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physio 2 last minute Flashcards

1
Q

When does effective refractory period take place

A

phase 0 to halfway to 3

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2
Q

What happens if you have an AP in relative refractory period

A

v-fib

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3
Q

What do nodal cells NOT have

A

sodium channels

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4
Q

What layer of the heart gets innervated first

A

inner most

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5
Q

Functino of purkinje

A

innervates ventricular mycotes, make sure that they all contract together

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6
Q

Hyperkalium

A

K doesnt want to move out, so the cell is depolarized. funny sodoim channels don’t open as well and HR slows down

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7
Q

How do Ca+ blockers work

A

reduce conduction through AV node, because they don’t have fast sodium channels

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8
Q

P wave

A

depolarization of atrial cells (1-2 small boxes)

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9
Q

QRS

A

depolarization of ventricular cells (3-5 small bozes)

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10
Q

Why does Q wave have a down tick?

A

septal depolarization

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11
Q

T wave

A

ventricule repolarization

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12
Q

PR

A

atrial depolarization to beginning of ventricular depolarization

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13
Q

ST segment

A

plataue phase of ventircular myocytes, ventricular contraction

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14
Q

QT interval

A

all electral events of ventircles

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15
Q

1st degree AV block

A

extra long PR, everthing else is normall

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16
Q

2nd degree AV block

A

p waves w/o QRS

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17
Q

3rd degree AV block

A

QRS without P waes

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18
Q

MI

A

elevated/lengthened ST, larger Q

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19
Q

3 waves in atrial pressure curve

A

A, C, V

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20
Q

C wave casued by

A

AV valves pushed into atria becasue of ventricular contraction

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21
Q

V wave

A

filling of atria, ventricle contraction

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22
Q

Where is the lowest point of veanous pressure

A

vena cava

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23
Q

Where is pulse pressure the fastest

A

arterioles

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24
Q

How do you caclulate SV

A

left end of diastole - left end of systole

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25
Q

s1

A

AV closure, isovolumic contraction

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26
Q

S2

A

semilunar valves, isobolumic relazation

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27
Q

Splitting during inhalation

A

normal

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28
Q

SPlitting during exhalation

A

problem, you are hearing pulmonary first

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29
Q

S3 in baby or old person

A

normal

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30
Q

When are you hearing in S3

A

during rapid filling

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31
Q

When are you hearing S4

A

right before S1

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32
Q

WHat do you innervate during increased force of contraction

A

sympahtetics, secrete epi, bind to beta 1 recetpros, increase Ca++ permeability

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33
Q

What do B1 receptors on SA node do

A

increase rate

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34
Q

isovolumic contraction V/A

A

ventricular contract

atrial relax

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35
Q

rapid ejection V/A

A

ventricular contract

atria relax

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36
Q

reduced ejection V/A

A

ventrciular contract

atrial relax

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37
Q

isobolumic relax V/A

A

venti releax

atrial relex

38
Q

rapid filling V/A

A

ventral relax

atrial releax

39
Q

reduced filling V/A

A

ventircular relax

atrial releax

40
Q

atrial systeol V/A

A

ventrial relax

atrial relax

41
Q

isobolumic contraction valve

A

both closed

42
Q

radid ejection valves

A

AV closed

P./A open

43
Q

reduced ejection valves

A

AV closed

P/A open

44
Q

isovolumic relax valves

A

both clsoed

45
Q

rapid filling valves

A

AV open

P/A cloed

46
Q

reduced filling valves

A

AV open

P/A clsoed

47
Q

atrial systeol vavles

A

AV open

P/A closed

48
Q

isovolumic contraction pressue

A

LV - pressure rising

aorta - pressure falling

49
Q

rapid jection pressure

A

LV - rising

aorta - rising

50
Q

reduced ejection pressure

A

LV -falling

aorta -falling

51
Q

isovolumic relax pressure

A

LV -falling

aorta - falling with uptick

52
Q

rapid filling pressure

A

LV -falling

aorta - falling

53
Q

reudced filling pressure

A

LV -rising

aorta -falling

54
Q

atrail systeol pressure

A

LV - rising

aorta - falling

55
Q

preload

A

how much/ how fast blood comes back to heart

56
Q

agterload

A

aortic pressur

57
Q

What happens when more blood is pumped out by right heart

A

more blood comes into left heart, more gets pumped out

58
Q

changes in contrability are independt of ____

A

volumn

59
Q

increased in contracbility

A

upward shift of afterload curve, increased SV

60
Q

decreased ocntrability

A

downward shift of afterlaod curve, decreased SV

61
Q

How can you get increased mean system filling pressure

A

increased blood volumne, vasoconstrictino, vneous massage

62
Q

What does positive inotrope cause

A

increased force of contraction, SV

63
Q

What happens during exercise

A

LVEDV increased, LVESV decreases, SV increases, CO increases

64
Q

Atrial pressure regulation is ____ of local blood flow or CO controls

A

independt

65
Q

tension

A

change in pressue x radius

66
Q

resistance

A

change in pressure / flow

67
Q

What has higher resistance right or left heart

A

left

68
Q

What contains the highest volume of blood

A

venous circuit

69
Q

What does decrease in O2 cause

A

vasodiliation

70
Q

What does build up of CO2 cause

A

vasodiliation

71
Q

What does build up of adenosine cause

A

vasodiliation

72
Q

What are things that can lead to edema

A

decreased colloid osmotic pressure, icnreased cap hydrostatic, lyumph obstructino, inflammatino in cap wall

73
Q

When is LV perfusion max

A

during diastole

74
Q

Wall tension

A

pressure x radius

75
Q

What are some thigns that can happen w/ bigger heaarts

A

greater radius, greater wall tension, decreased perfusion

76
Q

What is the most frequent place for MI

A

subendocardial arterial plexus

77
Q

What can increased HR cause

A

increased metabolism, hypoxia, increased ATP turnover, increased vasodilaition

78
Q

Vasodilaition

A

inhibits alpha1 recetpros, SANS

79
Q

vasoconstriction

A

activates alpha1 receptors, SANS

80
Q

increase HR

A

activate B1 recetpros

81
Q

decrease HR

A

activate cardioinhibitory center, stimulate vagus, PANS

82
Q

increase contrability

A

activate B1 recetpor, SANS

83
Q

decrease contrabtilibyt

A

activate cardioinhibitory center, stimulate vagus, PANS

84
Q

What are the major determinates of plasma osmotlati

A

Na, CL, HCO3, BUN ,glocuse

85
Q

What is the function of albumin

A

colloid osmotic pressure

86
Q

hydoalbumina

A

decreased osmotic pressue

87
Q

What does TPO stimulate

A

platelt production

88
Q

What does EPO stimulate

A

proudciton of RBCs

89
Q

Steps in erthyopeaus

A

erythroid progenitorys, erythroblasts, immature erythrmocytes, mature RBCs

90
Q

congeital polyctenia

A

VHL gene muated, way too much HIF1alpha, too many RBCs

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