approach to a case of narrow complex tachycardia

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narrow complex tachycardia is an important clinical cxondition to be known in acute medical care.......24/08/2011

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APPROACH TO A PATIENT

WITH NARROW

QRS COMPLEX

TACHYCARDIA

24-08-2011Dr.Nagula Praveen

My first CASE experience …

1.A 35 yr old female came to medicine OP with complaints of pounding sensation in the heart,dizziness.lightheadedness..the episode lasted for few minutes relieved spontaneously without any efforts..ending up in the patient passing urine after the absence of palpitations…on examination her heart heart was normal…there are no neck abnormalities…no other features..her BP is normal ..her thyroid status is normal ..What is the diagnosis was asked ?

SUPRAVENTRICULARTACHYCARDIA

CASE scenario

A 28 yr old woman has rapid palpitations accompanied by chest pain and dizziness while playing her cello.she is brought to an ED.she has a faint regular pulse of 180 bpm.her blood pressure is 100/70 mm Hg.cardiovascular signs reveals no signs of heart failure.an ECG show a regular tachycardia with a narrow QRS complex and no apparent Pwaves ..how should her case be managed?

Clinically

Patient complains of recurrent palpitations,chest fullness,light headedness,presyncope,syncope.

Ppt factors may be present – exercise,caffeine,cigarette smoking,alcohol.

h/o heart disease,pulmonary disease,post AFablation. CAUTION :H/O DIGOXIN USE On examination– neck pounding –cannon waves “frog’s sign “

– practically pathognomic of AVNRT. HR is a non specific feature in differentiating SVTs.

STEP wise

Look for QRS duration. QRS complex regular/irregular. Then look for presence of p waves. P waves morphology P waves and QRS relationship 1:1 AV block present. QRS alternation Termination initiation of tachycardia. Effect of BBB on tachycardia cycle length.

Decision tree schema by BAR and colleagues STEP 1 –FOR ANY FAILURE OF AV CONDUCTION –AV block present ectopic atrial tachycardia.

STEP 2 – QRS alternation –each QRS is different from subsequent one by 5 mm –AVRT ,other tachycardia also

STEP 4 – p wave morphology in frontal plane –negative in lead I LEFT SIDE BYPASS TRACT.

STEP 5 –P WAVE in horizontal plane .left side,right side ..

Ref–ncbl.org.in

In brief from the diagram clues

Response to carotid sinus massage or adenosine –with termination of arrhythmia with Pwave –AVNRT with atrial premature beat .

Tachycardia persists with AV block –AT,AFL,SANRT Pseudo r ‘ wave in V1 –AVNRT SHORT RP interval – AVNRT,AVRT Long RP interval – AT,SANRT,AVNRT atypical

NARROW COMPLEX QRS TACHYCARDIA

SHORT RP INTERVAL

TYPICAL AVNRT

AVRT

LONG RP INTERVAL

ATYPICA

L AVNRT

AVRT

slow retrograde

conduction

Permanent Form

junctional

tachycardia

ATRIAL TACHYCARDIA

SANRTINAPPROPRIATE ST

ECG findings

Main Mechanisms and Typical Electrocardiographic Recordings of Supraventricular Tachycardia.

Pwaves

no

Irregular R-R

intervalATRIAL

FIBRILLATIO

N

Regular

R-R interv

al

AVNRT

yes

NORMAL MORPHOLOGY

SINUS TACHYCARDIASINUS NODE REENTRY

INAPPROPRIATE SINUS TACHYCARDIA

Differentiation of AVNRT from AVRT

P wave present but not of same morphology as sinus rhythm

Pseudo r’ wave in

V1

AVNRT

Pseudo S wave on lead II

AVNRT

Pwave ST-T

changes

Positive in

lead I

AVRT

Right

posterosepta

lAccessor

y pathway

Negative

in lead

I

AVRT

Left side

d accessory pathwa

y

AVNRT

Presence of a narrow complex tachycardia with regular R-R intervals and no visible p waves.

P waves are retrograde and are inverted in leads II,III,AVF.

P waves are buried in the QRS complexes –simultaneous activation of atria and ventricles – most common presentation of AVNRT –66%.

If not synchronous –pseudo s wave in inferior leads ,pseudo r’ wave in lead V1---30% cases .

P wave may be farther away from QRS complex distorting the ST segment ---AVNRT ,mostly AVRT.

AV NODAL REENTRANT TACHYCARDIA

AFTER ADENOSINE

AV-nodal-re-entry-tachycardia-(AVNRT)-on-an-ECG-heart-monitor[www.savevid.com].flv

AVRT

Typical – RP interval < PR interval RP interval > 80 milli sec Atypical –RP interval > PR interval Concealed bypass tract – only retrograde conduction Manifest bypass tract– both anterograde and

retrograde. Electrical alternans –the amplitude of QRS complexes

varies by 5 mm alternatively. Rate related BBB occuring and the rate of tachycardia

is decreasing –then the bypass tract is on the same side of the block.

AV REENTRANT TACHYCARDIA

PRinterv

al RP

interval

PR interval

WPW syndrome

Two types Orthodromic Antidromic Antidromic is wide complex tachycardia In NSR detected by delta wave. Can ppt into AF and VF on use of AV nodal blockers MEMBRANE ACTIVE ANTIARRHTYHMIC DRUGS are safe. CONCEALED WPW syndrome – no delta wave .less risk of

AF

Orthodromic AVRT

LOWN GANONG LEVINE syndrome Short PR interval Normal QRS complex PSVT

Sinus Tachycardia

Focal Atrial Tachycardia

P wave morphology changes. PR interval > 0.12 sec . Second,third degree AV block can occur. Tachycardia terminates with a qrs complex .. Right atrial origin– p wave inverted in V1. If biphasic in V1—initially positive then negative. Upright in lead AVL Opposite if of left atrial origin Superior origin –upright p waves in inferior leads Inferior origin –p waves are inverted in inferior leads.

Focal atrial tachycardia (LA focus)

Multifocal Atrial Tachycardia

At least three consequtive p waves with different morphologies with a rate > 100 bpm to be present.

Isoelectric baseline between p waves. Also called as choatic atrial tachycardia Mostly seen in COPD ,electrolyte abn,theophylline Rate usually does not exceed 130-140 bpm.

Multifocal Atrial Tachycardia

SANRT

Microreentrant tachycardia Usually precipitated and terminated by

premature atrial complexes. Atrial rate is usually 120-150 bpm. IART - Large or small reentrant circuit. AV block can occur.

Junctional tachycardias Non paroxysmal – accelerated junctional rhythm Rate < 100 bpm Usually junctional node 40-60 bpm Paroxysmal or focal junctional tachycardia is rare –automaticity. 110-250bpm. P waves may be before or after QRS complex Infrequent and nonsustained episodes –no treatment Acute termination of SVT and establish the mechanism of SVT

in case of acute setting. Long term goal is abolishing the arryhthmia substrate. Precipitating factors – electrolyte

imbalance,hypoxia,ischemia,hyperthyroidism to be sought out.

Acute Treatment

Of SVT

A 12 lead ECG during tachycardia and NSR.

No delay in therapy if the mechanism of SVT is not known.

Perform CAROTID SINUS MASSAGE,or give 6mg bolus adenosine.

In case of severe hemodynamic compromise a synchronised cardioversion to be given.

Carotid sinus massage

Check for carotid bruit before massage. At the level of cricoid cartilage,at the angle of

mandible the carotid sinus is situated. Gentle pressure is applied over the carotid sinus

for 5 -10 seconds. ECG recording to be present. In case of no response – try on the other side. Simultaneous pressure not to be applied both sides. Alternative manuevres are valsalva,gag reflex,ice

water pouring over the face.

If SVT is suspected to be AVnode dependent – drug of choice is adenosine and CCBs verapamil and diltiazem.

Useful for sustained cases of AV node independent tachycardias.

But digoxin,BBs,CCBs better control of ventricular response in atrial tachycardias

Class I agents to be combined with AV nodal blocking drugs – to eliminate 1:1 conduction of atrial to ventricles.

HEMODYNAMIC STATUS

STABLE BP >90/60 mmHg

Narrow QRSand regular

R-RVagal

maneuveresIV

adenosineIV

verapamil,diltiazemIV sotalolRefractor

y

Wide QRScomplex

Vagal

manuevresIV

adenosine

procainamid

e

Digoxin

Verapam

il Are contraindicated

UNSTABLEBP< 90/60 mmHg

Direct cardioversion

DRUG DOSE SIDE EFFECTS

AV NODAL BLOCKERS

ADENOSINE 6-12 mg bolus Flushing ,dyspneaChest pain

VERAPAMIL 0.15 mg/kg over 2 min

Hypotension bradycardia

DILTIAZEM 0.25-0.35 mg/kg -2 min

same

DIGOXIN 0.5-1.0 mg --- 2-10 min

Digoxin toxicity

PROPANOLOL 1-3mg over I min Hypotension bradycardia

CLASS I AAD

QUINIDINE 6-10MG/KG at 10 mg/min

hypotension

PROCAINAMIDE 10-15mg/kg at 50 mg/min

hypotension

DISOPYRAMIDE 1-2 mg/kg at 10 mg/min

hypotension

PROPAFENONE 1-2mg/min at 10 mg/min

Bradycardia,GI disturbance

FLECAINIDE 2 mg/kg at 10 mg/min

Bradycardia,dizziness

CLASS III SOTALOL 1-1.5mg/kg at 10 mg/min

Hypotension,proarrythmic

AMIODARONE 1.5 mg/kg during 15 min

Hypotension,bradycardia

Pharmacologic Agents for Short-Term Treatment of Supraventricular Tachycardia (SVT).

Delacrétaz E. N Engl J Med 2006;354:1039-1051.

AFTER ADENOSINE

Algorithm for Short term management

of SVT

Algorithm for long term

Management of SVT

Refractory cases

Narrow QRS complexes

IV adenosine

IV procainami

deIV

amiodarone

Atrial pacingDirect

cardioversion

Wide QRS Complexes

Atrial pacingDirect

cardioversion

Pill in the pocket approach In whom recurrences are infrequent. But sustained.well tolerated hemodynamically. Patients who have had only a single episode of SVT.. 100-200mg of flecainide at the onset of SVT is a reasonable

approach…until he reaches the hospital. 40-160 mg verapamil –without preexcitation, Betablockers Propafenone 150-450 mg. 80% cases interrupted with a combination of CCBand BB in 2

hrs…

Long term control of SVT Frequency and severity of episodes. LVF Cost benefits of radiofrequency ablation

over the pharmacotherapy . Pharmacotherapy is considered in patients

who defer catheter ablation,whom in which ablation failed,or carries a risk of AV block.

Multifocal atrial tachycardia Trial and error Accessory pathway – class Ia,Ic,III AV node blocking drugs Young patients – Ia drugs Class I agents LVD < 35% not used.

Long term treatment

Membrane active

AAD

Catheter

ablation

Curative surgery

Antitachycardia pacing

Adenosine

not to be used in bronchospastic pulmonary disease.

Adenosine precipitates asthma Given rapidly in 1-2 sec. If given by peripheral vein uplift the arm.. Max dose is 30 mg 6- 12-12 mg Terminates AVNRT .AFL with 2:1 block Potentiated by dipyradimole,carbamazepine –

decrease dose to 3 mg.

Other drugs

Calcium channel blockers,beta blockers ,digoxin are the next drugs to be used if not responded to adenosine

Usually 60 % cases respond to a dose of 6 mg and 95 % cases at 12 mg.

Type 1 a AAD, 1c,iii,AMIODARONE in refractory cases.

Beta blockers not to used IV in heart failure.

Long term treatment in case of recuurent episodes,hemodynamic instability.

Catheter guided Radiofrequency Ablation

Several multipolar catheters are introduced High right atrium ,bundle of

his ,RVapex,Coronary sinus. Radiofrequency is delivered at the site of earlier

activation Success is defined by elimination of the

tachycardia or loss of pre excitation. 90-98% success in AV node dependent 60-80% in case of AV node independent. Cryoablation more useful…

Catheter Ablation of Cardiac Arrhythmias.

Pacemakers

Temporary role in case of digoxin toxicity. Permanent in case of long term control To terminate the tachycardia Revert into sinus rhythm Prevent the occurrence. Overdrive suppression RF induced atrial pacing are used

No role of surgery presently in PSVT rx .

ACUTE LONG TERM

PHYSIOLOGICAL rest ,sedation valsalva

Valsalva maneuvre Carotid sinus massage

Carotid sinus massage

PHARAMACOLOGICAL

vagomimmetic Suppress triggering arrhythmias

Direct effect on AV node

Change properties of reentrant pathways

Slow VR Control VR

CATHETER ABLATION SURGERY

Ablation or sectioning of reentrant pathway

ELECTRONIC DEVICES

Temp .pacing cardioversion

Permanent pacemakerAntitachycardia pacing

Some important points

Rxof PSVT given for patient comfort except in IHD,MS

When the QRS complex is wide and VT is mistaken as SVT with ABERRANT conduction IV verapamil – not recommended decreases BP.

If DC cardioversion to be avoided because of possible adverse response to digitalis adm …pacing Rt atrium and ventricle via temp pacing.

In WPW syndrome avoid VERAPAMIL,LIDOCAINE . Avoid digoxin. In SANRT ,IART –class IA,IC ,BB SANRT –digoxin.

Cont…

Rx of ectopic atrial tachycardia – consider digitalis toxicity,chronic lung disease,metabolic abn,electrolyte abnormalities,acute MI ----temporary pacing.

Unsuccessful is EC Removal or reversal of inciting factor Surgical excision of focus. Rx of MAT –chronic lung disease,metabolic,rare

is digitlais toxicity ---CCBS,BBs ..no role of cardioversion,devices ,surgery.

In case of WPW syndrome symptomatic concealed or manifested ..and evidence of preexcitation on NSR …send the patient for catheter ablation…

Our case

1. carotid sinus pressure 2.IV adenosine. 3.long term treatment depends upon episodes. 4.any underlying abnormality to be checked for. 5.definitive etiology only knon by EP study. 6.95% cases respond to RF ablation. 7.much less complications with cryoablation. 8.in case if SVT recurrs after ablation –opt for

pacemaker..

Lets have a look at the ECGs

SUPRAVENTRICULAR TACHYCARDIAS“You only get so many heart beats – you should save some for later in life” Dr. Samuel Levine

DIAGNOSIS IS ATRIAL FLUTTER

Sinus tachycardia was thought..

but it was AFL

AVNRT in structural heart disease

Look for the correct lead placement

AVNRT can occur in the background of acute MI

Special problems 1.Coexisting Double Tachycardias May not be identified during noninvasive

testing ..needs EP study. Ex—typical AVNRT and AT. Concentric –eccentric –concentric. AVNRT –both APC,VPC AT only APC 2.Pseudo AF- infrequent presentation of PSVT. Occurs during onset and termination of tahcycardia. Multiple accessory AV pathways. In young who have AF without other risk factors. 5% of AVNRT. Group beating is seen

REFERENCES CARDIOLOGY third edition –Michael. H.Crawford HURST’S THE HEART – 12 th edition. BRAUNWALD’S HEART DISEASE –A TEXTBOOK OF CARDIOVASCULAR

MEDICINE – 7 th ED HARRISON’S PRINICPLES OF INTERNAL MEDICINE -17 th ED SUPRAVENTRICULAR TACHYCARDIA –NEJM 2006 CARDIOVASCULAR MEDICINE – SVT – JERONIMO FERRE’ BASIC AND BEDSIDE ELECTROCARDIOGRAPHY –ROMULO.F.BALTAZAR SCHAMROTH –ELECTROCARDIOGRAPHY www.medscape.com www.ecglibrary.com www.googleimages.com www.acc.org. www.clinicaltrials.gov www.nejm.org

Aim for any case of cardiology

Than

k youSagittari

an

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