Arrhythmia a A

8/3/2019 Arrhythmia a A

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Presented by :Bashirah Mohd Nor

Izza Najiha binti ZaidinNorashikin binti Naim

Abdul Hamid bin Omar

ARRHYTHMIAS


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>The heart muscle has the abilityto initiate an electrical impulse

without external stimulus(Automaticity)

>The action potentials that

originate in any myocyte can be

transmitted to other myocyte.

>SA node is the pacemaker of the

normal heart.

>if the sinus rate becomes slow, a

lower center may assume the role

of the pacemaker

ARRHYTHMIA = abnormality/disturbance of cardiac rhythm


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Normal Sinus Rhythm

ECG Characteristics: Regular rhythm

Rate 60-100 bpm

Each QRS complex is preceded by a P wave

P wave is upright in lead II, III, aVF & down going in lead

aVR

It shows normal sequence of conduction, originating in the sinus node and proceeding

to the ventricles via the AV node and His-Purkinje system.

www.uptodate.com


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Mechanisms

tachycardia

1. accelerated automaticity

Due to increasing rate ofdiastolic spontaneous

depolarisation

2. Re-entry

Initiated by ectopic beat andsustained by a re-entry circuit

3. Triggered activity Due to secondary

depolarisation arising from anincompletely repolarised cellmembrane

bradycardia

1. Reduced automaticity

2. blocked/ abnormally slow

conductionThe AV node normally the only

electrical pathway connecting the atria

and ventricles

When accessory pathways exist, itsable to transmit the impulse

retrogradely back into the atria, thus

completing a circuit and initiating a

self sustaining re-entry tachycardia.


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Sinusbradycardia

Failure ofimpulse

formation

Heart block

Failure ofimpulse

conduction

HR :


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Sinus bradycardia

causesExtrinsic

Hypothermia

Hypothyroidism

Increase ICP Beta-blockers

Antiarrhythmic drugs

Intrinsic

Acute ischaemia andinfarction of sinusnode

fibrosis


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2nd degree heart block Mobitz 1 block (wenckebach phenomenon) Progressive lengthening of PR interval and then

failure of conduction of atrial beat and followed byshorter PR interval with conducted beat.

Mobitz 2 block Constant PR interval but occasionally without QRS

complex

2:1 AV block

Every 2 P waves will be followed by a QRS complex


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Wenckebach phenomenon

Mobitz type 2

2:1 AV block


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3rd degree (complete) heart block

Fails of all atrial activity to the ventricles

Thus ventricular activity is maintained by anescape rhythm:

AV node or Bundle of His narrow QRS

Distal Purkinje tissues broad QRS


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Bundle brunch block

QRS complex > 0.12 seconds

RBBB

RSR' in V1 (rabbit ears)

presence of wide (or deep) S wave in V6 widely split S2 on auscultation

LBBB

M pattern in lead V6

W pattern in lead V1 paradoxically split S2 on auscultation


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RBBB

LBBB


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RBBB

Congenitalheart disease

Pulmonary

disease Myocardialdisease

LBBB

Leftventricularoutflowobstruction

CAD


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MANAGEMENT Asymptomatic pt and rate >40bpmno Rx

Symptomatic pt or rate


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BY : NORASHIKIN BINTI NAIM


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Arise from atrium / AV junction conduction is via the His-

Purkinje system.

Causes :

Sinus tachycardia Atrial fibrillation

Atrial flutter Atrial tachycardia

AV nodal re-entry tachycardia (AVNRT) AV reciprocating tachycardia (AVRT) complexes

Multifocal atrial tachycardia

Accelerated junctional tacycardia


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Secondary phenomenon due to variety of stress

Causes :

ECG Normal P wave preceeding QRS complex

Management Investigate & treat the underlying cause

Exercise Pain Fever

Hypovolemia Sepsis Acute Heart failure Acute pulmonaryembolism

Pregnancy Thyrotoxicosis


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Common arrhythmia 5-10% of pts >65 years old

Condition resulting in atrial pressure/muscle mass/fibrosis,inflammation/infiltration of the atrium chaotic, IRREGULAR atrialrhythm (300-600 bpm) AV node response intermittently irregularventricular rhythm

Causes : I HAVE A FIB

Symptoms asymptomatic, palpitation, SOB, LOC

Signs irregularly irregular rhythm

I - Ischemic heart disease/ Idiopathic(lone AF)

H

hypertension / hyperthyroidismA - acute pericarditisV - valvular heart disease (mitralstenosis)E- embolus (pulmonary)A - atrial septal defectF - failure (cardiac)I - infection (pneumonia)B - booze/alcohol


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Treat the underlying illness - MI, pneumonia

Rhythm control

Anti-arrhythmic drugs - amiodarone DC cardioversion

Rate control Digoxin, beta blockers, CCB (verapamil/diltiazem)

Transvenous catheter radiofrequency ablation

Prevention of thromboembolism Warfarin/heparin/aspirin


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Large re-entry circuit within the right atrium encircling thetricuspid annulus organized/REGULAR atrial rhythm

Chrd by atrial rhythm with a rate between 250-350 bpm

Causes : Paroxysmal : pericarditis, postcardiac surgery Persistent : LV dysfunction, RHD, congenital heart disease

Treatment :

DC cardioversion if haemodynamically unstable

Medication Rate control beta-blocker, CCB Rhythm control amiodarone in recurrent episodes Anticoagulant

Catheter ablation - >85% cure rate, in recurrent &troublesome symptoms


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Regular sawtooth-like atrial activity between QRS complex, bestseen in inferior leads.

Flutter waves have constant amplitude, duration & morphologythrough the cardiac cycle.

Regular ventricular rate. Variable AV conduction can be seen, commonly 2:1 / 3:1


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Ventricular tachyarrhythmias can be considered

under the following headings:

Ventricular premature beats

Normal heart ventricular tachycardia

Life-threatening ventricular tachyarrhythmias

Sustained ventricular tachycardia

Ventricular fibrillation

Torsades de pointes

non-sustained ventricular tachycardia


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Ventricular Premature Beats (VPB)

The origin of premature beats in the ventricle at sites

remote from the Purkinje network produces slowventricular activation and a wide QRS complex that is

typically >120 ms in duration.

Aetiology:

Occur in normal person ( with ages)Myocarditis, CAD, valve heart disease, hyperthyroidism

Drug toxicity (digoxin, quinidine and anti-anxiety drug)

Electrolyte disturbance, anxiety, drinking, coffee

Manifestation:Asymptomatic

Haemodynamic instability

(palpitation,dizziness,syncope)

Pulsus BigeminusMultifocal

PVC's

Compensatory pause

after the occurance of a PVC

R on Tphenomemon

Ventricular Ectopic Beat


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Actually, a "retrograde p-wave may sometimes be

seen on the right hand side of beats that originate in

the ventricles, indicating that depolarization has

spread back up through the atria from the ventricles

QRS is wide and much different ("bizarre") looking than the

normal beats. This indicates that the beat originatedsomewhere in the ventricles and consequently, conduction

through the ventricles did not take place through normal

pathways. It is therefore called a ventricular beat

There is no preceding p wave, indicating that the beat

did not originate anywhere in the atria

fully compensatory pause

Pattern of VPB


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Pattern of VPB

Bigeminy Every sinus beat is followed by a VPC

Trigeminy Two sinus beats are followed by a VPC

MultiformedDifferent morphologies

Pairs or coupletsTwo successive VPCs.Vent.Tachycardia (VT) = 3 consecutive VPCs + rate is

>100 bpm

Nonsustained VT repetitive VPCs terminate

spontaneously and are more than three beats in

duration.

Treatment

Therapy: treat underlying disease, antiarrhythmia

No structure heart disease:

Asymptom: no therapy

Symptom caused by PVCs: antianxiety agents, -

blocker and mexiletine to relief the symptom.

With structure heart disease (CAD)

Reassurance & -blocker


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Ventricular rhythm that is characterized by 3complexes at a rate

40bpm 120 due to abnormal automaticity.

AIVR = "slow" VT???Both rhythms can manifest rates between 90 and 120 beats/min.

Benign rhythm ,has a characteristic gradual onset and offset and morevariability in cycle length. It is typically a brief, self-limiting arrhythmia.

Aetiology:

absence of any structural heart disease acute myocardial infarction (esp during reperfusion), acute myocarditis,

Cocaine @ digoxin intoxication

and postoperative cardiac surgery.

The rhythm is usually transient and rarely causes significant hemodynamiccompromise or symptoms.

Treatment is rarely necessary.

If symptomatic (impaired hemodynamics) => lidocaine, atropine (accelerate thesinus rate to overdrive the ventricular rhythm)


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Definition : a run of 3 consecutive PVC at arate of 120 and 220 bpm.

Etiology: often in organic heart disease

CAD, MI, DCM, HCM, HF,

long QT syndrome

Brugada syndrome

Sustained VT (>30s), Nonsustained VT Monomorphic VT, Polymorphic VT


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NON SUSTAINED SUSTAINED

DEFINITION Ventricular tachycardia that is 5

consecutive beats but lasts

< 30 s

VT that persists for 30 s or requires

termination because of hemodynamic

collapse.

ETIOLOGY 6% = normal hearts

> 6080% with heart disease.

CAD with MI

DCM @ HCM , metabolic disorders,

drug toxicity, or prolonged QT syndrome

SYMPTOM Asymptomatic pre-syncope (dizziness), syncope,

hypotension ,angina,SOB and cardiac arrest

TREATMENT Normal Heart => no treatment Haemodynamic compromise

(e.g. hypotensive or pulm. oedema)

DC cardioversion may be required.

No Haemodynamic compromise

Lidocaine, Amiodarone, Type Ia.

DC cardioversion ( X med. Therapy)PROGNOSIS GOOD ( low risk of sudden death)

3fold greater risk of death

than a comparable group of patients

without this arrhythmia.

POOR = 1st 6 weeks following AMI

75% mortality rate at 1 year.


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Torsades de points (Tdp):

A special type of polymorphic VT (twisting of

the point) + QT prolongation.Ventricular rate 100bpm (150 300bpm)

Treatment :

Correct underlying causes.

IV Mg, temporary pacing, IV Isoproterenol (C/I

congenital Long QT syndrome)


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Ventricular Fibrillation

Very rapid and irregular ventricular activation

with no mechanical effect.Aetiological

Often occur in severe organic heart disease:AMI, ischemia heart disease

Proarrhythmia (especially produce long QTand Tdp), electrolyte disturbance

Anaesthesia, lightning strike, electric shock,heart operation

Its a fatal arrhythmia

Manifestation:

Unconsciousness, no blood pressure andpulse and cardiac arrest.

Therapy:

Cardio-Pulmonary Resuscitate(CPR)

ICD 1st therapy


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Management

Pharmalogical

Non Pharmalogical

Radiofrequency Catheter Ablation

Implantable Cardioverter Defibrillator (ICD)


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Mxn of symptomatic tachyarrhythmias.

Performed by placing 3 or 4 electrodecatheters into the heart chamber.

Indication:

AV Nodal re-entry tachycardia (AVNRT)

AVRT + accessory pathway inc WPW synd.

1st line therapy.

Normal heart VT

Atrial flutter, Tachycardia or AF


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ICD recognizes ventricular tachycardia or fibrillation

and automatically delivers pacing or a shock to the

heart to cause cardioversion to sinus rhythm.

The following groups of patients may merit

prophylactic ICD placement:

Patients with coronary artery disease; significant

impairment of left ventricular function (LVEF 35

40%),spontaneous non-sustained ventricular

tachycardia in whom sustained ventricular tachycardia

was induced by pacing the heart during an

electrophysiological study.

Patients with very poor LV function post-MI (LVEF

35%).

Patients with dilated and particularly hypertrophic

cardiomyopathy, long QT syndrome and Brugada

syndrome or other channelopathies who have a strong

family history of sudden cardiac death.

Date post:	07-Apr-2018
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Arrhythmia a A

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