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APEX > Unit 1 - Respiratory Physiology > Flashcards

Unit 1 - Respiratory Physiology Flashcards

1
Q

what is tidal volume?

A

the amount of gas that is inhaled and exhaled during a breath

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2
Q

where does Vt go when you take a breath?

A
  • part goes to the respiratory zone, where gas exchange occurs
  • remainer sits in conducting zone (dead space)
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3
Q

normal dead space in a healthy ~70 kg adult

A

~2 mL/kg or 150 mL

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4
Q

normal removal of gas with exhalation

A
  • conducting zone gas removed first
  • followed by exhalation of respiratory zone gas
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5
Q

consequence of any condition that increases dead space

A

makes it more difficult to eliminate expiratory gases from lungs
- widens PaCO2-EtCO2 gradient
- causes CO2 retention

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6
Q

what is ventilation rate

A

volume of air moved into and out of lungs in a given period of time

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7
Q

what is minute ventilation (VE)?

A

amount of air in a single breath (Vt) multiplied by RR

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8
Q

what is alveolar ventilation?

A

fraction of VE that is available for gas exchange

= (Vt - Vd) x RR

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9
Q

calculating VA in relation to PaCO2

A

= CO2 production / PaCO2

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10
Q

VA is directly proportional to:

A

CO2 production
- higher CO2 production stimulates body to breathe deeper and faster to eliminate more CO2

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11
Q

VA is inversely proportional to:

A

PaCO2
- faster and deeper breathing reduces PaCO2

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12
Q

How does Vd (dead space) affect the PaCO2-EtCO2 gradient?

A

any condition that increases dead space also increases the gradient

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13
Q

how does atropine affect the PaCO2-EtCO2 gradient

A

increases
- bronchodilator, so it increases anatomic dead space by increasing volume of the conducting zone

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14
Q

how does hypotension affect PaCo2-EtCO2 gradient

A

increases
- reduced pulmonary blood flow = increased alveolar dead space

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15
Q

how does PPV affect PaCO2-EtCO2 gradient?

A

increases
- increases alveolar pressure, which increases ventilation relative to perfusion (dead space increases)

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16
Q

examples of decreased dead space

A

reduced by anything that reduces the volume of the conducting zone or increases pulmonary blood flow
- ETT
- LMA
- neck flexion

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17
Q

what is anatomic dead space?

A

air confined to conducting airways

nose & mouth to terminal bronchioles

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18
Q

what is alveolar dead space?
examples?

A

alveoli that are ventilated but not perfused

decreased pulmonary blood flow

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19
Q

what is physiologic dead space?

A

anatomic Vd + alveolar Vd

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20
Q

what is apparatus dead space?

examples?

A

Vd added by equipment

facemask, HME

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21
Q

what is the dead space to tidal volume ratio (Vd/Vt)

A

fraction of Vt that contributes to dead space

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22
Q

Vd to Vt ratio in spontaneously ventilating 70 kg pt

A

Vd/Vt = 150 mL/450 mL = 0.33

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23
Q

why does mechanical ventilation increase the Vd/Vt ratio to 0.5 (50%)?

A

mechanical ventilation increases alveolar pressure, which increases ventilation relative to perfusion

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24
Q

most common cause of increased Vd/Vt under GA

A

reduced CO

r/o hypotension with acute EtCO2 decrease before considering other causes of increased dead space

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25
Q

what does it mean if something increases Vd?

A

more of the Vt is lost to dead space and alveolar ventiltion will decrease

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26
Q

what does it mean for something to decrease Vd

A

less of the Vt is lost to dead space; alveolar ventilation will increase

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27
Q

how does an LMA reduce Vd

A

it bypasses much of the anatomic Vd between the mouth and glottis (similar to ETT)

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28
Q

how does neck position affect Vd

A
  • extension = increased Vd
  • flexion = decreased Vd
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29
Q

how do surgical positions affect Vd

A
  • sitting: increased
  • supine, trendelenburg: decreased
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30
Q

how to maintain a constant PaCO2 with increased dead space

A

increase minute ventilation (RR, Vt, or both)

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31
Q

why do patients with chronic bronchitis retain CO2?

A

Vd/Vt ratio is increased
(minute ventilation must increase to 30-50 L/min to maintain a normal PaCO2 - difficult to maintain)

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32
Q

where does dead space begin in a circle system

A

at the y-piece

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33
Q

does increasing the length of the circuit impact dead space?

A

no - anything proximal to the y-piece does not influence dead space, nor does increasing the length of the circuit

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34
Q

when can the proximal circle circuit become dead space?

A

incompetent valve - the entire limb with the faulty valve becomes apparatus dead space

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35
Q

what is the equation used to calculate physiologic dead space?

A

Bohr equation

compares PaCO2 in the blood vs. PCO2 in exhaled gas (greater difference in values = greater amount of dead space)

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36
Q

Bohr equation

A

Vd/Vt = (PaCO2 - PeCO2) / PaCO2

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37
Q

gross estimation of dead space

A

difference between PaCO2 and EtCO2

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38
Q

ventilation and perfusion values in the textbook patient

normal V/Q ratio in this patient?

A

ventilation is 4 L/min
perfusion is 5 L/min
V/Q - 0.8

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39
Q

what is alveolar compliance

A

a change in alveolar volume for a given change in pressure

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40
Q

what part of the lungs contain the largest alveoli?

A

the alveoli near the apex

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41
Q

how does volumetric change affect alveolar ventilation

A

an alveolus that undergoes a greater degree of volumetric change during a breath is going to be better ventilated (aka better gas exchange) vs. smaller degree of volumetric change

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42
Q

compliance =

A

change in volume/change in pressure

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43
Q

in what part of the lung is ventilation the greatest

A

lung base d/t higher alveolar compliance

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44
Q

in what part of the lungs is perfusion the greatest

A

lung base
d/t gravity

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45
Q

alveoli with the poorest ventilation

A

alveoli in the apex bc they have the poorest compliance

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46
Q

alveoli with the greatest ventilation

A

alveoli in the base

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47
Q

why are there higher V/Q ratios towards the apex and lower ratios towards the base

A
  • gravity and hydrostatic pressure affect distribution of blood flow to the lung
  • when standing upright, there’s less blood flow towards apex of lung and more blood flow towards the base
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48
Q

how is ventilation affected in the apex of the lungs in the upright position and in the non-dependent lung in lateral position

A
  • decreased alveolar ventilation
  • decreased alveolar compliance
  • decreased PACO2
  • increased PAO2
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49
Q

how is ventilation affected in the base of the lungs in the upright position and dependent lung in lateral position

A
  • increased alveolar ventilation
  • increased alveolar compliance
  • increased PACO2
  • decreased PAO2
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50
Q

how is perfusion affected in the nondependent lung in lateral position and in the apex of the lung in upright position

A
  • decreased blood flow
  • decreased vascular pressure
  • increased vascular resistance
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51
Q

how is perfusion affected in the dependent lung in lateral position and base of lung in upright position

A
  • increased blood flow
  • increased vascular pressure
  • decreased vascular resistance
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52
Q

dependent and non-dependent lung regions in sitting position

A

dependent: base
non-dependent: apex

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53
Q

dependent and non-dependent lung regions in supine position

A

dependent: posterior
non-dependent: anterior

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54
Q

dependent and non-dependent lung regions in left lateral position

A

dependent: left lung
non-dependent: right lung

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55
Q

dependent and non-dependent lung regions in right lateral decubitus

A

dependent: right lung
non-dependent: left lung

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56
Q

how does V/Q mismatch normally affect the A-a gradient

A

usually increases

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57
Q

what determines the final partial pressures of oxygen and carbon dioxide in the bood

A

balance between ventilation and perfusion in each unit and throughout the lung

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58
Q

V and Q in apex and base of lungs in sitting position

A

apex: V > Q
base: Q > V

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59
Q

Q=

A

pulmonary blood flow or cardiac output

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60
Q

most common cause of hypoxemia in PACU

A

V/Q mismatch (specifically atelectasis)

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61
Q

consequences of decreased FRC with anesthesia and surgery

A
  • less radial traction to keep airways open
  • atelectasis, R-L shunt, V/Q mismatch, hypoxemia
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62
Q

treatment of V/Q mismatch d/t atelectasis

A
  • humidified O2
  • maneuvers to reopen airways (mobility, coughing, deep breathing, incentive spirometry)
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63
Q

consequences of V/Q mismatch in underventilated alveoli

A

blood passing through underventilated alveoli tends to retain CO2 and can’t take in enough O2

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64
Q

consequences of V/Q mismatch in overventilated alveoli

A

blood passing through tends to give off excessive amount of CO2

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65
Q

oxyhemoglobin dissociation curve with overventilated alveoli

A
  • flat curve (blood can elminate a large amount of CO2 but can’t take up a proportionate amount of O2)
  • once PaCO2 reaches 100 mmHg, hgb is fully saturated and any additional O2 in blood must be dissolved in blood

(alveolus can transfer much more CO2 than it can O2)

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66
Q

why does the PACO2-PaCO2 gradient usually remain small with V/Q mismatch

A

a lung with V/Q mismatch eliminates CO2 from overventilated alveoli to compensate for underventilated alveoli

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67
Q

why is the PAO2-PaO2 gradient usually large with V/Q mismatch

A

a lung with V/Q mismatch can’t absorb more oxygen from overventilated alveoli to compensate for underventilated alveoli

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68
Q

how does the body compensate for V/Q mismatch

A
  • bronchioles constrict to minimize ventilation of poorly perfused alveoli
  • HPV reduces pulmonary blood flow to poorly ventilated alveoli to combat shunting
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69
Q

what does V/Q = infinity mean

A

dead space

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70
Q

what does V/Q = 0 mean

A

shunt

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71
Q

variables in the law of Laplace

A
  • tension
  • pressure
  • radius
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72
Q

describes the relationship between pressure, radius, and wall tension

A

law of Laplace

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73
Q

equation for tension in a cylinder

examples

A

pressure * radius

ex. blood vessels, cylindrical aneurysms

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74
Q

equation for tension of a sphere

examples

A

(pressure * radius) / 2

ex. alveoli, cardiac ventricles, saccular aneurysm

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75
Q

according to the law of Laplace, the tendency of an alveolus to collapse is directly proportional to:

A

surface tension

more tension = more likely to collapse

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76
Q

according to the law of Laplace, the tendency of an alveolus to collapse is indirectly proportional to:

A

alveolar radius

smaller radius = more likely to collapse

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77
Q

why are alveoli prone to collapse?

A

they’re coated with a thin layer of water, which increases surface tension and promotes collapse

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78
Q

function of surfactant

A

modulates surface tension and prevents alveolar collapse

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79
Q

which alveoli have more surfactant?

A

each alveolus has the same amount of surfactant

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80
Q

what variable impacts the concentration of alveolar surfactant

A

radius

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81
Q

what prevents smaller alveoli from collapsing and emptying into larger alveoli

A

as radius changes, so does concentration of surfactant - this keeps alveolar pressures constant

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82
Q

when do type 2 pneumocytes start producing surfactant

when does production peak

A

22-26 weeks gestation

peaks at 35-36 weeks

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83
Q

what determines the V/Q ratio of each alveolar unit

A

relative pressures between alveolus (PA), arterial capillary (Pa), venous capillary (Pv), and interstitial space (Pist)

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84
Q

Pa, Pv, and PA in all 4 lung zones

A

1: PA > Pa > Pv
2: Pa > PA > Pv
3: Pa > Pv > PA
4: Pa > Pis > Pv > PA

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85
Q

which lung zone usually does not occur in a normal lung

A

zone 1 (dead space)
ventilation without perfusion

???

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86
Q

what factors increase zone 1 (dead space)

A
  • hypotension
  • PE
  • excessive airway pressure
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87
Q

compensation for zone 1 (dead space)

A

bronchioles of unperfused alveoli constrict to reduce dead space

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88
Q

in which zone does V/Q = 1

A

zone 2
ventilation and perfusion (V/Q = 1)

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89
Q

how is it possible for a zone 2 unit to transiently change to zone 1 or zone 3

A

because pulmonary capillary pressure and alveolar pressure change throughout the respiratory cycle

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90
Q

relationship between blood flow and Pa/PA

A
  • blood flow is directly proportional to the difference in Pa - PA
  • the greater the differences between Pa-PA, the greater the blood flow
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91
Q

why should the tip of a PAC be placed in zone 3

A

the pressure in the capillary is always higher than the alveolus, so the vessel is always open and blood is always moving through it

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92
Q

what is an anatomic shunt?

A

any venous blood that empties directly into the left side of the heart (bypasses lungs and never has opportunity to saturate with O2)

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93
Q

sites that contribute to normal anatomic shunt

A
  • thesbian veins (drain L heart)
  • bronchiolar veins (drain bronchial circulation)
  • pleural veins (drain bronchial circulation)
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94
Q

classic example of zone 4

A

pulmonary edema

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95
Q

2 phenomena normally responsible for pulmonary edema

A
  1. fluid is pushed across capillary mebrane by significant increase in hydrostatic pressure (ex. fluid overload)
  2. fluid is pulled across capillary membrane by profound reduction in pleural pressure (NPPE)
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96
Q

purpose of alveolar gas equation

A

estimate the partial pressure of oxygen in the alveoli

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97
Q

how does supplemental oxygen affect hypoxemia and hypercarbia

A
  • can easily reverse hypoxemia
  • no effect on hypercarbia
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98
Q

what does the alveolar gas equation tell us about PAO2

A

the max PAO2 that can be achieved in a given FIO2

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99
Q

alveolar oxygen equation

A

FiO2 * (Pb - PH2O) - (PaCO2 / RQ)

  • Pb = barometric pressure
  • PH2O = humidity of inspired gas
  • RQ = respiratory quotient
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100
Q

what is PH2O assumed to be

A

47 mmHg

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101
Q

what is RQ assumed to be

A

0.8

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102
Q

is FiO2 always higher or lower than partial pressure of O2 in alveoli? why?

A

always higher
- inspired air becomes 100% humidified as it moves towards alveoli, which dilutes O2 concentration
- inspired air mixes with expired air, which dilutes the concentration of oxygen going toward alveoli

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103
Q

how does supplemental oxygen affect PaO2 and PAO2

A

can increase both

(masks hypoventilation, doesn’t treat cause)

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104
Q

what does an RQ > 1 suggest

A
  • lipogenesis
  • occurs with overfeeding
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105
Q

what does an RQ of 0.7 suggest

A

lipolysis
occurs with starvation

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106
Q

equation for RQ

A

CO2 production (200 mL/min) / O2 consumption (250 mL/min) = 0.8

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107
Q

5 causes of hypoxemia

A
  1. hypoxic mixture
  2. hypoventilation
  3. diffusion limitation
  4. V/Q mismatch
  5. shunt
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108
Q

what is the A-a gradient in hypoxic mixture and hypoventilation

A

normal

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109
Q

what PaO2 defines hypoxemia

A

< 80 mmHg

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110
Q

hypoxemia vs. hypoxia

A
  • hypoxemia = low concentration of O2 in blood
  • hypoxia = state of insufficient O2 to support tissues
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111
Q

does supplemental O2 fix A-a gradient in hypoxemia caused by a shunt

A

nope

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112
Q

what does a large difference in PAO2 and PaO2 imply

A

significant degree of shunt, V/Q mismatch, or diffuse defect across alveolar-capillary membrane

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113
Q

5 things that increase A-a gradient

A
  • aging
  • vasodilators
  • R-L shunt
  • diffusion limitations
  • V/Q mismatch
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114
Q

why does aging increase the A-a gradient

A

closing capacity increases relative to FRC

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115
Q

how do vasodilators affect A-a gradient

A

increase due to decreased HPV

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116
Q

how does R-L shunt affect A-a gradient

A

increases d/t atelectasis, pneumonia, bronchial intubation, intracardiac defect

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117
Q

how do diffusion limitations affect the A-a gradient

A

increase d/t alveolarcapillary membrane thickening hindering O2 diffusion

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118
Q

how to calculate A-a gradient

A

PAO2 - PaO2

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119
Q

how to estimate degree of shunt in relation to A-a gradient

A

increases by 1% for every 20mmHg of A-a gradient

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120
Q

normal inspiratory reserve volume in a healthy 70 kg male

A

3,000 mL

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121
Q

what is IRV?

A

inspiratory reserve volume - volume of gas that can be forcibly inhaled after a tidal inhalation

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122
Q

what is Vt? what is normal Vt in 70 kg healthy male?

A

volume of gas that enters and exits lungs during tidal breathing

500 mL

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123
Q

what is ERV?

normal in healthy 70 kg male?

A

expiratory reserve volume - volume of gas that can be forcibly exhaled after a tidal exhalation

1100 mL

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124
Q

what is closing volume?

A

the volume above residual volume where the small airways begin to close

variable
- ~30% at age 20
- ~55% at age 70

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125
Q

what is RV?

what’s normal for a healthy 70 kg man?

A

residual volume - volume of gas that remains in lungs after a complete exhalation

1200 mL

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126
Q

-

A

-

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127
Q

can residual volume be exhaled from lungs?

A

no

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128
Q

what is total lung capacity

A

IRV + TV + ERV + RV

5800 mL in healthy 70kg male

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129
Q

what is vital capacity

A

IRV + TV + ERV

normal: 4500 mL

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130
Q

what is FRC

A

RV + ERV

lung volume at end expiration

normal: 2300 mL

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131
Q

what is closing capacity?

A

RV + CV
- absolute volume of gas contained in lungs when small airways close

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132
Q

normal vital capacity

A

65-75 mL/kg

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133
Q

lungs volumes in males vs. females

A

~25% smaller in females

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134
Q

lung volumes in patients with obstructive lung disease

A

increased RV, CC, and TLC d/t air trapping

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135
Q

can spirometry measure TLC or FRC?

A

no, since it can’t measure RV

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136
Q

dynamic measurements that assess small airway closure

A

closing capacity
closing volume

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137
Q

reservoir of oxygen that prevents hypoxemia during apnea

A

FRC

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138
Q

normal FRC

A

35 mL/kg

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139
Q

what is static equilibrium

A

at FRC, the inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall

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140
Q

3 ways FRC can be indirectly measured

A
  1. nitrogen washout
  2. helium wash-in
  3. body plethysmography
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141
Q

how can we estimate the amount of time a pt can be apneic before desaturation

A

FRC / VO2

VO2 = oxygen consumption

142
Q

what happens to zone 3 when FRC is reduced

A

increases (intrapulmonary shunt)

143
Q

how do ARMs and PEEP restore FRC

A

by reducing West zone 3

144
Q

how does general anesthesia affect FRC and why

A
  • decreases
  • diaphragm shifts cephalad ~4 cm d/t decreased insp muscle tone and increased exp muscle tone
145
Q

FRC in obesity

A

decreased d/t decreased chest wall compliance and increased airway collapsibility

146
Q

FRC in pregnancy

A
  • decreased
  • diaphragm shifts cephalad as a result of gravid uterus, decreased chest wall compliance
147
Q

FRC in neonates

A
  • decreased
  • less alveoli = decreased lung compliance
  • cartilaginous ribcage is prone to collapse during inspiration
148
Q

FRC in advanced age

A
  • increased
  • dec lung elasticity = inc air trapping = inc RV = inc FRC
149
Q

FRC in lithotomy and trendelenburg

A

decreased

150
Q

in what positions is FRC increased

A
  • prone
  • sitting
  • lateral
151
Q

now do NMBs affect FRC

A
  • decreased
  • diaphragm shifts cephalad and decreases lung volumes
152
Q

how does light anesthesia affect FRC

A

decreased d/t straining and forceful expiration causing decreased lung volumes

153
Q

how do excessive IV fluids affect FRC

A
  • decreased
  • fluid accumulation in dependent lung regions favor zone 3 development
154
Q

how does high FiO2 affect FRC

A
  • decreased
  • absorption atelectasis = shunt
155
Q

suggested FiO2 to prevent absorption atelectasis

A

< 80% at emergence + PEEP or CPAP

156
Q

how does PEEP affect FRC

A

increases d/t recruitment of collapsed alveoli, partially overcoming affect of GA, and decreased venous admixture = increased PaO2

157
Q

how do sigh breaths affect FRC

A

increase (recruits collapsed aleoli)

158
Q

6 factors that increase closing volume

A

CLOSE-P
- COPD
- LV failure
- Obesity
- Surgery
- Extremes of age
- Pregnancy

159
Q

what determines if airways collapse during tidal breathing

A
  • relationship between FRC and closing capacity
  • normally, FRC > CC and airways don’t collapse during tidal breathing
160
Q

what happens when CC > FRC

A
  • airway closure occurs during tidal breathing
  • contributes to intrapulmonary shunting and hypoxemia
161
Q

when does airway closure occur in a young healthy pt vs. an older patient

A
  • young & healthy: just above residual volume
  • old: pleural pressure becomes progressively higher and small airwas close sooner and at higher volumes
162
Q

what happens to FRC, CC, RV, and VC with aging

A
  • increased FRC
  • increased CC
  • increased RV
  • decreased VC
163
Q

how do anesthesia and age affect closing capacity?

A
  • by 30, CC ~ FRC under GA
  • by 44, CC ~ FRC when supine
  • by 66, CC ~ FRC when standing
164
Q

how does increased CC relative to FRC affect oxygenation

A

anything that decreases FRC relative to CC or anything that increases CC relative to FRC will convert normal V/Q units to low V/Q units or shunt units

165
Q

what is CaO2?

A

oxygen content - measure of how much oxygen is present in 1 deciliter (100 mL) of blood

166
Q

how is O2 transported by the blood

A
  1. reversibly binds with hgb (97%)
  2. dissolves in plasma (3%)
167
Q

calculation for CaO2

A

(1.34 * hgb * SaO2) + (PaO2 * 0.003) = 20 mL O2 per dL

168
Q

theoretical max of molecular oxygen that can be carried by each gram of hgb

A

1.39 mL
- often see 1.34 because hgb usually contains a small amount of methemoglobin

169
Q

normal hgb and hct values for men vs. women

A

men: 15 g/dL and 45%
women: 13 g/dL and 39%

170
Q

how is O2 that is dissolved in plasma measured

A

PaO2

171
Q

what should a PaO2 measurement be used to determine

A

gas exchange in the lungs, not as a measurement of oxygen content in the blood

172
Q

what gas law explains O2 dissolving in the plasma

A

Henry’s law

173
Q

solubility coefficient for oxygen

A

0.003 mL/dL/mmHg

174
Q

what tells us how fast a quantity of o2 is delivered to tissues

A

oxygen delivery (DO2)

175
Q

what is the driving mechanism of DO2

A

cardiac output

176
Q

what principle is used to calculate oxygen consumption

A

fick’s principle/law

177
Q

what does Fick’s law assume about VO2

A
  • that it is the difference between amount of O2 that leaves the lungs and the amount of O2 that is returned to the lungs
  • difference in values is the amount of O2 consumed by the body
178
Q

equation for VO2

A

cardiac output * (CaO2 - CvO2) * 10

179
Q

normal value for VO2

A
  • 3.5 mL/kg/min
  • approx 250 mL/min in healthy 70 kg male
180
Q

what does the oxyhgb curve plot

A

hgb saturation (SaO2) vs. oxygen tension in blood (PaO2)

181
Q

what is P50?

A

the PaO2 where hgb is 50% saturated with oxygen

182
Q

what causes a decreased P50? what does this do to oxyhgb curve?

A
  • left shift (hgb has a stronger bond on O2)
  • ex. Hgb F, hypocarbia, carboxyhemoglobin
183
Q

what causes increased P50? what does this do to the oxyhgb curve?

A
  • shift to right (hgb more willing to release O2)
  • acidosis, hyperthermia, increased 2,3 DPG
184
Q

what does a left shift in the oxyhgb dissociation curve mean

A
  • increased affinity of hgb to O2
  • occurs in the lungs

left = love

185
Q

what does a right shift of oxyhgb dissociation curve mean

A
  • decreased affinity for O2 (right = release)
  • occurs near metabolically active tissue
186
Q

how does acidosis affect oxyhgb dissociation curve

A

right shift

187
Q

what happens to the oxyhgb curve with increased and decreased P50

A

lower P50 = left shift
higher P50 = right shift

188
Q

when does maximal O2 loading occur

A

PaO2 of ~100 mmHg

189
Q

will FiO2 increase binding of O2 to hgb if PaO2 is already 105 mmHg?

A

no - further increase in Fio2 will increase amount of oxygen dissolved in blood but won’t increase binding

190
Q

examples of common hemoglobinopathies
how do they affect the oxyhgb dissociation curve

A

left shift

  • fetal hgb
  • methemoglobin
  • carboxyhemoglobin
191
Q

what is the Bohr effect

A

CO2 and hydrogen ions cause a confirmational change in the hgb molecule and facilitates the release of O2

(increased partial pressure of CO2 and decreased pH cause Hgb to release O2)

192
Q

what is 2,3-DPG?

A
  • produced during RBC glycolysis
  • maintains oxyhgb curve in slightly right shift at all times
  • important compensation mechanism in chronic anemia
193
Q

what happens to 2,3-DPG in hypoxia

A

increased production - facilitates O2 offloading

194
Q

2,3 DPG concentration in banked blood

A

decreased - shifts oxyhgb dissociation curve to left and reduces amount of O2 available at tissue level

195
Q

what explains why Hgb F has a left shift

A

Hgb F doesn’t respond to 2,3-DPG

196
Q

1 molecule of glucose converts to ____ molecules ATP

A

38

197
Q

what produces ATP

A

oxidation of proteins, carbs, and fats

198
Q

primary substrate for ATP synthesis

A

glucose

199
Q

which produces more ATP - aerobic or anaerobic metabolism

A

aerobic

200
Q

primary goal of glycolysis

A

convert 1 glucose to 2 pyruvic acid molecules

201
Q

what happens to pyruvic acid with and without oxygen

A
  • no oxygen available = converted to lactate in cytoplasm
  • oxygen available = transported into mitochondria
202
Q

net gain of glycolysis

A

2 ATP

203
Q

how does glycolysis affect 2,3 DPG

A

the more glucose molecules that go through glycolysis, the more 2,3 DPG is produced

204
Q

where does the Krebs cycle take place

A

matrix of mitochondria

205
Q

when does the Krebs cycle begin and end

A
  • begins when oxaloacetic acid and acetylCoA react to produce citric acid
  • ends with production of oxaloacetic acid, NADH, and CO2
206
Q

primary goal of Krebs cycle

A

produce a large quantity of H+ ions in form of NADH - used in electron transport

207
Q

net gain from krebs cycle

A

2 ATP

208
Q

what happens to NADH in oxidative phosphorylation

A

split into NAD+, H+, and 2 electrons

209
Q

what drives ATP synthesis

A

electrons from NADH split are fed into chemiosmotic mechanism, generating a proton gradient across membrane

has help from ATP synthase

210
Q

net gain from oxidative phosphorylation

A

34 ATP

211
Q

final electron acceptor in electron transport

A

oxygen

212
Q

what is the lactic acid pathway

A

provides an alternative mechanism to convert pyruvic acid to ATP (just 2 molecules)

213
Q

what is the basis of altered homeostasis in setting of acidosis

A

body’s enzymes tend to not function properly in acidic environment

214
Q

how is serum lactate primarily cleared

A

liver

215
Q

what causes lactic acid build up

A

if there is no oxygen to accept electrons in electron transport, pyruvic acid isn’t used and concentration increases

lactic acid pathway converts pyruvic acid into ATP

lactic acid is a byproduct of this pathway

216
Q

primary byproduct of aerobic metabolism

A

CO2

217
Q

how is CO2 transported in blood

A
  1. as bicarbonate (70%)
  2. bound to hgb as carbamino compounds (23%)
  3. dissolved in plasma
218
Q

how is CO2 transported to lungs

A

venous blood

219
Q

PvCO2 vs. PaCO2

A

PvCO2 is about 5 mHg higher than PaCo2

220
Q

what is the Haldane effect

A

increased CO2 loading on hgb in acidic environment

221
Q

what is carbonic anhydrase

A

an enzyme that facilitates formation of carbonic acid (H2CO3) from H2O and CO2

222
Q

what does carbonic acid rapidly dissociate into

A

H+ and HCO3-

223
Q

what buffers H+

A

hgb and HCO3-

224
Q

what is the Hamburger shift

A

chloride shift
Cl- is transported into erythrocyte to maintain neutrality

225
Q

how does the Hamburger effect impact venous circulation

A

chloride shift adds osmotically active ions (Cl-) to erythrocyte in venous cirulation. erythrocyte swells and cell volume is increased relative to plasma volume

  • this explains why venous hct is ~3% higher than arterial hct
226
Q

solubility coefficient of dissolved Co2

A

0.067 mL/dL/mmHg

227
Q

solubility is a function of which gas law

A

Henry’s

228
Q

what is the Haldane effect

A
  • at a given PaCO2, deoxygenated hgb can carry more CO2
  • in the presence of deoxygenated hgb, the CO2 dissociation curve shifts to the left
229
Q

Bohr effect vs. Haldane effect

A
  • Bohr: says that CO2 and decreased pH cause erythrocyte to release O2
  • Haldane: says that O2 causes erythrocyte to release CO2 (deoxygenated blood can carry more CO2)
230
Q

what happens to the CO2 dissociation curve in the presence of oxygenated hgb

A
  • shifts to the right
  • blood has decreased affinity for CO2
231
Q

what happens to co2 dissociation curve in presence of deoxygenated hgb

A
  • shifts to left
  • blood has increased affinity for CO2
232
Q

where does increased deoxygenated hgb occur

A

in systemic capillaries to facilitate loading and subsequent transport of CO2

233
Q

where in the body is the CO2 dissociation curve right shifted

A

in the lungs to facilitate unloading of CO2 so it can be excreted

234
Q

..

A

..

235
Q

how does deoxygenated hgb shift the CO2 dissociation curve

A

left shift (blood can hold more CO2)

236
Q

what is hypercapnia

A

PaCO2 > 45 mmHg

237
Q

how is PaCO2 calculated

A

CO2 production / alveolar ventilation

238
Q

3 causes of hypercapnia

A
  • increased CO2 production
  • decreased CO2 elimination
  • rebreathing
239
Q

examples of increased co2 production that cause hypercapnia

A
  • sepsis
  • overfeeding
  • MH
  • intense shivering
  • prolonged sz activity
  • thyroid storm
  • burns
240
Q

examples of decreased CO2 elimination that contribute to hypercapnia

A
  • airway obstruction
  • increased dead space
  • increased Vd/Vt
  • ARDS
  • COPD
  • resp center depression
  • drug overdose
  • inadequate NMB reversal
241
Q

3 things that can cause rebreathing

A
  • exhausted soda lime
  • incompetent unidirectional valve in circle system
  • inadequate FGF with Mapelson circuit
242
Q

patho of hypoxemia with hypercapnia

A

increased alveolar CO2 displaces alveolar O2 and causes arterial hypoxemia

243
Q

how does hypercarbia affect cardiac muscle

A
  • myocardial depressant
  • also activates SNS, increases catecholamine release from adrenal medulla
  • SNS stim. offsets cardiac depression and vasodilatoin unless acidosis is severe
244
Q

how does hypercarbia affect cardiac rate and rhythm

A
  • tachycardia
  • dysrhythmias
  • prolonged QT
245
Q

CO2 is a smooth muscle dilator. what’s the exception to this?

A

the pulmonary vasculature - increases PVR and right heart workload

246
Q

how does hypercarbia affect minute ventilation

A

increases - CO2 is a resp stimulant

247
Q

what happens to K+ in hypercarbia

A

increased - hypercarbia activates H+/K+ pump, which buffers CO2 acid in exchange for releasing K+ in plasma

248
Q

calcium in hypercarbia and why

A
  • increased
  • iCa competes with H+ for binding sites on plasma proteins
249
Q

how does hypercarbia affect heart in presence of acidosis

A

plasma proteins buffer H+ and release Ca2+, increasing inotropy and offsetting acidosis-induced cardiac depression

250
Q

effect of increased Ca2+ in alkalosis

A

plasma proteins release H+ and Ca2+, which decreases inotropy

251
Q

how does hypercarbia affect ICP

A
  • increased ICP
  • CO2 freely diffuses across BBB
  • dec CSF pH = dec cerebrovascular resistance = increased CBF and volume
252
Q

at what point does CO2 narcosis occur

A

PaCO2 > 90 mmHg

253
Q

how does hypercarbia affect blood pH

A
  • resp acidosis: kidneys excrete H+ and conserve bicarb to return pH to normal
  • begins with hours
  • full compensation may take several days
254
Q

how does PaCO2 affect pH in acute respiratory acidosis

A

for every 10 mmHg increase above 40 mmHg pH decreases by 0.08

255
Q

how does PaCO2 affect pH in chronic respiratory acidosis

A

for every 10 mmHg increase above 40 mmHg, pH decreases by 0.03 due to HCO3- retention in the kidneys

256
Q

what is the primary monitor of PaCO2

A

central chemoreceptor in medulla

257
Q

what plays a secondary role in monitoring PaCo2

A

peripheral chemoreceptors in carotid bodies and transverse aortic arch

258
Q

when PaCO2 is between ___ and ___, minute ventilation increases in a linear fashion

A

20-80 mmHg

259
Q

what is a MAC of CO2

A

200 mmHg

260
Q

causes of a right shift of the CO2 ventilatory response curve

A
  • metabolic alkalosis
  • CEA
  • natural sleep
  • volatiles
  • opioids
  • NMBs
261
Q

causes of a left shift of the CO2 ventilatory response curve

A
  • hypoxemia
  • metabolic acidosis
  • surgical stim
  • CNS etiologies: inc ICP, fear, anxiety
  • salicylates
  • aminophylline
  • doxapram
  • norepinephrine
262
Q

what do a left shift and increased slope of CO2 ventilatory response curve indicate

A
  • Vm is higher than expected for a given PaCO2
  • creates respiratory alkalosis
263
Q

what is apneic threshold

A

highest PaCo2 at which a person won’t breathe

264
Q

what is implied by a right vs left shift of CO2 ventilatory response curve

A
  • left: implies apneic threshold has decreased
  • right: implies apneic threshold has increased
265
Q

what is the pacemaker for normal breathing?

A

dorsal respiratory center

new evidence: pre-Botzinger complex

266
Q

primarily responsible for expiration

A

ventral respiratory center

267
Q

where is neural control of RR and pattern

A

respiratory center in medulla

268
Q

where is chemical control of RR and pattern

A
  • central chemoreceptors in medulla
  • peripheral chemoreceptors in carotid bodies/aortic arch
269
Q

where does the resp center receive afferent input

A
  • central and peripheral chemoreceptors
  • stretch receptors in lungs
270
Q

where do efferent respiratory center pathways terminate

A

diaphragm, intercostals, and accessory muscles

271
Q

where is the respiratory center located

A

in RAS in medulla and pons

272
Q

primary job of respiratory center

A

determine RR and depth

273
Q

4 components of the respiratory center

A
  1. pneumotaxic center
  2. apneustic center
  3. dorsal respiratory group
  4. ventral respiratory group
274
Q

when is the dorsal respiratory group primarily active

A

during inspiration

275
Q

where are the pneumotaxic and apneustic centers located

A

pons
- pneumotaxic: upper
- apneustic: lower

276
Q

what does the pneumotaxic center do

A

inhibits DRG ( inhibits pacemaker)

277
Q

what does the apneustic center do

A

stimulates DRG (stimulates pacemaker)

278
Q

where are central chemoreceptors located

A

just a few microns below surface of anterolateral aspect of medulla

279
Q

function of central chemoreceptors in medulla

A
  • respond to PaCo2 indirectly
  • sends stimulatory impulses to dorsal respiratory center
280
Q

CO2, H+, HCO3- and the BBB

A
  • CO2 freely diffuses
  • H+ and HCO3- do not
281
Q

most important stimulus for central chemoreceptor

A

hydrogen ion concentration in CSF

282
Q

what drives the respiratory pacemaker in the dorsal respiratory center

A

H+

283
Q

what happens to H+ with an acute rise in PaCO2

A

increased H+ in CSF and increased Vm (Ve)

284
Q

what happens to H+ with an acute decline in PaCO2

A

decreased H+ in CSF and decreased Ve

285
Q

do non-volatile acids affect Ve?

A
  • on a short term basis, no (don’t pass BBB)
  • on a long term basis, yes
286
Q

how long does HCO3- equilibration between blood and CSF take

A

begins after a few hours and peaks at ~2 days

287
Q

does hyperventilation affect PaCO2?

A

effect limited to the time before HCO3- equilibrates between blood and CSF (~ 2 days)

288
Q

what happens to pH of CSF after equilibration of HCO3-

A

restored to normal (7.32) as a result of active transport of HCO3- from plasma to CSF

289
Q

what stimulates and depresses central chemoreceptor

A
  • stimulated by hypercarbia and hypoxemia
  • depressed by profound hypercarbia and hypoxenia
290
Q

what is the primary stimulus at the central chemoreceptor?

A

H+

291
Q

If H+ can’t pass through the BBB, how does it stimulate the central chemoreceptor?

A

CO2 diffuses across BBB and spontaneously combines with H2O to become H+ and HCO3-

292
Q

what do the central chemoreceptors primarily respond to?
peripheral ?

A

central - PaCO2
peripheral - PaO2

293
Q

what are type 1 glomus cells

A
  • sensors that transduce PaO2 into an action potential
  • mediate hypoxic drive
294
Q

what is the afferent limb of carotid chemoreceptors

A
  • Hering’s nerve
  • glossopharyngeal nerve (CN 9)
295
Q

how does CEA affect function of peripheral chemoreceptors

A

impairs function on operative side

296
Q

chief responsibility of the carotid body

A

monitor for hypoxemia
(don’t respond to SaO2 or CaO2)

297
Q

secondary responsibilities of carotid body

A
  • monitoring PaCo2
  • monitoring H+
  • perfusion pressure
298
Q

PaO2 < ____ closes oxygen-sensitive K+ channels in type 1 glomus cells

A

60 mmHg

299
Q

steps of the hypoxic ventilatory response

A
  1. PaO2 < 60 mmHg closes O2-sensitive K channels in type 1 glomus cells
  2. RMP increases, Ca2+ channels open, inc release of ACh and ATP
  3. AP propagated along Hering’s nerve to CN 9
  4. afferent pathway terminates in inspiratory center in medulla
  5. minute ventilation increases to restore PaO2
300
Q

why can’t we do bilateral CEA simultaneously or close together

A

CEA severs afferent limb of hypoxic respiratory response - takes the body time to recalibrate

301
Q

why is postop hypoxia not always countered by reflexive increase in minute ventilation

A
  • subanesthetic doses (0.1 MAC) of inhalation and IV anesthetics depress HPV
  • volatiles impair diaphragmatic, intercostal, and upper airway muscle function
302
Q

name 2 conditions that affect tissue oxygenation that do not impair HPV

A

anemia and carbon monoxide poisoning

303
Q

how do the carotid bodies respond to oxygen

A

they increase minute ventilation when PaO2 < 60 mmHg

304
Q

purpose of Hering-Breuer inflation reflex

A

prevents alveolar overdistention by stopping inflation when lung volume is too large

305
Q

how do the lungs influence respiratory control

A

stretch receptors transduce pressure conditions in the airway and transmit this information along CN 10 to dorsal respiratory center

306
Q

when does the Hering-Breuer inflation reflex “turn off” the dorsal respiratory center

A

when lung inflation is > 1.5 L above FRC (x3 normal Vt)

307
Q

is Hering-Breuer inflation reflex active during normal inspiration

A

nope

308
Q

what is the Hering-Breuer deflation reflex

A
  • stimulates the patient to take a breath when lung volume is too small
  • helps prevent atelectasis
309
Q

function of J receptors

A
  • activated by things that Jam traffic in pulmonary vasculature (PE or CHF)
  • stimulation causes tachypnea
310
Q

what is the paradoxical reflex of head

A

causes a newborn baby to take first breath

311
Q

steps of the Hering-Breuer inflation reflex

A
  1. central respiratory activity
  2. phrenic nerve activity to diaphragm
  3. inspiration stops
  4. lung inflation > 1.5 L
  5. vagus nerve stim
  6. inspiratory off switch
312
Q

only region in the body that responds to hypoxia with vasoconstriction

A

pulmonary vascular bed

313
Q

function of HPV

A
  • within seconds, selectively increases PVR in poorly ventilated areas to minimize shunt flow to these regions
  • full effect in about 15 minutes
314
Q

how do anesthetics affect HPV

A
  • volatiles > 1.5 MAC reduce effectiveness
  • IV anesthestics do NOT affect HPV
315
Q

how do vasodilators, PDE inhibitors, dobutamine, and some calcium channel blockers affect HPV?

A

increase shunt flow by inhibiting HPV

316
Q

how do phenylephrine, epinephrine, and dopamine affect HPV

A

constrict well-oxygenated vessels and increase shunt flow

317
Q

how does volume status affect HPV

A
  • hypervolemia (LAP > 25 mmHg) and elevated CO may distend constricted vessles and increase shunt flow
  • hypovolemia may cause pulmonary vasoconstriction to well ventilated alveolar units
318
Q

2 critical functions of ventilation

A
  1. deliver O2 to hgb to support aerobic metabolism
  2. eliminate CO2 from blood
319
Q

muscles of expiration

A

TIREs
Transverse abdominis
Internal oblique
Rectus abdominis
External oblique

320
Q

function of diaphragm and external intercostals during inspiration

A

contraction

321
Q

when does exhalation become active

A
  • when minute ventilation increases
  • pts with lung disease (COPD)
322
Q

vital capacity required for an effective cough

A

at least 15 mL/kg

323
Q

which airway division is anatomic dead space

A

conducting zone

324
Q

parts of airway in conducting zone

A
  • trachea
  • bronchi
  • bronchioles
325
Q

where does the conducting zone begin and end

A
  • begins at nares
  • ends with terminal bronchioles
326
Q

last structures perfused by bronchial circulation

A

terminal bronchioles

327
Q

what does the transitional zone contain

A

respiratory bronchioles

328
Q

function of transitional zone

A

dual function: air conduit and gas exchange

329
Q

airway zone in which gas exchange takes place

A

respiratory zone

330
Q

where does the respiratory zone begin and end

A
  • begins at alveolar ducts
  • extends to alveolar sacs
331
Q

why are bronchioles and alveolar ducts susceptible to external compression

A

they don’t contain cartilage

332
Q

what is transpulmonary pressure

A

alveolar pressure - intrapleural pressure

333
Q

is TPP positive or negative with airway collapse

A

negative

334
Q

TPP during tidal breathing

A

always positive

335
Q

TPP at FRC

A

+5

336
Q

TTP and airflow during expiration

A

TTP = +7
airflow = in

337
Q

TTP and airflow during end inspiration

A

TTP = +8
airflow = none

338
Q

TTP and airflow during quiet expiration

A

TTP = +6
airflow = out

339
Q

TTP and airflow during forced expiration

A

TTP = -1
airflow = out

340
Q

muscles of inspiration

A
  • diaphragm
  • external intercostals
  • anterior scalene
  • posterior scalene
  • sternocleidomastoid
341
Q

normal A-a gradient breathing room air

A

15 mmHg

342
Q

2 etiologies of hypoxemia with normal A-a gradient

A

low FiO2
hypoventilation

343
Q

supplemental O2 can improve oxygenation in all causes of hypoxemia except

A

shunt

344
Q
A

A = IRV
B = FRC
C = IC
D = VC

345
Q

3 key processes involved in aerobic glucose metabolism

A

glycolysis
Kreb’s cycle
electronic transport

346
Q

cells that mediate HPV

A

type 1 glomus cells

347
Q

peripheral chemoreceptors in carotid body primarily respond to:

A

PaO2

348
Q

predicted PaO2 by age

A

110 - (age * 0.4)

349
Q

primary determinant of CO2 elimination

A

alveolar ventilation

350
Q
A

A = insp reserve volume
B = FRC
C = inspiratory capacity
D = vital capacity

APEX (54 decks)

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