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Cardiology > Cardiovascular pharmacology > Flashcards

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
Q

Class IB Lidocaine

A

typically used for numbing - it is injectable

but it is used for MI with constant V tach

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26
Q

Lidocaine CI

A

Liver failure

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27
Q

Lidocaine SE

A

CNS effects of dizziness, paresthesia, disorientation, tremor, agitation, seizures and respiratory arrest

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28
Q

Class IB mexiletine

A

It is a pill

Typically sent on home in place of lidocaine to control their arrythmias

typically for scar-mediated
often a combo drug

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29
Q

Mexiletine SE

A

N/V

major neurologic - same as lidocaine

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30
Q

Class IC Flecainide

A

Slows velocity and widens QRS (not QT)

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31
Q

Indication of Flecainide

A

afib/flutter

heart is completely fine otherwise - NOT for heart with other effects

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32
Q

SE of flecainide

A

Neuro

33
Q

SE of propafenone

A

Same effect as flecanide, but the SE is metallic taste

34
Q

Class II

A

BBs

35
Q

What is the MC used BB

A

metoprolol

not a good anti-HTN, because it does not reduce HR that much

36
Q

What BB do you use IV

A

esmolol because it is short acting

37
Q

Indications of BB

A

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
Q

SE of BB

A

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
Q

What does class III lead to

A

Widen QRS and prolong QT

need to worry about other QT prolonging drugs

40
Q

What psych med can you not be on for class III?

A

Lexipro = no

41
Q

MC class III drug

A

amiodarone

42
Q

MOA of amiodarone

A

Works on ALL cardiac cells, all 4 classes

Primarily a K+ channel blocker

43
Q

Effect of amiodarone

A

Used for anything except slow HR

No negative iontropic effect (can use for low EF)

44
Q

CI of amiodarone

A

NO cardiac contraindications!

45
Q

amiodarone halflife

A

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
Q

SE of amiodarone for pulm

A

Pulm toxicity: annual lung exam (PFT or CXR) to make sure there is no interstitial fibrosis. Stop immediately especially if acute

47
Q

SE of amiodarone for thyroid

A

MC SE = hypothyroidism (because of iodine)

need to scan TSH levels

Hypothyroidism = still stay on
Hyperthyroidism = change

48
Q

SE of amiodarone for eyes

A

Deposits in eyes (only need to stop if it effects visual field or if there is neuropathy/neuritis)

Need annual eye exams

49
Q

SE of amiadaone for GI

A

Livertoxicity

need LFTs

50
Q

SE of amiadaone for neuro

A

tremors, peripheral neuropathy, insomnia

stop if these appear

51
Q

SE of amiadaorone for derm

A

blue/gray

typically men, refuse to wear a hat

sunscreen needs to be on

look like papa smurf

52
Q

DDI for amiadarone

A

Potent CYP 3A4 inhibitor
can raise digoxin
Warfarin

53
Q

Overview of amiadrone

A

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
Q

Sotalol Class III

A

BB properties (not a BB though)

effects contractility

Not something you hold and restart

QT prolongation

55
Q

CI of sotalol

A

Not for LV dysfunction because it decreases contractility

56
Q

When to discontinue sotalol

A

Discontinue if QT interval > 550 ms
Avoid combining with other QT prolonging drugs

57
Q

SE of sotalol

A

BB SE

58
Q

Monitoring of sotalol

A

Need to monitor for QT prolongation before they leave the hosptial (for like 24-48 hours)

59
Q

Dofetilide major concern

A

QT prolongation

other SEs are not

60
Q

Dofetilide monitoring

A

6 doses (2 doses a day) for three days

need to monitor EKG for QT prolongation

61
Q

What can be used for HF

A

dofetilide and amiodarone

62
Q

Dofetilide clearance

A

Renally cleared, so do not use in patients with CrCl < 20 mL/min

63
Q

Dronedarone

A

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
Q

Ibutilide (Corvert) only inditaion

A

Only for afib/flutter cardioversion

can cause tarsades
electrolytes need to be normal

65
Q

2 CCB used for antiarrythmias

A

Verapamil and dilatezam

not for LV dysfunction (HF)

66
Q

Digoxin MOA

A

AV node block by blocking Ca2+ and has cholinergic properties

67
Q

Indication of digoxin

A

slowing the ventricular rate in afib/flutter, as well as terminating reentrant arrhythmias involving the AV node

68
Q

Major EKG changes of digoxin

A

Diffuse PR prolongation and ST segment depression not better explained by LBBB, LVH

leave them on their digoxin

69
Q

Digoxin administeration

A

IV or oral

gut flora helps stop toxicity, so if there is meds that effect flora, there could be toxicity

70
Q

How long does it take to clear dig?

A

36 hour half-life

71
Q

When do you need to lower dose of digoxin?

A

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
Q

Digoxin toxicity

A

Any arrhythmia (which is why it can lead to a paradoxical increased HR)
Orange/yellow vision
GI effects N/V/D

73
Q

Adenosine MOA

A

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
Q

SE of Adenosine

A

Chest discomfort, dyspnea, flushing, and headache

75
Q

Atropine MOA

A

Speeds everything up

parasympatholytic drug that enhances both sinus nodal automaticity and AV nodal conduction through direct vagolytic action

shortens AV node pause

76
Q

Use of atropine

A

SYMPTOMATIC bradycardia

works for a few minutes

they need to be actively DYING

77
Q

If someone becomes tachycardiac with an MI, what do you do with atropine?

A

May worsen it

78
Q

What can Mobitz type II lead to?

A

third degree AVB

Cardiology (22 decks)

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