Anti-arrythmics Flashcards

1
Q

What are the possible underlying causes of arrhythmias?

A

Disorders of impulse formation:
Automaticity
Triggered activity

Disorder on impulse conduction:
reentry

Combination of both

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2
Q

What is automacity?

A

Ability of the cardiac cell to initiate an impulse without need a prior stimulation:
–> For sinus node and other focal pacemaker cells this is normal but can be enhanced and lead to an accelerated rate.

Cells that do not normally initiate an impulse can do so:
–> Multiple possible mechanisms (changes in K channels, increased Ca release from SR activating different Ca or N channels, etc)

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3
Q

What is triggered activity?

A

Impulse initiation in cardiac fibres caused by depolarizing oscillations within in membrane voltages (after depolarization). They are the consequence of preceeding action potential(s):

Early afterdepolarization (EAD)
Delayed afterdepolarization (DAD)

When large enough to reach threshold, will trigger an action potential.

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4
Q

What are the classes in Vaughn-Williams classification?

A

Class 1: Na channel blockers
- Membrane stabilising. Slow the rate of depolarization and may inhibit the arrhythmia by decreasing the cells responsiveness to excitation

Class 2: Cathecholamine blockade (b-blockers)

Class 3: K channel blockers
- Increasing in refractory period

Class 4: Calcium channel blockade
-Depress inward Ca current, prolonging conduction and refractoriness.
Some block potassium channels

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5
Q

How many subgroups are there for Class 1?

A
Class 1A - quinidine, procainamide
Class 1B - lidocaine, (being replaced by amiodarone ie. class 3)
Class 1C - propafanone, fleicainide
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6
Q

What is procainamide?

A

Class 1A drug

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7
Q

How does procainamide work?

A

Prolongs the action potential duration and refractoriness of atrial and ventricular tissue.

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8
Q

What is procainamide used for?

A

Used in both supraventricular and ventricular arrhythmias.

–> Atrial fibrillation in WPW

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9
Q

What is a side effect of procainamide?

A

Prolonged QT/Torsades de pointes
Hemolytic anemia, thrombocytoepnia, neutropenia
Hypotension
SLE like syndrome

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10
Q

How does lidocaine work?

A

Increases the stimulation threshold and leads to suppression of automaticity (esp in Purkinje fibres)

Shortens the action potential duration and also can shorten QT in diseased tissues

  • -> Used commonly for VF in ACS
  • -> NOT GOOD FOR SUPRAVENTRICULAR
  • -> good for post-MIs
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11
Q

What are side effects of lidocaine?

A

Hypotension, bradycardia
Neurological (confusion, headache, tremor, somnolence)
Seizure

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12
Q

What is Flecainide/Propafenone used in?

A

Used mainly for Atrial fibrillation. Also may have a use in PVCs.

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13
Q

What additional drud needs to be coadminitered with Flecainide/Propafenone?

A

Needs to be used with a B-blocker. (1:1 atrial flutter causing increased ventricular rate)

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14
Q

What are some risks using class 1C drugs?

A

Increases mortality in post MI patients, therefore not used in patients with ischemic heart disease. Also not used if any structural heart disease.

Increased risk of ventricular arrhythmias in chronic atrial fibrillation

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15
Q

What are class 2 drugs work?

A

Beta-blockers:

1) Blocks the sympathomimetic amine effects on Ifunny currents (phase 4) of nodal tissues.
SA node: slowing HR
AV node: prolonging refractory period.
Terminating SVT (re-entry)
Decrease ventricular response
2) Attenuation of sympathetic electrophysiological consequences
Shortening of action potential duration
Augmenting ventricular conduction
Increasing vent. Automaticity
Decreasing VF thresholds
Reversal of anti-arrhytmic drugs
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16
Q

What are Class 3 drugs?

A

Potassium channel blockers

17
Q

How do class 3 drugs work?

A

Action on phase 3 of AP waveform

–> Delays repolarization, lengthens APD

18
Q

What is the drug of choice for ventricular arrythmias?

A

Amiodarone

Also used for: For A.fib/fl:
Ventricular rate control
Conversion to SR
Maintaining SR
**

19
Q

What is the first line antiarrythmic agent in cardiac arrest?

A

amiodarone

20
Q

What are the effects of amiodarone?

A

Multiple actions

K, Na, Ca channels, B-blocker, CCB

21
Q

What kind of monitoring should be done for amiodarone?

A

Pulmonary toxicity/infiltrates/hypersensitivity
–> Q3-6 month PFTs

Thyroid
–> Hypo and hyperthyrois
TSH at baseline and q 3-6 months

Liver cirrhosis is rare
–> Follow liver enzymes, stop if > 3x normal

Ocular
–> Microdeposits common and not required to discontinue

Optic neuritis/atrophy leading to vision loss

Blue skin pigmentation

Prolonged QT

22
Q

What are class 3 drugs?

A

amiodarone and sotalol

23
Q

What are effects of sotalol?

A

K channel and B-blocker effects

24
Q

What is solatol used for?

A

Also used in Atrial fib and Ventricular tachycardias

25
Q

T or F: sotalol has less side effects

A

T but…

Increased risk of torsades de pointes due to increased effect on QT (need to check QT on ECG 1 week after initiation)
Caution in EF< 40%

26
Q

How does Adenosine work?

A

electrophysiological effects like ACh
decreases sinus rate; decreases A-V conduction
useful for supraventricular tachycardias

27
Q

What is an example of cardiac glycoside?

A

Digoxin

28
Q

How does digoxin work?

A

Direct action:
blocks Na/K atpase –> Increased intracellular Na –> decreased activity of Na/Ca exchanger (Na in for Ca out) –> increased intracellular Ca. More intracellular Ca for future muscle contractions.
- Increased contractility and excitability

Indirect action: increased vagal tone
Decreased impulse generation and propagation in nodal tissue

29
Q

What is digoxin’s use?

A

occasionally used for atrial fibrillation

associated increases in contractility (CHF)

30
Q

T or F: digoxin toxicity is common

A

T

31
Q

What side effect may digoxin cause?

A

heart blocks, arrhythmias, enhancement of effects seen
with therapeutic dose and generation of
early and delayed afterdepolarizations