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Physiology 4 > Longmuir > Flashcards

Longmuir Flashcards

1
Q

What are the 6 primary symbols?

A

P = pressure (units: mmHg (most common), cmH2O (which is a smaller pressure unit))
o 760 mmHg = 1 standard atmosphere

V = volume (units: L, mL)

T = temperature (units: *C, K)
o 0C = 273 K

A dot above adds time dimension (in these notes “X*”)

V* = flow or volume of gas/unit time (units: L/sec, mL/min)

F = fractional concentration of a gas in a gas mixture (no units, ranges 0-1)
o Refers to DRY GAS ONLY (no water vapor, it must be first subtracted out)

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2
Q

What is P?

A

pressure (units: mmHg (most common), cmH2O (which is a smaller pressure unit))
o 760 mmHg = 1 standard atmosphere

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3
Q

What units volume?

A

L, mL

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4
Q

What units for temperature?

A

C, K

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5
Q

What is Vdot measured in?

A

L/sec mL/min

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6
Q

What is F? Refers to what type of gas?

A

fractional concentration of a gas in a gas mixture (no units, ranges 0-1)

Refers to DRY GAS ONLY (no water vapor, it must be first subtracted out)

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7
Q

What are the 4 secondary symbols?

A

I = inspired gas that has been saturated with water vapor & warmed to 37*C
o Aka “tracheal air”
o Contains O2, N2 & H2O vapor

A = alveolar gas that has been saturated with water, warmed to 37*C & contains CO2
o Contains O2, N2, H2O vapor & CO2

B = barometric or barometric pressure

E = exhaled gas (usually contains CO2)

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8
Q

Primary symbols denote?

A

a Physical quantity

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9
Q

Secondary symbols denote?

A

Location

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10
Q

Tertiary symbols denote?

A

a particular type of gas such as O2, N2, H2O, CO2, Ne, CO, etc.

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11
Q

P_IO2 means?

A

Partial pressure of O2 in the airways (inspired, saturated, and warmed to 37)

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12
Q

What is the fractional concentration of O2 and N2 in the atmosphere?

A

FO2=0.21

FN2=0.79

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13
Q

What is I? Properties? What does it contain?

A

inspired gas that has been saturated with water vapor & warmed to 37*C
o Aka “tracheal air”
o Contains O2, N2 & H2O vapor

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14
Q

What is A? Properties? What does it contain?

A

alveolar gas that has been saturated with water, warmed to 37*C & contains CO2
o Contains O2, N2, H2O vapor & CO2

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15
Q

What is B?

A

Barometric pressure

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16
Q

What is E?

A

Exhaled gas (usually contains CO2)

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17
Q

What is FCO2?

A

0.0004 (usually ignored)

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18
Q

What is Pb?

A

760 mmHg

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19
Q

Descrbie Dalton’s law

A

Total Pressure = Sum of Partial Pressures = Barometric (usually)

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20
Q

Describe Dalton’s Law for Pressure. For Volume?

A

Pz=Ptot x Fz

Vz=Vtot x Fz

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21
Q

Describe the process of saturating gas with water vapor in the airways

A

As air enters the airways, it becomes saturated with H2O vapor that exerts its own partial pressure
(vapor pressure) that’s dependent on the temperature of the air & independent of the total
barometric pressures; thus, the total pressure remains the same (760 mmHg)

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22
Q

At body temperature, what is the saturating vapor pressure of water?

A 
P_IH2O
47 mmHg (at 37 C)
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23
Q

Where does gas exchange occur?

A

The alveoli

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24
Q

What is the respiratory exchange ratio?

A

R=CO2 production / O2 Consumption

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25
Q

Describe R for different fuels burned

A

R=1 for glucose, R<1 when fat is burned too

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26
Q

What is P_ACO2?

A

The partial pressure of CO2 in the aveoli

Very tightly regulated to 40 mmHg

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27
Q

Describe ideal gases in the human lung? Exceptions?

A

At room temperature & 1 atmospheric pressure, most gases that we’re concerned about behave as
ideal gases; we can use the ideal gas law & it’s derivatives to understand the human lung

 Note: water doesn’t behave like an ideal gas; as you condense it, the water vapor pressure
remains the same because some is condensed

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28
Q

What is BTPS? What is reported in BTPS?

A

body temperature & pressure, saturated

(all lung volumes are reported as BTPS)

P = barometric, T = 37*C, saturated with H2O

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29
Q

What is ATPS?

A

The volume of gas at ambient temperature and pressure, and which is saturated with water vapor.

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30
Q

What is STPD?

A

The volume of a gas at standard temperature and pressure, dry.

T = 0 °C; P = 760 mm Hg; PH2O = 0 mm Hg

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31
Q

What is Tidal Volume?

A

the volume of gas inspired or exhaled

during normal, quiet breathing

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32
Q

What is Vital capacity?

A

the maximal volume that can be exhaled after maximal inspiration
o By far the most clinically important

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33
Q

What is functional residual capacity?

A

the volume of gas in the lungs at the resting expiratory level (when no muscles are engaged)

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34
Q

What is residual volume?

A

Volume of gas in the lungs at the end of maximal expiration

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35
Q

What is total lung capacity?

A

The volume of gas in the lungs at the end of maximal inspiration

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36
Q

What can be measured using spirometry?

A

Tidal Volume

Vital Capacity

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37
Q

What needs to be measured using other techniques? What can be derived from that?

A

FRC (like nitrogen washout)

Then can calculate RV and TLC

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38
Q

Describe the nitrogen washout test

A

Test is started when the lungs are at FRC (resting expiratory level, just ask patient to relax)

Have the patient breath in O2 while hooked up to a machine; O2 will flush out the N2 into the
collection bag such that only O2 & CO2 remain in the lungs

The volume of gas in the bag & fractional concentration of N2 is measured to determine the Vol of N2 at FRC & then FRC is calculated

Since Vol N2 = FRC x 0.8, FRC = Vol of N2 @ FRC/0.8

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39
Q

How do we calculate RV, TLC, and FRC from vital capacity? (Approximately)

A 
RV = 0.25 VC
TLC = 1.25 VC
FRC = 0.5 TLC
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40
Q

What is forced vital capacity?

A

The volume of air exhaled during forced expiration

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41
Q

What is FVC - 0.5?

A

The volume of air exhaled during forced expiration in the first 0.5 seconds

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42
Q

What is FVC - 1.0?

A

The volume of air exhaled during forced expiration in the first 1 seconds

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43
Q

What is Forced Expiratory Flow (FEF_25-75)?

A

The average rate of gas flow measured between 25% and 75% of forced vital capacity

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44
Q

Describe lung function with height and age?

A

Lung function is positively correlated with height & negatively correlated with age
(downhill after age 20)

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45
Q

Describe how to use a nomogram for normal values of forced expiration

A

Use a ruler to draw a line across the age & height of a person to read off the various
predicted lung functions

There is a wide range of normal values (to include 95% of the population, one needs to
include 2 standard deviations; thus a person would have to lose 1/3 of his/her lung
function before being considered abnormal)
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46
Q

Describe normal FVC, FEV1.0/FVC, and TLC

A

o FVC 70% of predicted value (using nomogram)

o FEV1.0/FVC 75% (means that a person should be able to expel most of their air in less than 1 sec)

o TLC 70% of the predicted value (obtained by multiplying predicted FVC by 1.25)

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47
Q

What is obstructive ventilatory defect?

A

decreased rate of flow out of the lungs due to narrowed/blocked airways

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48
Q

What is the pattern for obstructive ventilatory defect?

A

A. FVC reduced < 70% of predicted value
(some exceptions in emphysema)

B. FEV1.0 / FVC < 75% (always)

C. TLC normal or above normal

D. FRC normal or above normal

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49
Q

What causes obstructive ventilatory defects?

A

asthma, chronic bronchitis, emphysema & COPD

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50
Q

What is restrictive ventilatory defect?

A

decrease in total volume of air the lungs can hold, often due to decreased elasticity or a problem related to the expansion of the chest wall during inhalation

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51
Q

What is the pattern for restrictive ventilatory defect?

A

A. FVC reduced < 70% of predicted value

B. FEV1.0 / FVC >= 75%

C. TLC reduced

D. FRC reduced

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52
Q

What are the causes of restrictive ventilatory defect?

A

Causes: fibrosis, chest wall deformities, pneumothorax, pleural fluid & neuromuscular impairment (notice that usually nothing’s wrong with the lungs, it’s the surrounding that’s abnormal)

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53
Q

For flow-volume loops, what are the axes?

A

X axis = volume

Y axis = flow rate

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54
Q

Flow volume loop for an asthmatic would show?

A

no problem breathing
in but exhaling is troublesome
(look at V*50)

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55
Q

What is anatomical dead space? How is it estimated?

A

Anatomical dead space = the volume of the conducting airways (i.e. trachea)
o Almost never changes in pulmonary disease
o Rule of thumb: body weight (lb) approximately equals to anatomical dead space volume (ml)

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56
Q

What is apparatus dead space?

A

the dead space created by adding a breathing device & thus tidal volume needs to be adjusted accordingly

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57
Q

What is physiological dead space?

A

the volume of the conducting airways + non-functioning alveolar regions (ventilated with air but not perfused with blood)

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58
Q

What is physiological dead space usually measured as?

A

VD/VT (ratio of dead space to tidal volume)

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59
Q

Physiological dead space effect on partial pressure of CO2?

A

Doesn’t evolve CO2; hence, the partial pressure of CO2 in the exhaled gases is lower than the partial pressure of CO2 in the alveoli

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60
Q

What is normal physiological dead space? Diseased?

A

VD/VT = 0.25 is normal; VD/VT = 0.5 is diseased; VD/VT = 0.75 is very diseased but survivable

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61
Q

What is the Bohr equation?

A

VD/VT = (PACO2 – PECO2)/PACO2

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62
Q

What does the Bohr equation state?

A

States that physiological dead space is tidal volume multiplied by a fraction that represents
the dilution of alveolar PCO2 by dead-space air, which doesn’t participate in gas exchange &
therefore doesn’t contribute CO3 to expired air

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63
Q

How do we use Bohr equation to get physiological dead space?

A

Exhaled gas is used to obtain PECO2

Arterial blood sample (PaCO2) is used to obtain PACO2

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64
Q

What is f?

A

Respiratory frequency (breaths per minute)

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65
Q

What is the ventilatory rate?

A

f x Tidal volume

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66
Q

What is dead space volume?

A

Tidal Volume X (Dead space volume/Tidal Volume)

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67
Q

What is alveolar ventilation?

A 
f x (V_T - V_D)
How much air gets to alveolar region
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68
Q

In lung mechanics, what are pressures measured to? What is assumed if the glottis is open?

A

all pressures are relative to atmospheric (thus, Patm = 0 cm H2O)

o If the glottis is open, no air flow is occurring & no mechanical device is attached to the mouth, the alveolar pressure is always equal to the atmospheric pressure

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69
Q

How is pressure difference calculated?

A

measured as inside minus outside ΔP = pressure(in) – pressure(out)

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70
Q

What is transpulmonary pressure?

A

Transpulmonary pressure (pressure difference across the lung wall) = PA – Ppl

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71
Q

What is the pressure difference across the chest wall?

A

Pressure difference across the chest wall = Ppl – Patm

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72
Q

Describe elastic recoil

A

If you have to apply a + pressure to inflate the lung, there must be a force trying to collapse the lung (elastic recoil)
o If you apply negative (subatmospheric) pressure around the lungs, the lungs will inflate

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73
Q

What does elastic recoil depend on? What is it independent of?

A

Elastic recoil depends on lung volume but is independent of the method by which the lungs are inflated

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74
Q

Describe the lungs within the thoracic cage when there is no muscular effort and the glottis is open

A

When there’s no muscular effort & the glottis is open, the lungs are at FRC & PA = Patm = 0 cm H2O

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75
Q

Describe elastic recoil of the lungs

A

Elastic recoil of the lungs = PA – Ppl
this is positive, meaning the lungs will collapse

NB. Elastic recoil pressure is drawn inward on lungs by convention

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76
Q

Describe elastic recoil of the chest wall

A

Elastic recoil of the chest wall = Ppl – Patm
this is negative, meaning the chest wall will expand

NB. Elastic recoil pressure is drawn inward on lungs by convention

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77
Q

Why is the respiratory system stable at FRC (no muscles, and glottis open)?

A

The balance of forces (lung tendency to collapse & chest wall tendency to expand outward) makes the respiratory system stable at FRC

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78
Q

What happens if air enters the pleural space?

A

Respiratory system is stable as long as the system is sealed; if air enters the pleural space, the lungs will collapse
o Pneumothorax = air in lungs (i.e. GSW); hemothorax = blood in lung (i.e. stab wound)

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79
Q

How is subatmospheric pleural space maintained?

A

Physiologically maintain the subatmospheric pleural space by (1) gas reabsorption into the venous circulation & (2) fluid reabsorption by osmotic forces (pleural fluid has less protein than plasma)

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80
Q

What is the function of pleural fluid?

A

Pleural fluid simultaneously acts as a lubricant to allow the lung & chest wall to slide over one another and a glue to allow the chest wall & lung to adhere to one another

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81
Q

What is lung compliance? (in words)

A

LUNG COMPLIANCE = Indicates how easy (higher values) or hard (lower values) it is to inflate the lung

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82
Q

Compliance is defined by? How is it measured?

A

Compliance = elastic recoil as a function of lung volume = ΔV / ΔP

 Measured (infrequently) by measuring volume change using a spirometer & pressure difference across the lung via a swallowed esophageal balloon

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83
Q

Describe compliance in stiff lungs? Emphysema? Fibrosis?

A

Stiff lungs = low compliance or high elastic recoil
Emphysema = less elastic recoil & more compliant
Fibrosis = more elastic recoil & less compliant

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84
Q

Describe surface tension using water

A

1 water molecule can make up to 4 H-bonds with surrounding water molecules in a 3D arrangement

o If you place a H2O molecule on a surface, at least 1 H-bond is broken & this is thermodynamically insulting

o H2O will respond by trying to minimize surface area to maximize H-bonds; this behavior is surface tension

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85
Q

How do we calculate elastic recoil pressure as a function of surface tension?

A

Elastic recoil pressure due to surface tension forces: P = 2γ/r
[γ = surface tension & r = alveolar radius]

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86
Q

Describe the balancing of surface tension

A

When the pressure-volume work trying to inflate the lung is balanced by the surface tension-area
work trying to deflate the lung, lung stability results

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87
Q

Describe the balance of surface tension at FRC

A

At FRC, the following forces exist & are balanced (no muscular effort is required):

  1. Air pressure difference between alveoli & pleural space working to inflate the lung
  2. Combination of surface tension forces & tissue elastic forces to collapse the lung
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88
Q

Are alveoli lined with water?

A

Alveoli aren’t lined with water (if they are, they would collapse)

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89
Q

What accounts for the majority of lung elastic recoil?

A

Alveolar surface tension accounts for most of the lung elastic recoil

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90
Q

Describe what lines the alveoli. Composition? Relation to premature infants?

A

Alveoli are lined with a secreted material called pulmonary surfactant that’s mostly phosphatidylcholine

(FA chains don’t form H-bonds thus strong surface tension forces don’t exist)

 Premature infants discover this because they don’t make surfactant until the last month

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91
Q

What is alveolar surface tension usually?

A

<10 dynes/cm

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92
Q

Describe surfactant surface tension as a function of lung volume

A

Surfactant surface tension has to change with lung volume (if not, the smaller one would collapse & empty into the large one); this quality results from compression/expansion of FA

 Surface tension decreases with decreasing surface area & lung volume; surface tension increases with increasing surface area & lung volume)

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93
Q

Fractional concentration refers to what type of gas

A

DRY GAS

MUST always subtract PH20 of 47 mmHg at body temp

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94
Q

Describe the 4 steps to generating an airflow in the breathing cycle?

A

Generating an Airflow
1. The lung itself is incapable of breathing
2. Breathing is accomplished by (1) muscular effort to contract the diaphragm and (2) muscular
effort to expand the rib cage outward (inspiration) or force the rib cage inward (forced expiration)
3. There are no tissue elements connecting the diaphragm and rib cage to the lung
4. The lung is mechanically coupled to the diaphragm/rib cage by pleural fluid hydraulically

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95
Q

The lung is connected to the diaphragm/rib cage how?

A

The lung is mechanically coupled to the diaphragm/rib cage by pleural fluid hydraulically

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96
Q

Describe the 4 steps to inspiration

A
  1. Contract diaphragm to expand the size of the thoracic cavity
  2. Since lung’s hydraulically-coupled to the diaphragm/chest wall by pleural fluid, lung expands also
  3. Now the same amount of air in the lungs is in a larger volume meaning the alveolar pressures
    become sub-atmospheric
  4. Air flows in until alveolar pressure = Patm (air flows in response to pressure gradient)
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97
Q

How do we calculate the direction of airflow?

A

ERlung = PA – Ppl always holds & can be used to determine airflow direction; solve for PA & if

PA = 0 cm H2O then no flow; PA > 0 cm H2O then air flows out; PA < 0 cm H2O then air flows in

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98
Q

How do we classify airway splits?

A

Airway Classification: 1 splits into 2 & so they are generations: at generation x, we have 2^x airways

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99
Q

What is cross-sectional area in lung context? how calculated?

A

CROSS SECTIONAL AREA: CSA = πr2 While the

CSA of an individual bronchiole is much smaller than the trachea, there are many more such that the CSA of the trachea is the least & so it is the bottleneck!

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100
Q

What is the bottleneck of airway?

A

CSA is smallest in trachea

Bronchioles have small CSA but there are many of them to increase total effective CSA

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101
Q

How is flow velocity calculated?

A

Velocity = rate of airflow/CSA

the linear velocity of air is faster in the trachea than in a bronchiole

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102
Q

Describe the classification difference between central and peripheral airways

A

By convention, airways > 2 mm are “central airways” and airways < 2 mm are “peripheral airways”

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103
Q

Describe the formulaic relationship of rate of airflow to driving pressure and resistance. Units?

A

Rate of airflow = driving pressure/resistance reworking of Ohms law: F = P/R

Units of flow = L/sec, units of pressure = cm H2O & units of resistance are cmH2O/(L/sec)

Airway resistance is rarely measured

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104
Q

Describe laminar flow. Resistance is proportional to?

A

LAMINAR FLOW  silent; occurs in peripheral airways (because of amount of cross sectional area)

Resistance is proportional to 1/r^4

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105
Q

Laminar flow resistance is proportional to?

A

1/r^4 (pressure is 1:1)

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106
Q

Describe turbulent flow. Resistance is proportional to? Pressure?

A

TURBULENT FLOW makes noise; occurs in central airways, particularly during forced expiration

R 1/ r5 AND increases proportionally with airflow (i.e. if flow doubles, driving pressure must
increase by a factor of 4 [i.e. diaphragm & accessory muscles contract more forcefully])

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107
Q

Describe the relationship of pressure and resistance to turbulent flow

A

resistance is proportilow onal to 1/r^5

flow proportional to P^2 (e.g. to double airflow, pressure must be quadrupled)

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108
Q

What are the ground rules for dynamic compression

A

Ground rules: (1) Occurs only during forced expiration (2) occurs only when pleural pressures are positive

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109
Q

During forced expiration, pleural pressures are ….than Patm

A

Greater than

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110
Q

Describe the pressures during forced expiration

A

During a forced expiration, the alveolar pressure is positive & counterbalances the pleural pressure & ERlung that are working to
compress/squeeze on the alveolus

ERlung = PA – Ppl; thus, PA = ERlung + Ppl
Air will flow out down the pressure gradient & as it flows the driving pressure will be dissipated & the pressure will drop

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111
Q

What is the equal pressure point?

A

Equal pressure point = point where the air pressure in the airways equals the pleural pressure

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112
Q

Describe the areas between equal pressure point and the mouth

A

Between the equal pressure point & the mouth, pleural pressure is greater than the pressure in the airway & airway compression occurs Dynamic compression primarily occurs in central airways

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113
Q

Describe increasing pleural pressure and flow rate response

A

Above about +10 cm H2O pleural pressure (a mild expiratory effort), further increases in expiratory effort
(as indicated by increase in pleural pressure) produce NO increase in flow rate

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114
Q

What is the purpose of diffusion?

A

The purpose of diffusion is to make the partial pressure of oxygen in the capillary equal to the partial pressure of oxygen in the alveolar gas [mixed venous blood has a textbook value of PO2 = 40 mmHg)

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115
Q

Mixed venous blood has a textbook value of PO2 of?

A

~40 mmHg

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116
Q

Describe the states of oxygen from the air to blood

A

The oxygen must undergo a phase change from a gas in air to a gas dissolved in a liquid

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117
Q

How do we determine the partial pressure of oxygen?

A

Partial pressure of oxygen in air is determined by Dalton’s law: PO2 = FO2 x (Ptotal – PH2O)

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118
Q

Describe the relationship between partial pressure of oxygen in air and in liquid

A

Partial pressure of oxygen in liquid = the partial pressure of oxygen in air when the air & the liquid are in equilibrium

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119
Q

What does partial pressure of oxygen in blood include?

A

Partial pressure of oxygen in a blood doesn’t include O2 bound to Hb, just dissolved O2

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120
Q

Describe what determines diffusion (5 things)

A

Area: increasing area increases diffusion

Diffusion properties of the gas: depends on MW of the gas

Thickness: longer path for diffusion makes diffusion lower (increased with pulmonary fibrosis)

Capacity of blood for the gas: depends on amount of Hb (decreased with anemia (lungs normal))

Partial pressure of gas in the alveoli: diffusion process is slower at high altitudes

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121
Q

What effect does area have on diffusion?

A

Increased by larger person, at TLC vs. RV or during exercise

Decreased by lung resection & emphysema

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122
Q

Describe properties of gas on diffusion

A

Diffusion properties of the gas: depends on MW of the gas

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123
Q

Describe thickness effect on diffusion. Disease state?

A

Thickness: longer path for diffusion makes diffusion lower (increased with pulmonary fibrosis)

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124
Q

Describe the capacity of blood for gas?

A

depends on amount of Hb (decreased with anemia (lungs normal))

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125
Q

Describe the partial pressure of gas effect on diffusion.

A

diffusion process is slower at high altitudes

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126
Q

Describe the generalized diffusion capacity of the lung equation

A

Vgas = DL x (PA – PC)

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127
Q

What is D_L?

A

Diffusing Capacity of the Lung (DL) is these terms lumped (A, diffusion properties of gas, thickness, capacity of blood for the gas, partial pressure of gas in the alveoli)

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128
Q

Describe CO diffusion equation

A

CO bings Hb tightly so that the partial pressure of CO in the capillary is essentially 0… VCO = DLCO x PACO

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129
Q

Describe the steady state technique for measuring diffusion capacity

A

Patient breaths a gas mixture with very dilute CO

Consumption of CO is measured over several minutes (what went in – what comes out)

Average PACO is estimated by mathematical approximations

D_LCO = V*CO /PACO

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130
Q

What are the components of D_L?

A

1/DL = 1/DM + 1/(ΘVC)

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131
Q

What is D_M? What reduces it?

A

DM = membrane diffusing capacity (gas has to cross the membrane)

Reduced in lung resection & emphysema

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132
Q

What is V_C?

A

VC = pulmonary capillary blood volume (gas has to find its way through the plasma) = 100 mL

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133
Q

What affects V_C?

A

↑during exercise due to capillary distension & recruitment of other capillaries in the lung

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134
Q

What is theta? What reduces it?

A

Θ = capacity of 1 ml of blood for O2 (gas has to combine with Hb) - Reduced in anemia

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135
Q

What is the transit time for a red blood cell in the pulmonary capillary bed?

A

V_c/C.O. = 1.2 sec

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136
Q

What is dissolved oxygen defined as?

A

Dissolved oxygen = oxygen in blood NOT bound to Hb

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137
Q

How do we calculate dissolved O2?

A

Amount of dissolved O2 = (Solubility) x (PO2)

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138
Q

What is the solubility of O2 in blood (IMPORTANT)?

A

Solubility of O2 in blood = 0.003 mL O2/(100 mL blood x mmHg)

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139
Q

How is dissolved O2 expressed?

A

Dissolved O2 can be expressed as, example, 0.3 mL O2/100 mL blood OR 0.3 vol%

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140
Q

Oxygen binds to Hb at what level?

A

1 gram of Hb binds 1.39 mL O2

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141
Q

What is oxygen capacity?

A

amount of oxygen bound to Hb per 100 mL blood when the Hb is fully saturated

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142
Q

How is oxygen capacity calculated?

A

Oxygen capacity = (g Hb/100 mL blood) x (1.39 mL O2/1 g Hb)

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143
Q

Is 1.39 mL O2/g Hb ever achieved? Why?

A
  1. 39mLO2/gHb is a theoretical maximum that’s never met because:
    1) Methemoglobin = when ferrous (F2+) has been oxidized to ferric (F3+) & can’t bind O2
    2) Carboxyhemoglobin = when Hb binds CO
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144
Q

What is oxygen content?

A

actual amount of O2 bound to Hb plus dissolved O2

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145
Q

How is oxygen content calculated?

A

O2 content = (O2 capacity x Saturation) + (amount dissolved O2)

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146
Q

What is used to calculate percent saturation of hemoglobin with oxygen?

A

Given a PO2, one can use an oxyhemoglobin dissociation curve to determine the % saturation

For example:

Arterial blood has PO2 ~100 mmHg & Hb has 97% saturation
Mixed venous blood has a PO2 ~ 40 mmHg & Hb has 75% saturation

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147
Q

What is larger dissolved oxygen or bound oxygen?

A

Amount of O2 bound to Hb is much larger than that dissolved

148
Q

Oxygen capacity refers to?

A

Oxygen capacity only refers to Hb & does NOT include dissolved O2

149
Q

Oxygen content refers to?

A

Oxygen content refers to both the amount of O2 on Hb & the dissolved O2 (Even though it’s small)

150
Q

What determines PO2?

A

Dissolved O2 is the only thing that determines PO2

151
Q

What is the Bohr effect?

A

Bohr effect: ↑PCO2 in blood shifts the oxyhemoglobin dissociation curve to the right (less saturation for a given PO2)

152
Q

What causes the Bohr effect?

A

Results from the fact that when CO2 is added to blood, both dissolved CO2 & H+ rise

1) H+ binds Hb & reduces the affinity of Hb for oxygen [primary reason]
2) CO2 forms carbamino compounds with Hb that reduce Hb’s affinity for O2

153
Q

Describe effect of temperature on bound hemoglobin

A

increasing temperature shifts the curve to the right

154
Q

Describe 2,3 DPG levels on the hemoglobin dissociation curve. Explain what happens at altitude

A

shifts the curve to the right

People at high altitude hyperventilate & blow off CO2, decreasing PCO2 & (Bohr effect)
causing the curve to shift left. Over time, levels of 2,3-DPG increase & the curve is
shifted back towards normal (not all the way & doesn’t overshoot)

155
Q

What does right shift mean on a oxyhemoglobin dissociation curve?

A

Right shifts make it so that more O2 is made available for unloading into tissues (affinity of
Hb for O2 is decreased)

156
Q

Describe what things cause right shift for hemoglobin curve

A

Summary: Increases in 2,3-DPG, dissolved CO2, H+ or temperature cause right shifts

(CADET face Right)

157
Q

What is the rate limiting step in O2 consumption?

A

The rate limiting step is the cardiovascular system (transfer of O2 in blood)

158
Q

Describe the body’s relation to CO2

A

CO2 is a metabolic waste product that must be eliminated constantly; paradoxically, a steady-state level of CO2 must be retained in order to maintain acid-base status

159
Q

Describe CO2 in the plasma

A
  1. Dissolved CO2
  2. Carbonic acid, H2CO3 (negligible)
  3. Bicarbonate anion (HCO3-)
160
Q

Describe CO2 in the red cell

A
  1. Dissolved CO2
  2. Carbonic acid, H2CO3 (negligible)
  3. Bicarbonate anion (HCO3-)
  4. Carbamino compounds (-NH2 +
    CO2 -> -NH-COO- + H+)
161
Q

CO2 makes what carbamino compound?

A

-NH2 + CO2 -> -NH-COO- + H+

162
Q

CO2 composition in whole blood?

A

5% is dissolved CO2
5% is carbamino compounds
90% is bicarbonate anion

163
Q

Describe the equilibrium of CO2 in the blood and lungs.

A

[eliminated by lungs] CO2(gas) ↔ CO2+ H2O (blood) ↔ H2CO3 ↔ H+ + HCO3
- [eliminated by kidneys]

164
Q

HCO3 is eliminated by? CO2?

A

HCO3 is kidneys

CO2 is lungs

165
Q

CO2 is what type of gas?

A

CO2is a volatile acid (you can breathe it away as a gas)

166
Q

Non-volatile metabolites are removed by?

A

Other acids produced by metabolism are nonvolatile & are eliminated by the kidneys

167
Q

What are the units of measurement of CO2 in the plasma?

A

Vol% = mL of CO2 in all forms/100 mL of blood

Mmol/L or mM  used to refer to CO2 in the plasma, especially when considering acid-base
problems; usually used to refer to specific forms of CO2 (i.e. mM dissolved CO2)

168
Q

How is dissolved CO2 calculated?

A

Dissolved CO2 = solubility x PCO2

169
Q

What is the solubility of CO2 in blood?

A

solubility of CO2 in blood = 0.0301mM/mmHg

170
Q

What is PCO2 in arterial blood? Corresponding amount of dissolved CO2?

A

In arterial blood, PCO2 is approximately 40 mmHg so dissolved CO2 = 1.2 mM

171
Q

Diffusion is driven by partial pressure or concentration?

A

Partial pressure (when going from liquid to gas or from liquid 1 to liquid 2)

172
Q

Dissolved CO2 combines to form what?

A

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3
-

173
Q

What is the henderson hasselback equation?

A

pH=6.1+log([HCO3]/[CO2])

pH=6.1+log([HCO3}/(0.0301 mM/mmHg *PCO2))

174
Q

How does a blood gas machine work?

A

Inject sample into center compartment & a pH electrode measures pH

CO2 diffuses (H+ doesn’t); CO2 makes right side solution acidic (measured by pH electrode)

Oxygen diffuses into the left compartment that contains an oxygen electrode

175
Q

What is the ratio of bicarbonate to CO2 in plasma?

A
176
Q

Normal PaCO2 is defined as?

A

Normal: (arterial) PaCO2 ~ 40 mmHg

177
Q

Respiratory acidosis is defined as?

A

Arterial PCO2 > 45 mmHg

178
Q

Effects of respiratory acidosis?

A

Concentrations of all compounds increase (CO2, H+, HCO3-); more CO2 = more acid

179
Q

Causes of respiratory acidosis

A

Causes: anything that reduces ventilatory drive (1. Holding your breath, 2. Drug overdoses that
reduce ventilatory drive, 3. Obstructive lung disease)

180
Q

What is respiratory alkalosis?

A

Arterial PCO2 < 35 mmHg; less CO2 = less acid thus alkalosis

181
Q

Effects of respiratory alkalosis?

A

Concentrations of all components decrease (CO2, H+, HCO3-)

182
Q

Causes of respiratory alkalosis?

A

Causes: 1. Hypoxic drive (ascent to high altitude) 2. Mechanical over-ventilation 3. Pain &/or
anxiety (“psychogenic hyperventilation”)

183
Q

Describe the function of buffering in response to protons in blood

A

In the simulated respiratory acidosis, pH decreased & bicarbonate increased solely by added CO2 gas

CO2 + H2O ↔ H+ + HCO3

Some of the H+ remains free while most binds to blood buffers

184
Q

Which is superior buffer, blood or plasma? Why?

A

Blood is a superior buffer compared to plasma, mainly due to blood buffers like Hb

In anemia, for a given increase in PCO2, the blood will become more acidic compared to normal

185
Q

What is the haldane effect?

A

as oxygen is added to blood, CO2 is driven off

186
Q

What is bohr effect?

A

as CO2 is added to blood, O2 is driven off Hb

187
Q

How does the haldane effect occur?

A
  1. When O2 binds to Hb, H+ ions are released
    Hb-H+ + O2 -> Hb-O2 + H+
    Then H+ + HCO3 -> CO2 + H2O (eliminated by lungs)
  2. Hb forms fewer carbamino compounds in the presence of O2
188
Q

Describe the relationship between O2 and CO2 according to Haldane

A

the lower the PO2, the lower the PCO2 needed to achieve the same blood CO2 content

189
Q

Describe cardiac output to the lungs

A

The most important feature of the pulmonary circulation is that it receives the entire cardiac output

190
Q

Describe the filter effects of the lung

A

The lung is a filter : lung sees the entire venous return & can remove particulate matter from the circulation

Physiologically : lung removes small emboli (blood clots) via proteases

Non-physiologically : dust/dirt/other particulate matter injected by drug users

191
Q

Function of lung filter?

A

The filtration function of the lungs keeps the arterial circulation clear of particulate matter; cerebral & coronary circulations are particularly vulnerable to occlusions while it’s not serious if a small region of pulmonary circulation is blocked by particulate matter

192
Q

Describe the metabolites/hormones affected by the lungs

A 
Angiotensin I is converted to AII in one pass
Angiotensin II is untouched
Bradykinin is 80% removed in 1 pass
Serotonin is 90% removed in 1 pass
Epinephrine is not affected
Norepinephrine is up to 30% removed
193
Q

Lung effect on angiotensin I

A

Converted to Angiotensin II in one pass

194
Q

Lung effect on angiotensin II

A

No effect

195
Q

Lung effect on bradykinin

A

80% removed in 1 pass

196
Q

Lung effect on serotonin

A

90% removed in 1 pass

197
Q

Lung effect on epi

A

Not effected

198
Q

Lung effect on norepi

A

30% removed

199
Q

Resistance and pressure in pulmonary circuit?

A

The pulmonary circulation is a low pressure/low resistance circuit

200
Q

Describe pulmonary arterial pressure (values)

A

Pulmonary arterial pressure: 25 mmHg/8 mmHg (mean arterial pressure is 15 mmHg)

201
Q

What is the mean pulmonary venous pressure

A

Mean pulmonary venous pressure is 2 mmHg & is virtually the same as left atrial pressure

202
Q

Describe capillary pressures in the pulmonary circulation

A

Capillary pressures are in between; unlike systemic system, capillaries contribute significantly to the total pulmonary resistance & a lot of driving pressure from the right ventricle is dissipated across the pulmonary capillary bed

203
Q

Describe pulmonary blood flow in the capillaries

A

Pulmonary blood flow is pulsitile in the capillaries & probably doesn’t impair gas exchange

204
Q

What is pulmonary capillary resistance (values)?

A

Resistance is around 2-3 mmHg per L/min or about 10 fold less than systemic circulation

205
Q

As CO increases, what happens to pulmonary resistance?

A

Pulmonary resistance decreases with increasing cardiac output; thus, pulmonary arterial pressure
does not increase substantially during exercise

206
Q

How does pulmonary resistance decrease?

A

↓ in pulmonary resistance is a passive phenomenon due to (1) distention of the vessels
that are already well-perfused & (2) recruitment (opening up) of vessels not perfused

207
Q

What is hypoxic vasoconstriction?

A

(unique to pulmonary circulation) -> pulmonary resistance increases with hypoxia

208
Q

What happens to the lung in low PO2?

A

When lung is hypoxic (low PO2), arterioles constrict & pulmonary vascular resistance increases dramatically

209
Q

What is the physiologic advantage to hypoxic vasoconstriction?

A

Major physiologic advantage: fetal lung  there’s no need for blood to flow thru the pulmonary capillary
bed; fetal lung is hypoxic & high vascular resistance causes venous blood flow to the arterial circulation by:
 A. the ductus arteriosus (pulmonary artery to aortic arch)
 B. Foramen ovale (right atrium to left atrium)
o With 1st breath, O2 causes an immediate ↓in pulmonary resistance & blood flows immediately through lungs

210
Q

Describe localized hypoxic vasoconstriction. Overall effect on the lung resistance?

A

If the hypoxia is localized, vessels (arterioles) constrict in that region; hypoxic vasoconstriction occurs only in that region & blood flow is re-directed to regions of the lung that have better ventilation

This localized vasoconstriction does little to increase pulmonary vascular resistance

211
Q

Describe generalized hypoxic vasoconstriction. What does this lead to?

A

Generalized hypoxic vasoconstriction is seen most commonly in people living at high altitude

Vasoconstriction throughout entire lung & resistance of the entire pulmonary vasculature is ↑; thus,
pulmonary arterial pressure rises & there’s pulmonary hypertension resulting in a change in right ventricular structure (called Cor Pulmonale): dilation (acute phase) &/or hypertrophy (chronic
adaptation) of the right ventricle due to this increase in the resistance of the pulmonary vasculature

212
Q

Describe the regional differences in lung ventilation

A

Regional Differences in Ventilation & Perfusion of the Lung

o In the lung, there’s less ventilation & perfusion at the apex of the lung compared to the base due to gravity
o Three Zone Model of Lung Perfusion (3 zones are called the “West Zones”)

213
Q

Describe zone 1 (west zone)? Exist in humans?

A

Zone 1: apex (PA > Pa > PV)

No perfusion (perfusion pressure can’t overcome gravity)

Alveolar pressure > arterial & venous pressures = collapsed capillary

In humans, there’s just enough driving pressure from the right ventricle to overcome the force of gravity on the column of blood such that the apex is perfused & there’s probably no zone 1 in humans

214
Q

Describe zone 2 (west zone)?

A

Zone 2: mid-region (Pa > PA > PV)

Arterial pressure is high enough to pump the blood up to this region

Arterial P > alveolar pressure = capillary is open (on the arterial side)

Venous pressure isn’t enough to maintain a column of blood from the heart up to Z2 so capillary constriction occurs towards the venous side

215
Q

Describe zone 3 (west zone)?

A

Zone 3: base (Pa > PV > PA)

Both arterial & venous pressures exceed atmospheric pressures & no vessel collapse or constriction is seen

216
Q

What is the respiratory quotient?

A

ratio of CO2 produced to O2 consumed; depends on what your body is burning for fuel

217
Q

What is RQ for glucose? For Fat? Mixed?

A

Glucose : Ratio is 1
Fat Ratio is 0.703

People burn a mixture of sugars & fats so the RQ = 0.8

218
Q

How is RQ measured?

A

Measure: pt breathes room air, collect exhaled gases, analyze for the amount of O2 removed & CO2 added

RQ = V_dot_CO2 / V_dot_O2

219
Q

What is RQ?

A

CO2/O2 produced/consumed by tissues

220
Q

Describe the effect of RQ on the alveolar air equation

A

Since O2 consumption per breath > CO2 production, have to accommodate for the O2 consumption in alveoli

221
Q

Suppose the RQ = R = 1, PB = 760 mmHg, PIH2O = 47 mmHg, PIO2 = 150 mmHg & PIN2 = 563 mmHg…calculate the effect on pressures

A

If R = 1, PAH2O = 47 mmHg, PACO2 = 40 mmHg, PAO2 = 150-40 = 110 mmHg & PAN2 = 563 mmHg

 Total = 760 mmHg

222
Q

Suppose the RQ = R = 0.8, PB = 760 mmHg, PIH2O = 47 mmHg, PIO2 = 150 mmHg & PIN2 = 563 mmHg…calculate the effect on pressures

A

If R = 0.8, PAH2O = 47 mmHg, PACO2 = 40 mmHg, PAO2 = 150-50 = 100 mmHg & PAN2 = 563 mmHg

 Total = 750 mmHg  alveolar regions are subamospheric!

223
Q

Effect of O2 diffusion into blood on alveolar air pressures

A

Since more O2 diffused into the capillaries than was replaced by CO2, alveolar regions are subatmospheric

224
Q

Describe what happens to account for the alveolar depletion of O2 when RQ doesnt equal 1. What is used?

A

To respond to the pressure drop, the alveolar regions being in more fresh air (passively) from the airways

o The flow in will be 2 parts O2 & 8 parts N2, which will restore alveolar pressure to Patm
o The subatmospheric pressure was caused by diffusion of O2 into the blood & was replaced by a
combination of mostly N2 & some O2

225
Q

If RQ=1 or FIO2 is 100% what is PAO2?

A

PAO2 = PIO2 – PACO2

226
Q

If FIO2 is 21% or RQ =0.8 what is PAO2?

A

PAO2 = PIO2 – PACO2 x 1.2

227
Q

How is PIO2 calculated?

A

PIO2 = (PB – 47 mmHg) x FO2

228
Q

What is arterial hypoxemia?

A

abnormally low PO2 in the arterial blood (low PaO2)

229
Q

Do people with anemia have arterial hypoxemia?

A

Note: people with anemia (low Hb) do NOT have arterial hypoxemia; they have a normal PaO2

230
Q

What are the major causes of arterial hypoxemia?

A

Causes: (1) hypoventilation, (2) diffusion limitation (3) shunt (4) ventilation-perfusion mismatching

231
Q

What is the alveolar-arterial oxygen difference? Typical value?

A

A-a difference = PAO2 – PaO2 should be low since O2 normally equilibrates

232
Q

What is the alveolar ventilation equation?

A

V_dot_A = 863 x V_dot_CO2/PaCO2

233
Q

What happens if CO2 production doubles, according to the alveolar ventilation equation?

A

States that if your CO2 production doubles, you must double alveolar ventilation to maintain constant PaCO2

234
Q

Hypoventilation is the same as? Defined by?

A

same as respiratory acidosis: Defined as PaCO2 > 45 mmHg

235
Q

When PAO2 decreases, what happens to Hb saturation? Why?

A

PAO2 decreases; Hb saturation is lower because

(1) PaO2 can’t be higher than PAO2
(2) The acidosis (from the CO2) shifts the O2-Hb dissociation curve to the right

236
Q

What causes hypoventilation?

A

(1) reduced ventilatory drive (2) obstructive lung disease (3) mechanical underventilation

237
Q

What are the 3 major features of hypoventilation as an arterial hypoxemia?

A
  1. PaO2 lower than normal (by definition)
  2. PaCO2 > 45 mmHg
  3. A-a difference normal (O2 normally equilibrates between alveolar gas & arterial blood)
238
Q

What is diffusion limitation arterial hypoxemia? When is it seen?

A

least common of arterial hypoxemias; mostly seen in emphysema & pulmonary fibrosis

239
Q

What causes diffusion limitation arterial hypoxemia?

A

low diffusing capacity of the lung (as measured by DLCO)

240
Q

Describe the physiology of diffusion limitation

A

Diffusion limitation occurs when the RBC is not fully oxygenated by the time it leaves the pulmonary capillary. At rest, the transit time of a RBC in the pulmonary capillary is about 1 sec & normally oxygenation is complete in 0.2-0.3 secs. In a diffusion limitation, oxygenation isn’t completed during the transit period.

There’s a small percentage of Hb that should have been loaded with O2 but was not

241
Q

What are the 3 features of diffusion limitation arterial hypoxemia?

A

1) A substantial alveolar-arterial oxygen difference (O2 doesn’t equilibrate)
2) Alveolar-arterial oxygen difference is eliminated with elevated inspiration
3) Diffusion limitation is much more severe with exercise due to shorter transit time & lower Hb
saturation in venous blood

242
Q

What are shunts?

A

a pathway thru which venous blood enters arterial circulation without any gas exchange whatsoever

243
Q

How are shunts reported quantitatively?

A

Usually reported as a percentage or fraction of the cardiac output: QS/QT (shunt/C.O.)

244
Q

Describe the physiologically normal shunts

A

Normal shunts: Thebesian veins (drain into L ventricle) & bronchial circulation (drain into pulmonary vein)

245
Q

What are two examples of abnormal shunts?

A

Abnormal shunts: (1) Pulmonary edema (“pulmonic shunts”) [blood flows but no oxygen because alveoli are closed off] & (2) Septal defects (“right-to-left shunts”)

246
Q

Describe the most distinguishing factor of shunt arterial hypoxemia

A
  1. Alveolar-arterial oxygen difference is high with room air

2. A-a oxygen difference is enormous when breathing elevated inspired air (such as 100% oxygen)

247
Q

Describe the reason why A-a oxygen difference is high in shunt arterial hypoxemia

A

Suppose that
o (a) patient has a 10% shunt [for every 100 mL of cardiac output, 90 mL comes from the lungs (oxygenated) &
10 mL comes from the shunt (not oxygenated)],
o (b) PB = 760 mmHg
o (c) Oxygen capacity of the blood is 20 vol% & the person breathes 100% O2

 Patient is now given 100% oxygen to breathe…
 For every 100 mL of blood flow, 90 mL is passing through the lungs & receives oxygen
o PAO2 = (PB-47)x1-PaCO2 = (760-47)x1-40=673 mmHg
o Hb becomes 100% saturated with oxygen (anytime the PaO2 > 150 mmHg, we consider Hb saturation 100%)
o Dissolved O2 = 0.003x673 = 2mL O2/100 mL blood or 1.8 mL O2 per 90 mL blood
 For every 100 mL of blood flow, 10 mL is passing through the shunt & doesn’t receive O2
o Hb is 75% saturated (same as mixed venous blood)
o Dissolved O2 is negligible (relative to the amount of dissolved oxygen in the blood coming from the lungs)
o O2 capacity is 20 mL O2/100 mL blood, but we’re considering 10 mL so O2 capacity is 2 mL O2/10 mL blood
o Since Hb saturation is 75%, it means that Hb has 1.5 mL O2 on it & an 0.5 mL O2 is needed to fully saturate

 1.8 mL dissolved O2 from lung blood mixes w/ negligible dissolved O2 from shunt blood
 The result is 100 mL
o 0.5 mL of dissolved O2 from the blood from the lungs is used to saturate the Hb in the blood from the shunt
o Dissolved O2 left per 100 mL is 1.8-0.5 = 1.3 mL
o PaO2 = dissolved O2/0.003 = 1.3/0.003 = 433 mmHg
o A-a difference = 673 mmHg – 433 mmHg = 240 mmHg

 Some of the dissolved oxygen coming from the oxygenated blood is used to saturate the Hb coming from the shunted
blood; it’s only dissolved O2 that determines the PO2 in blood so when dissolved O2 is used to oxygenate Hb, the PO2
falls & leads to the substantial alveolar-arterial difference

248
Q

What are the major features of ventilation-perfusion mismatching?

A

1) A large alveolar-arterial O2 difference breathing room air
2) Corrected by increasing the PIO2

249
Q

Give two examples of ventilation-perfusion mismatching

A

Ventilatory: Obstructive lung disease (because airway obstruction is rarely uniform), regional
differences in compliance

Circulatory: Pulmonary embolism

250
Q

What is the most common cause of ventilation-perfusion mismatching?

A

Most common cause: aging

 A young adult will have an Alveolar-arterial O2 difference approximately 5
 An old adult may have an Alveolar-arterial O2 difference approximately 20
 This is not usually a cause for concern

251
Q

What is the ventilation-perfusion ratio?

A

(VA/Q) = ratio of the rate of alveolar ventilation to pulmonary blood flow

*=dot

252
Q

What are the normal values for the ventilation-perfusion ratio?

A

Normally, VA = 4 L/min & Q = 5 L/min so VA/Q is normally 0.8

253
Q

Describe the ideal O2 and CO2 exchange

A

Ventilation & perfusion matching is important to achieve ideal O2 & CO2 exchange; usually, the ventilation perfusion
ratios throughout the lung are close to the overall ventilation-perfusion ratio of 0.8

254
Q

Give examples of V-P mismatch (the overall as well as extremes)

A

Region of lung is well ventilated but poorly perfused: VA/Q = [3 L/min]/[1 L/min] = 3

Region of the lung that’s poorly ventilated & well perfused: VA/Q = [1 L/min]/[4 L/min] = 0.25

But overall: VA/Q = [3 L/min+1 L/min]/[1 L/min+4 L/min] = 4/5 = 0.8

255
Q

Describe what happens with no ventilation in arterial hypoxemia (ventilation-perfusion mismatch)

A

No ventilation such that VA/Q = 0 (a shunt)

If there’s no ventilation, the air inside the alveolus (if it hasn’t collapsed which it usually does) will have the same partial pressures as the mixed venous blood passing through the pulmonary capillary

For example, PAO2=40 and PACO2=45 and so do blood partial pressures (P_Vdot)

256
Q

Describe what happens with no perfusion in arterial hypoxemia (ventilation-perfusion mismatch)

A

If there’s no perfusion, then the air inside the alveolus will have the same partial pressures as the inspired gases in the airways

E.g. PIO2=150 and PICO2=0 and blood matches

257
Q

Describe a normal alvelous in terms of ventilation perfusion matching. What are the values?

A

If there is both ventilation & perfusion, the alveolus will have gas partial pressure in between that of the inspired gases and the gases in the mixed venous blood. The exact values are determined by computer simulation/numerical approximations.

PIO2=150 PICO2=0
PAO2=100 PACO2=40
P_VdotO2=40 P_VdotCO2=45

258
Q

Describe what happens when the ventilation perfusion ratio increases

A

As the ratio of ventilation to perfusion increases, the partial pressure of CO2 in the alveolus falls & the partial pressure of O2 rises

259
Q

Describe the physiological response to ventilation perfusion mismatch

A

In a ventilation perfusion mismatch, you see both poorly ventilated regions (Low VQ ratio) & well ventilated regions (High VQ ratio) because total ventilation must remain the same in order to maintain a normal PaCO2 CO2 is retained in the poorly ventilated regions & extra amount of CO2
“blown off” in the well-ventilated region

260
Q

Describe CO2 and O2 levels resulting from ventilation perfusion mismatch

A

1) A well-ventilated region of the lung can
compensate for the abnormal accumulation of CO2 in a poorly-ventilated region (linear curve)

2) A well-ventilated region of the lung
cannot compensate for the abnormal loss
of O2 in a poorly ventilated region (non-linear curve)

261
Q

Describe CO2 as a chemical factor in blood with regard to ventilation

A

CO2 : mainly dissolved CO2, not bicarbonate/carbamino compounds (ventilation is sensitive to PaCO2)

Hypercapnia = elevated PaCO2

262
Q

Describe O2 as a chemical factor in blood with regard to ventilation

A

O2 : In particular, dissolved O2 not oxygen bound to Hb (thus, the rate of ventilation is sensitive to PaO2)

Hypoxia = reduced PaO2

263
Q

Describe pH as a chemical factor in blood with regard to ventilation

A

(acidosis = reduced pH)

A) from CO2 in a respiratory acidosis
B) from non-volatile acids in a metabolic acidosis (lactic acid, diabetic ketoacidosis)

264
Q

What are central receptors?

A

Central receptors  usually referred to as the ”Chemosensitive Area of the Brain” (CSA) aka Central chemoreceptor, aka CO2 chemoreceptor; located in the medulla

265
Q

Where is the CSA located? How does it work?

A

The CSA is located on the brain side of the blood-brain barrier, but senses dissolved CO2 in the blood

 The dissolved CO2 diffuses across the blood brain barrier (but not H+ or bicarbonate)
 Once in the CSF, the CO2 combines with water to form H+ & HCO3

 Data indicates that it’s the H+ that binds in the CSA to regulate ventilation; but, note, that H+ isn’t
coming from the blood but from the dissolved CO2 that diffuses across the blood-brain barrier

266
Q

What is the peripheral receptor in humans?

A

Carotid bodies

267
Q

The carotid bodies account for?

A

1) All ventilatory response to low PaO2 (hypoxic drive)
2) About ¼ of the response to changes in PaCO2
3) All the response to changes in pH in a metabolic acidosis/alkalosis

268
Q

Why are carotid bodies well suited for measuring arterial blood?

A

The carotid bodies are particularly well suited to sense arterial blood partial pressures because the rate of blood flow is very high relative to metabolism; this means that the partial pressure of, for example, oxygen is similar in both the arterial blood & the venous blood of the carotid or

 PaO2 PVO2
 This means that the carotid body is bathed with dissolved O2 that is essentially equal to PaO2

269
Q

Describe the response to CO2 increase

A

Essentially, if PaCO2 rises, ventilation rises to compensate & does so quite
dramatically

The ventilatory rate increases almost 2x per mmHg rise in PaCO2

Ventilatory responses serve to keep the PaCO2 within a few mmHg of the set point (at sea level, 35-40 mmHg)

270
Q

What is the CO2 set point?

A

Ventilatory responses serve to keep the PaCO2 within a few mmHg of the set point (at sea level, 35-40 mmHg)

This is achieved via ventilation modification

271
Q

When is response to hypoxia triggered?

A

occurs significantly when PaO2 falls below about 60-70 mmHg

Sensed by carotid bodies

272
Q

What is del V_40?

A

ΔV40 = difference in ventilatory rate when the PaO2 is 40 mmHg vs. a PaO2 of 150 mmHg

273
Q

What is hypoxic drive?

A

hyperventilation, a ventilatory rate faster than that needed to maintain a normal PaCO2

274
Q

What results in the alveolus due to hypoxic drive?

A

Alveolar ventilation ↑ due to the hypoxic drive & thus PaCO2 ↓due to hyperventilation (blow off CO2)

275
Q

Describe the mathematics of hypoxic drive step by step from AV equation to result in PAO2

A

AV equation: PaCO2=VCO2/VA * 863
To decreases PaCO2, we increase V*A

PAO2=PIO2-PaCO2x1.2
Decrease in PaCO2, increases PAO2

276
Q

What are the physiologic advantages to the rise of PAO2 in hypoxic drive?

A

1) It raises the arterial oxygen (PaO2) & increases Hb saturation
2) It reduces hypoxic vasoconstriction

277
Q

Describe acute hypoxic drive

A
  1. Hypoxia stimulates neural activity at the carotid body causing an increase in ventilatory rate
  2. Hyperventilation ↓ PaCO2, making the CSF pH more alkaline causing CSA to ↓ventilatory rate

 Thus, from the carotid bodies, a signal to ↑ ventilation & from the CSA a signal to ↓ ventilation
 Net result: a small increase in ventilatory rate in the acute stage (first 24 to 48 hours)

278
Q

Describe chronic adjustment to hypoxic drive

A
  1. Over hours/day, the pH of the CSF is restored toward normal by a reduction of bicarbonate

pH=6.1+log([HCO3]/(0.0301xPCO2))
Decrease PCO2 has to have corresponding increase in bicarbonate to maintain pH

  1. The result: the signal from the carotid bodies to increase ventilation is unopposed by a signal
    from the CSA & the full effect of hypoxic drive is felt (chronic higher ventilatory rate)
279
Q

What is respiratory acidosis? Response?

A

Respiratory acidosis = increase in CO2

 The increase in PaCO2 increases [H+] of the CSF causing an increase in ventilatory rate
 Increase in [H+] of the blood stimulates carotid body activity causing an increase in ventilatory rate
 Result: ventilatory stimulation from both the carotid bodies & the CSA

280
Q

What is metabolic acidosis? Response?

A

Metabolic acidosis = increase in acids from other sources (e.g. lactic acid, diabetic ketoacidosis)

 Same acute/chronic phases seen in hypoxic drive & for the same reasons

281
Q

Describe acute phase of metabolic acidosis repsonse

A
  1. Low pH stimulates neural activity at the carotid body & causes an ↑ ventilatory rate
  2. Hyperventilation ↓PaCO2 making the CSF pH more alkaline & causing a ↓ ventilatory rate.

Net result: a small increase in ventilatory rate in the acute stage

282
Q

Describe chronic adjustment to metabolic acidosis

A
  1. pH of the CSF is restored towards normal (via bicarb)
  2. Inhibition of ventilatory rate from the CSA becomes insignificant
  3. The stimulus from the carotid bodies (due to the ↑ in blood [H+]) causing an increase in
    ventilatory rate is unopposed by the CSA & higher ventilatory rate is observed chronically
283
Q

What is the equilbirum expression for CO2-Bicarbonate?

A

CO2+H2) H2CO2 H+ + HCO3-

284
Q

What is the ratio of CO2:H2CO3:HCO3-?

A

340:1:6800

285
Q

Can we ignore carbonic acid at pH 7.4

A

Yes, very small component of total products

286
Q

What is Ka’ defined as?

A

Ka’=[H+][HCO3-]/[CO2]

Not that Ka’=Ka*[H2O]

287
Q

What is the numerical value of Ka’?

A

800 x 10^-9 M

288
Q

What is normal concentration of H+?

A

40 nM

289
Q

What is normal concentration of HCO3-?

A

24 mM

290
Q

What is normal concentration of CO2?

A

1.2 mM

291
Q

If we increase hydrogen ions in the body via a metabolic acid, what happens?

A

Increase in hydrogen is countered by decrease in bicarbonate (combines) and production of CO2

(Use quadratic formula e.g. -X for protons and bicarb, and +X for CO2 and use Ka’)

292
Q

Why is CO2 ventilation a better buffer system that closed?

A

Removing CO2 created by acid challenge via ventilation results in less new hydrogen ion level and therefore a more normal pH (bicarb levels are approximately the same)

293
Q

What is PCO2 isobar?

A

PCO2 is maintained by CO2 blow off and therefore the change in bicarb as a function of pH is very vertical

294
Q

How do we calculate the PCO2 isobar?

A

Calculate pH from Ka’=[H+]{HCO3]/[CO2]=800 nM

  1. Initial conditions:
    [H+] = 40 nM, [HCO3-] = 24 mM, [CO2] = 1.2 mM
  2. Choose an amount of H+ to add
  3. Using previous analysis, solve for new H+ & pH
  4. Solve for the new [HCO3-]
  5. Plot [HCO3-] (y-axis) vs. pH (x-axis)

Use HH equation pH=6.1+log([HCO3]/(0.03018*PCO2))

  1. Select a constant PCO2
  2. Choose various concentrations of bicarbonate
  3. Use the equation to solve for pH
  4. Plot these x, y pairs (pH & [HCO3-] on the pH-bicarbonate diagram
295
Q

Describe PCO2 isobars if strong acid or base added to system

A

If a strong acid or base is added & ventilation
keeps PCO2 constant, the new pH & [HCO3-] will
be on the same PCO2 isobar

296
Q

What happens if PCO2 changes to a PCO2 isobar?

A

If PCO2 changes, new values of pH & [HCO3-] will be somewhere on a different isobar
Where that somewhere is depends on the other
body buffers

297
Q

Why does the body have other buffer systems from the CO2-bicarb?

A

We need other buffer systems because CO2 cannot buffer itself

If you add more CO2, then you need other buffers to remove H+ without regenerating the CO2

298
Q

What happens in a metabolic acid challenge (not CO2)?

A

results in addition of H+, equilibrium shifts to the right & excess CO2 is removed by ventilation (blown off)

299
Q

How does the body respond to respiratory acid challenge (CO2) (assume only CO2 bicarb system)?

A

Respiratory (CO2) acid challenge without other buffers results in the addition of CO2 & not much else happening such that the pH is unacceptably acidic

300
Q

If there were no other buffer systems, what would happen?

A

CO2 is constantly generated by tissues & carried away by the venous circulation to the lungs; if this was the only buffer system, the blood would be very acidic

301
Q

Describe generally what happens with other buffer systems responding to CO2 increase

A

When CO2 levels increase, H+ ions that are generated combine with other body buffers & pulls the CO2-bicarbonate equilibrium to the right such that most of the CO2 introduced into the system is carried away as
bicarbonate

o CO2 + H2O  HCO3- + H+ ( body buffers)
o Other buffers are needed to (1) buffer H+ ion produced by excess CO2 & (2) carry CO2 as HCO3- & not dissolved CO2 (pull the equilibrium to the right)

302
Q

What are the body’s other buffer systems?

A
  1. Phosphate: H+ + HPO4 ↔ H2PO4
  2. Plasma protein: H+ + (Protein) ↔ (Protein-H+)
  3. Red Cell
  4. Other cells
  5. Bone buffering
303
Q

Red Cell buffers?

A

buffers CO2 only & does not buffer non-volatile acids

o Note: Volatile acid = CO2; nonvolatile acids = fixed acids

304
Q

How does Red Cell buffer?

A

A. Dissolved CO2 enters the RBC
B. Some CO2 remains as dissolved CO2
C. Some becomes carbamino compounds (combines with Hb, H+ ions released & buffered by Hb)
D. Most dissociates to become H+ and HCO3- (first converted by carbonic anhydrase to carbonic
acid & then immediately dissociates)

 H+ is buffered by Hb
 HCO3- diffuses out in exchange for chloride (“chloride shift)

 Net result: the CO2 produced by metabolism is carried as HCO3- & carbamino compounds

305
Q

What is the chloride shift?

A

HCO3- diffuses out in exchange for chloride in red cell buffering

306
Q

How do other cells buffer?

A

Buffer H+ generated both by CO2 & non-volatile acids; either:

A. H+ enters the cell & a Cl- follows to maintain neutrality
B. H+ enters the cell & a Na+ or K+ leaves

o This can lead to an elevation in K+ in the extracellular fluid (hyperkalemia)

307
Q

Why does other cell buffering lead to hyperkalemia?

A

H+ enters the cell & a Na+ or K+ leaves

308
Q

Describe bone buffering

A

Calcium-CO3-Na + H+ + Cl- ↔ Calcium-Cl + Na+ + HCO3

309
Q

Compare Buffering of CO2 vs. buffering of non-carbonic acid

A

In response to strong acid (metabolic acidosis), most of the buffering is carried out by CO2-bicarb (<50%) system and cellular buffers; there’s no red cell buffering

In response to elevated CO2 (respiratory acidosis), there’s no CO2-bicarb buffering & mainly cellular buffering (red cell buffering (~30%))

310
Q

Other cells buffer what insults?

A

CO2 and non-volatile acids

311
Q

Describe the time course of buffering

A

Extracellular fluid or ECF (misnamed because it includes the RBC)
A. Plasma & RBC: seconds to minutes
B. Interstitial fluid: 10 – 30 minutes

o Cellular compartments (other than the RBC): 2-4 hours
o Bone: hours – days
o Kidney: days

312
Q

What does extracellular fluid include as buffer? How fast do these systems respond?

A

A. Plasma & RBC: seconds to minutes

B. Interstitial fluid: 10 – 30 minutes

313
Q

What is a buffer value?

A

the body’s ability to buffer a CO2 challenge

314
Q

Buffer value is equal to? Units

A

Buffer value = Delta_HCO3/Delta_pH

Units mmol/L/pH aka. slyke (sl)

315
Q

High buffer value means?

A

High buffer value (a good thing): when CO2 rises, large amounts of HCO3- are formed & the pH changes little

316
Q

Low buffer value means?

A

Low buffer value (a bad thing): when CO2 rises, HCO3- changes little & pH becomes more acidic

317
Q

Buffer value denotes what? What is being buffered?

A

Buffer value is the ability of body buffers OTHER THAN CO2-BICARB to

 1) bind H+
 2) convert CO2 to HCO3- by pulling the equilibrium to the right

318
Q

What are the buffer values for plasma, whole blood, ECF?

A 
Plasma (poor buffer): 4 mmol/L per pH unit
Whole blood (good buffer): 25 mmol/L per pH unit ECF = plasma (poor) + RBC (good) + interstitial fluid (poor) = 11 mmol/L per pH unit
319
Q

What is a buffer line?

A

Buffer value on the pH-bicarbonate diagram (the “buffer line”)

 Buffer value = ΔHCO3- = -(buffer value) x ΔpH [note: this is y = (slope)(x)]

 The ECF line is the most important for acid-base problems

320
Q

Describe the sequence of events in retention of CO2

A

Suppose a person retains CO2 & PCO2 begins to rise: During the first 10-30 minutes, the increasing acidity equilibrates with the blood/interstitial fluid & the change in pH & bicarb follow the ECF buffer line During the next several hours, H+ equilibrates with the intracellular space & pH/bicarb change according to a new buffer line

Over the next 24 hours or so, (1) buffering by bone takes place & (2) kidney retains HCO3- to
change pH toward normal

321
Q

Describe what happens to the buffer line over time for CO2 retention

A

Becomes more vertical i.e. pH is stablized and bicarb levels matter less (no effect on pH)

322
Q

What is the normal range of acid-base for arterial blood?

A

o pH 7.35 to 7.45
o PCO2 35 to 45 mmHg
o HCO3- 22 to 26 mmHg

323
Q

When does acid-base disorder occur?

A
  1. There is a respiratory &/or renal abnormality

2. Acid/base load exceeds the capacity of the respiratory &/or renal system to handle it

324
Q

What is the clincial term for pH outside of normal range?

A

acidemia (lower than normal) & alkalemia

higher than normal

325
Q

What is respiratory acid-base disorder?

A

When the initial (“primary”) abnormality is a change in PCO2, it’s called respiratory acidosis
(hypoventilation) or respiratory alkalosis (hyperventilation)

326
Q

What is metabolic acid-base disorder?

A

When the initial (primary) abnormality is due to (1) a gain/loss of non-carbonic acid (non-volatile acids) or
(2) a gain/loss of bicarbonate, it’s called metabolic acidosis or metabolic alkalosis

327
Q

What is compensation? What happens?

A

When a primary acid-base disturbance occurs, a compensatory change occurs (called “compensation”) that restores the pH towards normal but not all the way.

o Either the PCO2 or the bicarb or both will become further away from the normal value as a result

o [H+] = 800 nM*[CO2]/[HCO3]

 If the primary abnormality is an increase in CO2 (↑ PCO2), compensation is to increase bicarb
 If the primary abnormality is a decrease in bicarbonate, then compensation is to decrease PCO2

328
Q

What happens in metabolic acidosis generally?

A

Ded pH
Inc [H]

Distrubance is Dec [HCO3]

Compensation Hyperventilation to dec PaCO2

329
Q

What happens during metabolic alkalosis generally?

A

Inc pH
Dec [H]

Distrubance is Inc [HCO3]

Compensation Hypoventilation to inc PaCO2

330
Q

What happens during respiratory acidosis generally?

A

Dec pH
Inc [H]

Disturbance is Inc PaCO2

Compensation is Inc HCO3 by inc reabsorption

331
Q

What happens during respiratory alkalosis generally?

A

Inc pH
Dec [H]

Disturbance is Dec PaCO2

Compensation is Dec HCO3 by Dec reabsorption

332
Q

What is the primary disorder of metabolic alkalosis?

A

(1) more alkaline pH (2) increase in bicarbonate

333
Q

What is the compensation for metabolic alkalosis

A

Increase PCO2 via hypoventilation

334
Q

What causes metabolic alkalosis (3)?

A

A. GI loss of H+

B. Hypokalemia

C. Contraction alkalosis

335
Q

What is GI loss of H+?

A

In normal digestion, elevation of bicarbonate is transient because the pancrease then secretes bicarb to neutralize gastric acid in the small intestine

Excessive secretion of H+ into the lumen leads to excessive accumulation of bicarb in the
plasma

Alkalosis occurs as the result of vomiting

336
Q

Why does hypokalemia cause metabolic alkalosis?

A

K+ leaves the cell to restore [K+] to normal & so H+ enters the cell in exchange such that the ECF becomes alkaline

337
Q

What is contraction alkalosis?

A

both salt (NaCl) & water are lost but not HCO3-

Usually occurs more commonly with diuretics

Causes contraction of ECF & so the concentration of bicarb increase (same amount but now in a smaller volume)

Maintaining volume takes priority over maintaining pH & the kidney saves bicarbonate in
order to maintain volume

338
Q

Describe the acute phase for metabolic alkalosis response

A
  1. Carotid body senses alkalosis & signals a decrease in ventilatory rate
  2. Chemosensitive area of the brain (CSA) senses the increase in PCO2 & signals an
    increase in ventilatory rate

Net: small decrease in ventilation

339
Q

Describe the chronic phase response to metabolic alkalosis

A

over time, the pH of the CSF is rest & more hypoventilation occurs (signal from thecarotid is unopposed by signals from the CSA)

340
Q

What limits hypoventilation in metabolic alkalosis?

A

Hypoxic drive ultimately limits the magnitude of the hypoventilation

 Recall: PAO2 = PIO2 – PaCO2 x 1.2

 Once PaO2 falls below about 70-80 mmHg, hypoxic drive occurs & prevents further hypoventilation

341
Q

What is the primary disorder of metabolic acidosis?

A

(1) more acid pH (2) decrease in bicarb

342
Q

What is the compensation for metabolic acidosis?

A

decrease PCO2 (hyperventilation)

343
Q

What are the three causes of metabolic acidosis?

A

A. Inability to excrete dietary H+ usually due to renal disease

B. Increased H+ load (lactic acidosis or diabetic ketoacidosis)

C. Bicarbonate loss (diarrhea, renal disease)

344
Q

What is the plasma anion gap? Normal range?

A

Plasma anion gap (no relation to urinary anion gap) = [Na+] – ([Cl-] + [HCO3-])

 Normal range: 8 to 16 nM

345
Q

What is hyperchloremic acidosis?

A

metabolic Acidosis with NO CHANGE in anion gap (ex. Infusion of HCl)

346
Q

Describe the physiology of hyperchloremic acidosis

A

With buffering by the CO2-bicarbonate system, this results in a 1 for 1 replacement of bicarbonate (lost) with chloride (gained)

Physiological examples: in diarrhea or renal disease, where NaHCO3 is lost, the kidney saves NaCl to maintain extracellular fluid volume

347
Q

Describe metabolic acidosis with increase in ion gap

A

when bicarb is replaced by an “unmeasured” anion

 Ex. Lactic acidosis
 MUDPILES: Methanol, uremia, diabetic ketoacidosis, paraldehyde/propylene glycol,
infection/ischemia/isoniazid, lactate, ethelyene glycol/ethanol & salicylates/starvation

348
Q

What is MUDPILES?

A

Methanol, uremia, diabetic ketoacidosis, paraldehyde/propylene glycol,
infection/ischemia/isoniazid, lactate, ethelyene glycol/ethanol & salicylates/starvation

Leads to metabolic acidosis with increase in anion gap

349
Q

How does metabolic acidosis resolve?

A

increase in plasma bicarb without a corresponding increase in H+

 1. Administer NaHCO3  adds bicarb w/o an associated H+
 2. Physiologically, the kidney must restore normal bicarbonate levels (secretion of excess H+ in urine)

350
Q

What is the primary disorder of respiratory acidosis?

A

Primary disorder (1) more acid pH (2) increased PCO2/increased [HCO3]

Due to hypoventilation

351
Q

Describe compensation to respiratory acidosis

A

Primary event (retention of CO2) causes a (small) increase in plasma bicarbonate & the
compensation by the kidney also causes increased bicarb; however, the primary event is
accompanied by an increase in H+ caused by CO2 retention.

The compensation is not accompanied by an increase in H+ because the kidney secretes the H+ in the urine

352
Q

What are the causes of respiratory acidosis?

A

Ventilation not appropriate for the level of CO2 production; PCO2 rises to a higher steady-state level

A. Inapproproate control of ventilation
B. Obstructive lung disease
C. Chest wall &/or muscle disorders
D. Pulmonary fibrosis

353
Q

Describe the acute phase of respiratory acidosis

A 
Acute stage (10-30 min): change in pH & HCO3- follows the ECF buffer line on the CO2-bicarbonate
diagram
354
Q

Describe renal compensation to respiratory acidosis

A

Renal compensation: increase in PCO2 stimulates H+ secretion into the lumen & new bicarbonate that’s created as a result enters the plasma

355
Q

When is respiratory acidosis most commonly seen?

A

Most often seen in chronic obstructive lung disease (smokers) & pulmonary fibrosis

356
Q

What is the primary disorder of respiratory alkalosis?

A

(1) more alkaline pH (2) decreased PCO2/decreased [HCO3-]

Hyperventilation

357
Q

Describe compensation to respiratory alkalosis

A

over several days, the kidney decreases plasma bicarbonate further

 Primary event (reductive of CO2) causes a (small) decrease in plasma bicarbonate; compensation by the kidney also causes a (much larger) decrease in bicarbonate that moves pH back toward normal

primary disturbance is ↓PCO2 & compensation (renal) is ↓[HCO3-]

358
Q

What are the causes of respiratory alkalosis?

A
  1. Hypoxia (hypoxic drive)

2. Stimulation of respiratory center (pain, anxiety) 3. Mechanical overventilation

359
Q

Describe the acute phase of respiratory alkalosis

A

rise in pH & fall in HCO3- follow the ECF buffer line

360
Q

Describe renal compensation in respiratory alkalosis

A

fall in PCO2 causes the kidney to retain H+ & eliminate HCO3- in the urine (about 5 mM fall in bicarb for each 10 mmHg call in PCO2)

361
Q

How to tell what type of acid-base imbalance?

A

First, look at pH (alkalosis or acidosis?)
Then look at bicarbonate (metabolic or respiratory?)

Metabolic:
What’s the appropriate compensation?
Is the compensation occurring?

Respiratory:
Is the value on the ECF buffer line? If yes, it’s
acute. If no, it’s chronic (cellular buffering, bone
buffering & renal compensation)

362
Q

Describe the levels and compensation for metabolic alkalosis

A 
PaCO2 = 52 mmHg; HCO3- = 38 mM; pH = 7.49
pH = alkalosis; bicarbonate puts in quadrant for metabolic alkalosis (just example numbers)

Appropriate compensation is hypoventilation & yes, it’s happening, because PaCO2 is above normal

363
Q

Describe the levels and compensation for metabolic acidosis

A 
PaCO2 = 25 mmHg; HCO3 = 10 mM & pH = 7.22
pH = acidosis; bicarb = metabolic acidosis

Appropriate compensation is hyperventilation which is occurring because PaCO2 is below normal

364
Q

Describe the levels and compensation for respiratory alkalosis

A 
PaCO2 = 23 mmHg, HCO3 = 21.8 mM & pH= 7.6
pH = alkalosis; bicarb puts in quadrant for respiratory alkalosis

On the ECF line so acute respiratory alkalosis (no renal compensation yet)

ECF line recall is Bicarb ~ -11*pH

365
Q

Describe the levels and compensation for respiratory acidosis

A 
PaCO2 = 75 mmHg; HCO3 = 35 mM & pH = 7.29
pH = acidosis, bicarb in respiratory alkalosis quadrant

Not on the ECF line so chronic respiratory acidosis

Physiology 4 (4 decks)

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