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Unit 1 Respiratory 2: Physiology Flashcards

1
Q

What does contraction of inspiratory muscle result in? What law is this an example of?

A

Reduced thoracic pressure and increases thoracic volume.

Boyle’s law (pressure and volume)

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2
Q

What are the muscles of inspiration?

A

Diaphragm
External intercostals
Accessory muscles: sternocleidomastoid and scalene

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3
Q

What drives exhalation?

A

Exhalation is a passive process that is driven by recoil of the chest wall.

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4
Q

When active exhalation occurs, what are the muscles?

A

Abdominal muscles: rectus abdominis, transverse abdominis, interval and external obliques
Mneumonic: I let the air out of my TIREs

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5
Q

When does exhalation become an active process?

A

When minute ventilation increases
Lung disease (like COPD)
Cough

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6
Q

How much vital capacity is required for an effective cough?

A

At least 15 mL/kg

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7
Q

What are the 3 zones of the airway?

A

Conducting zone
Respiratory zone
Transitional zone

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8
Q

What is the conducting zone? Where does it start and end?

A

An atomic dead space.

Starts at the nares/mouth and ends with the terminal bronchioles.

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9
Q

What is the respiratory zone? Where does it start and end?

A

Where gas exchange takes place.

Begins at the respiratory bronchioles, includes the alveolar ducts and sacs

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10
Q

What is transitional zone? What parts does it include?

A

Portion of the airway that serves a dual function of air conduit and gas exchange.
Respiratory bronchioles and alveolar ducts.
Not all texts recognize transitional zone.

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11
Q

How many generations are in the bronchial tree?

A

23

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12
Q

Where is cilia located in the bronchial tree?

A 
Trachea
Bronchi
Bronchioles
Respiratory bronchioles (some)
None lower than this
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13
Q

Where is cartilage located in the bronchial tree?

A

Trachea
Bronchi - patchy
None lower

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14
Q

Where is smooth muscle located in the bronchial tree?

A 
Trachea
Bronchi
Bronchioles
Respiratory bronchioles (some)
Alveolar ducts (some)
None in the alveolar sacs
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15
Q

In order to prevent airway collapse, where must the pressure always be greater?

A

The pressure inside the airway must be greater than the pressure outside the airway.

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16
Q

What is alveolar pressure?

A

Pressure inside the airway

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17
Q

What is intrapleural pressure?

A

Pressure outside the airway

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18
Q

What is transpulmonary pressure?

A

The difference between the pressure inside the airway and pressure outside the airway.

TPP = alveolar pressure - intrapleural pressure

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19
Q

If TPP is a positive value, what does this mean for the airway? What about when TPP is negative?

A

+ It stays open.

- It collapses

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20
Q

During tidal breathing what happens with TPP? Intrapleural pressure? Alveolar pressure?

A

TPP: is always positive to keep airway open
Intrapleural pressure: is always negative to keep lungs inflated
Alveolar pressure: becomes slightly negative during inspiration and slightly positive during expiration

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21
Q

When are the only times intrapleural pressure becomes positive?

A

Pathologic states like pneumothorax

During forced expiration

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22
Q

When is there no airflow during tidal breathing?

A

At FRC or at end-expiration

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23
Q

What is Vt?

A

Tidal volume is the amount of gas that is inhaled and exhaled during the breath.

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24
Q

When you take a breath, what are the 2 zones that parts of the Vt is delivered to?

A

Respiratory zone - gas exchange occurs here

Conduction zone - dead space

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25
Q

How much Vt sits in the conducting zone in a healthy 70 kg adult?

A

About 2 mL/kg or 150 mL

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26
Q

During exhalation what zone is removed first removed from?

A

The conducting zone followed by the respiratory zone.

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27
Q

Conditions that increase what zone make it more difficult to eliminate expiratory gases?

A

Any condition that increases dead space (conducting zone).

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28
Q

Increased Vd (dead space) widens what gradient? Leading to what?

A

PaCO2 - EtCO2 gradient

This causes CO2 retention

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29
Q

Define ventilation rate.

A

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

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30
Q

What 2 ventilation rates do we care about?

A

Minute ventilation and alveolar ventilation

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31
Q

What is minute ventilation?

A

VE: the amount of air in a single breath (Vt) multiplied by the number of breaths per minute (RR).
VE = Vt x RR

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32
Q

What is alveolar ventilation?

A

VA: only measure the fraction of VE (minute ventilation) that is available for gas exchange (removes dead space from minute ventilation).
VA = (Ve - Vd) x RR

VA = CO2 production / PaCO2

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33
Q

VA (alveolar ventilation) is directly proportional to what?

A

Carbon dioxide production

- a higher CO2 production stimulates the body to breath deeper and faster

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34
Q

VA (alveolar ventilation) is inversely proportional to what?

A

PaCO2

- faster and deeper breathing reduce PaCO2

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35
Q

How do anticholinergics affect Vd?

A

They cause bronchodilation and increase Vd.

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36
Q

What are the 4 types of dead space?

A

Anatomic: conducting airways
Alveolar: alveoli that are ventilated but not perfused
Physiologic: anatomic Vd + alveolar Vd
Apparatus: equipment (face mask, HME)

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37
Q

What is Vd/Vt?

A

The dead space to tidal volume ratio is the fraction of tidal volume that contributes to dead space.

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38
Q

In a spontaneously ventilating patient, what is the assumed dead space? In a 70 kg patient?

A

2 mL/kg

or 1/3 of tidal volume

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39
Q

Why does mechanical ventilation increases the Vd/Vt ratio?

A

Mechanical ventilation increases alveolar pressure, which increases ventilation relative to perfusion.

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40
Q

What is the most common cause of increased Vd/Vt under general anesthesia?

A

Reduced cardiac output.

- if EtCO2 acutely decreases rule out hypotension first

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41
Q

What things related to airway (devices) increase Vd?

A

Face mask
HME
PPV

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42
Q

What things related to airway (devices) decrease Vd?

A

ETT
LMA
Tracheostomy

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43
Q

What does old age do to Vd?

A

Increases Vd.

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44
Q

How does neck position affect Vd?

A

Extension: increases Vd
Flexion: decreases Vd

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45
Q

What pathophysiology increases Vd?

A

Decreased CO
Decreased pulmonary blood flow
COPD
PE

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46
Q

How does posture affect Vd?

A

Sitting: increases Vd

Supine and head down positions: decrease Vd

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47
Q

If dead space increases, what must occur in order to maintain a constant PaCO2?

A

Minute ventilation (RR, Vt, or both) must increase

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48
Q

In a circle system, where does Vd begin?

A

At the Y-piece. Nothing proximal to the Y affects Vd, nor does increasing the length of the circuit.

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49
Q

With what exception does the entire limb of the circuit become Vd?

A

With an incompetent valve in the circle system

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50
Q

What equation can be used to calculated physiologic dead space?

A

The Bohr equation.

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51
Q

What does the Bohr equation compare? How do you interpret it?

A

The partial pressure of CO2 in the blood vs the partial pressure of CO2 in exhaled gas.
The greater the difference between the two, the greater the amount of dead space.

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52
Q

What is the actual Bohr equation?

A

Vd/Vt = (PaCO2 - PeCO2) / PaCO2

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53
Q

In a text book patient what is ventilation in L/min, and what is perfusion in L/min? What does this make V/Q ratio?

A

Ventilation: 4 L/min
Perfusion: 5 L/min

V/Q: 0.8

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54
Q

What is the importance of compliance?

Compliance =

A

An alveolus that undergoes a greater degree of volumetric change during a breath is going to be better ventilated.

Change in volume / change in pressure.

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55
Q

Which alveoli have the poorest ventilation? Why?

A

Alveoli in the apex.

because they have the poorest compliance

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56
Q

Which alveoli have the greatest ventilation? Why?

A

Alveoli in the base.

Because they have the greatest compliance

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57
Q

What 2 factors affect distribution of blood flow to the lung?

A

Gravity

Hydrostatic pressure

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58
Q

Where are V/Q ratios higher? Where are they lower?

A

V/Q is higher towards the apex and lower toward the base.

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59
Q 
In a non-dependent region of the lung, what occurs with:
Ventilation
Alveolar ventilation
Alveolar compliance
PACO2
PAO2
PAN2

Perfusion
Blood flow
Vascular pressure
Vascular resistance

V/Q

A 
Alveolar ventilation - decreases
Alveolar compliance - decreases
PACO2 - decreases
PAO2 - increases
PAN2 - =

Blood flow - decreases
Vascular pressure - decreases
Vascular resistance - increases

Increased V/Q

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60
Q 
In a dependent region of the lung, what occurs with:
Ventilation
Alveolar ventilation
Alveolar compliance
PACO2
PAO2
PAN2

Perfusion
Blood flow
Vascular pressure
Vascular resistance

V/Q

A 
Alveolar ventilation - increases
Alveolar compliance - increases
PACO2 - increases
PAO2 - decreases
PAN2 - =

Blood flow - increases
Vascular pressure - increases
Vascular resistance - decreases

V/Q decreased

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61
Q

Dead space is defined as:

A

Ventilation without perfusion.

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62
Q

Shunt is defined as:

A

Perfusion without ventilation

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63
Q

Dead space and shunt rarely exist in true form? T/F

A

True

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64
Q

What is the most common cause of hypoxemia in the PACU?

A

V/Q mismatch specifically atelectasis

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65
Q

Dead space V/Q =

A

♾

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66
Q

Shunt V/Q =

A

0

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67
Q

How does a lung with V/Q mismatch compensate? What happens with PACO2-PaCO2 gradient and PAO2-PaO2 gradient?

A

Eliminates CO2 fro over ventilated alveoli to compensate for underventilated alveoli. PACO2-PaCO2 gradient remains small.
Absorbs more O2 from overventilated alveoli to compensate for underventilated. PAO2-PaO2 is usually large.

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68
Q

What constitutes failure of V/Q mismatch compensation mechanism?

A

CO2 retention.

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69
Q

What is the Law of Laplace? Equations?

A

Describes the relationship between pressure, radius, and wall tension.

Cylinder shape: tension = pressure x radius

Spherical shape: tension = (pressure x radius) / 2

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70
Q

According to the law of Laplace, the tendency of an alveolus to collapse is directly proportional to? And inversely proportional to?

A

Directly: surface tension
Inversely: alveolar radius

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71
Q

What type of pneumocytes produce surfactant?

A

Type 2

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72
Q

Each alveoli contain the same amount of surfactant? T/F

A

True

Larger alveoli just have a relatively smaller concentration of surfactant, and small ones a relatively larger concentration of surfactant.

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73
Q

When do type 2 pneumocytes begin producing surfactant?

A

Between 22-26 weeks gestation

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74
Q

When is the peak production of surfactant production?

A

35 weeks

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75
Q

What can hasten fetal lung maturity?

A

Corticosteroids (betamethasone)

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76
Q

Zone 1 is considered? What is the relative pressure between PA, Pa, Pv?

A

Dead space

PA > Pa > Pv

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77
Q

What is the V/Q of zone 1?

A

♾

There is ventilation but no perfusion

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78
Q

Zone 1 does not occur in the normal lung? T/F

A

T

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79
Q

What conditions increase zone 1?

A

Hypotension
PE
Excessive airway pressure

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80
Q

How does a the body combat zone 1?

A

The bronchioles of under fused alveoli constrict to reduce dead space

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81
Q

What is zone II? What is the relative pressures between PA, Pa, Pv?

A

Waterfall

Pa > PA > Pv

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82
Q

What is the V/Q of zone II?

A

V/Q = 1

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83
Q

Blood flow is directly proportional to the difference in what to pressures in the lungs? What makes greater blood flow?

A

Pa - PA

The greater the difference between the 2, the great the blood flow

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84
Q

What is zone III? What is the relative pressures between PA, Pa, Pv?

A

Shunt

Pa > Pv > PA

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85
Q

What is the V/Q of zone III?

A

V/Q = 0

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86
Q

How does the body combat zone III?

A

Hypoxic pulmonary vasoconstriction reduces pulmonary blood flow to underventilated units

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87
Q

What zone should the tip of a pulmonary artery cather be place? Why?

A

Zone III
The pressure in the capillary is always higher than the alveolus, the vessel is always open and blood is always moving through it.

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88
Q

What 3 sites contribute to the normal anatomic shunt? What do they drain?

A

Thebesian veins - drains left heart
Bronchioles veins - drains bronchial circulation
Pleural veins - drain bronchial circulation

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89
Q

What is zone IV? What is the relative pressures between PA, Pa, PV, and Pist (interstitial space)?

A

Pulmonary edema : shen the interstitial space exceed the pressure in the pulmonary capillaries and alveolus.
Pa > Pist > Pv > PA

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90
Q

Zone IV is usually the result of what 2 phenomena? Examples of each.

A
  1. Fluid is pushed across the capillary membrane by a significant increase in capillary hydrostatic pressure : fluid overload, mitral stenosis, severe pulmonary vasoconstriction.
  2. Fluid is pulled across the capillary membrane by a profound reduction in pleural pressure : laryngospasm or inhalation against a closed glottis -> negative pressure pulmonary edema.
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91
Q

What is the alveolar gas equation?

A

Alveolar oxygen = FiO2 x (Pb - H2O) - PaCO2/RQ

Pb - barometric pressure
H2O - humidity of inhaled gas
RQ - respiratory quotient

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92
Q

What is the assumed humidity of inhaled gas?

A

47 mmHg

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93
Q

What is the assumed respiratory quotient?

A

0.8

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93
Q

What is the alveolar gas equation used to determine?

A

The partial pressure of oxygen inside the alveolus

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94
Q

What 3 important points does the alveolar gas equation illustrate?

A
  1. Hypoventilation can cause hypercarbia and hypoxemia
  2. Supplemental O2 can easily reverse hypoxemia, but does nothing for hypercarbia
  3. Hypercarbia can go undetected in the patient breathing supplemental O2
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95
Q

Why is the FiO2 always higher than the PAO2?

A

Inspired air becomes 100% humidified as it moves towards the alveoli, taking up space and diluting oxygen concentration.
Inspired air mixes with expired air diluting the concentration of oxygen going towards the alveoli.

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95
Q

What is the equation for respiratory quotient?

A

RQ = carbon dioxide production / oxygen consumption

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96
Q

What does an RQ of > 1 suggest? What about an RQ of 0.7?

A

> 1 : lipogenesis - over feeding

0.7 : lipolysis - starvation

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97
Q

What is the A-a gradient and what does it help determine?

A

The difference between the PAO2 and PaO2.

It helps diagnose the cause of hypoxemia by indicating the amount of venous admixture.

97
Q

When breathing room air, what is the normal A-a difference? Why?

A

Less than 15 mmHg.
The Thebesian, bronchiolar, and pleural beings bypass the alveolar-capillary interface and deliver deoxygenated blood to the left side of the heart (physiologic shunt).

98
Q

What 2 things can cause hypoxemia with a normal A-a gradient? Which can/cannot be fixed with supplemental O2

A
  1. Reduced FiO2 - not enough O2 in inspired gas - yes

2. Hypoventilation - inadequate air transfer in and out of the lungs - yes

99
Q

What 3 things can cause hypoxemia with an increased A-a gradient? Which can/cannot be fixed with supplemental O2?

A
  1. Diffusion limitation - capillary thickening hinders O2 diffusion - yes
  2. V/Q mismatch - yes
  3. Shunt - pulmonary blood bypasses alveoli - no
99
Q

What 4 factors increase the A-a gradient? Examples.

A
  1. Aging - closing capacity increases relative to FRC
  2. Vasodilators - decreased HPV
  3. Right to left shunt - atelectasis, pneumonia, bronchial intubation, intracardiac defect
  4. Diffusion limitation - alveolocapillary thickening hinders O2 diffusion
100
Q

Shunt increases ____ % for every ____ mmHg of A-a gradient

A

1%

20

101
Q

How many lung volumes and how many lung capacities are there?

A

4 and 4

101
Q

Define IRV, normal value?

A

Inspiratory reserve volume: amount of gas that can be forcibly inhaled after a tidal inhalation.
3000 mL

102
Q

Define Vt, normal value?

A

Tidal volume: amount of gas that enters and exits the lungs during tidal breathing.
500 mL

103
Q

Define ERV, normal value?

A

Expiratory reserve volume: volume of gas that can be forcibly exhaled after a tidal exhalation.
1100 mL

103
Q

Define RV, normal value?

A

Residual volume: volume of gas that remains in the lungs after complete exhalation.
1200 mL

104
Q

Define CV, normal value?

A

Closing volume: the volume above residual volume where the small airways begin to close.
Variable amount.

105
Q

Define TLC, normal value?

A

Total lung capacity: IRV + TV + ERV + RV

5800 mL

105
Q

Define VC, normal value?

A

Vital capacity: IRV + TV + ERV

4500 mL

106
Q

Define IC, normal value?

A

Inspiratory capacity: IRV + TV

3500 mL

107
Q

Define FRC, normal value?

A

Functional residual capacity: RV + ERV

2300 mL

107
Q

Define CC, normal value?

A

Closing capacity: RV + CV

Variable amount

108
Q

Tidal volume is _____ mL/kg

A

6-8

109
Q

Vital capacity is ____ mL/kg

A

65-75

109
Q

Functional residual capacity is ___ mL/kg

A

35

110
Q

Lung volumes are ~ how much smaller in females?

A

25%

111
Q

Lung volumes tend to get smaller with what body position?

A

Supine

111
Q

Patients with asthma, emphysema, and bronchitis have what increases in lung volumes/capacities and why?

A

Obstructive lung disease causes air trapping.

Increase residual volume, closing capacity, and total lung capacity

112
Q

What can spirometry NOT measure?

A

Residual volume, total lung capacity or function residual capacity.
Closing volume and capacity.

113
Q

What is the importance of FRC?

A

It is the reservoir of oxygen that prevents hypoxemia during apnea.

113
Q

How CAN FRC be measured?

A

Nitrogen wash-out
Helium wash-out
Body plethymography

114
Q

When FRC is reduced what zone is increased?

A

Zone III - shunt

115
Q

How does PEEP help restore FRC?

A

Restore FRC by decreasing zone III.

115
Q

What does general anesthesia do to FRC? How?

A

Decreases FRC.
Diaphragm shifts cephalosporin ~ 4cm as a result of decreased inspiratory muscle tone and increased expiratory muscle tone

116
Q

How does obesity affect FRC? How?

A

Decreases it.

Decreased chest wall compliance and increased airway collapsibility

117
Q

How does pregnancy affect FRC?

A

Decreases it.
Diaphragm shift cephalad as a result of the gravity uterus.
Decreased chest wall compliance

118
Q

How is FRC affected in neonates?

A

Decreased.
Less alveoli means less lung compliance.
Cartilaginous rib cage is prone to collapse.

119
Q

How does advanced age affect FRC?

A

Increases it.

Decreased elastic lung tissue mean air trapping therefore an increase in RV and FRC

121
Q

How does position affect FRC?

A 
Decreases it:
-supine
-lithotomy 
-T-burg
 Increases it:
-Prone
-sitting
-lateral - can also have no effect
122
Q

How does paralysis affect FRC?

A

Decreases it.

Diaphragm moves cephalad and decreases lung volumes

123
Q

How does inadequate anesthesia affect FRC?

A

Decreases it.

Straining leads to forceful exhalation and decreased lung volumes

125
Q

How does excessive IV fluids affect FRC?

A

Decreases it.

Fluid accumulation in dependent lung favors zone III

126
Q

How does high FiO2 affect FRC?

A

Decreases it.

Absorption atelectasis leads to conversion of low V/Q units to shunt like

127
Q

How does reduced pulmonary complicate affect FRC?

A

Decreases it.

Acute lung injury, pulmonary edema, pulmonary fibrosis, atelectasis, pleural effusion

129
Q

How does obstructive lung disease affect FRC?

A

Increases it.

Air trapping increases RV and FRC

130
Q

How does PEEP affect FRC?

A

Increases it.
Recruiters collapsed alveoli
Partially overcomes effects of GA
Decreases venous admixture therefore increasing PaO2

131
Q

How do sign breaths affect FRC?

A

Increases it.

Recruits collapsed alveoli

136
Q

How does age affect closing capacity?

A

In the young and healthy airway closure occurs just above residual volume, as we age pleural pressure becomes progressively higher such that the small airways being to close sooner and at higher lung volumes.

137
Q 
How are the follow affected by aging:
FRC
CC
RV
VC
A

FRC: increase
CC: increase
RV: increase
VC: decrease

137
Q

By age ___ CC ~ FRC when under general anesthesia

A

30

138
Q

By age ___ CC ~ FRC when supine.

A

44

139
Q

By age ___ CC ~ FRC when standing.

A

66

139
Q

How is closing capacity measured?

A

By tracer gas, nitrogen or xenon-133. This gas is inhaled at residual volume, and the measurement is taken as the patient exhales from TLC.

140
Q

What is CaO2?

A

Oxygen content: a measure of how much oxygen is present in 1 deciliter of blood.

141
Q

What causes airways to close during exhalation?

A

As a person exhales, there is point where pleural pressure exceeds airway pressure. This external force collapses the small airways that lack cartilage and traps gas distally in the alveoli.

142
Q

Define closing volume.

A

The point at which dynamic compression of airways begins.

The volume above RV where the small airways begin to close during exhalation.

143
Q

Define closing capacity.

A

The absolute volume of gas contained in the lungs when the small airways begin to collapse.
CC = CV + RV

144
Q

What relationship determines if the airways will collapse during tidal breathing?

A

The relationship between functional residual capacity and closing capacity

145
Q

When happens if closing capacity exceeds FRC?

A

Airway closure occurs during tidal breathing

146
Q

What factors increase closing volume? Mnemonic.

A 
CLOSE-P
COPD
Left ventricular failure 
Obesity 
Supine
Extremes of age
Pregnancy
147
Q

What 2 ways is oxygen transported by the blood? What % by each?

A
  1. Reversibly bound by hemoglobin - 97%

2. Dissolved in the plasma - 3%

147
Q

What is the equation for CaO2?

A

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

148
Q

How much oxygen can each gram of Hgb carry?

A

Maximum of 1.39 mL, but Hgb usually contains a small amount of methemoglobin and carboxyhemoglobin so 1.34 or 1.32 is used in the CaO2 equation instead.

149
Q

What is the normal H/H for men? Women?

A

Men: 15 g/dL and 45%
Women: 13 g/dL and 39%

149
Q

How is dissolved O2 in the plasma measured?

A

By PaO2.

150
Q

Oxygen dissolves in the plasma by which law?

A

Henry’s law

151
Q

What is Henry’s law?

A

At a constant temperature, the amount of gas that dissolves in a solution is directly proportional to the partial pressure of that gas over the solution. The higher the gas pressure, the more of it will dissolve into a liquid.

151
Q

What is the solubility coefficient of oxygen?

A

0.003 mL/dL/mmHg

152
Q

What is the difference in solubility in O2 vs CO2

A

CO2 is 20x more soluble than O2.

153
Q

What is DO2? What is the deriving mechanism?

A

Oxygen delivery: how fast a quantity of O2 is delivered to the tissues.
Cardiac output is the deriving mechanism of DO2.

153
Q

What is the equation for DO2?

A

DO2 = CaO2 x CO x 10

154
Q

What is the 10 in the DO2 equation?

A

Conversion factor since Hgb is measured in g/dL and CO is measured as L/min

155
Q

What is VO2? Equation?

A

Oxygen consumption

VO2 = CO x (CaO2 - CvO2) x 10

155
Q

What is a normal VO2?

A

3.5 mL/kg/min

~ 250mL/min in a 70kg male

156
Q

On the oxyhemoglobin dissociation curve what does a left shift mean? What causes it?

A

Hemoglobin has an increased affinity to bind oxygen.

Decreased Temp
Decreased 2,3-DPG
Decreased CO2
Decreased H+

Increased pH
Increased HgbMet
Increased HgbCO
Increased HgbF

157
Q

On the oxyhemoglobin dissociation curve what does a right shift mean? What causes this?

A

Hemoglobin has a decreased affinity for oxygen.

Increased temp
Increased 2,3-DPG
Increased CO2
Increased H+

Decreased pH

158
Q

What is P50? What is normal? What does a lower P50 mean? Higher?

A

The PaO2 where Hgb is 50% saturated by oxygen.
Normal: 26.5
Lower: left shift
Higher: right shift

159
Q

Maximum O2 loading occurs at a PaO2 of ~ ?

A

100 mmHg

159
Q

What purpose does a PaO2 above 100 mmHg serve?

A

A PaO2 above 100 mmHg does not improve O2 loading, but it does increase the amount of O2 dissolved in plasma.

160
Q

What is the Bohr effect?

A

CO2 and H+ cause a conformation change in the Hgb molecule and this facilitates the release of O2.

161
Q

Where does 2,3-DPG come from?

A

It is produced during RBC glycolysis d

161
Q

Why is 2,3-DPG important?

A

It maintains the oxyhemoglobin dissociation curve in a slightly right shifted position at all times.

161
Q

What does hypoxia do to 2,3-DPG production?

A

Hypoxia increases 2,3-DPG production, this facilitates O2 offloading.

162
Q

In what condition does 2,3-DPG play an important compensation mechanism role?

A

Chronic anemia

163
Q

What happens with 2,3-DPG in banked blood?

A

The concentration falls, shifting the oxyhemoglobin dissociation curve to the left and reduces the amount of O2 available at the tissue level

163
Q

What type of hemoglobin does not respond to 2,3-DPG?

A

Hgb F - this explains why it has a left shift (P50 = 19 mmHg)

165
Q

What is the Haldane effect?

A

It describes CO2 carriage.

It says that oxygen causes the RBC to release CO2

167
Q

What is the Bohr effect?

A

It describes O2 carriage.

It says that CO2 and decreased pH cause the RBC to release O2

168
Q

What is the Haldane effect basically stating?

A

That deoxygenated hemoglobin can carry more CO2

169
Q

In the presence of oxygenated Hgb, which way is the CO2 dissociation curve shift? What does this mean?

A

It is shifted to the right.

This means Hgb has a decreased affinity for CO2, this occurs in the lungs in order to facilitate the unloading of CO2.

171
Q

In the presence of deoxygenated Hbg, which way is the CO2 dissociated curve shifted? What does this mean?

A

It is shifted to the left.
This means Hgb has an increased affinity for CO2, this occurs in the systemic capillaries in order to facilitate the transport of CO2.

171
Q

A lower PO2 means less/more CO2 is carried?

A

More

173
Q

A higher PO2 means less/more CO2 is carried?

A

Less

174
Q

Whare are the 3 primary causes of hypercapnia?

A

Increased production of CO2
Decreased elimination of CO2
Rebreathing

175
Q

Hypercapnia = PaCO2 > ?

A

45 mmHg

176
Q

What is the equation for PaCO2?

A

PaCO2 = CO2 production / alveolar elimination

178
Q

What are the 9 consequences of hypercapnia?

A 
Decreased PaO2 - hypoxemia
Increased P50 - O2 dissociation curve shifted right
Depression of cardiac/smooth muscle
Stimulation of SNS
Increased alveolar ventilation
Increased K+
Increased Ca+2
Increased ICP
Decreased LOC
179
Q

How does hypercapnia lead to hypoxemia?

A

Increased alveolar CO2 displaces alveolar O2 -> arterial hypoxemia

180
Q

How does hypercapnia lead to increased P50?

A

The O2 dissociation curve is shifted to the right releasing more oxygen at the tissues. This partially compensates for hypoxemia.

181
Q

How does hypercapnia lead to cardiac/smooth muscle depression?

A

Acidosis inside muscle affects contractile protein and enzymatic function -> myocardial depression and vasodilation

183
Q

How does hypercapnia lead to stimulation of the SNS?

A

CO2 activates the SNS and increases catecholamine release.

  • unless acidosis is severe this offsets cardiac/smooth muscle depression
  • tachycardia -> increased myocardial O2 consumption and decreased myocardial O2 delivery
  • vasoconstriction -> increased SVR -> increased myocardial O2 consumption
  • dysrhythmias
  • prolonged QT interval
  • oculocardiac reflex is more common following precipitating event
183
Q

How does hypercapnia lead to increased alveolar ventilation?

A

CO2 is a respiratory stimulant

185
Q

How does hypercapnia lead to increased K+?

A

Hypercapnia activates the H+ / K+ pump

-buffers CO2 acid in exchange for releasing K+ into the plasma

186
Q

How does hypercapnia lead to increased Ca+2?

A

Ionized calcium competes with H+ for binding sites on plasma proteins.

  • acidosis -> plasma proteins buffer H+ and release Ca+2 -> increased inotropy
  • alkalosis -> plasma proteins release H+ and bind Ca+2 -> decreased inotropy
187
Q

How does hypercapnia lead to increased ICP?

A

CO2 freely diffuses across the BBB

-decreased CSF pH -> decreased cerebrovascular resistance -> increased CBF and volume

188
Q

How does hypercapnia lead to LOC depression?

A

CO2 narcosis occurs when PaCO2 > 90mmHg

190
Q

How does hypercarbia affect blood pH?

A

During respiratory acidosis, the kidneys excrete H+ and conserve bicarbonate. This process begins within hours, but full compensation can take days.

191
Q

What does the CO2 ventilators response curve describe?

A

The relationship between PaCO2 and minute ventilation

192
Q

What is the primary monitor of PaCO2?

A

The central chemoreceptors in the medulla

193
Q

Where are the secondary monitors of PaCO2?

A

The peripheral chemoreceptors in the carotid bodies and transverse aortic arch

195
Q

Within what range of PaCO2 does minute ventilation increase with PaCO2 in a linear fashion?

A

Between PaCO2 of 20-80 mmHg

195
Q

When does CO2 become a respiratory depressant?

A

When PaCO2 exceeds 80-100 mmHg

197
Q

What is the MAC of CO2?

A

200 mmHg

198
Q

What does a left shift of the CO2 ventilators response curve mean?

A

A left shift and increased slope indicate that Ve is higher than expected for a given PaCO2, this creates respiratory alkalosis.

199
Q

What does a right shift of the CO2 ventilators response curve mean?

A

A right shift and decreased slope indicate that Ve is lower than expected for a given PaCO2, this creates respiratory acidosis.

200
Q

What is apneic threshold?

A

The highest PaCO2 at which a person will not breathe.

201
Q

What does a left shift in the CO2 ventilatory response curve say about apneic threshold?

A

A left shift implies that the apneic threshold has decreased

202
Q

What does a right shift in the CO2 ventilatory response curve say about apneic threshold?

A

A right shift implies that the apneic threshold has increased

203
Q

Causes of a left shift of the CO2 ventilatory response curve

A 
Hypoxemia
Metabolic alkalosis
Surgical stimulation
CNS: increased ICP, fear, anxiety
Drugs: salicylates, aminophylline, doxapram, norepinephrine
204
Q

Causes of a right shift of the CO2 ventilatory response curve

A

Metabolic acidosis
Carotid endarterectomy
Natural sleep
Drugs: volatile anesthetics, opioids, NMB

206
Q

Do opioid antagonists affect the CO2 ventilatory response curve?

A

In the absence of opioids, opioid antagonists do not affect the curve

207
Q

Where are the respiratory centers located?

A

In the brainstem, within the medulla and the pons

208
Q

Dorsal Respiratory Group:
Where is it located?
What is its function?

A

Located in the medulla.
It is the pacemaker of the respiratory system.
It always causes inspiration.
Ramp signal. Turning off the ramp increases RR.
Sends signal for phrenic nerve to fire.

209
Q

Ventral Respiratory Group:
Where is it located?
What is its function?

A

Located in the medulla.
Not active during normal respiration. Contributes to extra respiratory drive.
When respiratory drive for increased ventilation becomes greater than normal, signal “spills over” into VRG.
Contributes to both inspiration and expiration.
Primarily active during expiration.

210
Q

Pneumotaxic Center:
Where is it located?
What is its function?

A

Located in the pons.
Inhibits DRG triggering the end of inspiration. Shuts off ramp.
A strong stimulus -> rapid shallow breathing.
A weak stimulus -> deep slow breathing.

211
Q

Apneustic Center:
Where is it located?
What is its function?

A

Located in the Pons.
Stimulated DRG. Antagonizes the pneumotaxic center -> inspiration.
Signals DRG and sustains ramp.
It’s affects are not obvious unless pneumotaxic center fails.
Action is inhibited by pulmonary stretch receptors (J receptors).

211
Q

Where are the central chemoreceptors that control ventilation located?

A

Below the surface of the anterolateral aspect of the medulla.

211
Q

What do the central chemoreceptors that control ventilation respond to? Where do they send their signals?

A

PaCO2.

Signals are sent to the DRG.

212
Q

What is the most important ion in the CSF that is stimulus for the central chemoreceptor?

A

Hydrogen ion concentration.

As H+ rises, the rate and depth of respirations increase until a new steady state for Ve is achieved.

212
Q

How do the hydrogen ions get into the CSF?

A

H+ can not cross the BBB.

CO2 freely diffuses across the BBB, then reacts with carbonic a hydrate and dissociates into H+ and HCO3-

213
Q

How does bicarbonate affect the central chemoreceptor?

A

Bicarb does not cross the BBB, but is created when carbonic acid dissociates into bicarb and H+.
HCO3- equilibrates between the blood and CSF beginning after a few hours and peaking at about 2 days.
So hyperventilation’s effect on PaCO2 is limited to this window.
After equilibration the CSF pH is returned to normal 7.32 as a result of active transport of HCO3- from the plasma to the CSF.

213
Q

Where are the peripheral chemoreceptors that control ventilation located?

A

In the adventitia of the carotid bodies, at the bifurcation of the common carotid artery, and in the transverse aortic arch.

215
Q

What is the chief responsibility of the carotid body to monitor? What are the secondary responsibilities?

A

Hypoxemia (PaO2 < 60 mmHg).

Monitoring PaCO2, H+, and perfusion pressure.

216
Q

Do carotid bodies respond to SaO2 or CaO2?

A

No

218
Q

Describe the hypoxic ventilatory response.

A
  1. PaO2 < 60 mmHg closes the O2-sensitive K+ channels in Type 1 Glomus cells.
  2. This raises RMP, opens Ca+2 channels, and increases neurotransmitter release (Ach and ATP).
  3. An action potential is propagated along Hering’s nerve then along the glossophyrngeal nerve (CN IX).
  4. The afferent pathway terminates in the inspiratory center in the medulla.
  5. Minute ventilation increases to restore PaO2.
219
Q

What conditions impair the hypoxic ventilatory response?

A
  1. Carotid endarterectomy severs the afferent limb of the hypoxic ventilatory response. This is why bilateral CEA is not done, or even very close to each other, it takes time for the body to recalibrate.
  2. Sub-anesthetic inhalation and IV anesthetics (0.1 MAC) depress the hypoxic ventilatory drive, so post op hypoxia is not always countered by a reflexive increase in Ve.
221
Q

Do anemia and carbon monoxide poisoning trigger the hypoxic ventilatory response?

A

No. Even though arterial oxygen content (CaO2) is reduced with anemia and carbon monoxide poisoning, the PaO2 is usually normal.

222
Q

Where do stretch receptors in the smooth airway muscle transmit information?

A

Information is transmitted along the vagus nerve (CN X) to the DRG.

224
Q

What is the Hering-Breuer Inflation Reflex?

A

When lung inflation is > 1.5 L above FRC (x3 normal Vt), this reflex “turns off” the dorsal respiratory center, stopping further inspiration.
This reflex is not active during normal respiration.

225
Q

What is the Hering-Breuer Deflation Reflex?

A

When lung volume is too small, it helps prevent atelectasis by stimulating the patient to take a deep breath.

227
Q

What are J receptors and where are they located?

What is their function?

A

J receptors are pulmonary C fiber receptors in the lungs.

J receptor stimulation causes tachypnea.

228
Q

How are J receptors activated?

A

The J receptors are activated by things that Jam traffic in the pulmonary vascular use, such as pulmonary embolism of CHF.

230
Q

What is Paradoxical Reflex of Head?

A

Causes a newborn baby to take their first breath.

231
Q

What causes hypoxic pulmonary vasoconstriction?

A

Reduction in alveolar oxygen tension (NOT arterial PO2).

233
Q

What is unique about the pulmonary vascular bed during hypoxia?

A

It is the only region in the body that responds to hypoxia with vasoconstriction.

235
Q

What is the purpose of HPV?

A

HPV selectively increases the pulmonary vascular resistance in poorly ventilated areas to minimize shunt flow to these regions.

237
Q

How quickly does the response of HPV occur, and when does it achieve full effect?

A

Response begins within seconds

Full effect in about 15 minutes

238
Q

What drugs impair HPV? (3)

A
  1. Volatile anesthetics > 1.5 MAC reduce effectiveness of HPV
  2. Vasodilators, phosphodiesterase inhibitors, dobutamine, and some CCB increase shut flow by inhibiting HPV
  3. Vasoconstrictive drugs ie phenylephrine, epinephrine, and dopamine may constrict well-oxygenated vessels and increase shunt flow
240
Q

What drugs do NOT affect HPV?

A

IV anesthetics: ketamine, propofol, fentanyl etc.

242
Q

How can hypervolemia (LAP > 25mmHg) affect HPV? Hypovolemia?

A

Hypervolemia and elevated CO may distend constricted vessels and increase shunt flow.
Hypovolemia may cause pulmonary vasoconstriction to well ventilated alveolar units.

244
Q

How can PEEP and tidal volumes affect HPV?

A

Excessive PEEP or high tidal volumes increase dead space (zone 1) and reduce optimal V/Q matching.

245
Q

What is the primary goal of glycolysis?

A

To convert 1 glucose into 2 pyruvic acid

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