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Pharmacology Exam II > Cardio-Antiarrythmics > Flashcards

Cardio-Antiarrythmics Flashcards

1
Q

Class I Anti-arrythmics MOA

A

block fast inward Na channels

in conductive tissues of the heart

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2
Q

Class 1A agents (3)

A

Quinidine
Procainamide
Disopyramide

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3
Q

Class 1B agents (2)

A

Lidocaine

Mexiletine

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4
Q

Class 1C agents (2)

A

Propanefone

Flecainamide

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5
Q

Class I Anti-Arrythmics Uses

A

Ventricular dysrhythmias and/or digitalis or MI-induced arrythmia

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6
Q

Clinical applications of quinidine

A

refractory patients

to convert AFib or FLutter, Prevent recurrences of AFib, treat life-threatining ventricular arrythmias

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7
Q

Procainamide MOA

Physiolgical effects

A

blocks Na channels

blocks K channels

Slowed conduction, automaticity, excitability

Prolongs APD and refractoriness

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8
Q

Procainamide clinical uses

A

Acute treatment of:
reentrant SVT
A-Fib
Atrial flutter associated with WPW Syndrome

Life-threatening ventricular arrythmias

HAS TO BE DELIVERED SLOWLY OVER TIME

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9
Q

Procainamide Adverse Effects

A

Cardiac - arrythmia aggravation, torsades, long QT syndrome

Non-cardiac: SLE-like syndrome, GI nausea and vomiting

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10
Q

Lidocaine Clinical Uses

Pharmacologic implications

A

second choice for life-threatening/sympotmatic arrythmias

Extensive 1st pass metabolism - needs IV use with multiple loading doses and a maintenance infusion

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11
Q

Propafenone MOA

Physiological effects

A

strong inhibitor of Na channels

strong effects on phase 0 depolarization

lengthened QRS and APD, PR as well

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12
Q

Propanefone clinical uses

A

atrial arrythmias, PSVT

ventricular arrythmias in patient with no or minimal heart disease and PRESERVED VENTRICULAR FUNCTION

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13
Q

Flecainide MOA

Clinical use

A

strong Na inhibitor

severely slows ventricular conduction

REFRACTORY life-threatening ectopic ventricular arrythmia

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14
Q

Class II Anti-arrythmics MOA

A

Beta-adrenergic antagonists

Decreased SA node automaticity, Decreased AV node conduction, Decreased Ventricular contractility

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15
Q

Class II Anti-arrythmics Clinical uses

only drugs found to what?

A

supra-ventricular tachycardias d/t increased sympathetic activity

preventing sudden death in patients with prior MI

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16
Q

Class III Agents MOA

A

Potassium (HIGHEST EFFECT), Calcium, and Na channels

Beta-receptor blockers

Main effect = Prolong phase 3 repolarization = increased QT interval

17
Q

Class III Anti-arrythmics (5)

A 
Dronedarone
Amiodarone
Sotalol
Ibutilide
Defetilide
18
Q

Class III Anti-arrythmics Clinical uses

A

wide range of different arrythmias

19
Q

Amiodarone MOA and Effects

A

Blocks K+ channels - prolongs refractoriness and APD

Blocks Na+ channels that are in the inactivated state

Block Ca2+ channels - slows SA node phase 4

Slows conduction through the AV node

20
Q

Amiodarone important clinical use

A

acute termination of V-tac or V-fib

21
Q

Important Clinical Pharmacology Points for Amiodarone

A

highly lipid-soluble (high Vd)

Metabolized to DEA - has even higher anti-arrythmic potency than amiodarone

Wide range of half life

rapidly redistributed out of myocardium until all tissues are saturated

22
Q

Amiodarone adverse effects (only 3-4% of people)

A

High dose IV can decrease cardiac contractility and hypotension

Interstitial pneumonitis (MAJOR SIDE EFFECT)

Hyper or hypothyroidism

23
Q

Class IV Anti-arrythmics

A

Verapamil

Diltiazem

24
Q

Major Cardiovascular sites of Class IV MOA

A

Vascular smooth muscle
Cardiac myocytes
SA and AV nodes

25
Q

Do CCB’s bind to all pores of the L-type Calcium channels?

A

No, only Motif IV

26
Q

Two Classes of CCB’s

A

Dihydropyridine - Nifedipine

Non-dihydropyridine - Verapamil, Diltiazem

27
Q

Dihydropyridinemainly effects?

Non-dihydropyridine mainly effects?

A

vasculature

heart

28
Q

Major Cardiovascular Actions of CCB’s

A

more marked vasodilation in arterial/arteriolar vessels - DECREASES AFTERLOAD

Negative chronotropic/dromotropic - NDHP agents only

29
Q

Main Clinical Applications of CCB’s

A

Systemic HTN
Angina Pectoris
SVT
Post-Infarct protection

30
Q

Verapamil Clinical application

A

Supraventricular tachycarida

Rate control in A-Fib

31
Q

Verapamil Adverse effects (2)

Contraindications

A

Constipation
EXACERBATE CHF

WPW syndrome with A-Fib
V-Tac

32
Q

Miscellaneous Anti-arrythmics

A

Adenosine, digoxin, ….

33
Q

Adenosine MOA

A

activates A1 receptor in SA and AV nodes

increases cAMP-independent, ACh/Adosensitive K channels

Activates A2 receptors in vasculature - potassium channel - vasodilation

34
Q

Adenosine physiological effect

A

SA node hyperpolarization

Decreased firing rate

Shortened AP duration of atrial cells

Depression of AV Conduction

35
Q

Adenosine clinical applications

Clinical pharmacology

A

Conversion of paroxysmal SVT caused by re-entry

Must use IV Bolus to a central vein

10-15 second half-life

36
Q

Sinus tachycardia, PSVT -treatment

A

vagal stimulation through carotid sinus massage or valsalva maneuver

Pharmacology Exam II (5 decks)

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