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pharmacology 2 > cardiovascular 2 > Flashcards

cardiovascular 2 Flashcards

1
Q

What is an example of a cardiac glycoside that acts on the contractile force of the heart?

A

Digoxin

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2
Q

What is digoxin used to manage?

A

Supraventricular tachydysrhythmias like atrial tachycardia, atrial flutter, and atrial fibrillation with rapid ventricular rate.

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3
Q

Describe the mechanisms by which digoxin manages supraventricular tachydysrhythmias.

A
  1. Slows conduction through the AV node to reduce ventricular rate
  2. Increases parasympathetic nervous system activity to decrease SA node activity
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4
Q

What type of arrhythmia is one at risk for when using digoxin?

A

Ventricular fibrillation

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5
Q

What was digoxin originally used to treat?

A

CHF, but it is no longer considered a first-line therapy.

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6
Q

How does digoxin increase contractility of the heart (inotropic)?

A

Digoxin inhibits the Na-K ATP transport system. This causes an increase in intracellular Na, which increases intracellular calcium, which causes contractility of the heart.

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7
Q

Which patient type should you be careful giving digoxin to?

A

Renal patients, because it digoxin is renally cleared.

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8
Q

What does digoxin’s protein binding tell us?

A

Digoxin is only 25% protein bound, so there are higher free drug concentrations. That means it is primarily eliminated unchanged by the kidneys, and is strongly influenced by renal function.

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9
Q

Describe the therapeutic range of digoxin. (Narrow? Wide?)

A

It has a NARROW therapeutic range. Its therapeutic effects are at 35% of its fatal dose.

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10
Q

What is the therapeutic range vs. the toxic range of digoxin?

A

Therapeutic range: 0.5-2.5 ng/mL

Toxic range > 3 ng/mL

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11
Q

What is toxicity of digoxin precipitated by?

A

Potassium depletion, such as by diuretics or alkalosis

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12
Q

What are the symptoms of digoxin toxicity?

A

Nausea/vomiting vision changes (yellow-green halos), atrial/ventricular dysrhythmias

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13
Q

How do you treat digoxin toxicity?

A
  1. Identify/correct inciting cause (hypoK, hypoMg, hyperCa)
  2. Treat dysrhythmias (phenytoin, lidocaine, atropine)
  3. Artificial pacing if complete heart block
  4. Fab fragments (digitalis antibodies)
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14
Q

Which drugs have interactions with digoxin?

A

Quinidine & Sympathomimetics

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15
Q

How does quinidine interact with digoxin?

A

Quinidine displaces digoxin from tissue binding sites.

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16
Q

How do sympathomimetics interact with digoxin?

A

Sympathomimetics could precipitate dysrhythmias.

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17
Q

What are examples of Class I antiarrhythmic drugs?

A

Quinidine, procainamide, lidocaine, phenytoin, flecainide

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18
Q

What kind of drugs are quinidine, procainamide, lidocaine, phenytoin, flecainide?

A

Class I antiarrhythmics - Sodium channel blockers

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19
Q

What kind of channels do Class I Antiarrhythmics block?

A

Sodium channels

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20
Q

How do Class I antiarrhythmics work?

A

They decrease intracellular sodium levels, which decreases intracellular calcium levels. This decreases myocardial depolarization rate and conduction velocity.

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21
Q

Which antiarrhythmic drug is often used for treatment of ventricular tachycardia and suppression of PVCs? What dose?

A

Lidocaine, 2 mg/kg IV – then 1-4 mg/min infusion

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22
Q

How is lidocaine metabolized?

A

Hepatically

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23
Q

What are symptoms of CNS toxicity by lidocaine?

A

Depression, apnea, seizure

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24
Q

What are examples of Class II antiarrhythmics?

A

Beta-blockers

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25
Q

What are examples of Class III antiarrhythmics?

A

Amiodarone, sotalol, bretylium

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26
Q

What type of channel blockers are Class III antiarrhythmics?

A

Potassium

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27
Q

How do Class III antiarrhythmics work?

A

They block potassium channels to prolong cardiac depolarization and action potential duration. This decreases the proportion of the cardiac cycle when the myocardium is excitable.

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28
Q

Which Class III antiarrhythmic prolongs the refractory period in ALL cardiac tissues?

A

Amiodarone

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29
Q

What type of effects does amiodarone have aside from Class III?

A 
Class I (Na channel blocking)
Class II (B blocking)
Class IV (Ca channel blocking)
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30
Q

which calcium blocker drug is the first line medication for supraventricular tachydysrhythmia

A

Diltiazem (cardizem)

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31
Q

diltiazem blocks CA2+ channel of _____node

A

AV

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32
Q

what is the dose of Diltiazem

A

0.25mg/kg (~20mg) slow IV bolus over 2min
second dose: 0.35mg/kg, given 2-15 min after 1st dose

infusion rate of 5-15mg/hr (most start at 10mg/hr)

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33
Q

Diltiazem has some role in control of _______

A

chronic HTN,

cause peripheral arterial vasodilation

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34
Q

Diltiazem has the elimination half life of ____

A

4-6 hrs, 20hr for metabolites

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35
Q

what are the side effects of Diltiazem?

A

dizziness, headache, flushing gingival hyperplasia (overgrowth of gum)

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36
Q

diltiazem is avoided with which pt histories

A

pt with actue MI, Hypotension, 2nd-3rd degree heart block

37
Q

diltiazem is an oral medication for management of ______,_____, and _____________

A

angina, HTN, Afib/Aflutter

38
Q

verapamil treats _______________

A

supraventricular tachydysrhythmia

39
Q

how doe verapamil treat SVTs

A

AV node depression thus cause bradycardia

40
Q

you see pts take Verapamil for ________,_________,_________, and/or_________

A

angina pectoris , hypertension, migraine, cluster headaches

41
Q

how does verapamil treat angina and hypertension

A

coronary and peripheral artery dilation

42
Q

what are the side effects of verapamil?

A

Hypotension, constipation, headaches, flushing , gingival hyperplasia

43
Q

verapamil has the elimination half life of _____

A

6-12 hr

44
Q

which calcium blockers are heart rate specific?

A

diltiazem, verapamil

45
Q

which calcium blockers are vascular specific ?

A 
Nifedipine (procardia)
nimodipine
nicardipine (cardene)
clevidipine (cleviprex)
amloidipine (norvasc)
46
Q

nifedipine treats angina pectoris, especially _________ vasospasm by vasodilating ________ and __________ arteries

A

nifedipine treats angina pectoris, especially CORONARY vasospasm by vasodilating CORONARY and PERIPHERAL arteries

47
Q

Nimodipine is a lipid-soluble analogue of ________

A

nifedipine

48
Q

which drug crosses the blood brain barrier to prevent cerebral vasospasm

A

Nimodipine

49
Q

Much like verapamil, nicardipine (cardene) treats _________ and _________, however it has no effect on_______ and_________

A

treats Angina pectoris and HTN

has no effect on SA node and AV node

50
Q

what is the IV infusion rate of Nicardipine

A

start at 5mg/hr, increase by 2.5 mg/hr every 5 min up to 15 mg/ hr

51
Q

Nicardipine is a tocolytic drug , what does tocolytic mean ?

A

inhibits labor

52
Q

the problem of nicardipine is _________ so clevidipine came into market

A

nicardipine is slow

53
Q

clevidipine (clevioprex) is like nicardipine but differs in ________

A

in a lipid emulsion , so looks like propofol

elimination half life of 1 min

54
Q

clevidipine (clevioprex) is very potent because

A

it has a elimination half life of 1 min ,

it is metabolized by plasma/tissue esterase ( NOT PSUEDOESTERASE)

55
Q

what is the starting infusion rate for clevidipine

A

1-2 mg/hr up to 16 mg/hr

56
Q

this drug is an oral med taken by pt at home similar to nifedpine/ nicardipine used for management of HTN

A

Amlodipine ( Norvasc)

57
Q

which calcium blocker drugs drops BP?

A

Verapamil, diltiazem, nifedipine, nicardipine, clevidipine

58
Q

which calcium blocker drugs drops HR?

A

verapamil and diltiazem

59
Q

which calcium blocker drugs drops myocardial contractility ?

A

Verapamil, diltiazem, nifedipine, nicardipine, clevidipine

60
Q

which calcium blocker drugs drops SA node activity ?

A

Verapamil, diltiazem

61
Q

which calcium blocker drugs drops AV node conductivity?

A

Verapamil, diltiazem

62
Q

which calcium blocker drugs increase coronary and peripheral arteries perfusion more than the other

A

nifedipine, nicardipine, clevidipine increase coronary and peripheral arteries perfusion more than Verapamil, diltiazem

63
Q

what effects do nifedipine, nicardipine, clevidipine have on the SA node?

A

no effect

64
Q

what effects do nifedipine, nicardipine, clevidipine have on the AV node

A

no effect

65
Q

Amiodarone is most effective for:

A

SVTs, PVCs, VTach, and defibrillation resistant Vfib

66
Q

This drug may also have some effect on the conversion of Afib:

A

amiodarone

67
Q

What is the IV bolus of amiodarone for pulseless Vfib or VTach?

A

300 mg IV bolus

68
Q

What is the initial dose of amiodarone for non life threatening tachdysrrhythmias?

A

1000 mg given over 24 hours:
150 mg slow IV bolus over ten minutes
then 360 mg over 6 hours (1 mg/min)
then 540 mg over 18 hours (0.5 mg/min)

69
Q

What is the elimination half time of amiodarone?

A

29 days

70
Q

Why is the elimination half time of amiodarone so long?

A

due to extensive protein binding and large volume of distribution

71
Q

What are side effects of amiodarone?

A

pneumonitis, hypotension (vasodilation), photosensitivity, rash, hypo- or hyperthyroidism (high iodine content)

72
Q

Adenosine is an endogenous nucleoside which works as a potent coronary __________ (dilator or constrictor) and _________ (increases or decreases) myocardial O2 consumption.

A

dilator; decreases

73
Q

What is the half time of adenosine?

A

0.6-1.5 seconds

74
Q

How does adenosine work?

A

It stimulates supraventricular potassium channels (these channels are not present in ventricular myocytes). This stimulation causes hyperpolarization and decreased depolarization.

75
Q

What is adenosine used for?

A

To treat AV nodal supraventricular tachyarrhythmias (reentrant tachycardia, atrial tachycardia)

76
Q

What is the starting dose of adenosine?

A

6 mg IV rapid bolus

77
Q

What is the second dose of adenosine?

A

12 mg IV, can be repeated

78
Q

What is adenosine known to do?

A

causes transient heart block (AV node); brief ventricular asystole

79
Q

Adenosine is ineffective for:

A

atrial fibrillation, atrial flutter, or ventriclar tachycardias

80
Q

What are side effects of adenosine?

A

flushing, dyspnea, chest pain, bronchospasm, metallic taste

81
Q

What are some other uses of adenosine?

A

controlled hpotension; pharmacologic stress testing; temporary asystole during aneurysm clipping or deployment of endovascular heart valve

82
Q

How do calcium channel blockers work?

A

they bind to L-type voltage gated calcium channels and cause a decrease in intracellular calcium.

83
Q

A decrease in intracellular calcium will cause:

A

decreased myocardial contractility
decreased heart rate
decreased SA node activity and/or AV node conductivity
vascular smooth muscle relaxation

84
Q

Use caution in using calcium channel blockers on patients with

A

impaired LV function or hypovolemia

85
Q

Are calcium channel blockers protein bound?

A

highly protein bound

86
Q

What organ metabolizes calcium channel blockers?

A

liver

87
Q

Calcium channel blockers potentiate the effects of:

A

neuromuscular blocking drugs and local anesthetic activity

88
Q

What is the common dosing for calcium channel blockers?

A

usually given as a single bolus or as a continuous infusion

pharmacology 2 (4 decks)

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