Pharm 24: Heart rhythm Flashcards

1
Q

Antiarrhythmic classes

A

I: Na+ block
II: β adrenergic block
III: K+ block
IV: Ca+ channel blockers

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2
Q

Na+ channel blockers MOA

A

decrease automaticity in SA nodal cells by shifting the threshold to more positive potentials and decreasing the slope of phase 4 depolarization

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3
Q

Na+ blockers and defib

A

Higher voltages are needed

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4
Q

NA+ blockers action on ventricular myocites

A

Decrease Phase 0 velocity, decrease automaticity

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5
Q

Class 1A effects

A

Moderate Na+ Block (phase 0)
Prolonged repolarization

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6
Q

Class 1B effects

A

Mild Na+ Block (phase 0)
Shortned repolarization

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7
Q

Class 1C effects

A

Marked Na+ Block (phase 0)
No change in repolarization

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8
Q

Quinidine class /MOA

A

1A

Also anticholinergic by blocking K+ after M2 stimulation.

Can increase AV conduction speed

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9
Q

Qunidine metabolism

A

P450 (bc of this bad to give w/ digoxin)

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10
Q

Procainamide Class/MOA and uses

A

1A

Used for rentry tachycardia

No anticholinergic effects

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11
Q

Chronic procainimide therapy leads to

A

Lupus like syndrome

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12
Q

Procainimide kinetics

A

Acetylated to N-Acetyl-procainimide (NAPA)

This is a class III for some reason

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13
Q

Disopyramide MOA/class and use

A

1A Na+

Used for VTACH

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14
Q

Lidocaine MOA use and class

A

1B

Bind to open and closed channels

Use for Vtach

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15
Q

What class exhibits use dependent block

A

1B

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16
Q

Lidocaine side effects

A

NOT torsades

CNS effects mostly

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17
Q

Mexilitine MOA and use

A

1B

Basically Oral Lidocaine

used as adjunct (usually w/ amio)

18
Q

Phentoyn use and MOA

A

Mostly antiepileptic but also some 1B

Sometimes used for congenital long QT in kids

19
Q

Class 1C names

A

Flecainide (main)
Ecainide
Moricizine
Propafenone

20
Q

Flecinide class/MOA and use

A

1C

Afib with normal heart

21
Q

β Blocker generations (effects

A

1: Nonselective β antagonist
2: Selective for β1 at low dose
3: β1 and also vasodilation

22
Q

β Blocker generations (names)

A

1) Propanalol
2) Atenolol, Metoprolol, Acebutolol, Bisprolol
3) Labetalol and carvedilol

23
Q

Pindolol MOA and uses

A

β1 and β2 partial agonist

use in Hypertensive bradycardia

24
Q

Nevibolol MOA

A

β1 blocker and also NO production for vasodilation

25
Labetalol/ Carvedilol MOA
β1 and also α-adrenegic antagonist for vasodilation
26
Class II effects on action potential
Decrease phase 4 depolarization
27
Class III effects on action potential
Prolonged repolarization
28
Reverse use dependency (what is it and what drugs)
Action potential prolongation most pronounced at slow rates Ibultide, Dofetilide and Sotalol (*NOT AMIO*)
29
Ibultilide class and MOA and use
Class III Prolongs repol Used to terminate Atrial rhythms
30
Deofetilide MOA, use and class
Class III Oral agent Used for atrial shit
31
Sotalol class, MOA and use
Mixed II/III Non selective β block and also K+ block
32
Amiodarone class and MOA
Mostly III but it does what it wants Mechanism is lipid membrane alterations Lengthens refractory period Use dependent class I
33
Amio Adverse effects
Pneumonitis w/ fibrosis Thyroid problems (hyper or hypo ) Negative inotrope when chornic Neuro shit Corneal deposits Liver shit
34
Ca2+ blockers work preferentially at
SA and AV node
35
Verapamil use
HTN and printzmetal angina
36
Verapamil + _____ = kill
Beta blockers Killing happens via heart failure
37
Adenosine MOA
P1 receptor -> G-protein K+ chanell opens —> inhibition of SA and AV conduction Also inhibits Ca2+ channel potentiation by cAMP
38
Adenosinne MOA
Boronchoconstriction in asthma
39
Ranolazine MOA and use
Stable angina
40
Ivabradine MOA and use
Ivabradine inhibits the *If* current responsible for phase 4 depolarization in SA nodal cells, slowing the heart, decreasing oxygen demant
41
Reverse use dependency seen in _______
Class III antiarrhythmics