Post on 30-Jul-2018
transcript
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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Dr. Ahmed Elberry, MD 2
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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Dr. Ahmed Elberry, MD 17
berry_ahmed@yahoo.com
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