Antiarrythmics

Question 1

Class I antiarrythmics mechanism?

Answer 1

Block voltage gated sodium channels in open/inactivated state -> slow heart rate and slow conduction velocity -> stop after depolarisations, stop re-entry loops

Question 2

Class IA e.g. Quinidine

Answer 2

Moderate Na channel blockers, increase AP duration, decrease heart rate and conduction velocity -> prolong QT and QRS

Question 3

Class IB e.g. Lidocaine

Answer 3

Weak Na blockers, shorten ERP, slow conduction in ISCHAEMIC tissue only! (Selectively block ectopic pacemaker activity!)

Question 4

Class IC e.g. Flecainide

Answer 4

Strong Na blockers, ERP increases, reduce heart rate and prolong QRS complex

Question 5

Class I uses?

Answer 5

Atrial fibrillation/flutter (IA, IC)
Ventricular tachycardia (IA, IB)
Wolfe Parkinson White (IC)

Question 6

Class I ADRs

Answer 6

Proarrythmic (IA, IC)
Dizziness and confusion (all!)
GI effects (IA, IC)

Question 7

Class II uses?

Answer 7

SVT (including AF), prevent arrythmic death post MI/in CHD, exercise induced arrythmia

Question 8

Class III- mechanism?

Answer 8

K+ channel blockers, increase length of plateau (increase ERP), increase AP duration -> slows conduction

Question 9

Amioderone -mechanism?

Answer 9

K+ blocker, and Na effects (decrease slope of upstroke, decrease conduction velocity), increase repolarisation phase (Ca+, beta blockers)

Question 10

Amioderone- uses?

Answer 10

All arrythmias!! (Not long term!)

Question 11

Amioderone- ADRs

Answer 11

Long term uses-> pulmonary fibrosis, hepatic injury, thyroid disease, photosensitivity

Question 12

Amioderone DDIs?

Answer 12

Digoxin and warfarin- monitor drug levels!

Question 13

Class IV e.g. Verapamil mechanism?

Answer 13

Block L-type calcium channels -> prolong plateau (increase AVN ERP), decrease slope of pacemaker potential (slow HR)

Question 14

Class IV uses?

Answer 14

Decrease AV re-entry -> SVTs

Question 15

Class IV ADRs

Answer 15

GI problems, negative inotropy-> reduced CO, AVN block, hypotension (peripheral vasodilation)

Question 16

Adenosine- mechanism?

Answer 16

A1 receptor agonist -> increase K+ out of SA/AVN = hyperpolarisation!! (Removes all channels from inactivated state!)

Question 17

Adenosine uses?

Answer 17

Converts re-entrant SVT to sinus rhythm :D

Question 18

Adenosine ADRs?

Answer 18

Hypotension, syncope

Question 19

Digoxin- mechanism

Answer 19

Inhibits Na pump -> reverses NCX -> increase Ca in cell -> increase force of contraction (positive inotrope) and decrease HR

Question 20

Digoxin uses?

Answer 20

A. Fib, flutter

Heart failure

Question 21

Digoxin ADRs

Answer 21

GI disturbance, yellow-green visual halos, confusion, TOXICITY! (Vomiting, bradycardia, yellow vision -> long half life so takes long time to clear it!)