Flashcards in EXAM #2: CV PHARM 3 Deck (32):
What are the Class IV antiarrhythmics?
Verapamil and Diltiazem; these are Ca++ blockers that specifically act on cardiac tissue
What is the general mechanism of the Class IV antiarrhythmics?
Ca++ channel antagonists with PRIMARY effects on nodal phase 0 depolarization
What are the physiologic effects of the Class IV antiarrhythmics?
- Depressed SA nodal automaticity and AV nodal conduction
- Decreased ventricular contractility
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.****
What are the cardiovascular sites of action of Ca++ blockers?
1) Vascular smooth muscle cells
2) Cardiac myocytes
3) SA and AV nodal cells
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
Which subunit of the Ca++ channel contains pores?
What are the main classes of CCBs? What do these different classes mainly effect?
- Dihydropyridine= vasculature
- Non-dihydropyridine= heart
What is the hallmark drug of the DHP group?
What are the two drugs in the non-dihydropyridine class of CCB?
What are the major cardiovascular effects of the NDHP class CCBs?
2) Negative chonotropy
3) Negative dromotropy
4) Negative ionotropy
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
How do the ratios of vasodilation:negative ionotropy compare between the DHPs and NDHPs?
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.
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
What are the main clinical applications of the CCBs?
1) Systemic HTN
2) Angina Pectoris
4) Post-infarction protection
Which group of CCBs is indicated specifically for SVT?
NDHP i.e. Diltiazem and Verapamil
What is the specific mechanism of action of Verapamil?
Blockade of slow inward Ca++ channels in nodal tissue
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
Does Verapamil have effects on ventricular arrhythmia?
NO b/c no effect on Na+ channels
What are the clinical indications for Verapamil?
2) A-fib with RVR to control rate
What are the adverse effects of Verapamil?
2) Exacerbation of CHF
4) AV block
5) Headache, flushing, dizziness, and ankle edema
When is Verapamil contraindicated?
1) Sick sinus syndrome
2) Pre-existing AV nodal disease
3) WPW with a-fib
4) Ventricular Tachycardia
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
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******
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
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
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)
What are the clinical indications for Adenosine?
Conversion of acute PSVT caused by re-entry into accessory bypass pathways
What is the half-life of adenosine? What are the clinical implications?
10-15 seconds; must be given by a central IV
What are the adverse effects of Adenosine?
3) Heart Block