Pharmacology - Cardiac Dysrhythmias

Front 1

Where is the heart beat initiated?

Back 1

SA node

Front 2

What are the two broad types of clinically important dysrhythmias?

Back 2

Tachycardias: in atria=supraventricular tachycardias Bradycardias: heart block due to damage AV node/conducting tissue. external pacemaker rather than drugs needed.

Front 3

describe Atrial fibrillation.

Back 3

fast, uncoordinated, and ineffective muscle contraction. not impulse get through to the ventricles so very irregular heart beat.

Front 4

What are the three causes of dysyrhythmia?

Back 4

normally induced by ischaemia: abnormal pacemaker activity, early or delayed after depolarisation, Re-enty

Front 5

explain how abnormal pacemaker activity can cause dysrhythmias?

Back 5

induced by ischaemia or increased sympathetic activity, ectopic focus of pacemaker beat.

Front 6

explain the principle of delayed after depolarisation

Back 6

no phase 4 depolarisation in none pacemaker cells, but at high Ca2+ this can occur and and action potential can be induced.

Front 7

explain the principle of early after depolarisation

Back 7

Arrise in phase 2 or 3 when repolorisation is delayed and AP abnormally long (bradycardia). Can be caused by Type III antidysrhythmics.

Front 8

explain the principle of re-entry.

Back 8

normally AP one direction. but if damages occurs then circus rhythms can begin, providing site for abnormal cardiac excitation.

Front 9

describe briefly the 5 phases of a cardiac action potential.

Back 9

0=fast depolarising inward Na+ current
1=rapid partial repolarisation: Na+ current inactivation
2=Plateau: inward Ca2+ current
3= Ca2+ current inactivation:outward K+current
4=pacemaker depolarisation: increased Na+/Ca2+ currents reduced K+ currents

Front 10

Give an example, effect, mechanism, and use for class 1a,b, and c anti-dysrhythmics.

Back 10

Mechanism: Used dependent Na+ channel blockers, act on Phase 1
Use: Ventricular fibrillation, especially associated with MI
Examples 1a=Disopyramide 1b=Lidocaine 1c=flecainide
Effect: decrease rate of depolarisation, increase ERP, decrease AV conductance.
Subdivided: into different degrees of use dependance, Ib dissociates the fastest, Ia less rapidly, Ic least rapidly.

Front 11

Describe Class II antidysrhythmics + example

Back 11

Mechanism: beta-adrenoceptor antagonists dec Ca2+ influx, dec pacemaker activity, slows AV conduction, inhibits ectopic beats, thus dec force & rate
eg: propranolol, atenolol,
Effect: works on phase 2, and 4 to slow pacemaker activity, and increase AV refractory period,
Good for: dysrhythmia prevention in MI, paroxysmal atrial fib' due to sympathetic activity

Front 12

Describe Class III antidysrhythmics + example

Back 12

Mechanism: Work on phase 3 blocking K+ channels increase action potential duration and increases ERP.
eg: Amiodarone (also blocks beta receptor, and Na+ channel)
Good for: Afib' and Vfib'

Front 13

Describe Class IV antidysrhythmics + example

Back 13

Mechanism: Ca2+ clockers effecting phase 2 decrase APV slowed AV conduction
eg: Veramapil
Good for: supra-ventricular tachycardias and Afib'

Front 14

Other drugs of not classified by system.

Back 14

Digoxin: a K+ channel activator (vagal action) to slow AV conduction, Afib'
Adenosine: K+ channel activator slows pacemaker activity and slows AV conduction, i.v. for supra-ventricular tachycardias

Front 15

How is Lidocaine administered?

Back 15

i.v.

Front 16

How is propanolol activity maintained with only a t1/2 of 4h and significant first pass metabolism?

Back 16

it has an active metabolite

Front 17

Unwanted effects of anti-dysrhythmics?

Back 17

narrow therapeutic index. Ca2+ blockers should be avoided in heart failure. Class II not in asthmatic patients as it would aggravate bronchoconstriction.