EXAM #2: CV PHARM 3 Flashcards Preview

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Flashcards in EXAM #2: CV PHARM 3 Deck (32):
1

What are the Class IV antiarrhythmics?

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

2

What is the general mechanism of the Class IV antiarrhythmics?

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

3

What are the physiologic effects of the Class IV antiarrhythmics?

- Depressed SA nodal automaticity and AV nodal conduction
- Decreased ventricular contractility

4

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

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.****

5

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

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

6

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

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

7

Which subunit of the Ca++ channel contains pores?

Alpha-1

8

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

- Dihydropyridine= vasculature
- Non-dihydropyridine= heart

9

What is the hallmark drug of the DHP group?

Nifedipine

10

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

Verapamil
Diltiazem

11

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

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

12

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

Arterial/ arteriolar > veins

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

13

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

DHP= 10:1
NDHP= 1:1

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?

- 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.

15

What are the non-cardiac effects of the CCBs?

- 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

16

What are the main clinical applications of the CCBs?

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

17

Which group of CCBs is indicated specifically for SVT?

NDHP i.e. Diltiazem and Verapamil

18

What is the specific mechanism of action of Verapamil?

Blockade of slow inward Ca++ channels in nodal tissue

19

What are the physiologic effects of Verapamil?

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

20

Does Verapamil have effects on ventricular arrhythmia?

NO b/c no effect on Na+ channels

21

What are the clinical indications for Verapamil?

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

22

What are the adverse effects of Verapamil?

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

23

When is Verapamil contraindicated?

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

24

Why is Verapamil contraindicated in WPW with a-fib?

- 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

25

What is the mechanism of action of Adenosine?

- 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******

26

What are the physiologic effects of Adenosine?

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

27

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

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

Net effect is VASODILATION

28

What is the impact of stimulation of pulmonary stretch receptors?

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

29

What are the clinical indications for Adenosine?

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

30

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

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

31

What are the adverse effects of Adenosine?

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

32

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

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

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