Dysarrthymia Treatment

Question 1

What causes the repolarisation of cardiac muscle?

Answer 1

Combination of Calcium being pumped back and activation of K chennels

Question 2

main cause of long QT syndrome

Answer 2

(remember QT is contraction of the heart, complete refilling before next contraction)
Channelopathy (HER) channel causes sudden death

Question 3

treatment of long QT syndrome

Answer 3

beta blockers

Question 4

difference in SA node depolarisation vs. other cardiac depolarisation

Answer 4

SA: depolarisation driven by Ca channels (not Na), it is slower

don’t have rapid inactivation or the plateau phase

Question 5

Electrical discharge of the SAN is from what 3 things

Answer 5

1. decrease in K outflow
2. ‘funny’ Na current
3. slow inward Ca current

Question 6

3 classifications of the site of origins of the dysarhthmias

Answer 6

atrial (supraventricular)
junctional (AV nodal)
ventricular

Question 7

4 main categories of dysrhythmias

Answer 7

1. ectoptic pacemaker activity: when have rhythm in a different part to the SAN. Firing of electrical signal to the one you should be getting.
2. Delayed after depolarisations: when Ca fails to be pumped back out of cell (after contraction) via Na/Ca exchanger -> get APs when should be in repolarisation
3. Circus re-entry: failure of impulse travelling down conduction pathways, meeting itself and dying out. Keeps circulating and making conduction wildly increase.
4. Heart block: atria and ventricles beat at different rhythms (have had a falling out)

Question 8

Why would we want to block sodium channels for anti-dysrhythmics

Answer 8

Na channels drive the fast depolarisations during phase 0. Can restore normal function by blocking these channels

Question 9

Action of sodium channel blockers

Answer 9

bind to the open and refractor states of the channels so are USE dependent

Question 10

clinical uses of class 1a (and example)

Answer 10

for ventricular dysrhythmias, prevent recurrent AF triggered by vagal-overactivity eg. disopyramide

Question 11

clinical uses of class 1b (and example)

Answer 11

treat and prevent ventricular tachycardia and fibrillation during and immediately after MI eg. lignocaine

Question 12

clinical uses of class 1c (and example)

Answer 12

suppresses ventricular ectopic beats. Prevents paroxysmal AF and recurrent tachycardias associated with abnormal conducting pathways
eg. flecainide

Question 13

Action of beta blockers

Answer 13

B1 Rs blocked: this decreases rate of depolarisation, reduces calcium entry in phase 2 of cardiac AP.

= slow the heart and decrease cardiac output.

they also increase the refractory period of AV node (prevent recurrent supraventricular tachycardias)

Question 14

Clinical uses of class 2 (3 examples)

Answer 14

reduce mortality following MI and to prevent recurrent tachycardias provoked by increased sympathetic activity

eg. atenolol, bisoprolol, sotalol

Question 15

Action of class 3 drugs

Answer 15

Potassium channels blockers

prolongs the cardiac action potential by prolonging the refractory period (phase 3 of ventricular AP).

Question 16

Clinical uses of class 3 and example

Answer 16

amiodarone

• treats tachycardia associated with Wolff-Parkinson-White syndrome.
• also effective in other supraventricular tachycardias and ventricular tachyarrthythmias

Sotalol combines class 3 with class 2. Used in supraventricular dysrhythmias and suppresses ventricular ectopic bears and short runs of ventricular tachy.

Question 17

What is Wolff-Parkinson-White Syndrome?

Answer 17

Normally: nodal tissue acts as a filter
In AF: crazy electrical signals, don’t want this all to go to the ventricles (life threatening). Nodal tissue will filter some of this.

In WPW: there is alternative conduction pathway, can go via both ways.
Presents: recurrent episodes of abnormally fast HR.
Combo of WPW and AF can be life-threatening.

Question 18

action of class 4

Answer 18

Calcium Channel Blockers

blocks cardiac voltage-gated L-type calcium channels.
slow conduction through SA and AV nodes where conduction of AP relies on the slow Ca currents

Shorten the plateau of cardiac AP and reduce force of contraction on heart

Question 19

clinical uses of class 4 (examples 2)

Answer 19

Verapamil**
used to prevent recurrence of SVTs.
used to reduce ventricular rate in patients with AF (as long as don’t have WPW)
INEFFECTIVE AND DANGEROUS in ventricular dysrhythmias

Diltiazem (similar but more effect on smooth muscle calcium channels and less bradycardia)

Question 20

Adenosine production is _______

Where does it take effect in the body?

Answer 20

produced endogenously

effects on breathing, cardiac and smooth muscle, vagal afferent nerves and platelets

Question 21

Why is adenosine used to treat dysrrythmias

UNCLASSIFIED

Answer 21

A1 R has an effect on AV node.
These Rs are linked to same cardiac K channels activated by ACh.

So it hyperpolarises cardiac conducting tissue and slows heart rate. (Decreases pacemaker activity)

Used to terminate SVTs

Question 22

Why is digoxin used to treat dysrythmias

UNCLASSIFIED

Answer 22

they increase vagal efferent activity to the heart

this parasymp action on heart reduces SA firing rate and reduces conduction velocity of electrical impulses through the AV node

Question 23

What is the risk with treating with digoxin

Answer 23

Toxic concentrations disturb sinus rhythm.

Inhibition of Na/K pump cause depolarisation and cause ectopic beats