[USMLE] Respiratory Physiology Flashcards

1
Q

the volume inspired or expired with each normal breath

A

Tidal volume (TV)

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2
Q

the volume that can be inspired over and above the tidal volume; used during exercise

A

Inspiratory reserve volume (IRV)

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3
Q

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

A

Expiratory reserve volume (ERV)

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4
Q

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

A

Residual volume (RV)

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5
Q

the volume of the conducting airways

A

Anatomic dead space

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6
Q

Anatomic dead space is normally approximately

A

150 mL

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7
Q

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

A

Physiologic dead space

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8
Q

Physiologic dead space is approximately equal to the anatomic dead space in

A

normal lungs

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9
Q

Physiologic dead space may be greater than the anatomic dead space in lung diseases in which there are

A

ventilation/perfusion (V/Q) defects

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10
Q

Physiologic dead space equation

A

In words, the equation states that physiologic dead space is tidal volume multiplied by a fraction. The fraction represents the dilution of alveolar PCO2 by dead-space air, which does not participate in gas exchange and does not therefore contribute CO2 to expired air.

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11
Q

Minute ventilation is expressed as

A

Minute ventilation = Tidal volume × Breaths min

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12
Q

Alveolar ventilation is expressed as

A

Alveolar ventilation = (Tidal volume − Dead space) × Breaths min

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13
Q

is the sum of tidal volume and IRV

A

Inspiratory capacity

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14
Q

is the sum of ERV and RV

A

Functional residual capacity (FRC)

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15
Q

the volume remaining in the lungs after a tidal volume is expired; includes the RV; cannot be measured by spirometry

A

FRC

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16
Q

sum of tidal volume, IRV, and ERV;

volume of air that can be forcibly expired after a maximal inspiration

A

Vital capacity (VC), or forced vital capacity (FVC)

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17
Q

sum of all four lung volumes;
volume in the lungs after a maximal inspiration;
includes RV, so it cannot be measured by spirometry

A

Total lung capacity (TLC)

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18
Q

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

A

FEV1

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19
Q

FEV1 is normally

A

80% of the forced vital capacity

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20
Q

FEV1 / FVC =

A

0.8

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21
Q

In obstructive lung disease, such as asthma, what happens to FEV1 and FVC

A

FEV1 is reduced more than FVC so that

FEV1/FVC is decreased

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22
Q

In restrictive lung disease, such as fibrosis, what happens to FEV1 and FVC

A

oth FEV1 and FVC are reduced and FEV1/FVC

is either normal or is increased

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23
Q

most important muscle for inspiration.

A

diaphragm

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24
Q

When the diaphragm contracts, the abdominal contents are

A

pushed downward

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25
Q

the ribs are lifted ____________

A

upward and outward

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26
Q

what happens to its volume

A

increases the volume of the thoracic cavity

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27
Q

are not used for inspiration during normal quiet breathing;

used during exercise and in respiratory distress

A

External intercostals and accessory muscles

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28
Q

Expiration is normally

A

passive

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29
Q

the lung-chest wall system is

A

elastic

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30
Q

it returns to its resting position after

A

inspiration

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31
Q

expiratory muscles are used during

A

exercise or when airway resistance in increased because of disease (asthma)

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32
Q

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

A

Abdominal muscles

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33
Q

Internal intercostal muscles pull the ribs

A

downward and inward

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34
Q

distensibility of the lungs and chest wall;

slope of the pressure–volume curve

A

Compliance of the respiratory system

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35
Q

Compliance of the respiratory system equation

A

C= V/P

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36
Q

Compliance of the respiratory system is inversely related to

A

elastance and stiffness

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37
Q

elastance depends on the amount of

A

elastic tissue

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38
Q

When the pressure outside of the lungs (i.e., intrapleural pressure) is negative,

A

the lungs expand and lung volume increases

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39
Q

When the pressure outside of the lungs is positive,

A

the lungs collapse and lung volume

decreases

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40
Q

the difference in the inflation of the lungs (inspiration) and the deflation of the lungs (expiration)

A

hysteresis

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41
Q

In the middle range of pressures, compliance is

A

greatest

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42
Q

In the middle range of pressures, lungs are

A

most distensible

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43
Q

At high expanding pressures, compliance is

A

lowest

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44
Q

At high expanding pressures, the lungs are

A

least distensible

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45
Q

At high expanding pressures, curve

A

flattens

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46
Q

at rest, lung volume is

A

at FRC

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47
Q

at rest, the pressure in the airways and lungs is

A

equal to atmospheric pressure (i.e. zero)

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48
Q

at equilibrium conditions, there is

A

a collapsing force on the lungs and an

expanding force on the chest wall

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49
Q

at FRC, these two forces are

A

equal and opposite

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50
Q

intrapleural pressure is negative

A

subatmospheric

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51
Q

intrapleural space

A

pneumothorax

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52
Q

If air is introduced into the intrapleural space (pneumothorax), the intrapleural pressure

A

becomes equal to atmospheric pressure

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53
Q

In a patient with emphysema, what happens to lung compliance and the tendency of the lungs

A

lung compliance is increased and the tendency of the

lungs to collapse is decreased

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54
Q

In a patient with fibrosis, what happens to lung compliance and the tendency of the lungs

A

lung compliance is decreased and the tendency of the lungs to collapse is increased

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55
Q

results from the attractive forces between liquid molecules lining the alveoli

A

Surface tension of the alveoli

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56
Q

collapsing pressure that is directly proportional to surface tension and inversely
proportional to alveolar radius

A

Laplace’s Law

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57
Q

Laplace’s Law equation

A

P= 2T / r

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58
Q

Large alveoli (large radii) have

A

low collapsing pressures and are easy to keep open

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59
Q

Small alveoli (small radii) have

A

high collapsing pressures and are more difficult to keep

open

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60
Q

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

A

collapse (atelactasis)

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61
Q

lines the alveoli

A

surfactant

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62
Q

by disrupting the intermolecular forces between liquid molecules

A

surface tension is reduced

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63
Q

This reduction in surface tension prevents small alveoli from

A

collapsing and increases compliance

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64
Q

surfactant is synthesized by

A

type II alveolar cells

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65
Q

surfactant consists primarily of the phospholipid

A

dipalmitoyl phosphatidylcholine (DPPC)

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66
Q

Surfactant may be present as early as gestational

week 24 and is almost always present by

A

week 35

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67
Q

can occur in premature infants because of the

lack of surfactant

A

Neonatal respiratory distress syndrome

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68
Q

atelectasis

A

lung collapse

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69
Q

difficulty reinflating the lungs

A

decreased compliance

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70
Q

hypoxemia

A

decreased V/Q

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71
Q

Airflow is driven by, and is directly proportional to the

A

pressure difference between the mouth

(or nose) and the alveoli

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72
Q

Airflow is inversely proportional to

A

airway resistance

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73
Q

airflow equation

A

Q= (delta P) / R

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74
Q

is described by Poiseuille’s law

A

Resistance of the airways

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75
Q

Resistance of the airways equation

A

R = (8nl) / (pi*r^4)

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76
Q

major site of airway resistance

A

medium-sized bronchi

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77
Q

smallest airways would seem to offer the

A

highest resistance, but they do not because of their parallel arrangement

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78
Q

changes airway resistance by altering the radius of the airways

A

Contraction or relaxation of bronchial smooth muscle

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79
Q

Parasympathetic stimulation relationship to airways, radius and resistance to flow

A

Parasympathetic stimulation, irritants, and the slow-reacting substance of anaphylaxis (asthma) constrict the airways, decrease the radius, and increase the
resistance to airflow

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80
Q

Sympathetic stimulation and sympathetic agonists (isoproterenol) relationship to airways, radius and resistance to flow

A

Sympathetic stimulation and sympathetic agonists (isoproterenol) dilate the airways via a2 receptors, increase the radius, and decrease the resistance to
airflow.

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81
Q

alters airway resistance because of the radial traction exerted on the airways by surrounding lung tissue

A

lung volume

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82
Q

High lung volumes are associated with

A

greater traction and decreased airway

resistance

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83
Q

Patients with increased airway resistance (e.g., asthma)

A

“learn” to breathe at higher lung volumes to offset the high airway resistance associated with their disease

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84
Q

Low lung volumes are associated with

A

less traction and increased airway resistance even to the point of airway collapse

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85
Q

During a deep-sea dive, what happens to air density and resistance to airflow

A

both increased

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86
Q

Breathing a low-density gas what happens to the resistance to airflow

A

reduced

87
Q

At rest (before inspiration begins), alveolar pressure

A

equals atmospheric pressure

88
Q

at rest, intrapleural pressure

A

negative

89
Q

lung volume is the

A

FRC

90
Q

during inspiration inspiratory muscles _____ and the volume of the thorax _____

A

contract;

increase

91
Q

As lung volume increases, what happens to alveolar pressure

A

alveolar pressure decreases to less than atmospheric

pressure (i.e., becomes negative)

92
Q

what causes air to flow into the lungs

A

pressure gradient between the atmosphere and the alveoli

93
Q

during inspiration, intrapleural pressure becomes

A

more negative

94
Q

Because lung volume increases during inspiration, the what happens to the elastic recoil strength

A

also increases

95
Q

At the peak of inspiration, lung volume is the

A

FRC plus one TV

96
Q

during expiiration, Alveolar pressure becomes

A

greater than atmospheric pressure

97
Q

alveolar gas is compressed by the

A

elastic forces of the lung

98
Q

during a forced expiration, intrapleural pressure actually becomes

A

positive

99
Q

positive intrapleural pressure

A

compresses the airways and makes expiration

more difficult

100
Q

In COPD, airway resistance is

A

increased

101
Q

during expiration, lung volume

A

returns to FRC

102
Q

is characterized by decreased FVC, decreased FEV1, and decreased FEV1/FVC

A

Asthma; COPD

103
Q

in asthma, air that should have been expired is not, leading to

A

air trapping and increased FRC

104
Q

COPD

A

obstructive disease; increased lung compliance

105
Q

in COPD, air that should have been expired is not, leading to

A

air trapping, increased FRC, and a

barrel-shaped chest

106
Q

“Pink puffers” (primarily emphysema)

A

mild hypoxemia and normocapnia (normal PCO2)

107
Q

“Blue bloaters” (primarily bronchitis)

A

severe hypoxemia with cyanosis and hypercapnia (increased PCO2)

108
Q

is characterized by a decrease in all lung volumes. Because FEV1 is decreased less than
FVC, FEV1/FVC is increased (or may be normal).

A

fibrosis

109
Q

Dalton’s law of partial pressures

A

Partialpressure = Totalpressure × Fractionalgas concentration

110
Q

In dry inspired air, the partial pressure of O2 can be calculated as

A

760 mmHg * 0.21

111
Q

In humidified tracheal air at 37°C, the calculation is modified to correct for the partial pressure of H2O, which is

A

47 mm Hg

112
Q

The amount of gas dissolved in a solution (such as blood) is

A

proportional to its partial pressure

113
Q

The diffusion rates of O2 and CO2 depend on the

A

partial pressure differences across the membrane and the area available for diffusion

114
Q

is illustrated by N2O and by O2 under normal conditions.

A

Perfusion-limited exchange

115
Q

In perfusion-limited exchange, the gas equilibrates early along the

A

length of the pulmonary capillary

116
Q

The partial pressure of the gas in arterial blood becomes

A

equal to the

partial pressure in alveolar air

117
Q

diffusion of the gas can be increased only if

A

blood flow increases

118
Q

Diffusion-limited exchange is illustrated by CO and by O2 during

A

strenuous exercise

119
Q

O2 is carried in blood in two forms:

A

dissolved or bound to hemoglobin (most important)

120
Q

Hemoglobin, at its normal concentration,

A

increases the O2-carrying capacity of blood 70-fold

121
Q

Each subunit of the hemoglobin contains a

A

heme moiety, which is iron-containing porphyrin

122
Q

normal adult hemoglobin

A

α2β2

123
Q

In fetal hemoglobin, the β chains are replaced by

A

gamma chains

124
Q

fetal hemoglobin is called

A

α2 gamma 2

125
Q

O2 affinity in adult and fetal

A

The O2 affinity of fetal hemoglobin is higher than the O2 affinity of adult hemoglobin (left-shift) because 2,3-diphosphoglycerate (DPG) binds less avidly

126
Q

causes sickle cell disease

A

Hemoglobin S

127
Q

maximum amount of O2 that can be bound to hemoglobin in blood

A

O2-binding capacity of blood

128
Q

total amount of O2 carried in blood, including bound and dissolved O2

A

O2 content of blood

129
Q

O2 content of blood equation

A

O2 content = (O2 binding capacity * % saturation) + Dissolved O2

130
Q

Hemoglobin combines rapidly and reversibly with O2 to form

A

xyhemoglobin

131
Q

the result of a change in the affinity of hemoglobin as

each successive O2 molecule binds to a heme site (called positive cooperativity)

A

sigmoid shape of the curve

132
Q

affinity for the fourth O2 molecule

A

highest

133
Q

Alveolar gas has a PO2 of

A

100 mmHg

134
Q

The very high affinity of hemoglobin for O2 at a PO2 of 100 mm Hg facilitates the

A

diffusion process

135
Q

The curve is almost flat when

A

PO2 is between 60 and 100 mm Hg

136
Q

when the affinity of hemoglobin for O2 is decreased

A

Shifts to the right

137
Q

during exercise, the tissues produce

A

CO2, which decreases tissue pH and, through the Bohr effect, stimulates O2 delivery to the exercising muscle

138
Q

Increases in temperature (e.g., during exercise)

A

shift the curve to the right

139
Q

Increases in 2,3-DPG concentration

A

shift the curve to the right by binding to the β chains of deoxyhemoglobin and decreasing the affinity of hemoglobin for O2

140
Q

affinity of hemoglobin for O2 is increased

A

shift to the left

141
Q

shift to the left causes

A

decreased PCO2, increased pH, decreased temperature, and decreased 2,3-DPG concentration

142
Q

Decreased binding of 2,3-DPG results in

A

ncreased affinity of HbF for O2, decreased P50, and a shift of the curve to the left

143
Q

decrease in arterial PO2

A

hypoxemia

144
Q

alveolar gas equation

A

PAO2 = P_I_O_{2} - (P_A_C_{O} / R)

145
Q

normal A–a gradient is

A

< 10 mm Hg

146
Q

A–a gradient is increased (>10 mm Hg) if

A

O2 does not equilibrate between alveolar gas and arterial blood (e.g., diffusion defect, V/Q defect, and right-to-left shunt)

147
Q

decreased O2 delivery to the tissues.

A

Hypoxia

148
Q

O2 delivery equation

A

O2 delivery = Cardiac output * O2 content of blood

149
Q

hypoxia can be caused by

A

decreased cardiac output, decreased O2-binding

capacity of hemoglobin, or decreased arterial PO2

150
Q

CO2 is produced in the tissues and carried to the lungs in the venous blood in three forms:

A

Dissolved CO2, Carbaminohemoglobin, HCO3

151
Q

site where CO2 is being added

A

capillaries

152
Q

transport of HCO3 as CO2 in the lungs

A

In the lungs, all of the above reactions occur in reverse. HCO3 – enters the RBCs in exchange for Cl–. HCO3 – recombines with H+ to form H2CO3, which decomposes into CO2 and H2O. Thus, CO2, originally generated in the tissues, is expired.

153
Q

H+ is buffered inside the RBCs by

A

deoxyhemoglobin

154
Q

pressure in pulmonary vs systemic circulation

A

Pressures are much lower in the pulmonary circulation than in the systemic circulation.

155
Q

resistance in pulmonary vs systemic circulation

A

Resistance is also much lower in the pulmonary circulation than in the systemic circulation

156
Q

Cardiac output of the right ventricle is

A

pulmonary blood flow.

157
Q

Cardiac output of the right ventricle =

A

cardiac output of the left ventricle

158
Q

When a person is supine, blood flow is

A

nearly uniform throughout the lung

159
Q

When a person is standing, blood flow is

A

unevenly distributed because of the effect of gravity

160
Q

Blood flow is lowest at

A

the apex of the lung (zone 1)

161
Q

Blood flow is highest at

A

the base of the lung (zone 3)

162
Q

why is blood flow lowest in zone 1?

A

Alveolar pressure > arterial pressure > venous pressure

The high alveolar pressure may compress the capillaries and reduce blood flow in zone. 1. This situation can occur if arterial blood pressure is decreased as a result of hemorrhage or if alveolar pressure is increased because of positive pressure ventilation.

163
Q

why is blood flow medium in zone 2?

A

Arterial pressure > alveolar pressure > venous pressure
Moving down the lung, arterial pressure progressively increases because of gravitational effects on hydrostatic pressure.

also, blood flow is driven by the difference between arterial pressure and alveolar pressure

164
Q

why is blood flow highest in zone 3?

A

Arterial pressure > venous pressure > alveolar pressure

Moving down toward the base of the lung, arterial pressure is highest because of gravitational effects, and venous pressure finally increases to the point where it exceeds alveolar pressure.

In zone 3, blood flow is driven by the difference between arterial and venous pressures, as in most vascular beds.

165
Q

In the lungs, hypoxia causes

A

vasoconstriction

166
Q

in other organs, hypoxia causes

A

vasodilation

167
Q

Fetal pulmonary vascular resistance is very high because of

A

generalized hypoxic vasoconstriction; as a result, blood flow through the fetal lungs is low.

With the first breath, the alveoli of the neonate are oxygenated, pulmonary vascular resistance decreases, and pulmonary blood flow increases and becomes equal to cardiac output (as occurs in the adult).

168
Q

Right-to-left shunts results in

A

a decrease in arterial PO2 because of the admixture of venous blood with arterial blood

169
Q

pressure are higher on which side of the heart

A

left

170
Q

is lowest at the apex and highest at the base because of gravitational effects

A

blood flow

171
Q

V/Q ratio is

A

higher at the apex of the lung and lower at the base of the lung

172
Q

At the apex (higher V/Q), PO2 is highest and PCO2 is lower because

A

gas exchange is more efficient

173
Q

At the base (lower V/Q), PO2 is lowest and PCO2 is higher because

A

gas exchange is less efficient

174
Q

If the airways are completely blocked (e.g., by a piece of steak caught in the trachea), then ventilation is

A

zero

175
Q

If blood flow is normal, then V/Q is

A

zero, which is called a shunt

176
Q

If blood flow to a lung is completely blocked (e.g., by an embolism occluding a pulmonary artery), then blood flow to that lung is

A

zero

177
Q

If ventilation is normal, then V/Q is

A

infinite, which is called dead space

178
Q

The PO2 and PCO2 of alveolar gas will approach their values in

A

inspired air

179
Q

Sensory information (PCO2, lung stretch, irritants, muscle spindles, tendons, and joints) is coordinated in the

A

brain stem

180
Q

Medullary respiratory center is located in the

A

retricular formation

181
Q

is primarily responsible for inspiration and generates the basic rhythm for breathing

A

Dorsal respiratory group

182
Q

Input to the dorsal respiratory group comes from what nerves

A

vagus and glossopharyngeal nerves

183
Q

The vagus nerve relays information from

A

peripheral chemoreceptors and mechanoreceptors in the lung

184
Q

The glossopharyngeal nerve relays information

from

A

peripheral chemoreceptors

185
Q

Output from the dorsal respiratory group travels, via the ____ to the diaphragm

A

phrenic nerve

186
Q

is primarily responsible for expiration

A

Ventral respiratory group

187
Q

Ventral respiratory group is not active during

A

normal, quiet breathing, when expiration is passive

188
Q

Ventral respiratory group is activated during

A

exercise, when expiration becomes an active

process

189
Q

is located in the lower pons

A

Apneustic center

190
Q

Apneustic center stimulates

A

inspiration

191
Q

Apneustic center produces

A

a deep and prolonged inspiratory gasp (apneusis)

192
Q

is located in the upper pons

A

Pneumotaxic center

193
Q

Pneumotaxic center inhibits

A

inspiration

194
Q

Pneumotaxic center regulates

A

inspiratory volume and respiratory rate

195
Q

is limited by the resulting increase in PCO2 and

decrease in PO2

A

Hypoventilation (breath-holding)

196
Q

Central chemoreceptors in the medulla are sensitive to the

A

pH of the cerebrospinal fluid (CSF)

197
Q

CO2 diffuses from arterial blood into the

A

CSF because CO2 is lipid-soluble and readily

crosses the blood–brain barrier

198
Q

The aortic bodies are located

A

above and below the aortic arch

199
Q

Decreases in arterial PO2 stimulate the peripheral chemoreceptors and

A

increase breathing rate

200
Q

Increases in arterial PCO2 stimulate peripheral chemoreceptors and

A

increase breathing rate

201
Q

In metabolic acidosis, breathing rate is

A

increased (hyperventilation) because arterial

[H+] is increased and pH is decreased

202
Q

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

A

reflex

decrease in breathing frequency (Hering–Breuer reflex)

203
Q

During exercise, what happens to the ventilatory rate?

A

increases

204
Q

what happens to the mean values for arterial PO2 and PCO2

A

do not change

205
Q

Arterial pH does not change during moderate exercise, although it may decrease during
strenuous exercise because of

A

lactic acidosis

206
Q

what happend to PCO2 during exercise?

A

increases; because the excess CO2 produced by the exercising muscle is carried to the lungs in venous blood

207
Q

Pulmonary blood flow increases because

A

cardiac output increases during exercise

208
Q

what happens to alveolar PO2 at high altitude

A

decreased; because the barometric pressure is decreased

209
Q

stimulates the peripheral chemoreceptors and increases the ventilation rate (hyperventilation) at high altitude

A

hypoxemia

210
Q

at high altitude, hyperventilation produces

A

respiratory alkalosis

211
Q

at high altitude, 2,3-DPG concentrations are

A

increased

212
Q

when 2,3-DPG concentrations are increased, the hemoglobin–O2 dissociation curve shifts

A

to the right

213
Q

an increase in pulmonary arterial pressure, increased work of the right side of the heart against the higher resistance, and hypertrophy of the right ventricle

A

Pulmonary vasoconstriction