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Pharmacology Exam 3 > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

what is the normal heart rhymthm?

A

SA node (pacemaker)-> atrial muscle-> av node-> ventricles

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2
Q

what is arrhythmia?

A

alteration in the normal impulse pathway
alteration in the pacemaker
ectopic focus is source of rhythm start
alteration in the transmission pathway
ventricular fibrillation is lifethreatening
ventricular arrhythmias are the major cause of cardiac death

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3
Q

what is the electrophysiology of cardiac cell

A

Na2+ influx, Ca2+ influx, K+ efflux

recovery

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4
Q

what are some non-drug treatments of arrhythmia?

A

no treatment
non drug treatment is preferable
pacemaker implantation
cardioversion- global depolarization of heart
automatic defibrillator implanted
surgical removal of ectopic focus- ablation

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5
Q

what are the class 1 drugs?

A

sodium channel blockers
local anesthetics
decrease rate of depolarization

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6
Q

which drugs are in 1a?

A

quinidine, procainamide, disopyramide

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7
Q

tell me about quinidine

A 
sodium channel blocker class 1a
for all arrythmias 
depresses all muscle function
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8
Q

what are the side effects of quinidine?

A 
anticholinergic effects (antivagal effects)
GI- nausea, vomiting
naus
anorexia
CNS- tinnitus, altered color vision
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9
Q

tell me about procainamide

A 
sodium channel blocker class 1a
like quinidine
does not enter the cns
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10
Q

what are the side effects of procainamide?

A

lupus like syndrome in slow acetylators

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11
Q

tell me about disopyramide

A

sodium channel blocker class 1a

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12
Q

what are the side effects of disopyramide?

A

antimuscarinic effect

strong antivagal effects

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13
Q

what drugs are in 1b?

A

lidocaine

mexiletine

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14
Q

tell me about lidocaine

A

sodium channel blocker class 1b
given IV- first pass effect
less likely to cause arrhythmias
useful for treating ventricular tachycardia

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15
Q

side effects of lidocaine

A

can enter cns- tumors, seizures

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16
Q

tell me about mexiletine

A 
sodium channel blocker class 1b
like lidocaine but can be given orally
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17
Q

what are the class 2 drugs?

A

beta blockers
block b1 receptors in the heart
effectively slows heart rate
propranolol, metoprolol, esmolol

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18
Q

propranolol

A

decrease pacemaker firing rate

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19
Q

metoprolol

A

more selective- less B2 effects

selective B1

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20
Q

esmolol

A

more rapid onset of action

selective B1

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21
Q

side effects of class 2

A

brady cardia
hypotension
b2 effects (propranolol)-asthma

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22
Q

what are the class 3 drugs?

A

potassium channel blockers
sotalol
amiodarone
dronedarone

23
Q

tell me about sotalol

A

potassium channel blocker

beta blocker that also blocks potassium channels

24
Q

tell me about amiodarone

A

potassium channel blocker
acts like all 4 classes of antiarrhythmia
most effective antiarrhythmic
DOC in cases of cardiac arrest

25
Q

side effects of amiodarone

A 
potentially fatal pulmonary fibrosis
liver damage
corneal deposits- optic neuritis
deposition in skin-- causes blue grey skin coloration
gi upset
26
Q

tell me about dronedarone

A

potassium channel blocker
analog of amiodarone
fewer side effects, less efficacy

27
Q

what are the class 4 drugs

A

calcium channel blockers
verapamil
diltiazem
nifedipine

28
Q

verapamil
diltiazem
nifedipine

A

calcium channel blocker
block calcium transport in cardiac cells
increase refractory period
useful for all but ventricular arrhythmia

29
Q

tell me about adenosine

A 
given iv
binds to an adenosine receptor and decreases firing rate of av node
very short half life
for atrial tachycardia
coronary vasodilator
30
Q

definition of angina

A

not enough blood flow to heart muscle
chest pain
usually after exercise- if at rest, then it’s unstable angina
treatment by increase blood flow to the heart or decrease oxygen demand

31
Q

behavioral treatment of angina

A

exercise- develop collateral circulation

32
Q

what are the nitrates?

A 
glyceryl trinitrate (nitroglycerin)
isosorbide dinitrate
33
Q

tell me about glyceryl trinitrate (nitroglycerin)

A

generally given sublingual
treatment of angina
rapidly dilates all blood vessels (including coronary artery)
GTN->nitric oxide->activates guanylate cyclase->cGMP-> vascular dilation
can develop rapid tolerance to nitric oxide

34
Q

side effects of nitroglycerin

A

hypotension
skin flushing
headache

35
Q

tell me about isosorbide dinitrate

A

treatment of angina

slow release nitrate formulation- can be given orally

36
Q

what are the other agents used in treament about angina?

A

use agents that decrease heart work
beta blockers- olols
calcium channel blocker- ipine

37
Q

congestive heart failure definition

A

heart muscle doesn’t contract strongly enough
blood doesn’t leave heart fast enough
tissue doesn’t get enough oxygenated blood
heart begins to enlarge-> pulmonary congestion
decrease ability to breathe
kidney is not well perfused
kidney causes retention of sodium ions and fluid- peripheral edema

38
Q

what are the causes of congestive heart failure?

A

cardiac damage

39
Q

how does the heart adapts to congestive heart failure?

A

Apparent loss of blood because tissues are underperfused thus release of epinephrine, NE, Angiotensin II
Increase BP, increase HR, vasoconstriction
Increase blood volume→ Angiotensin II→ increase sodium retention→increase aldosterone secretion→ increase Na+ — K+exchange (increase Na+)
Enlargement of heart- increase force of contraction due to stretching of cardiac muscle
Heart works harder
These compensation actually damage the heart

40
Q

treatment of cardiac insufficiency

A

increase cardiac muscle contractility (inotropic agents- increase amount of calcium in the heart muscle)

41
Q

digoxin

A

cardiac glycoside

42
Q

digoxin mechanism of action

A

All about Ca2+
In order for muscle to relax after contraction, calcium must be removed
Digoxin inhibit the Na+/K+ ATPase
Na+ remains in cell, this prevents the loss of calcium (Na+/Ca2+ exchanger)- net result- Ca2+ remains high in system
Greater Ca2+→greater contractility

43
Q

SE of digoxin

A

Cardiac arrhythmia
CNS effects: yellow green tinting of vision
Hallucinations: activation of chemoreceptor trigger zone→severe nausea

44
Q

effects of digoxin is greatly enhanced in what individuals?

A

hypokalemic (low k+)

45
Q

what is digoxin poisoning treated with?

A

anti-digoxin antibody

46
Q

what other inotropic agents are used to treat congestive heart failure

A

dobutamine

47
Q

what is dobutamine

A

beta 1 agonist

strong inotropic effect- increase force of contraction

48
Q

current best treatment of congestive heart failure

A 
ace inhibitors
beta blockers
vasodilators
diuretics
want to decrease BP, decrease fluid retention,
decrease heart rate
49
Q

what are the agents that increase blood flow to selected organs?

A

Sildenafil
Vardenafil
Tadalafil
Avanafil

50
Q

how do the afils work?

A

Inhibitors of types of cGMP phosphodiesterase
Nitrates→ NO→ increase cGMP→smooth muscle relaxation
cGMP is broken down into 5’GMP by type 5 phosphodiesterase

51
Q

side effects of afils

A

Metabolized by p450→ drug interactions
Stroke, myocardial infraction
Visual disturbances- impaired blue/green color discrimination
NAION- some potential for damage to the retina induced by cGMP phosphodiesterase inhibitors

52
Q

cautions of using afils

A

Slight dec BP

Do not use with alpha 1 blockers or nitrates→ dramatic decrease in BP

53
Q

what else is afils useful for?

A

Useful for treatment of pulmonary hypertension

54
Q

what is alprostadil?

A

another agent for increase blood flow to selective organs

ingestable pge1- vasodilation- when injected directly into penis- lead to erection

Pharmacology Exam 3 (4 decks)

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