ARRHYTHMIA - kau arrhythmia.pdf · 12/12/2010 Dr. Ahmed Elberry, MD 1 1 ARRHYTHMIA Dr. Ahmed A....

12/12/2010

Dr. Ahmed Elberry, MD 1

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ARRHYTHMIA

Dr. Ahmed A. Elberry, MBBCH, MSc, MDAssistant Professor of Clinical Pharmacy

Faculty of pharmacy,KAU

SINUS RHYTHM SA node is cardiac pacemaker Normal sinus rhythm 60-100 beats/min Depolarisation triggers depolarisation of

atrial myocardium Conducts more slowly through AV node Conducts rapidly through His bundles &

Purkinje fibres to ventricles

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SA node is controlled by autonomicnervous system Parasympathetic system predominates

(M2 receptors) Sympathetic system (ß1 receptors)

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ECG

Recording of electrical activity of the heart Net sum of depolarisation & repolarisation potentials of

all myocardial cells P-QRS-T pattern

P - atrial depolarisation QRS - ventricular depolarisation T - ventricular repolarisation

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Pq

R

s

T

ARRHYTHMIA

It is an electrophysiological abnormality leading toloss of cardiac rhythm

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Pathophysiology of arrhythmia

Causes of arrhythmia: Disturbance of impulse formation: Disturbance of impulse conduction

Classification of arrhythmia: According to their site of origin Supraventricular &

ventricular According to heart rate tachycardia & bradycardia

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Normal

Re-entry

AV re-entry tachycardia (Wolf-Parkinson-White syndrome)

CLINICAL CLASSIFICATION OFARRHYTHMIAS

1. Bradyarrhytmiassinus block, sick-sinus syndrome, AV block

2. Tachyarrhytmiasa) Supraventricular (SV)

Atrial fibrillation (AF) or atrial flutter paroxysmal supraventricular tachycardia (PSVT) Wolf-Prkinson-White Syndrome (WPW) .

b) Ventricular premature ventricular complexes ventricular tachycardia

Torsade de pointes is a polymorphic VT ventricular fibrillation

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Atrial fibrillation (AF) or atrial flutter

AF Atrial flutter• More common• extremely rapid (400 to 600 atrial

beats/min) & irregular atrialactivation.

• There is loss of atrial contraction,resulting in irregular ventricularactivation and irregularly irregularpulse (120 to 180 beats/min).

• Less common• rapid (270 to 330 atrial

beats/min) but regular atrialactivation.

• The ventricular response usuallyhas a regular pattern and apulse of 300 beats/min.

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They have similar precipitating factors, consequences, and drug therapy.The mechanism of AF & atrial flutter is reentry, which is usually associated

with organic heart disease that causes atrial distention (e.g., ischemia orinfarction, hypertensive heart disease, valvular disorders).

Atrial Flutter

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• Most cases of atrial flutter are causedby a large reentrant circuit in the wallof the right atrium

• ECG Characteristics:• Biphasic “sawtooth” flutter

waves at a rate of ~ 300 bpm• Flutter waves have constant

amplitude, duration, &morphology

• There is usually either a 2:1 or4:1 block at the AV node,resulting in ventricular rates ofeither 150 or 75 bpm

Atrial Fibrillation

• AF is caused by numerous wavelets ofdepolarization spreading throughout theatria simultaneously absence ofcoordinated atrial contraction.

• ECG Characteristics:• Absent P waves• Presence of “fibrillatory” waves

which vary in amplitude &morphology

• Irregularly irregular ventricularresponse

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1st Degree AV Block

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Prolongation of the PR interval, which is constantAll P waves are conducted

2nd Degree AV Block

Progressive prolongation of the PR interval until a P wave is not conducted.As the PR interval prolongs, the RR interval actually shortens

3rd Degree (Complete) AV Block

No relationship between P waves and QRS complexesRelatively constant PP intervals and RR intervalsGreater number of P waves than QRS complexes

CLINICAL MANEFISTATION

Asymptomatic Symptomatic:

Palpitation dizziness or acute syncopal episodes symptoms of HF; angina; embolic stroke with AF irregular pulse

Diagnosis: with ECG

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TREATMENT OF ARRHYTHMIA

The use of antiarrhythmic drugs in USA isdeclining because: many trials showed increased mortality with their

use Pro arrhythmia is a significant side effect advancing technology of nondrug therapies as

ablation implantable cardioverter-defibrillator (ICD).

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Phases of the action potential:• Phase 0: activation of Na+ channels rapid Na+ influx. (excitability &

conductivity).• Phase 1: Inactivation of Na+ channels & K+ efflux.• Phase 2: activation of slow Ca++ channels slow Ca++ influx & K+ efflux.• Phase 3: Activation of K+ channels rapid K+ efflux.• Phase 4:

a) normal cardiac muscle fiber resting potential Activation of A.T.P ase Na+ / K+ pump restore the electrolyte balance.

b) S.A.N., conductive tissue & ectopic focus slow Na+ & Ca++ influx Slowdiastolic depolarization (automaticity)

13Atrium & Ventr. S.A node

Drugs blocking ion channels

Activated Na+ channels phase 0 excitability & conductivity.

Inactivated Na+ channels phase 4 automaticity. Slow Ca++ channels phase 4 automaticity

Short phase 2 K+ channel long phase 3 long (A.P.D) & long (E.R.P)

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Vaughan Williams Classificationof Antiarrhythmic Drugs:

(1) Class 1: Na+ channel blockers (see below)

(2) Class II: beta-blockers : Propranolol, acebutalol & esmolol.

(3) Class III:Block mainly K+ channel delay repolarization long phase 3 long APD& ERPExamples: Amiodarone - Bretylium - Sotalol - Ibutilide – Dofetilide

(4) Class IV: CCB: Verapamil & Diltiazem

(5) Unclassified: e.g: Adenosine - Atropine - Digitalis - Magnesium

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A) Group A:Block both Na+ & K+

B) Group B: C) Group C:

1. Moderate block of activatedNa+ channel moderate of phase 0 moderate conductivity & excitability.

2. Block inactivated Na+

channel phase 4 depress automaticity.

3. Block K+ channel delayrepolarization long phase3 long A.P.D. &E.R.P.

* Examples:Quinidine , Procainamide &Disopyramide

1. Minimal block of activatedNa+ channel minimal ofphase 0 minimal effect ofconductivity & excitability.

2. Block mainly inactivatedNa+ channel phase 4 automaticity.

1. May activate K+ channel rapid repolarization short phase 3 short APD& ERP.

* Example:Lidocaine , Mexiletine ,

Tocainide & Phenytoin

- Marked block ofactivated Na+ channel marked of phase0 marked ofconductivity & excitability.

* Examples:Flecainide - Encainide -

Lorcainide - Propafenone

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Indications:Maintain normal sinus rhythm in supraventricular arrhythmia

Adverse effects (common & serious) GIT: diarrhoea, nausea, vomiting (in up to 30% of treated patients)

CNS – “cinchonisms“: headache, vertigo, tinnitus, visual disturbances

haematological: thrombocytopenia, haemolytic anaemia

Skin: urticaria (rash), photosensitisation

Myalgia, arthralgia, SLE like, fever, hepatitis Cardiovascular system

• Ventricular tachycardia (Torsades de pointes)• HF, Bradycardia, heart arrest

Interactions: strong inhibitor of CYP 2D6

Class IA: QUINIDINE

PROCAINAMIDE• It is the drug of choice in WPW syndrome• Adverse effects

Hypotension, esp. after rapid i.v. infusion. Long QT syndrome & TdP Lupus-like syndrome: after long treatment (> 6 months):

• Syndrome disappear spontaneously after drug withdrawal Other: GIT (vomiting, diarrhoea), allergy, CNS (depressions,

hallucinations), haematological disturbances

DISOPYRAMIDE• Adverse reactions:

1. Antimuscarinic (dry mouth, visual disturbances, urinary retention,glaucoma worsening)

2. -ve inotropic: can precipitate HF

Class IA:

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Indications:• Acute ventricular arrhythmias esp. after M.I. & with digoxin

overdose (Phenytoin)

Adverse reactions: CNS – paresthesia, tremor, nausea, hearing and speaking disturbances In high doses - agitation and convulsions may appear (treatment -

diazepam), apnoea, negative inotropic action and hypotension Phenytoin: megaloblastic anaemia, Hirsutism & gum hypertrophy

Class IB:Lidocaine , Mexiletine , Tocainide,

Phenytoin

Indication: Supraventricular arrhythmia

Adverse effects1. Cardiac: AV block, ventricular tachyarrhythmias2. GIT : Nausea, vomiting, constipation & metallic taste with

propafenone3. CNS : tremor, restlessness, headache, sleeping disturbances

Class IC: Flecainide - Encainide -Lorcainide - Propafenone

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It is a broad spectrum antiarrhythmic

Adverse effects Cardiac

bradycardia, AV blockade long QT syndrome & TdP risk

Extracardiac1. Lungh fibrosis (in a serious form in up to 1% of patients)2. Hepatotoxicity

3. Skin deposits – fotodermatitis and coloured sun-exposed skin (blue-grey)4. Corneal microdeposits – detectable already after few weeks of treatment, it's

mostly asymptomatic, but may cause blurred vision in some patients5. Optic neuropathy/neuritis (rare) may result in blindness

6. Thyreoid dysfunction: hypofunction or hyperfunction

Class III: AMIODARONE

SOTALOLAdverse reaction: generally relatively tolerable drug (mostly

transient)• Long QT & TdP• Bradycardia, HF, hypotension, bronchoconstriction, sleep disturbances

Dofetilide Proarrhythmogenic – TdP, the QT monitoring is essential

Ibutilide indicated mainly for rapid pharmacological cardioversion of AF &

Flutter to sinus rhythm

Class III

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CLASS II & CLASS IV

Class II (BB): indicated in supraventricular & ventricular

arrhythmia

Class IV (CCB): Indicated in supraventricular arrhythmia (not

ventricular) Not combined with BB

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• Atropine:• Indicated in sinus bradycardia

• Adenosine: Used in Acute supraventricular arrhythmia (successful in 90-95%)

Adverse reactions: flush, headache, dyspnea (bronchoconstriction), palpitations, very rare

is induction of ventricular fibrillation

• Digoxin:• Used in supraventricular arrhythmia (CI in ventricular)

• Mg: Indicated in digoxin-induced tachyarrhythmias & TdP

Unclassified

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ATRIAL FIBRILLATION ORATRIAL FLUTTER

Goal of treatment: Ventricular rate control: Prevention of embolic stroke: by anticoagulants

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Ventricular rate control in AF

If symptoms aresevere

direct currentcardioversion (DCC)to restore sinusrhythm immediately.

If patients arehemodynamically stable

In patients withnormal LV function

(EF >40%)

- IV βB (propranolol,metoprolol, esmolol),OR- IV CCB (Diltiazemor verapamil)

In patients withEF ≤ 40%

IV digoxin oramiodarone shouldbe the 1st line therapy

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Anticoagulants in AF Anticoagulation should be initiated prior to cardioversion

because return of atrial contraction risk ofthromboembolism.

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Patients with AF for ˃48h or unknown duration: should receive warfarin

(target INR 2 to 3) for atleast 3 weeks prior tocardioversion

& continuing for at least 4weeks after effectivecardioversion .

Patients with AF ˂48 hin duration: do not require warfarin, but it is recommended to

give IV UFH or LMWH(SC) at presentation priorto cardioversion.

Maintenance therapy

1. Quinidine maintained sinus rhythm; however,1. 50% of patients had recurrent AF within 1 year,2. more importantly, quinidine increased mortality, presumably

due in part to proarrhythmia.

2. Type Ic (e.g., flecainide, propafenone) & type III(eg. amiodarone, sotalol, dofetilide)antiarrhythmics may be alternatives; however,

1. they are also associated with proarrhythmia.

Consequently, chronic antiarrhythmic drugs shouldbe reserved for patients with recurrent paroxysmal AF.

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Paroxysmal SupraventricularTachycardia

Acute therapy: Severe symptoms: (e.g., syncope, anginal pain, severe HF)

DCC is the treatment of choice Mild to moderate symptoms:

Nondrug measures that vagal tone to the AV node (e.g.,unilateral carotid sinus massage, Valsalva maneuver).

Adenosine is the drug of 1st choice

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Maintainanace therapy(1) those that vagal tone to the AV node (e.g., digoxin)(2) those that conduction through slow, Ca++-dependent tissue

(e.g., adenosine, βB, CCB)(3) those that conduction through fast, Na+-dependent tissue

(e.g., quinidine, procainamide, disopyramide, flecainide).

Ventricular Tachycardia

Acute or severe Ventricular Tachycardia Most patients require & respond to DCC. However, TdP tends to

be paroxysmal & often recurs rapidly after DCC. IV magnesium sulfate is considered the drug of choice for

preventing recurrences of TdP.

Mild or no symptoms IV amiodarone is recommended as first-line therapy.

Procainamide or lidocaine given IV is a suitable alternative.

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Ventricular Fibrillation

Epinephrine is a drug of first choice for treating VF

Vasopressin is a potent VC that Bl Pr & systemic vascular resistance.

Amiodarone is the preferred antiarrhythmic during cardiac arrest

Lidocaine is recommended as an alternative to amiodarone

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BRADYARRHYTHMIAS

Asymptomatic sinus bradyarrhythmias usually do notrequire therapeutic intervention.

Long-term therapy of choice for patients with significantsymptoms is a permanent ventricular pacemaker.

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AV Block

Atropine (0.5 mg IV given every 3 -5 min, up to 3 mg total dose)should be given as the pacing leads are being placed.

Infusions of epinephrine (2 -10 mcg/min) or dopamine (2 -10 mcg/kg/min) can be used if atropine failed.

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[email protected]

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ARRHYTHMIA - kau arrhythmia.pdf · 12/12/2010 Dr. Ahmed Elberry, MD 1 1 ARRHYTHMIA Dr. Ahmed A....

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