ARRHYTHMIAS

Presented by : Bashirah Mohd Nor Izza Najiha binti Zaidin Norashikin binti Naim Abdul Hamid bin Omar

>The heart muscle has the ability

to 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

Normal Sinus Rhythm

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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.

Mechanisms
tachycardia
1. accelerated automaticity
Due to increasing rate of diastolic spontaneous depolarisation

bradycardia 1. Reduced automaticity 2. blocked/ abnormally slow conduction

The AV node normally the only electrical pathway connecting the atria and ventricles
When accessory pathways exist, its able to transmit the impulse retrogradely back into the atria, thus completing a circuit and initiating a self sustaining re-entry tachycardia.

2. 3.

Re-entry
Initiated by ectopic beat and sustained by a re-entry circuit Due to secondary depolarisation arising from an incompletely repolarised cell membrane

Triggered activity

HR : <60bpm

Sinus bradycardia
Failure of impulse formation

Heart block
Failure of impulse conduction

Sinus bradycardia

causes
Extrinsic
Hypothermia Hypothyroidism Increase ICP Beta-blockers Antiarrhythmic drugs

Intrinsic
Acute ischaemia and infarction of sinus node fibrosis

1st degree heart block

PR interval > 0.2s

Atrial depolarization is followed by conduction to ventricles but with delay

Sign of : Coronary artery disease Acute rheumatic Carditis Digoxin toxicity Electrolyte disturbance

2nd degree heart block

Mobitz 1 block (wenckebach phenomenon)
Progressive lengthening of PR interval and then

failure of conduction of atrial beat and followed by shorter 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

Wenckebach phenomenon

Mobitz type 2

2:1 AV block

3rd degree (complete) heart block

Fails of all atrial activity to the ventricles

Thus ventricular activity is maintained by an

escape rhythm:
AV node or Bundle of His narrow QRS Distal Purkinje tissues broad QRS

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

RBBB

LBBB

RBBB Congenital heart disease Pulmonary disease Myocardial disease

LBBB Left ventricular outflow obstruction CAD

MANAGEMENT
Asymptomatic pt and rate >40bpm no Rx

Symptomatic pt or rate <40bpm IV atropine

If fails temporary pacing Asymptomatic 1st degree or Mobitz 1 block no

Rx Asymptomatic Mobitz 2 and 3rd degree heart block permanent pacemaker

BY : NORASHIKIN BINTI NAIM

 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

Exercise Pain Fever Hypovolemia Sepsis Acute Heart failure Acute pulmonary embolism

Pregnancy Thyrotoxicosis

Management
Investigate & treat the underlying cause

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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 atrial rhythm (300-600 bpm) AV node response intermittently irregular ventricular rhythm

Causes :

I - Ischemic heart disease/ Idiopathic (lone AF) H hypertension / hyperthyroidism A - acute pericarditis V - valvular heart disease (mitral stenosis) E- embolus (pulmonary) A - atrial septal defect F - failure (cardiac) I - infection (pneumonia) B - booze/alcohol

I HAVE A FIB

Symptoms asymptomatic, palpitation, SOB, LOC

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Signs irregularly irregular rhythm

 Absent P waves Irregular fine oscillations of the baseline = fibrillation/f waves Rapid, irregular QRS complex

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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 the

tricuspid 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, best seen in inferior leads. Flutter waves have constant amplitude, duration & morphology through the cardiac cycle. Regular ventricular rate. Variable AV conduction can be seen, commonly 2:1 / 3:1

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VENTRICULAR TACHYARRHYTHMIAS

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

Ventricular Premature Beats (VPB) The origin of premature beats in the ventricle at sites remote from the Purkinje network produces slow ventricular activation and a wide QRS complex that is typically >120 ms in duration.

Ventricular Ectopic Beat

Aetiology:
Occur in normal person ( with ages) Myocarditis, CAD, valve heart disease, hyperthyroidism Drug toxicity (digoxin, quinidine and anti-anxiety drug) R on T Electrolyte disturbance, anxiety, drinking, coffee phenomemon

Manifestation:
Asymptomatic Haemodynamic instability (palpitation,dizziness,syncope) Pulsus Bigeminus

Multifocal PVC's

Compensatory pause after the occurance of a PVC

QRS is wide and much different ("bizarre") looking than the normal beats. This indicates that the beat originated somewhere in the ventricles and consequently, conduction through the ventricles did not take place through normal pathways. It is therefore called a ventricular beat

fully compensatory pause

There is no preceding p wave, indicating that the beat did not originate anywhere in the atria 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

Pattern of VPB
Bigeminy Every sinus beat is followed by a VPC Trigeminy Two sinus beats are followed by a VPC Multiformed Different morphologies Pairs or couplets Two 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

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 more variability 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 hemodynamic compromise or symptoms. Treatment is rarely necessary. If symptomatic (impaired hemodynamics) => lidocaine, atropine (accelerate the sinus rate to overdrive the ventricular rhythm)

 Definition : a run of 3 consecutive PVC at a rate 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

NON SUSTAINED
DEFINITION Ventricular tachycardia that is 5 consecutive beats but lasts < 30 s

SUSTAINED
VT that persists for 30 s or requires termination because of hemodynamic collapse.

ETIOLOGY

6% = normal hearts > 6080% with heart disease.

Asymptomatic

CAD with MI DCM @ HCM , metabolic disorders, drug toxicity, or prolonged QT syndrome
pre-syncope (dizziness), syncope, hypotension ,angina,SOB and cardiac arrest

SYMPTOM

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)
POOR = 1st 6 weeks following AMI 75% mortality rate at 1 year.

PROGNOSIS

GOOD ( low risk of sudden death)

3fold greater risk of death than a comparable group of patients without this arrhythmia.

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)

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 QT and Tdp), electrolyte disturbance Anaesthesia, lightning strike, electric shock, heart operation Its a fatal arrhythmia Manifestation: Unconsciousness, no blood pressure and pulse and cardiac arrest. Therapy: Cardio-Pulmonary Resuscitate (CPR) ICD 1st therapy

Brugada Syndrome
Idiopathic ventricular fibrilation + NO evidence of causative structural cardiac disease. Common = young male adult and in South East Asia.

Manifestation :
Sudden death during sleep, resuscitated cardiac arrest and syncope Asymptomatic

20% = monogenic inheritable cond.

SCN5A GPD1LL CACNA1C

ICD is only succesful therapy.

Management
Pharmalogical Non Pharmalogical
Radiofrequency Catheter Ablation Implantable Cardioverter Defibrillator (ICD)

 Mxn of symptomatic tachyarrhythmias. Performed by placing 3 or 4 electrode catheters 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

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.