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Pharm test 3 > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

what is arrhythmia?

A

alteration in normal impulse pathway

alteration in transmission pathway

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2
Q

what is an ectopic focus?

A

source of rhythm start

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3
Q

are ventricular alterations life threatening?

A

yes

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4
Q

what are a major cause of sudden cardiac death?

A

ventricular arrhythemias

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5
Q

T/F drug treatment can cause arrhythmias

A

True

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6
Q

T/F non drug treatment is preferable?

A

True

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7
Q

what are some non drug treatments?

A

pacemaker
cadioversion- global depolarization of heart
automatic defibultaor implanted
surgeries to remove ectopic forcus- ablation

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8
Q

class 1 drugs fro arrhythmias are what

A

sodium channel blockers

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9
Q

class 2 drugs for arrhythmias are what

A

beta blockers

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10
Q

class 3 drugs for arrhythmias are what?

A

K channel blockers

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11
Q

how do class 1 work?

A

local anesthetics, decrease rate of depolarization

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12
Q

what are the 1a drugs?

A

qpd
quinidine
procainamide
disopyramide

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13
Q

quinidine

A

for ALL arrhythmias, depresses all muscle function

- anticholinergic effects (antivagel)

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14
Q

quinidine SE

A

GI- nausea, vomitting, anorexea

CNS- tinnitus, alteration in color/vision

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15
Q

procainamide

A

like quinidine. analog of cocain. does NOT enter CNS

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16
Q

procainamide

A

in slow acetylators, lupus like syndromes

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17
Q

disopyramide

A

strong antivegal effect

- antimuscarinic effects- dry mouth, constipation

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18
Q

1b drugs for arrhythmias

A

lidocaine

mexiletine

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19
Q

lidocaine

A

give IV, 1st pass metal.

- less likely to cause arrhythmias but can enter CNS, tremors, seizures

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20
Q

what is a good use of lidocaine?

A

use for treating ventricular tachcardia (fast heart beat)

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21
Q

mexiletine

A

like lidocaine but given orally. `

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22
Q

class 2 works how?

A

blocks beta 1 receptors on heart. slows HR

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23
Q

class 2 drugs

A

propranolol
metoprolol
esmolol

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24
Q

class 2 SE

A

bradycardia

hypotension

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25
Q

propranolol

A

decrease firing rate

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26
Q

metoprolol

A

more selective, less B2 effects

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27
Q

esmolol

A

more rapid onset of action

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28
Q

class 3 drugs

A

sotalol
amiodarone
dronedarone

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29
Q

sotalol

A

Beta blocker that also blocks K channels

30
Q

amiodarone

A

ultimate drug!
acts like all 4 classes of antiarrhythmias
most effective in cardiac arrest

31
Q

SE of amiodarone

A

Potentially fatal pulmonary fibrosis- alters lung tissue
liver damage
deposits in cornea and skin (cuz of iodine, blue/gray skin)
GI upset

32
Q

dronedarone

A

fewer SE, less efficacy, analog of amiodarone

33
Q

class 4 drugs are what

A

calcium channel blockers

34
Q

class 4 drugs

A

verapamil
nifedipine
diltiazem

35
Q

all Ca channel blockers work how?

A

blocks Ca transport in cardiac cells

increases refractory period

36
Q

class 4’s are not useful for what?

A

ventricular arrhythmias, they are also vasodilator

37
Q

“other” drugs for arrhythmias

A

adenosine

38
Q

adenosine

A

IV, binds to adenosine receptor, decrease firing rate of AV node. very short half-life.

39
Q

Angina

A

not enough blood flow to heart muscle, chest pain, usually after exercise, at rest its called “unstable angina”

40
Q

treatment of angina?

A

increase bloodflow to heart, decrease O2 demand.

41
Q

basic treatment of angina?

A

behavioral, diet, exercise, stop smoking.

42
Q

Drugs to treat angina?

A

nitrates
nitroglycerin
isosorbide dinitrate

43
Q

nitroglycerin

A

sublingually. rapidly dilates all blood vessels, including coronary arteries

44
Q

mechanism of nitro.

A

activates NO which activates guanylate cyclase which activates cGMP which causes vasodilation

45
Q

SE of nitro

A

hypotension, skin flossing, headache.

46
Q

one big problem of taking a lot of nitroglycerin?

A

rapid tolerance.

47
Q

what is another nitrate used for angina?

A

isosorbide dinitrate

48
Q

isosorbide dinitrate

A

slow release nitrate formulation. can be given orally.

49
Q

other angents used for angina

A
  • agents that decrease heart work
  • beta blockers
  • calcium channel blockers
50
Q

what is congestive heart failure?

A

heart doesn’t contract enough, rest of body doesn’t get enough blood flow.

  • tissue not oxygenated blood.
  • heart begins to enlarge which causes…
  • pulmonary congestion…which causes
  • decrease ability to breath and kidney not well perfused
  • kidney causes retention of sodium ions + H20- edema
51
Q

why is it called CONGESTIVE heart failure?

A

lots of fluid retention- pitting edema if not treated.

52
Q

how does the heart adapt to failure?

A
  1. apparent loss of blood- increase in E and NE and All.
    leads to increase BP, HR, and vasoconstriction
  2. increase blood volume- All, increase sodium retention, increase aldosterone secretion, increase sodium potassium exchanger.
  3. enlargement of heart- Incrase force of contraction due to stretching of cardiac muscle
53
Q

why are these compensations so dangerous?

A

are what actually is damaging the heart. its a cycle, heart can’t repair itself

54
Q

two basics treatments of cardiac insufficiency

A
  1. incrase force of muscle contraction

2. inotropic agents

55
Q

how do inotropic agents work?

A

all increase amount of calcium in heart muscle

56
Q

cardiac glycosides are naturally occurring? T/F

A

True, found in plants

57
Q

main cardiac glycosides

A

digoxin, given orally

58
Q

mechanism of action of digoxin?

A

all about Calcium
Digoxin inhibits the sodium potassium ATPase….Na remains high in the cell…meaning that Ca will not be exchanged as much…Ca will be high in the cell leading to greater contractility and also increase duration of contraction.

59
Q

in order for muscle to relax what must be removed

A

calcium

60
Q

toxic effects of digoxin

A
  1. cardiac arrhythmias- cuz you prolong contractility

2. CNS- yellow/green vision, hallucinations, severe nausea cuz chemoreceptors activated

61
Q

digoxin poisiing cured by what?

A

anti digtoxin antibodies

62
Q

digoxin has greater effects in someone who is

A

hypokalemia

63
Q

other inotropic agents?

A

dobutamine- beta 1 agonist- incrase force of contraction

64
Q

current best treatment of CHF

A
  1. ACE inhibitors. decrease BP, fluid retention
  2. Beta blockers. decrease fluid retention
  3. vasodilators. decrease BP
65
Q

what do all these drugs have in common?

A

agents that inhibit bodies compensatory changes in heart failure. (don’t want heart to work as hard)

66
Q

agents that increase blood flow to certain organs

A

vardenafil
avanafil
tadalafil
sildenafil

67
Q

the -nafils do what?

A

inhibit type V cGMP phosphodiesterase, leads to more smooth muscle relaxation instead of cGMP getting broken down

68
Q

SE of these drugs

A
  • slight decrease in BP
  • do not use with alpha blockers or nitrates- major BP drop
  • stroke, heart attack
  • impaired blue green color
  • NAION- damage to retina
69
Q

what are these drugs also useful for?

A

pulmonary hypertension- pulmonary artery also has cGMP PDE that can be inhibited.

70
Q

alprostadil

A

injectable prostaglindin E1 PGE1, causes vasodilation when injected dirtily into penis

Pharm test 3 (4 decks)

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