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Apex- Respiratory Physiology Flashcards

1
Q

Anatomic dead space begins in the mouth and ends in the:

A. Small airways
B. Terminal bronchioles
C. REspiratory Bronchioles
D. Alveolar Ducts

A

B. Terminal bronchioles

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2
Q

What is the conducting zone known as?

A

Anatomic dead space

mouth/nose > terminal bronchials

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3
Q

Which respiratory zone is where gas exchange occurs?

A. Conducting Zone
B. Respiratory zone
C. Transitional Zone

A

B. Respiratory Zone

respiratory bronchials > alveoli

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4
Q

The diaphragm and external intercostals contract during (inspiration/expiration).

A

Inspiration

(exhalation is usually passive and driven by chest recoil)

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5
Q

2 accessory muscles for inspiration

A

Sternocleidomastoid
& Scalene muscles

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6
Q

Acessessory muscles for active expiration (5)

A

Internal & External obliques
Transverse & rectus abdominis

& Internal intercostals

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7
Q

A vital capacity of at least _____mL/Kg is required for an effective cough.

A

15ml/Kg

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8
Q

What is the difference between alveolar pressure and pleural plessure called?

A

Transpulmonary pressure

Alveolar pressure - pressure inside an airway

Pleural pressure = pressure outside the airway

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9
Q

Under nomral conditions, airways stay open if the transpleural pressure (TPP) is (postive/negative) and will collapse if the TPP is (postive/negative)

A

stays open +
collapses -

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10
Q

Muscle of inspiration or expiration:

external intercostals vs internal intercostals

A 
inspiration = external 
expiration = internal

(opposite)

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11
Q

Contraction of the inspiratory muscles (increases/reduces) thoracic pressure and (increases/decreases thoracic volume)

What law?

A

reduces pressure, increases volume

(think intrathoracic pressure needs to be more negative than ATM to create that pressure gradient to draw air into the lungs)

-Boyle’s law!
Pressure change for volume change?

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12
Q

What are the last structures perfused by the bronchial circulation?

A

The terminal broncioles

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13
Q

What makes up the transitional respiratory zone? Does gas exchange occur here?

A

The Respiratory bronchioles

*also serves as a air conduit

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14
Q

Where does the respiratory zone begin and end?

A

Alveolar ducts > alveolar sacks

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15
Q

Transpulmonary pressure vs intrapleural pressure…which ones are always negative vs positive

A

Transpulmonary pressure = always positive (keeps airway open)

(alveolar pressure - intrapleural pressure)

Intrapleural pressure = always negative (keeps lungs inflated)

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16
Q

What is the primary determinant of CO2 elimination?

A. Minute Ventilation

B. Tidal Volume

C. Alveolar ventilation

D. Respiratory rate

A

C. Alveolar ventilation

MV = TV x RR

AV = (TV -DEADSPACE) x RR

*dead space doesn’t contribute to gas exchange, so only a fraction of the tidal volume that reaches the resp zone contributes to gas exchange!

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17
Q

What is tidal volume (definition and number)

A

The amount of gas inhaled and exhaled during a breath

Vt ~ 6-8ml/kg

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18
Q

Normal Vd (deadspace ventilation) in the adult

A

2ml/kg

~150mls

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19
Q

Calculate the minute ventilation vs alveolar ventilation for a patient with a Vt of 500mls and RR of 10bpm

A

VE = 5,000ml/min (500ml x 10bpm)

VA= 3,500ml/min (500-150ml deadspace = 350ml x 10bpm)

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20
Q

Alveolar ventilation is directly vs indirectly proportional to:

CO2 production

PaCO2

A

directly proportional to CO2 production - higher CO2 production from body stimulates body to breathe deeper and faster so it can eliminate more CO2

inversely proportional to PaCO2 - faster and deeper breathing reduces PaCO2

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21
Q

How does deadspace ventilation affect the PaCO2 - EtCO2 gradient?

A

increase in deadspace ventilation, increases the PacO2-EtCO2 gradient

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22
Q

How would you calculate the following Vd/Vt ratio?

TV = 473

Dead space = 189

A

39%

189/473 = 0.392934

=39%

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23
Q

What would the PaO2 of a 33 year old breathing room air be?

A

96.8

Predicted PaO2 by age = 110 - (Age x 0.4)

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24
Q

Which conditions will MOST likely increase the PaCO2 to EtCO2 grident? (select 3)

  • Positive pressure ventilation
  • LMA
  • Hypotension
  • ETT
  • Neck flexion
  • Atropine
A

-Positive pressure ventilation

> increases alveolar pressure > increases ventilation relative to perfusion (dead space increases)

-Hypotension

-reduces pulmonary blood flow; ventilation > perfusion (dead space increases)

-Atropine

>bronchodilator, increases anatomic dead space by increases the volume of air moving through the conducting zone

*Anything that increases dead space ventilation essentially, whether it be reduced pulmonary blood flow or increased volume of the conducting zone.

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25
Q

Explain the 4 types of dead space:

  • Antatomic:
  • Alvolar:
  • Physiologic:
  • Apparatus:
A

-Antatomic: Air in the conduting airways

-Alvolar: Alveoli that are ventilated but not perfused

-Physiologic: Anatomic Vd + Alveolar Vd

-Apparatus: Vd added by equipment

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26
Q

What equation calculates physiologic dead space

A

The bohr equation

-compares partial pressure of CO2 in the blood vs partial pressure of CO2 exhaled in the lungs

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27
Q

What does the Vd/Vt ratio tell us

(dead space ventilation/tidal volume)

A

the % of tidal volume that is allocated to dead space.

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28
Q

Increases or decreases dead space ventilation (ie Vd to Vt ratio):

neck flexion vs neck extension

A

neck flexion decreases

neck extension increases

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29
Q

Increases or decreases dead space ventilation (ie Vd to Vt ratio):

ETT, LMA, Face mask

A

Increase = face mask

Decrease = ETT, LMA

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30
Q

T/F- the most common cause of increased Vd/Vt (dead space ventilation) under GA is mechanical ventilation

A

FALSE

*reduction in cardiac output > decreased BP increases dead space bc less pulmonary blood flow than ventilation

-mechanical ventilation does increase dead space ventilation bc it increases alvolar pressure relative to perfusion but it’s not the mos tcommon cause

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31
Q

Increases or decreases dead space ventilation (ie Vd to Vt ratio):

Sitting vs supine vs trendlenberg

A

Sitting = increased

Supine and trend = decreased

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32
Q

Increases or decreases dead space ventilation (ie Vd to Vt ratio):

COPD vs PE

A

both increase Vd

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33
Q

In the circle system, deadspace begins at the _________; anything proximal does not influence deadspace besides what one exception?

A

Y- Piece

  • invompetent valve in the circle system - entire limb with the faulty valve becomes apparatus dead space
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34
Q

What is the normal Vd/Vt ratio?

A

33%

150 (Vd) /450 (Vt)

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35
Q

Increases or decreases dead space ventilation (ie Vd to Vt ratio):

old age

A

Increased dead space

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36
Q

A patient is in the sitting position. When comapred to the apex of the lung, which of the following are higher in the base. (Select 2)

  • Blood Flow
  • Partial Pressure of Alveolar O2
  • V/Q ratio
  • Partial Pressure of CO2
A

- Blood Flow

-Partial Pressure of CO2

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37
Q

In the textbook patient, ventilation is ____L/min and perfusion is _____L/min, yielding an overall V/Q ratio of ______

A

vent = 4L/min

perfusion = 5L/min

VQ = 0.8

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38
Q

Define alveolar compliance

A

change in alvolar volume for a given change in pressure

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39
Q

Where is alveolar ventilation vs alveolar perfusion greatest in the lung?

A

both are greatest in the lung base

ventilation greatest in lung base due to greater alveolar compliance

perfusion greatest in the lung base due to higher pulmonary blood flow

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40
Q

V/Q ratios are higher towards the (apex/base) and lower torwards the (apex/base)

A

higher towards the apex (V>Q)

lower towards the base (V

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41
Q

Identify the statements that represent hte MOST accurate understanding of V/Q mismatch (select 2):

  • Bronchioles constrict to minimize zone 1
  • The A-a gradient is usually small
  • Blood passing through underventilating alveoli tends to retain CO2
  • Hypoxic pulmonary vasoconstriction minimizes dead space
A

-Bronchioles constrict to minimize zone 1

-Blood passing through underventilating alveoli tends to retain CO2

(HPV minimizes shunt - not dead space)

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42
Q

Deadspace vs Shunt

(words and equations)

A

Deadspace = ventilation, no perfusion (V/Q = infinity- dead for life)

Shunt = perfusion, no ventilation (V/Q = 0)

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43
Q

Atelectasis is the most common cause of hypoxemia in the PACU. Does it lead to deadspace ventilation or shunting?

A

right-to-left shunt

(collapsed alveoli arent getting perfused, persion no ventilation = shunt)

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44
Q

Do patients with V/Q mismatch tend to have more trouble with oxygenation or CO2 elimination?

A

Oxygenation

-CO2 retention suggesta a severe V/Q mistmatch

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45
Q

CO2 diffuses _____x faster than oxygen

A

20x

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46
Q

Why is the A-a gradient usually small with CO2 and big with O2 in a lung with VQ mismatch?

A

bc a lung with CO2 is eliminated from overfilled alveoli to compensate for the underventilated alveoli.

& a lung with a VQ mismatch cannot absorb more o2 from overfilled alveoli to compensate for underfilled ones

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47
Q

How does the body attempt to combast dead space ventilation?

what about shunt?

A

to combat dead space, the bronchioles constrict in attempt to minimize ventilation of the poorly perfused aolveoli

to combat shunt, HPV reduces pulmonary blood flow to poorly ventilated alveoli

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48
Q

Variables describe by the law of Laplace include all of the following EXCEPT:

  • tension
  • pressure
  • radius
  • density
A

-density

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49
Q

What does the law of laplace say?

A

As the radius of a sphere or cylinder becomes larger, the wall tension increases as well.

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50
Q

P = 2T/R

A

Law of la palce

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51
Q

According to the law of Lapalce, the tendency of an alveolus to collapse is:

Directly/indirectly proportional to

alvolar radius/surface tension

A

Directly proportional to surface tension (more tension = more likely to collapse)

Indirectly proportional to alveolar radius (smaller radius = more likely to collapase)

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52
Q

What prevents smaller alveoli from collapsing and emptying into larger ones?

A

Surfactant - it equalizes the effect of surface tension by keeping alveolar pressures constant

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53
Q

Type 2 pneumocytes begin producing surfactant between _______ weeks

Peak production =

How can fetal lung maturity be hastened in premature labor?

A

starts at 22-26 weeks

peaks at 35-36 weeks

Hastend by corticosteroids such as betamethasone

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54
Q

PA vs Pa

A

PA = alveolar pressure

Pa = arterial capillary pressure

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55
Q

Chart of Zones 1 - 4

A

PA > Pa > Pv

Pa > PA > Pv

Pa > Pv > PA

Pa > PIST > Pv > PA

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56
Q

Match - lung zones to:

shunt, dead space, waterfall, pulmonary edema

A

1- dead space (PA > Pa > Pv)

2 - Waterfall: (Pa > PA > Pv)

3 - Shunt: (Pa > Pv > PA)

4- Pulmonary Edema (Pa > Pist > Pv > PA)

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57
Q

What does “anatomic” shunt describe?

3 sites that contribute to a the normal anatomic shunt

A

Any venous blood that empties directly into the left side of the heart

(since it bypasses the lungs, it never has the opportunity to saturate with oxygen)

thebasian, bronciolar, pleural veins

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58
Q

What 3 conditions is zone 1 ventilation (deadspace) increased by?

A
  1. hypotension (air coming in, no blood to pick it up)
  2. pulmonary embolus (air coming in, no blood to pick it up)
  3. excessive airway pressure (compression of blood vessels)
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59
Q

where should the tip of a pulmonary artery catheter always be placed?

A

zone 3

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60
Q

What do the thebasian viens drain and where

A

they drain venous blood from the left heart back into the left heart

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61
Q

What drains bronchial venous blood into the left heart?

A

Bronchiolar veins and pleural veins

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62
Q

2 mechanisms in which pulmonary edema can occur

A

so fluid can be pushed across the capillary membrane by a significant increase in capillary hydrostatic pressure

>fluid overload, mitral stenosis, severe pulmonary vasoconstriction

  1. fluid can be pulled across the capillary membrane by a profound reduction in pleural pressure

>laryngospasm or mullers manuever (inhalation agaisnt a closed glottis) (negative pressure pulm. edema)

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63
Q

A patient is breathing room air at sea level. The ABG =

PaO2 60mmHg and a PaCO2 of 70mmHg

Calculate the patient’s alveolar o2 concentration

A

Alveolar O2 = FiO2 x (ATM - PH20) - (PaCO2/RQ)

0.21 x (760 - 47) - (70/0.8)

= 62.23 ~ 62mmHg

(bolds are constants)

So if normal ATM- you’d do (FIO2 x 713) - (PaCO2/RQ)

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64
Q

Causes of an increased A-a gradient include: (select 2)

  • hypoventilation
  • V/Q mismatch
  • hypoxic mixture
  • diffusion limitation
A

Diffusion limitation

VQ mismatch

looking at what is the difference between PAO2 (alveolar o2) and PaO2 (arterial o2)

Anytime your answering about A-a gradients- ask if the condition impairs ability to exchange - if no, not the cause

  • hypoventilation doesn’t impair your ability to exchange, your just doing it slower
  • hypoxic mixture doesn’t impair your ability to exchange, just dont have enough o2
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65
Q

What is the A-a gradient?

How are each measured?

A

The difference between alveolar o2 (PAO2) and arterial o2 (PaO2)

PAO2 is obtained from the alveolar gas equation

PaO2 is obtained via ABG

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66
Q

Etilogies of hypoxemia with a normal A-a gradient include what 2 things?

A
  1. low FiO2
  2. hypoventilation
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67
Q
A
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68
Q

3 Etilogies of hypoxemia with an increased A-a gradient

A
  1. diffusion limitation
  2. V/Q mismatch
  3. Shunt
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69
Q

Supplemental o2 can improve oxygenation in all cases of hypoxemia with the exception of what?

A

Shunt

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70
Q

What would constitute a diffusion impairment as a cause of hypoxemia? (3)

A

Pulmonary fibrosis, emphysema, intersistial lung disease

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71
Q

When breathing room air, what is the normal A-a gradient

A

< 15 mmHg

-bc the thebesian, bronchiolar, and pleural veins bypass the alveolar-capillary interface and deliver deoxygenating blood to the left heart, accounting for a very small physiologic shunt

72
Q

4 things that can increase the A-a gradient

A
  1. Aging (closing capacity increases relative to FRC)
  2. Vasodilators (decreased HPV)
  3. Right-to-left shunt (atelectasis, pna, bronchial intubation, intracardiac defect)
  4. Diffusion limitation (alveolar thickening hinders o2 diffusion)
73
Q

If your A-a graident is 218mmHg, what % shunt would you have?

A

1% shunt for every 20mmHg of A-a gradient

218/20 = 11%

74
Q

What are the 5 grousp of lung volumes and their mL’s

A
  1. Inspiratory reserve volume = 3,000mls
  2. Tidal volume = 500mls
  3. Expiratory volume = 1100mls
  4. Residual volume = 1200mls
  5. Closing volume = variable
75
Q

What makes up:

  1. TLC:
  2. VC:
  3. IC:
  4. FRC:
    5: CC:
A

1. TLC: RV + ERV + Vt + IRV (5.8L)

2. VC: ERV + Vt + IRV (4.6L)

3. IC: Vt + IRV (3.5L)

4. FRC: RV + ERV (2.3L)

5: CC: variable

76
Q

Since spirometry cannot measure __________; it als ocant measure what other 4 things?

A

Residual volume

> TLC, FRC, CC, CV

77
Q

What is vital capacity in ml/kg

A

65-75ml/kg

78
Q

What is FRC in mls/kg

A

35ml/kg

79
Q

True or false, lung volumes are 25% smaller in females

A

true

80
Q

What conditions reduce functional resdiual capcity (select 2)

  • advanced age
  • pulmonary edema
  • COPD
  • Obesity
A

Pulmonary edema & Obesity

81
Q

What is considered the volume of air in the lungs at end-expiration?

A

FRC (ERV + RV)

82
Q

What 3 things can be used to measure FRC indirectly

A
  1. Nitrogen washout
  2. Helium wash-in
  3. Body plethysmography
83
Q

Closing capacity = _____ + _______

A

closing volume + RV

84
Q

What is the volume above residual volume where the small airways begin to close during expiration

A

Closing volume

85
Q

Factors that increase closing volume mneumonic

A

CLOSE-P

COPD

LV failure

Obesity

Surgery

Extremes of age

Pregnancy

86
Q

T/F: under normal circumstances, the FRC is greater than CC

A

True - airways do not collapse during tidal breathing

87
Q

What happens with CC is > FRC

What can reverse this?

A

airway closure occurs during tidal breathing contributing to intrapulmonary shunting and hypoxemia

PEEP can reverse it by increasing the FRC relative to CC

88
Q

Aging effects on lung volumes/capacities (4)

A
  1. increased FRC
  2. increased CC
  3. Increased RV
  4. increased VC
    - as we age, pleural pressure becomes progressively higher (less chest recoil + less compliance = more RV/air trapping)
89
Q

At what age does CC approximate FRC under general anesthesia?

A

30

90
Q

At what age does closing capacity approximate FRC under when standing?

A

66yo

91
Q

What is CaO2?

What does it tell us?

What law?

Calculation

A

CaO2 = oxygen content

-tells us how much o2 is present in 1dL of blood

Henry’s law

CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.003)

92
Q

What is O2 carrying capacity vs O2 delivery

A

CaO2 = O2 carrying capacity

DO2 = O2 delivery

How much o2 is in the blood compared to how much is delivered to the tissues per minute

93
Q

Calculation for DO2= (oxygen delivery to the tissues)

A

DO2 = CaO2 x CO x 10

94
Q

What’s a normal CaO2?

A

20ml O2 per dL

95
Q

What’s a normal DO2?

A

1,000ml O2 per min

96
Q

What’s a normal VO2 (o2 consumption) - difference between the amount of o2 that leaves the lungs and returns to the lungs

ml/min &

ml/kg/min

A

250ml/min or

3.5ml/kg/min

97
Q

After o2 diffuses through the alveolar capillary membrane, it is transported by the blood in what 2 ways?

A
  1. 97% bound to hemoglobin (reversibly binds)
  2. 3% dissolved in plasma
98
Q

Formula to figure out O2 bound to hemoglobin

A

1.34 x hgb x SpO2

99
Q

Formula to figgure out O2 dissolved in the plasma

A

PaO2 x 0.003

100
Q

Normal H/H for males vs females

A

Males 15 & 45%
>14-18

Females 13 & 39%
>12-14

101
Q

Oxygen dissolves in the plasma according to what law?

A

Henry’s law

0The concentration of gas in a solution is directly proportional to the partial pressure of gas above the solution

102
Q

O2 bound + O2 dissolved =

A

CaO2

O2 content in the blood

103
Q

What is the driving force of DO2?

A

Cardiac output

104
Q

What law is used to calulate o2 consumption (VO2)?

A

Fick’s law

105
Q

The oxyhemoglobin dissociation curve plots the hgb saturation (SaO2) vs what?

What is P50?

A

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

P50 is where the hemoglobin is 50% saturated with O2

106
Q

A (right/left) shifted oxyhemoglobin dissociation curve means hemoglobin has a (higher/lower) affinity for oxygen.

Which occurs at the tissue level vs in the lungs?

A

right = lower affinity (right = release > tissues)

left = higher affinity for o2 (left = love > lungs)

107
Q

A lower P50 reflects a (right/left) shift

A

lower p50 = LEFT

(left/lower/love/lungs)

higher p50 = Right shift

108
Q

3 big things tha cause a left shift in the oxyhemoglobin curve

A
  1. alkalosis (decreased H+ ions)
  2. hypothermia (decreased temp)
  3. decreased 2-3 DPG
109
Q

3 big things that cause a right shift (increased P50)

A
  1. acidosis (increased H+ ions)
  2. hyperthermia (increased temp)
  3. increased 2-3 DPG
110
Q

What are the 3 hemoglobin species and which way do they shift the curve?

A
  1. Fetal hemoglobin
  2. Methemoglobin
  3. Carboxyhemoglobin

*all shift LEFT* (less room for O2 so they are going to hold on to as much of it as they can)

111
Q

Above a PaO2 of _______mmHg, increasing the FiO2 further will increase the amount of o2 dissolved in blood but won’t cause any additional o2 to bind to hemoglobin

A

100mmHg

112
Q

What states that an increased in partial pressure of CO2 and a decreased pH causes the hgb to release O2?

A

The Bohr effect

113
Q

When is 2,3-DPG produced? By what pathway?

A

During RBC glycolysis

Rapoport-Luebering pathway

114
Q

Hypoxia (increases/decreases) 2,3-DPG production

A

increases (facilitates O2 offloading by shifting curve to the right)

115
Q

T/F: Hgb F doesn’t respond to 2,3-DPG

A

True - which is why Hgb F has a left shift (P50 - 19mmHg)

116
Q

What do you know about banked blood and the concentration of 2,3-DPG

A

it falls and shifts the curve to the left, reducing the amount of O2 available at the tissue level

117
Q

1 mole of glucose converts to _____ ATP

A

38

118
Q

What is the currency for energy in the body?

A

Adenosine Triphosphate (ATP)

119
Q

What is the primary substrate used for ATP synthesis

A

Glucose

120
Q

What are the 3 key processes involved in aerobic metabolism

A
  1. Glycolysis = 2 ATP
  2. Krebs cycle = 2ATP
  3. Oxidative phosphorylation = 34 ATP
121
Q

When is pyruvate acid converted to lactic acid?

A

In the obsence of o2 (anaerobic metabolism)

122
Q

Lactic acid vs CO2

A

lactic acid is the primary byproduct of anerobic metabolism

CO2 is the primary byproduct of aerobic metabolism

123
Q

What is the citric acid cycle?

A

The krebs cycle

124
Q

Importation of which ion maintains electroneutrality during the hambuger shift?

A

chloride

125
Q

what are the 3 primary ways CO2 is transported (buffered) in the blood?

A
  1. As bicarbonate (70%)
  2. Bound to hemoglobin (23%)
  3. Dissolved in plasma (7%)
126
Q

What enzyme facilitates the formation of carbonic acid (H2CO3) from H20 and CO2?

A

Carbonic anhydrase

127
Q

A more acidic enviornment enhances O2 offloading from hemoglobin (________effect) and increases CO2 loading into the blood (________effect)

A

O2 offloading = bOhr effect

CO2 loading = haldane effect

128
Q

Venous blood is has about ____mmHg higher CO2 than arterial blood

A

5mmHg

129
Q

Solubility is a function of what law?

A

Henry’s

130
Q

Solubility coefficient of CO2

A

0.067

131
Q

The Haldane effect states that in the presence of deoxygenated hemoglobin, the carbon dioxide dissociation curve shifts:

  • To the right
  • To the left
  • up
  • down
A

To the left

O2 gets dropped off to the tissues, and the CO2 curve shifts left to load CO2 onto the hgb from the tissues

132
Q

P50 = PaO2 of what

A

26.5mmHg

133
Q

Where in the body is the CO2 curve right shifted vs left shifted

A

right = lungs to release co2 to be exhaled

left = tissues, for co2 from the tissues to be loaded onto the hgb

134
Q

Consequences of hypercapnia include: (select 2)

  • Hypokalemia
  • Increased myocardial o2 demand
  • increased o2 carrying capacity
  • hypoxemia
A
  • Increased myocardial o2 demand
  • hypoxemia
135
Q

CO2 is a smooth muscle dilator causing vasodilation, what’s the exception?

A

The pulmonary vasculature

CO2 increases PVR > increased workload of the right heart

136
Q

CO2 narcosis occurs when PaCO2 > what

A

90mmHg

137
Q

For every 10mmHg increase above a PaCO2 above 40mmHG, pH decreases by how much in acute respiratory acidosis vs chronic

A

acute resp acidosis - pH decreases by 0.08

chornic respiratory acidoisis- pH decreases by 0.03 (due to HCO3 retention by the kidneys)

138
Q

T/F hypercapnia INCREASES intraocular pressure

A

True

139
Q

What conditions increase minute ventilation for a given PaCO2? (select 3)

  • sugrical stimulation
  • salicylates
  • hypoxemia
  • sevoflurane
  • CEA
  • Resp alkalosis
A
  • surgical stimulation
  • Salicylates
  • hypoxemia
140
Q

A (right/left) shift in the CO2 response curve means the respiratory center is (more/less) sensitive to CO2

A

Right shift = less sensitive

Left shift = more sensitive

141
Q

Primary and secondary monitors of PaCO2

A

Primary = central chemoreceptor in the medulla

Secondary = peripheral chemoreceptors in the carotid bodies & aortic arch

142
Q

What is the apneic threshold defined as

A

the highest PaCO2 at which a person will not breathe. Once the PaCO2 exceeds the apneic threshold, the patient will begin to breathe.

143
Q

What does the slope of the CO2 response curve represent

A

The respiratory apparatus’s sensitivity to PaCO2

144
Q

MAC of CO2

A

200mmHg

145
Q

A left shift and increased slope in the CO2 response curve indicates that Ve is (higher/lower) than expected for a given PaCO2

A

Higher

ie) surgical stimulation - your paco2 can be normal but it makes you breathe faster anyway

146
Q

a left shift in the co2 response cureve implies that the apneic threshold has (increased/decreased)

A

decreased

147
Q

What is the pacemaker for normal breathing?

  • Pneumotaxic center
  • Apneustic center
  • Dorsal respiratory center
  • Ventral respiratory center
A
  • DRG
  • think dorsal column of spinal cord = sensory; this senses when the body needs to breathe, like how a pacemaker senses and fires , so does the DRG
148
Q

What respiratory center is primarily responsible for expiration/exhalation?

A

Ventral respiratory center

149
Q

What respiratory center inhibits the dorsal respiratory center?

A

The pneumotaxic

-it taxes/blocks it

150
Q

What respiratory center stimulates the dorsal respiratory center?

A

apneustic center

-think APNEa stimulates someone to breathe

151
Q

Where is the respiratory center located?

A

In the RAS in the medulla and the pons

152
Q

What 2 centers are found in the medullary respiratory centers vs pontine

A

medullary respiratory centers = DRG and VRG

Pontine respiratory centers = pneumotaxic (upper pons) & apneustic (lower pons)

153
Q

The central chemoreceptor:

  • is located on the dorsal surface of the medulla
  • responds to PaCO2 and PaO2
  • is stimulated by pH changed in the CSF
  • is unaffected by bicarbonate in the serum
A

-is stimulated by pH changed in the CSF

154
Q

T/F the central chemoreceptor is located on the dorsal surface of the medulla

A

false- the ventral surface

155
Q
A
156
Q

The central chemoreceptors respond (directly/indrectly) to PaCO2

A

indirectly

157
Q

What happens afte CO2 diffuses across the BBB

A

it combines with water to make carbonic acid

CO2 + H20 = H2CO3

H2CO3 dissoicates into HCO3- and H+

it’s the H+ that stimulates the DRG

158
Q

T/F- non-volatile acids (such as lactic acid) do NOT pass through the BBB

A

True! get outta herreeeee!

159
Q

What is the primary stimulus at the central chemoreceptor?

A

H+

160
Q

Select the statements that BEST describe the carotid chemoreceptors (select 2):

  • They are more sensitive to SaO2 than PaO2
  • Hering’s nerve is part of the afferent limb
  • They are more sensitive after CEA
  • Type 1 Glomus cells mediate hypoxic ventilatory drive
A
  • Hering’s nerve is part of the afferent limb
  • Type 1 Glomus cells mediate hypoxic ventilatory drive

(type 1 glomus cells = sensors that transduce PaO2 into an action potential which is the npropagated along the affarent limb, consisting of Hering’s nerve and CN9)

161
Q

Hypoxemia is defined as a PaO2 < what

A

PaO2 < 60mmHg

162
Q

Why don’t we do bilateral CEA’s simultaneously or close to eachother?

A

because CEA severs the afferent limb of the hypoxic ventilatory response (herrings nerve and CN 9) - it takes time for the body to recalibrate

163
Q

Where are the peripheral chemoreceptors found and what do they monitor for?

A

Carotid bodies and aortic arch

monitor for hypoxemia (PaO2 <60)

164
Q

What’s the biochemical stuffs that happens when PaO2 drops below 60mmHg

A

the oxygen-sensitive K+ channels in Type 1 Glomus cells close

  • this raises RMP
  • CA++ channels open
  • NT release increases (ACH and ATP)
  • Action potential propragates along Hering’s nerve > CN 9 > medulla

Ve increases to restore PaO2

165
Q

Two conditions that affect tissue oxygenation but do not impaire the hypoxic ventilatory response

A
  1. anemia
  2. CO poisioning
166
Q

Which reflex prevents alveolar overdistension?

  • Hering-Breuer deflation reflex
  • Paradoxical reflex of Head
  • Hering-Breuer inflation reflex
  • Pulmonary chemoreflex
A
  • Hering-Breuer inflation reflex
  • stops inhalation when lung volume is too large
167
Q

What reflex helps prevent atelectasis by activating the respiratory drive when the lung volume is too small?

A

Hering-Breuer Deflation reflex

168
Q

What kind of receptors increase the respiratory rate in the setting of pulmonary embolism or CHF

A

J- receptors (pulmonary C-fiber receptors) [stretch receptrs]

169
Q

What does the paradoxical reflex of the head stimulate?

A

the first breath of a newborn

170
Q

Stretch receptors transmit signals to the DRG via what CN

A

CN 10

171
Q

Which agent is MOST likely to increase intrapulmonary shunt?

  • Etomidate
  • Ketamine
  • Desflurane
  • Propofol
A
  • Desflurane (Devil)
  • agents that impair HPV increase the shunt fraction and reduce PaO2 - all halogenated agetns >1-1.5MAC

*IV anesthetics preserve HPV

172
Q

What is the only region in the body that responds to hypoxia with vasoconstriction?

A

The pulmonary vascular bed (HPV)

173
Q

What 5 things is HPV inhibited by

A

volatile anesthestics >1.5 MAC

PEEP (excessive)

Large tidal volumes

Hypervolemia

PDE inhibitors and dobutamine

174
Q

Which lung volume correlates with the point where dynamic compression of the airwayas begins?

  • ERV
  • TV
  • RV
  • CV
A

-Closing volume

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

175
Q

A patient presents with SOB. Labs show

PAO2 98, PaO3 68, PaCO2 37, HCO3 24

Supplemental o2 fails to improve the patients o2; what is the MOST likely etilogy of this patient’s hypoxemia?

A. Opioid OD

B. Right to left cardiac shunt

C. Anemia

D. Pulm fibrosis

A

B. Right to left cardiac shunt

CaO2 = (1.34 x hgb x SaO2) + (PaO2 x 0.003)

9.38 +

Respiratory (5 decks)

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