Treatment of Dysrhythmias Flashcards
Dysrhythmia
Underlying Physiology
Dysrhythmia (arrhythmia) describes conditions where the co-ordinated sequence of electrical activity in the heart is disrupted
Dysrhythmia
Underlying Physiology
causes
- Changes in the heart cells
- Changes in the conduction of the impulse through the heart
- Combinations of these
classifications of dysrhythmias
- atrial (supracentricular)
- junctional (associated with AV node)
- ventricular
tachycardia and bradycardia
Dysrhythmias (arrhythmias) arise from four broad categories of event:
- Ectopic pacemaker activity
- Delayed after-depolarisations
- Circus re-entry
- Heart block
1a: -Sodium channel blockers
disopyramide
• Ventricular dysrhythmias, prevention of recurrent atrial
fibrillation triggered by vagal over activity.
1b: -Sodium channel blockers
lignocaine
- Treatment and prevention of ventricular tachycardia and fibrillation during and immediately after MI.
1c: -Sodium channel blockers,
flecainide
- Suppresses ventricular ectopic beats. Prevents paroxysmal atrial fibrillation and recurrent tachycardias associated with abnormal conducting pathways.
2: -b-adrenoreceptor blockers,
sotalol
3: -Potassium channel block,
amiodarone
4: -Calcium channel blockers
verapamil
Unclassified:
adenosine and digoxin
Class 1-Sodium Channel Blockers
- Inhibit action potential propagation and they reduce the rate of cardiac depolarisation during phase 0.
- Subdivision to class a, b and c is based on the properties of the drugs in binding to sodium channels in their various states such as open, refractory and resting.
- Depolarisation switches channels from resting to open states- known as activation. Maintained depolarisation causes the channels to move to a refractory state - known as inactivation.
- Cardiac myocytes must repolarise to reset the sodium channels back to resting state.
- These drugs bind to the open and refractory states of the channels and so are viewed as use-dependent i.e. work more effectively if there is high activity and so are more effective against abnormal high frequency activity and not so much against normal beating rates.
Class 2 drugs- b blockers.
• Block b-1 receptors slow the heart and decrease cardiac
output.
• b-1 receptor activation increases the rate of depolarisation of the pacemaker cells so blocking them decreases this.
• b-1 receptor activation enhances calcium entry in phase 2 of the cardiac action potential so blocking them reduces this.
• b-blockers increase the refractory period of the AV node so prevent recurrent attacks of supraventricular tachycardias.
• Basically increased sympathetic drive and influence tend to promote dysrhythmias and so attenuating their influence will slow the heart and decrease their occurrence.
Class 2 drugs- b blockers. uses
• Sotalol, bisoprolol, atenolol. Clinical uses are to reduce mortality following MI and to prevent recurrence of tachycardias provoked by increased sympathetic activity.
Class 3 drugs – potassium channel blockers.
Amiodarone - prolongs the cardiac action potential by prolonging the refractory period.
• Amiodarone
tachycardia associated with the Wolff- Parkinson-White syndrome. Wolff-Parkinson-White syndrome is a heart condition featuring episodes of an abnormally fast heart rate. Episodes can last for seconds, minutes, hours or (in rare cases) days. They may occur regularly, once or twice a week, or just once in a while
is also effective in many other supreventricular and ventricular tachyarrhythmias.
Sotalol
combines class 3 with class 2 actions. It is used in supraventricular dysrhythmias and suppresses ventricular ectopic beats and short runs of ventricular tachycardia.
Class 4 drugs – Calcium Channel
Blockers.
• Verapamil and diltiazem.
Class 4 drugs – Calcium Channel
Blockers. mechanism
- Blocks cardiac voltage- gated L-type calcium channels.
- Slow conduction through the SA and AV nodes where the conduction of the AP relies on the slow calcium currents.
- They shorten the plateau of the cardiac AP and reduce the force of contraction of the heart.
• Verapamil
Used to prevent recurrence of supraventricular tachycardias
(SVTs)
• And to reduce the ventricular rate in patients with atrial fibrillation provided they do not have Wolff-Parkinson-White syndrome.
• It is ineffective and dangerous in ventricular dysrhythmias. (Diltiazem is similar but has more effect on smooth muscle calcium channels and less bradycardia
Unclassified - Adenosine
- Produced endogenously with effects on breathing, cardiac and smooth muscle, vagal afferent nerves and platelets.
- A1 receptor is responsible for the effect on the AV node.
- These receptors are linked to the same cardiac potassium channels that are activated by ACh. and so it hyperpolarises cardiac conducting tissue and slows the heart rate. It decreases pacemaker activity.
- Used to terminate SVTs.
Unclassified - Digoxin
- Cardiac glycosides are a family of compounds that are derived from the foxglove plant (Digitalis purpurea).
- Increase vagal efferent activity to the heart (by unknown mechansim)
- This parasympathomimetic action of digoxin reduces sinoatrial firing rate (decreases heart rate) and reduces conduction velocity of electrical impulses through the atrioventricular node
- Toxic concentrations disturb sinus rhythm. Inhibition of Na+/K+ pump cause depolarisation – ectopic beats
