular Tachycardia (VT)
  • Non-sustained VT: last < 30 sec
    • Self terminate
    • May consider primary prevention in high risk groups to prevent conversion to sustained VT
  • Sustained VT last > 30 sec
    • Requires intervention to prevent VF or SCD
ventricular tachycardia vt1
Ventricular Tachycardia (VT)
  • Causes:
    • Ischemia: MI (very common)
    • Stimulant use:
      • Caffeine, cocaine abuse
    • Metabolic abnormalities:
      • Acidosis, hypoxemia, hyperkalemia, hypokalemia, hypomagnesemia
    • Drugs:
      • Digoxin, theophylline, antipsychotics, TCA, AAD: flecainide, dofetilide, sotalol, quinidine
ventricular tachycardia vt2
Ventricular Tachycardia (VT)
  • Treatment:
    • correction of the underlying precipitating factors
    • acute episode of VT (with a pulse)
      • Severe symptoms:
          • DCC
          • Long term AAD is not needed if there was precipitating factors
        • Mild symptoms:
          • AAD: procainamide, amiodarone, sotalol and lidocaine
          • Assess patient’s risk for recurrence
ventricular tachycardia vt3
Ventricular Tachycardia (VT)
  • Treatment of chronic, recurrent, sustained VT :
    • Empiric amiodarone
    • Catheter ablation: if idiopathic
    • Implantable cardioverter-defibrillator (ICD)
      • +/- amiodarone or sotalol
        •  frequency of VT/VF episodes >>  frequency of shocks
        •  rate of VT >> can be terminated with BB
        •  episodes of concomitant supraventricular arrhythmias
        • minimize patient discomfort
        • prolong the battery life of the ICD
ventricular tachycardia vt4
Ventricular Tachycardia (VT)
  • Primary prevention of SCD in VT/VF
    • High risk: CAD, LV dysfunction, and nonsustained VT
      • Undergo electrophysiologic testing to guide subsequent therapy
        • No inducible sustained VT/VF, chronic AAD therapy is unnecessary
        • If inducible sustained VT/VF, implantation of an ICD is warranted.
  • Secondary prevention of SCD in VT/VF:
    • ICD is the first-line treatment
torsade de pointes tdp
Torsade de Pointes (TdP)
  • TdP is a rapid form of polymorphic VT
  • ECG:
    • long QT interval or prominent U waves (Delayed ventricular repolarization)
  • Etiology of TdP:
    • Genetic, electrolyte disturbances ( K,  Mg), subarachnoid hemorrhage, myocarditis, arsenic poisoning, severe hypothyroidism, or drug therapy (most common)
torsade de pointes tdp1
Torsade de Pointes (TdP)
  • Drugs that can cause TdP:
  • AAD: Quinidine, Procainamide, Disopyramide, Amiodarone, Dofetilide, Dronedarone, Sotalol and Ibutilide
  • Psychotropics
    • Phenothiazines (e.g., thioridazine, chlorpromazine) TCA (Haloperidol, Pimozide) Atypical antipsychotics (e.g., quetiapine, ziprasidone)
  • Organophosphate insecticides
  • Arsenic Antibiotics
    • Pentamidine, Macrolides (erythromycin and clarithromycin), Trimethoprim-sulfamethoxazole, Fluoroquinolones (levofloxacin, moxifloxacin, gemifloxacin) and Voriconazole
torsade de pointes tdp2
Torsade de Pointes (TdP)
  • Risk factors for drug-induced TdP:
    • High dose (quinidine, TdP at low doses)
    • concurrent structural heart disease
    • Evidence of mild QT prolongation at baseline
    • Evidence of mild QT prolongation after initiation of drug
    • Female gender
  • QT interval prolongation has been used as a measurement of risk of TdP
    • If baseline QTc interval > 450 msec AVOID drugs that can prolong QT
    • If QTcinterval is 560 msec after the initiation of the drug >> discontinue or reduce dose of the drug
torsade de pointes tdp3
Torsade de Pointes (TdP)
  • Treatment of Acute TdP
    • DCC
    • Followed by IV magnesium sulfate to prevent recurrence
    • Discontinue all drugs that prolong the QT interval
    • Correct exacerbating factors (e.g., hypokalemia or hypomagnesemia)
ventricular fibrillation vf
Ventricular Fibrillation (VF)
  • A Tachyarrhythmia
  • The most common underlying rhythm of cardiac arrest
  • If not treated: pulseless electrical activity, asystole
  • no cardiac output leads to rapid fatality
  • Causes:
  • frequently associated with CAD (only 20% patients rescued from VF have evidence of evolving MI)
treatment of pulseless vt or vf
Treatment of pulseless VT or VF
  • ABCs
  • CPR until defibrillator attached
  • Check pulse between every intervention (except sequential shocks with persistent VF
  • defibrillate up to 3 times as needed for V fib or pulseless VT (200 joules, 300 J, 360 J)
  • if no pulse and persistent or recurrent VF/VT –
    • CPR, intubation, establish IV access
    • epinephrine, defib 360, lidocaine, defib 360, bretylium, repeat epi/defib, consider bicarbonate, defib 360, bretylium, defib 360, repeat lidocaine or bretylium, defib 360, magnesium, procainamide
vf treatment
VF Treatment
  • Prevention of recurrence:
    • long-term therapy implantable cardioverter-defibrillator (ICD)
      • Amiodarone or beta blockers often added
    • if ICD shocks are frequent, consider adding sotalol, amiodarone or mexiletine; if shocks recur, radiofrequency catheter ablation
sinus bradycardia
Sinus Bradycardia
  • Heart rate <60 beats/min
  • Not always pathologic
  • Symptoms:
    • fatigue, dizziness, inability to concentrate, forgetfulness, syncope
  • Causes:
    • sinus node dysfunction: aging, accompanying a conduction disease (e.g. AV block, AF), CHD
  • Treatment:
    • treat the underlying cause,
    • atropine
    • Pacemaker if patient is hemodynamicallycompromised
av nodal block
AV Nodal Block
  • A type of bradyarrhythmia
  • Types
    • 1st-degree heart block—PR interval >0.1ms; AV conduction remains 1:1
    • 2nd-degree heart block-- progressive prolongation of PR interval AV conduction <1:1
    • 3rd-degree heart block—no AV conduction, atria & ventricles contract independently from 1 another
  • Causes:
    • Use of AV nodal blocking agents (digoxin, -blockers, nondihydropyridine CCBs, amiodarone, dronedarone), hyperkalemia
  • Treatment
    • treat underlying cause;
    • symptomatic patients: atropine 0.5mg IV Q3–5min up to total 3mg,
    • transcutaneous pacing; permanent pacemaker needed in patients without underlying treatable cause
paroxysmal supraventricular tachycardia psvt
Paroxysmal Supraventricular Tachycardia (PSVT)
  • HR >100bpm,
  • ECG: narrow QRS complexes
  • Symptoms: chest pressure or discomfort, dyspnea, fatigue, lightheadedness, dizziness, palpitations;
  • Treatment:
    • hemodynamicallystable patients: vagal maneuvers to sympathetic tone are 1st line;
    • Adenosine
wolff parkinson white wpw syndrome
Wolff-Parkinson-White (WPW) Syndrome
  • Atype of SVT
  • Etiology:
    • accessory pathway that bypasses AV node & causes tachycardia; HR >200bpm,
  • life-threatening, may lead to VF
  • Symptoms:
    • chest pain or tightness, dizziness, lightheadedness, fainting, palpitations, SOB
wolff parkinson white wpw syndrome1
Wolff-Parkinson-White (WPW) Syndrome
  • Treatment:
    • Avoid AV nodal blocking agents (b-blockers, non-DHP CCBs, adenosine, lidocaine, & digoxin)
    • short term electrical cardioversion:
      • amiodarone150mg IV over 10min;
      • procainamide LD 20mg/min IV until arrhythmia resolves, hypotension, or QRS widens by >50% or total of 17mg/kg; continuous infusion 1–4mg/min
    • long term catheter ablation