Dysarrthymia Treatment Flashcards
What causes the repolarisation of cardiac muscle?
Combination of Calcium being pumped back and activation of K chennels
main cause of long QT syndrome
(remember QT is contraction of the heart, complete refilling before next contraction)
Channelopathy (HER) channel causes sudden death
treatment of long QT syndrome
beta blockers
difference in SA node depolarisation vs. other cardiac depolarisation
SA: depolarisation driven by Ca channels (not Na), it is slower
don’t have rapid inactivation or the plateau phase
Electrical discharge of the SAN is from what 3 things
- decrease in K outflow
- ‘funny’ Na current
- slow inward Ca current
3 classifications of the site of origins of the dysarhthmias
atrial (supraventricular)
junctional (AV nodal)
ventricular
4 main categories of dysrhythmias
- ectoptic pacemaker activity: when have rhythm in a different part to the SAN. Firing of electrical signal to the one you should be getting.
- 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
- Circus re-entry: failure of impulse travelling down conduction pathways, meeting itself and dying out. Keeps circulating and making conduction wildly increase.
- Heart block: atria and ventricles beat at different rhythms (have had a falling out)
Why would we want to block sodium channels for anti-dysrhythmics
Na channels drive the fast depolarisations during phase 0. Can restore normal function by blocking these channels
Action of sodium channel blockers
bind to the open and refractor states of the channels so are USE dependent
clinical uses of class 1a (and example)
for ventricular dysrhythmias, prevent recurrent AF triggered by vagal-overactivity eg. disopyramide
clinical uses of class 1b (and example)
treat and prevent ventricular tachycardia and fibrillation during and immediately after MI eg. lignocaine
clinical uses of class 1c (and example)
suppresses ventricular ectopic beats. Prevents paroxysmal AF and recurrent tachycardias associated with abnormal conducting pathways
eg. flecainide
Action of beta blockers
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)
Clinical uses of class 2 (3 examples)
reduce mortality following MI and to prevent recurrent tachycardias provoked by increased sympathetic activity
eg. atenolol, bisoprolol, sotalol
Action of class 3 drugs
Potassium channels blockers
prolongs the cardiac action potential by prolonging the refractory period (phase 3 of ventricular AP).
Clinical uses of class 3 and example
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.
What is Wolff-Parkinson-White Syndrome?
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.
action of class 4
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
clinical uses of class 4 (examples 2)
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)
Adenosine production is _______
Where does it take effect in the body?
produced endogenously
effects on breathing, cardiac and smooth muscle, vagal afferent nerves and platelets
Why is adenosine used to treat dysrrythmias
UNCLASSIFIED
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
Why is digoxin used to treat dysrythmias
UNCLASSIFIED
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
What is the risk with treating with digoxin
Toxic concentrations disturb sinus rhythm.
Inhibition of Na/K pump cause depolarisation and cause ectopic beats
