Anti arrhythmic medication

Question 1

myocardial action potential

Answer 1

zero depolarisation
action potential (Na+)

early repolarisation (transient opening of K+)

plateau phase (ca2+ balance)

rapid repoloarization

depolarisation.

Question 2

what are arrhythmias

Answer 2

disturbance in cardiac rhythm
tachy / Brady

can be due to genetic defects, ischaemia, drugs or hormones

ion channels control ionic balance (target these in anti arrhythmic drugs)

Question 3

the 3 mechanism of arrhythmias

Answer 3

increased automaticity (ability of the cells to generate an AP?)

re-entry

triggered activity

Question 4

automacity

Answer 4

the property of cardiac myocytes to undergo spontaneous depolarisation, imitating an electircal impulse
(SA and AV node)
(pacemaker cells)

they have self automaticity (that’s why there is a slope in the resting potential due to inward Na+) then inward Ca2+
then outward K+

(looks this up)

Question 5

which cells can generate their own automaticity?

Answer 5

sinus node
AV node/junction (atria)
His-Purkinjee system (ventricles)

Question 6

heart block with wide QRS

Answer 6

needs urgent admission and pacemaker as soon as possible.

cardiac arrest

Question 7

normal automaticity

Answer 7

sympathetic effect

parasympathetic effect

Question 8

sympathetic automaticity

Answer 8

sympathetic: norepinephrine from sympathetic nerve fires and epinephrine by adrenal glands via beta 1 adrenergic receptors. the slope for depolarisation increases = automatic and increased HR

Question 9

increased automaticity

Answer 9

enhanced normal automaticity (only occurs in pacemaker cells)

• stimulates sympathetic nervous system
• inhibition of parasympathetic
• ATP depletion (hypoexemia, ischaemic)
• digoxin toxicity
• hyopkalaemia

abnormal automaticity
(occurs only within non pacemaker cells) acute ischaemic/reperfusion, congestive HF

Question 10

re-entry

Answer 10

most common mechanism of tachycardia

look up slide

the electrical impulse doesn’t cease at the end of one cardiac cycle and persists and re-excites the heart as part of self propagating mechanism

Question 11

re-entry ….

Answer 11

fast pathway (fast conduction with long refractory prime)

slow pathway (slow conduction, short refractory time)

Question 12

triggered activty

Answer 12

small action potentials that are generated over the normal and have the capacity to trigger another action potential

e.g. drug induced

Question 13

how do we manage arrhythmias?

Answer 13

treat cause
cardio version (defibrillator)
pacemakers
drugs 
ablation

Question 14

anti arrhythmic drugs - what makes them ideal properties?

Answer 14

good for all types of arrhythmia
prevents re-entry
increases refractory period
blocks the effect of catecholamines
reduces excitability
little or no effect on contractility (isotropy)
use deponent block

! in the wrong circumstances, drugs can actually trigger arrhythmias because the therapeutic window can be small

Question 15

four classes of anti arrhythmic drugs

Answer 15

class Ia agents (double quarter pounder)

class Ib agents (mayo, lettuce, pickles)

class Ic (more, fries, please)

look on slide for this.

Question 16

class Ia agents anti arrhythmic drugs.

Answer 16

class Ia agents. block the fast Na+ channels.
used in WPW, ventricular tacky arrhythmias, paroxysmal recurrent AF.

Question 17

class Ib agents

Answer 17

block the Na+
shorten the AP duration

lidocaine
mexiletine
phenytoin

Question 18

class Ic agents

Answer 18

large effect without significantly shifting of the AP.
block Na+ channels in the activated state.

flecanide (pill in the pocket)
moricizine
propafenone

Question 19

class II agents

Answer 19

beta blockers
acts on the sympathetic nervous system
AV node

increases refractoriness

preventing arrhythmias in ischaemia (MI) (scar tisse= re-entry circuit)

Question 20

class III agents

Answer 20

potassium channel blockers

block K+ channels = increases the duration of AP

amiadorone
*can be very toxic (photosensitivity, thyroid) need to test thyroid and liver and X-ray first

need 10mg
cannot be used to fix immediately ? can enhance other treatments. used for chronic tx.

Question 21

class IV channel blockers

Answer 21

verapamil
dilitazem

block the L type ca2+ blocker
directly blocks them (AVN)

used in atrial arrhythmias

Question 22

class V agents

Answer 22

cannot be classified under any of the classes:

digoxin
adenosine
magnesium sulfate

Question 23

digoxin

Answer 23

inhbition of Na+/K+ ATPase in the myocardium
decreases sodium gradient
increases ca2+
increases iontropy (contractility)

toxic drug and can trigger arrhythmias

controls ventricular rate in AF

digitalis effect (ECG changes)
downsloping of ST depression
Salvador Dali sagging appernace
biphasic T wave at the end of the QRS complex

Question 24

toxicity of glycosides

Answer 24

potentially fatal

uncommon

Question 25

adenosine

Answer 25

acts on adenosine receptors. increases K+ efflux, cell hyper polarisation= transient heart block in AV node uses in AV re-entry tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT)

Question 26

magnesium sulfate

Answer 26

used in Torsades de points which is triggered by K+ also indicated in pre-eclampsia