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mod 2 CC > framework > Flashcards

framework Flashcards

1
Q

3 determinants of O2 supply

A
  1. arterial O2 saturation- % hgb, 97% O2 bound to Hgb
  2. O2 transport in blood- Hgb level and affinity
  3. Cardiac output- SV x HR
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2
Q

what is a key determinant of O2 saturation?

A

Alveolar gas exchange- cross A-C membrane

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3
Q

oxygenation is influenced by what 3 things

A
  1. Ventilation- ability
  2. V/Q matching- concentration of O2
  3. Diffusion- effectiveness
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4
Q

PaCO2 is determined primarily by?

A

Ventilation

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5
Q

minute ventilation?

A

RR x Vt

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6
Q

hyperventilation does what to CO2

A

decreases. more is blown off

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7
Q

how do you measure PaO2

A

arterial blood sample

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8
Q

what is V/Q matching

A

relationship between air reaching alveoli (vent) and blood reaching alveoli (perfusion- Q)

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9
Q

what 4 things determine diffusion

A
  1. driving pressure - difference in concentration gradient
  2. diffusion coefficient - how fast it can dissolve/diffuse
  3. anatomical surface area -pulm edema, fibrosis
  4. thickness of A-C mem - inflam process
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10
Q

what influences driving pressure?

A

Difference of concentration of gases.

the greater the difference the greater the driving pressure

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11
Q

what is diffusion coefficient

A

how readily a gas will diffuse across

CO2 is 20 x faster than O2

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12
Q

what influences anatomical surface area?

A

lobectomy, plural effusion

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13
Q

arterial O2 sat 2 main components

A
  1. vent

2. gas exchange

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14
Q

arterial O2 sat is influenced by? 3

A
  1. movement of air in and out
  2. concentration of inspired O2
  3. gas exchange at the A-C membrane
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15
Q

which process of ventilation is active? passive?

A

active - inhalation

passive - exhale

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16
Q

pressures when you inhale

A

increases the intrapulmonary pressure
decreases pulmonary pressure
- relative to atmospheric pressure

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17
Q

WOB functional residual capacity FRC

A
  • volume of air left in lungs after passive expiration

- needed for gas exchange

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18
Q

WOB vital capacity

A
  • vol of air breathed out after the deepest inhale
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19
Q

WOB tidal volume

A
  • amount of air moved into and out of the lungs during normal breathing aprox 500cc

shallow resps = decreased Vt

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20
Q

WOB is influenced by? 3

A
  1. resp muscle function
  2. lung compliance
  3. airway resistance
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21
Q

WOB is

A

overcoming elastic and resistance properties of lungs

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22
Q

lung compliance. 3

A
  • measure of distension ability. stretch and force required
  • chest wall elasticity
  • airway resistance
  • alveolar compliance

fibrosis

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23
Q

if a PT has poor lung compliance…

A

they will have rapid and shallow breaths

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24
Q

airway resistance

A

resistance of resp tract to airflow during inspire and expire. Diameter

wheezing, asthma

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25
Q

arterial O2 content.

A

amount to O2 being carried by blood. includes O2 bound to Hgb and O2 dissolved in plasma

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26
Q

determinants of O2 transport in blood

A
  1. Hgb level

2. Affinity (dissociation curve)

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27
Q

stroke vol =

A

amount of blood ejected from heart

mls/beat

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28
Q

stroke vol is influenced by 3

A
  1. preload
  2. contractility
  3. afterload
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29
Q

contractility

A

ability of heart myofibrils to change their strength of contraction

SNS response

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30
Q

preload

A

volume of blood in the ventricles at the end of diastole

crackles, CVP, JVD norm 2-6), tachycardia
- increased force of diastole = increased preload

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31
Q

preload is influenced by

A

circulating vol and venous return

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32
Q

afterload

A

force or resistance against which the vents have to pump in order to eject blood

DBP, PP, cap refill, skin temp, periph pulses, pt hx

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33
Q

primary determinant of afterload

A
  1. diameter of arterioles

2. arotic impedance (valve stenosis, vasoconstrict)

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34
Q

contractility primary determinant

A

preexisting medical condition

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35
Q

aortic impedance

A

the sum of external forces that resist left vent ejection

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36
Q

oxygen demand is influenced by 3

A
  1. temp (normal 36.4-37.6)
  2. physical activity
  3. stress physiological or perceived
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37
Q

type 1 alveolar cell

A

more surface area. cover 90-95 %

gas exchange

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38
Q

type 2 alveolar cells

A

smaller only 5%

secrete pulm surfactant to decrease surface tension

found at blood/air barrier

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39
Q

minute ventilaion

A

relationship with blood and CO levels

RR x Vt = min vol

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40
Q

central chemoreceptors

A

CNS
located in ventrolateral medulary surface of cranial nerves

  • sensitive to pH of environment of CSF of altered O2 and CO2** levels
  • a rise in CO2 causes = tension of arteries
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41
Q

periph chemoreceptors

A

PNS
in carotid and aortic bodies

  • sensitive to chemical concentrations in blood.
  • low O2 (hypoxia)**, high CO2, hypoglycemia

when O2 in arterial blood falls, send message to brain to increase ventilation

**only when O2 falls below 60mmHg*

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42
Q

how much O2 is inhaled through the air?

A

21%

some gets dissolved into humidity

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43
Q

how much atmospheric pressure is inspired O2

A

159mmHg (21% of atmospheric pressure of 766mmHg)

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44
Q

humidification of upper airways drops pressure to

A

150mmHg

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45
Q

pressure pulm/arterial O2 level

A

40mmHg

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46
Q

alveolar partial pressure = ?

A

100mmHg

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47
Q

arterial PaO2 is dependant on 2 factors?

A
  1. inspired O2 pressure (FiO2)

2. FRC

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48
Q

2 main factors that influence ventilation and CO2 level

A
  1. RR

2. Vt

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49
Q

aterial CO2 is dependent on 2?

A
  1. CO2 production

2. CO2 removal

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50
Q

when FRC is decreased?

A

there is less air in the lungs at the end of expire

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51
Q

deadspace

A

vol gas that passes through the lung that is not perfused and does not take part in gas exchange

  • decreases Vt
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52
Q

anatomical shunt

A

blood that passes through venous to arterial circulation that does not take part in gas exchange

  • septal or vent defects
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53
Q

physiological shunt

A

alveoli perfused but not ventilated

pneumonia

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54
Q

lung compliance dependent on 3 factors

A
  1. chest wall elasticity
  2. airway resistance
  3. alveolar compliance
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55
Q

during inspiration 3:

A
  1. intrathoracic and intrapulmonary pressure decreases
  2. diaphragm contracts
  3. intercostal muscles contract and thoracic cavity increases in size
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56
Q

resp gas is not exchanged in

A

terminal bronchioles

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57
Q

what decreases airway resistance

A

SNS

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58
Q

the most sensitive region of resp tract for trigger cough

A

carina- the biforcation of trachea that separates L and R broncioles

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59
Q

pulm surfactant 4:

A
  1. prevent alveolar collapse
  2. reduce alveolar surface tension
  3. increases lung compliance
  4. secreted by type 2 cells
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60
Q

peripheral chemoreceptors are located in

A

aortic arch

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61
Q

V/Q mismatch primarily affects?

A

O2 levels in arterial blood

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62
Q

external vs. internal compliance

A

ex- stab wound, corset, deformity. prob with diaphragm, broken ribs

in- fibrosis

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63
Q

airway resistance is influenced by?

A

diameter of airway.

wheezing, bronchospasms, increased secretions

64
Q

respiratory muscle function

A

MS, Guillain Barre, poor nutrition, broken robs, abd ascites, ALS

PT would need mechanical vent to replace muscle function for thoracic abnormalities

65
Q

for CCN what are the significant pulmonary volumes?

A

VC, Vt, FRC

increased WOB = decreased Vt = increased RR

Assess PTs RR and tidal vol

66
Q

Vital Capacity

A

indicates if a PT can cough and clear their throat. Do determine if the PT can be extubated.

can they protect their airway?

67
Q

FRC

A

functional residual capacity

amount of air left in lungs at the end of exhale.

many small airways remain open post-exhale. If airway collapse it is more WOB to open on the next inhale

increased FRC = decreased WOB
decreased FRC = decreased arterial oxygenation = decreased O2 supply to tissues

68
Q

ABG gold standard for ventilation

A

PaCO2

Alveoli should have a lower concentration of CO2 than in the blood for the CO2 to be expelled toward lower concentration.

Shunt/shunt-like - reduces clearance of CO2 from alveoli disrupting concentration gradient and CO2 cant diffuse out of blood will build up as PaCO2

69
Q

tidal volume

A

amount of air inhaled with each breath. inverse relationship with RR

hypervent = decreased TV
shallow = decresed TV
70
Q

what are chemoreceptors

A

plays feedback that incresaes ventilation. central and peripheral both sensitive to CO2 levels in blood

sense change and send message to brainstem to increase ventiation by increasing RR and/or depths of breath

71
Q

PaCO2 is the primary influence on?

A

ventilation

72
Q

< 60mmHg O2 in arterial blood =

A

moderate degree of hypoxemia

73
Q

what is the key determinant to O2 saturation and supply?

A
  1. alveolar gas exchange
74
Q

diffusion is influenced by?

A
  1. thickness of membrane

2. difference in concentration of gasses

75
Q

external respiration

A

takes place in lungs and across alveolar mem

76
Q

internal respiration

A

gas exchange across the membrane that separate tissues and cells of body organs from blood

77
Q

what is alveolar gas exchange

A

physical movement of gas by diffusion across A-C membrane (ACM)

78
Q

what are the two components of gas exchange?

A
  1. diffusion

2. V/Q matching

79
Q

4 main factors that influence diffusion in lungs

A
  1. thickness of A-C mem
  2. driving pressure -concentration gradient. supplemental O2 NP
  3. anatomical surface area
  4. diffusion coefficient - what is more diffusable, CO2
80
Q

CO2 levels determined primarily by

A

ventilation

81
Q

when ventilation inadequate what happens to driving pressure

A

decreased CO2 exhaled = Pa CO2 increases = decreases driving pressure

82
Q

the movement of O2 across the membrane is influenced by? 2

A
  1. ventilation

2. diffusion

83
Q

diffusion impared

A

O2 less diffusable that CO2. decresaed surface area would impact decrease O2sat

84
Q

when V/Q properly matched…

A

optimal gas exchange

85
Q

what happens to air if person lying on their side

A

the lung below will receive more air = more blood

ex. if PT has right lung pneumonia - position PT on left side

86
Q

shunt/shunt-like

A

alveoli partial or non-ventilated but fully perfused

part: secretions, bronchoconstrict
shunt: pneumonia, atelectasis

87
Q

dead space/dead space-like

A

alveoli fully ventilated but not perfused

dead-like : person with low CO

dead : PE

88
Q

ventilation influenced by factors that affect getting air into and out of the lungs : 3

A
  1. compliance
  2. resistance
  3. resp muscle strength

vent assessed by PaCO2 values

89
Q

why does hypoxemia occur in V/Q mismatch?

A

causes local or regional hypoxia, triggering vasoconstricion

O2 cannot pass the barrier (A-C mem) and then less in bloodstream for tissues

90
Q

what affects Hgb dissociation curve

A
  1. pH
  2. PaCO2
  3. temp
91
Q

right shift curve

A

decreased pH (acidic), increased CO2 and increased Temp

decreased affinity- increases cellular oxygenation but could cause depletion eventually

Right Release

92
Q

left shift curve

A

increased pH (alkolitic), decreased CO2, decreased Temp

increased affinity - Hgb remains saturated but PaO2 driving pressure affected impacting cellular oxygenation

Left

93
Q

normal PaO2 =
normal SaO2 =
normal PaCO2 =

A

PaO2 = 80-100mmHg
<80- >60 = mild hypoxemia
<60- >40 =mod hypoxemia
<40 = severe hypoxemia

SaO2 = 93-100%

PaCO2 = 35-45

94
Q

Hgb O2 trasport:

A

inspired O2 meets prefusion–> PaO2 in plasma binds to Hgb becomes SaO2 (oxyhemaglobin)–> released back into plasma again as PaO2 to diffuse into cells to meet demand

95
Q

% SaO2 in blood to Hgb

A

97% to Hgb and 3% left in plasma

96
Q

what percent of O2 carried in blood is used at cellular level?

A

25%

75% venous returns to heart and lungs remains saturated

97
Q

diffusion is reliant on

A

driving pressure

concentration gradient

98
Q

if there is low Hgb then what happens to O2

A

there will be less avail for O2 to bind with Hgb so less to be transported to tissues

99
Q

if there is a left shift then…

A

the increased affinity means that for any given SaO2, the PaO2 will be lower than normal.

need SaO2 higher to ensure adequate PaO2

less avail for tissues

drive more O2, warm her up, give PRBC transfuse

100
Q

CO =

A

HR x SV (amount of blood in one beat mls)

the amount of blood pumped out of the heart in 1 min

75mls of blood per beat, HR 70/min x 75mls = 5250 mls or 5.2L/min

101
Q

S1 is associated with

A

closure of mitral and tricuspid valves

high pitched and heard at apex

102
Q

S2

A

aortic and pulmonary valves closing

103
Q

pulse pressure is? normal number

A

difference between systolic and diastolic 120-80 = 40

104
Q

these decrease contractility 3

A
  1. decreased O2
  2. Inotropic drugs
  3. electrolyte imbalance
105
Q

veins can be referred to as

A

capacitance vessels (active constriction)

106
Q

veins contain what % of circulating blood vol?

A

75%

107
Q

stimulation of SNS =

A
  1. increased HR

2. increased contractility

108
Q

primary pacemaker of heart

A

SA node

109
Q

optimal stretch of cardiac myofibrils that support optimal contractility =

A

starlings law

110
Q

tone of vessels?

A

diameter and elasticity

111
Q

primary indicators of preload

A
  1. CVP
  2. S3- hear second dubb = PT need lasix
  3. POCUS - point of care ultrasound
  4. JVD? (right side heart)
112
Q

secondary indicators of preload

A
  1. crackles - decide if HF issue or infectious issue (left side heart)
  2. edema
  3. skin turgur
  4. mucus membranes
  5. in/outs / daily weights
113
Q

common afterload assess parametres:

A
  1. PP (norm 40)
  2. DBP <80 = dilated, >80 = constricted
  3. cap refill
  4. color limbs
  5. temp limbs
  6. periph pulses
114
Q

vasoconstriction is what type of response?

A

SNS and RAAS

115
Q

what happens to CO and SV if vasodialted?

A

SV increased. vents can eject more

CO - increased even though BP low

116
Q

vasoconstricted

A

can have normal BP but low CO because heart is working harder to eject through narrow arteries

117
Q

diastolic BP is the best indicator of?

A

Tone. indicates the degree of vasodilate/constrict

118
Q

PP is altered by

A

force of contraction of vent, arterial tone and vessel diameter

119
Q

what is a good indicator of organ perfusion?

A

Mean BP or MAP

often used to titrate drugs and fluid therapy

2distolic + systolic / 3 = organ perfusion

120
Q

what will the body do if contractility of heart impaired?

A

SV will fall so HR will increase to maintain CO

compensatory response by SNS

121
Q

SV has 3 determinants

A
  1. contractility
  2. preload
  3. afterload
122
Q

increased preload examples 5

A
  1. excess circulating vol
  2. decrease intrathoracic pressure
  3. increase vent filling time
  4. constrict veins (decreases venous capacitance)
  5. increase venous return
123
Q

decreased preload ex. 6

A
  1. decreased circulate vol
  2. increased intrathoracic pressure (harder for blood to return to heart)
  3. decreased vent filling time
  4. dilated veins
  5. decreased venous return
  6. tachycardia
124
Q

if preload is decreased what happens to contractility

A

decreased

125
Q

frank starling law =

A

if you increase the vol into heart, CO will increase to a point when the actin/myosin molecules cannot stretch any farther then contractility can be impaired and over stretched

  • increased preload = increased contractility
  • increased pressure = increased stretch myofibrils
  • overstretched myofibrils = decreased contractility
126
Q

what happens to contractility and preload if a PT has HF?

A

If contractility imapired then vents dont empty effectively during systole = more vol left in vents at end systole (increased ESV) = heart fills with more blood during diastole = greater than normal amount to blood in vents at end of diastole (increased EDV) = increase in preload.

less stretch = greater pressure

vents less distensible = less compliant

127
Q

what happens to afterload if you decrease contraction?

A

decreases SV and blood flow leaving heart

128
Q

how do you assess vessel diameter? and what does that affect?

A

measure the pulse pressure

<40 = narrow/ vasoconstriced = increased afterload and resistance

129
Q

what does the inflammatory response and hyperthermia do to afterload?

A

decreases

130
Q

what are catecholimines? and what do they do to afterload?

A

epi/norepi (from adrenal glands)

increase

131
Q

name things that determine contractility

A
  1. preload
  2. SNS
  3. amount of Ca+ in myocardial cell
132
Q

name things that decrease contractility

A
  1. low O2 supply to the heart
  2. negative inotropis drugs (BB’s, CCB’s)
  3. electrolyte imbalance
  4. preexist medical cond
133
Q

name things that increase contractility

A
  1. electrolyte imbalance
  2. circulating catecholemines (epi/norepi)
  3. inotropic drugs (digoxin, dopamine, dobutamine)
134
Q

how is ejection fraction measured?

what is normal %?

what is measured?

if EF < 30% = ?

A

Echo

> 50%

% blood going into right left atrium and % leaving left vent

if < 30 = decreased contractility

135
Q

the ANS key role 3:

A
  1. regulate cardiovascular system
  2. alters HR
  3. changes SV by exerting influence on contractility and arterial tone.

these manipulate CO and vessel diameter and are important in mntning organ perfusion.

136
Q

the ANS has 2 divisions:
SNS and PNS

which neurotransmitters are for SNS? PNS?

A

SNS: epi and norepi (adrenergic or adrenalin)

PNS: acetlylcholine (cholinergic)

137
Q

PNS receptors location and 2 main effects

maybe not important

A

atria, AV junction and vents of heart

leaves brain to vegas nerve

  1. slow down rate of impulse at SA node
  2. slow transmissions of impulses through the AV node

= decreased HR

138
Q

SNS receptors location and innervates:

maybe not important

A

receptors in:

  1. systemic vasculature
  2. skin
  3. lungs
  4. GI system
  5. kidneys

innervates: SA node, AV node, ventricular myocardium

139
Q

SNS receptors 2 main types

what is it designed for?

A

Alpha and Beta

short term action. in chronic PTs SNS in overdrive = increased cell metabolism and O2 demand

140
Q

Beta 1 receptors located? what do they do?

A

one heart
located: SA node, AV node and myocardial cells

they:

  1. increase HR,
  2. speed on conduction,
  3. automaticity (firing of cell) and
  4. force of contraction
141
Q

Beta 2 receptors located? results in ?

A

two lungs/two legs
located: smooth muscles of bronchioles and arterioles supplying skeletal muscle

they:

  1. vasodilate arterioles**
  2. bronchodilation**
  3. increase intestinal motility
  4. increase breakdown of glycogen and lipids
142
Q

Alpha receptors located and results?

A

located: skin, peripheral circulation, gut and kidneys**

they:
1. vasoconstrict** arterioles in skin and peripheral circulation

  1. vasoconstrict** in gut and kidneys

= increase BP

143
Q

what do BB do?

A

block beta receptors so neurotransmitters cannot connect inhibiting the effects of SNS

= decrease HR, conduction, firing and contraction

144
Q

what does inotropic drugs so?

A

dopamine and dobutamine…

mimic action of SNS stimulating beta receptors

= increased HR, conduction, firing and contraction

145
Q

norepiepherine does what

A

vasoconstricts

drug of choice for excess dilation like sepsis

146
Q

key source of input to regulate the ANS? sensed by what?

A

BP

sensed by barroreceptors

147
Q

where are barroreceptors located? what do they do?

A

aortic body and carotid sinuses .

sense changes of stretch of vessel wall

148
Q

factors influencing metabolic and O2 demands 3.

A
  1. temp
  2. physical activity
  3. stress
149
Q

3 main compensatory mechanisms

A
  1. neurological: SNS
  2. hormonal :RAAS
  3. chemical: action from chemoreceptor response
150
Q

if CO decreases, explain compensatory mechanisms…

if decreases to alveoli perfusion is deminished (creating dead space or dead space-like)…

A
  • decrease in pressure changes will be sensed by the baoreceptors
  • triggers ANS to compensate: SNS will increase HR, increase contractility and vasoconstrict
  • arterial O2 falls and will be sensed by chemoreceptos to stimulate resp centers in brainstem to increase RR and depth (when PaO2 < 60mmHg)
  • the increase in ventilation will increase O2 avail at A-C membrane, support diffusion, and help O2 saturation = increase O2 supply from source
151
Q

if CO drops that blood flow though kidneys is reduced (and urine output drops)?

A
  • kidneys will respond by releasing hormones in RAAS which will increase circulating preload, and BP by increasing afterload (vasoconstrict)
152
Q

what 4 outcomes does the RAAS provide?

A
  1. increased preload
  2. increased afterload
  3. increased CO
  4. increased BP
153
Q

what does angiotensin 2 do? 3

A
  1. potent vasoconstrictor = increased afterload and BP
  2. stimulate release aldosterone from adrenal cortex = reabsorbs Na+ and H2O = increased vol and preload
  3. triggers production of vassopressin (ADH) = reabsorb H2O = increased vol and preload
154
Q

what happens to the chemoreceptors if SaO2 is decreased?

what else is activated?

A

chemorecptors trigger resp center to increase RR and Vt.

SNS also activated

both attempt to restore O2 supply

155
Q

what will the SNS do if there is decreased Hgb

A

Hgb = deceased transport = SNS to increase HR

156
Q

how do cells get from aerobic to anaerobic?

A

hypoxia cells shift from aerobic to anaearobic = lactic acid.

locally this causes - pre-capillary sphincters to relax = increased blood flow and O2 supply

globally - chemoreceptors sense decrease in pH and trigger center responses = increase RR and Vt, increase vent and SaO2

NOTE: this also increases cardiac work, resp work, and muscle work = increase O2 demand

mod 2 CC (3 decks)

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