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Cardiopulmonary > Midterm > Flashcards

Midterm Flashcards

1
Q

Aorta is derived from what embryonic structure

A

truncus arteriosus

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2
Q

pulmonary trunk is derived from what embryonic structure

A

truncus arteriosus

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3
Q

smooth part of R and left ventricle (concus cordis and aortic vestibule) are derived from what embryonic structure

A

bulbus cordis

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4
Q

L and R atrium are derived from

A

primitive atrium

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5
Q

smooth part of RA and oblique v. of L. atrium are derived from

A

sinus venous

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6
Q

where is M2 receptor found, G subunit and mechanism?

A

heart, Gi, decreased cAMP, increased K

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7
Q

Where is m3 found, g subunit, and mechanism

A

everywhere, Gq, increased ip3 and DAG

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8
Q

m4 found where? g subunit and mechanism

A

neurons, Gi, decreased cAMP, decreased ACh release

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9
Q

Alpha post ganglionic adrenergic affinity NE or EPI

A

NE>epi

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10
Q

Beta post ganglionic adrenergic affinity-NE or EPI

A

epi>NE

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11
Q

Alpha 1 g subunit

A

Gq

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12
Q

Alpha 2 G subunit

A

Gi

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13
Q

Beta 1-3 G subunit

A

Gs

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14
Q

Eyes sympathetic response-m. and receptor too

A

dilate
radial muscle-contracts-alpha 1, dilate pupil
ciliary muscle-relax and flatten- beta- allow distance vision

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15
Q

Cardiovascular sympathetic receptors

A

beta1> beta2

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16
Q

vasculature adrenergic receptors

A

alpha 1-vasoconstrict and send blood away

beta 2-dilate and increase blood flow

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17
Q

pulmonary adrenergic receptors

A

bronchodilation-beta 2

secretions- beta-2 humidify more air, alpha 1- decrease secretions

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18
Q

Gi tract sympathetic recptors

A

alpha 1- increase sphincter tone
alpha 1 and beta- decrease motility
alpha 2- decrease secretions

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19
Q

liver sympathetic response

A

alpha 1 and beta 2 to increase glucose release

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20
Q

adipose tissue sympathetic response

A

alpha1, beta 1, and beta 3 to increase FFA release

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21
Q

male sex organs sympathetic response

A

alpha- ejaculation

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22
Q

eyes parasympathetic resposne

A

M- activate sphincter muscle of eye- constrict pupil

M- contraction ciliary muscle muscle of lens-near vision

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23
Q

heart PS response

A

M2- decrease rate

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24
Q

smooth muscle PS receptor

A

M3-vasodilation except for abdominal viscera, kidneys and veins

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25
Q

lungs PS response

A

M3- bronchial SM contraction and gland secretion

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26
Q

digestive organs PS response

A

m3- increase motility, secretion and relax sphincter

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27
Q

male sex organs PS response

A

M-erection

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28
Q

urinary system PS response

A

m3-micturition

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29
Q

Smooth muscle has what receptors

A

mACHRs and adrenergic

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30
Q

ACh does what to SM

A

gut SM m. contraction, relaxation in other tissues

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31
Q

NE/epi does what to SM

A

vascular SM contraction, gut SM relaxation

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32
Q

NO does what to SM

A

inhibits SM

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33
Q

PKA is activated through what G protein and does what to SM

A

Gs, blocks myosin light chain kinase it results in inhibition of contraction (decreased cross bridge cycling)

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34
Q

Skeletal muscle Organization, innvervation, NTs, Action of NTs, mode of transmission and NT receptors

A

Thick/thin filaments organized, alpha-motorneuron, ACh, Excitatory only, Specialized NMJ, nAChRs at motor end plate

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35
Q

Smooth muscle Organization, innvervation, NTs, Action of NTs, mode of transmission and NT receptors

A

Thick/thin filaments randomly arranged, intrinsic and ANS innervation, NTs=ACh, NE/epi, NO, Excitatory or inhibitory, uses varicosities with no motor end plate, Multiple receptors located over cell membrane

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36
Q

What is Thrombopoietin, where is it from and where does it bind

A

From liver, stimulates megakaryocytes to make platelets and binds MPL receptor

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37
Q

What do platelets contain

A 
Mitochondria
Actin
Myosin
Cox1 
Vesicles-contain serotonin
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38
Q

5 steps of hemostasis

A

Vascular spasm, Platelet plug, Blood clotting, repair and removal

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39
Q

Describe vascular spasm

A

platelets release serotonin which vasoconstricts

also release thromboxane A2 which is a prostaglandin that increases IP3 of SM, which leads to inc Ca++

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40
Q

Describe platelet plug

A

Vascular damage leads to collagen being exposed and binding/activating receptors on platelets

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41
Q

Platelet and collagen are held together via

A

Von willebrand factor and is associated with collagen type 6, collagen also binds to integrin to platelet membrane

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42
Q

What does an activated platelet do in platelet plug

A

swells, extends podocytes
then contracts, releases calcium, actin and myosin interact to squeeze out granules
ADP and thromboxane A2 are release which attracts other platelets
*may be sufficent to stop bleeding

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43
Q

Decribe clot retraction

A

requires platelets, which bind fibrin and contract to pull fibrin closer together,
also requires calcium and the final product squeezes liquid out which solidifies clot

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44
Q

what happens during repair of damage?

A

PDGF released by platelets which stimulates fibroblasts to repair

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45
Q

Describe clot removal

A

Plasmin is an enzyme that digests fibrin
Plasminogen is inactive form of plasmin, made by liver, found in blood
tPA activates plasminogen-plasmin
tPA is released by damaged tissue
Delayed activation due to tPA inhibitor in blood… so you won’t actually start using tPA until the blood goes away/the damage is healed
*Protein C inactivates tPA inhibitor

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46
Q

How do endothelial factors within blood vessel prevent clots?

A

Smooth surface of vessel makes it harder for platelets to grab on
Membrane proteins on endothelial cells such as Glycocalyx repels platelets and clotting factors. Thrombomodulin inhibits thrombin and leads to protein C activation

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47
Q

How does Prostacyclin/PGI2 prevent clots?

A

It is made near the injury and causes vasodilation, which prevents agregation

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48
Q

How dose antithrombin III prevents clots?

A

anticoagulant, binds and inhibits thrombin

*Heparin: increases antithrombin efficacy-Heparin is from mast cells

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49
Q

What is happening in a systolic murmur?

A

Systolic: between S1 and S2
Mitral/tricuspid regurg: blood moving back into atria when AV valve should be closed
Aortic/pulmonic stenosis: hard to push blood out

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50
Q

What is happening in a diastolic murmur?

A

Diastolic: between S2 and S1
Mitral/tricuspid stenosis: hard to push blood through into
ventricle
Aortic/pulmonic regurg: blood moving back into ventricle when these valves should be closed

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51
Q

Define preload

A

end diastolic volume or right atrial pressure

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52
Q

define afterload

A

aortic/pulmonary a. pressure

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53
Q

what is frank starling relationship

A

increased preload=increase ventricular fiber length= increased tension and CO

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54
Q

Increased preload leads to what

A

increased SV and wider loop on chart

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55
Q

increased afterload leads to what

A

increased aortic pressure, decreased SV, higher LV pressure

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56
Q

increased contractility leads to what

A

greater tension during systole, which means higher SV, dec end systolic volume and higher LV pressure

57
Q

increased TPR leads to what

A

decreased CO and decreased venous return for certain RA pressure

58
Q

positive inotropy leads to what

A

increase CO and decrease RA pressure

59
Q

phase 0 of ventricles, atria and purkinje myocytes

A

inward Na current and depolarization

60
Q

phase 1 of ventricles, atria and purkinje myocytes

A

outward K current +
decreased inward Na current
rapid repolarization

61
Q

phase 2 of ventricles, atria and purkinje myocytes

A

inward Ca current +(slow ca++ channels open)
increased outward K current(via calcium activated potassium channels, although closing of special, voltage gated K channel)
plateau

62
Q

phase 3 of ventricles, atria and purkinje myocytes

A

decreased inward Ca current (ca channels close)
increased outward K current (special K channels open)
repolarization

63
Q

phase 4 of ventricles, atria and purkinje myocytes

A

inward and outward K
currents are equal
RMP

64
Q

Phase 4 of SA/AV node

A

inward Na current (“funny current,” activated by
repolarization from preceding AP)
slow depolarization

65
Q

Phase 0 of SA/AV node

A

inward Ca current (opening of slow ca++ gates), closing of special K gates
depolarization

66
Q

Phase 3 of SA/AV node

A

outward K current (opening special K+ gates)
closing of ca++ gates
repolarization

67
Q

define inotropy

A

how hard the cardiac muscle contracts,
based off [intracellular Ca]
*Ejection fraction

68
Q

define chronotropy

A

Chronotropy: how fast the cardiac muscle contracts,
based off firing rate of SA node
HR, length of phase 4 depolarization

69
Q

define dromotropy

A

Dromotropy: the conduction velocity through the AV

node (PR interval)

70
Q

What is happening in P wave, PR interval, QRS, T wave, QT interval and ST segment? and what phase is each one?

A

P wave: atrial depolarization (phase 0 atrial m.)
PR interval: depends on conduction velocity through AV
node
QRS complex: ventricular depolarization (phase 0 ventricles)
T wave: ventricular repolarization (phase 3 ventricles)
QT interval: entire period of depolarization and
repolarization of ventricles (includes Q, R, S, T waves)
ST segment: period of ventricular depolarization (stops
right before T wave)

71
Q

phase 0 of ventricles, atria and purkinje myocytes

A

inward Na current and depolarization

72
Q

phase 1 of ventricles, atria and purkinje myocytes

A

outward K current +
decreased inward Na current
rapid repolarization

73
Q

phase 2 of ventricles, atria and purkinje myocytes

A

inward Ca current +
increased outward K current
plateau

74
Q

phase 3 of ventricles, atria and purkinje myocytes

A

decreased inward Ca current
increased outward K current
repolarization

75
Q

phase 4 of ventricles, atria and purkinje myocytes

A

inward and outward K
currents are equal
RMP

76
Q

st depression means

A

subendocardial problem- ischemia has not made it all the way through the wall, just endocardium

77
Q

Phase 0 of SA/AV node

A

inward Ca current

depolarization

78
Q

Phase 3 of SA/AV node

A

outward K current

repolarization

79
Q

define inotropy

A

how hard the cardiac muscle contracts,
based off [intracellular Ca]
*Ejection fraction

80
Q

define chronotropy

A

Chronotropy: how fast the cardiac muscle contracts,
based off firing rate of SA node
HR, length of phase 4 depolarization

81
Q

how to measure turbulence

A

reynolds number= densitydiametervelocity/ viscosity

if greater than 2000 then turbulent (bruits and arteriosclerosis)

82
Q

What is happening in P wave, PR interval, QRS, T wave, QT interval and ST segment?

A

P wave: atrial depolarization
PR interval: depends on conduction velocity through AV
node
QRS complex: ventricular depolarization
T wave: ventricular repolarization
QT interval: entire period of depolarization and
repolarization of ventricles (includes Q, R, S, T waves)
ST segment: period of ventricular depolarization (stops
right before T wave)

83
Q

definition for compliance

A

Compliance= change in V/ Change in pressure

84
Q

Septal leads are

A

V1 and V2

85
Q

how is atrial pressure calculated

A

pulmonary wedge pressure

catheter measures pressure in pulmonary a (slightly overestimates)

86
Q

lateral leads are? and look at what coronary artery?

A

I, aVL, V4, V5, V6 (l circumflex)

87
Q

starling forces pushing fluid out are

A

capillary hydrostatic pressure +interstitial oncotic pressure = Pc + πi

88
Q

st depression means

A

subendocardial problem- ischemia has not made it all the way through the wall, just endocardium

89
Q

equation for blood flow

A 
Velocity= flow rate (Q)/ area (cm)
Q= pressure gradient/ resistance
90
Q

equation for cardiac output

A 
CO= SV x HR
CO= (arterial-venous pressure)/ TPR
91
Q

When muscles contract and temporarily compress arteries, the increased flow after relaxation is called

A

reactive hyperemia

92
Q

Equation for resistance

A

R= (8n(viscosity)length)/ pir^4

93
Q

how to measure turbulence

A

reynolds number= densitydiametervelocity/ viscosity

if greater than 2000 then turbulent (bruits and arteriosclerosis)

94
Q

define shear

A

the difference in velocities of adjacent layers of blood, shear is higher at periphery because greatest difference of blood velocity of adjacent layers

95
Q

definition for compliance

A

Compliance= change in V/ Change in pressure

96
Q

Mean arterial pressure is calculated how

A

diastolic + 1/3 pulse pressure

97
Q

how is atrial pressure calculated

A

pulmonary wedge pressure

catheter measures pressure in pulmonary a (slightly overestimates)

98
Q

Starling forces keeping fluid in are

A

capillary oncotic pressure +interstitial hydrostatic pressure = πc + Pi

99
Q

starling forces pushing fluid out are

A

capillary hydrostatic pressure +interstitial oncotic pressure = Pc + πi

100
Q

what does histamine and bradykinin do

A

arteriolar dilation,venous constriction

it is released in response to tissue damage and increases capillary porosity. This can cause edema

101
Q

what does serotonin do to blood vessels

A

arteriolar vasoconstriction

102
Q

what do lactate, adenosine and inc K do to skeletal muscle

A

local vasodilation (active hyperemia)

103
Q

When muscles contract and temporarily compress arteries, the increased flow after relaxation is called

A

reactive hyperemia

104
Q

Name all the things angiotensin II does

A

aldosterone secretion by adrenal cortex leads to increased Na reabsorption and H2O follows
increases Na/H exchange in PCT in kidney-H2O follows
increases thirst-increased H2O intake
vasoconstriction of arterioles
stimulates ADH secretion from posterior pituitary-fluid retention +vasoconstriction

105
Q

anterior leads are

A

v3-4

106
Q

inferior leads are

A

2,3, avf

107
Q

blood islands are first seen _____

A

in the Yolk sac

108
Q

Blood islands arise from ___ and are induced to become___

A

mesoderm cells, hemangioblasts

109
Q

what binds to mesenchymal cells to form hemangioblasts

A

FGF2

110
Q

central cells become

A

HSC

111
Q

peripheral cells become

A

angioblasts-endothelium of blood vessels

112
Q

what arterial systems have only alpha receptors

A

skin and mucosa, salivary glands, and brain

113
Q

Erythropoietin source, trigger for release, control of hormone, receptor, cells expression receptors and effect

A

kidney, low o2 to kidney, HIF accumulation in renal cell, receptor is EPoR, pluripotent stem cells and RBC precursors, increased erythroid division

114
Q

thrombopoiesis source, trigger for release, control of hormone, receptor, cells expression receptors and effect

A

liver and possibly others, constitutive release, controled by internalization of TPO by plateltes, MPL is receptor, Platelets and Hematopoietic cell lines express receptor and it increases ALL blood cell lineages.

115
Q

blood coagulation 3 steps

A

formation of prothrombin activator
activation of thrombin
creation of fibrin from fibrinogen

116
Q

binding of thrombin to thrombomodulin activates ___?

____ can then inactive _____?

A

protein C, which can then inactive the plasmin inhibitor

117
Q

what does primary heart field form

A

form left and right side

Atria, Left ventricle, and PART of right ventricle

118
Q

secondary heart field forms

A

form remainder of right ventricle and outflow tract (consisting of conus cordis & truncus arteriosus)

119
Q

where are timed k gates opening in the ventricles-atria

A

t wave

120
Q

P WAVE ECG Characteristics

A

upright in 1,2 v4-6, AVF,
inverted in AVR
all others are variable

121
Q

wolff parkinson white is

A

ventricular preexcitation syndrome

122
Q

qrs duration, q duration and see 1-2 mm in which leads

A

.05-.11, .03, normal in 1 AVL, AVF, v5-6

123
Q

t wave shape, height and leads seen in

A

1,2, v3-6, inverted in AVR
shape is slightly round and asymmetrical
heigh is not greater than 5 mm in standard leads and not greater than 10 mm in precordial leads

124
Q

qrs greater than .12 sec

A

BBB

125
Q

CUSHING REACTION

A

hypertension because of intracranial pressure too low and body tries to compensate

126
Q

where do you see stemi

A

v2-v3 J point greater than 2mm (1.5 woman), or 1mm in 2 or more contiguous leads

127
Q

describe nstemi

A

st segment depression, t wave inversion, chest pain and elevated cardiac enzymes

128
Q

Zones of infarction- you see infarction, injury and ischemia at what respective waves/segments

A

infarction-q
injury-st segment shifts
ischemia- t wave changes

129
Q

MI LAD- Area and leads

A

Anterior wall infarction v1-7

130
Q

MI RCA- area and leads are

A

inferior wall infarction, 2,3,AVF

131
Q

MI circumflex artery

A

Lateral wall, 1, AVL v5-6

132
Q

posterior descending

A

posterior wall infarction v1-3

133
Q

ekg first several hours post MI

A

T wave peak

134
Q

EKG first day after MI

A

St elevation marked and r wave amplitude diminshing

135
Q

EKG 2nd day after MI

A

R wave nearly gone, T wave inversion, St elevation may decrease and significant q wave

136
Q

EKG after 2/3 days

A

No r wave, Deep t wave inversion, marked q wave, st may be at baseline

137
Q

EKG weeks post MI

A

some r wave may return, t wave less inverted, st elevation may persist in aneurysm develops and q wave persists

138
Q

lab values post MI

A

WBC increased 12-15000 hours to 2-4 days after

CRP increased and BNP increased because of ventricular wall stress and fluid overload

139
Q

Caridac biomarkers of necrosis

A 
troponin I (cTnI) or T
1-4 hours s/p MI
10-24 hours peak
persists for 5-14 days
renal failure may give false positive

Cardiopulmonary (8 decks)

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