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Pharm > Cardio III > Flashcards

Cardio III Flashcards

1
Q

What are the class IV types of drugs? MAO?

A

Verapamil
Diltiazem

Ca channel antagonists that affects nodal phase 0 depolarization

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2
Q

What are the major effects of class IV drugs?

A

Depressed SA nodal automaticity and AV nodal conduction

Decreased ventricular contractility

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3
Q

The metabolism of quinidine is inhibited by what other drug interaction? Induced by?

A

Inhibited by cimetidine

Stimulated by phenytoin, phenobarbital, rifampicin

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4
Q

What type of drug is phenytoin?

A

Class Ib antiarrhythmic

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5
Q

What type of drug is Mexiletin?

A

Class Ib antiarrhythmic

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6
Q

What type of drug is tocainide?

A

Class Ib antiarrhythmic

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7
Q

Why is it that blockage of Ca channels by class IV agents results in slowed pacemaker?

A

Because nodal tissues is regulated by Ca influx

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8
Q

How do class IV agents cause arrhythmias?

A

Cause an AV block if suppress long enough

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9
Q

What is the effect of Class IV agents on LV funx?

A

Lower

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10
Q

What is the effect of class IV drugs on HR?

A

Decrease

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11
Q

What are the two types of channels that class IV drugs block?

A

L and T type Ca channels

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12
Q

Can CCBs bind to all pores of Ca channels? Why is this important?

A

No, so it doesn’t stop HR all together

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13
Q

What are the three places that CCBs affect?

A
  1. vascular smooth muscle
  2. Cardiac myocytes
  3. SA and AV nodal cells
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14
Q

What is the overall effect of CCBs?

A

Diminish the degree to which the Ca channel pores open in response to voltage depolarization

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15
Q

What are the two main classes of CCBs?

A

Dihydropyridine (DHP)

Non-dihydropyridine (NDHP)

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16
Q

What is the main DHP?

A

Nifedipine

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17
Q

What are the two non DHP drugs?

A

Verapamil

Diltiazem

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18
Q

What are the tissues that the DHP drugs mainly affect? What is the effect here?

A

Vasculature–vasodilation and reflex tachycardia

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19
Q

Are DHPs used an antiarrhythmics?

A

No

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20
Q

What tissue do NDHPs affect?

A

Heart–used an antiarrhythmic

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21
Q

What drugs are phenylalkylamines?

A

Verapamil and derivatives

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22
Q

What drugs are benzothiazepines?

A

Diltiazem and derivatives

23
Q

What is the effect of CCbs on chronicity and dromoticity?

A

Negative for NDHP agents only

24
Q

What are the inotropic effects of CCBs?

A

Negative, but this may be offset by reflex tachycardia that DHPs produce

25
Q

Drugs that have a -dipine suffix are what type of drugs?

A

DHPs

26
Q

What is the ratio of vasodilation to negative inotropy for DHPs? NDHPs?

A 
DHPs = 10:1
NDHPs = 1:1
27
Q

What are the effects of CCBs on smooth muscle? Skeletal?

A

Little to none

28
Q

What are the main clinical applications of CCBs? (4) Which are only for NDHPs?

A

Systemic HTN
Angina
SVT (NDHPs only)
Infarct protection (NDHPs only)

29
Q

What is the MOA of verapamil?

A

CCB
Decreases SA automaticity
Decrease AV conduction
Cardiac depression

30
Q

How does verapamil increase the PR interval?

A

Decreases AV conduction

31
Q

Verapamil has no effect on ventricular Na conduction. What is the significance of this?

A

Ineffective on ventricular arrhythmia

32
Q

What are the clinical applications of verapamil?

A

SVT

Rate control a-fib

33
Q

How does verapamil rate control a-fib?

A

Slows the rate of conduction from the AV node

34
Q

What are the adverse effects of verapamil?

A

constipation

Exacerbate CHF

35
Q

What are the two contraindications of verapamil?

A

WPW w/afib

Ventricular tachycardia

36
Q

How can verapamil cause constipation?

A

Decrease smooth muscle contraction

37
Q

How can verapamil exacerbate CHF?

A

Decrease HR when heart is overloaded

38
Q

Why don’t you want to give verapamil if there is an issue with the sinus node?

A

Decreases conduction

39
Q

Why does WPW contraindicate verapamil?

A

Will force all signals down the fast pathway, causing ventricular tachycardia

40
Q

What is the MOA of adenosine as an antiarrhythmic?

A

Activates A1 receptor on SA and AV node, to increase K channel sensitivity

41
Q

What is the effect of adenosine on the SA node?

A

SA node hyperpolarization and decrease firing

42
Q

What is the effect of adenosine on the AP duration of the atrial cells?

A

Shortens

43
Q

What is the effect of adenosine on the av velocity?

A

Depresses

44
Q

What is the effect of adenosine on the vasculature (MOA)?

A

Activates A receptor, causing an increase in NO production,and K hyperpolarization

45
Q

What is the effect of adenosine on the pulmonary stretch receptors?

A

Stimulates

46
Q

What are the clinical applications of Adenosine?

A

ACute conversion of paroxysmal SVT caused by a bypass pathway

47
Q

How do you administer adenosine? What is its half life?

A

IV bolus via central line

10-15 seconds

48
Q

What are the adverse effects of adenosine?

A

Hypotension
Heart block
Dyspnea

49
Q

How does atropine work to stop bradycardia?

A

Blocks M2 receptors on the heart (and all M receptors elsewhere)

50
Q

How does isoproterenol work to treat bradycardia?

A

B1 agonist causes an increase in HR

51
Q

What is the last resort for treating chronic bradycardia?

A

Pacemaker

52
Q

What is the indication for vagal stimulation through carotid sinus massage, or the valsalva maneuver?

A

Sinus tachycardia, PSVT

53
Q

What is the normal QRS complex length?

A

120 ms

Pharm (73 decks)

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