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Block 13 - The Development of Cardiorespiratory Disease > ALS Lecture 13 - The Pharmacology of Rhythm Control DONE > Flashcards

ALS Lecture 13 - The Pharmacology of Rhythm Control DONE Flashcards

1
Q

2 types of heart cells

A

pacemaker, myocyte

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2
Q

Type 1 heart cells, pacemaker (4)

A

depolarise without stimulation, SA node, AV node, conduction tissue

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3
Q

Type 2 heart cells, myocytes (3)

A

fire when stimulated, atria, ventricles

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4
Q

muscle cells in diastole (phase 4) remain at

A

resting membrane potential of -90mv till stimulated

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5
Q

3 properties of cardiac cells

A

automaticity, excitability, refractoriness

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6
Q

automaticity

A

spontaneous depolarisation till threshold potential reached when cell fires (phase 0)

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7
Q

spread of excitation sequence (8 steps)

A
  1. SA node
  2. atria
  3. AV node
  4. bundle of His
  5. bundle branches
  6. Purkinje fibres
  7. endocardium to epicardium
  8. apex to base
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8
Q

label the diagram of the phases of excitation (A)

A

done

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9
Q

phase 0 of cardiac action potential

A

rapid depolarisation, fast Na+ inflow

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10
Q

phase 1 of cardiac action potential

A

initial rapid repolarisation due to Na+ closure, Cl- influx, outflow of K+

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11
Q

phase 2 of cardiac action potential

A

plateau, delayed repolarisation by slow inward Ca+ and outflow of K+

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12
Q

phase 3 of cardiac action potential

A

2nd period of repolarisation, continual K+ outflow and Ca2+ inflow

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13
Q

what class is digoxin?

A

5

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14
Q

what effect does digoxin do? (5)

A

slow HR, reduced AV conduction, increased contraction force, rhythm disturbance, increased ectopic pacemaker

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15
Q

digoxin MOA (4 steps)

A
  1. inhibits Na+K+ATPase pump
  2. increased Na+, decreased K+
  3. Na+/Ca2+ transported gets rid of Na+, bringing in Ca2+
  4. strengthens ventricular contraction so more blood each beat
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16
Q

Vaughan Williams classification, Class 1 agents interfere with

A

sodium channel

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17
Q

Vaughan Williams classification, Class 1a agents

A

lengthen action potential

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18
Q

Vaughan Williams classification, Class 1b agents

A

shorten action potential

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19
Q

Vaughan Williams classification, Class 1c agents

A

no significant effect on action potential

20
Q

Vaughan Williams classification, Class 2 agents inhibit

A

sympathetic nervous system

21
Q

Vaughan Williams classification, Class 2 agents are mostly

A

beta-blockers

22
Q

Vaughan Williams classification, Class 3 agents inhibit

A

potassium channel

23
Q

Vaughan Williams classification, Class 4 agents inhibit (2)

A

calcium channels, AV node

24
Q

Vaughan Williams classification, Class 5 agents work by (2)

A

other, unknown

25
Q

fill in the table of different Vaughan Williams classification drugs (B)

26
Q

look at the diagrams of class 1a - 2 Vaughan Williams classification drugs (C)

27
Q

problems with Vaughan Williams classification drugs (2)

A

some have multiple effects, does not include important anti-arrhythmics

28
Q

fill in the table of Vaughan Williams classification class 5 drugs (D)

29
Q

label the diagram of drugs affecting cardiac action potential (E)

30
Q

3 disadvantages of using drugs in comparison with DC shock

A

may take days, side effects, useful adjunct

31
Q

3 disadvantages of using DC shock in comparison with drugs

A

doesn’t always work, needs GA

32
Q

label the diagram of the heart and the nodes (F)

33
Q

lignocaine MOA (3)

A
  1. sodium channel blocker
  2. raises depolarisation threshold
  3. heart less likely to initiate APs that may cause arrhythmia
34
Q

beta blockers examples (5)

A

bisoprolol, metoprolol, atenolol, carvedilol, nebivolol

35
Q

beta blockers are used in (5)

A

HTN, angina, post MI, arrhythmias, stable heart failure

36
Q

beta blockers MOA (4)

A
  1. beta adrenergic receptor antagonists
  2. inhibits sympathetic stimulation
  3. reduces heart rate, contractility, blood pressure
  4. reduces excitability and arrhythmia
37
Q

beta blockers contraindications (4)

A

asthma, cardiogenic shock, hypotension, AV block

38
Q

beta blocker side effects (5)

A

fatigue, cold extremities, bronchospasm, nightmares, impotence

39
Q

amiodarone MOA (3)

A
  1. K+ channel blocker
  2. extends action potential, delays repolarisation
  3. blocks abnormal signals, arrhythmia
40
Q

amiodarone is first line use for (2)

41
Q

amiodarone is given

42
Q

calcium channel blockers are used in (3)

A

HTN, angina, arrhythmia

43
Q

calcium channel blockers MOA (2)

A
  1. slows movement of calcium

2. reduces HR, Lv contraction, BP

44
Q

calcium channel blockers contraindications (4)

A

pregnancy, cardiogenic shock, bradycardia, heart failure

45
Q

calcium channel blockers side effects (5)

A

low bp, slow HR, drowsiness, flushing, ankle oedema

Block 13 - The Development of Cardiorespiratory Disease (14 decks)

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