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Pharm 2 final > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

P wave in EKG

A

first positive deflection

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2
Q

what does P wave represent?

A

atrial depolarization

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3
Q

QRS complex in EKG

A

3 waves in one:

  1. if 1st wave is downward then called Q wave
  2. 1st upward wave is called R wave
  3. if there is a downward wave after R wave, it’s called S wave
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4
Q

what does Q wave represent on EKG?

A

septal depolarization

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5
Q

what does QRS complex on EKG represent?

A

ventricular depolarization and implies contraction

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6
Q

what does T wave on EKG represent?

A

re-polarization of ventricles

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7
Q

you should be aware of T waves that what?

A
  1. deflect downward

2. are tall and pointy

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8
Q

volume-pressure diagram

A
  1. mitral valve opens
  2. end-systolic volume at 50 mL in left ventricle
  3. end-diastolic volume at 120 mL in left ventricle
  4. mitral valve closes (when ventricular pressure > atrial pressure)
  5. isovolumetric contraction
  6. aortic valve opens at 80 mm Hg (b/c ventricular pressure > aortic pressure)
  7. period of ejection
  8. aortic valve closes at 100 mm Hg (b/c aortic pressure > ventricular pressure)
  9. isovolumetric relaxation
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9
Q

period of contraction on volume-pressure diagram

A
  1. ventricular pressure rises as contraction begins
  2. initially the pressure is not sufficient to open aortic valve
  3. no emptying occurs
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10
Q

how much pressure is required to push open aortic valve according to volume-pressure diagram?

A

pressure >80 mm Hg

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11
Q

what percent of blood is ejected in first 1/3 of ejection period on volume-pressure diagram?

A

70%

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12
Q

what percent of blood is ejected in remaining 2/3 of ejection period on volume-pressure diagram?

A

30%

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13
Q

what causes period of relaxation on volume-pressure diagram?

A
  1. ventricles relax quickly
  2. blood in aorta pushes back and closes aortic valve
  3. ventricles continue to relax, but the volume doesn’t change
  4. also when left ventricle is perfused
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14
Q

when is the left ventricle perfused?

A

during isovolumetric relaxation

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15
Q

in what phase does cardiac cell depolarizes?

A

phase 0

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16
Q

what happens to membrane during phase 0 (depolarization)?

A

becomes more positive causes fast Na channels to open and sodium rushes in

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17
Q

what happens when membrane potential reached +20mV in phase 0 (depolarization) of cardiac cell?

A

fast sodium channels close

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18
Q

in what phase does cardiac cell repolarize?

A

phase 1 and 3

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19
Q

what happens after fast sodium channels close in phase 1 (initial repolarization)?

A

cell begins to repolarize and potassium channels open causing potassium ions to flow out

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20
Q

in what phase does cardiac cell plateaus?

A

phase 2

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21
Q

what happens after slow calcium channels open in phase 2 (plateau)?

A

potassium channels remain open

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22
Q

what happens when potassium channels remain open during phase 2 (plateau)?

A

net balance of membrane charge causing repolarization to be temporarily delayed

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23
Q

in what phase of cardiac muscle action potential does slow calcium channels close?

A

phase 3 (rapid repolarization)

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24
Q

what happens after slow calcium channels close during phase 3 (rapid repolarization)?

A

potassium channels stay open and potassium rushes out causing cell to repolarize

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25
Q

phase 4 (resting membrane potential)

A

cell membrane averages -90 mV

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26
Q

Ohm’s law

A

V = I x R

V = voltage
I = current
R = resistance
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27
Q

how is Ohm’s law applied to hemodynamics?

A

P = F x R

P = pressure = mean arterial pressure (MAP)
F = flow = cardiac output (CO)
R = resistance = systemic vascular resistance (SVR)
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28
Q

Ohm’s law and hemodynamics

A

MAP = CO x SVR

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29
Q

how can blood pressure (MAP) be raised?

A
  1. increasing HR
  2. increasing SV
  3. increasing SVR
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30
Q

location of alpha 1 adrenergic receptors

A

vasculature

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31
Q

actions of alpha 1 adrenergic receptors

A

vasoconstriction

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32
Q

locations of alpha 2 adrenergic receptors

A
  1. brain

2. nerves

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33
Q

actions of alpha 2 adrenergic receptors

A
  1. sedation

2. sympathetic inhibitions

34
Q

locations of beta 1 adrenergic receptors

A

heart

35
Q

actions of beta 1 adrenergic receptors

A
  1. inotrophy
  2. chronotropy
  3. dromotropy
36
Q

locations of beta 2 adrenergic receptors

A
  1. lung

2. vasculature

37
Q

actions of beta 2 adrenergic receptors

A
  1. bronchodilation

2. vasodilation

38
Q

effect of alpha adrenergic receptors

A
  1. mydriasis
  2. increase glycogenolysis
  3. decrease insulin secretion
  4. lipolysis
  5. vasoconstriction
39
Q

effect of beta adrenergic receptors

A
  1. bronchodilation
  2. increase inotropy
  3. increase chronotropy
  4. increase automaticity
  5. vasodilation
40
Q

parent compound of catecholamine

A

beta phenylethylamine

41
Q

catechol group consists of what?

A

hydroxyl substitution on #3 and #4 carbons on benzene ring of beta phenylethylamine

42
Q

T/F: drugs that have a catechol group are often called “catecholamines” and are usually vasoactive

A

true

43
Q

effect of hydroxyl substitutions on catecholamine

A

increase beta and alpha activity

44
Q

amine substitutions on catecholamine has what effect?

A

larger substitutions increases beta activity but no or smaller substitution (i.e.-CH3) gives less beta activity

45
Q

effect of side chain distance on catecholamine

A
  1. length increases sympathomimetic activity

2. substitution increases duration of action

46
Q

dopamine is a naturally occurring what?

A

sympathomimetic

47
Q

where is dopamine synthesized?

A

in kidney

48
Q

dopamine bind to which receptors?

A
  1. alpha 1
  2. beta 1
  3. delta 1
49
Q

T/F: dopamine can also be a central neurotransmitter (“feel good” neurotransmitter)

A

true

50
Q

at low levels, dopamine binds to D1 and causes what?

A

increased renal flow

51
Q

at moderate levels, dopamine binds to which receptor?

A

beta 1

52
Q

what happens when dopamine binds to B1 receptor at moderate levels?

A

increases BP and HR

53
Q

at high levels, dopamine binds to which receptor?

A

alpha 1

54
Q

what happens when dopamine binds to a1 receptors at high levels?

A

causes vasoconstriction

55
Q

epinephrine is a naturally occurring what?

A

sympathomimetic

56
Q

epinephrine is synthesized, stored and released by what type of cells in response to what?

A

chromaffin cells in adrenal medulla in response to stress

57
Q

non-selective epinephrine binds to which receptors?

A
  1. alpha 1
  2. beta 1
  3. beta 2
58
Q

effects of non-selective epinephrine

A
  1. vasoconstriction
  2. increased inotropy
  3. increased chronotropy
  4. bronchodilation
  5. mast cell stabilization
59
Q

uses of epinephrine

A
  1. cardiac arrest
  2. anaphylaxis
  3. asthma
60
Q

how much epinephrine should be given to pts under cardiac arrest?

A

1 mg every 3-5 minutes

61
Q

how much epinephrine is given to pedo patients undergoing anaphylaxis?

A

150 mcg

62
Q

how much epinephrine is given to adult patients undergoing anaphylaxis?

A

300 mcg

63
Q

how much epinephrine is given to patients for asthma?

A

11.25 mg nebulized racemic epi

64
Q

norepinephrine is a naturally occurring what?

A

sympathomimetic

65
Q

where is norepinephrine synthesized?

A

adrenal medulla and sympathetic neurons

66
Q

what is the primary post-ganglionic adrenergic neurotransmitter?

A

norepinephrine

67
Q

where does norepinephrine bind predominantly at?

A

alpha 1 but also beta 1

68
Q

effect of norepinephrine

A

causes intense increase in systemic vascular resistance

69
Q

catecholamine synthesis pathway

A

phenylalanine –> L-tyrosine –> L-dopa –> dopamine –> norepinephrine –> epinephrine

70
Q

phenylephrine is a synthetic what?

A

non-catecholamine

71
Q

where does phenylephrine bind?

A

alpha 1

72
Q

effect phenylephrine

A
  1. causes intense vasoconstriction
  2. increase preload and blood pressure
  3. reflex bradycardia (can cause asystole)
73
Q

T/F: phenylephrine must be diluted before use

A

true

74
Q

ephedrine is synthetic what?

A

non-catecholamine

75
Q

where does ephedrine bind?

A
  1. alpha 1
  2. beta 1
  3. beta 2
76
Q

effect of ephedrine

A

tachphylaxis because of norepinephrine depletion

77
Q

when is ephedrine contraindicated?

A

with MAOIs (phenezine/Nardil)

78
Q

digoxin

A

cardiac glycoside

79
Q

effect of digoxin

A

increases contractility by inhibiting Na+K+ATPase which causes increase in intracellular Ca2+

80
Q

what was digoxin traditionally used for?

A

heart failure and ventricular control in patients with a-fib

81
Q

T/F: digoxin has an extremely low therapeutic index and is not used much anymore

A

true

82
Q

signs of digoxin toxicity

A
  1. confusion
  2. vomiting
  3. anorexia
  4. blurry vision
  5. arrhythmias

Pharm 2 final (10 decks)

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