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Cardio > Cardio L8 Drug therapy 1 > Flashcards

Cardio L8 Drug therapy 1 Flashcards

1
Q

Mechanism of Cardiac AP:

A 
Phase 4 (Diastolic period)
Phase 0
Phase 1
Phase 2 
Phase 3
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2
Q

Phase 4 (Diastolic period)
Process
Notes

A
  • Inward K current and Na/K pump current
  • Na, Ca channels closed
  • Inward current in nodal cells gradually depolarizes cells

→Due to Ii and NCK

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3
Q

Phase 0
Process
Notes

A

Na channels open Inward current causes rapid depolarisation to >+40 mV

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4
Q

Phase 1
Process
Notes

A

Initial rapid repolarization
Gives rise to notch, not seen in nodal tissue
Due to I10,Icl

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5
Q

Phase 2
Process
Notes

A

Plateau mainly due to:

  1. Outward K currents
  2. Inward Na, Ca and NCX currents
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6
Q

Phase 3
Process
Notes

A

Repolarization
Increasing K current (s)
Inactivation of inward Na, Ca currents

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7
Q

Electrical activation sequence

A

Abnormalities in electrical behaviour will give rise to abnormalities in contraction. The risk arises from a reduced ability to pump blood.

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8
Q

Normal Sinus Rhythm:

A

ECG (EKG) shows sequence of activation starting in SA node and atria and passing to ventricles via the AV node and his-Purkinje system.
Note the normal ECG characteristics:
1. Regular narrow complex
2. Rate 60-100 bpm
3. Each QRS has a P wave with constant delay
4. T wave ‘normal’

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9
Q

Atrial flutter

A

Atrial re-entry (with conduction block?)

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10
Q

Atrial fibrillation

A

Like flutter but on a finer physical scale

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11
Q

Paroxysmal supraventricular tachycardia

A

Episodic VT from nodal re-entry

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12
Q

Ventricular tachycardia

A

High V rate – possibly atrial driven or re-entrant

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13
Q

Polymorphic ventricular tachycardia

A

Episodic VT from nodal re-entry

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14
Q

Ventricular tachycardia

A

High V rate – possibly atrial driven or re-entrant

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15
Q

Polymorphic ventricular tachycardia

A

VT with unstable ECG

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16
Q

Ventricular fibrillation

A

Fine re-entry and fatal

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17
Q

Causes of arrhythmias:

A

Abnormality in action potential
Abnormality in conduction
Abnormality in excitability

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18
Q

Abnormality in action potential

A
  1. Genetic (channelopathies)
  2. Ischemia
  3. Electrolyte disturbances
  4. Drugs
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19
Q

Abnormality in conduction

A
  1. Anatomy
  2. Ischemia, infarct
  3. Electrolyte disturbances
  4. Secondary to AP and electrical
  5. Drugs
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20
Q

Abnormality in excitability

A
  1. Increased sympathetic drive
  2. Surgery
  3. Drugs
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21
Q

Early after depolarization

A

Prolonged action potential duration

Membrane oscillations

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22
Q

Delayed after-depolarization

A
  1. Abnormal oscillatory Ca release from SR (caused by Ca overload)
  2. Elevated cytosolic Ca causes (late) inward current by channels and Na/Ca exchange
    • Leading to oscillatory depolarization of cell membrane
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23
Q

Re-entry prerequisites:

A
  1. Unidirectional conduction block or inhomogeneous conduction in circuit
  2. The refractory period in healthy tissue is shorter than the time taken for conduction of re-entering AP
  3. The re-entered beat must pass the conduction defect before the next normal AP arrives
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24
Q

What determines refractory period?

A
  1. Action potential Duration
  2. Average Membrane Potential
  3. Recovery time of Sodium Channel (from inactivation)
  4. In nodal tissue with less Na current, recovery of Ca current plays a role.
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25
Q

Mechanism of Action of Antiarrhythmic Drugs:

A

To stop automaticity

To stop re-entry

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26
Q

To stop automaticity function

A
  1. Can increase membrane threshold
  2. Hyperpolarize membrane
  3. Block sympathetic activity
  4. Inhibit sodium entry
  5. Inhibit calcium entry
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27
Q

To stop re-entry function

A
  1. Convert Unidirectional Block to Bidirectional Block

2. Abolish Unidirectional Block

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28
Q

Objectives of antiarrhythmic therapy:

A

Improve Ventricular Function
Prevent progression to VF
May not need to treat PCV –

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29
Q

Improve Ventricular Function

why

A
  • Symptomatic
  • Slowing Ventricular rate → thereby increasing ventricular filling. This should help increase cardiac output.
  • Make contraction more efficient
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30
Q

Prevent progression to VF

A

Prophylactic

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31
Q

May not need to treat PCV –

A

If infrequent

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32
Q

Class Ia: example

A

Quinidine

33
Q

Class Ia: function

A

Prolong AP duration and reduce upstroke

Decrease sodium entry into the cell

34
Q

Class Ia: MOA

A

Bind to inactivated Na channel in a use-dependent manner.

35
Q

Class Ia: process

A

Slow binding and unbinding to and from receptors

→Also slows phase 4 depolarization and suppresses propagation of automaticity.

36
Q

Class Ia: useful in

A

Ventricular arrhythmias

Prevention of paroxysmal recurrent atrial fibrillation (triggered by vagal overactivity).

37
Q

Class Ib:Example

A

Lignocaine

38
Q

Class Ib function

A

Decrease AP duration and reduce upstroke
Suppress automaticity:
1. Prolong refractory period (bind to inactive state)
2. Decrease conduction (especially in ischemic and therefore more depressed tissue)
3. Decrease Na influx

39
Q

Class Ib useful for

A

Treatment (and prevention) during and immediately after myocardial infarction.

40
Q

Class Ib risk

A

A systole

Ventricular tachycardias

41
Q

Class Ic: example

A

Propafenone

42
Q

Class Ic: function

A

Blocks sodium entry
Minimal change in action potential duration
Suppress automaticity
Increase refractory period

43
Q

Class Ic: useful in

A

WPW syndrome and recurrent tachyarrhythmias arising in abnormal conduction system

44
Q

Class Ic: contraindicated in + why

A

Decrease cardiac contractility – hence contraindicated immediately post MI
→ Flecainide may inhibit CPVT via SR release block

45
Q

Class Ii: example

A

Atenolol

46
Q

Class Ii: type II agents are

A

Beta-Blocker

47
Q

Class Ii: action

A

Suppress automaticity (decreased sympathetic rdrive:

  1. Shorten action potential duration
  2. Prolong refractory period
  3. Decrease conduction in SA and AV nodes
  4. Hemodynamic depression especialy if heart failure is present (with some exceptinos)
48
Q

Class Ii: use

A
  • In supraventricular tachycardias

* Improves survival post MI

49
Q

Class III example

A

Amiodarone

50
Q

Class III function

A

Prolong action potential duration (secondary to K channel blockade)
Prolong refractory period

51
Q

Class III characterised

A

Less haemodynamic depressant (but watch out)

52
Q

Class III undesired possible effects

A
  1. Sotalol → is also Beta blocker

2. Bretylium → adrenergic neurone blocker

53
Q

Class III useful for

A
  • Wolff-parkinson-White syndrome

* Ventricular tachycardias and atrial fibrillation

54
Q

Class Iv example

A

Verapamil

55
Q

Class Iv MOA

A

Calcium channel blockers

56
Q

Class Iv function

A

Block AV node (good for supraventricular tachyarrhythmia, bad if AV node already blocked)
May reduce O2 demand and cardiac work

57
Q

Class Iv may affect

A

Ventricular arrhythmias but not very useful for this purpose.

58
Q

Class Iv useful for

A

Can prevent recurrence of paroxysmal supraventricular tachycardia
Reduce ventricular rate in patients with atrial fibrillation

59
Q

Class Iv perferential for

A

Cardiac (verapamil and diltiazem) vs. vascular Ca channels (nifedipine).

60
Q

SA Node drugs

A

Beta-blockers, atropine, digitalis

61
Q

Atrial muscle drugs

A

Quinidine, amiodarone, digitalis, disopyramide, procainamide, flecainide

62
Q

AV node drugs

A

Beta-blockers, verapamil, digitalis

63
Q

Bypass tract drugs

A

Quinidine, disopyramide, amiodarone, flecainide, procainamide, digitalis

64
Q

Ventricle drugs

A

Lignocaine, quinidine, Beta-blockers, amiodarone, disopyramide, amidarone,mexiletine, breylium, sotalol, tocainine

65
Q

Physiological agents

A

Magnesium

Adenosine

66
Q

Magnesium function

A

Reduces calcium entry through the sarcolemma
Plays an important role in the intracellular space as an agent, which binds ATP and is involved in regulating metabolic processes.

67
Q

Magnesium depeleted in

A

Ischemic cells

68
Q

Magnesium valuable in

A

Ventricular arrhythmias in ischemic cells, especially if there is hypomagnesemia

69
Q

Adenosine use for

A

SVT

70
Q

Adenosine enhances

A

K current in atrial tissues

71
Q

Adenosine side effects

A

Transient flushing

Breathlessness

72
Q

Vagal Stimulants example

A

digoxin

73
Q

Vagal Stimulants classified as

A

Class V

74
Q

Vagal Stimulants function

A

Suppress AV conduction

Decrease ventricular rate

75
Q

Vagal Stimulants dont always

A

Stop arrhythmias

76
Q

Vagal Stimulants used in

A

Supraventricular tachyarrhythmias

77
Q

Side effects:

Antiarrhythmic agents

A

may be pro-arrhythmic

78
Q

Antiarrhythmic agents may be pro-arrhythmic

Incidence:

A
  1. Inhomogeneity in conduction and refractoriness
  2. Prolongation of action potential duration (Early after depolarization)
  3. Apparent, due to lack of efficacy
  4. Pre-existing severe cardiomyopathy

Cardio (108 decks)

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