Fs Exam 2 - Respiratory

Front 1

Two ways of looking at barometric/atmospheric pressure

Back 1

1. 1 square of air from earth to space weights 14.7 lbs
2. Air column will push mercury 760 mmHg in vacuum barometer

Front 2

Atmospheric pressure values

Back 2

760 mm Hg, 1 atm, 14.7 lb/in^2, 30 in Hg

Front 3

What alters atmospheric pressure

Back 3

Drops with elevation
Increases underwater – doubles for each 33 feet.

Hint 3

//fce-study.netdna-ssl.com/2/images/upload-flashcards/94/11/60/15941160_m.png

Front 4

Partial pressure of gas

Back 4

Partial pressure of gas = fractional concentration * total barometric pressure

Front 5

Ambient air fractional concentrations

Back 5

21% oxygen
79% nitrogen
0.04% CO2 –> Pco2 in air is approximately 0.

Front 6

Gas dissolved

Back 6

Solubility coefficient * partial pressure of gas
(Sc * Pgas)

Front 7

Arterial blood gas

Back 7

Obtain blood from artery, analyze dissolved gases.
Includes pH, PPO2, PPCO2, and O2 sat

Front 8

Ways to express amount of gas in solution

Back 8

1. Gas dissolved (concentration) – mL gas/dl blood
2. Partial pressure – arterial blood gas (ABG) expresses free gas in plasma and does not include Hb bound gas

Front 9

PO2 and PCO2 in arterial blood

Back 9

PO2 = 100 mmHg, PCO2 = 40 mmHg

Front 10

O2 Dissociation curve

Back 10

Expresses effect of PO2 on percent Hb saturation and oxygen concentration.

As increase PO2, dissolved O2 goes up slightly.

Hint 10

//fce-study.netdna-ssl.com/2/images/upload-flashcards/94/13/88/15941388_m.png

Front 11

Formula for Hb–bound O2

Back 11

(Hb concentration in g/dl * 1.4 Oxygen/g Hb) * O2 saturation


First term is maximum O2 concentration

Front 12

Formula for free O2 in blood

Back 12

gas dissolved = solubility constant * Pgas
0.003 mL O2/dl blood for every mmHg O2 * PaO2


0.003 mL O2/dl blood is solubility of free oxygen in blood

Front 13

Total Oxygen concentration

Back 13

Sum of Hb–bound O2 and free O2 in blood


(Hb concentration in g/dl * 1.4 Oxygen/g Hb) * O2 saturation
+
0.003 mL O2/dl blood for every mmHg O2 * PaO2


Note that PaO2 impacts both portions (O2 sat and PaO2)

Hint 13

//fce-study.netdna-ssl.com/2/images/upload-flashcards/94/14/03/15941403_m.png

Front 14

What does partial pressure of gas include?

Back 14

Includes both Hb–bound and free oxygen.
Can be used to determine % Hb saturation

Front 15

Dissolved and Hb–bound O2 at very high PaO2

Back 15

At very high PaO2, dissolved O2 rises more than Hb–bound O2 because Hb is already mostly saturated. Total O2 rises.

Hint 15

//fce-study.netdna-ssl.com/2/images/upload-flashcards/94/14/45/15941445_m.png

Front 16

Dissolved and Hb–bound O2 at very low PaO2

Back 16

At very low PO2, dissolved O2 slowly declines and Hb–bound O2 falls off rapidly

Hint 16

//fce-study.netdna-ssl.com/2/images/upload-flashcards/94/14/48/15941448_m.png

Front 17

PCO2 plasma arterial baseline level

Back 17

Brain controls PCO2 plasma at 40 mmHg

Front 18

Forms of CO2 in blood

Back 18

Free gas in plasma
Hemoglobin–bound
Bicarbonate–bound

Front 19

CO2 dissociation curve

Back 19

Linear relationship between PCO2 and concentration in plasma that is steeper than O2 dissociation curve.

Hint 19

//fce-study.netdna-ssl.com/2/images/upload-flashcards/94/14/81/15941481_m.png

Front 20

Why is CO2 dissociation curve steeper than O2 dissociation curve?

Back 20

1. CO2 is more soluble in plasma than O2
2. Bicarbonate is added CO2 reservoir
3. Hb has more CO2 binding sites than O2 binding sites.

Front 21

O2 delivery formula

Back 21

Arterial O2 concentration x Cardiac Output

Front 22

Mixed venous O2

Back 22

What is not consumed by tissues
"Mixed" refers to pulmonary artery because different tissues have different consumption.
Mixed venous O2 < arterial O2, because some used up

Front 23

Mixed venous CO2

Back 23

Measured as mixed venous partial pressure (PVCO2) or total mixed venous CO2 concentration
Mixed venous CO2 > arterial CO2

Front 24

Respiratory quotient

Back 24

Ratio of CO2 production to O2 consumption
VCO2 / VO2


Carbohydrate–rich diet – 1
Lipid–rich diet – 0.7
Normal value – 0.8

Hint 24

//fce-study.netdna-ssl.com/2/images/upload-flashcards/94/17/87/15941787_m.png

Front 25

Normal values for arterial and venous O2

Back 25

Arterial PaO2 = 100 mmHg
Total arterial O2 concentration = 20 mL O2/dl


Venous PvO2 = 40 mmHg
Total mixed venous O2 concentration = 15 mL O2/dl

Front 26

Normal values for arterial and venous CO2

Back 26

Arterial PCO2 = 40 mmHg
Total arterial CO2 concentration = 48 mL CO2/dl


Venous PvCO2 = 46 mmHg
Total mixed venous CO2 concentration = 52 mL CO2/dl

Front 27

AV concentration differences for O2 and CO2

Back 27

Difference between arterial and venous O2 concentration – 5 mL O2/dl
Difference between arterial and venous CO2 concentration – 4 mL CO2/dl


About the same for O2 and CO2

Front 28

AV Partial Pressure differences for O2 and CO2

Back 28

Difference between arterial and venous O2 partial pressure – 60 mmHg
Difference between arterial and venous CO2 partial pressure – 6 mmHg

Front 29

Why is there a big difference between AV partial pressure between O2 and CO2 but not a big difference for AV concentration differences?

Back 29

CO2 is more soluble than O2 and has dissociation curve has a steeper slope than O2 dissociation curve.


For O2, small concentration drop associated with very large partial pressure drop. For CO2, same concentration drop associated with smaller partial pressure drop.

Hint 29

//fce-study.netdna-ssl.com/2/images/upload-flashcards/94/18/14/15941814_m.png

Front 30

Anemia – Hb levels

Back 30

Normal – 15 g/dlAnemic – <13 g/dl

Front 31

How does anemia change total arterial oxygen concentration?

Back 31

Total arterial oxygen concentration = Hb–bound O2 + dissolved O2


Anemia lowers Hb–bound O2 by lowering concentration of Hb (Hb * 1.4 mL O2/g Hb * O2 sat). Thus lowers total arterial oxygen concentration

Front 32

PaO2 in anemia

Back 32

PaO2 is normal at 100 mmHg

Front 33

Total mixed venous O2 concentration in anemia

Back 33

Lowered total mixed venous O2 concentration

Front 34

Treatment for anemia

Back 34

Stop bleeding, transfuse blood if necessary

Front 35

How does anemia change saturation curve?

Back 35

Must change O2 concentration axis to reflex less Hb. % Hb saturation is unchanged.

Hint 35

//fce-study.netdna-ssl.com/2/images/upload-flashcards/94/18/35/15941835_m.png

Front 36

Carbon monoxide

Back 36

Odorless, colorless gas that binds Hb 240x more avidly than O2.
Displaces O2 from binding site and prevents O2 binding

Front 37

Effect of CO toxicity on total arterial O2 concentration formula

Back 37

Reduces mL O2/g Hb, which is normally 1.4. Thus lowers maximum Hb–bound O.

Front 38

O2 dissociation curve for carbon monoxide poisoning

Back 38

O2 dissociation curve does not work because PO2 correlation with percent saturation is dramatically changed.
O2 dissociation curve is shifted to the left.

Front 39

Total arterial O2 partial pressure in CO toxicity

Back 39

PaO2 = 100 mmHg – unchanged diffusion of O2 into blood

Front 40

Ways to measure O2 saturation (especially in CO poisoning)

Back 40

1. Use O2 dissociation curve – extrapolate from PO2. Altered in CO poisoning
2. Finger pulse oximeter – cheap but can't differentiate between O2 and CO
3. Multiwavelength spectrophotometer – only way to assess CO toxicity.

Front 41

Treatment of CO toxicity

Back 41

Treat with hyperbaric oxygen to outcompete carbon monoxide for Hb binding sites.
Hyperbaric oxygen reduces half life of Hb–CO from 4–5 hours to 20 minutes.

Front 42

How does hyperbaric oxygen affect dissolved oxygen?

Back 42

Increase FiO2 from 21% to 100%
Increase PB from 1 atm to 3 atm (760 * 3 = 2500 mmHg)


Thus increases arterial oxygen

Front 43

Ventilation

Back 43

Process of moving air in and out of chest ro provide O2 and remove CO2

Front 44

Dead space

Back 44

Area in lungs not exposed to capillary blood. Has ventilation but no perfusion.


Total dead space = anatomic dead space (trachea) + alveolar dead space (parenchyma in lung disease)

Front 45

Tidal volume

Back 45

Amount of air inspired at normal resting breath


VT = VD + VA
VT (L/breath) = Dead space component (no exchange) + alveolar component

Front 46

Minute ventilation

Back 46

Multiply tidal volume formula by respiratory rate (breaths/min)


Expiratory minute ventilation = dead space ventilation + alveolar ventilation
Measured in L/min

Hint 46

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/01/53/15960153_m.png

Front 47

Normal tidal volume, alveolar volume, minute ventilatoin, alveolar ventilation, and respiratory rate

Back 47

VT = 500 mL
VA = 100 mL
VE = 5L/min
VA = 4L/min
Respiratory rate = 10 breaths/min

Front 48

What gas pressure does brain maintain

Back 48

Brain mantains PCO2 at around 40 mmHg

Front 49

Measuring mean alveolar values

Back 49

PAO2/FAO2 and PACO2 and FACO2 are hard to measure. Can't average al alveoli because dead space alveolar–capillary units do not contribute

Front 50

What controls mean alveolar O2 and mean alveolar CO2?

Back 50

Amount of alveolar ventilation controls mean alveolar O2 and mean alveolar CO2.

Front 51

Alveolar ventilation equation

Back 51

VCO2 (Tissue CO2 production) = VA (alveolar ventilation) * FACO2 (fractional concentration of CO2)


Modified:
PaCO2 (arterial partial pressure of CO2) = (VCO2 (tissue CO2 production)/VA (alveolar ventilation)) * K


K accounts for change from FACO2 to VCO2
Also note that FACO2 (alveolar) changed to PaCO2 (arterial)

Hint 51

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/02/67/15960267_m.png

Front 52

Why can PaCO2 substitute for FACO2 in alveolar ventilation equation?

Back 52

Equal because:
1) CO2 dissociation curve is linear and steep so constant relationship between partial pressure and total CO2 concentratoin.
2) CO2 is very soluble – unlikely to be diffusion limited.

Front 53

Can PaO2 substitute for FAO2?

Back 53

No!

Front 54

What happens when change ventilation in alveolar ventilation equation?

Back 54

If VCO2 is constant at around 200 mL/min and brain regulates FACO2 at 40 mmHg, then:
If decreaes ventilation, PaCO2 goes up (hypercapnea)
If increase ventilation, PaCO2 go down.

Hint 54

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/02/79/15960279_m.png

Front 55

Hypercapnea

Back 55

High PaCO2
60–70 mmHg is moderately high and 100 mmHg is very high
Causes drowsiness, unconsciousness, respiratory arrest
Metabolic acidemia
Tolerated worse than hypoxia

Front 56

How does hypoventilation occur?

Back 56

1 Total minute ventilation is low (so alveolar ventilation is low). Due to depressed respiratory center in brainstem and narcotics or excessive work of breathing (asthma, COPD)
2. Low alveolar ventilation because of increased dead space ventilation with normal minute ventilation.

Hint 56

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/04/11/15960411_m.png

Front 57

Mixed expired CO2 (FECO2)

Back 57

Fractional concentration of CO2 in entire tidal volume breath. Greater amount of dead space => lower mixed expired CO2 concentration.

Front 58

Dead Space Fraction

Back 58

VD/VT = 150 mL/500 mL = 0.3, normally

Front 59

Bohr Equation of dead space fraction

Back 59

VD/VT = (FACO2–FECO2)/FACO2
More dead space = lowered FECO2
If no dead space, FACO2 = FECO2. Not possible.

Front 60

Bohr Equation expressed in pressure

Back 60

VD/VT = (FACO2–FECO2)/FACO2 = (PaCO2 – PECO2)/PaCO2


Equate alveolar CO2 to arterial CO2 and change fractional concentration to partial pressure

Hint 60

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/08/07/15960807_m.png

Front 61

Distribution of ventilation in lungs

Back 61

Most of ventilation goes to lower lobes of lung.

Hint 61

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/08/49/15960849_m.png

Front 62

Distribution of profusion in lungs

Back 62

Most of profusion goes to lower lungs because of gravity.

Hint 62

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/08/55/15960855_m.png

Front 63

Emphysema

Back 63

Destruction of normal matrix in lungs –> compliant lungs
Almost exclusively caused by smoking
Detected 95% by radiography. Large conglomerate air spaces with small amount of surrounding capillary flow (high ventilation, low profusion)

Front 64

Pulmonary fibrosis

Back 64

Excess deposition of matrix in lungs
Stiff, noncompliant lungs

Front 65

Fick's Law of Diffusion

Back 65

Vgas = A/t * D * (P1–P2)
D is proportional to solubility/sqrt(MW)

Front 66

Solubility of CO2, O2, and CO

Back 66

CO2 is 25 times more soluble than O2. CO is about as soluble as O2. Solubility is directly related to Vgas by D, diffusion constant

Hint 66

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/09/99/15960999_m.png

Front 67

Partial pressure of gas includes...

Back 67

Partial pressure of gas includes only plasma, not Hb–bound gas.

Front 68

Change in partial pressure of gases across capillary – figure

Back 68

Partial pressure of gases in capillary approach partial pressure of gas in alveolus. Diffusion occurs until partial pressures are equal.

Hint 68

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/10/20/15961020_m.png

Front 69

Change in partial pressure of nitrous oxide across capillary

Back 69

Initial concentration of 0 mmHg in capillary.
Inspire N2O into alveolar space. Diffuses across alveolar capillary membrane –> gas as plasma (PcN2O). No combination with Hb.
Because no H binding, PcN2O rises rapidly until equates with PAN2O – no further flow.
Perfusion–limited – only way to add more PCN2O is to move more air into alveolus.

Hint 69

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/10/23/15961023_m.png

Front 70

Change in partial pressure of carbon monoxide across capillary.

Back 70

Inspire CO into alveolar space. Diffuse across alveolar capillary membrane –> transiently xists as free gas –> almost all binds to Hb
PCCO never rises very much and never equates to PACO.
Transfer of CO is diffusion limited – because PCCO isn't close to PACO, can increase PCCO by Fick's law properties

Hint 70

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/10/89/15961089_m.png

Front 71

Change in partial pressure of oxygen across capillary

Back 71

Inspire O2 into alveolar space (PAO2). Begins at given mixed venous pressure of O2 and diffuses across alveolar capillary membrane –> exists both as free gas and Hb–bound.
Normal circumstances – PCO2 rises fairly rapidly until it reaches PAO2. Perfusion–limited because can only increase PAO2 by bringing more air in.
Disease conditions – PCO2 does not equate to PAO2 – governed by factors of diffusion so diffusion–limited.

Hint 71

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/11/43/15961143_m.png

Front 72

Diffusion–limited or perfusion–limited

Back 72

Diffusion–limited if end capillary value does not equate to alveolar pressure.
Perfusion–limited if end capillary value does equate to alveolar pressure.

Front 73

RBC travel time at rest and exercise

Back 73

At rest, PO2 in capillary reaches PAO2 after 1/3 of capillary.
In exercise, travel time reduced from 3/4 sec to 1/4 second. PCO2 no longer reaches PaO2 – diffusion–limited.

Front 74

What kind of limitation does thickening of lung lead to?

Back 74

PCO2 cannot reach PAO2 = diffusion–limitation. e.g. pulmonary fibrosis

Hint 74

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/11/79/15961179_m.png

Front 75

Alveolar hypoxia

Back 75

PAO2 drops from 100 mmmHg –> 50 mmHg
Normal curve is less steep because (P1–P2) is less
Takes longer to equate to PO2

Hint 75

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/11/97/15961197_m.png

Front 76

Diffusion limitation

Back 76

Altering diffusion constants and values can change whether reaches diffusion limitation.
Exercise reduces likelihood of hitting diffusion limitation.

Front 77

Diffusion capacity for carbon monoxide test

Back 77

Patient inhales small amount of CO, holds breath, then exhales.
Measures amount of CO that moved to capillary, calculated by measuring how much CO is exhaled.

Front 78

Why can't measure O2 for O2 diffusion capacity? Why is CO a good substitute?

Back 78

No CO in blood at baseline, so O2 is harder to measure.
If patient can't transfer CO appropriately, also cant transfer O2.

Front 79

Forster Equation for DL

Back 79

1/DL = 1/DM + 1/(theta – Vc)
Reciprocals because D is a conductance – can add resistance but not conductance in series.
1/DM reflects diffusion process itself.
1/(THETA*Vc) reflects time for O2 or CO2 to react with Hb.

Hint 79

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/12/36/15961236_m.png

Front 80

Values in Forster equation

Back 80

DL: Diffusion capacity of lungs
DM: True diffusing capacity of membrane separating alveolus from blood.
Theta – Affinity of Hb for CO
VC – Total mL of blood in capillaries exposed to arterial gas on one time.

Front 81

DL depends on three factors:

Back 81

1. Amount of surface area present for gas exchange
2. Amount of capillary blood exposed to alveolar gas
3. Amount of Hb present.

Front 82

What reduces diffusion capacity?

Back 82

DL is reduced by diseases which reduce functioning of alveolar capillary units.

Front 83

Exercise and DLCO

Back 83

Exercise increases diffusion capacity because vasodilation increases amount of capillary blood exposed to alveolar gas at a time.

Front 84

Effect of raising or lowering O2 tension on DLCO

Back 84

100% O2 reduces DLCO because O2 competes with CO for Hb binding sites.


Less CO taken up.

Hint 84

//fce-study.netdna-ssl.com/2/images/upload-flashcards/96/12/60/15961260_m.png

Front 85

Causes of hypoxemia and impaired CO2 gas exchange

Back 85

Hypoventilatoin, diffusion limitation, shunt, ventilation–perfusion inequality

Front 86

What determines steady state concentrations of mean alveolar values (PAO2/FAO2 or PACO2 or FACO2)?

Back 86

Alveolar ventilation

Front 87

Equation for partial pressure of gas

Back 87

Pxgas = Fxgas * PB, PB = 760 mmHg

Front 88

PACO2 formula

Back 88

PaCO2 = VCO2/VA * K = PACO2

Front 89

Air, alveolar, and arterial PO2

Back 89

Ambient air PO2 = 160 mmHg
Alveolar PAO2 = 100 mmHg
Arterial PaO2 = 100 mmHg

Front 90

Hypoventilation

Back 90

Low alveolar ventilation given PACO2.
Rate of 60 breaths/minute may be normal for PACO2 of 40.

Front 91

Alveolar ventilation equation (PaCO2)

Back 91

PaCO2 = VCO2/VA * K
To keep PaCO2 around 40, need around 4L of VA based on amount of CO2 produced.

Hint 91

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/84/20/16038420_m.png

Front 92

VCO2 – Alveolar gas equation

Back 92

VCO2 = VA * FACO2
VCO2 = VA * PACO2/K


Assume FICO2 = 0

Front 93

VO2 – Alveolar gas equation

Back 93

VO2 = VA * (FIO2 – FAO2)
VO2 = VA * (PIO2 – PAO2)/K


Need two fractional concentratoins because present in both air and blood (as oppose to CO2, which is only present in blood)

Front 94

Alveolar gas equation

Back 94

PAO2 = PIO2 – PACO2/R

Hint 94

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/85/04/16038504_m.png

Front 95

PIO2 formula

Back 95

PIO2 = FIO2 (PB–PH2O), usually around 150 mmHg
PB = 760 mmHg, PH2O = 47 mmHg

Hint 95

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/84/95/16038495_m.png

Front 96

FIO2

Back 96

21% oxygen in ambient air. More if supplemental

Front 97

PB

Back 97

Barometric pressure. Varies with altitude, 760 mmHg at sea level.

Front 98

PiO2 in trachea

Back 98

FiO2 (PB – PH2O)
0.21 (760–47) = 150

Front 99

R value

Back 99

Ratio of CO2 production to O2 consumption
Usually from 0.8 to 1.0

Hint 99

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/85/25/16038525_m.png

Front 100

Alveolar ventilation at sea level

Back 100

PaO2 = 100 mmHg when PaCO2 = 40 mmHg

Hint 100

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/85/46/16038546_m.png

Front 101

Why is room level PO2 at 160 mmHg while PaO2 is 100 mmHg?

Back 101

1. Consuming O2 at tissue level
2. Mixed venous blood coming into alveolar capillary unit is at 40 mmHg.

Front 102

PAO2 when put on supplemental oxygen

Back 102

FiO2 = 100%
PAO2 = 1.0 (760–47) – 40/0.8 = 650 mmHg


No change in alveolar ventilation (40/0.8), changing concentration of inspired gas

Hint 102

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/86/03/16038603_m.png

Front 103

PAO2 when hypoventilating (PaCO2 of 80)

Back 103

FiO2 = 21%, PaCO2 = 80 mmHg
PAO2 = 0.21 (760–47) – 80/.8 = 50 mmHg

Front 104

Hypoxemia vs hypoxia

Back 104

Hypoxemia – Low arterial (blood) partial pressure of O2. Less than 70 mm Hg
Hypoxia – Low air or tissue O2

Front 105

Overcoming hypercapnea and hypoxemia

Back 105

Hypercapnea – Requires mechanical ventilation until underlying disease is addressed.Hypoxemia – usually overcome by giving supplemental oxygen – increase PIO2

Front 106

Diffusion limitation and PO2

Back 106

Normal conditions – PO2 quickly equates to alveolar value
Mildly abnormal conditions – equates less quickly
Grossly abnormal conditions – may not equate with alveolar value = diffusion abnormality


Exercise shortens time to 0.25s from 0.75 s – adds diffusion limitation in mildly abnormal conditions

Hint 106

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/90/29/16039029_m.png

Front 107

CO2 diffusion along capillary length

Back 107

CO2 is very soluble. By 1/3 of capillary, equates to PACO2
Rarely diffusion limited (diffusion limitation occurs when end capillary and alveolar pressures do not equate).

Hint 107

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/90/62/16039062_m.png

Front 108

What determines PCO2/PO2 of individual alveolar units?

Back 108

1. Composition of inspired gas (FIO2)
2. Composition of mixed venous blood (PVO2)
3. Ventilation–perfusion ratio
4. Slopes and positions of O2/CO2 dissociation curves

Front 109

Dead–space

Back 109

High V/Q ratio – high perfusion, low perfusion

Hint 109

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/94/31/16039431_m.png

Front 110

Shunt

Back 110

Low V/Q ratio – low ventilation, high perfusion

Hint 110

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/94/34/16039434_m.png

Front 111

Low V/Q ratio is caused by:

Back 111

Alveoli filled with infection, water, protein, collagen
Alveolar collapse
Mucus plugging or edema at small airways


In presence of maintained capillary blood flow

Front 112

High V/Q ratio is caused by:

Back 112

Capillary obstruction from vascular disease or blood clots


In presence of maintained ventilation to alveolus
(or increased ventilation with normal perfusion)

Front 113

What does end capillary blood resemble in low and high V/Q?

Back 113

Low V/Q – resembled mixed venous blood
High V/Q – resembles inspired air
V/Q of 1 – normal arterial values (100, 40)

Front 114

Normal O2 and CO2 values in arteries

Back 114

PaO2 = 100 mmHg, 20 mL O2/dl
PvO2 = 40 mmHg, 15 mL O2/dl


PaCO2 = 40 mmHg, 48 mL O2/dl
PvCO2 = 46 mmHg, 52 mL CO2/dl

Front 115

Normal O2 and CO2 in inspired air

Back 115

PIO2 = 150 mmHg
PICO2 = 0 mmHg

Front 116

V/Q Ratio Equation

Back 116

Used to calculate individual alveolar capillary unit values with differing VQ ratios

Hint 116

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/95/81/16039581_m.png

Front 117

Graph for V/Q ratio equation

Back 117

PO2 ranges from 40–150 mmHg with 100 mmHg at V/Q of 1
PCO2 ranges from 46–0 mmHg with 40 mmHg at V/Q of 1
O2 concentration runs with PO2 but plateaus when Hb is fully saturated.

Hint 117

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/96/95/16039695_m.png

Front 118

Main concern of high V/Q ratio

Back 118

Blood readily exchanges gas but small amount of blood so little contribution to blood gas. Concern is that it increases dead space ventilation, lowering alveolar ventilation.


VE = VA + VD

Hint 118

//fce-study.netdna-ssl.com/2/images/upload-flashcards/03/98/63/16039863_m.png

Front 119

Describing V/Q ratio with PO2/PCO2 curve

Back 119

Increasing V/Q ratio – PO2 increases and PCO2 decreases.
Decreasing V/Q ratio – PO2 decreases and PCO2 increases.

Front 120

PE in left lung – initial changes in VE, VD, VA

Back 120

No change in VE (5 L/min)
VA – 2L/min in right lung, 0 L/min in left lung
VD – 0.5L/min in left lung, 2.5 L/min in left lung


VA drops to half (4 –> 2), so PCO2 rises 2x by equation PaCO2 = VCO2/VA * K

Hint 120

//fce-study.netdna-ssl.com/2/images/upload-flashcards/04/00/58/16040058_m.png

Front 121

In PE, what happens to blood going to affected lung?

Back 121

Redirected to other lung

Front 122

PE in left lung – compensation

Back 122

Increase total minute ventilation to maintain alveolar ventilation
Increase Ve to 9 L/min
VA = 4L/min in right lung, 0 L/min in left lung
VD = 0.5 L/min in right lung, 4.5 L/min in left lung


Maintained VA so PACO2 does not drop.

Hint 122

//fce-study.netdna-ssl.com/2/images/upload-flashcards/04/02/32/16040232_m.png

Front 123

Mild increases in minute ventilation to overcome dead space ventilation

Back 123

Not a problem – keep VA normal to keep PaCO2 normal and then keep PaO2 normal.

Hint 123

//fce-study.netdna-ssl.com/2/images/upload-flashcards/04/02/50/16040250_m.png

Front 124

Severe increases in minute ventilation to overcome dead space ventilation

Back 124

May be ok
Or may not be able to – inability to maintain VE –> respiratory muscle failure
VE falls, followed by decrease in VA because increase in VD.
Decrease in VA causes hypercapnea and hypoxemia.

Front 125

How can hypoventilation occur?

Back 125

1) Low total VE – narcotic overdose, excessive work of breathing (COPD, asthma)
2) Low VA because of increased dead space (high minute ventilation)

Front 126

What does end capillary blood look like for low V/Q ratio?

Back 126

Mixed venous blood

Front 127

Causes of low V/Q

Back 127

Alveoli villed with infection, pus, water, protein, collagen
Mucus plugging or edema of small airways
With maintained capillary blood

Front 128

Normal concentration of O2 in mixed venous and arterial blood

Back 128

Comes in at 15 mL O2/dl, exits at 20 ml O2/dl

Hint 128

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/84/17/16068417_m.png

Front 129

Low V/Q ratio in right upper lobe – effect on right lung

Back 129

Right – Mixed venous blood comes in at 15 mL O2/dl, exits at 16 mL O2/dl

Hint 129

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/84/68/16068468_m.png

Front 130

Low V/Q ratio in right upper lobe – effect on left lung

Back 130

Breathe faster to create high V/Q in left lung (increased ventilation)
Mixed venous blood comes in at 15, leaves at 20.5
PO2 is higher but small change in oxygen concentration because of flattening of O2 dissociation curve

Hint 130

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/84/77/16068477_m.png

Front 131

Left atrium O2 concentration when low V/Q of right upper lung (with left lung compensation)

Back 131

Left atrium O2 concentration is low (18 mL )2/dl blood). PaO2 = 50 mmHg.


Cannot maintain PaO2.

Front 132

Treatment of hypoxemia in low V/Q

Back 132

Supplemental O2 – nasal prongs or mask
Increases FiO2 from 0.21 to 0.5 or 1.0 so PiO2 increases (PiO2 = Pb*FiO2)
Increases PaO2 mainly of affected lung because hemoglobin already saturated in normal lung.
V/Q and PO2 curve shifts left so at given V/Q ratio, PO2 increases.

Hint 132

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/85/67/16068567_m.png

Front 133

Normal mixed venous and arterial CO2 concentrations

Back 133

Mixed venous blood comes in at 52 mg/dl, exits at 48.

Hint 133

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/86/03/16068603_m.png

Front 134

Pneumonia in right upper lobe, effect on right lobe mixed venous and arterial CO2

Back 134

Right lung – mixed venous comes in at 52 mg, exits at 51 mg/dl

Hint 134

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/86/57/16068657_m.png

Front 135

Pneumonia in right upper lobe, compensation effect on left lobe mixed venous and arterial CO2

Back 135

Hyperventilation increases V/Q in left lung.
Mixed venous comes in at 52 mg, exits at 45 mg/dl.
Because linear relationship between partial pressure and concentration for CO2, lowering pressure does lower concentration

Hint 135

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/86/75/16068675_m.png

Front 136

Pneumonia in right upper lobe, effect on concentration of CO2 and PCO2 in left atrium

Back 136

Normal 48 mL CO2/dl blood
PaCO2 = 40 mmHg

Front 137

Low V/Q with compensation – effect on arterial O2 and CO2 levels

Back 137

Systemic arterial hypoxemia but normocapnea

Front 138

Treatment of low V/Q pneumonia in right upper lobe

Back 138

Ventilation and antibiotics

Front 139

Shunt

Back 139

Extremely low V/Q of 0
End capillary gas concentrations = mixed venous concentrations.
Cannot overcome O2 changes with supplemental O2 – does not reach lobe. Ventilation can't offset global hypoxemia but can offset CO2 – same as low V/Q.

Front 140

A–a gradient

Back 140

Used to assess patient's oxygenation.
A–a = PAO2 – PaO2


Remember: PAO2 = PIO2 – PACO2/R
In healthy lungs, no A–a gradient

Hint 140

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/88/88/16068888_m.png

Front 141

Elevated A–a gradient

Back 141

Not caused by hypoventilation – mean alveolar O2 (PAO2) causes reduction in PaO2.
Occurs with:
Diffusion abnormality – PaO2 does not reach PAO2
Or mostly low V/Q or shunt mismatch – low ventilation reduces PaO2 compared to PAO2 (where there is a PAO2) because PAO2 depends on PIo2 which is normal.

Front 142

V/Q ratio changes as descend lung

Back 142

Top of lung has higher V/Q ratio than bottom of lungs
As descend, ventilation increases at slower rate than does blood flow (gravity). So, V/Q goes down as you go down lung.

Hint 142

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/90/29/16069029_m.png

Front 143

Muscle movements of inspiration

Back 143

Contract diaphragm and expand chest wall

Front 144

Mechanical movements of expiration

Back 144

Normally passive, can forcefully exhale

Front 145

Diaphragm innervation

Back 145

Phrenic nerve (C3–5) – injury impairs breathing

Front 146

Tidal volume

Back 146

Volume of one inspiration/expiration

Hint 146

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/92/33/16069233_m.png

Front 147

Total lung capacity

Back 147

Volume of active breath in and out

Hint 147

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/92/30/16069230_m.png

Front 148

Residual volume

Back 148

Residual volume left after complete exhalation

Hint 148

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/92/21/16069221_m.png

Front 149

Functional residual capacity

Back 149

Volume remaining at end of normal tidal volume exhalation.

Hint 149

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/92/18/16069218_m.png

Front 150

Lung recoil pressure

Back 150

Inwards (towards lower volume)
Because of intrinsic properties – elastin, fibronectin, collagen and surface tension

Front 151

Chest wall recoil pressure

Back 151

Outwards (higher volume) except at very high volumes

Front 152

Pleural space and fluid

Back 152

Pleural space = potential space between visceral and parietal pleura
Small amount of pleural fluid in this space (radiographically undetectable) mechanically couples lungs and chest wall.
Pleural fluid transmits force of diaphragm and inspiratory muscle to lungs

Front 153

Subatmospheric intrapleural pressure

Back 153

<760 mmHg because inward lung recoil and outward chest wall recoil.
Verify by puncturing chest wall – air follows pressure gradient into chest

Hint 153

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/92/69/16069269_m.png

Front 154

Pneumothorax

Back 154

Uncouples lung and chest wall
Lung recoils to smaller volume and chest wall to larger volume
Can occur due to puncturing of either lung or chest wall.

Hint 154

//fce-study.netdna-ssl.com/2/images/upload-flashcards/06/93/08/16069308_m.png

Front 155

Figure of Lung capacity vs airway pressure

Back 155

Middle line – relaxation pressure of 0.
Lung is on right – wants to recoil inwards (so manometer reads positive airway pressure). Increase in volume increases inwards recoil force.


Chest wall is on left – wants to recoil outwards (so manometer reads negative airway pressure) – except at high pressures, at which wants to recoil inwards.

Hint 155

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/09/67/16070967_m.png

Front 156

Figure of lung capacity vs airway pressure – summation of chest wall and lung and FRC

Back 156

Summation line crosses airway pressure of 0 at functional residual capacity (FRC) – this is the volume at which lung inward recoil force equals chest outward recoil force.

Hint 156

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/10/30/16071030_m.png

Front 157

Intrapleural pressure during breath

Back 157

Inspiration – intrapleural pressure becomes more subatmospheric
Expiration – passively returns to resting subatmospheric pressure

Hint 157

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/10/69/16071069_m.png

Front 158

Emphysema and gas exchange

Back 158

Emphysema destroys ECM. Leads to high V/Q ratio.

Front 159

Fibrosis and gas exchange

Back 159

Fibrosis has excess ECM deposition. Some areas of low V/Q and others of high V/Q

Front 160

Pressure–volume curve of lung

Back 160

Inspiration – intrapleural pressure becomes more negative and volume increases.
Curve is steep at first – small change in pressure needed for large change in volume (high compliance)
Curve eventually flattens – more pressure needed to change volume (less compliant)

Hint 160

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/10/93/16071093_m.png

Front 161

Compliance

Back 161

Measures distensibility
dV/dP

Front 162

Elastance

Back 162

1/Compliance
Measures ability to return to original position

Front 163

Compliance in fibrosis and emphysema

Back 163

Emphysema – high compliance – small pressure to generate same volume
Fibrosis – low compliance – larger pressure to generate same volume

Hint 163

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/11/29/16071129_m.png

Front 164

Model of elastic recoil

Back 164

Elastic recoil causes lung to recoil to lower volume and tethers small airways open (preventing collapse) when springs are stretched during inspiration

Hint 164

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/11/53/16071153_m.png

Front 165

Alteration of recoil during emphysema

Back 165

Emphysema – decreased elastic recoil (overly compliant) – reduced tethering of small airways = increased tendency for airway collapse

Front 166

Alteration of recoil during fibrosis

Back 166

Fibrosis – larger inward recoil of lung (low compliance) and increased tethering of airways, preventing small airway collapse. But requires more energy to distend lungs.

Front 167

Surface tension

Back 167

Partly responsible for compliance.
Forces acting along 1 cm line on surface of liquid at gas–liquid interface
Cohesion between water is stronger than adhesion to air
Acts on small amount of liquid lining alveolus to make liquid surface area and alveolus volume as small as possible

Front 168

Surfactant

Back 168

Phospholipid secreted by type 2 alveolar cells into alveolar space linings
Lowers surface tension of fluid lining alveolus

Front 169

Surface tension and compliance – saline experiment

Back 169

If fully fill lung with saline, surface tension forces are obliterated. Leads to steeper PV curve (greater compliance), similar to emphysema..


Demonstrates that surface tension reduces compliance.

Hint 169

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/12/46/16071246_m.png

Front 170

Infant respiratory distress syndrome (RDS)

Back 170

Developmental deficiency in surfactant
More surface tension = lower compliance. PV curve similar to fibrosis.
Treat with exogenous surfactant replacement

Hint 170

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/12/58/16071258_m.png

Front 171

Law of Laplace and alveoli

Back 171

Law of Laplace – P = 4T/r
As alveolus gets smaller, greater recoil pressure (P) inwards. Thus, small alveoli have greater tendency to collapse

Hint 171

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/12/88/16071288_m.png

Front 172

Surfactant and small alveoli

Back 172

Surfactant has lower surface tension at lower surface area.
Stabilizes small alveoli from Law of Laplace effects, preventing collapse.

Hint 172

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/13/06/16071306_m.png

Front 173

Hysteresis in saline and air–filled lungs

Back 173

Time lag in 2 associated events.
Air filled lung surface tension –> hysteriesis
Saline –> no surface tension forces –> no hysteresis


Surface tension forces are responsible for hysteresis.

Hint 173

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/14/05/16071405_m.png

Front 174

Why is ventilation higher in lower lobes than upper?

Back 174

Upper portion has more recoil forces inward than bottom because of gravity.


Upper lobe alveoli are higher on PV curve = larger volume at rest but less change in volume with inspiration because less compliant.
Basal alveoli are lower on PV curve – lower resting volume but more compliant, so greater change in V with inspiration.

Hint 174

//fce-study.netdna-ssl.com/2/images/upload-flashcards/07/14/53/16071453_m.png

Front 175

What does pressure differnce over tube depend on?

Back 175

Rate and pattern of flow

Front 176

Ohms Law

Back 176

Resistance = P1–P2/Flow

Front 177

Pulmonary Vascular Resistance equation (Ohm's Law)

Back 177

(MPAP–Left Atrial (Wedge) Pressure)/CO

Front 178

Pouiseuille's Law

Back 178

R=8nl/PIr^4


Resistance is proportional to length and viscosity and inversely proportional to radius^4

Front 179

Turbulent flow

Back 179

Nonlinear pressure–flow relationship
Pressure is proportional to (flow rate)^2
Generally, higher airway resistance because larger drop in pressure
Increase in gas density increases resistance

Hint 179

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/43/73/16094373_m.png

Front 180

Heliox

Back 180

Gas mixture of helium and oxygen. Helium is less dense than oxgen so lowers resistance

Front 181

Airway resistance varies with lung volume

Back 181

Airway resistance decreases with increase in lung volume (because of increase in radius)

Hint 181

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/43/97/16094397_m.png

Front 182

Chief site of airway resistance

Back 182

Large airways (larynx and trachea) because have lowest overall cross–sectional area.
40,000 small areas and 1 trachea/larynx.

Hint 182

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/44/21/16094421_m.png

Front 183

Reynold's number

Back 183

Determines whether flow is laminar or turbulent.
Re = 2rvd/n
Velocity, density, radius are positively correlated and viscosity is negatively correlated with turbulent flow.
Reynolds > 2000 indicates turbulent flow.

Front 184

Gas density and Reynold's number

Back 184

Gas density increases with atmospheric pressure and molecular weight (i.e. Nitrogen vs Helium)
Increases Reynold's number –> turbulent flow

Front 185

Intraalveolar and intrapleural pressure at FRC

Back 185

No flow.
Atmospheric intraalveolar pressure
Subatmospheric intrapleural pressure

Front 186

Intraalveolar and intrapleural pressure during inspiration

Back 186

Slightly subatmospheric intraalveolar pressure
Further subatmospheric intrapleural pressure

Front 187

End–inspiration intraalveolar and intrapleural pressure

Back 187

Atmospheric intraalveolar pressure
Minimal subatmospheric intrapleural pressure

Front 188

Intraalveolar and intrapleural pressure during normal passive expiration

Back 188

Slightly atmospheric intraavlveolar pressure
Subatmospheric intrapleural pressure returns to rest subatmospheric pressure

Front 189

Intraalveolar and intrapleural pressure during forced expiration

Back 189

Intraalveolar pressure rises substantially above atmospheric
Intrapleural pressure also rises substantially above atmospheric
Both rise to same degree, depending on degree of muscular effort

Front 190

Airway collapse during forced expiration

Back 190

Airway pressure drops from alveolus to mouth. At some point, airway pressure drops below pleural pressure and airway collapse.
Pressure behind collapse causes airway to open. Pressure drop causes it to close again. Called a starling resistor.

Front 191

Determining factor for airway collapse during forced expiration

Back 191

Difference between alveolar and pleural pressure
Depends on elastance of lung

Front 192

Effect of emphysema and fibrosis on likelihood of airway collapse during forced expiration

Back 192

Emphysema – decreased elasticity/inward recoil. Less subatmospheric intrapleural pressure –> lesser difference between pressure –> greater tendency to collapse


Fibrosis – increased elasticity/inward recoil. Greater subatmospheric intrapleural pressure –> greater difference between pressures –> lesser tendency to collapse

Front 193

FEV1

Back 193

Amount of volume can exhale in 1 second

Front 194

FEV1/VC

Back 194

FEV1/VC is usually 75%. Limited by airway collapse.

Front 195

FEV1/VC in emphysema

Back 195

FEV1/VC is around 40% in emphysema – more likely to collapse so exhale less before collapse occurs.

Front 196

FEV1/VC in fibrosis

Back 196

FEV1/VC is around 90% in fibrosis – less likely to collapse so exhale more before collapse occurs.

Front 197

Is flow generally effort–dependent or independent in forced expiration?

Back 197

Generally effort–independent because effort doesn't change difference between pleural and alveolar pressure.

Front 198

Is flow effort–dependent at beginning of forced expiration?

Back 198

No – greater effort results in more flow at beginning of forced expiration.
Because at high volumes, airways are so distended that they will not collapse even if tendency to collapse.

Hint 198

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/48/14/16094814_m.png

Front 199

Importance of hypercapnea

Back 199

Indicates critical illness – represents failure to regulate PCO2.

Front 200

Is hypoxemia critical?

Back 200

Hypoxemia is abnormal but not as reflective as emergency.Hypoxemia does not trigger response until it reaches 50 mmHg.

Front 201

Pulmonary circulation pressures

Back 201

Pulmonary circulation is low pressure
Pulmonary artery has pressure of 25/10 instead of 120/80. MPAP is 15.
Increased MAP of 30–50 under pulmonary hypertension.

Front 202

Measuring pulmonary artery pressures

Back 202

Use pulmonary artery catheter
Insert in any vein, access vena cavae, thread into right atrium and then pulmonary artery and wedge into small arteriole.
Balloon catheter – inflated and carried by cardiac output

Hint 202

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/50/90/16095090_m.png

Front 203

Compliance of pulmonary vasculature

Back 203

Highly compliant with little smooth muscle – little work required

Front 204

Pulmonray Vascular Resistance equation

Back 204

Pulmonary Vascular Resistance = (MPAP – Left Atrium Pressure)/Cardiac Output
Expressed in Wood units. Normal value is < 3

Front 205

PVR response to increase in vascular pressure or flow

Back 205

Falls because of intrinsic changes in response to increase in pressure/flow – (a) Recruitment (opening of closed capillaries) and (b) Distension of open capillaries
Counterintuitive – by PVR = Pressure/CO, PVR should rise when pressure rises

Hint 205

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/51/11/16095111_m.png

Front 206

Alveolar and extraalveolar vessels and associated forces

Back 206

Capillaries are alveolar vessels – exposed to alveolar forces
Arterioles are extraalveolar vessels – exposed to recoil forces

Hint 206

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/51/26/16095126_m.png

Front 207

Effect of lung volume on PVR

Back 207

Low volumes – extraalveolar vessels are small – high PVR
High volumes (TLC) – capillaries are stretched – increased PVR


Lowest point is at middle volume (FRC)

Hint 207

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/51/44/16095144_m.png

Front 208

Starling resistor effect

Back 208

Water can flow through 2 pathways
A – if chamber pressure exceeds downstream pressure, flow is independent of downstream pressure
B – if downstream pressure exceeds flow pressure, flow depends on upstream to downstream difference

Hint 208

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/51/71/16095171_m.png

Front 209

West Zone 1

Back 209

Top of lung
PA > Pa > Pv
No flow because alveolar pressure is too high

Hint 209

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/52/55/16095255_m.png

Front 210

West Zone 2

Back 210

Middle of lung
Waterfall or starling effect
Pa > PA > Pv
PA is close to Pa – vessel collapses, increaseing Pa, reopening vessel which then collapses again.

Hint 210

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/52/52/16095252_m.png

Front 211

West Zone 3

Back 211

Bottom of lung
Pa > Pv > Pa
Alveolar pressure is irrelevant. Flow determined by afferent–to–efferent pressure drop

Hint 211

//fce-study.netdna-ssl.com/2/images/upload-flashcards/09/52/46/16095246_m.png

Front 212

Central controllers of ventilation

Back 212

Brainstem (automatic, involuntary)
Cerebral cortex (voluntary

Front 213

Central controllers locations

Back 213

Medulla – intrinsic, automatic rhythm of ventilation
Lower and upper pons

Front 214

What are three things chemoreceptors change?

Back 214

PaCO2 – depressed by age, sleep, narcotics
pH – goes along with PaCO2
PaO2 – doesn't change ventilation until below 50 mmHg

Front 215

Central chemoreceptors location

Back 215

Ventral surface of medulla
Surrounded by ECF and CSF

Front 216

What do central chemoreceptors sense?

Back 216

Responds to [H+] – increase stimulates ventilation, decrease inhibits ventilation


Rise in [H+] occurs when CO2 is high and diffuses into brain, converted by carbonicc anhydrase

Front 217

Peripheral chemoreceptors

Back 217

Located at carotid body bifurcation and aortic arch
Respond to all three but less important than central:


1. Decrease in PaO2 – completely responsibly for hypoxia response
2. Decrease in pH
3. Increase in pCO2