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B3 Clinical Application > B3 Ibe CPR > Flashcards

B3 Ibe CPR Flashcards

1
Q

medicines block Ca2+ channels in myocardial action potentials

A

Nitrendipine, nimodipine, nifedipine
bind DHPR
Class of calcium blocking so block muscle contracation

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2
Q

t tubule in cardiac contraction

A

large ca stores (diameter 5x)
mucopolysacchardies bind calcium ions

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3
Q

increasing dose of caclium channel blockers

A

decreases impulse conduction
decrease in contraction

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4
Q

hyperkalemia

A

raise rest potential
promote K+ efflux
reduce conduction velocity
decrease rate of phase 0

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5
Q

hypokalemia

A

lower rest potential
reduce K+ efflux (excess in cell)
take longer get back to resting potential (longer 3)

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6
Q

acetylcholine effect phase 4 nodal contraction

A

decrease rate of diastolic depolarization
decrease HR

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7
Q

catecholamine effect phase 4 nodal contraction

A

increase depolarization
increase HR

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8
Q

sympathetic stimulation phase 4 nodal contract

A

increase chance funny channel open
increase HR

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9
Q

refractoriness determinant of

A

susceptibility to arrythmias
facilitate reentry & arrythmia

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10
Q

prevent tetany in cardiac

A

refeactory period
allow heart chamber time refill

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11
Q

slow action potential locations

A

SA node
AV node

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12
Q

fast action potential locations

A

atrial myocyte, ventricular myocyte, purkinje, bundle His

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13
Q

positive dromotropic

A

increase in conduction velocity
increase Ca vis SNS

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14
Q

negative dromotropic

A

decrease conduction velocity
decrease Ca, Increase K via PNS

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15
Q

cause of heart block via conduction velocity

A

increase PNS
damage to AV node

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16
Q

Stokes Adams syndrome

A

delaay in pickup heartbeat
5-20s lack blood to brain
delay in HR = syncope

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17
Q

specialized excitatory/conductive tissue

A

nodal pacemakers
automaticity
own contraction
excitatorymsystem control HR

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18
Q

distribution of blood in body determine by

A

output L ventricle
contractile state of arterioles

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19
Q

where are greatest pressure drop

A

arterioles

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20
Q

max resistance location

A

arterioles

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21
Q

receptors in arterioles

A

alpha 1
beta 2

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22
Q

receptors venules/veins

A

alpha 1

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23
Q

vein resevoirs

A

spleen, liver, large ab veins, venous plexus

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24
Q

cardiac factors affect cardiac out[put

A

heart rate
myocardial contractility

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25
Q

coupling factors affect cardiac output

A

afterload
preload
functional coupling between heart & blood vessels

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26
Q

flow of adult

A

5L

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27
Q

determine blood fllow

A

pressure difference ends of vesel
resistance of vessel

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28
Q

cause turublent blood flow

A

high velocity
sharp turns
rough surfaces
rapid narrow
causes murmurs

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29
Q

thrill

A

palpable murmur

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30
Q

S1

A

close AV valves
hear in mitral (L, 5th intercostal)

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31
Q

S2

A

close Semilunar
hear L sternal (2nd intercostal)

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32
Q

S3

A

abnormal, early diastole
rapid ventricular filling
apex

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33
Q

S4

A

abnormal
turbulent flow
ventricle non-compliance
apex

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34
Q

aortic stenosis murmur

A

crescendo-decrescendo
systolic ejection
LV greater pressure than aorta in systole
radiate to carotid

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35
Q

aortic stenosis can lead to what on exertion

A

Syncope
Angina
Dyspnea

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36
Q

Mitral/Tricupsid Regurgitation sound

A

holosystolic, high pitch
blowing

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37
Q

cause mitral regurge

A

ischemic heart disease
mitral valv prolapse
left ventricle ddilation

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38
Q

cause tricupsid regurge

A

right ventricle dilation

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39
Q

mitral valve prolapse sound

A

late systolic
crescendo with midsystolic click

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40
Q

cause of mitral valv prolapse

A

sudden tense chordae tendineae

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41
Q

ventricular septal defect sound

A

holosystolic
harsh sound
hear @ tricupsid (5th intercostal, midclavicular)

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42
Q

aortic regurge sound

A

high pitch blowing
early diastolic
decrecendo
hear @ aortic root dilate or L sternal border

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43
Q

symptom aortic regurge

A

hyperdynamic puls (bounding)
head bobbing

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44
Q

causes of aortic regurge

A

Bicupsid aortic valve
Endocarditis
Aortic root dilate
Rheumatic fever

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45
Q

aortic regurge progress to

A

left sided heart failure

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46
Q

mitral stenosis sound

A

mid to late diastolic
follows opening snap

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47
Q

mitral stenosis a sign of

A

rheumatic fever, pulmonary congestion, hypertension, left atrial dilaiton, atrial fibrillation

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48
Q

patent ductus arteriosus sound

A

continuous machine like
L infraclavicular

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49
Q

causes of patent ductus arteriosus

A

congenital rubella
premature birth

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50
Q

polycythemia effect on blood flow

A

decrease flow (increasing viscosity)
increase resistance
excess of RBC makes too difficult to mvoe

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51
Q

anemia effect blood flow

A

increase flow (decreasing viscosity)
decrease resistance

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52
Q

vascular conductance

A

measure of blood flow through vessel for given pressure change

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53
Q
A
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54
Q

series vs parrallel arrangement

A

series are within same organ
parrrallel are across multiple organs (independent flow regulation)

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55
Q

what holds most/least volume blood

A

least - arteries
most - veins

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56
Q

MAP drives

A

blood to organs and capillaries

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57
Q

R atrial pressure

A

5

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58
Q

R ventricle pressure

A

25/5

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59
Q

pulmonary trunk pressure

A

25/10

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60
Q

L atrial pressure

A

<12

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61
Q

L ventricle pressure

A

130/10

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62
Q

aortic pressure

A

130/90

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63
Q

veins more distensible than arteries

A

8x

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64
Q

aged arteries

A

least amount of capitance & compliance

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65
Q

why aged arteries decrease compliance

A

walls stiffer, less compliant
arterial pressure increse

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66
Q

veins & cardaic output

A

constricted = lots bl.ood move to heart
increase output

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67
Q

factors affect opulse pressure

A

stroke volume (direct correlation)
arterial compliance (inverse correlation)

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68
Q

arteriosclerosis pulse pressure

A

stiffer, less compliant
increase pulse pressure

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69
Q

aortic stenosis pulse pressure

A

SV descreased
all pressures decreased

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70
Q

PDA pulse pressure

A

low diastolic, high systolic
high piulse

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71
Q

aortic regurge pilse pressure

A

backward flow
high pulse pressure

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72
Q

factors increase R atrial pressure

A

increase blood volume
increased venous tone
dialte arterioles
decrease cardiac function

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73
Q

P wave represent

A

atrial depolarization

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74
Q

PR interval represent

A

initial depolarization of atria to initial depolarization of ventricles

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75
Q

QRS represent

A

ventricles depolarize

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76
Q

T wave represent

A

repolarization ventricles

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77
Q

QT interval represent

A

first ventricular depolarization to last ventricular repolarization

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78
Q

PR interval length

A

0.12-0.2s

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79
Q

QRS interval length

A

0.06-0.11s

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80
Q

QT interval length

A

0.36-0.44s

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81
Q

repolarizations towards & away from reference electrode are …. deflections in EKG

A

towards: negative
away: positive

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82
Q

inferior leads of heart

A

II, III, aVF

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83
Q

lateral leads

A

I, aVL, V5, V6

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84
Q

right side lead

A

aVR, V1

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85
Q

anterior leads

A

V2, V3, V4

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86
Q

aVR electrode locations & vector

A

+ R arm
- L arm
- L leg
-150 degree

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87
Q

aVL electrode location & vector

A

+L arm
- R arm
- L leg
-30 degree

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88
Q

aVF electrode location ^ vector

A

+L leg
- R arm
- L arm
90 degree

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89
Q

first vs second half p wave

A

first: R atrial depolarization
second: L atrial depolarixation

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90
Q

normal leads to see variant of Q wave

A

III & aVR may have deeper Q

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91
Q

hyperkalemia change EKG

A

peak T
wide PR
widen QRS
none/flat P

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92
Q

hypokalemia change EKG

A

long QT
flat T wave

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93
Q

wolf parkinson white ekg

A

delta wave with wide QRS
supraventricular tachicardia

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94
Q

abnormla impulses of wolff parkinsosn white syndrom

A

extra connection of impulse from ventricle back to atria
lead to tachy

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95
Q

atrial fibrillation ekg

A

no P wave
weird R-R

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96
Q

risk factors of atrial fibrillatoin

A

Hypertension
coronary artery disease
holiday heart - excessive alcohol

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97
Q

atrial flutter EKG

A

sawtooth pattern
back-back atrial depolarization

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98
Q

ventricular fibrillation EKG

A

irratic
she crazy

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99
Q

EKG first degree block

A

long PR, >0.2

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100
Q

EKG 2 degree TI block

A

R-R varies (regularly irregular)
PR lengthen until beat drop

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101
Q

EKG 2 degree TII block

A

drop beat but no change PR interval
preogreess to 3 degree

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102
Q

third degree block

A

disassoc ventricle & atria
no rhythm to PQRS

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103
Q

one cause of third degree block

A

Lym3 disease

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104
Q

Einthoven Law

A

potential of anyh limb = sum pf pther two

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105
Q

what does heart axis represent

A

average direction of ventricular depolarization during ventricle contraction

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106
Q

L axis deviation

A

Positive in lead I
Negative lead II

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107
Q

R axis deviation

A

Negative lead I
Positive lead II

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108
Q

causes L axis deviation

A

laying down, expiration, fat
hypertrophy of Left ventricle (hypertension, aortic stenosis, aortic regurge)

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109
Q

Is right axis deviation ever normal

A

yes in newbornscau

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110
Q

causes R axis deviation

A

R ventricular hypertrophy ( pulmonary hypertension, pulmonary valve stenosis, IV septal defect, situs invertus)

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111
Q

L ventricular hypertrophy EKG

A

R wave of aVL >11mm
R wave V5-6 >35mm
S wave if V1 >35 mm

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112
Q

pathologic Q wave indicate what

A

prior mI
absence of electricity
scar is electrically dead

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113
Q

Qwave pathological if :

A

> 1mm wide
2mm deeo
25% depth QRS

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114
Q

EKG sinus arrythmia

A

inconsistent R-R

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115
Q

EKG sinus arrest

A

<3s duration of dropped beat

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116
Q

EKG PAC

A

no T wave
irregular R-R
abnormal P wave

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117
Q

EKG PAC bigeminy

A

every other beat is PAC

118
Q

EKG atrial tachy

A

P waveinvert

119
Q

Junctional EKG

A

regular R-R
40-60bpm
abnormal P wave

120
Q

Left bundle branch b lock EKG

A

V1 shows W looking QRS
V6 shows M looking QRS

WiLLiaM

121
Q

R bundle branch block EKG

A

V1 hsow M looking QRS
V6 show W looking QRS

MoRRoW

122
Q

PVC EKG

A

QRS with no P
same shape if unifocal

123
Q

ventricular pacemaker EKG

A

spike make wide QRS

124
Q

atrial pacemaker

A

spike where P wace should be

125
Q

AV pacemaker EKG

A

first spike with p wave
second spike make wide QRS

126
Q

AC interference EKG

A

electronic device or pacemaker near patiuent

127
Q

muscle tremor EKG

A

lots of random spike

128
Q

wandering baseline

A

undulates
somethign between electrode & machine

129
Q

mitral stenosis P changes

A

pulmonary capillary wedge pressure is greater than end diastolic presure

130
Q

prelead

A

stretch of myocardium
EDV

131
Q

afterload

A

systemic vascular resistance
ESV

132
Q

increase preload causes

A

increase cardiac output
increase force of contraction
increase vlood volume

133
Q

when does frank starling graph line curve to plateau

A

high level of EDV
ventricle reach limit and can’t maintain venous return amount of blodd

134
Q

what happen to systole on frank starling law graph as volume reaches maximum

A

systole decreases as actin/myosin no longer close to each other

135
Q

phases of pressure volume loop

A

1- filling ventricles (EDV)
2 - isovolumetric contract ventricles
3 - eject of ventricle
4 - isovolumetric relax of ventricle (ESV)

136
Q

increase preload cuases

A

greater EDV
greater SV

137
Q

increase afterload cuases

A

decrease SV
increase ESV

138
Q

increased contractility causes

A

increase SV
ESV decrease

139
Q

4 factor that inacrease contractility
positive ionotropi agents - B1 receptors

A

increased calcium entry - more AP & more trnsion created
increased troponin C affinity fro Ca
force increases when stretch more (frnak starling)
Cardiac glycosides

140
Q

S4 heart sound

A

turbulence from ventricle non-compliance
vibrate ventricular wall in atrial contraction

141
Q

S1 noise

A

AV valve closes, start systole

142
Q

why does ventricular volume decrease during rapid ejev=ction

A

SV ejected in this phase & ready for atrial fill

143
Q

Pressure changes during reduced ejection

A

ventriclar pressure fall slightly
aortic pressure decreases
atrial pressures rise (venous return increased)

144
Q

splitting of S2

A

inspiration delays close pulmonary valve
both aortic & pulmonary valve close here

145
Q

what is peak L atrial pressure named in isovol relax

A

V wave
increase volume against closed tricupsid

146
Q

when is S3 sound normal

A

kids and pregnant peoiple

147
Q

wide splitting of S2 occur when

A

pulmponic stenosis, R bundle block
delayed pulmonic as delay R ventricle empty

148
Q

fixed splitting S2 occure\ when d

A

delayed pulmonic closure
independent of respiration

149
Q

change in pressure-volume loop aortic stenosis

A

incerase afterload
increase ESV

150
Q

change in pressure-volume loop aortic regurge

A

increase preload
increase EDV

151
Q

change in pressure-volume loop mitral stenosis

A

decrease EDV & ESV

152
Q

change in pressure-volume loop mitral regurge

A

decrease ESV
increase EDV

153
Q

4 reasons venour return oncrease SV in exercise

A

veins contstrict
skeletal miuscle pump
thoracic pump
sympathetic stimulation

154
Q

SV declione in prolong exercise

A

high bT
redistribute blood flow to skin
excess fluid loss
decrease plasma volume
dehydrate

155
Q

formula cardaic output

A

CP = SV * HR

156
Q

fick formula cardiac output

A

CO = (O2 consumed)/(arterial O2 - venous O2)

157
Q

CO maintain in exercise

A

early: increase HR & SV
later: increase HR
diastolic shorten with increase HR

158
Q

factors directly affect CO

A

metabolism
exercise
age
body size

159
Q

caffeine affect CO

A

stimulatory afffect
increase HR by increase depolarization

160
Q

ion concentration affect CO

A

increase SAA nodal cell or contracility

161
Q

abnormla body temp affect CO

A

decrease temp = decrease metabolism
lower HR & force contract

162
Q

resistance to venous return determinants

A

2/3 by venous resistance
1/3 byu arterial resistance

163
Q

effect increase blood volume on mean vasc fxn curve

A

increase mean systemic fill pressure (venous return shift R)
cardiac output & atrial pressure increase

164
Q

increase TPR on vasc fxn curve

A

decrease CO, decrease venous return

165
Q

normal interpleural presure & how changes

A

-4mmHG
if increased require more R atrial pressure

166
Q

risk factors & features of hypertension

A

increased age, diabetes, inactivity, high sodium, excess alcohol, smoking, black
90% cases related increased CO or increased TPR

167
Q

hypertensive urgency

A

180/120, no organ damage

168
Q

hypertensve emeregncy

A

180/120 with end organ damage
stroke, hemorrhage, MI, aortic dissection etc

169
Q

determinants of BP

A

cardiac output
total peripheral resistance

170
Q

short term regualtion BP

A

baroreceptors (seconds)
chemoreceptors
CNS

171
Q

intermediate regulation BP

A

RAAS (minutes)lon

172
Q

long term regulation BP

A

kidney Na/H2O (hours to dyas)

173
Q

stimulation baroreceptors effect

A

from increased BP causing stretch
cardioinhibitory stimulated
vasodilation occur
decrease CO & restore BP

174
Q

carotid sinus & barorecepturs

A

has afferent limb - glossopharyngeal N
efferent - vagus N
decrease in BP as vasodilate

175
Q

conditions predispuise carotid sinus syndromw

A

atherosclerosis
more senstive
light touhc = bradycardia

176
Q

RAS

A

decrease BP
baroreceptors secrete renin
angiotensinogen become angiotensin I
ACE in lung makes it angiotensin II
make aldoserone
icnreases Na and H2O reabsorb
increase plasma volume = increase out put = increase BP

177
Q

exercise & BP

A

up to 85% total outpt to muscles if strenuouus
only modest increase mean BP due to vasodilate in active muscles

178
Q

what does SNS not innervate

A

capillaries, precapillary sphincters

179
Q

PNS on heart

A

responsible for control HR
not affect contractibility

180
Q

vasoconstrictor effect

A

kidney, gut, spleen, skin

181
Q

vasomotor center components

A

vasodilator
vasoconstrictor
sensry

182
Q

functions VMC

A

partial state of contraction via sympathetic tone
Lateral - heart activitt by increase HR/contract
medial - signal via vagus ot decrease HR

183
Q

VMC & arterial presssure

A

increase by constricting arterioles/large vessels
increasing CO/HR

184
Q

where are baroreceptors located

A

carotid sinus
walls of aortic arch

185
Q

carotid sinus baroreceptor respond to

A

pressure 60-180 mmHGd

186
Q

most senstive baroreceptor @

A

100mmHg

187
Q

what happen baroreceptor as pressure increase

A

impulses increases - lead to inhibition of constrictor, activate vagal

188
Q

orthostatic hypotension

A

impaired baroreceptor reflex
when go from laying to standing, should increase SNS to compensate

189
Q

vasovagal syncope

A

from cardioinhibitory & vasodepressor response
increased PNS

190
Q

carotid/aortic chemoreceptors respond when

A

lack of oxygen
excess CO2
excess H+
pressure below 80mmHg

191
Q

Response to blood loss

A

decrease blood volume = decrease CO & arterial pressure
carootid sinus sense decrease and increase SNS
if present with ischemia, chemoreceptors inobvlved
if arteriolar vasoconstriction senseed they decrease capillary pressure & favor absorbtion
adrenal medulla release Epi/NEpi
RAAS activated and angtiotensin II vasoconstricts, aldosterone increase NaCL reabsorb

192
Q

Cushing reaciton

A

specuial CNS ischemic response
inccrease pressure of CSF cut blood to brain

193
Q

Bainbridge reflex

A

prevent damming of blood
atrial stretch = increase HR

194
Q

Valsalva maneuver

A

monitor change BP/HR with brief strain
done regularly

195
Q

hypotension & baroreceptor

A

increase BP, vasoconstrict
important for big hemorrhage

196
Q

ANP

A

from atrial myocyte
respond to increase blodd volume
vasodilate afferent, constrict efferent and aldosterone escape

197
Q

Brain NP

A

ventricular myocyte
help diagnose hearfailure
increase Na absorbtion

198
Q

What isAV shunt & where located

A

connect arteriole to veing, bypass capillary
if dilate & relax, arteriole send blood to venule
nose, lip, penis

199
Q

contunuous non fenestrated capillary location

A

muscle, skin, fat, nerve tissue

200
Q

fenestrated capillary line

A

intestines, kidneys, endocrine

201
Q

sinusoidal capillary location/fxn

A

vascular channel mve lots blood
bone marrow, liver, spleen

202
Q

why is it imoprtant that endothelium lines capillaries

A

derived relaxing factor that is sensative to NO
M3 receptors activate synthesis of NO
allow vasodilation

203
Q

how much of blood is reabsorbed on venous side of cpaillary

A

85%

204
Q

solid structures in interstitium

A

collagen fibers
proteoglycan filaments

205
Q

lymph affect by hyrostatic pressure

A

increase interstitial fluid hyrostatic pressure creates increas lymph flow

206
Q

Peripheral Artery disease

A

impaired arteriolar autoregultaion
can’t adjust to metabolic needs
ischemia and pain as can’t dilate in response

207
Q

ultrafiltration & its determinmants

A

process blodd plasma filters across capillary to make interstitial fluid
capillary hydrostatic pressure
interstitial fluid pressure
plasma colloid osmotic pressure
interstitial fluid colloid osmotic pressure

208
Q

captillary hydrostatic pressure fxn

A

pull fluid out from capillary

209
Q

interstitial fluid pressure fxn

A

push fluid into capillary

210
Q

plasma colloid osmotic pressure fxn

A

pull fluid back into capillary

211
Q

interstitial fluid colloid osmotic pressure fxn

A

pull fluid out of capillary

212
Q

how to increase capilary pressure

A

decrease arteriole resistance
increase venous pressure

213
Q

what is another namoe for plasma colloid osmotic pressure

A

plasma protein

214
Q

diseases that lead to decreased plasma colloid osmotic presure & effect

A

cirrhosis, nephrosis, dilutional
decreases means interstitial fluid colloid osmotic is unapposed and can pull fluid to cause edema

215
Q

factors determine plasma colloid osmotic pressure

A

75% from albumin
25% globulins

216
Q

capillaru factors decrease filtration

A

creates decrease interstitial fluid
decease capillary pressure (constrict arteriole)
decrease osmotic tissue pressure (more lymph, less edema)
increase osmptoc colloid pressure (dehydration)

217
Q

capillary factors increase filtration

A

interstitial fluid form
increase capillary pressure (dilate arterioles)
increase osmotic tissue pressure (block lymph)
decrease osmotic colloid pressure (liver fail)

218
Q

4 causes of edema

A

increase capillary hydrostatic pressure
loss plasma protein
increased capillaru permeability
blockage of lymph return

219
Q

what can increase capillary hydrostatic pressure

A

hypertension, heart failure

220
Q

causes loss plasma proteins

A

nephrosis, burns, wounds, liver disease
particularly albumin loss

221
Q

cause of lymph block

A

infection or cancer
local edema

222
Q

cause of increased capillary permeability

A

allergic rxn/burn
localized but can spread

223
Q

thirst mechanism

A

osmoreceptors in hypothalamus

224
Q

antidieuretic hormone fxn

A

reabsorb water into blood from kidney
prevent water lloss

225
Q

aldosterone fxn

A

resorption of sodium ions & water

226
Q

Atrial natriuretic peptide fxn

A

increase glomerular filtration rate
inhibit ADH
Inhibit renin secreation

227
Q

hyperemia

A

increased amount blood in vessls of organ or tissue

228
Q

active hyperemia

A

increased metabolic = increased metabolites
causes increased dilation & flow

229
Q

reactive hyperemia

A

after an occlusion occurs
during ischemia metabolites build up
excess blood flow required to wash away after

230
Q

blood flow determinant & equation

A

pressure difference & resistance
Q = (P1-P2)/(R)

231
Q

vasodilators for blood flow control

A

adenosine
CO2
lactic acid
ADP compounds
histamine
K+
H+

232
Q

precapillary sphincters & tissue demand

A

numper of sphincter open at any time is about same as requirerment for nutirtion of tissu
meet metabolic ozygen needsmetab

233
Q

metabolic autoregulation theory

A

as arterial P decreases, oxygen decreases
cause vasodilator release

234
Q

myogenic autoregulation theory

A

as arterial P decrease, artieroles will dilate
in response to wall tension

235
Q

kidney blood flow control

A

feedback of tubules & arterioles

236
Q

brain blood flow conrol

A

CO2 & H+ concentration

237
Q

Laplace law & hypertension

A

wall thickens as adaption to minimize wall tension
minimize oxygen demand as a result

238
Q

long term local blood flow regulation occur by

A

change size and number of vascular vessels

239
Q

when does angiogenesis occur

A

factors release from
ischemic tissue
rapid growing tissue
tisue with high metabolic rattes

240
Q

humoral blood flow regulation - vasoconstrictors

A

NEpi & Epi
Angiotension II
Vasopressin
Endothelin

241
Q

humoral blood flow regulation - vasodilators

A

Bradykinin
serotonin
histamine
prostoglandins
NO
adenosine

242
Q

acute response heart fail

A

increase SNS

243
Q

chronic response heart failure

A

sympathetic contract kidney arterioles
decrease filtration & urine
Na/H2o retention
increase volume, decrease resistance
BNP excerete extra Na = strong heart fail indicator

244
Q

progressive change in CO curve after MI show

A

heart never recovers to intital cpacity

245
Q

moderate cardiac damage fluid retention

A

lower CO & flow to kidneys
moderate retention

246
Q

sever cardiac damge fluid retention

A

excessive retention weakens heart more
0 urine outpit

247
Q

decompensated heart failure

A

CO can’t sustain renal fxn
fluid retention
elevate mean fill pressure
elevate right atrial pressure

248
Q

L heart fail

A

forward
R side continues normal
pulmonary congestion

249
Q

acute pulmonary edema

A

with chronic heat fail, increase load on already weak hearttre

250
Q

treat acute pulmonary edema

A

fast dieuretics
oxygen
cardiotonic drug

251
Q

arterio-venous fistula

A

blood bypass resistance = low TPR
CO must increase to maintain BO
chronic elevation leads to excess venous return & heart fail

252
Q

Beriberi

A

b1 deficent for peripheral tissues
extreme vasodilate in peripheral with low TPR
high CO
seen in alcoholics

253
Q

what predominates coronary blood flow

A

metabolic effects (vasodilation)
even if SNS active

254
Q

Circle of Willis

A

arterial blood continuous to tissues

255
Q

most to least oxygen in fetus

A

umbilical
atrium
internal ilian ratery
inferior vena cava

256
Q

autoregulation lungs factor

A

hypoxia cause vasoconstrict

257
Q

autoregulation heart factor

A

vasodilatory metabolites
NO, CO2, low O2

258
Q

brain autoregualtion factors

A

casodilatory metaboiltes
CO2, H+

259
Q

kidney autoregulation factors

A

myogenic, tubuloglomerular feedback

260
Q

skeletal muscle autoregulation factors

A

vasodilatory metabolites in exercise
sympathetic tone @ rest

261
Q

vasodilatory metabolites in exercise

A

CHALK
CO2, H+, Adenosine, Lactate, K+

262
Q

skin autoregulation factors

A

sympathetic vasoconstriction

263
Q

key events hemostasis

A

vessel spasm (constrict)
form plug (gp1b)
blood coagulation (intrinsic vs extrinsic)
clot retraction (polymerize fibrin)
clot lysis (plasmin)

264
Q

ligand for platelet adhesion

A

Von Willebrand facotr
bind to gp1b/1a

265
Q

platelet alpha granules

A

vWF, factor V, fibrinogen, growth factors

266
Q

platelet dense granules

A

ATP, ADP serotonin, Ca

267
Q

coagulation factors

A

vWF, fibrinogen, Factor V/XI/XII

268
Q

adhesion factpors

A

gp1b/1a, gpIIb/111a

269
Q

what does vWF bind

A

Gp1b/1a activates more plateletes & bridges form

270
Q

fibrinogen bind

A

GpIIb/IIIa
platelet plug

271
Q

prothrombin dependent on

A

vitamin K
for clotting

272
Q

fibrinogen depend on

A

synthesis in liver
intravascular for clotting

273
Q

extrinsic clot patheay

A

Ca with factor VII makes VIIa
more Ca, VIIa & factor X form activated X
with factor V activates prothrombin activator
Prothrombin + platelet phospholipid + prothomabin + Ca makes thrombin
Thrombin can then make more factor 5 to continue

274
Q

Intrinisc clot pathway

A

XII to XI to IX with CA
VIII with thrombin & Ca activates factor X\Calcium ads to & activate prothrombin
makes thrombin

275
Q

thrombin-thrombomodulin

A

activate protein C (also need protein S)
inactivates factors V & VIII

276
Q

regulation of fibrinolysis

A

plasminogen activator inhibitor 1 & 2
prevent breakdown and leave as clots

277
Q

vitamin K defieency

A

lack bile production/delivery cause fat malabsorption
inactivates VII, IX, X & Protein C+S

278
Q

Factor II (Prothrombin) deficiency

A

excessiive bleed/hemorrhange
dyspro(…) = abnormal structure
Hypo(…) = inadequaate productionhem

279
Q

hemophilia A

A

deficeny of factor 8
85% all hemophilias
family history of
lab will show prolong PTT

280
Q

hemophilia B

A

deficiency factor 9

281
Q

hemophilia C

A

defciency facto 11

282
Q

Disseminated Intravascular Coagulation (DIC)

A

decrease in all cloting factors
increase fibrin degradfing factor
bleed out

283
Q

bleed tiem

A

1-6 minutes
platelet fxn

284
Q

clotting time

A

6-10min

285
Q

Prothrombin Time

A

extrtinsic pathway assess
12s

286
Q

Partial Thromboplastin Time

A

assess intrinsic
factor 8

287
Q

bernard soulier syndrome

A

d=defect in adhesion with decrease GpIb

288
Q

glanzmann thrombasthenia

A

defect in aggregation
decrease GpIIb/IIIa
no platelet clump

289
Q

immune thrombocytopenia

A

destruction platelet in splee
anti-gpIIb/IIIa antibodies

290
Q

Von Willebrand disease

A

decreas vWF
decrease factor 8
increases PTT

291
Q

factor V Leiden

A

mutant factor 5
resistant to degradation by protein C
lead to thrombosis, DVT

292
Q

protein C or S deficency

A

decrease ability to inactivate factors V & VIII
Protein C cancels & Protein S stops coagulation

B3 Clinical Application (5 decks)

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