SUPRVENTRICULAR TACHYARRHYTHMIAS

Mohammad Hassan Khedr MD Cardiology

Case #1

Q. A 32 year old female is treated in the emergency room for palpitations. The first ECG is tachycardia and the second is after adensosine.What is the arrhythmia?

A. AVNRT B. ORT C. Atrial tachycardia D. Atrial fibrillation

Answer: AVNRT (A)

A small R’ is seen is lead V1 with pseudo-S waves in the inferior leads that are absent after termination of the arrhythmia. These represent retrograde atrial activation with a very short RP interval.

Q. A 42 year old smoker presents to the ED with palpitations. His blood pressure is 110/60. The following rhythm strip is obtained . What is the next appropriate step?

Emergent cardioversion for polymorphic VT. B. I.V. procainamide C. I.V. lidocaine D. diltiazem drip to obtain rate control.

Approach to classification of SVT1) Clinical behavior (ie. Paroxysmal, persistent,

permanent, incessant, sustained, nonsustained, chronic, and repetitive)

2) Mechanism (ie, ectopic, automatic, reenterant, orthodromic, antidromic)

3) ECG appearance (narrow or wide)4) Location (sinus, atrial, AV nodal/ juntional)

Mechanism

All cardiac tachyarrhythmias are produced by one or more mechanisms including:

1) Disorders of impulse initiation 2) Abnormalities of impulse conduction.

Mechanisms of Arrhythmia

Abnormal automaticity automatic impulse generation from unusual site

or overtakes sinus node Triggered activity

secondary depolarization during or after repolarization

Dig toxicity, Torsades de Pointes Reentry

90 % of arrhythmiasythmias

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

Altered Automaticity

Reentry

Most common mechanism

Requires two separate paths of conduction

Requires an area of slow conduction

Requires unidirectional block

Symptoms

palpitations fatigue lightheadedness Chest discomfort dyspnea Presyncope Polyurea (release of atrial natriuretic peptide in

response to increased atrial pressures from contraction of atria against a closed AV valve)

Syncope (rare)

Clues from Symptoms

Regular vs. Irregular Premature depolarizations,

AF, MAT AVNRT, AVRT

Sudden onset and offset No clear precipitating

factor

AT Gradual onset of

symptoms and get more rapid over time (warm-up)

Particular maneuver or position provokes the syndrome

Supraventricular TachycardiasDiagnosis

ECG is cornerstone Observe zones of transition for clues as to

mechanism: onset termination slowing, AV nodal block bundle branch block

Regular SVT in adults

90% reentrant 10 % not reentrant 60% AV nodal reentrant tachycardia (AVNRT) 30% orthodromic reciprocating tachycardia

(ORT) 10% Atrial tachycardia 2 to 5% involve WPW syndrome

Differential Dx of Regular SVT

Short RP tachycardia AV nodal reentrant

tachycardia ORT( Orthodromic

reciprocating tachycardia)

Atrial tachycardia when associated with slow AV nodal conduction (rare)

Short RP interval

Differential Dx of Regular SVT

Long RP tachycardia Atrial tachycardia Sinus node reentry Sinus tachycardia Atypical AV nodal

reentrant tachycardia

Long RP interval

Sinus Tachycardia

Appropriate physiological stimulus (eg, exercise) or to an excessive stimulus (eg, hyperthyroidism).

Pyrexia Hypovolemia Anemia Drugs

caffeine, alcohol, nicotine Prescribed compounds

(eg, salbutamol, aminophylline, atropine, catecholamines)

Recreational/illicit drugs (eg, amphetamines, cocaine, “ecstasy,” cannabis

Anticancer treatments

Physiological Stimulus Pathological Causes

Management

Treat underlying mechanism Beta blockade for physiological symptomatic

sinus tachycardia triggered by emotional stress and other anxiety related disorders

Other Long RP tachycardias

Sinus node reentrant abrupt onset and

offset P wave complex

same as sinus Amenable to calcium

channel blockers, much less responsive to beta blockers

Amenable to catheter ablation

Syndrome of inappropriate sinus tachycardia typical sinus

tachycardia with lowest rate on Holter of 130 bpm

Treated with high dose beta blockers

Poor results with catheter ablation

AV Nodal Reentrant Tachycardia

2 pathways within or limited to perinodal tissue anterograde

conduction down fast pathway blocks with conduction down slow pathway, with retrograde conduction up fast pathway.

Slow pathway

Fast pathway

Fast Conduction PathSlow Recovery

Slow Conduction PathFast Recovery

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)

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

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

Fast Conduction PathSlow Recovery

Slow Conduction PathFast Recovery

Cardiac Conduction

Tissue

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

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

Fast Conduction PathSlow Recovery

Slow Conduction PathFast Recovery

Cardiac Conduction

Tissue

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

Initiation of AV Nodal Reentrant Tachycardia

PAC = premature atrial complex (beat)

PAC

PAC

Sustainment of AV Nodal Reentrant Tachycardia

Rate 150-250beats per min

P waves generatedretrogradely(AV node→ atria) andfall within orat tail of QRS

May have very short RP interval with retrograde P wave visible as an R’ in lead V1 or psuedo-S wave in inferior leads in 1/3 of cases .

No p wave seen in 2/3

Tachycardia Algorithm (1 of 2)38

Tachycardia Algorithm (2 of 2)39

Narrow QRS Tachycardia40

AV Nodal Reentrant Tachycardia

Responds to vagal maneuvers in 1/3 cases

Very responsive to AV nodal blocking agents such as beta blockers, Ca channel blockers, adenosine.

Recurrences are the norm on medical therapy

Catheter ablation 95% successful with 1% major complication rate

Determining AV Nodal Participation in SVT by Transiently Depressing AV Nodal Conduction

Vagotonic Maneuvers Carotid sinus massage Valsalva maneuver (bearing down) Facial ice pack (“diving reflex;” for kids)

Adenosine (6-12 mg I.V.) If SVT “breaks,” a reentrant mechanism

involving the AV node is likely If atrial rate unchanged, but ventricular rate

slows (#P’s > #QRS’s), SVT is atrial in origin

Carotid Sinus Massage

Stimulation of carotid sinus triggers baroreceptorreflex and increased vagaltone, affectingSA and AV nodes

Termination of SVT by Vagotonic Maneuver (Carotid Sinus Massage)

SVT

Carotid Sinus Massage

Junctional Tachycardias

1) Focal Junctional Tachycardia (automatic orparoxysmal junctional tachycardia)

2) Non paroxysmal Junctional Tachycardia

Focal Junctional Tachycardia

- Uncommon- Pediatrics or post-

op

The ECG features: HR 110 to 250 bpm A narrow complex or

typical BBB conduction pattern

Atrioventricular dissociation is often present

Nonparoxysmal Junctional Tachycardia Narrow complex

tachycardia with rates of 70 to 120 bpm

A typical “warm-up” and “cool-down” pattern

The arrhythmia mechanism enhanced automaticity

arising from a high junctional focus or

in response to a triggered mechanism

it may be a marker for a serious underlying condition, such as digitalis toxicity, postcardiac surgery, hypokalemia, or myocardial ischemia

Ex . RT. Ante ro s e p ta l AP

AVRT

Orthodromic tachycardia- 95%

ORT with a concealed accessory pathway (retrograde only conducting pathway)

Antidromic tachycardia- 5%

Sustainment of Orthodromic AV Reciprocating Tachycardia

Atria

AP

AVN

Ventricles

Retrograde P’s fall in the ST segmentwith fixed, short RP

Rate 150-250beats per min

Accessory Pathway with Ventricular Preexcitation(Wolff-Parkinson-White Syndrome)

“Delta” Wave

APPR < .12 s

QRS ≥ .12 s

Sinusbeat

Hybrid QRS shape

In sinus rhythm, every ventricular activation is a fusion between accessory pathway and AV nodal conduction

Varying Degrees of Ventricular Preexcitation

ORT

Amenable to AV nodal blocking agents in absence of anterograde conduction of pathway

Amenable to catheter ablation with 95% success and 1% rate major complication

Conduction down AVnode

Up accessory pathway

WPW syndrome The diagnosis of WPW

syndrome is reserved for patients who have both pre-excitation and tachyarrhythmias

AVRT is the most common arrhythmia, accounting for 95% of re-entrant tachycardias that occur in patients with an accessory pathway

Louis Wolff, Sir John Parkinson and Paul Dudley

Classic ECG pattern

Accelerated AV conduction PR <120 msec

Prolonged QRS > 120 msec Abnormal slurred upstroke of QRS ( delta

wave) Abnormal depolarization and

repolarization may lead to pseudoinfarction pattern

WPW epidemiology

Present in 0.3% of the population

Risk of sudden death 0.15% to 0.39% over 3- to 10-year follow-up

Sudden death due to atrial fibrillation with rapid ventricular conduction

Atrial fibrillation often induced from rapid ORT

ORT(orthodromic reciprocating tachycardia

Markers associated with increased sudded cardiac death1) a shortest pre-excited R-R interval less than 250 ms during spontaneous or induced AF2) a history of symptomatic tachycardia3) multiple accessory pathways4) Ebstein’s anomaly

The detection of intermittent preexcitation, which is characterized by an abrupt loss of the delta wave and normalization of the QRS complex, is evidence that an accessory pathway has a relatively long refractory period and is unlikely to precipitate VF.

The loss of pre-excitation after administration of the antiarrhythmic drug procainamide has also been used to indicate a low-risk subgroup.

Antiarrhythmic drugs that primarily modify conduction through the AV node include: digoxin, verapamil, beta blockers, adenosine, and diltiazem

Antiarrhythmic drugs that depress conduction across the accessory pathway include: Class I drugs, such as procainamide, disopyramide,

propafenone, and flecainide, as well as class III antiarrhythmicdrugs, such as ibutilide, sotalol, and amiodarone.

Atrial Fibrillation and WPW

Atrial fibrillation is a potentially life-threatening arrhythmia in patients with WPW syndrome.

If an accessory pathway has a short anterograde refractory period, then rapid repetitive conduction to the ventricles during AF can result in a rapid ventricular response with subsequent degeneration to VF.

Atrial Fibrillation and WPW

AV nodal blocking agents may paradoxically increase conduction over accessory pathway by removing concealed retrograde penetration into accessory pathway. Concealed penetration into the

pathway causes intermittent block of pathway conduction

Management of Atrial Fibrillation with WPW

Avoid AV nodal blockers IV procainamide to slow accessory pathway

conduction Amiodarone if decreased LVEF DC cardioversion if symptomatic with

hypotension

Management of Patients with WPW

All patients with symptomatic AF & WPW should be evaluated with EPS

Accessory pathways capable of conducting faster than 240 BPM should be ablated

Patients with inducible arrhythmias involving pathway should be ablated

WPW patients in high risk professions should be ablated.

Atrial Tachycardia

Atrial rate between 100 and 250 bpm Does not require AV nodal or infranodal

conduction P wave morphology different than sinus P-R interval > 120 msec differentiating from

junctional tachycardia

Atrial tachycardia P wave upright lead V1 and negative in aVL

consistent with left atrial focus. P wave negative in V1 and upright in aVL

consistent with right atrial focus. Adenosine may help with diagnosis if AV block

occurs and continued arrhythmia likely atrial tachycardia

Atrial Tachycardia

Most are due to abnormal automaticity and have right atrial focus

May be reentry particularly in patients with previous atriotomy scar, such as CABG or congenital repair patients

it is often associated with

underlying cardiac abnormalities