Pharmacological Treatment of Dysrhythmias Flashcards

1
Q

what causes delayed after depolarisation event? what are examples of places with high intracellular calcium levels?

A

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
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2
Q

what is the vaughan williams system of drugs used to treat dysrhythmias?

A

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

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3
Q

What are the 2 drugs unclassified on the VW scale but used to treat dysrhythmias?

A
  • adenosine

- digoxin

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4
Q

what is the mechanism of action of class 1 sodium channel antagonists?

A
  • 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
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5
Q

class 1 drugs are use-dependent. what does this mean?

A
  • 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
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6
Q

what is an example of a 1a drug? what are its clinical uses?

A
  • Disopramide

- ventricular dysrhythmias, prevention of recurrent atrial fibrillation

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7
Q

what is an example of a 1b drug? what are its clinical uses?

A
  • lignocaine

- treatment/prevention of ventricular tachycardia and fibrillation during and immediately after MI

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8
Q

what is an example of a 1c drug? what is its clinical use?

A
  • flecanide

- suppresses ventricular ectopic beats

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9
Q

what are the side effects/dangers of using antidysrhythmic drugs?

A

-given at wrong concentration they can cause dysrhythmias since they alter conduction pathways

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10
Q

what are the dangers of using class 1 drugs?

A
  • decrease contractility of the heart

- change rate of depolarisation occurring and the amount of calcium taken back into cell decreasing the SV

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11
Q

how do b adrenoreceptors normally function?

A
  • 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
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12
Q

what is the mechanism of action of class 2 drugs?

A
  • 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
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13
Q

what is an example of a class 2 drug?

A

Sotalol

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14
Q

what are the clinical uses of class 2 drugs?

A
  • reduce mortality following MI

- prevent recurrence of tachycardias

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15
Q

what is special about the class 2 drug stall?

A

it also has class 3 drug properties

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16
Q

what is the mechanism of action of class 3 drugs?

A

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

17
Q

what is the clinical use of class 3 drugs?

A

-preventing or reducing affect of re-entry mechanisms which lead to dysrhythmias

18
Q

what is the disadvantage of using class 3 drugs?

A
  • prolong the QT interval
  • increase the time for calcium fluxing into the cell
  • higher intracellular calcium levels can lead to dysrhythmias
19
Q

what is an example of a class 3 drug? what is it used to treat?

A
  • amiodarone
  • wolf parkinson white syndrome
  • supraventricular and ventricular tachyarrythmias
20
Q

what are the two types of calcium antagonist?

A
  • DHP blockers

- rate limiting

21
Q

what are 2 examples of rate limiting calcium antagonists? what are they used to treat?

A
  • verapamil and diltiazem

- reduce tachycardias and dysrhythmias

22
Q

What is the mechanism of action of the rate limiting calcium channel antagonists?

A
  • 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
23
Q

what are class 4 drugs used to treat?

A
  • prevent supra ventricular tachycardia

- useful for patients with atrial fibrillation

24
Q

where are adenosine receptors located? what happens if bound to?

A
  • Av node and on cardiac muscle cells

- cAMP activates protein kinase which phosphorylates channels

25
Q

what happens if adenosine binds to a1 receptors on AV node?

A

hyper polarise conducting tissue slowing HR decreasing pacemaker activity

26
Q

what is adenosine used to treat?

A

used to terminate supraventricular tachycardias

27
Q

what are the two mechanisms of action of digoxin?

A
  • increase vagus activity slowing heart rate down

- changes what happens with calcium storage

28
Q

what is there disadvantage of using digoxin?

A

inhibits NaK pump can cause ectopic beats due to chucking out of Na and Ca in