Cardiovascular pharmacology III Flashcards

1
Q

what are the effects of class IV antiarryhtmics?

A
  1. calcium channel blockers - primary effects on nodal phase 0
  2. depressed SA nodal automaticity, AV conduction, decreased ventricular contractility
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2
Q

what are the cardiovascular sites of action for the calcium channel blockers?

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

how do the calcium channel blockers work?

A

interfere with entry of calcium into cells through voltage dependent L and T type calcium channels

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4
Q

what are the two classes of calcium channel blockers?

A
  1. dihydropyridine (DHP)

2. non-dihydropyridine (NDHP)

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5
Q

what is the DHP class drug? where are its effects?

A
  1. nifedipine

2. vasculature - vasodilation and reflex tachycardia

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6
Q

what are the NDHP class drugs? where are their effects?

A
  1. verapamil and diltiazem

2. heart - tx for arrhythmias

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7
Q

what are the major cardiovascular actions of the calcium channel blockers?

A
  1. vasodilation (arteries more than veins)
  2. negative chronotropic and dromotropic (NDHP ONLY)
  3. negative inotropic
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8
Q

what are the main clinical applications for calcium channel blockers?

A
  1. systemic hypertension
  2. angina pectoris
  3. SVT
  4. post-infarct protection
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9
Q

what is the mechanism of action of verapamil?

A
  1. blocks slow inward calcium channels
  2. decrease AV conduction - increase PR interval
  3. cardiac depression
  4. ineffective on ventricular arrhythmia
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10
Q

what ECG changes occur during calcium channel blocker use?

A

increased PR interval (decreased AV conduction)

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11
Q

what are the clinical applications for verapamil?

A
  1. SVT - want to decrease spontaneous activity

2. rate control in Af

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12
Q

what are the adverse effects of verapamil?

A
  1. exacerbate CHF

2. constipation

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13
Q

what are the contraindications for verapamil?

A
  1. WPW syndrome with Af

2. ventricular tachycardia

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14
Q

what is the mechanism of action of adenosine?

A
  1. activates a1 receptor in SA and AV nodes
  2. SA node hyperpolarization and decreased firing rate - INCREASE MAXIMUM DIASTOLIC POTENTIAL
  3. shortening of AP duration of atrial cells
  4. depression of AV conduction velocity
  5. activates a2 receptors in vasculature - vasodilation
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15
Q

what are the clinical applications of adenosine?

A

acute conversion of paroxysmal SVT caused by reentry involving accessory bypass pathways

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16
Q

what are the adverse effects of adenosine?

A
  1. hypotension
  2. complete heart block
  3. CNS
  4. dyspnea