EXAM #2: CV PHARM 3

Question 1

What are the Class IV antiarrhythmics?

Answer 1

Verapamil and Diltiazem; these are Ca++ blockers that specifically act on cardiac tissue

Question 2

What is the general mechanism of the Class IV antiarrhythmics?

Answer 2

Ca++ channel antagonists with PRIMARY effects on nodal phase 0 depolarization

Question 3

What are the physiologic effects of the Class IV antiarrhythmics?

Answer 3

• Depressed SA nodal automaticity and AV nodal conduction

- Decreased ventricular contractility

Question 4

What channels are effected by the Ca++ blockers? What part of the channel is affected?

Answer 4

L and T-type Ca++ channels

• Channels are composed of 4 subunits
• Alpha subunit contains the Ca++ pore

**It is important to note that no CCB completely blocks Ca++ movement through the pores in the alpha subunit.*

Question 5

What are the cardiovascular sites of action of Ca++ blockers?

Answer 5

1) Vascular smooth muscle cells
2) Cardiac myocytes
3) SA and AV nodal cells

Question 6

What is the specific effect of Ca++ blockers on Ca++ pores?

Answer 6

Diminished degree to which the alpha subunit pores open in response to voltage change

Question 7

Which subunit of the Ca++ channel contains pores?

Answer 7

Alpha-1

Question 8

What are the main classes of CCBs? What do these different classes mainly effect?

Answer 8

• Dihydropyridine= vasculature

- Non-dihydropyridine= heart

Question 9

What is the hallmark drug of the DHP group?

Answer 9

Nifedipine

Question 10

What are the two drugs in the non-dihydropyridine class of CCB?

Answer 10

Verapamil

Diltiazem

Question 11

What are the major cardiovascular effects of the NDHP class CCBs?

Answer 11

1) Vasodilation
2) Negative chonotropy
3) Negative dromotropy
4) Negative ionotropy

Question 12

Where is the site of action of the NDHPs in the vasculature?

Answer 12

Arterial/ arteriolar > veins

I.e. blockade of Ca++ channels in the arterial circulation to a greater degree than the venous

Question 13

How do the ratios of vasodilation:negative ionotropy compare between the DHPs and NDHPs?

Answer 13

DHP= 10:1 
NDHP= 1:1

Question 14

How do CCBs compare in the management of HTN? How would you decide which class of CCB to use to treat a patient with CVD?

Answer 14

• DHP= increase in HR b/c of reflex tachycardia
• NDHP= decrease in HR

Thus, NDHP may be a good option for patients with ischemia i.e. CVD.

Question 15

What are the non-cardiac effects of the CCBs?

Answer 15

• CCB’s have little effect on smooth muscle outside of the vasculature
• No effect on skeletal muscle

EXCEPTION= some effect on uterine contraction and can be used to prevent pre-term labor

Question 16

What are the main clinical applications of the CCBs?

Answer 16

1) Systemic HTN
2) Angina Pectoris
3) SVT
4) Post-infarction protection

Question 17

Which group of CCBs is indicated specifically for SVT?

Answer 17

NDHP i.e. Diltiazem and Verapamil

Question 18

What is the specific mechanism of action of Verapamil?

Answer 18

Blockade of slow inward Ca++ channels in nodal tissue

Question 19

What are the physiologic effects of Verapamil?

Answer 19

1) Decreased SA automaticity= decreased HR
2) Decreased AV conduction= increased PR interval
3) Cardiac depression i.e. decrease ventricular rate and contraction

Question 20

Does Verapamil have effects on ventricular arrhythmia?

Answer 20

NO b/c no effect on Na+ channels

Question 21

What are the clinical indications for Verapamil?

Answer 21

1) SVT
2) A-fib with RVR to control rate
3) Angina
4) HTN

Question 22

What are the adverse effects of Verapamil?

Answer 22

1) Constipation
2) Exacerbation of CHF
3) Hypotension
4) AV block
5) Headache, flushing, dizziness, and ankle edema

Question 23

When is Verapamil contraindicated?

Answer 23

1) Sick sinus syndrome
2) Pre-existing AV nodal disease
3) WPW with a-fib
4) Ventricular Tachycardia

Question 24

Why is Verapamil contraindicated in WPW with a-fib?

Answer 24

• WPW= fast conductive pathway
• Blocking Ca++ in slow pathway–> conduction all follows FAST pathway

Thus, it can lead to an INCREASE in ventricular response rate

Question 25

What is the mechanism of action of Adenosine?

Answer 25

• Activation of A1 (adenosine) receptors in SA and AV nodes
• Activates K+ channels that HYPERPOLARIZE the SA node and DECREASE firing rate

Increase in maximum diastolic potential*

Question 26

What are the physiologic effects of Adenosine?

Answer 26

1) Hyperpolarization of the SA node slows conduction
2) Shortened AP duration in atrial cells
3) Slowed atrial-ventricular conduction velocity

Question 27

What is the effect of adenosine activation of A2 receptors in the vasculature?

Answer 27

• K+ channel activation and HYPERPOLARIZATION which,
• Increases Ca++ influx that in turn increases NO release

Net effect is VASODILATION

Question 28

What is the impact of stimulation of pulmonary stretch receptors?

Answer 28

The tension/bearing down you see patients do upon administration of adenosine is partly a result of the pulmonary stretch receptor (and cardiac pause)

Question 29

What are the clinical indications for Adenosine?

Answer 29

Conversion of acute PSVT caused by re-entry into accessory bypass pathways

Question 30

What is the half-life of adenosine? What are the clinical implications?

Answer 30

10-15 seconds; must be given by a central IV

Question 31

What are the adverse effects of Adenosine?

Answer 31

1) Hypotension
2) Flushing
3) Heart Block
4) Dyspnea

Question 32

What drugs can be used to treat symptomatic bradycardia? Why?

Answer 32

1) Atropine– antagonizes M2 receptors in the heart to increase HR
2) Isoproterenol to agonize B1 receptors and increase HR