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Pharmacology > L6: Antiarhythmics > Flashcards

L6: Antiarhythmics Flashcards

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1
Q

What is the depolarizarion phase of nodal tissue?

A

Phase 4

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2
Q

What is the depolarization phase of atrio-ventricular tissue (NON-nodal)?

A

Phase 0

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3
Q

In non-nodal tissue what channel is responsible for:
1. Phase 4
2. Phase 0
3. Phase 1
4. Phase 2
5. Phase 3

A
  1. -
  2. Na
  3. Na
  4. Ca
  5. K
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4
Q

In non-nodal tissue what does each phase represent?
1. Phase 4
2. Phase 0
3. Phase 1
4. Phase 2
5. Phase 3

A
  1. Rest
  2. Depolarization
  3. AP firing
  4. Early repol plateau
  5. Late repol
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5
Q

In nodal cells, what does each phase represent?
1. Phase 4
2. Phase 0
3. Phase 1
4. Phase 2
5. Phase 3

A
  1. Rest
  2. Depol
  3. NONE
  4. NONE
  5. Repolarization
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6
Q

What channel is responsible for each phase in Nodal cells?
1. Phase 4
2. Phase 0
3. Phase 1
4. Phase 2
5. Phase 3

A
  1. Funny channel
  2. Ca channel
  3. NONE
  4. NONE
  5. K channel
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7
Q

What are the three causes of arrythmias?

A
  1. Failure of impulse initiation
  2. Failure of impulse propagation
  3. Enhanced automaticity
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8
Q

What is the result of failure of impulse initiation?

A

Slow HR because AP is not initiated in the SA node

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9
Q

What is the result of failure of impulse propagation from atria to ventricles?

A

Heart block bc AP isnt making it through the AV node

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10
Q

What are three mechanisms of enhanced automaticity?

A

A. Triggered automaticity
B. And reentry
C. Rapid HRs

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11
Q

What is anatomical reentry?

A

A collection of dead cells that the AP has to physically go around.

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12
Q

What is functional reentry?

A

Electrical impulses have to go around cells that dont work due to drug toxicity or mutation in a channel.

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13
Q

In a perfect world, what would a Sodium channel blocker do?

A

Slow phase 0 and slow impulse of the conduction veloicity while also increasing the threshold for firing the AP

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14
Q

In a perfect world, what does a potassium channel blockade do?

A

Increase AP duration and increase refractoriness (longer repol)

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15
Q

In a perfect world, what would a CCB do to the heart rhythm?

A

Inhibit excitability of nodal tissues and inhibit early repol of AV tissues (longer Depol)

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16
Q

What antiarrhythmic drugs are class Ia?

A

Quinidine
Procainamide

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17
Q

What antiarrhythmic drugs are class Ib?

A

Lidocaine and mexiletine

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18
Q

What antiarrhythmic drugs are class Ic?

A

Flecainide
Propafenone

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19
Q

What type of channel do class 1 drugs block?

A

Sodium channels

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20
Q

What drugs are class II?

A
  • Propranolol
  • Acebutolol
  • Esmolol
  • Metroprolol
  • Atenonol
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21
Q

What type of drug are class II antiarrythymic?

A

Beta blockers

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22
Q

What drugs are Class III antiarryhtmics?

A
  • Amiodarone
  • Dronedarone
  • Ibutilide
  • Dofetilide
  • D
  • I sotalol
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23
Q

What type of antiarrythmics are class III drugs?

A

Potassium channel blockers

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24
Q

What antiarrythmias are class IV?

A

Verapimil
Diltiazem

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25
What type of drug are class IV antiarrythmics?
Calcium channel blockers
26
What is the MOA of quinidine?
Binds to open and inactivated NA channels. Decreases reentrant arrythmias by decreasing conduction velocity and increasing action potential duration and refraction.
27
What are the theraputic uses of quinidine?
* Afib * Aflutter * Malaria
28
Side effects of Quinidine:
* VT * Torsades * Cinchonism
29
What is the MOA of procainamide?
Binds to open and inactivated NA channels and blocks K+ channnels tp prolong phase 3 repol.
30
What are the theraputic uses for procainamide?
Ventircular and atrial tachyarrythmias
31
What are the theraputic uses for procainamide?
Ventircular and atrial tachyarrythmias
32
What are the side effects of procainamide?
Lupus-like symptoms and torsades
33
What is the MAO of lidocaine?
Rapidly associates and dissociates from NA channe;s and shortens repolarization and AP duration to suppress abnormal automaticity arrythmias.
33
What is the MAO of lidocaine?
Rapidly associates and dissociates from NA channe;s and shortens repolarization and AP duration to suppress abnormal automaticity arrythmias.
34
What are the theraputic uses of lidocaine?
Ventricular tachycardia, Vfib
35
What are the side effects of lidocaine?
Agitation, confusion, seizures and arrythmias
36
What is the MOA for mexiletine?
Rapidly dissociates from NA channe;s and shortens phase 3 repol by decreasing action potential duration and supresses abnormal automaticity and arrythmias
37
What are the theraputic uses for mexiletine?
VT
38
What are the side effects of mexiletine?
Tremors and GI upset
39
What is the MOA of Flecainide?
Slowly associates and disscociates from resting NA channels and supresses the phase 0 upstroke to slow conduction.
40
What are the theraputic uses of flecainide?
* Afib * Aflutter * VT
41
What class of drugs do you absoluteley not give to pts with heart disease?
1C
42
What are the side effects of Flecainide?
Blurred vison, prolonged PR, QRS and QT and increased mortality in pts with MI
43
What is the MOA of propafenone?
Slowly associates and dissociates from resting Na channels to supress phase 0 upstroke to slow conduction
44
What are the clinical uses for propafenone?
AFib and Aflutter
45
What is the MOA of Class II antiarrythmiucs?
Decreased Phase 4 depolarization to prolong AV conduction
46
What is the MOA of Class II antiarrythmiucs?
Decreased Phase 4 depolarization to prolong AV conduction
47
What are the theraputic uses of class II antiarrythmics?
Afib Aflutter SVT
48
What are the side effects of Class II antriarrythmics?
* ED * AFlutter * Fatigue
49
What is the MOA of class III antiarrythmics?
K channel blocker similar to thyroid hormone that increases AP duration and refraction
50
What drug is consididered a dirty drug and why?
Amidarone because it blocks Na, K, Ca and alpha and beta receptors
51
What are the theraputic uses for class III antiarrythmics?
* Afib * Aflutter * VT and VF
52
What are the side effects of amiodarone?
* Hyper/hypothyroidism * Interstitial pulmonary fibrosis
53
What is the side effect of Dronedarone?
Increased mortality in pts with HF
54
What is the MOA of d,l Sotalol?
K+ channel blocker, NS BB that increases the effective refractory period.
55
Theraputic uses of d,l, Sotalol
Afib and ventricular arrythmias
56
What are the side effects of d,l Sotalol?
Torsades and increased mortality in HF pts
57
What antiarrythmic requires physicians to be extra trained to use it?
Dofetilide
58
What antiarrythmic requires physicians to be extra trained to use it?
Dofetilide
59
What is the MOA of class IV antiarrythmics?
Binds to open votage gated Ca channels to decrease nodal tissue exciteability and increase refraction
60
Theraputic uses of class IV antiarrythmics:
Afib Aflutter PSVT
61
What are the side effects of class IV antiarrythmics?
Negative inotropic Hypotension Arrythmia
62
What is the MOA of adenosine?
Adenosine receptor agonist activates potassium current to hyperpolarize nodal tissue and depress excitability
63
Clinical use of adenosine?
Abolishing and diagnosing SVT

Pharmacology (8 decks)

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