atrial fibrillation - virginia veterinary medical ... · •atrial depolarization rate –extremely...

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10/2/2018 1 Atrial Fibrillation How to make ORDER out of CHAOS Julia Shih, VMD, DACVIM (Cardiology) October 27, 2018 Depolarization & ECG Depolarization & ECG Depolarization & ECG Micro-reentrant circuits Requires large atria Atrial depolarization rate Extremely rapid Atrial Fibrillation Loss of atrial contraction Reduction in stroke volume Irregularly irregular rhythm Due to AV nodal properties Loss of atrial contraction Normally ~10-15% of total cardiac output At rapid heart rates, accounts for up to 30% ventricular filling Tachycardia reduces diastolic filling time Hemodynamic Consequences Further drop in stroke volume and cardiac output Tachycardia increases myocardial work and oxygen demand Chronic tachycardia results in myocardial failure Structural and electrical remodeling

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Page 1: Atrial Fibrillation - Virginia Veterinary Medical ... · •Atrial depolarization rate –Extremely rapid Atrial Fibrillation yp –Loss of atrial contraction –Reduction in stroke

10/2/2018

1

Atrial FibrillationHow to make ORDER out of CHAOS

Julia Shih, VMD, DACVIM (Cardiology)

October 27, 2018

Depolarization & ECG

Depolarization & ECG Depolarization & ECG

• Micro-reentrant circuits

• Requires large atria

• Atrial depolarization rate– Extremely rapid

Atrial Fibrillation

y p

– Loss of atrial contraction

– Reduction in stroke volume

• Irregularly irregular rhythm– Due to AV nodal properties

• Loss of atrial contraction– Normally ~10-15% of total cardiac output

– At rapid heart rates, accounts for up to 30% ventricular filling

• Tachycardia reduces diastolic filling time

Hemodynamic Consequences

– Further drop in stroke volume and cardiac output

• Tachycardia increases myocardial work and oxygen demand

• Chronic tachycardia results in myocardial failure

• Structural and electrical remodeling

Page 2: Atrial Fibrillation - Virginia Veterinary Medical ... · •Atrial depolarization rate –Extremely rapid Atrial Fibrillation yp –Loss of atrial contraction –Reduction in stroke

10/2/2018

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• Lone atrial fibrillation– Absence of overt cardiac disease

– Giant breed dogs

Lone vs. Acquired

• Acquired atrial fibrillation– Secondary to cardiac disease resulting

in secondary atrial enlargement

– Dogs: DCM, CVD

– Cats: HCM, RCM, UCM

• Lone AF– Incidental finding– Mild exercise

intolerance

• Acquired AF

Diagnosis: History, Clinical Signs

Acquired AF– Weakness– Lethargy– Syncope– Cough– Tachypnea– Dyspnea

• Auscultation– Irregularly irregular rhythm

– Variable intensity S1, S2, S3

– Absent S4

+/ H t

Diagnosis: Physical Exam

– +/- Heart murmur

– +/- Tachycardia

– +/- Tachypnea, Dyspnea,

Crackles, Dull lung sounds (pleural effusion)

• Variable pulse quality

• +/- Jugular venous distension, abdominal fluid wave, pale mucous membranes

• ECG Findings– Irregularly irregular rhythm

• Irregular R-R intervals

– Absent P waves

Diagnosis: ECG

– Presence of fibrillation waves (F waves)• Fine baseline undulation

• May not be apparent

– Narrow/supraventricular QRS morphology

– Tachycardia

Diagnosis: ECG Diagnosis: ECG

50mm/s

Atrial Fibrillation

25mm/s

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Differential Diagnoses (ECG)

Atrial Flutter

Differential Diagnoses (ECG)

Atrial Fibrillation with LBBBAtrial Fibrillation with LBBB 

Ventricular Tachycardia 

Differential Diagnoses (ECG)

Multiform ventricular tachycardia 

OR

Atrial fibrillation with a right bundle branch block and VPCs

Differential Diagnoses (ECG)

Atrial fibrillation with a right bundle branch block

Differential Diagnoses (ECG)

Focal atrial tachycardia with right bundle branch block

Other Diagnostics

• Blood Work

• Thoracic Radiographs

• Echocardiography

Page 4: Atrial Fibrillation - Virginia Veterinary Medical ... · •Atrial depolarization rate –Extremely rapid Atrial Fibrillation yp –Loss of atrial contraction –Reduction in stroke

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Methods of Treatment

• Rhythm Control - Cardioversion– Restoration of sinus rhythm

– Electrical or pharmacological cardioversion

– Patients may revert back to atrial fibrillation

• Rate Control– Slow the heart rate

– Improves diastolic filling (cardiac output)

Electrical Cardioversion

• Options– Transthoracic

• Monophasic vs. Biphasic Shock

– Intracardiac (TVEC)

– Transesophageal

Electrical Cardioversion

Synchronization Shock Sinus Rhythm

Electrical Cardioversion

SynchronizationMode Off

Shock Ventricular Fibrillation

Electrical Cardioversion - Risks

• Overall Safe – Complications Rare

• Theoretical Risks:– Anesthetic complications

– Shock induced myocardial damage

– Thromboembolic complications

– Induction of ventricular arrhythmias

– Induction of bradycardia

– Sudden death

Electrical Cardioversion

• Success Rate > 90%

• Maintenance of Sinus Rhythm– Lone AF: 690 days

– Acquired AF: 73 days

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Pharmacological Cardioversion

• Greatest success with recent onset atrial fibrillation

• Atrial fibrillation begets atrial fibrillation

• Limited success

• Requires continuous cardiac monitoring for:– Sinus node dysfunction

– Atrioventricular block

– Ventricular arrhythmias

– Atrial flutter

Pharmacological Cardioversion

• Quinidine– Sodium Channel Blocker (Class I Antiarrhythmic)

– Dose• PO: 5-20 mg/kg PO q2-6h

Sid Eff t– Side Effects • Weakness, lethargy

• Ataxia, seizures

• Gastrointestinal (anorexia, vomiting, diarrhea)

• Myocardial depression

• Proarrhythmia (QT prolongation, Torsade de Pointes)

• Drug Interactions (ex. digoxin, antacids, thiazides)

Pharmacological Cardioversion

• Amiodarone– Potassium Channel Blocker (Class III Antiarrhythmic)

– Also has class I, II, IV activity

– IV Dose2 /k IV l 5 10 i• 2 mg/kg IV slow over 5-10 min

• Repeat up to a dose of 10 mg/kg

– Post-Cardioversion• Oral amiodarone 10-25mg/kg PO q12h for ~1 week

• Reduce to 5mg/kg PO q24h over 2-3 weeks

Pharmacological Cardioversion

• Amiodarone– Side Effects

• Gastrointestinal

• Neutropenia

• Thrombocytopenia• Thrombocytopenia

• Hepatotoxicity ***

• Hypothyroidism

• Keratopathy

• Drug Interactions – (antiarrhythmics, theophylline, methotrexate, cyclosporine)

• Hypersensitivity

Pharmacological Cardioversion

• Diltiazem– Calcium Channel Blocker (Class IV Antiarrhythmic)

– Not technically used for cardioversion

– DoseIV 0 1 0 25 /k IV l di d f ll d b• IV: 0.1 - 0.25 mg/kg IV loading dose followed by a

2 - 6 mcg/kg/min CRI

• PO: 0.5 - 4 mg/kg PO q8h

Pharmacological Cardioversion

• Other Options– Lidocaine

• 2mg/kg IV

– Procainamide6 8 /k IV l• 6 – 8 mg/kg IV slow

(up to 20mg/kg IV)

• 20-50 mcg/kg/min CRI

– Humans:• Propafenone (Class Ic)

• Flecainide (Class Ic)

• Dofetilide (Class III)

• Ibutilide (Class III)

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Maintaining Sinus Rhythm

• Humans: Only 20% of successfully cardiovertedpatients maintain NSR without chronic antiarrhythmic therapy

• Best Antiarrhythmic Choices:A i d– Amiodarone

– Sotalol

• What to do about lone

atrial fibrillation?

Rate Control

• Prolong AV Refractory Period & Slow Conduction

• “ABCD for SVT”

- Amiodarone- Beta-blockers

- Calcium Channel Blockers- Digoxin

Rate Control – Amiodarone

• Amiodarone– Potassium Channel Blocker (Class III Antiarrhythmic)

– Also has class I, II, IV activity

– IV Dose (Nexterone) – Numerous protocols2 5 /k IV l 5 10 i• 2.5 mg/kg IV slow over 5-10 min

• Follow by 0.8 mg/kg/hr for 6 hours

• Then 0.4 mg/kg/hr for 18 hours

– Chronic Oral Dosing• 10-25mg/kg q12-24 PO

• Goal: Reduce to 5mg/kg PO q24h over 2-3 weeks

– Numerous Side Effects

Rate Control – Beta Blockers

• β-Blockers– IV

• Esmolol 0.25 – 0.5 mg/kg IV slow followed by a 50 – 200 mcg/kg/min CRI

– PO– PO• Atenolol D: 0.25 – 1.5 mg/kg PO q12-24h

C: 6.25 – 12.5 mg/cat PO q12-24h

• Metoprolol D: 0.4 – 1.0 mg/kg PO q8-12h

C: 2 – 15 mg/cat PO q8h

• Propanolol D: 0.2 - 1.0 mg/kg PO q8h

C: 2.5 – 5.0 mg/cat PO q8-12h

Rate Control – CCBs

• Calcium Channel Blockers– Not affected by sympathetic drive

– Diltiazem: • IV: 0.1 - 0.25 mg/kg IV slow followed by a

2 6 /k / i CRI2 - 6 mcg/kg/min CRI

• PO: 0.5 – 4 mg/kg PO q8h

– Give slowly IV

– Side Effects• Gastrointestinal

• Lethargy

Rate Control – Digoxin

• Digoxin– Parasympathetic activation, sympathetic inhibition

– Na+-K+ ATPase Inhibitor

– Negative chronotrope, positive inotrope

– Overridden by heightened sympathetic tone

– Slow onset, long t1/2

– Dose: • D: 0.003 – 0.005 mg/kg PO q12h

• C: 0.03125 mg/cat PO q48h

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Rate Control – Digoxin

• Digoxin Toxicity– Gastrointestinal (anorexia, vomiting, diarrhea)

– Proarrhythmia• AV Block

Bi i• Bigeminy

• Atrial and ventricular tachyarrhythmias

• Treat arrhythmias with Class I agents (e.g. lidocaine)

– Potentiated by hypokalemia and renal dysfunction

– Digoxin Levels• Check trough levels 6 - 8 hours post pill

• Goal Therapeutic Range: 0.6 - 1.2 ng/mL

Rate Control – Other Options

• Other Options– Combination Therapy

• Digoxin + β-Blockers

• Digoxin + Diltiazem

• Careful with CCB + β Blocker combinations• Careful with CCB + β-Blocker combinations

– Humans:• Adenosine, Flecainide, Propafenone

Goal Heart Rate

• Goal Heart Rate– 140-160 bpm

– Breed and patient dependent

• Large and giant breed dogs normally have a sinus t < 90 b t / i d i l l h trate < 90 beats/min and require a lower goal heart

rate

– Maintain cardiac output

• Monitor via Holter

Other Therapies

• Overdrive Pacing

• Catheter Ablation

• Cryoablation

• AV Nodal Ablation &

Ventricular Pacing

• Device Therapy– Atrial pacemakers

– Atrial defibrillators

To Treat or Not To Treat

• What to do with lone AF and a normal HR?

• What are the long term consequences of AF at normal heart rates?

• Does atrial fibrillation cause DCM?

Thank You!