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CardioMonday Oct.2005

Approach to narrow QRS tachycardias

EL-SAYED M.FARAG (Msc.Cardiology)

Definiton

Narrow QRS complex tachycardias(NCT) are defined as tachyarrhythmias with a rate faster than 100 beats/minute and a QRS duration of 120 msec (0.12 sec) or less, as demonstrated on the electrocardiogram (ECG) or cardiac

monitor .

The normal QRS duration reflects normally synchronous activation of both ventricles through the His bundle, bundle branches, and terminal Purkinje conduction system.

SA node

AV node

Bundleof His

Bundle Branches

Purkinje Fibres

Internodal Pathways

Beat Originates from SA ,atrial tissue or AV Node

QRS Complex: normal, narrow

Sinus tachycardia (ST) Inappropriate sinus tachycardia (IST) Sinoatrial nodal reentrant tachycardia (SNRT) Atrial tachycardia (AT) Multifocal atrial tachycardia (MAT) Atrial fibrillation (AF) Atrial flutter (AFl) Junctional ectopic tachycardia (JET) Nonparoxysmal junctional tachycardia (NPJT) Atrioventricular nodal reentrant tachycardia (AVNRT) Atrioventricular reentrant tachycardia (AVRT)

The narrow QRS complex tachycardias include:

Altered automaticity

Triggered activity

Reentry

Mechanisms

Hypothermia decrease, hyperthermia increase phase 4 slope

Hypoxia & hypercapnia both increase phase 4 slope

Cardiac dilation increases phase 4 slope

Local areas of ischemia or necrosis increases automaticity of neighboring cells

Hypokalemia increases phase 4 slope, increases ectopics, prolongs repolarization

Hyperkalemia decreases phase 4 slope; slow conduction, blocks

1. Altered Automaticity

2. Triggered Activity

Afterdepolarization reaches threshold

Early: interrupt repolarization

Delayed: after completion of AP.

3. Reentry

Requires: available circuit, unidirectional block, and different conduction speed in limbs of circuit

Exp: WPW reciprocating tachycardia, AV-nodal reentry, …..

Fast Conduction PathSlow Recovery

Slow Conduction PathFast Recovery

The “Re-Entry” Mechanism of Ectopic Beats & Rhythms.

Electrical Impulse

Cardiac Conduction

Tissue

Tissues with these type of circuits may exist:• in microscopic size in the SA node, AV node, or any type of heart tissue• in a “macroscopic” structure such as an accessory pathway in WPW



Premature Beat Impulse

Cardiac Conduction

Tissue

1. An arrhythmia is triggered by a premature beat

2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only

Repolarizing Tissue (long refractory period)


3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway



Cardiac Conduction

Tissue


4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit



Cardiac Conduction

Tissue


NCT WORKUPECGLab. Workup ( CBC,TFT,s.electrolyte,24 hour Holter monitorContinuous loop event recorderEchocardiogramTreadmill test ( with or after exercise)

ALL ARE NARROW BUT THE DIFFERENCE IS WIDE

!!

Tachycardias Arising From the Sinus Node Region

Sinus tachycardia and Inappropriate sinus tachycardia

Sinus node rentry tachycardia

Sinus node reentry tachycardia

Sinus node reentry tachycardia arises from a reentrant circuit involving the sinus node, producing P waves that are fairly similar if not identical to those during sinus rhythm .

sinus node reentry can be initiated and terminated abruptly by a premature atrial stimulus, which is consistent with its reentrant mechanism. It is usually nonsustained and associated with slower rates than inappropriate sinus tachycardia, making it clinically insignificant.

Carotid sinus massage and other vagal maneuvers typically slow or terminate sinus node reentry.

Inappropriate sinus tachycardiaIt is a clinical syndrome characterized by sinus tachycardia without an identifiable physiologic stimulus. Secondary causes for resting sinus tachycardia must be ruled out, such as anemia, hyperthyroidism, pheochromocytoma, and diabetes mellitus with autonomic dysfunction.

At least two clinical variants have been described: (1) resting heart rate of 100 beats/min or greater and (2) increased heart rate response to minimal exertion .Sinus rates greater than 200 beats/min are not characteristic of inappropriate sinus tachycardia, and paroxysmal increases in heart rate are not seen.

The mechanism of inappropriate sinus tachycardia is still speculative but is thought to be a primary abnormality of the sinus node complex characterized by a high intrinsic heart rate, beta-adrenergic hypersensitivity,

and accentuation by a depressed cardiovagal reflex.

Atrioventricular Node Reentrant Tachycardia

(AVNRT)

The most common form of paroxysmal SVT is AV node reentrant tachycardia (AVNRT), which accounts for greater than 60% of cases referred to an electrophysiology laboratory. Patients typically present in their 30s or 40s, with greater than 70% being women .Although the mechanism for AVNRT is reentry involving the AV node, the precise location of the reentrant circuit is uncertain but includes atrial tissue surrounding the AV node. The reentrant circuit consists of an anterograde limb and a retrograde limb.

Types of AVNRTCommon (Slow – Fast).

Uncommon :

*Fast-Slow

*Slow-Slow

Common AVNRT

Uncommon AVNRT

Atrioventricular Reentrant Tachycardia Mediated by Accessory Pathways.

The second most common form of paroxysmal SVT is AV

reentrant tachycardia (AVRT) using an accessory pathway

Accessory pathways are discrete bundles of myocardial tissue

bridging the atrium and ventricle along the tricuspid or mitral

valve annulus. More than half of accessory pathways are

situated in the left free wall, 20% to 30% occur in the

posteroseptal location, 10% to 20% occur in the right free wall,

and 5% to 10% occur in the anteroseptal location near the AV

node.

Because the accessory pathway conducts more rapidly

than the normal conduction system, the ventricle is

producing a short P-R interval and a delta wave on the

surface ECG .

In contrast, about 25% of accessory pathways conduct

only retrogradely and are not manifest on the ECG

during sinus rhythm (Concealed accessory pathway).

Orthodromic atrioventricular reentrant tachycardia

involving an accessory pathway,the tachycardia is narrow

complex because of anterograde conduction down the AV

node and His-Purkinje system. Retrograde atrial

activation over the accessory pathway results in a P wave

within the early ST segment .

Ex.RT.Anteroseptal AP

Atrial tachycardia is less common than AVNRT or AVRT,

accounting for fewer than 15% of patients referred for

electrophysiology study. It can occur in the pediatric

population, especially in children with surgically corrected

congenital heart disease. Atrial tachycardia usually arises from

a single localized atrial focus .

Atrial Tachycardia

Atrial Tachycardia (3:2 & 2:1)

Paroxysmal junctional reciprocating Tachycardia ( PJRT)

Multifocal atrial tachycardia (MAT)

Multifocal atrial tachycardia is a rare SVT. It involves more than one atrial focus and requires at least three distinct P wave morphologies to be diagnosed on the surface ECG.

Because the foci fire independently of one another, the atrial rate is irregular and typically averages 100 beats/min. The P-R interval also may vary depending on the location of the foci relative to the AV node

The mechanism for multifocal atrial tachycardia has not been defined clearly but may be due to enhanced automaticity or triggered activity. Most patients with this arrhythmia have exacerbations of severe

underlying pulmonary disease with hypoxia.

Jnctional TachycardiaJunctional tachycardias arise from a discrete focus within the AV node or the His bundle. In the pediatric population, junctional tachycardia also is known as junctional ectopic tachycardia .

Junctional ectopic tachycardia presenting before 6 months of age usually is associated with underlying heart disease that carries a high mortality. In contrast, adult junctional tachycardia has a more benign prognosis and typically develops after the acute phase of myocardial infarction, digitalis intoxication, and acute myocarditis.

Although the precise mechanism for junctional tachycardia has not been defined, it is likely due to enhanced impulse initiation in the region of the AV node by automaticity or triggered activity rather than reentry

Nonparoxysmal atrioventricular junctional tachycardia in a healthy young adult. Top, This tachycardia occurs at a fairly regular interval (“W-shaped” complexes) and is interrupted intermittently with sinus captures that produce functional right and left bundle branch blocks. Middle, Two P waves are indicated by arrowheads. The junctional discharge rate is approximately 120 beats/min (cycle length = 500 milliseconds) and the rhythm irregular, sometimes shortened by sinus captures or delayed by concealed conduction that resets and displaces the junctional focus. Bottom, Carotid sinus massage slows the junctional as well as the sinus discharge rates.

Atrial Flutter

Atrial flutter is an atrial arrhythmia characterized by a regular rate, a uniform morphology, and a rate

greater than 240 beats/min. Atrial flutter is usually accompanied by a fixed 2:1 ventricular response,

and it is this rapid ventricular response that results in most symptoms. Atrial flutter may be observed

transiently after cardiac surgery or may persist for months to years. Many different forms of atrial

flutter exist, which has led to multiple classification schemes.

Classification of atrial Flutter

Common (Typical)

- Isthmus dependant

- Non Isthmus dependant

Uncommon (Atypical)

Type I atrial flutter

Type II atrial Flutter

Atrial Fibrillation Atrial Fibrillation

Atrial fibrillation (AF) is the most common sustained cardiac rhythm disturbance occuring in approximately 0.4 to 1% of general population with increasing prevelance with age (10% over 80 years)AF may be:

Primary, no underlying disease Secondary to: HPT, IHD, MVD, …...

Increased MorbidityEmbolic complications (stroke)Reduced cardiac function; hemodynamic changesComplaints and symptomsIncreased mortality

Induction of atrial fibrillation by a premature atrial beat originating in the orifice of one of the pulmonary veins. These triggers can be caused by microreentrant circuits that occur in the transitional zone of cells as the pulmonary vein endothelium transitions into the left atrial endocardium

The trigger for the induction of intermittent atrial fibrillation is located in the pulmonary veins in 90% of patients and outside the pulmonary vein area in 10% of patients

IT IS TOO WIDE HOW TO NARROW??

Take home messege

Observe either the onest or the termination.

Note the P ,PR and RP.

Do vagal maneuver and adenosine.

STILL VAGUE?EPS

Electrophysiologic study

HRA

HIS ds

HIS px

CSp

CSds

RVa

CS

RV

HRA HIS

Abl

Ex. Concealed LLAP

Ex.SA reentry

Ex. PAF (RUPV)

EX.Atrial tachycardia by CARTO (electroantomic mapping)

HOW TO TREAT?

Priority order: •Ca2+ Channel blocker• B-Blocker• Digoxin• DC cardioversion• Consider procainamide, amiodarone, sotalolPriority order:

• No DC cardioversion• Amiodarone• Diltiazem

• No DC cardioversion• Amiodarone

• No DC Cardioversion• Amiodarone• B-Blocker• Ca2+ channel blocker

• No DC cardioversion• Ca2+ channel blocker• B-Blocker• Amiodarone

• No DC cardioversion• Amiodarone• Diltiazem

Preserved

Preserved

Preserved

EF<40%, CHF

EF<40%, CHF

EF<40%, CHF

Junctional tachycardia

Paroxysmal supraventricular tachycardia

Ectopic or multifocal atrial tachycardia

Attempt therapeutic diagnosis maneuver• Vagal stimulation• Adenosine

Narrow-Complex SupraventricularTachycardia, Stable

Non Pharmacologic AF therapy

Catheter ablation.

Atrial pacing (single or dual site pacing).

Intraatrial ICD.

AFFIRM TRIAL

RACE TRIAL

SPECIAL GROUP NEEDS SPECIAL TREATMENT

WHAT IS COLOUR OF THIS TISSUE!!???

Thank You Thank You

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Documents

slope slow conduction

terminal purkinje conduction

different conduction

fast conducting pathway

slow pathway

slow conducting pathway

accessory pathway

atrial tissue