mbbs antiarrhythmics 2014 class i [basics]

8/13/2019 MBBS Antiarrhythmics 2014 Class I [Basics]

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Myocardial cells are excitable!

[Impulse generation, conduction & contraction]

SA Node Impulse generation [Pace maker]

Atria Conduction, contraction

AV Node Conduction

HIS

purkinjesystem

Conduction

Ventricles Conduction, contraction2


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Rhythmic

Electrical and mechanical activity

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Arrhythmias

What is normal cardiac rhythm?

What is rhythm?

Any activity in the universeoccurring again and again at regularintervals

Arrhythmia-abnormal rhythm

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Normal cardiac rhythm

Impulse generation

Impulse propagation

Sinus

tachycardia

Atrial rhythm

WPW

syndrome

First degree

HB

Normal velocity

Rate-60-100 BPM

Pace maker-Sinus

Normal conduction pathways

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Types of arrhythmias

Bradyarrhythmias

Tachyarrhythmias

Supraventricular Atrial fibrillation [AF]

Atrial flutter [AFL]

Paroxysmal supraventricular

tachycardia [PSVT]

Ventricular Ventricular fibrillation & Flutter [VF,

VFL]

Ventricular tachycardia [VT]

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Activities in the heart

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Mechanical activity[contraction & CO]

Electrical activity [Imp.gen&cond.]

Action potentials

Depolarization

Repolarization

Ionic fluxes

Arrhythmias Anti arrhythmics


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K K

K

RP

-90

TP

-70

Symp

Para

Symp

4

01

2

3

K

K K

4

0 3

4

Nodal tissue Myocyte

TP

-40

RP

-60

++++

Cardiac action potential 21


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AP in non-pacemaker tissue

AP in pacemaker tissue

Ca NaKK

4

4

0

3

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Pathogenesis of arrhythmias

Abnormalities of impulse

generation

Abnormalities of spontaneous

automaticity

Abnormalities of triggered

automaticity

Abnormalities of impulse

propagation

Impulse block

Re-entry phenomenon

Anatomically defined Functionally defined18


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Triggered automaticity[Abnormality of impulse generation] Re-entry phenomenon

[Circus movement][Abnormality of impulse conduction]

Pathogenesis of arrhythmia[Mechanisms of arrhythmias]


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Pathogenesis of arrhythmiasAbnormalities of impulse

generation

Spontaneous automaticityAbnormalities of triggered

automaticity[ After depolarization]

Atrial and ventricular tachycardia

Not commonAcutely ill pts.

Underlying disease+

Treat the cause

Early after depolarization[EADs]

Delayed after depolarization[DADs]

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Pathogenesis of arrhythmias

Abnormalities of triggered

automaticity

Early after depolarization[EADs]

4

0

1, 2, 3

4

RMP

TP

E

A

D

K+ channels are defective-slow

[QT prolongation]-Torse-De-Pontes

Drugs[K+ channel blockers]

Hypokalemia

Low HR

[Tt increase HR]

If Phase 4 [repolarization] is prolonged voltage gated [Na or Ca] channels

may be activated prematurely to produce EADs 14


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Pathogenesis of arrhythmiasAbnormalities of triggered

automaticity

Delayed after depolarization [DADs]

4

0

1, 2,

3

4

RMP

TP

D

A

D

Fluctuations in baseline-due to Ca++ loading

-If baseline comes near TP -DAD may occur

Adrenergic stressDigitalis toxicity

Ischemia

E

A

D

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Pathogenesis of arrhythmiasAbnormalities of impulse

propagation

Impulse block[Heart blocks]

AV blocksBeta blockers

Calcium channel

blockers

Digitalis toxicityAdenosine

Ischemia

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Re-entry


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Re-entry

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Pathogenesis of arrhythmiasRe-entry phenomenon

Anatomically defined Functionally defined

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AVAVN

SAN

1. 2 pathways

2. Nearly parallel

3. Connected proximally and distally

4. Different velocities & RP


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1. Two roughly parallel conductingpathways must be present &

2. Connected proximally and distallyby conducting tissue, forming apotential electrical circuit

3. One pathway must have a longerrefractory period

4. Pathway with the shorterrefractory period must conduct

electrical impulses more slowly thandoes the opposite pathway

Re-entry phenomenon

Initiation of reentry

An appropriately timed, prematureelectrical impulse can be blocked inpathway B (which has a relatively longrefractory period)

While conducting down pathway A.

Because conduction down pathway A isslow, pathway B has time to recover,allowing the impulse to conductretrogradely up pathway B.

The impulse can then reenter pathwayA.

A continuously circulating impulse is thus

established. 9

B BA

A


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Types of arrhythmias

Bradyarrhythmias

Tachyarrhythmias

Supraventricular Atrial fibrillation [AF]

Atrial flutter [AFL]

Paroxysmal supraventricular

tachycardia [PSVT]

Ventricular Ventricular fibrillation & Flutter [VF,

VFL]

Ventricular tachycardia [VT]

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How do antiarrhythmics work?

Tachyarrhythmias mediated by changes inthe cardiac action potential

Drugs that alter the action potential altercardiac arrhythmias [By altering ionicfluxes]

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Effect AP

Change the shape of the cardiac AP.

1. Conduction velocity [CV].

2. Refractory period [RP]

3. Automaticity [AM]

Antiarrhythmic drugs do this by altering the

channels that control the flow of ions across

the cardiac cell membrane.


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Antiarrhythmics

Classification [Singh-Vaughan-Williams]Sodium-channel-

blockers

6

Beta-blockersPot.channel

blockers

Calcium channel

blockers

Conduction Velocity

Refractory Period

Automaticity


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Effect on AP

5

Increase RP[APD]

Decrease RP[APD]

1. 2 pathways

2. Nearly parallel

3. Connected proximally and

distally

4. Different velocities & RP


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Antiarrhythmics

Classification [Singh-Vaughn-Williams]Sodium-channel-

blockers

4

Beta-blockers

Propranolol

Pot.channel

blockers

Amiodarone

Calcium channel

blockers

Verapamil

Diltiazem

Miscellaneous

Adenosine

Magnesium

Digitalis

Atropine

Procainamide

Sotalol,CV-Moderately

, CV-Mild

, CV-Profound


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Na+ Channel blockers

Class 1A.Eg. Procainamide

.CVRP

.Atria & Ventricles

.Oral & i.v.

PK:Acetylation

Uses:AF, Reentrant

tachy,VT

.ADEs:

Anticholinergic

SLE, agranulocytosis

Proarrhythmic-

Torse-De-Pontes

3

Class 1BEg.Lignocaine

Na+ Channel

No action at low HR

User dependent

APD[RP]Only ventricles

i.v[bolus-infusion]

Use: Vent.arrhythmias

ADEs: CNS

Proarrhythmic-rare

Class 1CEg. Porpafenone

Conduction-V.potent

Oral

Beta blocker, -ve inotropic

Uses: atrial &

Vent.arrhythmias

ADEs: Visual disturbances

GIT effects

Reserve drug

Diisopyramide

[-ve inotropic]

Mexiletine[O] Flecanide

[No beta blockade]


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Class II-BetablockersEg.Propranolol

Mild, blunt arrhythmogenic effect

SA Node-Phase 4 is blunted-reduces automaticity

AV Node-slows conduction

Protective-Prevents reentrant tachycardias Uses:

Effective in arrhythmias where SA & AV nodes are involved

AF & AFL-Reduces ventricular response

Not effective in treating ventricular arrhythmias, but effectivelyprotects.

Yes, last slide!

mbbs antiarrhythmics 2014 class i [basics]

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