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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
What are examples of Class III antiarrhythmics?
Amiodarone, sotalol, bretylium
26
What type of channel blockers are Class III antiarrhythmics?
Potassium
27
How do Class III antiarrhythmics work?
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.
28
Which Class III antiarrhythmic prolongs the refractory period in ALL cardiac tissues?
Amiodarone
29
What type of effects does amiodarone have aside from Class III?
``` Class I (Na channel blocking) Class II (B blocking) Class IV (Ca channel blocking) ```
30
which calcium blocker drug is the first line medication for supraventricular tachydysrhythmia
Diltiazem (cardizem)
31
diltiazem blocks CA2+ channel of _____node
AV
32
what is the dose of Diltiazem
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)
33
Diltiazem has some role in control of _______
chronic HTN, | cause peripheral arterial vasodilation
34
Diltiazem has the elimination half life of ____
4-6 hrs, 20hr for metabolites
35
what are the side effects of Diltiazem?
dizziness, headache, flushing gingival hyperplasia (overgrowth of gum)
36
diltiazem is avoided with which pt histories
pt with actue MI, Hypotension, 2nd-3rd degree heart block
37
diltiazem is an oral medication for management of ______,_____, and _____________
angina, HTN, Afib/Aflutter
38
verapamil treats _______________
supraventricular tachydysrhythmia
39
how doe verapamil treat SVTs
AV node depression thus cause bradycardia
40
you see pts take Verapamil for ________,_________,_________, and/or_________
angina pectoris , hypertension, migraine, cluster headaches
41
how does verapamil treat angina and hypertension
coronary and peripheral artery dilation
42
what are the side effects of verapamil?
Hypotension, constipation, headaches, flushing , gingival hyperplasia
43
verapamil has the elimination half life of _____
6-12 hr
44
which calcium blockers are heart rate specific?
diltiazem, verapamil
45
which calcium blockers are vascular specific ?
``` Nifedipine (procardia) nimodipine nicardipine (cardene) clevidipine (cleviprex) amloidipine (norvasc) ```
46
nifedipine treats angina pectoris, especially _________ vasospasm by vasodilating ________ and __________ arteries
nifedipine treats angina pectoris, especially CORONARY vasospasm by vasodilating CORONARY and PERIPHERAL arteries
47
Nimodipine is a lipid-soluble analogue of ________
nifedipine
48
which drug crosses the blood brain barrier to prevent cerebral vasospasm
Nimodipine
49
Much like verapamil, nicardipine (cardene) treats _________ and _________, however it has no effect on_______ and_________
treats Angina pectoris and HTN has no effect on SA node and AV node
50
what is the IV infusion rate of Nicardipine
start at 5mg/hr, increase by 2.5 mg/hr every 5 min up to 15 mg/ hr
51
Nicardipine is a tocolytic drug , what does tocolytic mean ?
inhibits labor
52
the problem of nicardipine is _________ so clevidipine came into market
nicardipine is slow
53
clevidipine (clevioprex) is like nicardipine but differs in ________
in a lipid emulsion , so looks like propofol elimination half life of 1 min
54
clevidipine (clevioprex) is very potent because
it has a elimination half life of 1 min , | it is metabolized by plasma/tissue esterase ( NOT PSUEDOESTERASE)
55
what is the starting infusion rate for clevidipine
1-2 mg/hr up to 16 mg/hr
56
this drug is an oral med taken by pt at home similar to nifedpine/ nicardipine used for management of HTN
Amlodipine ( Norvasc)
57
which calcium blocker drugs drops BP?
Verapamil, diltiazem, nifedipine, nicardipine, clevidipine
58
which calcium blocker drugs drops HR?
verapamil and diltiazem
59
which calcium blocker drugs drops myocardial contractility ?
Verapamil, diltiazem, nifedipine, nicardipine, clevidipine
60
which calcium blocker drugs drops SA node activity ?
Verapamil, diltiazem
61
which calcium blocker drugs drops AV node conductivity?
Verapamil, diltiazem
62
which calcium blocker drugs increase coronary and peripheral arteries perfusion more than the other
nifedipine, nicardipine, clevidipine increase coronary and peripheral arteries perfusion more than Verapamil, diltiazem
63
what effects do nifedipine, nicardipine, clevidipine have on the SA node?
no effect
64
what effects do nifedipine, nicardipine, clevidipine have on the AV node
no effect
65
Amiodarone is most effective for:
SVTs, PVCs, VTach, and defibrillation resistant Vfib
66
This drug may also have some effect on the conversion of Afib:
amiodarone
67
What is the IV bolus of amiodarone for pulseless Vfib or VTach?
300 mg IV bolus
68
What is the initial dose of amiodarone for non life threatening tachdysrrhythmias?
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
What is the elimination half time of amiodarone?
29 days
70
Why is the elimination half time of amiodarone so long?
due to extensive protein binding and large volume of distribution
71
What are side effects of amiodarone?
pneumonitis, hypotension (vasodilation), photosensitivity, rash, hypo- or hyperthyroidism (high iodine content)
72
Adenosine is an endogenous nucleoside which works as a potent coronary __________ (dilator or constrictor) and _________ (increases or decreases) myocardial O2 consumption.
dilator; decreases
73
What is the half time of adenosine?
0.6-1.5 seconds
74
How does adenosine work?
It stimulates supraventricular potassium channels (these channels are not present in ventricular myocytes). This stimulation causes hyperpolarization and decreased depolarization.
75
What is adenosine used for?
To treat AV nodal supraventricular tachyarrhythmias (reentrant tachycardia, atrial tachycardia)
76
What is the starting dose of adenosine?
6 mg IV rapid bolus
77
What is the second dose of adenosine?
12 mg IV, can be repeated
78
What is adenosine known to do?
causes transient heart block (AV node); brief ventricular asystole
79
Adenosine is ineffective for:
atrial fibrillation, atrial flutter, or ventriclar tachycardias
80
What are side effects of adenosine?
flushing, dyspnea, chest pain, bronchospasm, metallic taste
81
What are some other uses of adenosine?
controlled hpotension; pharmacologic stress testing; temporary asystole during aneurysm clipping or deployment of endovascular heart valve
82
How do calcium channel blockers work?
they bind to L-type voltage gated calcium channels and cause a decrease in intracellular calcium.
83
A decrease in intracellular calcium will cause:
decreased myocardial contractility decreased heart rate decreased SA node activity and/or AV node conductivity vascular smooth muscle relaxation
84
Use caution in using calcium channel blockers on patients with
impaired LV function or hypovolemia
85
Are calcium channel blockers protein bound?
highly protein bound
86
What organ metabolizes calcium channel blockers?
liver
87
Calcium channel blockers potentiate the effects of:
neuromuscular blocking drugs and local anesthetic activity
88
What is the common dosing for calcium channel blockers?
usually given as a single bolus or as a continuous infusion

pharmacology 2 (4 decks)

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