[USMLE] Respiratory Physiology Flashcards
1
Q
the volume inspired or expired with each normal breath
A
Tidal volume (TV)
2
Q
the volume that can be inspired over and above the tidal volume; used during exercise
A
Inspiratory reserve volume (IRV)
3
Q
the volume that can be expired after the expiration of a tidal volume
A
Expiratory reserve volume (ERV)
4
Q
the volume that remains in the lungs after a maximal expiration; cannot be measured by spirometry
A
Residual volume (RV)
5
Q
the volume of the conducting airways
A
Anatomic dead space
6
Q
Anatomic dead space is normally approximately
A
150 mL
7
Q
the volume of the lungs that does not participate in gas exchange
A
Physiologic dead space
8
Q
Physiologic dead space is approximately equal to the anatomic dead space in
A
normal lungs
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
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.
11
Q
Minute ventilation is expressed as
A
Minute ventilation = Tidal volume × Breaths min
12
Q
Alveolar ventilation is expressed as
A
Alveolar ventilation = (Tidal volume − Dead space) × Breaths min
13
Q
is the sum of tidal volume and IRV
A
Inspiratory capacity
14
Q
is the sum of ERV and RV
A
Functional residual capacity (FRC)
15
Q
the volume remaining in the lungs after a tidal volume is expired; includes the RV; cannot be measured by spirometry
A
FRC
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)
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)
18
Q
volume of air that can be expired in the first second of a forced maximal expiration
A
FEV1
19
Q
FEV1 is normally
A
80% of the forced vital capacity
20
Q
FEV1 / FVC =
A
0.8
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
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
23
Q
most important muscle for inspiration.
A
diaphragm
24
Q
When the diaphragm contracts, the abdominal contents are
A
pushed downward
25
the ribs are lifted ____________
upward and outward
26
what happens to its volume
increases the volume of the thoracic cavity
27
are not used for inspiration during normal quiet breathing;
| used during exercise and in respiratory distress
External intercostals and accessory muscles
28
Expiration is normally
passive
29
the lung-chest wall system is
elastic
30
it returns to its resting position after
inspiration
31
expiratory muscles are used during
exercise or when airway resistance in increased because of disease (asthma)
32
compress the abdominal cavity, push the diaphragm up, and push air out of the lungs
Abdominal muscles
33
Internal intercostal muscles pull the ribs
downward and inward
34
distensibility of the lungs and chest wall;
| slope of the pressure–volume curve
Compliance of the respiratory system
35
Compliance of the respiratory system equation
C= V/P
36
Compliance of the respiratory system is inversely related to
elastance and stiffness
37
elastance depends on the amount of
elastic tissue
38
When the pressure outside of the lungs (i.e., intrapleural pressure) is negative,
the lungs expand and lung volume increases
39
When the pressure outside of the lungs is positive,
the lungs collapse and lung volume
| decreases
40
the difference in the inflation of the lungs (inspiration) and the deflation of the lungs (expiration)
hysteresis
41
In the middle range of pressures, compliance is
greatest
42
In the middle range of pressures, lungs are
most distensible
43
At high expanding pressures, compliance is
lowest
44
At high expanding pressures, the lungs are
least distensible
45
At high expanding pressures, curve
flattens
46
at rest, lung volume is
at FRC
47
at rest, the pressure in the airways and lungs is
equal to atmospheric pressure (i.e. zero)
48
at equilibrium conditions, there is
a collapsing force on the lungs and an
| expanding force on the chest wall
49
at FRC, these two forces are
equal and opposite
50
intrapleural pressure is negative
subatmospheric
51
intrapleural space
pneumothorax
52
If air is introduced into the intrapleural space (pneumothorax), the intrapleural pressure
becomes equal to atmospheric pressure
53
In a patient with emphysema, what happens to lung compliance and the tendency of the lungs
lung compliance is increased and the tendency of the
| lungs to collapse is decreased
54
In a patient with fibrosis, what happens to lung compliance and the tendency of the lungs
lung compliance is decreased and the tendency of the lungs to collapse is increased
55
results from the attractive forces between liquid molecules lining the alveoli
Surface tension of the alveoli
56
collapsing pressure that is directly proportional to surface tension and inversely
proportional to alveolar radius
Laplace's Law
57
Laplace's Law equation
P= 2T / r
58
Large alveoli (large radii) have
low collapsing pressures and are easy to keep open
59
Small alveoli (small radii) have
high collapsing pressures and are more difficult to keep
| open
60
In the absence of surfactant, the small alveoli have a tendency to
collapse (atelactasis)
61
lines the alveoli
surfactant
62
by disrupting the intermolecular forces between liquid molecules
surface tension is reduced
63
This reduction in surface tension prevents small alveoli from
collapsing and increases compliance
64
surfactant is synthesized by
type II alveolar cells
65
surfactant consists primarily of the phospholipid
dipalmitoyl phosphatidylcholine (DPPC)
66
Surfactant may be present as early as gestational
| week 24 and is almost always present by
week 35
67
can occur in premature infants because of the
| lack of surfactant
Neonatal respiratory distress syndrome
68
atelectasis
lung collapse
69
difficulty reinflating the lungs
decreased compliance
70
hypoxemia
decreased V/Q
71
Airflow is driven by, and is directly proportional to the
pressure difference between the mouth
| (or nose) and the alveoli
72
Airflow is inversely proportional to
airway resistance
73
airflow equation
Q= (delta P) / R
74
is described by Poiseuille’s law
Resistance of the airways
75
Resistance of the airways equation
R = (8*n*l) / (pi*r^4)
76
major site of airway resistance
medium-sized bronchi
77
smallest airways would seem to offer the
highest resistance, but they do not because of their parallel arrangement
78
changes airway resistance by altering the radius of the airways
Contraction or relaxation of bronchial smooth muscle
79
Parasympathetic stimulation relationship to airways, radius and resistance to flow
Parasympathetic stimulation, irritants, and the slow-reacting substance of anaphylaxis (asthma) constrict the airways, decrease the radius, and increase the
resistance to airflow
80
Sympathetic stimulation and sympathetic agonists (isoproterenol) relationship to airways, radius and resistance to flow
Sympathetic stimulation and sympathetic agonists (isoproterenol) dilate the airways via a2 receptors, increase the radius, and decrease the resistance to
airflow.
81
alters airway resistance because of the radial traction exerted on the airways by surrounding lung tissue
lung volume
82
High lung volumes are associated with
greater traction and decreased airway
| resistance
83
Patients with increased airway resistance (e.g., asthma)
“learn” to breathe at higher lung volumes to offset the high airway resistance associated with their disease
84
Low lung volumes are associated with
less traction and increased airway resistance even to the point of airway collapse
85
During a deep-sea dive, what happens to air density and resistance to airflow
both increased
86
Breathing a low-density gas what happens to the resistance to airflow
reduced
87
At rest (before inspiration begins), alveolar pressure
equals atmospheric pressure
88
at rest, intrapleural pressure
negative
89
lung volume is the
FRC
90
during inspiration inspiratory muscles _____ and the volume of the thorax _____
contract;
| increase
91
As lung volume increases, what happens to alveolar pressure
alveolar pressure decreases to less than atmospheric
| pressure (i.e., becomes negative)
92
what causes air to flow into the lungs
pressure gradient between the atmosphere and the alveoli
93
during inspiration, intrapleural pressure becomes
more negative
94
Because lung volume increases during inspiration, the what happens to the elastic recoil strength
also increases
95
At the peak of inspiration, lung volume is the
FRC plus one TV
96
during expiiration, Alveolar pressure becomes
greater than atmospheric pressure
97
alveolar gas is compressed by the
elastic forces of the lung
98
during a forced expiration, intrapleural pressure actually becomes
positive
99
positive intrapleural pressure
compresses the airways and makes expiration
| more difficult
100
In COPD, airway resistance is
increased
101
during expiration, lung volume
returns to FRC
102
is characterized by decreased FVC, decreased FEV1, and decreased FEV1/FVC
Asthma; COPD
103
in asthma, air that should have been expired is not, leading to
air trapping and increased FRC
104
COPD
obstructive disease; increased lung compliance
105
in COPD, air that should have been expired is not, leading to
air trapping, increased FRC, and a
| barrel-shaped chest
106
"Pink puffers” (primarily emphysema)
mild hypoxemia and normocapnia (normal PCO2)
107
“Blue bloaters” (primarily bronchitis)
severe hypoxemia with cyanosis and hypercapnia (increased PCO2)
108
is characterized by a decrease in all lung volumes. Because FEV1 is decreased less than
FVC, FEV1/FVC is increased (or may be normal).
fibrosis
109
Dalton’s law of partial pressures
Partialpressure = Totalpressure × Fractionalgas concentration
110
In dry inspired air, the partial pressure of O2 can be calculated as
760 mmHg * 0.21
111
In humidified tracheal air at 37°C, the calculation is modified to correct for the partial pressure of H2O, which is
47 mm Hg
112
The amount of gas dissolved in a solution (such as blood) is
proportional to its partial pressure
113
The diffusion rates of O2 and CO2 depend on the
partial pressure differences across the membrane and the area available for diffusion
114
is illustrated by N2O and by O2 under normal conditions.
Perfusion-limited exchange
115
In perfusion-limited exchange, the gas equilibrates early along the
length of the pulmonary capillary
116
The partial pressure of the gas in arterial blood becomes
equal to the
| partial pressure in alveolar air
117
diffusion of the gas can be increased only if
blood flow increases
118
Diffusion-limited exchange is illustrated by CO and by O2 during
strenuous exercise
119
O2 is carried in blood in two forms:
dissolved or bound to hemoglobin (most important)
120
Hemoglobin, at its normal concentration,
increases the O2-carrying capacity of blood 70-fold
121
Each subunit of the hemoglobin contains a
heme moiety, which is iron-containing porphyrin
122
normal adult hemoglobin
α2β2
123
In fetal hemoglobin, the β chains are replaced by
gamma chains
124
fetal hemoglobin is called
α2 gamma 2
125
O2 affinity in adult and fetal
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
causes sickle cell disease
Hemoglobin S
127
maximum amount of O2 that can be bound to hemoglobin in blood
O2-binding capacity of blood
128
total amount of O2 carried in blood, including bound and dissolved O2
O2 content of blood
129
O2 content of blood equation
O2 content = (O2 binding capacity * % saturation) + Dissolved O2
130
Hemoglobin combines rapidly and reversibly with O2 to form
xyhemoglobin
131
the result of a change in the affinity of hemoglobin as
| each successive O2 molecule binds to a heme site (called positive cooperativity)
sigmoid shape of the curve
132
affinity for the fourth O2 molecule
highest
133
Alveolar gas has a PO2 of
100 mmHg
134
The very high affinity of hemoglobin for O2 at a PO2 of 100 mm Hg facilitates the
diffusion process
135
The curve is almost flat when
PO2 is between 60 and 100 mm Hg
136
when the affinity of hemoglobin for O2 is decreased
Shifts to the right
137
during exercise, the tissues produce
CO2, which decreases tissue pH and, through the Bohr effect, stimulates O2 delivery to the exercising muscle
138
Increases in temperature (e.g., during exercise)
shift the curve to the right
139
Increases in 2,3-DPG concentration
shift the curve to the right by binding to the β chains of deoxyhemoglobin and decreasing the affinity of hemoglobin for O2
140
affinity of hemoglobin for O2 is increased
shift to the left
141
shift to the left causes
decreased PCO2, increased pH, decreased temperature, and decreased 2,3-DPG concentration
142
Decreased binding of 2,3-DPG results in
ncreased affinity of HbF for O2, decreased P50, and a shift of the curve to the left
143
decrease in arterial PO2
hypoxemia
144
alveolar gas equation
PAO2 = P_I_O_{2} - (P_A_C_{O} / R)
145
normal A–a gradient is
< 10 mm Hg
146
A–a gradient is increased (>10 mm Hg) if
O2 does not equilibrate between alveolar gas and arterial blood (e.g., diffusion defect, V/Q defect, and right-to-left shunt)
147
decreased O2 delivery to the tissues.
Hypoxia
148
O2 delivery equation
O2 delivery = Cardiac output * O2 content of blood
149
hypoxia can be caused by
decreased cardiac output, decreased O2-binding
| capacity of hemoglobin, or decreased arterial PO2
150
CO2 is produced in the tissues and carried to the lungs in the venous blood in three forms:
Dissolved CO2, Carbaminohemoglobin, HCO3
151
site where CO2 is being added
capillaries
152
transport of HCO3 as CO2 in the lungs
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
H+ is buffered inside the RBCs by
deoxyhemoglobin
154
pressure in pulmonary vs systemic circulation
Pressures are much lower in the pulmonary circulation than in the systemic circulation.
155
resistance in pulmonary vs systemic circulation
Resistance is also much lower in the pulmonary circulation than in the systemic circulation
156
Cardiac output of the right ventricle is
pulmonary blood flow.
157
Cardiac output of the right ventricle =
cardiac output of the left ventricle
158
When a person is supine, blood flow is
nearly uniform throughout the lung
159
When a person is standing, blood flow is
unevenly distributed because of the effect of gravity
160
Blood flow is lowest at
the apex of the lung (zone 1)
161
Blood flow is highest at
the base of the lung (zone 3)
162
why is blood flow lowest in zone 1?
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
why is blood flow medium in zone 2?
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
why is blood flow highest in zone 3?
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
In the lungs, hypoxia causes
vasoconstriction
166
in other organs, hypoxia causes
vasodilation
167
Fetal pulmonary vascular resistance is very high because of
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
Right-to-left shunts results in
a decrease in arterial PO2 because of the admixture of venous blood with arterial blood
169
pressure are higher on which side of the heart
left
170
is lowest at the apex and highest at the base because of gravitational effects
blood flow
171
V/Q ratio is
higher at the apex of the lung and lower at the base of the lung
172
At the apex (higher V/Q), PO2 is highest and PCO2 is lower because
gas exchange is more efficient
173
At the base (lower V/Q), PO2 is lowest and PCO2 is higher because
gas exchange is less efficient
174
If the airways are completely blocked (e.g., by a piece of steak caught in the trachea), then ventilation is
zero
175
If blood flow is normal, then V/Q is
zero, which is called a shunt
176
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
zero
177
If ventilation is normal, then V/Q is
infinite, which is called dead space
178
The PO2 and PCO2 of alveolar gas will approach their values in
inspired air
179
Sensory information (PCO2, lung stretch, irritants, muscle spindles, tendons, and joints) is coordinated in the
brain stem
180
Medullary respiratory center is located in the
retricular formation
181
is primarily responsible for inspiration and generates the basic rhythm for breathing
Dorsal respiratory group
182
Input to the dorsal respiratory group comes from what nerves
vagus and glossopharyngeal nerves
183
The vagus nerve relays information from
peripheral chemoreceptors and mechanoreceptors in the lung
184
The glossopharyngeal nerve relays information
| from
peripheral chemoreceptors
185
Output from the dorsal respiratory group travels, via the ____ to the diaphragm
phrenic nerve
186
is primarily responsible for expiration
Ventral respiratory group
187
Ventral respiratory group is not active during
normal, quiet breathing, when expiration is passive
188
Ventral respiratory group is activated during
exercise, when expiration becomes an active
| process
189
is located in the lower pons
Apneustic center
190
Apneustic center stimulates
inspiration
191
Apneustic center produces
a deep and prolonged inspiratory gasp (apneusis)
192
is located in the upper pons
Pneumotaxic center
193
Pneumotaxic center inhibits
inspiration
194
Pneumotaxic center regulates
inspiratory volume and respiratory rate
195
is limited by the resulting increase in PCO2 and
| decrease in PO2
Hypoventilation (breath-holding)
196
Central chemoreceptors in the medulla are sensitive to the
pH of the cerebrospinal fluid (CSF)
197
CO2 diffuses from arterial blood into the
CSF because CO2 is lipid-soluble and readily
| crosses the blood–brain barrier
198
The aortic bodies are located
above and below the aortic arch
199
Decreases in arterial PO2 stimulate the peripheral chemoreceptors and
increase breathing rate
200
Increases in arterial PCO2 stimulate peripheral chemoreceptors and
increase breathing rate
201
In metabolic acidosis, breathing rate is
increased (hyperventilation) because arterial
| [H+] is increased and pH is decreased
202
When lung stretch receptors are stimulated by distention of the lungs, they produce a
reflex
| decrease in breathing frequency (Hering–Breuer reflex)
203
During exercise, what happens to the ventilatory rate?
increases
204
what happens to the mean values for arterial PO2 and PCO2
do not change
205
Arterial pH does not change during moderate exercise, although it may decrease during
strenuous exercise because of
lactic acidosis
206
what happend to PCO2 during exercise?
increases; because the excess CO2 produced by the exercising muscle is carried to the lungs in venous blood
207
Pulmonary blood flow increases because
cardiac output increases during exercise
208
what happens to alveolar PO2 at high altitude
decreased; because the barometric pressure is decreased
209
stimulates the peripheral chemoreceptors and increases the ventilation rate (hyperventilation) at high altitude
hypoxemia
210
at high altitude, hyperventilation produces
respiratory alkalosis
211
at high altitude, 2,3-DPG concentrations are
increased
212
when 2,3-DPG concentrations are increased, the hemoglobin–O2 dissociation curve shifts
to the right
213
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
Pulmonary vasoconstriction
