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Cardiovascular pharmacology Flashcards

1
Q

For this lecture, what is important to know

A

You will likely not be using class 1 and 4 - those will be written by cardio

likely not hammered on boards

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2
Q

What does amiadorone cause?

A

Thyrotoxicity

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3
Q

What do drugs change?

A

Action potential

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4
Q

What is the action potential of an SA node

A

Does not have a flat segment that needs repolariztiation

phase 4 sodium INflux
phase 0 Ca++
phase 3 K+ EFflux (brings back to resting potential)

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5
Q

What happens if you block Ca++

A

Slows depolarization because less Ca2+ go in

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6
Q

What happens if you block phase 3

A

Block K+ efflux - meaning that it will take longer to fire again, causing bradycardia

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7
Q

What does an atrium AP look like

A
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8
Q

What cells have a flat resting potential?

A

Myocardial cell, meaning that it needs an impulse.

Na+ block takes it longer to meet threshold

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9
Q

What creates the plataue of a myocardial AP

A

K+ going out and Ca2+ coming in

(want a long squeeze, and then we relax)

blocking these will stretch it out the plateau (know this)

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10
Q

What causes arrythmias?

A

Arrhythmias are caused by abnormal pacemaker activity or abnormal impulse propagation.

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11
Q

What is the aim of arrythmia therapy

A
  1. The aim of therapy of the arrhythmias is to reduce ectopic pacemaker activity and modify conduction or refractoriness in reentry circuits to disable circus movement
  2. Antiarrhythmic drugs decrease the automaticity of ectopic pacemakers more than that of the SA node.

Lower the ability for abnormal pacemakers to fire on it’s own

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12
Q

What is a problem with arrhythmia therapy

A

Can cause blocks if you slow too much

and other cells can take over, and become the pacemakers themselves

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13
Q

What is the overview of how antiarrhtmics work?

A

Phase 4 (works on potassium)
Phase 1 (sodium)
Phase 3 (potaassium going out)

Decrease phase 4 slope
increase threshold
Increase maximum diastolic potential
increase actional potential duration

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14
Q

What are the 4 classes of drugs?

A
  1. class I drugs that block fast sodium channels
  2. those that are beta blockers (class II)
  3. those that block potassium channels (class III)
  4. those that are calcium channel blockers (class IV)
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15
Q

What are the class of CCB we use for arrhythmia

A

non-dihydropyrodine

verapmil
ditalzem

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16
Q

Class I antiarrythmias

A

Ia: quinidine, procainamide, disopyramide

Ib: lidocaine, mexiletine

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17
Q

Class IA MOA

A

prolongs ventricular depolarization and repolarization (prolongs the QT)

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18
Q

Class IB MOA

A

Mild effect

Work better on ischemic tissue (scar-mediated - during a heart attack)

small quick attachment and release - no prolong QT

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19
Q

Class IC MOA

A

Good block with a fast release

Widens QRS (depolarization)
Does not effect plateau and repolarization - so no prolong QT

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20
Q

Qunidine problems

A

QT prolongation
Can lead to Torsades
Works on SA and AV nodes - so you can cause other arrythmias

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21
Q

SE of qunidine

A

N/V/D
CYP3A4

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22
Q

Procainamide

A

Does not have anticholinergic activity of quinidine

for Wide complex SVT if stable
Widens QT
Lupus drug reaction,

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23
Q

Disopyramide use

A

for restrictive cardiomyopathy

negative iontropic property - so it relaxes myocardium

not used for weak hearts

Anticholinergic effects

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24
Q

Do we ever use class Ia?

A

NEVER pretty much

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25
Class IB Lidocaine
typically used for numbing - it is injectable but it is used for MI with constant V tach
26
Lidocaine CI
Liver failure
27
Lidocaine SE
CNS effects of dizziness, paresthesia, disorientation, tremor, agitation, seizures and respiratory arrest
28
Class IB mexiletine
It is a pill Typically sent on home in place of lidocaine to control their arrythmias typically for scar-mediated often a combo drug
29
Mexiletine SE
N/V major neurologic - same as lidocaine
30
Class IC Flecainide
Slows velocity and widens QRS (not QT)
31
Indication of Flecainide
afib/flutter heart is completely fine otherwise - NOT for heart with other effects
32
SE of flecainide
Neuro
33
SE of propafenone
Same effect as flecanide, but the SE is metallic taste
34
Class II
BBs
35
What is the MC used BB
metoprolol not a good anti-HTN, because it does not reduce HR that much
36
What BB do you use IV
esmolol because it is short acting
37
Indications of BB
ventricular dysrhythmias, as well as supraventricular dysrhythmias works on SA node and AV node Low level of efficacy - mainly used to control HR as a whole
38
SE of BB
bradycardia exercise intolerance (because they are not able to increase HR) Dizziness Fatigue Sexual dysfunction (often not for young folks) typically used with others
39
What does class III lead to
Widen QRS and prolong QT need to worry about other QT prolonging drugs
40
What psych med can you not be on for class III?
Lexipro = no
41
MC class III drug
amiodarone
42
MOA of amiodarone
Works on ALL cardiac cells, all 4 classes Primarily a K+ channel blocker
43
Effect of amiodarone
Used for anything except slow HR No negative iontropic effect (can use for low EF)
44
CI of amiodarone
NO cardiac contraindications!
45
amiodarone halflife
LOTS of SE because it has a super long half-life of 28 days because it breaks down and deposits everywhere - takes 10 grams of amiadrone to be therapeutic -need a few weeks to get fully loaded on amiadorone if you wanna switch drugs, you need to be off for at least a month!
46
SE of amiodarone for pulm
Pulm toxicity: annual lung exam (PFT or CXR) to make sure there is no interstitial fibrosis. Stop immediately especially if acute
47
SE of amiodarone for thyroid
MC SE = hypothyroidism (because of iodine) need to scan TSH levels Hypothyroidism = still stay on Hyperthyroidism = change
48
SE of amiodarone for eyes
Deposits in eyes (only need to stop if it effects visual field or if there is neuropathy/neuritis) Need annual eye exams
49
SE of amiadaone for GI
Livertoxicity need LFTs
50
SE of amiadaone for neuro
tremors, peripheral neuropathy, insomnia stop if these appear
51
SE of amiadaorone for derm
blue/gray typically men, refuse to wear a hat sunscreen needs to be on look like papa smurf
52
DDI for amiadarone
Potent CYP 3A4 inhibitor can raise digoxin Warfarin
53
Overview of amiadrone
Works very very well, but TONS of SEs over time good for older patients because they will likely die before the SEs Not good for patient with bad compliance
54
Sotalol Class III
BB properties (not a BB though) effects contractility Not something you hold and restart QT prolongation
55
CI of sotalol
Not for LV dysfunction because it decreases contractility
56
When to discontinue sotalol
Discontinue if QT interval > 550 ms Avoid combining with other QT prolonging drugs
57
SE of sotalol
BB SE
58
Monitoring of sotalol
Need to monitor for QT prolongation before they leave the hosptial (for like 24-48 hours)
59
Dofetilide major concern
QT prolongation other SEs are not
60
Dofetilide monitoring
6 doses (2 doses a day) for three days need to monitor EKG for QT prolongation
61
What can be used for HF
dofetilide and amiodarone
62
Dofetilide clearance
Renally cleared, so do not use in patients with CrCl < 20 mL/min
63
Dronedarone
like amiodarone (does not work as well) not used for Heart failure not used with liver usages bradycardia QT prolongation does not have pulm or thyroid toxicity seen in amiodarone
64
Ibutilide (Corvert) only inditaion
Only for afib/flutter cardioversion can cause tarsades electrolytes need to be normal
65
2 CCB used for antiarrythmias
Verapamil and dilatezam not for LV dysfunction (HF)
66
Digoxin MOA
AV node block by blocking Ca2+ and has cholinergic properties
67
Indication of digoxin
slowing the ventricular rate in afib/flutter, as well as terminating reentrant arrhythmias involving the AV node
68
Major EKG changes of digoxin
Diffuse PR prolongation and ST segment depression not better explained by LBBB, LVH leave them on their digoxin
69
Digoxin administeration
IV or oral gut flora helps stop toxicity, so if there is meds that effect flora, there could be toxicity
70
How long does it take to clear dig?
36 hour half-life
71
When do you need to lower dose of digoxin?
Amiodarone, quinidine, verapamil, diltiazem, itraconazole, propafenone, and flecainide decrease digoxin clearance - so you need lower dose Also renal insufficiency - as it is renally cleared
72
Digoxin toxicity
Any arrhythmia (which is why it can lead to a paradoxical increased HR) Orange/yellow vision GI effects N/V/D
73
Adenosine MOA
Activates potassium Blocks AV node to reset SVTs allows SA node to take over and become the pacemaker short half life (<10 seconds) DOES NOTHING FOR THE ATRIA
74
SE of Adenosine
Chest discomfort, dyspnea, flushing, and headache
75
Atropine MOA
Speeds everything up parasympatholytic drug that enhances both sinus nodal automaticity and AV nodal conduction through direct vagolytic action shortens AV node pause
76
Use of atropine
SYMPTOMATIC bradycardia works for a few minutes they need to be actively DYING
77
If someone becomes tachycardiac with an MI, what do you do with atropine?
May worsen it
78
What can Mobitz type II lead to?
third degree AVB

Cardiology (22 decks)

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