Supraventricular Tachycardia Teresa Menendez Hood, MD FACC Presbyterian Hospital of Dallas

Supraventricular Tachycardia

Teresa Menendez Hood, MD FACCPresbyterian Hospital of Dallas

Supraventricular Tachycardias

• AV nodal reentry tachycardia• AV reentry tachycardia - the WPW(Wolff-Parkinson White)

Syndrome• Atrial flutter• Atrial Fibrillation• Atrial Tachycardia• Sinus Tachycardia and Sinus Node Reentry

Atrial Fibrillation

• Unorganized, very rapid electrical foci in the atria• No contraction of the atria as a whole• In order to protect the ventricles, the AV node

blocks most of the atrial impulses from conducting through to the ventricles, thus protecting the ventricles

• Controlled rate = ventricular rate < 100 beats/min• Uncontrolled rate = ventricular rate > 100

beats/min

Atrial Fibrillation

• Characteristics of atrial fibrillation:– Ventricular rhythm is usually irregularly irregular

– Average ventricular rate is 160 – 180 beats/min on no drugs

– No P waves seen

– QRS interval is usually normal (narrow)

– If see discrete P waves…think of MAT• This clinical scenario is a cardiac or pulmonary patient in the ICU.

Thought to be due to a hyperadrenergic state and CCB and helpful.

Atrial Fibrillation

– Control the rate using IV calcium channel blockers or beta-blockers…IV dig does not work

– If the A-fib is chronic (> 48 hours)• Chemical cardioversion after a period of anticoagulation

• Electrical cardioversion only after anticoagulation

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

Classification of Atrial FibrillationThe 3 Ps

• Permanent - Conversion to sinus rhythm not possible

• Persistent - Capable of being converted to sinus rhythm

• Paroxysmal - Converts spontaneously to sinus rhythm

Gallagher MM and Camm AJ Clin Cardiol 1997;20:381

AF: Anticoagulation - General Points

• AF most common significant rhythm disorder – Prevalence: 1.5%-3% of patients in their 60s

5%-7% of patients in their 70s15% of patients in their 80s

• AF most potent common risk factor for stroke– Relative risk = 5

• Patients with AF can be stratified according to risk of stroke

Feinberg WM e al. Arch Intern Med 1995;155:469 Wolf PA et al. Stroke1991;22:983

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AF: Anticoagulation - General Points

• Anticoagulation (INR 2.0 - 3.0) can reduce risk of stroke by 2/3 1,2

• Aspirin has little effect on risk of stroke due to AF 3

1 Hylek EM and Singer DE. Arch Intern Med 1994;120:8972 Hylek EM et al. New Engl J Med 1966;335:5403 The Atrial Fibrillation Investigators. Arch Intern Med 1997;157:1237

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Risk Factors for Stroke in AF

Risk Factor

Prior stroke

Age

Hypertension

Diabetes

Relative Risk (multivariate)

2.5

1.4 (per decade)

1.6

1.7

Absolute RiskAge < 65 years and no risk factors, “lone AF”: 1%/yr.All others: 3.5%-8+%/yr lowered to ~1.5%/yr by warfarin

The Atrial Fibrillation Investigators Arch Intern Med 1994;154:1449

Elective Cardioversion of AFAnticoagulation

• Cardioversion appears to raise risk of embolism

– 1%-5% emboli within hours to weeks

– Anticoagulation well before and after greatly reduces risk

• Standard guideline for electrical or drug cardioversion

– INR 2 - 3 for 3 weeks before; and

– INR 2 - 3 for 4 weeks after NSR

– IF AF < 2 days’ duration, no anticoagulation

Laupacle A et al. Chest 1995;108Prystowsky EN et al. Circulation 1996;1262

Adequate Rate Control

• At office visits– Apical (not radial) heart rate (sitting): 80 /

min• On 24-hour Holter monitor

– Goal: average hourly heart rate 80 / min• Exercise testing

– Inadequate: 85% age-predicated maximum heart rate in stage I (Bruce) or 3 min of exercise

– Digoxin alone will never control the rate unless the patient has intrinsic AVN conduction system disease

Tachycardia - Induced Cardiomyopathy

• Chronic tachycardia in otherwise structurally normal heart as the sole cause of developing ventricular dysfunction

• Can follow any chronic cardiac tachyarrhythmia

Fenelon G et al. Pacing Clinical Electrophysiol 1996;19:95

Preference for Acute Cardioversion

• DC Cardioversion

• i.v. Ibutilide

• Other:

– Oral Flecainide

– Oral Propafenone

– i.v. Procainamide

Preference for Acute Cardioversioni.v. Ibutilide

• QTc 460 msec• Short duration of AF (<30 days)• No clinical CHF. K and Mg levels OK• Anesthesia risk (e.g., COPD)• Patient preference• Acute efficacy - flutter (63%), fib (31%)• Caution: risk of polymorphic VT (8%)

Stambler BS, et al. Circulation 1996; 94:1613-1621

Long term treatment

• Beyond the scope of this talk• Guided by patient symptoms• AFFIRM trial did not show any benefit of

NORMAL SINUS RHYTHM versus AFIB with rate control in patients who had minimal symptoms

• Ablation for AFIB is guided by patients’ symptoms and drug failures

Atrial Flutter

• Usually a single, irritable foci in the atria (right) • AV node protects the ventricles by blocking some of the

atrial impulses (decremental conduction)• P waves take on a “sawtooth” appearance and are called

F waves or flutter waves– Atrial rhythm and ventricular response are usually regular

– Atrial rate 250-350 beats/min. Ventricular rate varies depending on the number of impulses the AV node is blocking

– No P waves or PR interval

– QRS normal width or with aberrancy

Atrial Flutter• Treatment:

– Same as atrial fibrillation but often harder to slow the ventricular rate

– Long term treatment is ablation and NOT drugs!

RF Ablation of Atrial Flutter

• Atrial flutter involves a macro-reentry circuit within the right atrium.

• Critical areas of conduction within the right atrium are necessary to sustain atrial flutter.

• RF ablation of conduction within such critical sites (most commonly the inferior vena cava-tricuspid valve isthmus) abolishes atrial flutter in 85% of cases.

Cosio FG. Am J Cardiol. 1993;71:705-709.

Diagram of Atrial Flutter Circuit Within Right Atrium

Cosio FG. Am J Cardiol. 1993;71:705-709.

Inferior vena cava - tricuspid valve isthmus

Differential Diagnosis ofWide-Complex Tachycardia

• VT• SVT with aberrancy (atrial fibrillation/flutter)-i.e.

BB Block• Antidromic AV reentry –i.e. antegrade via WPW

accessory pathway• Atrial fibrillation, atrial flutter, atrial tachycardia, or

AV nodal reentry in setting of WPW with rapid conduction down accessory pathway that is activated as a bystander-I.e. not an integral part of the circuit.

Akhtar M. In:Zipes and Jalife. Cardiac Electrophysiology from Cell to Bedside. 1990:636.

Narrow QRS Wide QRS - BBB(Aberrant conduction)

Wide QRS - VTWide QRS - Preexcitation(Conduction via AP)

C D

A BAVN

HB

RB LB

Key ECG Signs

• Atrial activity

• QRS configuration

• R-R cycle length

• Aberrant ventricular conduction

• Response to vagal maneuvers

An EKG you will see on the Boards………..

• This has been on every Board exam I have ever taken. Please do give AVN blockers for this!When in doubt, treat as if you thought this was VT.

Atrial Fibrillation with Preexcitation

Electrocardiographic Differentiation of VT vs. SVT

with Aberrancy

• Clinical history – if the patient has had an MI in the past?…it is VT until proven otherwise

• AV dissociation

• QRS morphology

• QRS axis

• Fusion beat

• Capture beat

A-V Dissociation, Fusion, and Capture Beats in VT

Fisch C. Electrocardiography of Arrhythmias. 1990;134.

ECTOPY FUSION CAPTURE

V1 E F C

ECG Distinction of VT from SVT with Aberrancy

Favors VT Favors SVT

with Aberrancy

Duration RBBB: QRS > 0.14 sec. < 0.14 sec.LBBB: QRS > 0.16 sec. < 0.16 sec.

Axis QRS axis -90° to ±180° Normal

ECG Distinction of VT from SVT with Aberrancy

Favors VT Favors SVT

with AberrancyMorphology Precordial concordance

If LBBB: V1 duration > 30 msS wave > 70 msS wave notched or slurredV6: qR or QR R wave

If RBBB: V1: monophasic R waveqRIf triphasic, R > R1 R < R1

V6: R < S

Sinus Tachycardia

• Sinus node is still the pacemaker, but the rate is accelerated for some physiologic reason:– Rhythm is regular

– Rate > 100 beats/minute

– P wave, PR interval, and QRS complex are all normal

• Can look like Sinus Node Reentry – paroxysmal and less than 160 BPM; incidence of ~10% of all PSVT’s

Sinus Tachycardia

• Treatment:– Alleviate the underlying cause-anemia, pheo, hyperthyroid…

– Could be inappropriate ST- a type of autonomic dysfunction with HR consistently above 120

Paroxysmal Supraventricular Tachycardia

• Repeated episodes of tachycardia with an abrupt onset and ending (paroxysmal)

• SVT is usually due to a reentry mechanism.

• Could also be to abnormal automaticity or triggered activity but would have more of a warm-up and cool-down effect.

Supraventricular Tachycardia

• Characteristics:– Rhythm is regular– Rate 140-220 beats/minute– P waves may be buried in the QRS or the T wave

and may differ in morphology from sinus P waves– PR and QRS interval may be normal or prolonged.

Supraventricular Tachycardia

– Long term treatment is with ablation in most cases

– Response to vagal maneuvers is helpful

– Acutely: meds used to decrease the rate or convert the patient to NORMAL SINUS RHYTHM: Adenosine, IV Verapamil or Esmolol

– If patient is unstable: • Electrical cardioversion

Pearls

• ST depression is common during SVT and is not a marker of serious ischemia

• If the first dose of Adenosine does not work? Then add 6mg to the amount and give again (6-12-18)…do not repeat the same dose. (If given via central line then 3-6-9-12)

• Adenosine may put the patient in AFB…be ready to cardiovert.

Classification of PSVT

• Short R-P– AVRT(slow-fast)

– AVNRT

• Long R-P– Atypical forms of the AVNRT (fast-slow)or

AVRT(usually will have a negative P wave in 2,3,avf)

– Most atrial tachycardias, SNRT

– PJRT

Atrial Tachycardia

• Reentry, Automaticity and Triggered (rare) Activity have been found as causes

• Rates 120 to 150• Usually 1:1 AVN conduction and persistence

despite AV block• Usually from right atria (Ring of Fire)• Can be seen as an incisional tachycardia from

previous surgery..i.e. ASD repair• May see remission in children so do not attempt

ablation until adulthood.

AVN reentry

• Most common from of PSVT• Can occur at any age and more common in women• Typical form is down the slow and up the fast

pathway in the AVN region.• Adenosine is the drug on choice for conversion.

Need to be careful about pts with reactive airway disease and those on persantine. It may not work in pts with theophylline.

WPW

• Pre-excitation affects 3/1000 patients on routine screening….not all develop PSVT

• Antegrade (delta wave) and retrograde conduction

• More common in men• Most present in young adulthood• 15% incidence of AFIB• Multiple pathways in 10%