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Cardio > Cardio L8 Drug therapy 1 > Flashcards

Cardio L8 Drug therapy 1 Flashcards

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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
Mechanism of Action of Antiarrhythmic Drugs:
To stop automaticity | To stop re-entry
26
To stop automaticity function
1. Can increase membrane threshold 2. Hyperpolarize membrane 3. Block sympathetic activity 4. Inhibit sodium entry 5. Inhibit calcium entry
27
To stop re-entry function
1. Convert Unidirectional Block to Bidirectional Block | 2. Abolish Unidirectional Block
28
Objectives of antiarrhythmic therapy:
Improve Ventricular Function Prevent progression to VF May not need to treat PCV –
29
Improve Ventricular Function why
* Symptomatic * Slowing Ventricular rate → thereby increasing ventricular filling. This should help increase cardiac output. * Make contraction more efficient
30
Prevent progression to VF
Prophylactic
31
May not need to treat PCV –
If infrequent
32
Class Ia: example
Quinidine
33
Class Ia: function
Prolong AP duration and reduce upstroke | Decrease sodium entry into the cell
34
Class Ia: MOA
Bind to inactivated Na channel in a use-dependent manner.
35
Class Ia: process
Slow binding and unbinding to and from receptors | →Also slows phase 4 depolarization and suppresses propagation of automaticity.
36
Class Ia: useful in
Ventricular arrhythmias | Prevention of paroxysmal recurrent atrial fibrillation (triggered by vagal overactivity).
37
Class Ib:Example
Lignocaine
38
Class Ib function
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
Class Ib useful for
Treatment (and prevention) during and immediately after myocardial infarction.
40
Class Ib risk
A systole | Ventricular tachycardias
41
Class Ic: example
Propafenone
42
Class Ic: function
Blocks sodium entry Minimal change in action potential duration Suppress automaticity Increase refractory period
43
Class Ic: useful in
WPW syndrome and recurrent tachyarrhythmias arising in abnormal conduction system
44
Class Ic: contraindicated in + why
Decrease cardiac contractility – hence contraindicated immediately post MI → Flecainide may inhibit CPVT via SR release block
45
Class Ii: example
Atenolol
46
Class Ii: type II agents are
Beta-Blocker
47
Class Ii: action
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
Class Ii: use
* In supraventricular tachycardias | * Improves survival post MI
49
Class III example
Amiodarone
50
Class III function
Prolong action potential duration (secondary to K channel blockade) Prolong refractory period
51
Class III characterised
Less haemodynamic depressant (but watch out)
52
Class III undesired possible effects
1. Sotalol → is also Beta blocker | 2. Bretylium → adrenergic neurone blocker
53
Class III useful for
* Wolff-parkinson-White syndrome | * Ventricular tachycardias and atrial fibrillation
54
Class Iv example
Verapamil
55
Class Iv MOA
Calcium channel blockers
56
Class Iv function
Block AV node (good for supraventricular tachyarrhythmia, bad if AV node already blocked) May reduce O2 demand and cardiac work
57
Class Iv may affect
Ventricular arrhythmias but not very useful for this purpose.
58
Class Iv useful for
Can prevent recurrence of paroxysmal supraventricular tachycardia Reduce ventricular rate in patients with atrial fibrillation
59
Class Iv perferential for
Cardiac (verapamil and diltiazem) vs. vascular Ca channels (nifedipine).
60
SA Node drugs
Beta-blockers, atropine, digitalis
61
Atrial muscle drugs
Quinidine, amiodarone, digitalis, disopyramide, procainamide, flecainide
62
AV node drugs
Beta-blockers, verapamil, digitalis
63
Bypass tract drugs
Quinidine, disopyramide, amiodarone, flecainide, procainamide, digitalis
64
Ventricle drugs
Lignocaine, quinidine, Beta-blockers, amiodarone, disopyramide, amidarone,mexiletine, breylium, sotalol, tocainine
65
Physiological agents
Magnesium | Adenosine
66
Magnesium function
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
Magnesium depeleted in
Ischemic cells
68
Magnesium valuable in
Ventricular arrhythmias in ischemic cells, especially if there is hypomagnesemia
69
Adenosine use for
SVT
70
Adenosine enhances
K current in atrial tissues
71
Adenosine side effects
Transient flushing | Breathlessness
72
Vagal Stimulants example
digoxin
73
Vagal Stimulants classified as
Class V
74
Vagal Stimulants function
Suppress AV conduction | Decrease ventricular rate
75
Vagal Stimulants dont always
Stop arrhythmias
76
Vagal Stimulants used in
Supraventricular tachyarrhythmias
77
Side effects: | Antiarrhythmic agents
may be pro-arrhythmic
78
Antiarrhythmic agents may be pro-arrhythmic | Incidence:
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

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