respiratory physiology Flashcards

1
Q

anatomic dead space begins in the mouth and ends in the

A

terminal bronchioles (also called the conducting zone)

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2
Q

gas exchange occurs across the _______________ (type of cell) in the respiratory zone by _______________

A

flat epithelium (type 1 pneumocytes)
by diffusion

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3
Q

pneumonic for exhalation and muscles utilized:

A

I let the air out of my TIRES
Transverse abdominis
Internal oblique
Rectus Abdominis
External Oblique

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4
Q

where are the two parts of the airway where you will find cartilage

A

trachea and bronchi (NOT the bronchioles)

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5
Q

does the conducting zone participate in gas exchange

A

no because it is anatomic dead space

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6
Q

TPP (trans pleural pressure) =

A

alveolar pressure - intrapleural pressure

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7
Q

transpulmonary pressure is always

A

positive

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8
Q

intrapleural pressure is always

A

negative

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9
Q

alveolar ventilation =

A

(tidal volume - dead space) x RR

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10
Q

in a healthy adult, the normal dead space is

A

2mg/kg (or 150mL for 70kg)

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11
Q

how does atropine increase anatomic dead space

A

it is a bronchodilator so it increases the volume of the conducting zone

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12
Q

dead space is reduced by anything that does these 2 things (and 3 examples)

A

reduces conducting volume or increases pulmonary blood flow
ex) LMA, ETT, neck flexion

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13
Q

anatomic dead space definition and example

A

air confined to the conducting airways
example: nose and mouth to terminal bronchioles

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14
Q

alveolar dead space definition and example

A

alveoli that are ventilated but not perfused
example: decreased pulmonary BF

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15
Q

physiologic dead space definition and example

A

anatomic Vd and alveolar Vd
ex: variable

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16
Q

apparatus dead space definition and example

A

Vd added by equipment
ex: face mask, heat and moisture exchanger

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17
Q

Vd/Vt ratio definition

A

the fraction of Vt that contributes to Vd

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18
Q

in the circle system, dead space begins at the

A

y piece

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19
Q

the bohr equation compares

A

partial pressure of CO2 in the blood versus partial pressure of CO2 in exhaled gas

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20
Q

the bohr equation itself

A

Vd/Vt = (PaCO2 - PeCO2) /PaCO2

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21
Q

in the textbook patient, ventilation is ___L/min and perfusion is ___L/min

A

ventilation is 4L/min
perfusion is 5L/min

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22
Q

ventilation is greatest at the lung base due to

A

high alveolar compliance

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23
Q

perfusion is greatest at the lung base due to

A

gravity

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24
Q

what does HPV minimize

A

shunt aka zone 3 (not dead space)

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25
Q

Law of laplace

A

P=2T/R
pressure, tension, radius

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26
Q

with no surfactant, there is an increase in ___________ and likelihood that alveoli will collapse

A

surface tension

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27
Q

does each alveolus contain the same amount of surfactant?

A

yes, the concentration just varies

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28
Q

zone 1

A

dead space
PA>Pa>Pv

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29
Q

zone 2

A

waterfall (V/Q =1)
Pa>PA>Pv
-BF is directly proportional to the difference in Pa-PA

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30
Q

zone 3

A

shunt (V/Q=0)
Pa>Pv>PA

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31
Q

zone 4

A

pulmonary edema
Pa>Pis>Pv>PA

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32
Q

alveolar gas equation

A

FiO2 x (Pb-PH2O)-(PaCO2/RQ)
FiO2 x (760-47)-(____/.8)

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33
Q

how respiratory quotient (RQ) is calculated

A

= CO2 production / O2 consumption
= 200mL/250mL
=.8

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34
Q

hypoxemia is when PaO2 is technically <

A

<80

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35
Q

what is the A-a gradient of a healthy patient breathing room air?

A

105-95=10mmHg

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36
Q

things that increase A-a gradient include (4)

A

aging (closing capacity increases relative to FRC)
vasodilators (decreased HPV)
right to left shunt (atelectasis, PNA, intubation, intracardiac defect)
diffusion limitation (alveocapillary thickening)

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37
Q

shunt increases by what percent for every 20mmHg of A-a gradient

A

1%
ex) If Aa gradient is 218mmHg, then 218/20 ~11% shunt

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38
Q

normal IRV

A

3,000

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39
Q

normal ERV

A

1100

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40
Q

normal RV

A

1200

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41
Q

norrmal Closing volume

A

~30% TLC by age 20
~50% TLC by age 70

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42
Q

normal TLC and what its comprised of

A

5.8L
IRV + TV + ERV + RV

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43
Q

normal VC and what its comprised of

A

4.5L
IRV + TV + ERV

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44
Q

normal IC and what its comprised of

A

3.5L
IRV + TV

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45
Q

normal FRC and what its comprised of

A

2.3L
RV + ERV

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46
Q

normal closing capacity composition

A

RV + CV

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47
Q

VC = _______ mL/kg

A

65-75

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48
Q

FRC can be measured indirectly by (3)

A

nitrogen washout
helium wash in
body plesmythography

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49
Q

normal FRC mL/kg

A

35

50
Q

time until patient desaturates equation

A

FRC/VO2 (O2 consumption)

51
Q

when FRC is reduced, which west zone increases

A

west zone 3 (shunt)

52
Q

factors that increase closing volume

A

CLOSE-P
COPD
Left ventricular failure
Obesity
Surgery
Extremes of age
Pregnancy

53
Q

oxygen content equation (CaO2)

A

(1.34 x HGB x SaO2) + (PaO2 x .003)

54
Q

oxygen delivery equation (DO2)

A

CaO2 x CO x 10 OR
CaO2 x (HR x SV) x 10

55
Q

after oxygen diffuses through the capillary membrane, it is transported in the blood in 2 ways

A
  1. reversibly binds with HGB (97%)
  2. Dissolved in plasma (3%)
56
Q

each gram of HGB molecule can carry how many molecular mL of O2?

A

1.39 (but since all HGB carry some metHGB or carboxyHGB, thats why you see 1.34)

57
Q

VO2 (O2 consumption) equation

A

=CO x (CaO2 - CvO2) x 10

58
Q

VO2 = _______ mL/kg/min or ______ mL/min (assumes 70kg male)

A

3.5mL/kg/min
250mL/min

59
Q

decreased P50 = shift to the

A

left on the oxygHGB curve
ex)HgbF

60
Q

increased P50 = shift to the

A

right on the oxyHGB curve

61
Q

when PaO2 is >100mmHg, what happens to the O2 in the body

A

no additional O2 will bind to HGB but it will continue to dissolve in blood

62
Q

define bohr effect

A

Bohr effect happens in BLOOD
CO2 and H+ cause conformational change in HGB to facilitate O2 release of O2.
AKA increased partial pressure of CO2 and decreased pH causes HGB to release O2
O2 OFFLOADING

63
Q

what happens to 2,3 DPG in banked blood

A

concentration falls and shifts O2/HGB dissociation curve to the left and reduces amount of O2 available at tissue level

64
Q

when is 2,3 DPG produced

A

during RBC glycolysis

65
Q

does HgbF respond to 2,3 DPG?

A

no, which explains why it has a left shift (p=19mmHg)

66
Q

what happens during glycolysis

A

glucose –> pyruvic acid
1. 1 glucose molecule becomes 2 pyruvic acid molecules. (in the presence of O2, pyruvic acid is transported to mitochrondria. without O2 available, pyruvic acid becomes lactate in the cytoplasm)
2. the 2 pyruvic acid are converted to 2 acetyl coenzyme A

-2,3 DPG is produced about half way through glycolysis which is why increased glycolysis means increased 2,3 DPG

67
Q

what is the ATP net gain during glycolysis and the krebs cycle

A

2 ATP

68
Q

krebs cycle (citric acid cycle)

A
  1. oxaloacetic acid and acetyl coenzyme A react to produce citric acid in matrix of mitochondria.
  2. reaction ends with production of oxaloacetic acid, NADH, and CO2
  3. goal is to produce large quantity of H+ in form of NADH because its used for electron transport
69
Q

oxidative phosphorylation (and net gain)

A
  1. NADH is split into NAD, H+ and 2 electrons
  2. a gradient is generated which causes ATP synthesis with the help of ATP synthase
  3. O2 serves as final electron acceptor
  4. end product is 34 ATP and H2O
70
Q

primary byproduct of aerobic metabolism

A

CO2

71
Q

how is CO2 transported in the blood? (3)

A
  1. as bicarbonate (70%)
  2. bound to HGB as carbamino compounds (23%)
  3. dissolved in plasma (7%)
72
Q

describe Haldane effect

A

CO2 loading on HGB. O2 causes erythrocyte to release CO2

73
Q

what is the reaction for carbonic acid buffer r/t bicarbonate

A

H2O + CO2 <-> H2CO3 <-> H+ + HCO3-

74
Q

what is needed to facilitate the carbonic acid buffer

A

carbonic anhydrase (facilitates creation of carbonic acid)

75
Q

when talking about the solubility of CO2 relative to O2, which law is being referenced

A

henrys law (solubility)

76
Q

deoxygenated HGB causes CO2 dissociation curve to shift to the

A

left

77
Q

when referencing CO2 dissociation curve, explain the left shift

A

blood has increased affinity for CO2. we are referencing deoxygenated HGB.
- lower PO2 means more CO2 is carried

78
Q

when referencing CO2 dissociation curve, explain the right shift

A

blood has a decreased affinity for CO2. we are referencing oxygenated HGB.
-higher PO2 means less CO2 is carried.

79
Q

where in the body is the CO2 dissociation curve right shfited

A

lungs

80
Q

where in the body is the CO2 dissociation curve left shifted

A

capillaries

81
Q

PaCO2=

A

CO2 production / alveolar ventilation

82
Q

hypercapnia and K

A

activates H/K pump
buffers CO2 in exchange for releasing K into the plasma

83
Q

primary internal monitor of PaCO2

A

central chemoreceptors in medulla

84
Q

secondary monitors of PaCO2

A

peripheral chemoreceptors in aortic bodies and transverse aortic arch

85
Q

MV increases with PaCO2 in a linear fashion when PaCO2 is between

A

20-80mmHg

86
Q

a left shift in the CO2 ventilatory response curve implies that the apneic threshold has

A

decreased

87
Q

a right shift in the CO2 ventilatory response curve implies that the apneic threshold has

A

increased

88
Q

what is the respiratory pacemaker

A

dorsal respiratory center (in NTS of medulla)

89
Q

where does neural control of ventilation take place

A

medulla

90
Q

function of, location of pneumotaxic center

A

inhibits DRG, located in upper pons
triggers end of inspiration by inhibiting DRG

91
Q

function and location of ventral respiratory group

A

located in the medulla
primarily active during expiration, has pre botzinger complex

92
Q

function and location of apneustic center

A

in lower pons
stimulates DRG (stimulates pacemaker), causes inspiration.
action is inhibited by pulmonary stretch receptors (J receptors)

93
Q

what can and cant diffuse through BBB

A

CO2 can, H+ and HCO3- cannot

94
Q

primary stimulus at central chemoreceptor

A

H+

95
Q

if H+ cant pass through BBB, how can is stimulate central chemoreceptor

A

CO2 + H2O combine to become H+ and HCO3-

96
Q

what does the carotid body monitor for

A

hypoxemia (PaO2 < 60mmHg)
(secondary responsibilities include monitoring for PaCO2, H+ and perfusion pressure)

97
Q

hypoxic ventilatory response to hypoxemia

A
  1. PaCO2 <60mmHg closes oxygen sensitive K channels in type 1 gloms cells
  2. raises RMP, opens Ca2+ channels, increases neurotransmitter release (Ach and ATP)
  3. AP propagated among herrings nerve (CN9)
  4. afferent pathway terminates in inspiratory center in medulla)
  5. MV increases to restore PaO2
98
Q

which reflex prevents alveolar over distention

A

hering breuer INFLATION reflex

99
Q

which reflex is initiated when lung volumes are too small

A

Hering breuer DEFLATION reflex

100
Q

HPV occurs due to a reduction in

A

alveolar oxygen tension (NOT arterial PO2)

101
Q

drugs that can inhibit HPV

A

gases
vasodilators
PDE inhibitors
dobutamine
CCB’s
vasoconstrictive agents (neo, epi, dopa), may constrict well oxygenated vessels and increase shunt flow

102
Q

which conditions decrease O2 carrying capacity but do not initiate HPV response

A

anemia
carbon monoxide poisoning

103
Q

what does this graph tell us

A

towards the apex: V>Q
towards the base: V < Q

104
Q

label this graph

A
105
Q

what does increased Vd do to the PaCO2 EtCO2 gradient and CO2

A

widens gradient, increases CO2 retention

106
Q

VA is inversely proportional to

A

PaCO2. higher CO2 creates faster and deeper breathing thereby increasing VA (alveolar ventilation aka MV without dead space)

107
Q

CV v CC

A

CV: when dynamic compression of aw begins (CLOSE-P)
closing capacity: CV+RV. Volume of gas contained in lungs when airways begin to collapse

108
Q

which principle calculates O2 consumption

A

Ficks (VO2 is the difference between the amount of O2 that leaves the lungs and the amount of O2 that returns to the lungs)
VO2= CO x (CaO2-CvO2) x 10

109
Q

what happens to 2,3 DPG in banked blood and what does it do to the oxyhgb curve

A

decrease in 2,3 DPG and curve shifts to the left

110
Q

what is the energy currency in the body

A

ATP

111
Q

a more acidic environment and Bohr v Haldane

A

bohr enhances O2 offloading from Hgb (Bohr effect) and co2 loading onto Hgb (haldane)

112
Q

solubility is a function of which law (and example)

A

henrys
solubility of CO2 is 0.067

113
Q

CO2 ventilatory response curve describes relationship between

A

PaCO2 and MV

114
Q

what is the primary monitor of PaCO2

A

central chemoreceptor in medulla

115
Q

MV increases with PaCO2 in a linear fashion when it’s between

A

20-80mmHg

116
Q

left shift and increased slope in CO2 ventilatory response curve creates what

A

respiratory alkalosis

117
Q

right shift and decreased slope in CO2 ventilatory response curve creates what

A

resp acidosis

118
Q

a left shift in the CO2 ventilatory response curve implies that the apneic threshold has

A

decreased (things that make you breathe a lot to create that resp alkalosis on the left side)

119
Q

a right shift in the CO2 ventilatory response curve implies that the apneic threshold has

A

increased (things that make you breathe less to cause that resp acidosis on the right side)

120
Q

5 causes of hypoxemia and how A-a gradient is affected

A

normal A-a
- reduced FiO2 (hypoxic mixture)
-hypoventilation (opioid OD)

increased A-a
-diffusion limitation (p.fibrosis)
-V/Q mismatch (COPD)
-shunt (R-L, intracardiac)