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PY365 AF > Mechanistic approach to treatment of dysrhythmias > Flashcards

Mechanistic approach to treatment of dysrhythmias Flashcards

1
Q

How are bradydysrhythmias treated

A

Need to modify autonomic input
- anticholinergics
- beta blockers
- pacemakers

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2
Q

How are tachydysrhythmias treated

A

Increase automaticity
- decrease rate of depolarisation
- increase resting membrane potential (makes it more negative)
- make action potential threshold less negative
- treated by use of antidysrrhythnmic drugs

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3
Q

How are re-entrant rhythms treated

A
  • increasing refractory period
  • decreasing conduction velocity
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4
Q

How is triggered activity treated

A
  • shorten action potential duration
  • correct conditions of calcium overload
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5
Q

What are the signs of AF

A
  • multiple re-entrant loops
  • 350-600 action potentials per minute
  • irregularly irregular pulse (fast or slow)
  • loss of clear p waves on ECG
  • thrombi
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6
Q

What are the different classes of antiarrhythmic drugs

A
  1. class 1- Na+ channel blockade
  2. Class 2- B-adrenergic receptor blockade
  3. class 3- K+ channel blockade
  4. Class 4- Ca2+ channel antagonists
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7
Q

when are voltage gated sodium channels closed

A

at resting potential

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8
Q

when are voltage gated sodium channels open

A

in response to a nerve impulse, the gate opens and sodium enters the cell

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9
Q

when are voltage gated sodium channels inactivated

A

for a brief period following activation, the channel does not open in response to a new signal

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10
Q

How do Class 1 antiarrhythmic drugs work

A

bind to open or inactivated Na+ channels

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11
Q

What category in class 1 drugs are mainly used to treat cardiac dysrhythmias

A

main drugs used are class 1C

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12
Q

What is the difference between class 1A, 1B, and 1C drugs

A
  • 1A is a moderate Na+ channel block, with prolonged repolarisation
  • 1B is a mild Na+ channel block with shortened repolarisation
  • 1C is a marked Na+ channel block with no change in action potential duration
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13
Q

Explain how an Na+ channel blockade reduces re-entry

A

Decrease Phase 0 upstroke velocity and reduces conduction velocity, which decreases re-entry

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14
Q

What can trigger dysrhythmias

A

stress and emotion can trigger dysrhythmias (MI)

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15
Q

How do class 2 beta blockers decrease automaticity and re-entry

A

Decrease cardiac rate and increase refractory period in AV node
Reduce excitability in the ventricles

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16
Q

When are class 2 beta blockers used

A
  1. to control ventricular rate in AF or atrial flutter
  2. Post MI to reduce effects of adrenaline on damaged myocytes
  3. to treat re-entrant rhythms which use AV node
    - eg. metoprolol, atenolol
17
Q

what is the risk with class 2 beta blockers

A

Possible conduction block or bradycardia

18
Q

Explain how class 3 Potassium channel blockers work

A

prolong the action potential and increase refractory period and therefore decrease re-entrant rhythms and return rhythm to a normal sinus rhythm

19
Q

When are class 3 Potassium channel blockers used

A

Used to treat WPW and both atrial and ventricular fibrillation

20
Q

Give examples of Class 3 potassium channel blockers

A

amiodarone, dronedarone, sotalol

21
Q

What is the risk of using class 3 potassium channel blockers

A

may precipitate Torsades de Pointes

22
Q

Describe the chemical structure of amiodarone

A

-Resembles thyroxine
- CYP3A4 main route for metabolism, metabolite active
- both amiodarone and metabolite have long half lives

23
Q

how is amiodarone excreted

A

hepatic excretion

24
Q

Describe the chemical structure of dronedarone

A
  • No iodine so no thyroid side effects
  • less lipophilic than amiodarone so its half life is shorter and so is the half life of its active metabolite
25
Q

how is dronedarone excreted

A

Metabolised and excreted in liver

26
Q

what is an advantage of using dronedarone compared to amiodarone

A

less interactions than amiodarone

27
Q

describe how class 4 calcium channel antagonists decrease heart rate and re-entry

A
  • decrease automaticity in SA node and increase threshold potential of SA node
  • Slow conduction velocity through AV nodes and increase effective refractory period of AV node
28
Q

When are class 4 calcium channel antagonists used

A

used to regulate ventricular rate in supraventricular (SVT) tachycardias such as AF

29
Q

Give examples of class 4 calcium channel antagonists

A

diltiazem and verapamil

30
Q

what is the risk in the use of class 4 calcium channel antagonists

A

possible conduction block and bradycardia

31
Q

Give examples of class 5 miscellaneous drugs

A
  1. digoxin
  2. adenosine
32
Q

explain how digoxin decreases re-entry

A

increases refractory period in AV node
- stimulates parasympathetic system
- prolongs action potential duration

33
Q

what is the risk of using digoxin

A

possible conduction block or bradycardia

34
Q

How does adenosine have an effect on re-entry

A

targets AV node and increases k+ current and decreases node excitability

35
Q

What is the risk of using adenosine

A

Possible conduction block or bradycardia

PY365 AF (19 decks)

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