Ahmad Hersi Consultant Electrophysiologist Assistant Professor

Ahmad HersiConsultant Electrophysiologist

Assistant Professor

Dysrhythmias

• Ventricular Tachycardia (VT)• Ventricular Fibrillation (VF)• Torsade de point• Polymorphic VT

•Sinus Tachycardia• Atrial Tachycardia• Atrial Flutter• Atrial Fibrillation• AVRT• AVNRT•Junctional Tachycardia

Atrial fibrillation accounts for 1/3 of all

patient discharges with arrhythmia as principal diagnosis.

2% VF

Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.

34% Atrial

Fibrillation

18% Unspecified

6% PSVT

6% PVCs

4% Atrial Flutter

9% SSS

8% Conduction

Disease3% SCD

10% VT

Outline Atrial FibrillationDescription

Chaotic and disorganized atrial activity Irregular heartbeat Can be paroxysmal, persistent or

permanent (chronic) Most common sustained arrhythmia Can be symptomatic or asymptomatic Incidence increases with age

Atrial Fibrillation Demographics by Age

Adapted from Feinberg WM. Arch Intern Med. 1995;155:469-473.

U.S. population

Population withatrial fibrillation

Age, yr

<5 5-9

10-14

15-19

20-24

25-29

30-34

35-39

40-44

45-49

50-54

55-59

60-64

65-69

70-74

75-79

80-84

85-89

90-94

>95

U.S. populationx 1000

Population with AFx 1000

30,000

20,000

10,000

0

500

400

300

200

100

0

Atrial Fibrillation

Common and age-dependent2 - 4% over age 60

Significant risk of stroke4% per year (Framingham Study)

High risk of embolism with cardioversion

Incidence of AF

The Framingham Study 1982,The Framingham Study 1982, New England New England Journal of MedicineJournal of Medicine

Annual Incidence 0.1% Per YearAnnual Incidence 0.1% Per Year

Atrial Fibrillation: Causes

Cardiac Non-cardiac “Lone” atrial fibrillation

Atrial Fibrillation: Cardiac Causes Hypertensive heart disease Ischemic heart disease Valvular heart disease

– Rheumatic: mitral stenosis– Non-rheumatic: aortic stenosis, mitral regurgitation

Pericarditis Cardiac tumors: atrial myxoma Sick sinus syndrome Cardiomyopathy

– Hypertrophic– Idiopathic dilated (? cause vs. effect)

Post-coronary bypass surgery

Atrial Fibrillation: Non-Cardiac Causes

Pulmonary– COPD– Pneumonia– Pulmonary embolism

Metabolic– Thyroid disease: hyperthyroidism– Electrolyte disorder

Toxic: alcohol (‘holiday heart’ syndrome)

“Lone” Atrial Fibrillation

Absence of identifiable cardiovascular, pulmonary, or associated systemicdisease

Approximately 0.8 - 2.0% of patients with atrial fibrillation (Framingham Study)1

In one series of patients undergoing electrical cardioversion, 10% had lone AF.2

1 Brand FN. JAMA. 1985;254(24):3449-3453.

2 Van Gelder IC. Am J Cardiol. 1991;68:41-46.

Forms of AF

– Paroxysmal Paroxysmal lasting less than 48 hours, transient

– Persistent An episode of AF lasting greater than 48 hours, which can still be

cardioverted to sinus rhythm

– Permanent – Inability of pharmacologic or non-pharmacologic methods to restore

sinus rhythm

Symptoms

Palpitations Presyncope Fatigue Chest pain Dyspnea Syncope

Work-up

EKG ECHO TFT 24 h Holter Others…..

ECG Recognition

Atrial Rate: > 300 bpm Rhythm: Irregular

– Ventricular Rate: Variable • Dependent upon: • AV node conduction properties • Sympathetic and parasympathetic ton

Recognition: Absence of P waves

Atrial Fibrillation: Clinical Problems Embolism and stroke (presumably due to LA clot) Acute hospitalization with onset of symptom Congestive heart failure

– Loss of AV synchrony

– Loss of atrial “kick”

– Rate-related cardiomyopathy due to rapid ventricular response

Rate-related atrial myopathy and dilatation Chronic symptoms and reduced sense of well-being

Management Strategies

Prevention of Thromboembolis

Rate control

Restoration of sinus rhythm

Therapeutic Approaches to Atrial Fibrillation

Anticoagulation

Antiarrhythmic suppression

Control of ventricular response– Pharmacologic

– Catheter modification/ablation of AV node

Curative procedures– Surgery (maze)

– Catheter ablation

Prevention of Thromboembolis

Atrial Fibrillation and Stroke

Risk: 5 - 8% per year in high-risk patients

Anticoagulant therapy is clearly indicated and beneficial in rheumatic atrial fibrillation.

In non-rheumatic atrial fibrillation, major randomized trials have provided useful guidelines for identifying and treating patients at risk.

Predictors of Thromboembolic Risk in Atrial Fibrillation

Congestive Heart Failure

Hypertension

Age ≥75 years

Diabetes

Stroke or TIA

CHADS2

CHADS2 Score and Risk of Stroke

JAMA 2001;285:2864

Restoration of sinus rhythm

Antiarrhythmic Drugs to SuppressAtrial Fibrillation

Class I agents– IA: quinidine, procainamide, disopyramide

– IC: flecainide, propafenone

Class III agents– amiodarone, sotalol

Chronic1 month coumadin cardioversion (CV)

Uncertain durationStable 1 month coumadin CVUnstable TEE CV

Acute

Timing of Cardioversion for Atrial Fibrillation

coumadin repeat TEE CV

no clot

clot

Heparin TEECV coumadin

Rate control

Control of Ventricular Rate in Atrial Fibrillation

Digoxin

Calcium channel blockers

Verapamil, diltiazem

Beta blockers

Sinus Tachycardia (ST)

Clinical Conditions Associated with Persistent Clinical Conditions Associated with Persistent Sinus TachycardiaSinus Tachycardia

Fever

Volume depletion

Anemia

Sepsis (due to profound vasodilatation reflex tachycardia)

Pain / anxiety

Hypoxemia (PE / COPD)

Cardiac conditions decreased cardiac output (CHF / MI)

Medications (B2 agonists)

Drugs (crack / ephedrine)

Hyperthyroidism

Rx – Sinus TachycardiaRx – Sinus Tachycardia

Sinus tachycardia is almost always a physiologic response to a given stimulus or disease state

In most situations, do not treat sinus tachycardia, treat the underlying process

Focal Atrial Tachycardia

Causes – Atrial TachycardiaCauses – Atrial Tachycardia

Onset is often precipitated by increased sympathetic stimulation

Specific examples:• Digoxin toxicity (especially if AV block noted)• Theophylline (beta-agonist)• EtOH• Myocardial ischemia• Hypoxia

Rx – Atrial TachycardiaRx – Atrial Tachycardia

Rhythm often spontaneously resolves with normalization of sympathetic tone

If rhythm recurs repeatedly, consider Rx:• Step #1 – beta-blockers (BB)• Step #2 – amiodarone (not if dig toxic)• Step #3 – radio-frequency ablation is curative

Kowey PR. Arch Int Med. 1998; 158: 325

Atrial Flutter with 2:1 AV block

Background - Atrial FlutterBackground - Atrial Flutter

Underlying mechanism – large “macro re-entrant circuit” in the atrium, typically moves counter-clockwise

Atrial rate range: 250-350 bpm Ventricular response depends on the degree of AV block:

• 2:1 block ventricular rate = 150 bpm• 3:1 block 100 bpm• 4:1 block 75 bpm

Causes – Atrial FlutterCauses – Atrial Flutter

Most commonly occurs in male patients with dilated or distended atria with elevated left atrial pressure

Clinical scenarios:– Systolic CHF with low EF– Mitral regurgitation (MR)

Rx – Atrial FlutterRx – Atrial Flutter

Unstable pt (i.e. low BP / CP / AMS):• Synchronized cardioversion as per ACLS • 50J 100J 200J 300J 360J

Stable pt:• Rate control - just like atrial fibrillation (AFib)• Elective cardioversion - just like AFib• Anti-coagulation – just like AFib

Atrioventricular Nodal Re-entrant Tachycardia

(AVNRT) or AVRT

AVNRT or AVRT

Rx – AVNRT / AVRTRx – AVNRT / AVRT Unstable:

– Synchronized cardioversion start @ 50J (avoid if EF < 40%)

Stable:– Step #1 – attempt to terminate rhythm with vagal

maneuvers (carotid massage / Valsalva)– Step #2 – adenosine 6mg IVP 12mg 2min later

18mg 2min later– Step #3 – AV nodal blocking agents (BB / CCB > digoxin)– Step #4 – amiodarone 150mg IV over 10min 1mg/min

x 6hrs 0.5mg/min x 18hrs (max dose 2.2g/24hrs)

– Step #5 – in pts with bypass tracts not tolerating the medications, consider radio-frequency ablation

ACLS 2000 / Wang YS, et al. JACC. 1991; 18:1711

Wolf-Parkinson-White (WPW) Syndrome

Take Home Messages - WPWTake Home Messages - WPW Syndrome features:

• Short PR• Broad irregular QRS complexes due to Delta waves• Ventricular rates up to 300 bpm

Conduction along the accessory pathway:• Orthodromic – conduction to ventricles over normal AV

node-His-Purkinje path• Antidromic – conduction to ventricles via accessory path

Medical Rx:• 1st choice – procainamide 20mg/min IV (max 17mg/kg)• Drugs to avoid – AV nodal blocking agents!!!• Radio-frequency ablation curative > 95% cases

ACLS 2000 / Krahn AD. Ann Intern Med. 1992; 116: 456

So What Is Actually Meant By So What Is Actually Meant By Supraventricular Tachycardia?Supraventricular Tachycardia?

Arrhythmias of supraventricular origin using a re-entrant mechanism with abrupt onset & termination

AVNRT (60%)

AVRT (30%)

Atrial tachycardia (10%)

Ventricular Tachycardia (VT)

Brugada EKG Criteria for VTBrugada EKG Criteria for VT

AV dissociation

R-S interval > 100 ms

No RS morphology in pre-cordial leads

Dr. Brugada (Cardiology) @ Noon Conference – The Methodist Hospital 9/00

Classification - VTClassification - VT Duration:

– Sustained VT (> 30 seconds or hemodynamic compromise)

– non-Sustained VT (< 30 seconds)• Risk factor for sudden death among pts with heart dz

QRS morphology:– Monomorphic (common in pts with CAD)– Polymorphic (usually associated with a prolonged QT)

ACP - MKSAP 12. Cardiovascular Medicine: 24

Rx – VTRx – VT

Hemodynamically Unstable:– Unsynchronized cardioversion as per ACLS protocol for VF /

pulseless VT

Unstable (CP / AMS):– Synchronized cardioversion as per ACLS protocol

Rx – VTRx – VT Stable:

– Rx ischemia– Correct electrolytes (K / Mg / Ca)– Consider cardioversion (yes even in stable pts!!)– EF > 40%:

• Procainamide / sotalol (class IIa)• amiodarone (class IIb)

– EF < 40%:• amiodarone (class IIa)

Torsades de Pointes

Causes – Torsades de PointesCauses – Torsades de Pointes

Underlying Mechanism – prolongation of the QT interval coupled with R-on-T phenomenon

Medications (Class Ia anti-arrhythmics / TCAs)

Electrolyte abnormalities (Mg / K)

Bradycardia (usually s/p inferior MI)

Rx – Torsades de PointesRx – Torsades de Pointes

Unstable:• Cardioversion as per ACLS protocol for VT based on

hemodynamics (refer to prior slides)

Stable:• Correct electrolytes (K / Mg)• Hold any culprit medications • magnesium sulfate 2g IVP + repeat prn• Transcutaneous overdrive pacing

Summary - WideSummary - Wide

Ventricular tachycardia (VT)

Torsades de Pointes (sub-type of VT)

Any supraventricular tachycardia with aberrancy (e.g. sinus tach with pre-existing bundle branch block)