Brs Respiratory Physiology Set

Front 1

Describe Tidal Volume

Back 1

It is the volume of inspired or expired with each normal breath

Front 2

tidal volume

Back 2

volume inspired or expired with each normal breath

Front 3

What is the tidal volume?

Back 3

The volume inspired or expired during normal breathing

Front 4

What structures make up the conducting zone?

Back 4

The nose, nasopharynx, larynx, trachea, bronchi, bronchioles, and terminal bronchioles.

Front 5

Volume inspired and expired with each breath

Back 5

Tidal volume

Front 6

definition of tidal volume

Back 6

volume inspired with each normal breath

Front 7

Describe Inspiratory Reserve Volume

Back 7

-It is the volume that can be inspired over and above the tidal volume
-It is used during exercise

Front 8

inspiratory reserve volume

Back 8

volume inspired over and above TV ex. during exercise

Front 9

What is the inspiratory reserve volume?

Back 9

The volume that can be inspired beyond the tidal volume

Front 10

What is the function of the conducting zone?

Back 10

To warm, humidify, and filter the air before it reaches the critical gas exchange region.

Front 11

The volume that can be inspired over and above the tidal volume

Back 11

Inspiratory Reserve Volume

Front 12

definition of IRV

Back 12

volume that can be inspired over and above the tidal volume (with exercise)

Front 13

Describe Expiratory Reserve Volume

Back 13

It is the volume that can be expired after the expiration of a tidal volume

Front 14

expiratory reserve volume

Back 14

volume that can be expired after expiration of a tidal volume

Front 15

What is the expiratory reserve volume?

Back 15

The volume that can be expired after expiration of the tidal volume

Front 16

How many divisions of the trachea/bronchi/bronchiole system are there?

Back 16

There are 23 such divisions.

Front 17

What lung capacity is used during exercise

Back 17

IRV

Front 18

definition of ERV

Back 18

volume that can be expired after expiration of tidal volume

Front 19

Describe Residual Volume

Back 19

-It is the volume that remains in the lungs after a maximal expiration
-It cannot be measured by spirometry

Front 20

residual volume

Back 20

volume that remains in lungs after a maximal expiration
- cannot be measured by spirometry

Front 21

What is the residual volume?

Back 21

The volume that remains in the lungs after a maximal expiration

Front 22

What effects does sympathetic innervation have on the conducting airway?

Back 22

The walls of the conducting airways contains smooth muscle.
Sympathetic adrenergic neurons
activate β2 receptors on bronchial smooth muscle,
which leads to relaxation and dilation of the airways.

(and circulating epinephrine released from the adrenal medulla)

Front 23

Volume the remains in the lungs after maximal expiration

Back 23

Residual volume

Front 24

definition of residual volume

Back 24

volume that remains in the lungs after a maximal expiration... Cannot be measured by spirometry

Front 25

Describe Anatomic Dead Space

Back 25

-The volume of the conducting airways
-Approximately 150ml

Front 26

anatomic dead space

Back 26

volume of conducting pathways
approx. 150 ml

Front 27

Can residual volume be measured by spirometry?

Back 27

No

Front 28

What effects does parasympathetic innervation have on the conducting airway?

Back 28

Parasympathetic cholinergic neurons activate muscarinic receptors, which leads to contraction and constriction of the airways.

Front 29

What are the two dead spaces of the lungs?

Back 29

Anatomic and Physiologic

Front 30

definition of anatomic dead space

Back 30

volume of the conducting airways

Front 31

Describe Physiologic Dead Space

Back 31

-A functional measurement
-It is defined as the volume of the lungs that does not participate in gas exchange
-It is approximately equal to the anatomic dead space in normal lungs
-It may be greater than the anatomic dead space in lung diseases in which there are ventilation/perfusion (V/Q) defects

Front 32

physiological dead space

Back 32

- volume of lungs that does NOT participate in gas exchange

Front 33

What is anatomic dead space?

Back 33

The volume of the conducting airways,
Approximately 150 ml (or about 1 ml/lb of body weight)

Front 34

What type of drugs are used to treat asthma?

Back 34

β2-adrenergic agonists
(e.g. epinephrine, isoproterenol, albuterol),
which are used to dilate the airways.

Front 35

Volume of conducting airways

Back 35

Anatomic dead space

Front 36

what is the "normal" anatomic dead space

Back 36

approx. 150 ml

Front 37

What is the equation to define physiologic dead space?

Back 37

V_D=V_T* (P_ACO2-P_ECO2)/(P_ACO2)

V_D=Physiologic Dead Space
V_T= Tidal Volume
P_ACO2=P_CO2 of alveolar gas = P_CO2 of arterial blood
P_ECO2=P_CO2 of expired air

Front 38

calculation of physiological dead space (Vd)

Back 38

Vd = TV x (PaCO2 - PeCO2) / PaCO2

Front 39

What is physiologic dead space?

Back 39

It is the total dead space (the volume of the lungs that doesn't participate in gas exchange)
In normal lungs, physiologic dead space is approximately equal to anatomic dead space, but when there are V/Q defects, it is greater than anatomic dead space

Front 40

What structures make up the respiratory zone?

Back 40

Respiratory bronchioles, alveolar ducts, and the alveolar sacs.

Front 41

Defined as the volume of the lungs that does not participate in gas exchange

Back 41

Physiologic dead space

Front 42

definition of physiologic dead space

Back 42

volume of the lungs that does not participate in gas exchange

Front 43

Describe Minute Ventilation

Back 43

Minute Ventilation = TV*RR

Front 44

minute ventilation

Back 44

TV x breaths/min

Front 45

Formula for physiologic dead space

Back 45

Vd = Vt x [(PCO2 - PexpiredCO2) / PCO2]
Vt = tidal volume
Note that PCO2 is arterial/alveolar

Front 46

What are transitional structures?

Back 46

Respiratory bronchioles are transitional structures. Like the conducting airways, they have cilia and smooth muscle, but they are also considered part of the gas exchange region because alveoli occasionally bud off their walls.

Front 47

Is a the functional measurement of dead space

Back 47

Physiologic

Front 48

what is the equation for physiologic dead space?

Back 48

Vd = Vt * (PaCO2 - PeCO2)/PaCO2

Front 49

Describe Alveolar Ventilation

Back 49

Alveolar Ventilation = (TV-Dead Space)*RR

Front 50

alveolar ventilation

Back 50

alveolar ventilation = (TV - Vd) x breaths/min

Front 51

Formula for minute ventilation

Back 51

Minute ventilation = tidal volume x (breaths/min)

Front 52

How many alveoli does each lung contain?

Back 52

Approximately 300 million alveoli.

Front 53

PHYSIOLOGIC DEAD SPACE

May be greater than the anatomic in:

Back 53

Lung diseases with V/Q defects

Front 54

what is the equation for alveolar ventilation?

Back 54

alveolar ventilation = (Vt - Dead space) * breaths/min

Front 55

Describe Inspiratory Capacity

Back 55

The sum of Tidal Volume and IRV

Front 56

inspiratory capacity

Back 56

IRC = IRV + TV

Front 57

Formula for alveolar ventilation

Back 57

Alveolar ventilation = (tidal volume - dead space) x (breaths/min)

Front 58

What is the role of type II pneumocytes?

Back 58

Type II pneumocytes synthesize surfactant and have regenerative capacity for the type I and type II pneumocytes.

Front 59

How do you calculate the physiologic dead space? ie Formula

Back 59

Vd= Vt X (PaC02 - PeC02)/ PaC02
PaC02 = alveolar gas = PC02 of arterial
PeC02 = PC02 of expired air

Front 60

definition of functional residual capacity

Back 60

sum of ERV and RV;
volume remaining in lungs after Vt is expired

Front 61

Describe Functional Residual Capacity

Back 61

-The sum of ERV and Residual Volume
-The volume in the lungs after a tidal volume is expired
-Includes the residual volume so it cannot be measured by spirometer

Front 62

functional residual capacity

Back 62

FRC = ERV + RV

volume remaining after a tidal volume is expired --> cannot be measured

Front 63

What is the inspiratory capacity?

Back 63

Tidal volume + IRV

Front 64

Which structures of the conducting zone contain cartilage?

Back 64

Only the trachea and bronchi contain cartilage.

Front 65

Tidal volume X Breaths/min

Back 65

Minute ventilation

Front 66

what is the normal FEV1?

Back 66

80% of the FVC

Front 67

Describe Vital Capacity/Forced Vital Capacity

Back 67

-The sum of Tidal Volume, IRV, and ERV
-The volume of air that can be forcibly expired after a maximal inspiration

Front 68

vital capacity or forced vital capacity

Back 68

FVC = TV + IRV + ERV

Front 69

What is the functional residual capacity?

Back 69

ERV + RV
The volume remaining in the lungs after a tidal volume is expired

Front 70

Where is pulmonary blood flow the highest? The lowest? Why?

Back 70

Pulmonary blood flow is highest at the base of the lungs. It is lowest at the apex (top) of the lungs. This is due to gravitational effects.

Front 71

(Tidal volume - Dead space) X Breaths/min

Back 71

Alveolar ventilation

Front 72

What happens to FEV1 in obstructive lung diseases?

Back 72

FEV1 reduced more than FVC, so FEV1/FVC is decreased

Front 73

Describe Total Lung Capacity

Back 73

-The sum of all four lung volumes
-The volume in the lungs after a maximal inspiration
-Includes residual volume, so it cannot be measured by spirometry

Front 74

total lung capacity

Back 74

TLC = IRV + TV + ERV + RV

- cannot be measured by spirometry

Front 75

Can FRC be measured by spirometry?

Back 75

No, because it includes the residual volume

Front 76

What is tidal volume (Vt)?

Back 76

Normal, quiet breathing. It is approximately 500 mL and includes the volume of air that fills the alveoli plus the volume of air that fills the airways.

Front 77

The sum of tidal volume and IRV

Back 77

Inspiratory capacity

Front 78

What happens to FEV1/FVC in restrictive lung disease?

Back 78

e.g. fibrosis, both FEV1 and FVC are reduced and FEV1/FVC is normal or increased

Front 79

Describe Forced Expiratory Volume (FEV1)

Back 79

-FEV1 is the volume of air that can be expired in the first second of a forced maximal expiration
-Normally 80% of forced viral capacity

Front 80

forced expiratory volume (FEV1)

Back 80

volume of air that can be expired in the first second of forced maximal expiration

Front 81

What is the vital capacity?

Back 81

Also known as the forced vital capacity (FVC)
TV + IRV + ERV
This is the volume of air that can be forcibly expired after a maximal inspiration (total lung capacity except for the RV)

Front 82

What is inspiratory reserve volume?

Back 82

The additional volume that can be inspired above tidal volume. It is approximately 3000 mL.

Front 83

Sum of ERV and residual volume

Back 83

Functional Residual volume

Front 84

what is the most important muscle for inspiration?

Back 84

diaphragm

Front 85

Describe how FEV1 is affected by obstructive lung disease

Back 85

In obstructive lung disease, such as asthma, FEV1 is reduced more than FVC so that FEV1/FVC is decreased

Front 86

normal value of FEV1/FVC

Back 86

0.80

Front 87

What is the total lung capacity?

Back 87

The sum of all lung volumes; the volume in the lungs after a maximal inspiration

Front 88

What is expiratory reserve volume?

Back 88

The additional volume that can be expired below tidal volume, approximately 1200 mL.

Front 89

Volume remaining in the lungs after a tidal volume expiration

Back 89

FRC

Front 90

what is hysteresis

Back 90

the difference in the P-V curves of inspiration and expiration

Front 91

Describe how FEV1 is affected by restrictive lung disease

Back 91

In restrictive lung disease, such as fibrosis, both FEV1 and FVC are reduced and FEV1/FVC is either normal or is increased

Front 92

obstructive lung disease, such as (1), the FEV1/FVC ratio is (2)

Back 92

1 = asthma
2 = reduced

Front 93

Can TLC be measured by spirometry?

Back 93

No, because it includes RV

Front 94

What is the volume of gas that remains in the lungs after a maximal forced expiration?

Back 94

Residual volume, which is approximately 1200 mL. This cannot be measured by spirometry.

Front 95

Sum of tidal volume, IRV, and ERV

Back 95

Forced vital capacity

Front 96

what happens to the FRC in a patient with emphysema and why?

Back 96

FRC increases due to increased compliance of the lung.
The lung reduces its tendency to collapse
and "traps" the air that failed to be expired from a normal cycle.

Front 97

What are the muscles of inspiration?

Back 97

-Diaphragm
-External intercostals
-Accessory muscles

Front 98

restrictive lung disease, such as (1), the FEV1/FVC ratio is either (2) or (3)

Back 98

1 = fibrosis
2 = increased
3 = unchanged

Front 99

Can VC be measured by spirometry?

Back 99

Yes

Front 100

What is the inspiratory capacity (IC)?

Back 100

The inspiratory capacity is composed of the tidal volume plus the inspiratory reserve volume.
Approximately 3500 mL (500 + 3000)

Front 101

The volume of air that can be forcibly expired after a maximal expiration

Back 101

FVC

Front 102

What happens to the FRC in a patient with fibrosis?

Back 102

lung compliance is decreased,
and tendency of the lung to collapse is increased,
so FRC decreases

Front 103

Describe the Diaphragm

Back 103

-The most important muscle for inspiration
-When the diaphragm contracts, the abdominal contents are pushed downward and the ribs are lifted upward and outward, increasing the volume of the thoracic cavity

Front 104

what is the most important muscle for inspiration?

Back 104

diaphragm

Front 105

What is the forced expiratory volume?

Back 105

Abbreviated as FEV1
This is the volume of air that can be expired in the first second of a forced maximal expiration

Front 106

What is the functionary residual capacity (FRC)?

Back 106

FRC is the volume remaining in the lungs after a normal tidal volume is expired and can be thought of as the equilibrium volume of the lungs. It is composed of the expiratory reserve volume plus the residual volume.
Approximately 2400 mL (1200 + 1200)

Front 107

The volume in the lungs after maximal inspiration

Back 107

TLC

Front 108

what is the effect of surfactant on alveoli?

Back 108

it reduces the surface tension, and, therefore the opening pressure of the alveoli (Laplace's law). This results in a decreased tendency of alveoli to collapse

Front 109

Describe the external intercostals and accessory muscles

Back 109

-Not used for inspiration during normal quiet breathing
-Used during exercise and in respiratory distress

Front 110

which muscles are used for inspiration during exercise/respiratory distress?

Back 110

external intercostals
accessory abdominal muscles

Front 111

What is the normal value for FEV1/FVC?

Back 111

0.8 (80%)

Front 112

What is the vital capacity?

Back 112

Vital capacity is the volume that can be expired after maximal inspiration.
It is composed of the inspiratory capacity
plus the expiratory reserve volume.

Approximately 4700 mL (3500 + 1200)

Front 113

Sum of all four lung volumes

Back 113

TLC

Front 114

where is surfactant produced?

Back 114

type II alveolar cells

Front 115

What are the muscles of expiration?

Back 115

-Abdominal muscles
-Internal intercostal muscles

Front 116

muscles in quiet expiration?

Back 116

none --> passive recoil of lung tissue

Front 117

What happens to FEV1/FVC in obstructive lung disease?

Back 117

It decreases

Front 118

What is the volume of total lung capacity?

Back 118

Total lung capacity (TLC) includes all of the lung volumes (Vital capacity + residual volume).
It is approximately 5900 mL (4700 + 1200)

Front 119

Lung capacities that can't be measured

Back 119

FRC and TLC

B/C it includes residual volume, so cannot be measured by spirometry

Front 120

what is the primary composition of surfactant?

Back 120

dipalmitoyl phosphatidylcholine (DPPC)

Front 121

Describe the muscles of expiration

Back 121

-Expiration is normally passive
-Because the lung-chest wall system is elastic, it returns to its resting position after inspiration
-Expiratory muscles are used during exercise or when airway resistance is increased because of disease (e.g., asthma)

Front 122

expiratory muscles used during exercise or when airway resistance is increased?

Back 122

internal intercostals
abdominal muscles

Front 123

What happens to FEV1/FVC in restrictive lung disease?

Back 123

FEV1 and FVC are REDUCED

FEV1/FVC
Normal or increased

Front 124

What is the anatomic dead space? What is its volume?

Back 124

The anatomic dead space is the volume of the conducting airways, including the nose (and/or mouth), trachea, bronchi, and bronchioles. The volume is approximately 150 mL.

Front 125

The volume of air that can be expired in the first second of forced maximal expiration

Back 125

FEV1

Front 126

what is the earliest time surfactant is produced in the fetus?

Back 126

24 weeks

Front 127

Describe the role of abdominal muscles in expiration

Back 127

Compress the abdominal cavity, push the diaphragm up, and push air out of the lungs

Front 128

compliance of lungs

Back 128

describes distensibility of lungs and chest wall
- inversely related to elastance AND stiffness
- slope of pressure-volume curve

C = V/P

Front 129

Is asthma an example of obstructive or restrictive lung disease?

Back 129

Obstructive

Front 130

What is the definition of physiologic dead space?

Back 130

Physiologic dead space is the total volume of the lungs that does not participate in gas exchange.

Front 131

FEV1 is normally ______% of forced vital capacity

Back 131

80% of FVC

Front 132

how does one tell if a fetus is producing mature levels of surfactant?

Back 132

lecithin:sphingomyelin ratio > 2:1 in amniotic fluid

Front 133

Describe the role of internal intercostal muscles in expiration

Back 133

They pull the ribs downward and inward

Front 134

transmural pressure = (1) pressure - (2) pressure

Back 134

1 = alveolar pressure
2 = intrapleural pressure

Front 135

Is fibrosis an example of obstructive or restrictive lung disease?

Back 135

Restrictive

Front 136

What is a reason the physiologic dead space can become larger than the anatomic dead space?

Back 136

In normal persons, the physiologic dead space is nearly equal to the anatomic dead space. When the physiologic dead space is larger than the anatomic dead space, there may be a ventilation/perfusion defect.

Front 137

In obstructive lung diseases, what happens to the FEV1 and FVC

Back 137

FEV1 is reduced more than FVC so

FEV1/FVC is DECDREASED

Front 138

according to Poiseuille's law, what is the relationship between resistance of an airway and the radius?

Back 138

R is inversely proportional to the r^4

Front 139

Describe compliance

Back 139

-Describe the distensibility of the lungs and chest
-Is inversely related to elastance, which depends on the amount of elastic tissue
-Inversely related to stiffness
-The slow of the PV curve
-The change in volume for a given change in pressure. Pressure refers to the transmural or transpulmonary pressure (the pressure difference across pulmonary structures)

Front 140

when intrapleural pressure is negative, the lungs (1) and volume (2)

when intrapleural pressure is positive, the lungs (3) and volume (4)

Back 140

1 = expand
2 = volume increases
3 = collapse
4 = volume decreases

Front 141

What are the muscles that participate in inspiration?

Back 141

Diaphragm
External intercostals and accessory muscles -- only used during exercise and respiratory distress

Front 142

What is the equation to calculate the volume of physiologic dead space?

Back 142

Vd = Vt*(Paco2 - Peco2)/Paco2

Volume of the physiologic dead space is the tidal volume multiplied by a fraction that represents the dilution of alveolar Pco2 by dead space air.

Front 143

In restrictive lung disease, what happens to FEV1 and FVC?

Back 143

FEV1 and FVC are reduced so

FEV1/FVC are normal or increased

Front 144

where is the major site of airway resistance?

Back 144

medium-sized bronchi

Front 145

What equation describes compliance?

Back 145

C=V/P

C=Compliance
V=Volume
P=Pressure

Front 146

hysteresis

Back 146

difference between inspiration and expiration lung pressure-volume curves

Front 147

What is the role of the diaphragm in inspiration?

Back 147

The most important inspiratory muscle
When the diaphragm contracts, the abdominal contents move downward and the ribs move upward and outward
This increases the volume of the thoracic cavity

Front 148

What is the difference between minute ventilation and alveolar ventilation rates?

Back 148

Minute ventilation is the total rate of air movement into and out of the lungs. Alveolar ventilation rate is the same, but it corrects for the physiologic dead space.

Minute ventilation = Vt x Breaths/min

Alveolar ventilation Va = (Vt-Vd) x Breaths/min

Vt = tidal volume (mL)
Vd = physiologic dead space (mL)

Front 149

Name a common form of obstructive lung disease?

Back 149

Asthma, can't get air out

Front 150

What class (and example) of drug causes dilation of airways?

Back 150

Beta-2 agonists (e.g. isoproterenol)

Front 151

Describe the compliance of the lungs

Back 151

-Transmural pressure is alveolar pressure minus intrapleural pressure
-When the pressure outside of the lungs (ie intrapleural pressure) is negative, the lungs expand and lung volume increases
-When the pressure outside of the lungs is positive, the lungs collapse and lung volume decreases
-Inflation of the lungs (inspiration) follows a different curve than deflation of the lungs (expiration) (called hysteresis)
-In the middle range of pressures, compliance is greatest and the lungs are most distensible
-At high expanding pressures, complaince is lowest and the lungs are lead distensible ad the curve flattens

Front 152

when is lung compliance the highest?

Back 152

middle range of pressure on curve

Front 153

Is normal quiet expiration active or passive?

Back 153

Passive
Results from the elastic recoil of the inspiratory muscles

Front 154

What is forced vital capacity (FVC)?

Back 154

Forced vital capacity is the total volume of air that can be forcibly expired after a maximal inspiration

Front 155

Name a common form of restrictive lung disease?

Back 155

Fibrosis, can't get air in

Front 156

at what point in the breathing cycle is alveolar pressure equal to 0?

Back 156

at FRC, just before inspiration.

Front 157

Describe the compliance of the lung-chest wall system

Back 157

Less than that of the lungs alone or the chest wall alone

Front 158

compliance of the lung-chest wall system is (1) than that of lungs or chest (2)

Back 158

1 = less
2 = alone

Front 159

What are the expiratory muscles?

Back 159

Abdominal muscles -- compress the abdominal cavity and push the diaphragm upward
Internal intercostals -- pull the ribs down
Note that these muscles only participate during exercise or when airway resistance is increased due to lung disease

Front 160

What is FEV1?

Back 160

FEV1 is the volume of air that can be forcibly expired in the first second.

Front 161

In restrictive lung diseases name what happens to each: increase or decrease:
TLC
Residual Volume
FEV1
FVC
FEV1/FVC
Pa02
A-a gradient

Back 161

TLC= decreased
Residual volume = decreased
FEV1= decreased
FEV1/FVC = Normal to increased
Pa02 = Decreased
A-a gradient = Increased

Front 162

how does one measure intrapleural pressure?

Back 162

with a balloon catheter in the esophagus

Front 163

Describe the complaince of the lung-chest wall system at rest

Back 163

-Lung volume is at FRC and the pressure in the airway and lungs is equal to atmispheric pressure
-Under these equilibrium conditions, there is a collapsing force on the lungs and an expanding force on the chest wallAt FRC, these two forces are equal and opposite and therefore the combined lung-chest wall system neither wants to collapse nor expand

Front 164

pneumothorax

Back 164

lungs collapse
chest wall springs forward
(natural tendencies)

Front 165

What is respiratory compliance?

Back 165

Describes the distensibility of the lungs and chest wall
It is inversely related to elasticity (that is, as elasticity increases, compliance decreases)
Inversely related to stiffness
Compliance is the change in volume or a given change in pressure. The higher the compliance, the greater the change in volume for that pressure value

Front 166

What is the value of FEV1/FVC in a normal person?

Back 166

FEV1/FVC = ~0.8, meaning that 80% of the vital capacity can be forcibly expired in the first second.

Front 167

In obstructive lung diseases name what happens to each: increase or decrease
TLC
Residual Volume
FEV1
FVC
FEV1/FVC
Pa02
A-a gradient

Back 167

TLC= increased
Residual volume = increased
FEV1= decreased
FEV1/FVC = decreased
Pa02 = Decreased
A-a gradient = Increased

Front 168

why do patients with COPD expire through pursed lips?

Back 168

during forced expiration a positive intrapleural pressure is created that collapses the airways. Pursing the lips creates enough back-pressure to maintain airway patency

Front 169

Describe the intrapleural pressure at rest

Back 169

Negative due to the lungs collapsing in and the chest expanding out

Front 170

emphysema
- lung compliance is (1) and tendency of lungs to collapse is (2); tendency of lungs to collapse is (3) than tendency of chest wall to expand resulting in (4)

Back 170

1 = increased
2 = decreased
3 = less
4 = barrel-shaped chest

Front 171

Formula for respiratory compliance

Back 171

C = V/P
V = volume
P = transmural pressure

Front 172

What is the FEV1/FVC in a patient with asthma?

Back 172

In obstructive lung diseases like asthma, both FVC and FEV1 are decreased, but FEV1 is decreased more. Thus, FEV1/FVC is decreased.

Front 173

An increase in A-a gradient means

Back 173

Hypoxemia of pulmonary origin

Front 174

What are general characteristics of COPD?

Back 174

obstructive disease with increased lung compliance. FEV1 is markedly decreased, FVC is decreased, FEV1/FVC is decreased and FRC is increased

Front 175

Describe a pneumothorax

Back 175

-Air is introduced into the intrapleural space
-The intrapleural pressure becomes equal to atmospheric pressure
-The lungs will collapse (their natural tendency) and the chest wall will spring outward (its natural tendency)

Front 176

in fibrosis, lung compliance is (1) and tendency of lungs to collapse is (2); the tendency of lungs to collapse is (3) than tendency of chest wall to expand

Back 176

1 = decreased 3
2 = increased
3 = greater

Front 177

What is the transmural pressure?

Back 177

Alveolar pressure - intrapleural pressure

Front 178

What is the FEV1/FVC in a patient with fibrosis?

Back 178

In patients with restrictive lung diseases such as fibrosis, both FVC and FEV1 are decreased, but they decrease the same or FEV1 is decreased less than FVC. Thus, in fibrosis FEV1/FVC is the same or increased.

Front 179

Hypoxemia due to extrapulmonary causes has a _____ A-a gradient

Back 179

Normal

Front 180

What are characteristics of a "pink puffer"

Back 180

primarily emphysema, have mild hypoxemia, normocapnia.

Front 181

Describe the changes in lung compliance due to emphysema

Back 181

-Lung compliance is increased then the tendency of the lungs to collapse is decreased
-At the original FRC, the tendency of the lungs to collapse is less than the tendency of the chest wall to expand
-The lung-chest wall system will seek a new higher FRC so that the two opposing forces can be balances
-The patient's chest becomes barrel-shaped, reflecting this higher volume

Front 182

collapsing pressure (surface tension)

Back 182

P = 2 T / r

T = surface tension
r = radius

Front 183

What is intrapleural pressure?

Back 183

The pressure outside of the lungs, inside the thoracic cavity

Front 184

What is the most important muscle for inspiration?
What muscles are used for inspiration during exercise?

Back 184

The diaphragm.
During exercise, the external intercostal muscles and accessory muscles (scalene muscles and sternomastoids)

Front 185

Laplace's law states that larger alveoli are

Back 185

Less likely to collapse b/c collapsing pressure is directly proportional to surface tension and inversely proportional to size

Front 186

what are characteristics of 'blue bloaters?'

Back 186

primarily bronchitis, have severe hypoxemia with cyanosis, do not maintain alveolar ventilation --> hypercapnia; right ventricular failure and systemic edema. must have productive cough for >3 consecutive months in >= 2 years

Front 187

Describe the changes in lung compliance due to fibrosis

Back 187

-Lung complaince is decreased and the tendency of the lungs to collapse is increased
-At the original FRC the tendency of the lungs to collapse is greater than the tendency of the chest wall to expand
-The lung-chest wall system will seek a new, lower FRC so that the two opposing forces can be balanced

Front 188

in absent of surfactant, small alveoli have a tendency to (1) known as (2)

Back 188

1 = collapse
2 = atelectasis

Front 189

How does intrapleural pressure determine lung inflation and deflation?

Back 189

When the IPP is negative, the lungs expand, causing lung volume to increase
When the IPP is positive, the lungs collapse and lung volume decreases

Front 190

What muscles are used for expiration? During exercise?

Back 190

Expiration is normally a passive process.

During exercise (or disorders like asthma), the muscles of expiration include abdominal muscles, internal intercostal muscles, and internal and external obliques.

Front 191

Small alveoli are more likely to collapse b/c

Back 191

of increased pressure and tendency to collapse

Front 192

what are characteristics of pulmonary fibrosis?

Back 192

restrictive disease with decreased lung compliance. inspiration is impaired; decrease in ALL lung volumes, FEV1/FVC is increased

Front 193

what is the equation to correct for water vapor and PO2 in humidified tracheal air?

Back 193

P(total) = (760mmHg - 47mmHg) * 0.21 = 150 mmHg P(O2)

Front 194

Describe the surface tension of the alveoli

Back 194

-Results from the attractive forces between liquid molecules lining the alveoli
-Creates a collapsing pressure that is directly proportional to surface tension and inversely proportional to alveolar radius

Front 195

surfactant
- roles (2)
- synthesized where? (1)
- made of (3)?

Back 195

2 = decreases surface tension, increases compliance
1 = type II alveolar cells
3 = DPPC dipalmitoyl phosphatidylcholine

Front 196

What is hysteresis?

Back 196

When the volume-pressure relationship of the lungs is different for inspiration and expiration

Front 197

What happens during a pneumothorax?

Back 197

Normally, intrapleural pressure is -5 cm H2O. When a sharp object punctures the intrapleural space, air is introduced into the space, and intrapleural pressure suddenly becomes equal to atmospheric pressure.
- There is no longer a negative intrapleural pressure to hold the lungs open, and the lungs collapse.
- There is no longer a negative intrapleural pressure to keep the chest wall from expanding, and the chest wall springs out.

Front 198

Surfactant is synthesized in

Back 198

Type II pneumocytes

Front 199

what is the normal P(O2) in normal humidified tracheal air?

Back 199

150 mmHg

Front 200

Describe the surface tension of large alveoli vs small alveoli

Back 200

Large alveoli (large radius) have a low collapsing pressure and are easy to keep open

Small alveoli have high collapsing pressures and are more difficult to keep open

In the absence of surfactant, the small alveoli have a tendency to collapse

Front 201

Ratio of what reflects mature lungs?

Back 201

lecithin/sphingomyelin ratio of 2:1 in amniotic fluid

Front 202

At what pressures is compliance the greatest?

Back 202

Middle range of pressures
High compliance = greatest distensibility
At high pressures, compliance is low and the lungs are only slightly distensible

Front 203

What occurs when the volume is FRC?

Back 203

At FRC, because they are elastic structures, the lungs "want" to collapse and the chest wall "wants" to expand. At FRC, the collapsing force on the lungs is exactly equal to the expanding force on the chest wall. Thus, the combined system neither has a tendency to collapse nor to expand.

Front 204

Surfactant consist of

Back 204

DPPC, dipalmitoyl phosphatidycholine

Front 205

what limits gas exchange in pulmonary capillaries normally?

Back 205

perfusion --> partial pressures of gases equilibrate early in the capillary

Front 206

What is atelectasis?

Back 206

-Lack of gas exchange within alveoli, due to alveolar collapse or fluid consolidation
-In the absence of surfactant, the small alveoli have a tendency to collapse

Front 207

neonatal respiratory distress syndrome

Back 207

due to lack of surfactant
lungs collapse, difficulty reinflating and hypoxia

Front 208

How does the compliance of the chest-wall system compare to the compliance of the lungs or chest wall along?

Back 208

It is greater

Front 209

What occurs when the volume is less than FRC?

Back 209

When the volume in the system is less than FRC (i.e., the subject makes a forced expiration), there is less volume in the lungs and collapsing (elastic) force of the lungs is smaller. The expanding force on the chest wall is greater, however, and the combined system "wants" to expand.

Front 210

How do you know if a neonates lungs are mature?

Back 210

Lecithin:sphingomyelin ratio > 2:1

Front 211

what limits gas exchange in the pulmonary capillaries under strenuous exercise?

Back 211

diffusion --> perfusion is increased to a point that maximum gas exchange is achieved limited by the rate at which the gases can cross the alveolar membranes

Front 212

Describe surfactant

Back 212

-Lines the alveoli
-Reduces surface tension
-Syntehsized by type II alveolar cells and consists primarily of phospholipid dipalmitoyl phosphatidylcholine (DPPC)

Front 213

formula for airflow

Back 213

Q = P / R

Front 214

Describe the state of pressure and lung volume at rest

Back 214

Lung volume is at FRC
Pressure in the airways and lungs is equal to atmospheric pressure (0 mmHg)
There is a collapsing force on the lungs and an expanding force on the chest wall
These forces are equal and opposite, so the chest-wall system does not collapse or expand
These two opposing forces generate negative intrapleural pressure

Front 215

What occurs when the volume is greater than FRC?

Back 215

When the volume in the system is greater than FRC (i.e., the subject inspires from the spirometer), there is more volume in the lungs and collapsing (elastic) force of the lungs is greater. The expanding force of the chest wall is smaller, and the combined system "wants" to collapse.

Front 216

The major site of airway resistance in the lungs is

Back 216

the medium-sized bronchi

Front 217

what limits gas exchange in fibrosis?

Back 217

thickness of membrane increases

Front 218

Describe how surfactant reduces surfact tension

Back 218

-Disrupts the intermolecular forces between liquid molecules
-This reduction in surface tension prevents small alveoli from collapsing and increases compliance

Front 219

poiseuilles law for resistance

Back 219

R = 8 n l / (pi) r^4

Front 220

What happens during pneumothorax?

Back 220

Air is introduced into the intrapleural space
This causes the intrapleural pressure to equal atmospheric pressure
The lungs follow their natural tendency to collapse
The chest wall follows its natural tendency to expand

Front 221

What happens to compliance in patients with emphysema?

Back 221

Emphysema is associated with loss of elastic fibers in the lungs. As a result, the compliance of the lungs increases. As a result, at a given volume, the collapsing (elastic recoil) force on the lungs is decreased.

Front 222

Why don't the smallest airways offer the highest resistance based on Poiseuille's law?

Back 222

The smallest airways are connected in parallel

Front 223

what limits gas exchange in emphysema?

Back 223

surface area is decreased

Front 224

Describe surfactant synthesis in the fetus

Back 224

-Variable
-Surfactant may be present as early as gestational week 24 and is almost always present by gestational week 35
-Lecithin:sphingomyelin ratio greater than 2:1 in amniotic fluid reflects mature levels of surfactant

Front 225

where is the major site of airway resistance?

Back 225

medium bronchi

Front 226

What happens to lung compliance in a patient with emphysema?

Back 226

Lung compliance increases because the alveoli are eaten away
The tendency of the lungs to collapse is decreased
A new, higher FRC is established because air can't escape
The chest becomes barrel-shaped

Front 227

Why do patients with emphysema have a barrel-shaped chest?

Back 227

Because of the decreased tendency to collapse, the combined lung and chest-wall system seeks a new higher FRC, where the two opposing forces (expansion and collapse) can be balanced. A patient with emphysema breathes at higher lung volumes, and will have a barrel-shaped chest.

Front 228

How do the lungs change airway resistance?

Back 228

contraction or relaxation of bronchial smooth muscle

Front 229

what molecule causes off-loading of O2 from Hb in tissues?

Back 229

2,3-diphosphoglycerate

Front 230

Describe neonatal respiratory distress syndrome

Back 230

-Can occur in premature infants because of lack of surfactant
-Infant exhibits atelectasis (lungs collapse), difficulty reinflating the lungs (as a result of decreased compliance), and hypoxemia (as a result of decreased V/Q)

Front 231

What causes constriction of airways? (3)

Back 231

1 = PNS
2 = irritants
3 = slow reacting substance of anaphylaxis (asthma)

Front 232

What happens to lung compliance in a patient with fibrosis?

Back 232

Lung compliance decreases
The tendency of the lungs to collapse is increased
A new, lower FRC is established because the tendency of the lungs to collapse exceeds the tendency of the chest wall to expand

Front 233

What happens to compliance in patients with fibrosis?

Back 233

Fibrosis is associated with stiffening of lung tissues and decreased compliance. The lung and chest-wall system will seek a new lower FRC.

Front 234

What constricts the airways, decrease the resistance, and increase the resistance to flow?

Back 234

Parasympathetic stimulation
Irritants
Slow-reacting substance of anaphylaxis ASTHMA

Front 235

what is the composition of fetal Hb and how are its properties different from adult Hb?

Back 235

composition: 2 alpha and 2 gamma chains; this causes a left-shift in the saturation curve resulting in increased affinity for O2 due to decreased affinity to 2,3-DPG

Front 236

What causes dilation of airways? (2)

Back 236

1 = SNS stimulation
2 = SNS agonists i.e. isoproterenol that act on B2 AR

Front 237

What causes surface tension in the alveoli?

Back 237

Attractive forces between liquid molecules lining the alveoli
This creates a collapsing pressure that is directly proportional to surface tension and inversely proportional to alveolar radius

Front 238

What does the law of Laplace state?

Back 238

The law of Laplace states that the pressure tending to collapse an alveolus is directly proportional to the surface tension generated by the molecules of liquid lining the alveolus and inversely proportional to alveolar radius.

Front 239

What increases the radius, and decreases the resistance to airflow?

Back 239

Sympathetic stimulation
Sympathetic agonist

Front 240

what is the equation for O2 content of blood?

Back 240

O2 content = (O2-binding capacity * % saturation) + dissolved O2

Front 241

asthma is an (1) disease, with (2) FVC and (3) FEV1 and (4) FEV1/FVC ratio; functional residual capacity is (5)

Back 241

1 = obstructive disease
2 = decreased
3 = decreased
4 = decreased
5 = increased

Front 242

Laplace's Law

Back 242

P = 2T/r
P = collapsing pressure (pressure required to keep alveolus open)
T = surface tension
R - radius of alveolus

Front 243

What is the formula for collapsing pressure (Law of Laplace)?

Back 243

P = 2T/r

P = Collapsing pressure on alveolus (dynes/cm^2)
or Pressure required to keep alveolus open
T = Surface tension (dynes/cm)
r = Radius of the alveolus (cm)

Front 244

MOA for sympathetic dilation of airways

Back 244

B2 receptor activation

Front 245

which binding site of Hb has the highest affinity for O2? Why is this important?

Back 245

the fourth binding site --> it allows maximal loading of O2 in the lungs and unloading in the tissues

Front 246

COPD is an (1) disease with (2) lung compliance; characterized by (3) FCV, (4) FEV1 and thus, (5) FEV1/FVC ratio

Back 246

1 = obstructive disease
2 = increased lung compliance
3 = decreased
4 = decreased
5 = decreased

Front 247

How does collapsing pressure vary according to alveolar radius?

Back 247

Large alveoli (large radius) have low collapsing pressures, so it is easy to keep them patent
Small alveoli (small radius) have high collapsing pressures, and are easier to collapse

Front 248

In simple words, describe the law of Laplace.

Back 248

The tendency for an alveolus to collapse increases as the radius decreases.

Front 249

Isoproternol MOA on the lungs

Back 249

dilates via B2 stimulation

Front 250

What causes a right-shift in the Hb-O2 dissociation curve?

Back 250

increased P(CO2)
decreased pH
increased temperature
increased 2,3-DPG

Front 251

What is the most important constituent in surfactant?

Back 251

Dipalmitoyl phosphatidylcholine (DPPC).

Front 252

fibrosis is a (1) disease with (2) lung compliance characterized by a decrease in (3); FEV1/FVC ratio is (4)

Back 252

1 = restrictive disease
2 = decreased lung compliance
3 = decrease in all lung volumes
4 = increased (normal)

Front 253

What is atelectasis?

Back 253

Alveolar collapse

Front 254

Asthma is what type of disease?

Back 254

Obstructive lung disease

Front 255

What causes a left-shift in the Hb-O2 dissociation curve?

Back 255

decreased P(CO2)
increased pH
decreased temperature
decreased 2,3-DPG

Front 256

pink puffers

Back 256

emphysema
- mild hypoxemia
- maintain alveolar ventilation = normocapnia

Front 257

What happens if there is no surfactant?

Back 257

Small alveoli have a tendency to collapse (atelectasis)

Front 258

What occurs in neonatal respiratory distress syndrome?

Back 258

Surfactant is lacking. Infants born before gestational week 24 will never have surfactant, and infants born between weeks 24 and 35 will have uncertain surfactant status. Thus, without surfactant, small alveoli have increased surface tension and increased pressures, and will collapse. Lung compliance will be decreased and the work of inflating the lungs during breathing will be increased.

Front 259

What are the effects of Asthma on FEV and FVC?

Back 259

Decreased FEV1
Decreased FVC
Decreased FEV1/FVC ratio

Front 260

In asthma, air should have been expired is known as ______ leading to______

Back 260

Air trapping, a barrel shaped chest
Increased FRC

Front 261

what is normal pulmonary arterial pressure?

Back 261

15 mmHg

Front 262

blue bloaters

Back 262

bronchitis
- severe hypoxemia with cyanosis
- do not maintain alveolar ventilation = hypercapnia
- right ventricular failure and systemic edema

Front 263

How does surfactant reduce alveolar surface tension?

Back 263

Disrupts the intermolecular forces between liquid molecules
This prevents small alveoli from collapsing and increases compliance

Front 264

What is the formula for pulmonary vascular resistance (PVR)?

Back 264

PVR = P(pulm.artery) - P(L.atrium)/ Cardiac Output

P(pulm.artery) = pressure in pulmonary artery
P(L.atrium) = pulmonary wedge pressure

Front 265

Who are pink puffers

Back 265

Emphysema

Front 266

Describe the pressure and perfusion relationships in Zone 1 alveoli

Back 266

alveolar pressure > arterial pressure > venous pressure
Q is greatly decreased, V is decreased and V/Q is increased
blood flow is lowest

Front 267

Dalton's law of partial pressure

Back 267

PP = total pressure x fractional conc.

Front 268

How is surfactant produced?

Back 268

It is made by type II alveolar cells

Front 269

What does Poiseuille's law sate?

Back 269

Resistance is inversely proportional to the radius of an airway (to the fourth power), and directly proportional to the length of the airway and viscosity of inspired air.

Front 270

Why are emphysema people called pink puffers?

Back 270

They have mild hypoxemia with normal ventilation, normal pCO2
(normocapnia)

Front 271

Describe the pressure and perfusion relationships in Zone 2 alveoli

Back 271

arterial pressure > alveolar pressure > venous pressure
Q, V and V/Q are "normal"
gas transfer is maximized

Front 272

physiological shunt

Back 272

2% of systemic cardiac output bypasses pulmonary circulation making the PO2 of arterial blood slightly lower than that of alveolar air

Front 273

What is surfactant made of?

Back 273

Comprised mostly of the phospholipid dipalmitoyl phosphatidylcholine (DPPC)

Front 274

What is Poiseuille's law?

Back 274

R = 8ηl/πr^4

R = Resistance
η = Viscosity of inspired air
l = Length of the airway
r = Radius of the airway

Front 275

Who are blue bloaters?

Back 275

Bronchitis

Front 276

Describe the pressure and perfusion relationships in Zone 3 alveoli

Back 276

arterial pressure > venous pressure > alveolar pressure
Q is greatly increased, V is increased and V/Q is reduced
blood flow is highest

Front 277

perfusion limited exchange
- demonstrated by (1)
- gas equilibrates (2) along length of pulmonary capillary
- diffusion of gas can only be increased in blood flow (3)

Back 277

1 = N20, O2 under normal conditions, CO2
2 = early
3 = increases

Front 278

When during fetal development is surfactant produced?

Back 278

This is somewhat variable
Can be made as early as 24 weeks
Almost always present by 35 weeks
A lecithin:sphingomyelin ratio greater than 2:1 in the amniotic fluid generally reflects mature levels of surfactant

Front 279

What are the sites of highest airway resistance?

Back 279

The medium-sized bronchi. Because of the parallel arrangement of the smallest airways, the total resistance is less than the individual resistance.

Front 280

Why are people with Bronchitis called Blue Bloaters?

Back 280

B/c they have severe hypoxemia w/ Cyanosis
No alveolar ventilation, hypercapnia, increased pCO2
Right vent. Failure and systemic edema

Front 281

what is the effect of hypoxia on pulmonary vasculature?

Back 281

it causes vasoconstriction in order to redirect flow away from poorly ventilated hypoxic regions of the lung to those that are better ventilated

Front 282

diffusion limited exchange
- demonstrated by (1)
- gas (2) equilibrates along pulmonary capillary

Back 282

1 = CO, O2 under strenous exercise
2= does not equilbrate

Front 283

What is neonatal respiratory distress syndrome?

Back 283

Occurs in premature infants who have not manufactured sufficient amounts of surfactant
These infants have atelectasis (collapsed lungs), difficulty reinflating the lungs because of decreased compliance, and hypoxemia (decreased V/Q)

Front 284

What factors constrict the airways, decrease the radius, and increase the resistance to flow?

Back 284

Parasympathetic stimulation, irritants, and the slow-reacting substance of anaphylaxis (asthma)

Front 285

What is COPD?

Back 285

A combination of bronchitis and emphysema

Front 286

Where are right-to left shunts seen and what is the result?

Back 286

Tetralogy of Fallot; result in a decrease in arterial P(O2)

Front 287

subunits in fetal hemoglobin

Back 287

a2 y2

Front 288

What drives airflow?

Back 288

The pressure difference between the mouth or nose and the alveoli

Front 289

What factors relax the airways, increase the radius, and decrease the resistance to airflow?

Back 289

Sympathetic stimulation and sympathetic agonists (isoproterenol) dilate the airways via β2 receptors.

Front 290

What type of lung disease is COPD

Back 290

Obstructive lung disease with increased lung compliance and impaired expiration

Front 291

where are left-to-right shunts seen and what is the result?

Back 291

paten ductus arteriosus or traumatic injury; do not result in decrease in arterial P(O2). most are asymptomatic.

Front 292

fetal Hb has a (1) affinity for O2 than adult Hb bc 2,3BPG binds (2)

Back 292

1 = higher
2 = less tightly

Front 293

How is airflow related to airway resistance?

Back 293

Inversely proportional
The higher the airway resistance, the lower the airflow

Front 294

What is the difference in intrapleural pressure when expiration (passive) and forced expiration?

Back 294

In passive expiration, intrapleural pressure (which was -6 cm H2O during inspiration) returns to its resting value (-3). During a forced expiration, intrapleural pressure actually becomes positive. This positive intrapleural pressure compresses the airways and makes expiration more difficult.

Front 295

What happens to lung compliance in COPD?

Back 295

It's increased

Front 296

What is the normal V/Q ratio?

Back 296

0.8

Front 297

methemoglobin

Back 297

Fe3+
does not bind O2

Front 298

Equation for airflow

Back 298

Q = delta P / R
Q = airflow
delta P = pressure gradient
R = resistance

Front 299

What is asthma? What is it characterized by?

Back 299

Asthma is an obstructive disease in which expiration is impaired.
Characterized by:
Decreased FVC
Decreased FEV1
Decreased FEV1/FVC

Air that should have been expired is not, leading to air trapping and increased FRC.

Front 300

Which iron state binds oxygen?

Back 300

FE2+

Front 301

What are the partial pressures of CO2 and O2 in pulmonary capillaries of obstructed airways?

Back 301

in a physiologic shunt, Pa values approach venous values: Pa(O2) = 40 mmHg and Pa(CO2) = 46 mmHg

Front 302

What is COPD? What is it characterized by?

Back 302

COPD is a combination of chronic bronchitis and emphysema. It is an obstructive disease with increased lung compliance in which expiration is impaired.

Characterized by:
Decreased FVC, FEV1
Decreased FEV1/FVC

Air that should have been expired is not, leading to air trapping, increased FRC, and a barrel-shaped chest.

Front 303

O2 binding capacity of blood

Back 303

max amount of O2 that can be bound to Hb

- depends on Hb conc.

Front 304

Formula for airway resistance

Back 304

R = (8nl) / (pi x r^4)
n = viscosity
l = length of airway
r = radius

Front 305

What is the name for FE3+?

Back 305

Methemoglobin

Front 306

What are the partial pressures of CO2 and O2 in alveoli of obstructed pulmonary capillaries?

Back 306

in physiologic dead space, the partial pressures of O2 and CO2 approach that of humid air: P(O2) = 150 mmHg and P(CO2) = 0 mmHg

Front 307

What are "pink puffers"? "Blue bloaters"?

Back 307

"Pink puffers" (primarily emphysema) have mild hypoxemia and normocapnia (normal PCO2).

"Blue bloaters" (primarily bronchitis) have severe hypoxemia with cyanosis and hypercapnia (increased PCO2). They have right ventricular failure and systemic edema.

Front 308

SHIFT to the RIGHT of Hb-O2 curve

Back 308

increased PCO2
increased 2, 3 BPG
decreased pH
increased temp

Front 309

What is the relationship between airway resistance and radius of the airway?

Back 309

Resistance is inversely proportional to the fourth power of the airway

Front 310

What is the normal structure for adult hemoglobin?

Back 310

α2β2

Front 311

Where is the medullary respiratory center located?

Back 311

in the reticular formation

Front 312

LEFT SHIFT of Hb-O2 curve

Back 312

HbF
CO

---> affinity of Hb for O2 is increased

Front 313

What is the major site of airway resistance?

Back 313

Medium-sized bronchi

Front 314

What condition leads to a decrease in all lung volumes, decreased lung compliance in which inspiration is impaired, and an increased FEV1/FVC?

Back 314

Fibrosis (restrictive disease).

Front 315

What is the structure of fetal hemoglobin?

Back 315

α2γ2

Front 316

What is responsible for inspiration and generates basic rhythm of breathing?

Back 316

Dorsal respiratory group

Front 317

CO (1) the O2 content of the blood

Back 317

decreases

Front 318

What factors cause the bronchial smooth muscle to contract?

Back 318

Parasympathetic stimulation
Irritants
Slow-reacting substance of anaphylaxis (asthma)

Front 319

What are the values of partial pressure of O2 and CO2 for alveolar air, systemic arterial blood, and mixed venous blood?

Back 319

Alveolar air
PO2 = 100 mmHg
PCO2 = 40

Systemic Arterial Blood
PO2 = slighty <100 (due to physiologic shunt)
PCO2 = 40

Mixed Venous Blood
PO2 = 40 mmHg
PCO2 = 46

Front 320

Why does a left shift occur with fetal hemoglobin?

Back 320

Tighter O2 affinity
Less 2,3 DPG affinity

Front 321

From where does the input to the dorsal respiratory group come?

Back 321

vagus (chemoreceptors and mechanoreceptors) and glossopharyngeal (chemoreceptors) nerves

Front 322

hypoxemia

Back 322

decrease in arterial PO2

Front 323

What factors cause the bronchial smooth muscle to relax?

Back 323

Sympathetic stimulation
Sympathetic agonists
These things use beta 2 receptors

Front 324

In hemoglobin, what is the heme moiety?

Back 324

Iron-containing porphyrin. The iron is in the ferrous state (Fe2+), which binds O2. Iron in the ferric state (Fe3+) does not bind O2.

Mnemonic: Ferris (Ferrous) was with 2 (Fe2+) people on his adventure.

Front 325

What does %saturation measure?

Back 325

Amount of O2 bound to hemoglobin

Front 326

Where does the output of the dorsal respiratory group go?

Back 326

along the phrenic nerve to the diaphragm

Front 327

A-a gradient

Back 327

- used to compare causes hypoxemia
A-a gradient = alveolar PO2 - arterial PO2

Front 328

How does isoproterenol affect bronchodilation?

Back 328

It is a sympathetic agonist, and this causes the bronchioles to dilate

Front 329

What is hemoglobin F composed of?

Back 329

In fetal hemoglobin, the β chains are replaced by γ chains. Thus, fetal hemoglobin is α2γ2.

Front 330

O2 content is a measure of

Back 330

Total O2 in blood: bound to heme and dissolved O2

Front 331

What is the function of the ventral respiratory group and when is it activated?

Back 331

function is expiration, activated during exercise

Front 332

alveolar PO2

Back 332

alveolar PO2 = inspired Po2 - alveolar PCO2 / R

Front 333

How does lung volume contribute to airway resistance?

Back 333

Lung tissue exerts radial traction upon the airways
High lung volumes are associated with greater traction and decreased resistance
Low lung volumes exert less traction, and there can be resistance to the point of airway collapse

Front 334

At which values of PO2 is hemoglobin 100% saturated?
75% saturated? 50% saturated?

Back 334

100% saturated: PO2 = 100 mmHg
75% saturated: PO2 = 75 mmHg
50% saturated: PO2 = 50 mmHg

Front 335

What is the formuale for O2 content?

Back 335

= (O2-binding capacity x %sat) + dissolved O2

Front 336

What and where is the apneustic center?

Back 336

stimulates inspiration; located in lower pons

Front 337

What does a shift to the right in the hemoglobin-O2 dissociation curve indicate? What causes this?

Back 337

Shifts to the right occur when the affinity of hemoglobin for O2 is decreased.

Causes:
Increases in PCO2
Decreases in pH
Increases in temperature (e.g. during exercise)
Increases in 2,3-DPG concentration (e.g. living at high altitudes)

Front 338

normal A-a gradient

Back 338

is less than 10 mmHg

Front 339

How do the density and viscosity of an inspired gas affect airflow?

Back 339

They change the resistance to airflow
During deep-sea diving, air density increases and resistance increases
Low-density gases such as helium reduce airflow resistance

Front 340

What is on the x and y axis of Hemoglobin curve?

Back 340

X axis = PO2
Y axis = % sat.

Front 341

Where/what is the pneumotaxic center?

Back 341

located in the upper pons and inhibits inspiration

Front 342

Increased A-a gradient

Back 342

- if O2 does not equilibriate between alveolar and arterial blood

- diffusion defect
- V/Q defect
- right to left shunt

Front 343

What are the thoracic pressures at rest, before inspiration begins?

Back 343

Alveolar pressure = atmospheric pressure = 0
Intrapleural pressure is negative due to the opposing forces of the lungs trying to collapse and the chest wall trying to expand

Front 344

What does a shift to the left in the hemoglobin-O2 dissociation curve indicate?
What conditions cause this?

Back 344

Shifts to the left occur when the affinity of hemoglobin for O2 is increased.

Causes:
Decreased PCO2
Increased pH
Decreased temperature
Decreased 2,3-DPG concentration

Front 345

What is the pO2 of mixed venous blood?

Back 345

40 mm Hg

Front 346

where are the central chemoreceptors for breathing and what stimuli increase breathing rate?

Back 346

medulla; decreased pH (or increased CO2 which combines with water to make H+) of CSF

Front 347

what is the major form of CO2 in blood?

Back 347

HCO3

- small amounts of CO2 dissolved and as carbaminohemoglobin

Front 348

Equation for airflow

Back 348

Q = delta P / R
Q = airflow
delta P = pressure gradient
R = resistance

Front 349

What is 2,3-DPG? When does 2,3-DPG production increase?

Back 349

2,3-diphosphoglycerate (2,3-DPG) is a byproduct of glycolysis in red blood cells. 2,3-DPG binds to the β chains of deoxyhemoglobin and reduces their affinity for O2.

2,3-DPG production increases under hypoxic conditions (i.e. high altitude).

Front 350

At pO2 of 25 mm Hg, what is the % Hg sat. ?

Back 350

50%, aka P50, 2 out 4 heme groups are saturated

Front 351

where are the peripheral chemoreceptors for breathing and what stimuli increase breathing rate?

Back 351

carotid and aortic bodies; decreased P(O2) (if <60mmHg), decreased pH, increased P(CO2)

Front 352

main buffer of H+ in RBCs?

Back 352

deoxyhemoglobin

Front 353

Formula for airway resistance

Back 353

R = (8nl) / (pi x r^4)
n = viscosity
l = length of airway
r = radius

Front 354

Does HbF cause the curve to shift to the left? What about the binding of CO to hemoglobin?

Back 354

HbF: left shift.
HbF does not bind 2,3-DPG as strongly as adult hemoglobin, which results in increased affinity of HbF for O2.

Carbon monoxide (CO) poisoning: left shift

Front 355

Why is there a sigmoid shaped curve for Hg-O2 dissociation curve?

Back 355

Positive cooperativity, B/c of a change in affinity for hemoglobin with each O2 added.

Front 356

What are J receptors and what do they affect?

Back 356

located in alveolar walls, close to capillaries. they are activated by engorgement of pulmonary capillaries (as in left heart failure) to cause rapid shallow breathing

Front 357

pulmonary circulation vs. systemic circulation
- pressure is (1)
- resistance is (2)
- CO of RV = (3)

Back 357

1 = much lower (15 mmHg)
2 = lower
3 = pulmonary blood flow

Front 358

What is the relationship between airway resistance and radius of the airway?

Back 358

Resistance is inversely proportional to the fourth power of the airway

Front 359

What is the A-a gradient used for? What is the normal A-a gradient?

Back 359

A-a gradient = PAO2 - PaO2
Alveolar - arterial
A-a gradient can be used to compare causes of hypoxemia.

Normal A-a gradient < 10 mmHg

Front 360

Shifts to right in Heme-O2 dissociation curve are

Back 360

Occur b/c of Decreased O2 affinity
Increase in pCO2
Decrease in pH
Increase in Temp
Increase in 2,3 DPG

Front 361

what happens to the mean values of arterial P(O2) and P(CO2) during exercise

Back 361

they do not change

Front 362

blood flow is lowest in the (1) of lung and highest at (2)

Back 362

1 = apex (zone 1)
2 = base (zone 3)

Front 363

What is the major site of airway resistance?

Back 363

Medium-sized bronchi

Front 364

What is the A-a gradient for the following conditions?

High altitude
Hypoventilation
Diffusion defect (e.g. fibrosis)
V/Q defect
Right-to-left shunt

Back 364

High altitude: Normal
Hypoventilation: Normal
Diffusion defect (e.g. fibrosis): Increased
V/Q defect: Increased
Right-to-left shunt: Increased

Front 365

What happens to the P50 in rightward shifts of heme-o2 curve

Back 365

P50 is increased; O2 unloading occurs

Front 366

what happens to physiologic dead space during exercise?

Back 366

it decreases

Front 367

zone 1
- blood flow (1)
- alveolar pressure is (2) than arterial pressure

Back 367

1 = lowest
2 = greater than
--> high alveolar pressure compresses capillaries
--> hemorrhage or positive pressure ventilation

Front 368

What factors cause the bronchial smooth muscle to contract?

Back 368

Parasympathetic stimulation
Irritants
Slow-reacting substance of anaphylaxis (asthma)

Front 369

What are the three forms of CO2 in the blood?

Back 369

1. Dissolved CO2
2. Carbaminohemoglobin
3. HCO3- (major form, 90%)

Front 370

What is the Bohr effect?

Back 370

Decreasing the affinity for hemoglobin for O2 and facilitating the unloading of O2 in tissues

Front 371

what are physiologic adaptations in high altitude?

Back 371

alveolar P(O2) is decreased, arterial P(O2) is decreased (hypoxemia), hyperventilation, respiratory alkalosis, increased EPO, increased 2,3-DPG, hypoxic pulmonary vasoconstriction

Front 372

zone 2
- blood flow (1)
- alveolar pressure is (2) than arterial pressure

Back 372

1 = medium
2 = lower

Front 373

What factors cause the bronchial smooth muscle to relax?

Back 373

Sympathetic stimulation
Sympathetic agonists
These things use beta 2 receptors

Front 374

How does CO2 get converted to HCO3-? Where is it converted?

Back 374

CO2 diffuses into RBCs, where it combines with H2O to form H2CO3. This reaction is catalyzed by carbonic anhydrase.
H+ and HCO3- are dissociated from H2CO3. HCO3- leaves the RBC in exchange for Cl- (chloride shift).

Front 375

How does an increase in 2,3 DPG affect the heme-o2 curve?

Back 375

Rightward sift
By binding B-chains of deoxyhemoglobin and decreasing the affinity for heme O2

Front 376

What structures perforate the diaphragm and at what levels?

Back 376

IVC (T8), esophagus (T10), vagus (T10), aorta (T12), thoracic duct (T12), azygous vein (T12).

Front 377

zone 3
- blood flow (1)
- arterial pressure is the (2)

Back 377

1 = highest
2 - highest

Front 378

How does isoproterenol affect bronchodilation?

Back 378

It is a sympathetic agonist, and this causes the bronchioles to dilate

Front 379

What are the three zones? What is the comparison of the pressures?

Back 379

Zone 1: blood flow is lowest
Alveolar pressure > arterial pressure > venous pressure

Zone 2: blood flow is medium
Arterial pressure > alveolar pressure > venous pressure

Zone 3: blood flow is highest
Arterial pressure > venous pressure > alveolar pressure

Front 380

How does the body compensate for living in high altitude?

Back 380

Increases synthesis of 2,3 DPG which binds hemoglobin and Facilitates O2 unlaoding

Front 381

By what is the diaphragm innervated?

Back 381

phrenic nerve (C3, 4, 5) (keeps the diaphragm alive)

Front 382

In contrast to other organs, in lungs, hypoxia causes (1) which redirects blood away from poorly ventilated, hypoxic regions

Back 382

1 = vasoconstriction

Front 383

How does lung volume contribute to airway resistance?

Back 383

Lung tissue exerts radial traction upon the airways
High lung volumes are associated with greater traction and decreased resistance
Low lung volumes exert less traction, and there can be resistance to the point of airway collapse

Front 384

In the lung, what happens during hypoxia? Why?

Back 384

Hypoxia causes vasoconstriction. Physiologically, this effect is important because local vasoconstriction redirects blood away from poorly ventilated, hypoxic regions of the lung and toward well-ventilated regions.

Front 385

How does CO, CArbon monoxide affect the heme-O2 curve?

Back 385

Left-ward shift, b/c 250-times binding affinity
CO decrease the O2 content by binding direct to O2 sites

Front 386

What are the accessory muscles of inspiration?

Back 386

external intercostals, scalene muscles, sternocleidomastoids

Front 387

right to left shunts

Back 387

ex. tetralogy of fallot

--> always decrease arterial PO2

Front 388

How do the density and viscosity of an inspired gas affect airflow?

Back 388

They change the resistance to airflow
During deep-sea diving, air density increases and resistance increases
Low-density gases such as helium reduce airflow resistance

Front 389

What is the normal V/Q ratio?

Back 389

V/Q = 0.8

Front 390

What affect does respiratory alkalosis have on heme-O2 curve?

Back 390

A left-ward shift, Increase in pH

Front 391

what are the accessory muscles of expiration?

Back 391

rectus abdominis, internal and external obliques, transversus abdominis, internal intercostals

Front 392

V/Q ratio

Back 392

ratio of alveolar ventilation to pulmonary blood flow

Front 393

What are the thoracic pressures at rest, before inspiration begins?

Back 393

Alveolar pressure = atmospheric pressure = 0
Intrapleural pressure is negative due to the opposing forces of the lungs trying to collapse and the chest wall trying to expand

Front 394

Where is blood flow highest? Where is ventilation highest?

Back 394

Blood flow AND ventilation are highest at the base of the lungs.

Front 395

What affect does a left-ward shift have on P50?

Back 395

The P50 is decreased, unloading of O2 into tissues is difficult

Front 396

what molecule activates bradykinin?

Back 396

Kallikrein

Front 397

Where is the V/Q ratio highest? (apex or base)

Back 397

apex

Front 398

Which of the standard lung volumes is in the lungs at rest?

Back 398

The FRC

Front 399

Where is the V/Q ratio highest? Where is the V/Q ratio lowest?

Back 399

The V/Q ratio is highest at the apex (3.0), and lowest at the base (0.6).

Front 400

What is hypoxemia?

Back 400

Decreased in arterial pO2

Front 401

What is the effect of CO poisoning?

Back 401

causes a decrease in oxygen binding capacity of Hb with a left-shift in the oxygen dissociation curve

Front 402

apex has (1) regional arterial PO2 and (2) regional PCO2 bc gas exchange is more efficient

Back 402

1 = highest
2 = lower

Front 403

What happens to the thoracic pressures during inspiration?

Back 403

The inspiratory muscles contract and increase the thoracic volume
This causes the intrapleural pressure to become more negative
The increased transmural pressure on the alveoli causes the alveolar pressure to become negative
The pressure gradient between the alveoli and the air causes air to flow into the lungs

Front 404

What is a shunt? What can cause a shunt?

Back 404

V/Q = 0
When the airways are completely blocked (e.g. by a steak caught in the trachea).

Front 405

What is the A-a gradient?

Back 405

Pao2-Pa2, difference between alveolar and arterial pO2

Front 406

Calculation of pulmonary vascular resistance?

Back 406

PVR = [P(pulm artery) - P(wedge)] / Cardiac outupt

Front 407

dorsal respiratory group

Back 407

- inspiration
- generates basic rhythm of breathing

Front 408

How does lung volume relate to elastic recoil?

Back 408

Elastic recoil is greatest when the lungs contain high volumes

Front 409

What is dead space?

Back 409

V/Q = infinite.
When the blood flow to a lung is completely blocked (e.g. by an embolism)

Front 410

Why do we use the A-a gradient?

Back 410

Can distinguish if hypoxemia is from the lungs or outside the lungs

Front 411

ventral respiratory group

Back 411

- expiration
- not active during normal quiet breathing --> only active when expiration is an active process

Front 412

What do we measure when we want to know about the dynamic compliance of the lungs?

Back 412

Changes in intrapleural pressure during inspiration

Front 413

What nerves relay sensory information? Where does the information go?

Back 413

Vagus nerve and glossopharyngeal nerve relays information to the dorsal respiratory group.

Front 414

What is a normal A-a gradient?

Back 414

<10mm Hg, b/c O2 equilibrates between alveolar gas and arterial gas

Front 415

apneustic centre

Back 415

lower pons
- stimulates inspiration
- deep and prolonged inspiratory gasp

Front 416

Which of the standard lung volumes is in the lungs at the peak of inspiration?

Back 416

FRC + TV

Front 417

In what nerve does the output to the diaphragm travel?

Back 417

Phrenic nerve

Front 418

When the A-a is > 10 mm Hg what does it mean?

Back 418

O2 is not equilibrating so;
Diffusion defect
V/Q defect
Right-to-left shunt

Front 419

pneumotaxic centre

Back 419

upper pons
- inhibits respiration
- regulates depth and rate of breathing

Front 420

What happens to the thoracic pressures during expiration?

Back 420

The inspiratory muscles relax and the thoracic pressure becomes less negative
This causes the alveolar pressure to become positive
The pressure gradient causes air to flow from the lungs out the airway

Front 421

Where are the central and peripheral chemoreceptors located?

Back 421

Central chemoreceptors are in the medulla.
Peripheral chemoreceptors are in the carotid and aortic bodies.

Front 422

What is hypoxia?

Back 422

decreased O2 delivery to the tissues.

Front 423

central chemoreceptors

Back 423

- located in medulla
- sensitive to pH of CSF (decreases in pH increased breathing)

Front 424

What happens to intrapleural pressure during a forced expiration?

Back 424

It becomes POSITIVE
During quiet expiration, IPP becomes less negative, but never actually becomes positive
Positive IPP can compress the airways and make expiration more difficult

Front 425

How does increased CO2 activate the central chemoreceptors?

Back 425

CO2 diffuses from arterial blood into the CSF (CO2 is lipid soluble). In the CSF, CO2 combines with H2O to produce H+ and HCO3-. The resulting H+ acts directly on the central chemoreceptors. Thus, increases in PCO2 and [H+] stimulate breathing, and decreases in PCO2 and [H+] inhibit breathing.

Metabolic acidosis -> hyperventilation

Front 426

What is the equation for O2 delivery?

Back 426

= Cardiac output X O2 content of blood

Front 427

peripheral chemoreceptors
- location? (1)
- respond preferentially to? (2)

Back 427

1 = carotid and aortic bodies
2 = decreased PO2 (<60 mmHg)

Front 428

How is breathing altered in a patient with COPD?

Back 428

Airway resistance is increased
Patients learn to expire slowly with pursed lips
This prevents the airway collapse that can occur with a forced expiration

Front 429

In response to exercise, does the arterial PO2 and PCO2 change? What about the Venous PCO2? V/Q ratios?

Back 429

The arterial PO2 and PCO2 do not change in response to exercise. Venous PCO2 does increase.
The V/Q ratios are more evenly distributed in the lung during exercise.

Front 430

What does O2 content depend on?

Back 430

Hg concentration
O2-binding capacity
% saturation

Front 431

Hering-Breur Reflex

Back 431

receptors are stimulated by distension of lungs, the produce a reflex decrease in breathing reflex

Front 432

Which of the standard lung volumes is in the lungs at the end of a quiet expiration?

Back 432

The FRC

Front 433

In the context of adaptation to high altitude, what are the changes to the following parameters:

Alveolar PO2
Arterial PO2
Ventilation rate
Arterial pH
Hemoglobin concentration
2,3-DPG concentration
Hemoglobin-O2 curve
Pulmonary vascular resistance

Back 433

Alveolar PO2: decreased (resulting from decreased barometric pressure)
Arterial PO2: decreased (hypoxemia)
Ventilation rate: increased
Arterial pH: Increased (respiratory alkalosis)
Hemoglobin concentration: Increased (polycythemia)
2,3-DPG: Increased
Hemoglobin-O2 curve: shift to right
Pulmonary vascular resistance: increased (hypoxic vasoconstriction)

Front 434

What are the causes of hypoxia?

Back 434

Decrease CO
Decrease O2-binding capacity
Decreased arterial pO2

Front 435

J (juxtacapillary) receptors

Back 435

located in alveolar walls close to capillaries --> engorgement of capillaries i.e. left heart failure causes rapid, shallow breathing

Front 436

What is asthma?

Back 436

An obstructive disease where expiration is impaired
Patients have low FEV1/FVC
Air that should be expired is instead getting trapped, which causes the FRC to increase

Front 437

If a patient has a decreased Pao2 and normal A-a gradient, what should you think?

Back 437

1) Hypoventilation

2)High altitude

Distinguish by high altitude b/c low air/ barometric pressure:

Front 438

joint and muscle receptors and breathing

Back 438

early stimulation of breathing during exercise

Front 439

What is COPD?

Back 439

A combination of chronic bronchitis and emphysema
Obstructive disease with increased lung compliance, so expiration is impaired
Decreased FEV1/FVC
Air that should be expired is trapped, leading to increased FRC and a barrel-shaped chest

Front 440

Name all the diseases associated with restrictive lungs diseases

Back 440

1.Lung tissue abnormalities: pulmonary fibrosis, silicosis, asbestosis, tuberculosis
2. Pluera problems: Pneumonthorax, Pleural Effusion
3. Neuromuscular: Polio, Myasthenia Gravis

Front 441

What are "pink puffers?"

Back 441

COPD patients who primarily have emphysema
Mild hypoxemia
Normocapnia because alveolar ventilation is maintained

Front 442

Name all of the diseases associated with obstructive lung diseases.

Back 442

1. Obstructed airway lumen; chronic bronchitis, edema, or food aspiration
2. Asthma, constricted of airway muscles
3. Outside of airway; emphysema = lung tissue destruction

Front 443

What are "blue boaters?"

Back 443

COPD patients who primarily have bronchitis
Severe hypoxemia with cyanosis
Hypercapnia because alveolar ventilation is not maintained
Right ventricular failure and systemic edema

Front 444

Where does Asthma usually take place and how does it occur?

Back 444

Hypersensitivity reaction of the bronchioles; produces edema and bronchospasm

Front 445

What is fibrosis?

Back 445

Restrictive disease associated with decreased lung compliance, so inspiration is impaired
All lung volumes are decreased
FEV1/FVC is increased

Front 446

What is the PCO2 value when a person is hypercapnic and breathing rapidly and deeply

Back 446

60 to 75 mm Hg

Front 447

What is Dalton's law of partial pressure?

Back 447

Partial pressure = total pressure x fractional gas concentration

Front 448

At what level of PCO2 does a person become lethargic and semicomatose,

Back 448

80 -100 mm Hg pCO2

Front 449

What is the fractional concentration of oxygen in dry inspired air?

Back 449

21%

Front 450

What is the PCO2 value when a person is hypercapnic and breathing rapidly and deeply

Back 450

60 to 75 mm Hg

Front 451

When calculating the partial pressure of oxygen in humidified tracheal air, what do we have to do to calculate?

Back 451

You have to subtract the partial pressure of water (47 mmHg) from the total pressure before multiplying by the fractional concentration of oxygen

Front 452

At what level of PCO2 does a person become lethargic and semicomatose,

Back 452

80 -100 mm Hg pCO2

Front 453

Are the systemic and pulmonary circulations entirely separate?

Back 453

No
2% of cardiac output bypasses the pulmonary circulation (physiologic shunt), and this venous blood mixes with arterial blood
This makes the PO2 of arterial blood slightly lower than the PO2 of alveolar air

Front 454

How many forms of CO2 are carried in the blood? Name them

Back 454

3 forms
1: Dissolved CO2, free in solution
2: Carbaminohemoglobin, CO2 bound to heme
3: HCO3-, major form ~ 90%

Front 455

How much gas dissolves in solution?

Back 455

An amount that is proportional to the partial pressure

Front 456

How is CO2 carried in the RBC? IE Formula

Back 456

CO2 combines with H2O to form H2CO3-
H2CO3- dissociates into H+ + HCO3-

Front 457

Formula for dissolved gas in solution

Back 457

Dissolved gas = partial pressure of gas x solubility in blood

Front 458

how does HCO3- get out the RBC?

Back 458

HCO3- is exchanged for CL- ion
HCO3- is then transferred in the blood, the major form of CO2

Front 459

What factors impact the diffusion rates of O2 and CO2?

Back 459

The partial pressure difference across the membrane
The surface area available for diffusion

Front 460

What happens to H+ ion generated in the RBC from H2CO3- dissociation?

Back 460

H+ is buffered by deoxyhemoglobin

Front 461

What gases exhibit perfusion-limited exchange?

Back 461

N2O
O2 (under normal conditions)

Front 462

In the lungs, what reactions take place in the RBC?

Back 462

HCO3- enters the RBC
Cl- is kicked out in exchange
H+ recombines to form H2CO3
H2CO3 decomposes to CO2 and H2O
CO2 is expired

Front 463

What is perfusion-limited exchange?

Back 463

The gas equilibrates early along the length of the pulmonary capillary
The partial pressures of the gas in the arterial blood and alveolar air become equal
Diffusion of the gas can be increased only if blood flow increases

Front 464

What are the pressures in pulmonary circulation when compared to systemic?

Back 464

Lower, eg pulmonary artery is 15mm Hg and aortic is 100mm hg

Front 465

What gases exhibit diffusion-limited exchange?

Back 465

CO
O2 (emphysema, fibrosis, and during strenuous exercise)

Front 466

What is the resistance in pulmonary circulation vs systemic?

Back 466

Much lower

Front 467

What is diffusion-limited exchange?

Back 467

The gas does not equilibrate by the time the blood reaches the end of the pulmonary capillary
The partial pressure difference of the gas between the arterial blood and the alveolar air is maintained
Diffusion continues as long as there is a partial pressure gradient

Front 468

Pulmonary blood flow is equal to CO of ______

Back 468

Right ventricle

Front 469

How does fibrosis cause O2 to become diffusion-limited?

Back 469

Thickening of the alveolar membrane increases diffusion distance
This restricts the diffusion of O2

Front 470

Cardiac output of the right ventricle is equal to

Back 470

CO of the left ventricle

Front 471

How does emphysema cause O2 to become diffusion-limited?

Back 471

The surface area for gas diffusion is decreased

Front 472

If the pressure of pulmonary circulation are low how are they sufficient to pump CO?

Back 472

B/c the resistance in pulmonary circulation is low

Front 473

How is oxygen transported in the blood?

Back 473

Dissolved
Bound to hemoglobin (most important mechanism)

Front 474

Zone one blood flow in the lung is

Back 474

the lowest

Front 475

What is the structure of adult hemoglobin?

Back 475

Globular tetramer
Each subunit has a heme moiety, which is iron-containing porphyrin
The iron is in the ferrous 2+ state, which binds oxygen
If the iron is in the ferric 3+ state, it is methemoglobin and will not bind oxygen
Made of 2 alpha and 2 beta chains (normal adult Hb is known as a2B2)

Front 476

What is the sequence of pressures for zone? Eg alveolar, arterial, venous

Back 476

Alveolar>Arterial>venule

Front 477

What is the structure of fetal hemoglobin?

Back 477

The beta chains are replaced by gamma chains, so fetal Hb is known as a2y2

Front 478

Where is arterial pressure greater than alveolar and venule pressures?

Back 478

Zone 2
Arterial>Alveolar>Venule

Hint 478

Zones in the lung

Front 479

What is the difference in oxygen affinity between adult and fetal hemoglobin?

Back 479

Fetal Hb has higher oxygen affinity
This means the oxygen dissociation curve is left-shifted relative to the adult curve
Because of this phenomenon, a fetus will draw maternal oxygen across the placenta

Front 480

Where is venule pressure greater than alveolar?

Back 480

Zone 3
Arterial pressure>Venula>Alveolar

Front 481

How do fetal and adult hemoglobins differ with regard to 2,3-BPG binding?

Back 481

Fetal Hb binds 2,3-BPG less avidly

Front 482

How is blood flow driven in zone 2?

Back 482

By the difference in pressures between Arterial and Alveolar

Front 483

What is the oxygen-binding capacity of blood?

Back 483

The maximum amount of O2 that can be bound to hemoglobin in the blood
Is dependent upon the hemoglobin concentration of the blood
Limits the amount of O2 that can be carried in the blood

Front 484

How is blood flow driven in zone 3?

Back 484

By the difference in pressures between Arterial and Venous, like normal vascular beds.

Front 485

What is the oxygen content of the blood?

Back 485

The total amount of oxygen carried in blood, including Hb-bound and dissolved
Depends upon the Hb concentration, PO2, and the P50 of Hb

Front 486

How is pulmonary blood flow regulated in hypoxic conditions?

Back 486

Vasoconstriction, opposite of vascular beds, this redirects blood away from poorly ventilated areas

Front 487

Formula for oxygen content

Back 487

O2 content = (oxygen binding capacity x %saturation) + dissolved O2

Front 488

Right to left shunts always result in decrease in _______. Why?

Back 488

arterial PO2, b/c of mixture of venous blood

Front 489

What is the name of hemoglobin that is bound to oxygen?

Back 489

Oxyhemoglobin

Front 490

How can the magnitude of right-left shunt be measured?

Back 490

Have the pt breathe 100% O2 and measure the dilution of oxygenated to non-oxgenated

Front 491

What is the percent saturation of Hb at 100 mmHg (arterial blood)?

Back 491

100% saturated

Front 492

Which shunt is more common and Why?

Back 492

Left ot right b/c of higher pressures on the left

Front 493

What is the percent saturation of Hb at 40 mmHg (mixed venous blood)?

Back 493

75% saturated

Front 494

What are the usual causes of left ot right shunts?

Back 494

Congenital abnormalities eg patent ductus arteriousus
Traumatic Injury

Front 495

What is the percent saturation of Hb at 25 mmHg?

Back 495

25% saturated

Front 496

These do not result in a decrease in arterial PO2?

Back 496

Left to right shunts
PO2 will be elevated on the right b.c of mixture of blood

Front 497

What is the shape of the oxygen dissociation curve?

Back 497

Sigmoidal
This is because the affinity of hemoglobin increases as each successive oxygen molecule binds a heme (this is positive cooperativity)

Front 498

At the apex, PO2 is ______ and PCO2 is _____

Back 498

PO2 is Higher,
PCO2 is lower
more gas exchange in the upper

Front 499

How does the sigmoidal shape of the oxygen dissociation curve affect oxygen loading and unloading?

Back 499

Changing oxygen affinity facilitates oxygen loading in the lungs, and unloading in the tissues

Front 500

At the base, PO2 is ______ and PCO2 is ______

Back 500

PO2 is lower
PCO2 is higher
less gas exchange

Front 501

Why can people tolerate changes in atmospheric pressure and oxygen without compromising the oxygen-carrying capacity of Hb?

Back 501

Because the oxygen dissociation curve is almost flat between PO2 of 60 and 100 mmHg
However, below 60, the slope decreases sharply and small decreases in oxygen produce large changes in oxygen-carrying capacity

Front 502

If the airways are blocked, eg piece of steak, then ventilation is _______ and this is called

Back 502

Zero, V/Q is zero, physiologic shunt

Front 503

What happens to oxygen and hemoglobin in the lungs?

Back 503

Oxygen diffuses from alveolar gas to pulmonary capillary blood
The PO2 of alveolar gas is 100 mmHg, and oxygen affinity of Hb is very high at this concentration
This facilitates the diffusion process
By tightly binding oxygen, the free oxygen concentration and O2 partial pressure are kept low, which maintains the partial pressure gradient

Front 504

If there is no gas exchange in a lung that is perfused but not ventilated, what are the values of pumonary capillary blood?

Back 504

PO2 and PCO2 will approach their mixed values of blood, 40 mm Hg and 46 mm Hg respectively

Front 505

What happens to oxygen and hemoglobin in the peripheral tissues?

Back 505

O2 diffuses from the arterial blood to the cells
The gradient for diffusion is maintained because the cells consume O2 for metabolism, which keeps the tissue PO2 low
The lower affinity of Hb for O2 in this portion of the curve facilitates O2 unloading

Front 506

What happens to the A-a gradient in physiologic shunting?

Back 506

It's increased

Front 507

What factors cause the oxygen dissociation curve to be shifted to the right (that is, decrease the affinity of hemoglobin for O2)?

Back 507

Increased PCO2
Decreased pH
Increased temperature
Increased 2,3-BPG concentration

Front 508

In a pulmonary embolism, what are the expected V/Q findings?

Back 508

PE means no blood flow to the lung, V/Q is infinite, called dead space

Front 509

What is an adaptation to chronic hypoxemia at high altitudes?

Back 509

Increased production of 2,3-BPG to facilitate oxygen unloading in the tissues

Front 510

When there is no gas exchanged in a lung that is ventilated but not perfused, what are the PO2 and PCO2 findings?

Back 510

PO2 and PCO2 will approach the values of inspired air
150 mm Hg and 0 mm Hg

Front 511

What factors cause the oxygen dissociation curve to be shifted to the left (increase the affinity of hemoglobin for O2)?

Back 511

Decreased PCO2
Increased pH
Decreased temperature
Decreased 2,3-BPG concentration

Front 512

The central control of breathing is controlled by

Back 512

Medullary respiratory center

Front 513

Under what conditions is oxygen loading and unloading onto hemoglobin most difficult?

Back 513

Under conditions that left-shift the oxygen dissociation curve

Front 514

This is primarily responsible for inspiration and generates basic rhythm of breathing

Back 514

Dorsal Medullary respiratory center

Front 515

How does CO binding to hemoglobin affect O2 binding?

Back 515

CO competes with O2 for binding sites
Hb's affinity for CO is 200X higher than its affinity for O2
CO binds to Hb and decreases the O2 concentration of the blood
CO binding to Hb increases the affinity of the remaining Hb sites for O2, so this shifts the oxygen dissociation curve to the left

Front 516

Where is the the respiratory center located?

Back 516

Reticular formation

Front 517

What is hypoxemia?

Back 517

Decreased arterial PO2

Front 518

What is the A-a gradient?

Back 518

The difference between arterial and alveolar air PO2 concentrations

Front 519

What information does the vagus nerve relay to the dorsal respiratory center?

Back 519

Relays peripheral chemoreceptors and mechanoreceptors in the lungs

Front 520

Formula for A-a gradient

Back 520

Gradient = alveolar air PO2 - arterial PO2

Front 521

What information does the glossopharyngeal relay to the respiratory center?

Back 521

The glossopharyngeal nerve relays peripheral information

Front 522

Formula for alveolar air PO2

Back 522

Alveolar air PO2 = PIO2 - [arterial PCO2 / R)
PIO2 = PO2 of the inspired air
R = 0.8 usually

Front 523

What nerve does the output information travel to in the respiratory center?

Back 523

Via phrenic to the diaphragm

Front 524

What is the normal A-a gradient

Back 524

Less than 10 mmHg because O2 normally equilibrates between alveolar gas and arterial blood
If the gradient is increased, something is inhibiting equilibration (diffusion defect, V/Q defect, R-to-L shunt)

Front 525

What is the ventral respiratory center responsible for?

Back 525

EXPIRATION

Front 526

What is hypoxia?

Back 526

Decreased oxygen delivery to the tissues

Front 527

When is the ventral respiratory center active?

Back 527

During exercise, when expiration is an active process

Front 528

Formula for oxygen delivery

Back 528

O2 deliver = cardiac output x O2 content of blood

Front 529

Where is the apneustic center located?

Back 529

PONS

Front 530

How is CO2 transported in the blood?

Back 530

Dissolved
Bound to hemoglobin (carbaminohemoglobin)
Bicarbonate (major form of transport)

Front 531

What does the apneustic center do?

Back 531

Stimulates inspiration, produces a deep and prolonged inspiratory gasp

Front 532

How is CO2 transported as bicarbonate?

Back 532

CO2 is generated in the tissues, and it diffuses into the RBCs
Carbonic anhydrase generates H + HCO3
HCO3 leaves the RBCs in exchange for Cl; this is known as the chloride shift
HCO3 is transported to the lungs in plasma
In the lungs, HCO3 goes back into RBCs in exchange for Cl and carbonic anhydrase catalyzes the reverse reaction
CO2 diffuses out of the RBCs and is expired

Front 533

Where is the pneumotaxic center located?

Back 533

Located in the upper pons

Front 534

How is H buffered inside RBCs?

Back 534

It is buffered by deoxyhemoglobin (Hb with no O2)
DeoxyHb is a better buffer than oxyHb (oxygen-bound Hb), so it is helpful that blood has been deoxygenated by the time it reaches the venous end of the capillaries

Front 535

What does the pneumotaxic center do?

Back 535

Inhibits inspiration, regulates inspiratory volume and respiratory rate

Front 536

How does pulmonary circulation pressure compare to systemic circulation pressure?

Back 536

It is much lower (about 15 mmHg in the pulmonary artery vs 100 mmHg in the aorta)

Front 537

What is the role of the cerebral cortex in breathing?

Back 537

Provides voluntary control; hyperventilate or hypoventilate

Front 538

How does pulmonary circulation resistance compare to systemic circulation resistance?

Back 538

Resistance is much lower in pulmonary circulation

Front 539

What are the central chemoreceptors in the medulla sensitive to?

Back 539

pH

Front 540

What is the distribution of blood in the lung in the supine and standing positions?

Back 540

Supine -- evenly distributed
Standing -- blood tends to move downward due to gravity

Front 541

What affect does a low pH have?

Back 541

Causes an increase in breathing rate

Front 542

What are the zones of the lung?

Back 542

Zone 1 -- apex of the lung
Zone 2 -- middle of the lung
Zone 3 -- base of the lung

Front 543

What acts directly on the central chemoreceptors?

Back 543

H+ ion acts directly

Front 544

Which zones of the lung have the lowest and highest blood flow when standing?

Back 544

Zone 1 has the lowest flow because of gravity
Zone 3 has the highest flow

Front 545

Since H+ ions cannot cross the Blood-Brain barrier, how does the body know there is a change in pH?

Back 545

CO2 diffuses b/c it's lipid soluble
In the CSF, CO2 combines with H2O to produce H+ and HCO3-

Front 546

What is the order of the alveolar, arterial, and venous pressures (from highest to lowest) in zone 1 of the lung?

Back 546

Alveolar > arterial > venous

Front 547

Where are the peripheral chemoreceptors located?

Back 547

Carotid and Aortic Bodies

Front 548

What is the order of the alveolar, arterial, and venous pressures (from highest to lowest) in zone 2 of the lung?

Back 548

Arterial > alveolar > venous

Front 549

Where are the carotid bodies located?

Back 549

at the bifurication of the common carotid

Front 550

What is the order of the alveolar, arterial, and venous pressures (from highest to lowest) in zone 3 of the lung?

Back 550

Arterial > venous > alveolar

Front 551

Where are the aortic bodies located?

Back 551

Below the aortic arch

Front 552

How does high alveolar pressure affect blood flow in zone 1 of the lung?

Back 552

It may compress the capillaries and reduce blood flow
This can occur if arterial pressure is decreased from hemorrhage
Can also occur if positive-pressure ventilation has artificially increased the alveolar pressure

Front 553

What stimulates the peripheral chemoreceptors to increase breathing rate?

Back 553

1: A decrease in pO2
2:An increase in pCO2

Front 554

What happens to arterial pressure as you move down the lung?

Back 554

It increases due to hydrostatic pressure

Front 555

What stimulates the carotid bodies directly?

Back 555

Changes in H+ ions

Front 556

What is hypoxic vasoconstriction?

Back 556

Hypoxia causes vasoconstriction (unlike in other organs, where hypoxia causes vasodilation)
This directs blood away from poorly ventilated regions

Front 557

In metabolic acidosis, what happens to breathing rate?

Back 557

Increased, hyperventilation

B/c of increase in arterial H+ ions and pH decrease

Front 558

How much pulmonary vascular resistance is observed in the developing fetus?

Back 558

A lot
This is because of generalized hypoxic vasoconstriction
Therefore, blood flow through the fetal lungs is low

Front 559

When is breathing rate changed b/c of hypoxemic conditions?

Back 559

PO2 decrease to < 60mm Hg

Front 560

What happens to fetal lungs when the first breath begins?

Back 560

The alveoli become oxygenated
Pulmonary vascular resistance decreases
Pulmonary blood flow increases and becomes equal to cardiac output

Front 561

Where are the lung stretch receptors found?

Back 561

in the smooth muscle of airways

Front 562

What type of cardiac shunt is seen in tetralogy of Fallot?

Back 562

Right to left

Front 563

When the lung stretch receptors are stimulated by distention they produce a

Back 563

Reflex decrease in breathing frequency

Front 564

What is the effect of a right-to-left cardiac shunt upon arterial PO2?

Back 564

Decreases PO2 because there is mixture of venous and arterial blood

Front 565

What is the Hering-Breuer reflex?

Back 565

Reflexive decrease in breathing frequency when the lung stretch receptors are stimulated

Front 566

What type of cardiac shunt is most common and why?

Back 566

Left to right, because pressures are higher on the left side of the heart

Front 567

Where are J (Juxtacapillary) receptors located

Back 567

In the alveolar walls, close to the capillaries

Front 568

What is the effect of a left-to-right cardiac shunt upon arterial PO2?

Back 568

Arterial PO2 does not change
Venous blood PO2 increases because oxygenated blood is diverted to the right side of the heart

Front 569

What is the function of the J receptors?

Back 569

They cause rapid and shallow breathing, when pulmonary capillaries become engorged with blood, ie LHF

Front 570

What is the V/Q ratio?

Back 570

The ratio of alveolar ventilation to perfusion
Ideal exchange of O2 and CO2 depends upon ventilation and perfusion matching

Front 571

During exercise there is increase in O2 consumption and PCO2 production, how does the body compensate?

Back 571

By matching the ventilation rate

Front 572

What is the approximate V/Q ratio in a normal healthy patient

Back 572

0.8

Front 573

If you were sample in ABG during moderate exercise what would you expect and why?

Back 573

No change in PO2 or PCO2 in moderate
Matching of ventilation rate

Front 574

In what zone of the lung is ventilation the highest?

Back 574

zone 3

Front 575

What would you expect to find in the venous blood sample, CHEM 7, during moderate exercise?

Back 575

Venous PCO2 increases b/c of muscle CO2 production

Front 576

In what zone of the lung is V/Q highest? Lowest?

Back 576

Highest in zone 1
Lowest in zone 3

Front 577

How does the body respond in high altitude conditions

Back 577

PO2 is decreased so arterial PO2 is decreased in the high climate:
1:Hypoxemia stimulates the peripheral chemoreceptors
2:Hypoxemia stimulates EPO
3: 2,3 DPG concentrations are increased
4: Pulmonary vasoconstriction

Front 578

How does V/Q affect gas exchange in the different regions of the lungs?

Back 578

The apex (zone 1) has the highest V/Q, so there is more gas exchange. Therefore, PO2 is highest and PCO2 is lowest here
In the base (zone 3), V/Q is lower so there is less gas exchange, resulting in the lowest PO2 and highest PCO2

Front 579

Why does 2,3 DPG increase in High Altitudes?

Back 579

Help in dumping O2 to the tissues

Causes a right shift, 2,3 DPG binds with greater affinity and facilitates O2 unloading

Front 580

How does airway obstruction alter the V/Q ratio?

Back 580

V = 0, so V/Q = 0
This is a shunt

Front 581

What affect does EPO have on the blood?

Back 581

Increase RBC production, which increases Hg, increased O2 carrying capacity, increased O2 content

Front 582

What is the status of gas exchange in a region of the lung that is perfused but not ventilated?

Back 582

There is no gas exchange
V/Q = 0
Therefore, PO2 and PCO2 of the capillary blood approach their values in venous blood

Front 583

What is the response of the peripheral chemoreceptors in high altitude?

Back 583

increase ventilation rate, hyperventilation
Which produces respiratory alkalosis

Front 584

What happens to the A-a gradient if there is an airway obstruction?

Back 584

It increases because gas exchange is decreased

Front 585

What is treatment for respiratory alkalosis in high altitude

Back 585

Acetasolamide

Front 586

What happens to V/Q when there is a circulatory obstruction?

Back 586

This can happen in a pulmonary embolism
Q = 0, so V/Q is infinite
When V/Q is infinite, you have dead space

Front 587

What does pulmonary vasoconstriction due in to the heart in high altitude adjustment?

Back 587

Right ventricle hypertrophy
B/c an increase in pulmonary arterial pressure causes an increased work load of right side

Front 588

What are the PO2 and PCO2 values of alveolar gas when the lung is ventilated but not perfused?

Back 588

They approach their values in inspired air

Front 589

What part of the CNS contains the various centers that neurally control respiration?

Back 589

Sensory information (PCO2, lung stretch, irritants, etc) is coordinated in the brain stem
Brain stem output controls respiratory muscles and the breathing cycle

Front 590

What are the respiratory centers?

Back 590

Medullary respiratory center -- reticular formation
Apneustic center -- lower pons
Pneumotaxic center -- upper pons
Cerebral cortex

Front 591

What respiratory groups are found in the respiratory medullary centers?

Back 591

Dorsal respiratory group
Ventral respiratory group

Front 592

What does the dorsal respiratory group of the medullary respiratory center do?

Back 592

Responsible for inspiration
Generates the basic rhythm for breathing
Input to the DRG comes from the vagus (peripheral chemoreceptors, lung mechanoreceptors) and glossopharyngeal (peripheral chemoreceptors) nerves
Output from the DRG travels via the phrenic nerve to the diaphragm

Front 593

What does the ventral respiratory group of the medullary respiratory center do?

Back 593

Primarily responsible for active expiration
Not active during quiet breathing

Front 594

What does the apneustic center do?

Back 594

Stimulates deep and prolonged inspiratory gasps (apneusis)

Front 595

What does the pneumotaxic center do?

Back 595

Inhibits inspiration to regulate respiratory volume and respiration rate

Front 596

What does the cerebral cortex do (in the context of breathing)?

Back 596

Allows you to voluntarily control your breathing to a certain extent
Voluntary hypoventilation is limiting by increasing PCO2

Front 597

What are the types of chemoreceptors?

Back 597

Central chemoreceptors in the medulla
Peripheral chemoreceptors in the carotid and aortic bodies

Front 598

How do the central chemoreceptors work?

Back 598

Sensitive to the pH of the CSF
Decreased pH stimulates hyperventilation
Increased pH stimulates hypoventilation

Front 599

How is low pH detected in the CSF?

Back 599

H does not cross the blood-brain barrier very well, but CO2 does
In the CSF, CO2 reacts with water to give H and HCO3
It is this H that is detected by the central chemoreceptors

Front 600

How do the peripheral chemoreceptors work?

Back 600

Decreased arterial PO2 causes hyperventilation
Increased arterial PCO2 causes hyperventilation
Arterial H stimulates the carotid body receptors directly to cause hyperventilation

Front 601

In addition to chemoreceptors, what other types of sensory receptors are involved in the control of breathing?

Back 601

Lung stretch receptors
Irritant receptors
J (juxtacapillary receptors)
Joint and muscle receptors

Front 602

How do lung stretch receptors work?

Back 602

Found in the smooth muscle of the airways
When these receptors are stimulated by stretch, they decrease breathing frequency

Front 603

What is the Hering-Breuer reflex?

Back 603

Increased lung volume (stimulation of stretch receptors) causes a decrease in breathing frequency

Front 604

How do irritant receptors work?

Back 604

Found between airway epithelial cells
Stimulated by noxious substances

Front 605

How do J receptors work?

Back 605

Found in the alveolar walls
Engorgement of pulmonary capillaries stimulates them and causes rapid, shallow breathing

Front 606

How do the joint and muscle receptors work?

Back 606

They are activated during limb movement
Involved in the early stimulation of breathing during exercise

Front 607

What happens to gas exchange during exercise?

Back 607

Increased ventilatory rate, probably via joint and muscle receptors
This increases gas exchange in a given time period
Increased oxygen consumption
Increased CO2 production

Front 608

What happens to arterial and venous blood gas values during exercise?

Back 608

Mean arterial PO2 and PCO2 do not change
Arterial pH doesn't usually change, but severe exercise can cause lactic acidosis
Venous PCO2 increases because this is where exercise-produced CO2 is carried

Front 609

What happens to V/Q during exercise?

Back 609

Cardiac output increases and this increases pulmonary blood flow
More pulmonary capillaries are perfused and more gas exchange occurs
The distribution of V/Q throughout the lung becomes more even and there is a decrease in physiologic dead space

Front 610

What are some adaptations to high altitude?

Back 610

Decreased alveolar PO2, resulting in hypoxemia
Hypoxemia stimulates hyperventilation
Hypoxemia also stimulates RBC production, which increases the Hb concentratio in the blood
More 2,3-BPG is produced to right-shift the oxygen dissociation curve
Pulmonary vasoconstriction due to hypoxemia, causing increased pulmonary arterial pressure and hypertrophy of the right ventricle

Front 611

What is acetazolamide used for?

Back 611

Treatment of respiratory alkalosis from hyperventilation at high altitudes