Pharmacological Treatment of Dysrhythmias Flashcards
(28 cards)
what causes delayed after depolarisation event? what are examples of places with high intracellular calcium levels?
small peak of activity driven by calcium or calcium triggering places where you have high intracellular calcium levels:
- areas of ischaemic damage
- areas with high calcium deposits
what is the vaughan williams system of drugs used to treat dysrhythmias?
1a, b and c-sodium channel blockers all different types depending on what stage they bind to the voltage gated sodium channels and how strong or weak they affect
2- beta adrenoreceptor blockers
3-potassium channel blockers
4-calcium antagonists
What are the 2 drugs unclassified on the VW scale but used to treat dysrhythmias?
- adenosine
- digoxin
what is the mechanism of action of class 1 sodium channel antagonists?
- inhibit action potential propagation and reduce the rate of cardiac depolarisation in phase 1
- change where threshold will be so need a greater than normal voltage to cause depolarisation= decreasing ectopic events
- elongates the action potential
class 1 drugs are use-dependent. what does this mean?
- effectiveness of these drugs will increase as the rate of opening and closing of these voltage gated sodium channels occurs
- more frequent depolarisations= more effective drugs
- hence if you get a faster than normal rate of depolarisation occurring then the effectiveness of these drugs will increase to restore a normal rhythm
what is an example of a 1a drug? what are its clinical uses?
- Disopramide
- ventricular dysrhythmias, prevention of recurrent atrial fibrillation
what is an example of a 1b drug? what are its clinical uses?
- lignocaine
- treatment/prevention of ventricular tachycardia and fibrillation during and immediately after MI
what is an example of a 1c drug? what is its clinical use?
- flecanide
- suppresses ventricular ectopic beats
what are the side effects/dangers of using antidysrhythmic drugs?
-given at wrong concentration they can cause dysrhythmias since they alter conduction pathways
what are the dangers of using class 1 drugs?
- decrease contractility of the heart
- change rate of depolarisation occurring and the amount of calcium taken back into cell decreasing the SV
how do b adrenoreceptors normally function?
- G protein coupled receptor attached to B1/2 receptor
- catecholamine binds stimulating cAMP production and Protein Kinase A will modify calcium channels and alter where we store calcium in cell altering contractility
what is the mechanism of action of class 2 drugs?
- blocking reduces influx of Ca into the cell decreases contractility
- SA and AV node are under innervation by sympathetic nervous system blocking these channels increases refractory period and deals contraction through the AV node
what is an example of a class 2 drug?
Sotalol
what are the clinical uses of class 2 drugs?
- reduce mortality following MI
- prevent recurrence of tachycardias
what is special about the class 2 drug stall?
it also has class 3 drug properties
what is the mechanism of action of class 3 drugs?
act on signal which repolarises our membrane
block K by blocking K channels results in prolonging the QT interval
prolonging QT interval you increase cardiac cells refractory state
what is the clinical use of class 3 drugs?
-preventing or reducing affect of re-entry mechanisms which lead to dysrhythmias
what is the disadvantage of using class 3 drugs?
- prolong the QT interval
- increase the time for calcium fluxing into the cell
- higher intracellular calcium levels can lead to dysrhythmias
what is an example of a class 3 drug? what is it used to treat?
- amiodarone
- wolf parkinson white syndrome
- supraventricular and ventricular tachyarrythmias
what are the two types of calcium antagonist?
- DHP blockers
- rate limiting
what are 2 examples of rate limiting calcium antagonists? what are they used to treat?
- verapamil and diltiazem
- reduce tachycardias and dysrhythmias
What is the mechanism of action of the rate limiting calcium channel antagonists?
- block calcium channels which maintain plateau of ventricular depolarisation, so shorten plateau phase= less Ca influx= lower intracellular Ca= lower force of contraction
- DHP Ca channels in nodal tissue so slow conduction through SA and AV pathways changes speed at which heart is working
what are class 4 drugs used to treat?
- prevent supra ventricular tachycardia
- useful for patients with atrial fibrillation
where are adenosine receptors located? what happens if bound to?
- Av node and on cardiac muscle cells
- cAMP activates protein kinase which phosphorylates channels
