Cardio III

Question 1

What are the class IV types of drugs? MAO?

Answer 1

Verapamil
Diltiazem

Ca channel antagonists that affects nodal phase 0 depolarization

Question 2

What are the major effects of class IV drugs?

Answer 2

Depressed SA nodal automaticity and AV nodal conduction

Decreased ventricular contractility

Question 3

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

Answer 3

Inhibited by cimetidine

Stimulated by phenytoin, phenobarbital, rifampicin

Question 4

What type of drug is phenytoin?

Answer 4

Class Ib antiarrhythmic

Question 5

What type of drug is Mexiletin?

Answer 5

Class Ib antiarrhythmic

Question 6

What type of drug is tocainide?

Answer 6

Class Ib antiarrhythmic

Question 7

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

Answer 7

Because nodal tissues is regulated by Ca influx

Question 8

How do class IV agents cause arrhythmias?

Answer 8

Cause an AV block if suppress long enough

Question 9

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

Answer 9

Lower

Question 10

What is the effect of class IV drugs on HR?

Answer 10

Decrease

Question 11

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

Answer 11

L and T type Ca channels

Question 12

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

Answer 12

No, so it doesn’t stop HR all together

Question 13

What are the three places that CCBs affect?

Answer 13

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

Question 14

What is the overall effect of CCBs?

Answer 14

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

Question 15

What are the two main classes of CCBs?

Answer 15

Dihydropyridine (DHP)

Non-dihydropyridine (NDHP)

Question 16

What is the main DHP?

Answer 16

Nifedipine

Question 17

What are the two non DHP drugs?

Answer 17

Verapamil

Diltiazem

Question 18

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

Answer 18

Vasculature–vasodilation and reflex tachycardia

Question 19

Are DHPs used an antiarrhythmics?

Answer 19

No

Question 20

What tissue do NDHPs affect?

Answer 20

Heart–used an antiarrhythmic

Question 21

What drugs are phenylalkylamines?

Answer 21

Verapamil and derivatives

Question 22

What drugs are benzothiazepines?

Answer 22

Diltiazem and derivatives

Question 23

What is the effect of CCbs on chronicity and dromoticity?

Answer 23

Negative for NDHP agents only

Question 24

What are the inotropic effects of CCBs?

Answer 24

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

Question 25

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

Answer 25

DHPs

Question 26

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

Answer 26

``` DHPs = 10:1 NDHPs = 1:1 ```

Question 27

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

Answer 27

Little to none

Question 28

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

Answer 28

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

Question 29

What is the MOA of verapamil?

Answer 29

CCB Decreases SA automaticity Decrease AV conduction Cardiac depression

Question 30

How does verapamil increase the PR interval?

Answer 30

Decreases AV conduction

Question 31

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

Answer 31

Ineffective on ventricular arrhythmia

Question 32

What are the clinical applications of verapamil?

Answer 32

SVT | Rate control a-fib

Question 33

How does verapamil rate control a-fib?

Answer 33

Slows the rate of conduction from the AV node

Question 34

What are the adverse effects of verapamil?

Answer 34

constipation | Exacerbate CHF

Question 35

What are the two contraindications of verapamil?

Answer 35

WPW w/afib | Ventricular tachycardia

Question 36

How can verapamil cause constipation?

Answer 36

Decrease smooth muscle contraction

Question 37

How can verapamil exacerbate CHF?

Answer 37

Decrease HR when heart is overloaded

Question 38

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

Answer 38

Decreases conduction

Question 39

Why does WPW contraindicate verapamil?

Answer 39

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

Question 40

What is the MOA of adenosine as an antiarrhythmic?

Answer 40

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

Question 41

What is the effect of adenosine on the SA node?

Answer 41

SA node hyperpolarization and decrease firing

Question 42

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

Answer 42

Shortens

Question 43

What is the effect of adenosine on the av velocity?

Answer 43

Depresses

Question 44

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

Answer 44

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

Question 45

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

Answer 45

Stimulates

Question 46

What are the clinical applications of Adenosine?

Answer 46

ACute conversion of paroxysmal SVT caused by a bypass pathway

Question 47

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

Answer 47

IV bolus via central line 10-15 seconds

Question 48

What are the adverse effects of adenosine?

Answer 48

Hypotension Heart block Dyspnea

Question 49

How does atropine work to stop bradycardia?

Answer 49

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

Question 50

How does isoproterenol work to treat bradycardia?

Answer 50

B1 agonist causes an increase in HR

Question 51

What is the last resort for treating chronic bradycardia?

Answer 51

Pacemaker

Question 52

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

Answer 52

Sinus tachycardia, PSVT

Question 53

What is the normal QRS complex length?

Answer 53

120 ms