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ARRHYTHMIA

Arrhythmia HEART

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ARRHYTHMIA

Hazhar Faisal Abdullah

M.Pharm (Pharmacology) 2nd Sem

Faculty of Pharmacy

Amity University

DELHI-INDIA

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DEFINATION:

■Cardiac arrhythmia/cardiac dysrhythmia/irregular heart beat is a group of condition in which the heart beat is irregular, too fast or too slow.

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ABNORMAL RHYTHM:

CAN BE OF TWO EXTREME FORMS:

1. Bradycardia - Cardiac beats below 60 beats per minute .

2. Tachycardia – Cardiac beat above 100 beats per minute.

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ETIOLOGY (CAUSES):■ Coronary artery disease.■ Electrolyte and pH imbalances in your blood (such as sodium or

potassium).■ Changes in your heart muscle.■ Injury from a heart attack.■ Healing process after heart surgery.■ Irregular heart rhythms can also occur in "normal, healthy"

hearts.■ Ischemic Heart Disease■ Neurogenic and drug influences■ Others

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(SYMPTOMS)■ Palpitation (make you feel like your heart is beating too hard or

too fast characterized by awareness of cardiac muscle contractions in the chest )

■ Dizziness.

■ Shortness of breath or chest pain Dyspnea. Sincope or Fainting (a short loss of consciousness and muscle

strength) Unstable haemodynamic condition. Abnormal pulse. Precipitation of cardiac failure.

■ Sudden cardiac death

■ Swelling

■ Exercise Intolerance

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Normal cardiac rhythm:

For normal cardiac rhythm:I. Heart rate should be 80-100II. Impulse should originate from SA nodeIII. Cardiac impulse should propagate through normal

conduction pathwayIV. Normal velocity

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CARDIAC ACTION POTENTIAL:

■FAST CHANNEL AP SLOW CHANNEL AP

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CARDIAC CONDUCTION AND ECG:

Cardiac cycle P wave = atrial depolarization PR interval = pause between atrial

and ventricular depolarization QRS = ventricular depolarization T wave = ventricular

depolarization U wave=Perkinje fiber repolarization

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Mechanism of Arrhythmias 1) Enhanced/ectopic pacemaker activity2) After depolarisation

i. Early after-depolarisationii. Delayed after depolarisation

3) Reentryi. Circus movement typeii. Microentry circuit

4) Increased/decreased automaticity

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1-ENHANCED/ECTOPIC PACEMAKER ACTIVITY■ An ectopic pacemaker or ectopic foci is an excitable groups of cells that causes the

premature heart beat outside the normally functioning SA node of human heart....– Results due to pathological increase in phase 4 slope - accelerated pacemaker

rate– May result from current of Injury– Physiology: ACh reduces such pacemaker rate – by decreasing phase 4 and

hyperpolarization– Ventricular wall cells may also show such pace maker activity – due to ischemia.

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Blockage of Conduction from SA node AV node BlockageCauses• Ischemia • Fibrosis (the thickening and scarring of connective tissue, usually as a

result of injury or damage)• Viral Infection

RESULTS in HEART ATTACK

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2-AFTER DEPOLARISATION:

These are secondary depolarisation accompanying a normal or premature action potential.

EARLY AFTER DEPOLARISATION:repolarisation during phase 3 AP is interrupted and membrane

potential oscillates.If the amplitude of oscillation is sufficiently large, neighbouring tissue is

activated and series of impulses are propagated

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CONTINUE..

■ EAD are frequently associated with long QT interval.■ They result from depression of delayed rectifier K+ ion. DELAYED AFTER-DEPOLARISATION:• After attaining RMP a secondary deflection occurs which may reach

threshold potential and initiate a single premature AP.• Result from a Ca+ overload.

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Becaues an AP is needed to trigger after depolarisation, arrhythmia based on these have been called triggered arrhythmias.

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3-REENTRY:■ Due to primarily to abnormality of conduction, an impulse may

recirculate in the heart and cause repetitive activation without need for any new impulse to be generated.

■ One of the causes of the most arrhythmias■ Normally, impulses propagate in synchronized manners■ But, here one impulse reenters and re-excites areas of heart more

than once – no need for new impulse generation■ Re-entering of impulses may be

1. Anatomically defined reentry – Circus movement type2. Functionally defined reentry - Microentry circuit

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A- CIRCUS MOVEMENT TYPE:

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2.Re-entry Tachycardias Atrial Fibrillation

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B- MICRO ENTRY CIRCUIT:

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4-INCREASED OR DECREASED AUTOMATICITY or Fractionation of Impulse: Increased Vagal activity – Atrial ERP (effective refractory period )brief and inhomogeneous

Premature impulses get conducted by fibers having short ERP – then to the fibers with longer ERP and so on

Asynchronous activation of atrial fibers – inhomogeneity – Atrial fibrillation etc.

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Classification of Arrhythmia: NORMOTROPIC• Sinus tachycardia• Sinus bradycardia• Sinus arrhythmia ECTOPIC• Heart block• Extrasystole• Paroxysmal tachycardia• others

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Arrhythmia Conditions - Clinically■ Extrasystole: premature beats due to abnormal automaticity/after

depolarization – AES, VES or AV nodal ES■ Paroxysmal Supraventricular Tachycardia (PSVT): Sudden onset of atrial

tachycardia 150-200/minute (1:1), reentry phenomenon (AV node) ■ Atrial Flutter: 200-350/minute (2:1 to 4:1 AV block), reentrant circuit in right

atrium■ Atrial Fibrillation: Asynchronous activation of atrial fibres 350-550/min with

irregular 100 to 160 ventricular beats – due to electrophysiological inhomogenicity of atrial muscles (bag of worms)

■ Ventricular tachycardia: 4 or more consecutive extrasystole of ventricles – monomorphic or polymorphic

■ Ventricular Fibrillation: rapid irregular contractions – fatal (MI, electrocution)

■ Torsades de pointes: polymorphic ventricular tachycardia, rapid asynchronous complexes, rise and fall in baseline of ECG

■ Atrio-ventricular Block (A-V Block): vagal influence or ischaemia - 1st, 2nd and 3rd degree – slowed conduction, drop beat and no

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SINUS TACHYCARDIA:■ Rate: 101-160/min■ P wave: sinus■ QRS: normal■ Conduction: normal■ Rhythm: regular or slightly irregular

■ The clinical significance of this dysrhythmia depends on the underlying cause. It may be normal.

■ Underlying causes include: increased circulating catecholamine's CHF hypoxia (oxygen deficiency) increased temperature stress response to pain

■ Treatment includes identification of the underlying cause and correction.

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SINUS BRADYCARDIA:■ Rate: 40-59 bpm■ P wave: sinus■ QRS: Normal (.06-.12)■ Conduction: P-R normal or slightly prolonged at slower rates■ Rhythm: regular or slightly irregular■ This rhythm is often seen as a normal variation in athletes, during sleep, or in

response to a vagal maneuver. If the bradycardia becomes slower than the SA node pacemaker, a junctional rhythm may occur.

■ Treatment includes: treat the underlying cause, atropine, artificial pacing if patient is hemodynamically compromised.

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SINUS ARRHYTHIMIA:■ Rate: 45-100/bpm■ P wave: sinus■ QRS: normal■ Conduction: normal■ Rhythm: regularly irregular ■ The rate usually increases with inspiration and decreases with

expiration. ■ This rhythm is most commonly seen with respiration due to

fluctuations in vagal tone.■ The non respiratory form is present in diseased hearts and sometimes

confused with sinus arrset (also known as "sinus pause"). ■ Treatment is not usually required unless symptomatic bradycardia is

present.

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PAROXYSMAL ATRIAL TACHYCARDIA:■ Rate: atrial 160-250/min: may conduct to ventricles 1:1, or 2:1, 3:1, 4:1 into the

presence of a block. ■ P wave: morphology usually varies from sinus■ QRS: normal (unless associated with aberrant ventricular conduction). ■ Conduction: P-R interval depends on the status of AV conduction tissue and

atrial rate: may be normal, abnormal, or not measurable. ■ PAT may occur in the normal as well as diseased heart.

It is a common complication of Wolfe-Parkinson-White syndrome.(WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely)

■ This rhythm is often transient and doesn't require treatment. However, it can be terminated with vagal maneuvers. Digoxin, antiarrhythmics, and cardioversion (is a procedure that uses

external electric shocks to restore a normal heart rhythm) may be used.

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ATRIAL FIBRILLATION:■ Rate: atrial rate usually between 400-650/bpm.■ P wave: not present; wavy baseline is seen instead. ■ QRS: normal■ Conduction: variable AV conduction; if untreated the ventricular response is

usually rapid. ■ Rhythm: irregularly irregular. (This is the hallmark of this dysrhythmia). ■ Atrial fibrillation may occur paroxysmally, but it often becomes chronic. It is

usually associated with COPD, CHF or other heart disease. ■ Treatment includes:

Digoxin to slow the AV conduction rate. Cardioversion may also be necessary to terminate this rhythm.

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VENTRICULAR TACHYCARDIA:■ Rate: usually between 100 to 220/bpm, but can be as rapid as 250/bpm ■ P wave: obscured if present and are unrelated to the QRS complexes. ■ QRS: wide and bizarre morphology■ Conduction: as with PVCs■ Rhythm: three or more ventricular beats in a row; may be regular or irregular. ■ Ventricular tachycardia almost always occurs in diseased hearts.■ Some common causes are:

CAD acute MI digitalis toxicity CHF ventricular aneurysms.

■ Patients are often symptomatic with this dysrhythmia. ■ Ventricular tachycardia can quickly deteriorate into ventricular fibrillation.

Electrical countershock is the intervention of choice if the patient is symptomatic and rapidly deteriorating.

Some pharmacological interventions include lidocaine, pronestyl, and bretylium.

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TORSADE DE POINTES:■ Rate: usually between 150 to 220/bpm,

■ P wave: may be present

■ QRS: wide and bizarre morphology

■ Conduction: as with PVCs

■ Rhythm: Irregular 

■ Paroxysmal –starting and stopping suddenly

■ Hallmark of this rhythm is the upward and downward deflection of the QRS complexes around the baseline. The term Torsade de Pointes means "twisting about the points."

■ Consider it V-tach if it doesn’t respond to antiarrythmic therapy or treatments

■ Caused by: drugs which lengthen the QT interval such as quinidine electrolyte imbalances, particularly hypokalemia myocardial ischemia

■ Treatment: Synchronized cardioversion is indicated when the patient is unstable. IV magnesium IV Potassium to correct an electrolyte imbalance Overdrive pacing

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VENTRICULAR FIBRILLATION:■ Rate: unattainable■ P wave: may be present, but obscured by ventricular waves■ QRS: not apparent■ Conduction: chaotic electrical activity■ Rhythm: chaotic electrical activity■ This dysrhythmia results in the absence of cardiac output. ■ Almost always occurs with serious heart disease, especially acute MI. ■ The course of treatment for ventricular fibrillation includes:

immediate defibrillation and ACLS protocols.(Advanced cardiac life support (ACLS) in adults)

Identification and treatment of the underlying cause is also needed.

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HEART BLOCK■ DEPRESSED CONDUCTION OF IMPULSE FROM ATRIA TO VENTRICLES

■ AV NODE BECOMES DEFECTIVE AND IMPULSES (P-WAVES) ARE BLOCKED FROM BEING TRANSMITTED TO VENTRICLES

■ FIRST DEGREE

■ SECOND DEGREE

TYPE I

TYPE II

■ THIRD DEGREE

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1° HEART BLOCK■ PR INTERVAL > 0.20 SECONDS

■ CAUSES: MAY BE NORMAL VARIANT

INFERIOR WALL MI

DRUGS: DIGOXIN

VERAPAMIL

■ TREATMENT:

MONITOR

OBSERVE FOR SYMPTOMS

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2° HEART BLOCK■ ONE OR MORE P-WAVES ARE NOT CONDUCTED THROUGH THE

VENTRICLE

■ HEART RATE - VENTRICULAR RATE SLOW TO NORMAL

ATRIAL RATE MAY BE 2 – 4 X’s

FASTER THAN VENTRICULAR

PRI becomes progressively longer until drops QRS

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3° HEART BLOCK(COMPLETE HEART BLOCK)■ATRIAL IMPULSES & VENTRICULAR RESPONSE ARE

IN TOTAL DISASSOCIATION■P-WAVES ARE SEEN & ARE IRREGULAR■QRS COMPLEX ARE SEEN & ARE IRREGULAR

(ESCAPE RHYTHM)■NO CORRELATION BETWEEN P-WAVES & QRS

(RATE IS SLOW) – independent rhythms

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NSR(Normal sinus rhythm) vs 3RD Degree Block

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3° HEART BLOCK(COMPLETE HEART BLOCK)■TREATMENT

PACEMAKERTEMPORARY

ORPERMANENT

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Diagnosis of Arrhythmia:

■Medical history■Physical examination■Laboratory test

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Anti-arrhythmia Agents:

■Anti-tachycardia agents■Anti-bradycardia agents

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TREATMENT:Anti-tachycardia agents

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5-Others: Adenosine, Digital

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Anti-bradycardia agents

■Isoprenaline■Epinephrine■Atropine■Aminophylline

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Non-drug therapy:■Cardioversion: For tachycardia especially hemodynamic

unstable patient■Radiofrequency catheter ablation (RFCA): For those

tachycardia patients (SVT, VT, AF, AFL)■Artificial cardiac pacing: For bradycardia, heart failure

and malignant ventricular arrhythmia patients.

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CLASS 1:Na+ CHANNEL BLOCKERS

FURTHER CLASSIFIED INTO:• Class 1a-

Eg:quinidine,procainamide,disopyramide• Class 1b-Eg:lidocaine• Class1c-Eg:propafenone

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Quinidine:

■ Dextroisomer of Quinine: Na+ channel blocking and antivagal action■ Actions:

Inhibition of Na channel – slanted O phase and Decreases phase 4Prolongation of APD – due to K+ channel blockIncrease in ERP – due to delay in Na+ and K+ channel recoveryNet result is delay in conductivity and increase in refractorinessFall in BP – direct cardiac depressionOther actions include – alpha blockade, decreased skeletal muscle contractility,

uterine contractions, vomiting and diarrhoea etc. Kinetics: well absorbed orally, half life – 10 Hrs Uses:

Broad spectrum antiarrhythmic Atrial fibrillation and flutter, prevention of PSVT and prevention of ventricular

tachycardia Adverse effects: Not used now for adverse effects like Proarrhythmia (torsades de pointes), sudden

cardiac arrest or VF, cinchonism, angioedema, vascular collapse etc. Available as 200, 300 mg tabs. And 300 mg/ml Injections

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Procainamide:■ Procaine derivative (amide)■ Identical action with quinidine except:

– Minimal antivagal action– Lesser suppression of ectopic automaticity– Lesser depression of contractility and AV conduction– No alpha blocking action

■ Kinetics:– Absorbed orally and bioavailability is 80%– Metabolized in liver to N-acetyl-procainamide (NAPA) – blocks K channel and prolongs

repolarization

■ Dosage – 250 mg tabs and 1gm/ml injections – Antiarrhythmic – 0.5 to 1 gm oral followed by 0.25-0.50 mg every 2 Hrs

■ Uses: Mainly for monomorphic VTs and to prevent recurrences■ ADRs: Hypersensitivity, flushing, hypertension, torsedes de pointes and CNS

symptoms – mental confusion, hallucinations and weakness

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Lidocaine (Lignocaine) :

■ Popular antiarrhythmic and also local anaesthetic (membrane stabilizing action)■ Lowest potency for Na+ channel inactivated state – ECTOPIC Foci

– Enhance phase – 4 depolarization in partially depolarized or stretched PF – After depolarization antagonized – no effect on SAN

– Practically no action on Atrial fibres– Rate of 0 phase in AVN and ventricles – not affected– Reduction in APD in PF and ventricular myocardium

■ Actions:– Selective action on partially depolarized and cells with long APD – normal ventricular and

conducting fibres – not affected– Suppression of automaticity in ectopic foci (reentry) – one way or two way block– Enhanced phase-4 depolarization in partially depolarized – Little effects on cardiac contractility and arterial BP

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■ Kinetics: Ineffective orally, given IV lasts for 10-20 minutes. Therefore given as IV bolus

50-100 mg followed by 20-40 mg every 10-20 minutes. Half-life prolonged in CHF (coz.

Vd decreases) and 70-80% metabolized by liver

■ Adverse effects: Neurological – drowsiness, paresthesia, blurred vision, nystagmus and

fits etc.

– No proarrhythmic effects – no cardiotoxicity

■ Uses: 50-100 mg bolus and 10-20 mg every 20 minutes

– 1st line of drug in Arrhythmia following acute MI and cardiac surgery

– Prevention of ventricular tachycardia

– Digitalis toxicity – no AV block

■ LA lignocaine Vs Antiarrhythmic lignocaine ?

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CLASS 2:β BLOCKERS

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■ Drugs used are beta-blockers: Propranolol, Sotalol, Esmolol and Acebutlol

■ Suppression of adrenergically mediated activity■ Propranolol - Membrane stabilizing effect like quinidine on heart –

high doses – clinical dose: cardiac adrenergic blockade■ Clinical doses (antiarrhythmic effect) - Block beta-1 receptor in

heart and decreases heart rate1. Decrease in phase 4 depolarization and automaticity in SA node,

AVN, PF and other ectopic foci (Adrenaline causes ventricular ES and fibrilation by increasing the phase 4 depolarization !!!)

2. Prolongation of ERP of AVN – impede AV conduction

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Uses of Propranolol:■ Arrhythmias associated with increased sympathetic activity – sinus

tachycardia, atrial extrasystoles provoked by emotion and exercise■ Less effective in PSVT than adenosine and verapamil■ Propranolol is used to treat sympathetically mediated arrhythmias -

phaeochromocytoma and halothane anaesthesia– Sinus tachycardia, atrial and nodal extrasystole and nodal

extrasystole provoked by exerciseDoes not abolish AF or Afl but decreases ventriculsar rate

■ Reduce mortality after MI – anti-ischaemic action■ Esmolol IV – quickly terminates AF and fluttter and used in

emergency control of arrhythmia due to anaesthetics

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CLASS 3:K+ channel blockers

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■ Class III drugs K channel blockers prolong repolarization (increase

refractoriness) by blocking outward potassium conductance

– Prolongation of Cardiac action potential

– Increased ERP

■ Drugs – Amiodarone Ibutilide, dofetilide, sotalol (II + III action) and

bretylium

■ Bretylium is used only in life threatening arrhythmias

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Amiodarone:

Long acting and highly lipophillic and Iodine containing compoundMOA: - multiple actions1. Blocking of delayed rectifier K+ channel – prolongs APD2. Weak class I (lidocaine like) – depresses conducton in partially depolarized and long

APD3. II (beta- blocker) – NC alpha and beta; and class IV actions4. Also direct coronaray and peripheral vasodilator■ Overall – Slowed conduction and supressed automaticityKinetics: Incompletely and slowly absorbed – daily oral dose is given for several days for

actions to develop, t1/2 = 3-8 weeksDose: 400-600 mg/day p.o for many days followed by 100-200 mg/day as maintenance (100-

300 mg slow IV)

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Amiodarone:Uses:■ Most tachyarrhythmic conditions – ventricular and supraventricular■ Recurrent VT and VF■ WPW syndrome

Adverse effects:

■ Photosensitization – skin pigmentation

■ Peripheral neuropathy – weak shoulder and pelvic muscles

■ Myocardial depression – bradycardia

■ Pulmonary alveolitis and fibrosis – kept below 200 mg

■ Corneal micro deposits – on long term use

■ Hypothyroidism, goitre – inhibition of T4 to T3

Drug Interactions: Digoxin and warfarin (reduced renal clearance)

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CLASS 4:calcium channel blockers

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■ Three important classes:– Phenylalkylamines – hydrophillic Verapamil– Dihydropyridines – lipophilic Nifedepine– Benzothiazepines – hydrophilic Diltiazem

■ Verapamil and diltiazem: are useful in Arrhythmia■ Relatively selective AV nodal L-type calcium channel blockers –

depression of Ca++ mediated depolarization and delay recovery– Slows SA node automaticity – reduced phase 4 depolarization in SAN and PF – extinction of

latent pacemakers and DAD– Prolongation of AVN ERP – reentry terminated– Negative ionotropic action

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■Uses: Verapamil1. PSVT:

■For termination of attack – 5 mg IV over 2-3 minutes (reflex bradycardia)

■For prevention of attack 60-120 mg orally tds2. Reduce ventricular rate in Atrial fibrillation (AF) and

Atrial flutter – with digitalis

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Others: Adenosine, Digital

Adenosine:■ Endogenously produced important chemical mediator used in PSVT■ MOA:

– Activation of ACh sensitive K+ channel - membrane hyperpolarization of SA node (G-protein coupled adenosine receptor A1)

– depression of SA node and also slowing of AV conduction– shortening of action potential in atrium and reduced excitability– Also indirectly reduces Ca++ current in AV node – depression of reentry

in PSVT

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■ Very short half life – 20-30 sec. - Uptake by RBCs and endothelial cells (5-AMP and inosine)

■ Administered intravenously – available as free base or ATP– 6 - 12 mg/ATP 10 - 20 mg given as a rapid intravenous bolus

(administered over a 1-2 second period)– If the first dose does not result in elimination of the supraventricular

tachycardia within 1-2 minutes - 12 mg should be given as a rapid intravenous bolus

■ ADR: chest tightness, dyspnoea, fall in BP and flushing etc.

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REFERENCES: The pharmacological basis of therapeutics by goodman and gilman’s Essentials of medical pharmacology by KD Tripathi. Clinical pharmacy and therapeutics by walker whittlesea. Basic and Clinical Pharmacology Katzung 13 Edition Pharmacotherapy Handbook - Ninth Edition by Barbara G.

Wells (Author), Joseph T. Dipiro (Author), Terry L. Schwinghammer (Author) www.youtube.com - Pathophysiology of Cardiac Arrhythmias by Andrew Wolf Wikipedia http://www.rnceus.com/ekg/ekgsecond2.html ACLS Guidelines 2005 www.EMS-ED.net http://www.doctorshangout.com/forum/topics/acls-algorithms-1

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Thank You