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APPROACH TO TACHYARRYTHMIAS PROF.DR.MD.ZAKIR HOSSAIN PROFESSOR AND HEAD DEPARTMENT OF MEDICINE SZMCH

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Page 1: APPROACH TO TACHYARRYTHMIASbsmedicine.org/congress/2017/Prof._Md._Zakir_Hosasin.pdf · 2018. 12. 15. · APPROACH TO TACHYARRYTHMIAS PROF.DR.MD.ZAKIR HOSSAIN PROFESSOR AND HEAD DEPARTMENT

APPROACH TO TACHYARRYTHMIAS

PROF.DR.MD.ZAKIR HOSSAINPROFESSOR AND HEAD

DEPARTMENT OF MEDICINE

SZMCH

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TACHYARRYTHMIA

• Cardiac arrythmia is a disturbance ofelectrical rhythm of heart.

• Cardac arrythmia with rate above 100/min iscalled tachyarrythmia.

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Mechanism of tachyarrythmia

A. Increased automaticity.

B. Triggered activity.

C. Rentry.

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MECHANISM OF REENTRY

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Evaluation of tachyarrythmia

At the beginning of evaluation important points are

• Whether patient is haemodynamically stable or not.

• Rapid ECG evaluation to decide any emergencyintervention like cardioversion or defibrillation.

• Detailed evaluation can be done later on when patientis stable

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HISTORY

• Heart beat regular/irregular

• What is the approximate heart rate

• Continuous /intermittent

• Number and frequency of episodes

• Onset gradual/abrupt

• How an attack terminates

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• Any associated symptoms:

Chest pain , dyspnea ,lightheadedness, polyuria.

• Any history of triggers:

Exercise,alcohol,medication,heart failure, infection

• Any history of structural heart disease CAD,Vulvulardisease.

• Family history of arrhythmia or sudden death

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Physical examination

• Physical examination often unrevealing when tachycardia is

episodic and not ongoing at the time of examination.

• Detailed cardiac examination

Other relevant systemic examination including thyroid.

pulse Rate,rhythm,volume,character

BP HTN,Hypotension

JVP

precordium Apex location and character, heart sound and murmur

Page 10: APPROACH TO TACHYARRYTHMIASbsmedicine.org/congress/2017/Prof._Md._Zakir_Hosasin.pdf · 2018. 12. 15. · APPROACH TO TACHYARRYTHMIAS PROF.DR.MD.ZAKIR HOSSAIN PROFESSOR AND HEAD DEPARTMENT

INVESTIGATIONResting 12 lead ECG even if patient dosent havetachycardia at the time of ECG. May reveal:

Evidence of prior MIlong QT intervalIschemiaAtrial enlargement/hypertrophyVentricular enlargement/hypertrophyEvicence of preexcitation

ECG is particularly diagnostic if patient has tachycardiaat the time of recording.

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• Other ECG recording

• Echocardiograpy

• Exercise test

• Electrophysiology which is sometimes associated with therapeutic RFA.

HOLTER MONITOR Several episodes/day

EVENT MONITOR Less frequent episodes

IMPLANTABLE LOOP RECORDER

<2 episodes /month

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OTHER TESTS

• Serum electrolyte Ca, Mg , K, Na.

• CBC

• Thyroid function test

• Cardiac biomarkers

• Drug level in suspected drug toxicity

• Toxin screen

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Tachycardia with regular narrow QRS complex

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Sinus tachycardia

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AVNRT mechanism

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AVRT mechanism

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ATRIAL FLUTTER

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TYPES OF ATRIAL FLUTTER

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TACHYARRYTHMIA WITH NARROW IRREGULAR QRS COMPLEX

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Atrial flutter with variable block

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ATRIAL FIBRILLATION

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AF with Digoxin effect

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AF classification

ParoxysmalAF that terminates spontaneously or with intervention

within 7 days of onset though recurrent paroxysm may occur.

Persistent AF that persist for >7 days but < 12 months. sinus rhythm

can be restored and maintained.

PermanentSinus rhythm cant be restored or maintained.

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Causes of atrial fibrillation

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Multifocal atrial tachycardia

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Tachyarrythmiawith regular wide QRS complex

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Ventricular tachycardia

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SVT with aberrant conduction

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ACCELERATED IDIOVENTRICULAR RYTHM

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Tachyarrythmiawith irregular wide QRS complex

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ATRIAL FIBRILLATION WITH RBBB

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Irregular rhythm with variable QRS duration

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POLYMORPHIC VT

Two types

• Polymorphic VT with normal QT interval eg;post MI.

• Polymorphic VT with long QT eithercongenital or acquired called “torsades depointes’’.

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Torsades de pointes

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Management of SVT

If patient is haemodynmically stable:• Vagal menoeuvre• IV adenosine (6 mg IV push followed by 12 mg if needed.)• Alternative IV verapamil ( 5-10n mg IV over 5-10 min)

If patient is haemodynamically unstable – Emergency cardioversion

Long term management

• EPS and RFA of reentry circuit.• Drugs

Amiodarone, flecainide,propafenone,verapamil diltiazem,beta blocker.

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Management of atrial fibrillation

If AF occurs as a complication of acute illness likepneumonia or pulmonary embolism treatment ofprimary disorder will restore sinus rhythm.

Paroxysmal AF

Aim is to prevent attack

Drugs Beta blocker , flecainide or propafenone if no CAD or LV dysfunction,

amiodarone if CAD or LV dysfunction present.

RFAIsolation of pulmonary veins from left atrium

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Persistent and permanent AF

• Rhythm control if possible.

• Rate control accepting that restoration tosinus rhythm is not possible.

• Anticoagulation by assessing risk ofthromboembolism.

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Restoration to sinus rhythm is possible < 3 Months durationPatient is youngNo structural heart disease

Cardioversion

If AF duration is of <48 hoursImmediate cardioversion after IV heparin by IV flecainide in patient with no

structural heart disease or IV amiodarone in patient with structural heat disease orby DC cardioversion if pharmacological cardioversion failed.

If AF duration >48 hoursAt first patient must be anticoagulated by warfarin for at least for 4 weeks before

cardioversion and continue anticoagulation for further 3 months.

In case of urgent cardioversion TOE should be done to exclude LA thrombus.

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Rate controlIf sinus rhythm cant be restored, rate control is thegoal by drugs or by pace and ablation therapy.

AnticoagulationWith oral anticoagulants by risk stratification

with CHA2DS2VASc scoring. If score >2, oralanticoagulants like warfarin,dabigatran orrivaroxaban is used. If score <1 aspirin can beused. if score is O ,no need of anticoagulation.

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Atrial flutter

• Acute paroxysm if haemodynamically unstableby electrical cardioversion

• Pharmacological cardioversion by amiodaroneor flecainide if duration <48 hours.

• If >48 hours treatment strategy is similar to AF.

• Recurrent paroxysm may be prevented by drugslike amiodarone or by RFA of reentry circuit.

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Ventricular tachycardia

• Prompt restoration to sinus rhythm is the goal

• Synchronized DC cardioversion if systolic BP is <90 mm of Hg.

• If well tolerated and haemodynamically stable , IV amiodarone or IV lignocaine.

Prevention of attack

Drugs- amiodarone,beta blockerICD if poor LV functionRFA of scar tissue.

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Torsades de pointes

• Treatment of underlying cause

• IV magnesium

• Atrial pacing

• IV isoprenaline

• Beta blocker in congenital long QT

• ICD

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VENTRICULAR FIBRILLATION

Immediate defibrillation

In survivors

Prophylactic ICD Implantation.

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Simplified management optionsCardiac arrest due to VF or pulseless VT CPR and urgent Defibrillation

AF, Atrial tachycardia, SVT or any tachycardia causing haemodynamic instability

Urgent cardioversion

Regular narrow complex tachycardia with haemodynamic stability

Vagal menoeuvre or IV AdenosineMay terminate AVNRT or unmask Atrial tachycardia

New onset AF/A flutter<48 hoursPersistent /permanent AF or flutterAVNRT,AVRT

Electric or chemical cardiovesionRate control,anticoagulation,catheter ablationAntiarrythmic, catheter ablation

SVT with aberrancy If confusion treat as VTAdenosinre,verapamil/electrical cardioversion

Atrial fibrillation with aberrancy Immediate chemical or electrical cardioversionas chance of degeneration into VF

Polymorphic VT (torsades de pointes) Mg sulphate, electrical cardioversionoverdrivre pacing.Prevent and correct precipitating cause.

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Antiarrythmic drugs

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Catheter ablation can be done infollowing tachyarrythmia:

AV nodal re-entry tachycardia (AVNRT)

AV re-entry tachycardia (AVRT) with an accessory pathwayincluding WPW syndrome

Normal heart VT

Atrial flutter

Atrial tachycardia

Atrial fibrillation

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ICD

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