supraventricular tachycardia - achmad lefi, md, fiha.pdf

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CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

SUPRAVENTRICULARTACHYCARDIA

ANUDYA KARTIKA

ACHMAD LEFI


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CASE : One day at the ED…A 24 - year - old man is brought to ED with sudden - onset

rapid palpitations associated with chest tightness, breathlessness andfeeling dizzy and unwell. It started 30

minutes earlier, while playing football.

He is uncomfortable but alert and orientated. He is warm to touch and

looks well perfused.His BP is 92/55 mmHg, pulse 200 bpm, O2

saturations on 5 L/min via a face mask are 99% and his lung fields are

clear. The performed ECG was :

Cardiology: Clinical Cases Uncovered. By T. Betts, J. Dwight andS. Bull. Published 2010 by Blackwell Publishing.


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WHAT’S THE LIKELY DX??


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INTRODUCTIONSVT is a common entity in clinical practice and a relatively

common occurrence in the emergency department.

Estimated incidence of 35 per 100,000 person-years,with a prevalence of 2.29 per 1,000 persons AVNRT 50-60%,

AVRT 30%

Supraventricular tachycardias are not usually associated

with structural heart disease, although there are exceptions.

Issa ZF, Miller JM, Zipes DP.Clinical arrhythmology and electrophysiology: a companion to Braunwald’s heart disease 2nd ed.2012.


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ELECTROPHYSIOLOGY

MECHANISMAll cardiac tachyarrhythmias are produced by one or moremechanisms :

Tissues exhibiting abnormal automaticity that underlie SVT

in the atria, the AV junction, or vessels that communicatedirectly with the atria (vena cava or pulmonary veins).

Disorders of

impulse

formation

Disorders of

impulse

conduction

• Automaticity

• Triggered

activity

Re-entry

Issa ZF, Miller JM, Zipes DP.Clinical arrhythmology and

electrophysiology: a companion to Braunwald’s heart disease.2012.


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AUTOMATICITYAbility of cardiac cells to depolarize spontaneously, reach

threshold potential, & initiate a propagated action

potential in without of external electrical stimulation

Enhancedautomaticity

• accelerated generation of an action potential bynormal pacemaker tissue found in the sinusnode

• “latent pacemakers” may become the functional

pacemaker under certain conditions.

Abnormal

automaticity

• only when there are major abnormalities inmyocyte transmembrane potentials inparticular steady-state depolarization of themembrane potential (hypoxia, K+ imbalance)


electrophysiology: a companion to Braunwald’s heart disease

2nd ed. Elsevier Saunders 2012.


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DADs (Delayed Afterdepolarizations)

occur after completion of repolarization of the action potential (i.e., during phase 4).

EADs (Early Afterdepolarizations) occur during the action potential & interrupt

the orderly repolarization of the myocyte.


electrophysiology: a companion to Braunwald’s heart disease 2nd ed.

Elsevier Saunders 2012.

TRIGGERED ACTIVITYImpulse initiation in cardiac fibers caused by

afterdepolarizations that occur consequent to a preceding

impulse or series of impulses


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RE-ENTRYWhen a propagating impulse fails to die out after

normal activation of the heart and persists to

reexcite the heart after expiration of the refractory

period in repetitive cycles.

(A)An impulse (initiated from SA node) passes through AV nodal connection & an

accessory pathway.

(B) A premature atrial impulse occurs reaches recovering accessory pathway,

conduction can occur in the AV node.(C)the impulse takes time to circulate through AV node & across the ventricle to

allow the acc. pathway to recover its excitability & conduct the impulse back to

the atrium

Delacrétaz E. Supraventricular tachycardia. N Engl J Med 2006;354:1039-51


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AVNRT

Issa ZF, Miller JM, Zipes DP.Clinical

arrhythmology and electrophysiology: a

companion to Braunwald’s heart disease


• Most common type of SVT , mostly without any structural heart

disease.

• The group most often affected is young, healthy women.• Some underlying heart disease pericarditis, previous

myocardial infarction, or mitral valve prolapse

• The coexistence of slow and fast pathways in AV nodal tissue is

the basis of aberrant substrate for reentrant tachyarrhythmias


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Issa ZF, Miller JM, Zipes DP.Clinical arrhythmology and electrophysiology: a companion to Braunwald’s heart

disease 2nd ed. Elsevier Saunders 2012.


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In typical AVNRT :

Antegrade conduction down the slow AVnodal pathway & retrograde conduction up

the fast pathway

the retrograde P wave may not be seen or

may be visible early after the QRS complex.

When visible, it often appears as a pseudo R

wave in lead V1.


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AVNRT ECG

P wave

• In typical (slow-fast) AVNRT P wave is usually not visiblebecause of the simultaneous atrial and ventricular activation

QRS wave

• usually the same as in normal sinus rhythm.

P-QRSRelationshp

• In typical (slow-fast) AVNRT, the RP interval is very short (–40 to75 milliseconds).

Sohinki D et al. The Ochsner Journal 14:586–595, 2014


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AVRT Caused by accessory pathways (or bypass

tracts) that serve as aberrant conduits for impulses that pass from the SA node and travel

in an antegrade or retrograde fashion through

such tracts a reentry circuit.

Am Fam Physician. 2010;82(8):942-95


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WPW Kent accessory pathwayW P W p a tt er n the constellation of ECG abnormalities

related to the presence of an AV BT (short PR interval, delta

wave) in asymptomatic patients.

W P W s y n d r o m e a WPW ECG pattern + tachyarrhythmias.

Because the AV BT typically conducts faster than the AVN, the onset of

ventricular activation is earlier than if depolarization occurred only via the

AVN shortened PR (P-delta) interval.Issa ZF, Miller JM, Zipes DP.Clinical arrhythmology and




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ORTHODROMIC AVRTAVN-His Purkinje System serves as the anterograde limb of the

reentrant circuit (i.e., the pathway that conducts the impulse from

the atria to the ventricles), whereas an AV bypass tract serve sas

the retrograde limb


lectrophysiology: a companion to Braunwald’s heart disease



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ORTHODROMIC AVRT

Rate

• Inscribed within the ST-T wave segment with an RP interval that is usually lessthan half of the tachycardia R-R interval (i.e., RP interval < PR interval)

QRS wave

• generally normal and not preexcited, even whenpreexcitation is present during SR

P wave

• tends to be a rapid tachycardia, with rates ranging from 150->250 beats/min.


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SVT of AVRT ECG

Brady WJ, Truwit JD. Critical Decisions in Emergency & Acute Care Electrocardiography. Wiley Blackwell 2009.

P wave

• usually in the ST segment or T wave and is often visible betweensuccessive R waves

• negative in leads II, III, and aVF and a long RP interval (RP greater thanPR).

QRS wave

• wide (fully preexcited) QRS complex, usually regular R-R intervals, andventricular rates of up to 250 beats/min.


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CLINICAL

MANIFESTATIONS

Most often asymptomatic at the time of evaluation.

Fatigue, lightheadedness, chest discomfort, dyspnea, presyncope, or more rarely, syncope.

Premature beats are commonly described as pauses or nonconductedbeats followed by a sensation of a strong heartbeat, or they are

described as irregularities in heart rhythm


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PHYSICAL EXAM &

DIAGNOSTIC WORKUPEvaluation System or test Possible finding Significance

Focused

Physical

examination

Cardiovascular Murmur (s)

Friction rub

3rd Heart Sound

Cannon waves

Valvular heart disease

heart failure or

tachycardia

Pericarditis

Heart failure tachycardia

Possible AV Nodal

reentrant tachycardia or VT

Respiratory Crackle Heart failure tachycardia

Endocrine Enlarged or tender

thyroid gland

Hyperthyroidism or

thyroiditis tachycardia

Colucci RA, Silver MJ, Shubrook J. Common Types of Supraventricular Tachycardia : Diagnosis and Management.

Am Fam Physician. 2010;82(8):942-952


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Evaluation System or test Possible finding Significance

In office

testing

Vitals Hemodynamic

instability or febrile illness

Incite

tachyarrhythmia

Orthostatic

blood pressure

Autonomic or

dehydration

issues

Induce

tachyarrhythmia

Electrocardio-

graphy

Preexcitation Wolf-Parkinson-

White Syndrome

Wide versus

narrow complex

QRS Complex

Type of SVT versus

VT

Q Waves Ischemia VT

Colucci RA, Silver MJ, Shubrook J. Common Types of

Supraventricular Tachycardia : Diagnosis and

Management. Am Fam Physician. 2010;82(8):942-952


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PHYSICAL EXAM &

DIAGNOSTIC WORKUP


Am Fam Physician. 2010;82(8):942-952

Evaluation System or test Possible finding Significance

Blood work Complete blood

count

Anemia or

infection

All possibly

induce or incite

tachyarrhythmias

Thyroid

stimulating

hormone

Suppression or

hyperthyroidism

Basic metabolic

panel

Electrolyte

disturbance

B-type

Natriuretic

peptide

Congestive HF

Cardiac enymes MI or ischemia


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PHYSICAL EXAM &

DIAGNOSTIC WORKUPEvaluation System or test Possible finding Significance

Diagnostics Chest radiography Cardiomegaly Congestive HF

or

Cardiomyopathy

Holter monitor or

event recorder

Capture aberrant

rhythm, frequency,duration

Type of

tachyarrhythmia

Graded exercise

test

Preexcitation or

aberrant rhythm

Type of

arrhythmia

Echocardiography Structural or

valvular heart

disease

Possible

surgical

intervention


Am Fam Physician. 2010;82(8):942-952


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MANAGEMENT

Non-pharmacologic

PharmacologicElectrical

modality/Catheter ablation

A rapid assessment of the patients airway, breathing, and circulation

should be conducted, and all vital signs should be documented.


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ACC/AHA/ESC guidelines for the

management of patients with

supraventricular arrhythmias

—executive summary.

J Am Coll Cardiol. 2003;42(8):1493-1531


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ACC/AHA/ESC guidelines for the management of patients with

supraventricular arrhythmias


J Am Coll Cardiol. 2003;42(8):1493-1531


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ACC/AHA/ESC guidelines for the management of

patients with supraventricular arrhythmias


J Am Coll Cardiol. 2003;42(8):1493-1531


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MANAGEMENTNon pharmacologic

The initial strategy for terminating a

PSVT a vagotonic maneuver

• Carotid sinus massage

• Coughing

• Cold stimulus to the face

• Straining

Evaluate CAROTID BRUIT (ie,

abnormal sound) before

attempting this maneuver (esp in

elderly).

Reported complications

VF

hemiplegia cervicomediastinal

hematoma.

Straining hypotension


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MANAGEMENTPharmacologic

IV antiarrhythmic drugs should be administered for

arrhythmia termination in hemodynamically stable patients.

The advantage of adenosine relative to IV calcium-channel or betablockers relates to its rapid onset and short half-life.

ACC/AHA/ESC guidelines for the management of patients with

supraventricular arrhythmias—executive summary. J Am Coll

Cardiol. 2003;42(8):1493-1531.


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ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary. J Am

Coll Cardiol. 2003;42(8):1493-1531.


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MANAGEMENTElectrical Modality

Immediate DC cardioversion hemodynamically

unstable tachycardias

ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary. J Am

Coll Cardiol. 2003;42(8):1493-1531.


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RHYTHM CONTROL : CATHETER ABLATION

percutaneous, catheter-based techniques designed to modify or

eliminate fast-pathway conduction.

Energy (initially diagnostic cath &

later RadioFrequency) was applied in the region of the apex of Koch’s triangle,

along the superior aspect of the tricuspid annulus


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SUMMARY

Supraventricular tachycardia is a common entity in clinical practice and arelatively common occurrence in the emergency department

Knowledge of the mechanism of each SVT is important in determiningmanagement at the bedside.

ECG features can help to distinguish between atrioventricular nodal re-entrant tachycardia and atrioventricular re-entrant tachycardia

The management consists of non-pharmacologic, pharmacologic, and

electrical modality (DC cardioversion & ablation catheter).


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THANK YOU

supraventricular tachycardia - achmad lefi, md, fiha.pdf

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