Respiratory Physiology

Question 1

1. Which of the following lung volumes or capacities can be measured by spirometry?

(A) Functional residual capacity (FRC) (B) Physiologic dead space
(C) Residual volume (RV)
(D) Total lung capacity (TLC)
(E) Vital capacity (VC)

Answer 1

E. Residual volume (RV) cannot be measured by spirometry.  Therefore, any lung volume or capacity that includes the RV cannot be measured by spirometry. Measurements that include RV are functional residual capacity (FRC) and total lung capacity (TLC).  
Vital capacity (VC) does not include RV and is, therefore, measurable by spirometry. 
Physiologic dead space is not measurable by spirometry and requires sampling of arterial PCO2 and expired CO2.

Question 2

2. An infant born prematurely in gestational week 25 has neonatal respiratory distress syndrome. Which of the following would be expected in this infant?

(A) Arterial PO2 of 100 mm Hg 
(B) Collapse of the small alveoli 
(C) Increased lung compliance 
(D) Normal breathing rate 
(E) Lecithin:sphingomyelin ratio of greater than 2:1 in amniotic fluid

Answer 2

B. Neonatal respiratory distress syndrome is caused by lack of adequate surfactant in the immature lung. Surfactant appears between the 24th and the 35th gestational week. In the absence of surfactant, the surface tension of the small alveoli is too high.
When the pressure on the small alveoli is too high (P = 2T/r), the small alveoli collapse into larger alveoli. There is decreased gas exchange with the larger, collapsed alveoli, and ventilation/perfusion (V/Q) mismatch, hypoxemia, and cyanosis occur.
The lack of surfactant also decreases lung compliance, making it harder to inflate the lungs, increasing the work of breathing, and producing dyspnea (shortness of breath).
Generally, lecithin:sphingomyelin ratios greater than 2:1 signify mature levels of surfactant.

Question 3

3. In which vascular bed does hypoxia cause vasoconstriction?

(A) Coronary
(B) Pulmonary 
(C) Cerebral 
(D) Muscle 
(E) Skin

Answer 3

B. Pulmonary blood flow is controlled locally by the PO2 of alveolar air. Hypoxia causes pulmonary vasoconstriction and thereby shunts blood away from unventilated areas of the lung, where it would be wasted.
In the coronary circulation, hypoxemia causes vasodilation.
The cerebral, muscle, and skin circulations are not controlled directly by PO2.

Question 4

A 12-year-old boy has a severe asthmatic attack with wheezing. He experiences rapid breathing and becomes cyanotic. His arterial PO2 is 60 mm Hg and his PCO2 is 30 mm Hg.

4. Which of the following statements about this patient is most likely to be true?

(A) Forced expiratory volume/forced vital capacity (FEV1/FVC) is increased (B) Ventilation/perfusion (V/Q) ratio is increased in the affected areas of his lungs
(C) His arterial PCO2 is higher than normal because of inadequate gas exchange
(D) His arterial PCO2 is lower than normal because hypoxemia is causing him to hyperventilate
(E) His residual volume (RV) is decreased

Answer 4

D. The patient’s arterial PCO2 is lower than the normal value of 40 mm Hg because hypoxemia has stimulated peripheral chemoreceptors to increase his breathing rate; hyperventilation causes the patient to blow off extra CO2 and results in respiratory alkalosis.
In an obstructive disease, such as asthma, both forced expiratory volume (FEV1) and forced vital capacity (FVC) are decreased, with the larger decrease occurring in FEV1. Therefore, the FEV1/FVC ratio is decreased.
Poor ventilation of the affected areas decreases the ventilation/perfusion (V/Q) ratio and causes hypoxemia.
The patient’s residual volume (RV) is increased because he is breathing at a higher lung volume to offset the increased resistance of his airways.

Question 5

A 12-year-old boy has a severe asthmatic attack with wheezing. He experiences rapid breathing and becomes cyanotic. His arterial PO2 is 60 mm Hg and his PCO2 is 30 mm Hg.

5. To treat this patient, the physician should administer

(A) an  α1-adrenergic antagonist 
(B) a  β1-adrenergic antagonist 
(C) a  β2-adrenergic agonist 
(D) a muscarinic agonist 
(E) a nicotinic agonist

Answer 5

C. A cause of airway obstruction in asthma is bronchiolar constriction. β2-adrenergic stimulation (β2-adrenergic agonists) produces relaxation of the bronchioles.

Question 6

6. Which of the following is true during inspiration?

(A) Intrapleural pressure is positive
(B) The volume in the lungs is less than the functional residual capacity (FRC) (C) Alveolar pressure equals atmospheric pressure
(D) Alveolar pressure is higher than atmospheric pressure
(E) Intrapleural pressure is more negative than it is during expiration

Answer 6

E. During inspiration, intrapleural pressure becomes more negative than it is at rest or during expiration (when it returns to its less negative resting value).
During inspiration, air flows into the lungs when alveolar pressure becomes lower (due to contraction of the diaphragm) than atmospheric pressure; if alveolar pressure were not lower than atmospheric pressure, air would not flow inward.
The volume in the lungs during inspiration is the functional residual capacity (FRC) plus one tidal volume (TV).

Question 7

7. Which volume remains in the lungs after a tidal volume (TV) is expired?

(A) Tidal volume (TV)
(B) Vital capacity (VC)
(C) Expiratory reserve volume (ERV) (D) Residual volume (RV)
(E) Functional residual capacity (FRC) (F) Inspiratory capacity
(G) Total lung capacity

Answer 7

E. During normal breathing, the volume inspired and then expired is a tidal volume (TV). The volume remaining in the lungs after expiration of a TV is the functional residual capacity (FRC).

Question 8

8. A 35-year-old man has a vital capacity (VC) of 5 L, a tidal volume (TV) of 0.5 L, an inspiratory capacity of 3.5 L, and a functional residual capacity (FRC) of 2.5 L. What is his expiratory reserve volume (ERV)?

(A) 4.5 L 
(B) 3.9 L 
(C) 3.6 L 
(D) 3.0 L 
(E) 2.5 L 
(F) 2.0 L 
(G) 1.5 L

Answer 8

G. Expiratory reserve volume (ERV) equals vital capacity (VC) minus inspiratory capacity. [Inspiratory capacity includes tidal volume (TV) and inspiratory reserve volume (IRV)].

Question 9

11. Which of the following is the site of highest airway resistance?

(A) Trachea 
(B) Largest bronchi 
(C) Medium-sized bronchi 
(D) Smallest bronchi 
(E) Alveoli

Answer 9

C. The medium-sized bronchi actually constitute the site of highest resistance along the bronchial tree. Although the small radii of the alveoli might predict that they would have the highest resistance, they do not because of their parallel arrangement. In fact, early changes in resistance in the small airways may be “silent” and go undetected because of their small overall contribution to resistance.

Question 10

9. When a person is standing, blood flow in the lungs is

(A) equal at the apex and the base
(B) highest at the apex owing to the effects of gravity on arterial pressure (C) highest at the base because that is where the difference between arterial and venous pressure is greatest
(D) lowest at the base because that is where alveolar pressure is greater than arterial pressure

Answer 10

C. The distribution of blood flow in the lungs is affected by gravitational effects on arterial hydrostatic pressure. Thus, blood flow is highest at the base, where arterial hydrostatic pressure is greatest and the difference between arterial and venous pressure is also greatest. This pressure difference drives the blood flow.

Question 11

12. A 49-year-old man has a pulmonary embolism that completely blocks blood flow to his left lung. As a result, which of the following will occur?

(A) Ventilation/perfusion (V/Q) ratio in the left lung will be zero
(B) Systemic arterial PO2 will be elevated
(C) V/Q ratio in the left lung will be lower than in the right lung
(D) Alveolar PO2 in the left lung will be approximately equal to the PO2 in inspired air
(E) Alveolar PO2 in the right lung will be approximately equal to the PO2 in venous blood

Answer 11

D. Alveolar PO2 in the left lung will equal the PO2 in inspired air. Because there is no blood flow to the left lung, there can be no gas exchange between the alveolar air and the pulmonary capillary blood. Consequently, O2 is not added to the capillary blood.
The ventilation/perfusion (V/Q) ratio in the left lung will be infinite (not zero or lower than that in the normal right lung) because Q (the denominator) is zero.
Systemic arterial PO2 will, of course, be decreased because the left lung has no gas exchange.
Alveolar PO2 in the right lung is unaffected.

Question 12

15. Which volume remains in the lungs after a maximal expiration?

(A) Tidal volume (TV)
(B) Vital capacity (VC)
(C) Expiratory reserve volume (ERV) (D) Residual volume (RV)
(E) Functional residual capacity (FRC) (F)Inspiratory capacity
(G) Total lung capacity

Answer 12

D. During a forced maximal expiration, the volume expired is a tidal volume (TV) plus the expiratory reserve volume (ERV). The volume remaining in the lungs is the residual volume (RV).

Question 13

16. Compared with the systemic circulation, the pulmonary circulation has a

(A) higher blood flow 
(B) lower resistance 
(C) higher arterial pressure 
(D) higher capillary pressure 
(E) higher cardiac output

Answer 13

B. Blood flow (or cardiac output) in the systemic and pulmonary circulations is nearly equal; pulmonary flow is slightly less than systemic flow because about 2% of the systemic cardiac output bypasses the lungs. The pulmonary circulation is characterized by both lower pressure and lower resistance than the systemic circulation, so flows through the two circulations are approximately equal (flow = pressure/resistance).

Question 14

17. A healthy 65-year-old man with a tidal volume (TV) of 0.45 L has a breathing frequency of 16 breaths/min. His arterial PCO2 is 41 mm Hg, and the PCO2 of his expired air is 35 mm Hg. What is his alveolar ventilation?

(A) 0.066 L/min 
(B) 0.38 L/min 
(C) 5.0 L/min 
(D) 6.14 L/min 
(E) 8.25 L/min

Answer 14

D. Alveolar ventilation is the difference between tidal volume (TV) and dead space multiplied by breathing frequency.
TV and breathing frequency are given, but dead space must be calculated.
Dead space is TV multiplied by the difference between arterial PCO2 and expired PCO2 divided by arterial PCO2. Thus: dead space = 0.45 × (41 –35/41) = 0.066 L.
Alveolar ventilation is then calculated as: (0.45 L –0.066 L) × 16 breaths/min = 6.14 L/min.

Question 15

18. Compared with the apex of the lung, the base of the lung has

(A) a higher pulmonary capillary PO2 (B) a higher pulmonary capillary PCO2 (C) a higher ventilation/perfusion (V/Q) ratio
(D) the same V/Q ratio

Answer 15

B. Ventilation and perfusion of the lung are not distributed uniformly. Both are lowest at the apex and highest at the base.
However, the differences for ventilation are not as great as for perfusion, making the ventilation/perfusion (V/Q) ratios higher at the apex and lower at the base. As a result, gas exchange is more efficient at the apex and less efficient at the base.
Therefore, blood leaving the apex will have a higher PO2 and a lower PCO2 because it is better equilibrated with alveolar air.

Question 16

19. Hypoxemia produces hyperventilation by a direct effect on the

(A) phrenic nerve 
(B) J receptors 
(C) lung stretch receptors 
(D) medullary chemoreceptors 
(E) carotid and aortic body chemoreceptors

Answer 16

E. Hypoxemia stimulates breathing by a direct effect on the peripheral chemoreceptors in the carotid and aortic bodies.
Central (medullary) chemoreceptors are stimulated by CO2 (or H+).
The J receptors and lung stretch receptors are not chemoreceptors. The phrenic nerve innervates the diaphragm, and its activity is determined by the output of the brain stem breathing center.

Question 17

20. Which of the following changes occurs during strenuous exercise?

(A) Ventilation rate and O2 consumption increase to the same extent
(B) Systemic arterial PO2 decreases to about 70 mm Hg
(C) Systemic arterial PCO2 increases to about 60 mm Hg
(D) Systemic venous PCO2 decreases to about 20 mm Hg
(E) Pulmonary blood flow decreases at the expense of systemic blood flow

Answer 17

A. During exercise, the ventilation rate increases to match the increased O2 consumption and CO2 production.
This matching is accomplished without a change in mean arterial PO2 or PCO2.
Venous PCO2 increases because extra CO2 is being produced by the exercising muscle. Because this CO2 will be blown off by the hyperventilating lungs, it does not increase the arterial PCO2.
Pulmonary blood flow (cardiac output) increases manyfold during strenuous exercise.

Question 18

21. If an area of the lung is not ventilated because of bronchial obstruction, the pul monary capillary blood serving that area will have a PO2 that is

(A) equal to atmospheric PO2 
(B) equal to mixed venous PO2 
(C) equal to normal systemic arterial PO2 
(D) higher than inspired PO2 
(E) lower than mixed venous PO2

Answer 18

B. If an area of lung is not ventilated, there can be no gas exchange in that region. The pulmonary capillary blood serving that region will not equilibrate with alveolar PO2, but will have a PO2 equal to that of mixed venous blood.

Question 19

22. In the transport of CO2 from the tissues to the lungs, which of the following occurs in venous blood?

(A) Conversion of CO2 and H2O to H+ and HCO3–in the red blood cells (RBCs)
(B) Buffering of H+ by oxyhemoglobin (C) Shifting of HCO3–into the RBCs from plasma in exchange for Cl
(D) Binding of HCO3–to hemoglobin (E) Alkalinization of the RBCs

Answer 19

A. CO2 generated in the tissues is hydrated to form H+ and HCO3–in red blood cells (RBCs).
H+ is buffered inside the RBCs by deoxyhemoglobin, which acidifies the RBCs.
HCO3–leaves the RBCs in exchange for Cl–and is carried to the lungs in the plasma.
A small amount of CO2 (not HCO3–) binds directly to hemoglobin (carbaminohemoglobin).

Question 20

23. Which of the following causes of hypoxia is characterized by a decreased arterial PO2 and an increased A–a gradient?

(A) Hypoventilation 
(B) Right-to-left cardiac shunt 
(C) Anemia 
(D) Carbon monoxide poisoning 
(E) Ascent to high altitude

Answer 20

B. Hypoxia is defined as decreased O2 delivery to the tissues. It occurs as a result of decreased blood flow or decreased O2 content of the blood. Decreased O2 content of the blood is caused by decreased hemoglobin concentration (anemia), decreased O2-binding capacity of hemoglobin (carbon monoxide poisoning), or decreased arterial PO2 (hypoxemia). Hypoventilation, right-to-left cardiac shunt, and ascent to high altitude all cause hypoxia by decreasing arterial PO2. Of these, only right-to-left cardiac shunt is associated with an increased A–a gradient, reflecting a lack of O2 equilibration between alveolar gas and systemic arterial blood. In right-to-left shunt, a portion of the right heart output, or pulmonary blood flow, is not oxygenated in the lungs and thereby “dilutes” the PO2 of the normally oxygenated blood.
With hypoventilation and ascent to high altitude, both alveolar and arterial PO2 are decreased, but the A–a gradient is normal.

Question 21

24. A 42-year-old woman with severe pulmonary fibrosis is evaluated by her physician and has the following arterial blood gases: pH = 7.48, PaO2 = 55 mm Hg, and PaCO2 = 32 mm Hg. Which statement best explains the observed value of PaCO2?

(A) The increased pH stimulates breathing via peripheral chemoreceptors
(B) The increased pH stimulates breathing via central chemoreceptors (C) The decreased PaO2 inhibits breathing via peripheral chemoreceptors
(D) The decreased PaO2 stimulates breathing via peripheral chemoreceptors
(E) The decreased PaO2 stimulates breathing via central chemoreceptors

Answer 21

D. The patient’s arterial blood gases show increased pH, decreased PaO2, and decreased PaCO2. The decreased PaO2 causes hyperventilation (stimulates breathing) via the peripheral chemoreceptors, but not via the central chemoreceptors. The decreased PacO2 results from hyperventilation (increased breathing) and causes increased pH, which inhibits breathing via the peripheral and central chemoreceptors.

Question 22

25. A 38-year-old woman moves with her family from New York City (sea level) to Leadville Colorado (10,200 feet above sea level). Which of the following will occur as a result of residing at high altitude?

(A) Hypoventilation
(B) Arterial PO2 greater than 100 mm Hg
(C) Decreased 2,3-diphosphoglycerate (DPG) concentration
(D) Shift to the right of the hemoglobin–O2 dissociation curve
(E) Pulmonary vasodilation
(F) Hypertrophy of the left ventricle
(G) Respiratory acidosis

Answer 22

D. At high altitudes, the PO2 of alveolar air is decreased because barometric pressure is decreased. As a result, arterial PO2 is decreased (<100 mm Hg), and hypoxemia occurs and causes hyperventilation by an effect on peripheral chemoreceptors.
Hyperventilation leads to respiratory alkalosis.
2,3-Diphosphoglycerate (DPG) levels increase adaptively;
2,3-DPG binds to hemoglobin and causes the hemoglobin–O2 dissociation curve to shift to the right to improve unloading of O2 in the tissues.
The pulmonary vasculature vasoconstricts in response to alveolar hypoxia, resulting in increased pulmonary arterial pressure and hypertrophy of the right ventricle (not the left ventricle).

Question 23

26. The pH of venous blood is only slightly more acidic than the pH of arterial blood because

(A) CO2 is a weak base
(B) there is no carbonic anhydrase in venous blood
(C) the H+ generated from CO2 and H2O is buffered by HCO3–in venous blood
(D) the H+ generated from CO2 and H2O is buffered by deoxyhemoglobin in venous blood
(E) oxyhemoglobin is a better buffer for H+ than is deoxyhemoglobin

Answer 23

D. In venous blood, CO2 combines with H2O and produces the weak acid H2CO3, catalyzed by carbonic anhydrase. The resulting H+ is buffered by deoxyhemoglobin, which is such an effective buffer for H+ (meaning that the pK is within 1.0 unit of the pH of blood) that the pH of venous blood is only slightly more acid than the pH of arterial blood. Oxyhemoglobin is a less effective buffer than deoxyhemoglobin.

Question 24

27. In a maximal expiration, the total volume expired is

(A) tidal volume (TV)
(B) vital capacity (VC)
(C) expiratory reserve volume (ERV) (D) residual volume (RV)
(E) functional residual capacity (FRC) (F) inspiratory capacity
(G) total lung capacity

Answer 24

B. The volume expired in a forced maximal expiration is forced vital capacity, or vital capacity (VC).

Question 25

28. A person with a ventilation/perfusion (V/Q) defect has hypoxemia and is treated with supplemental O2. The supplemental O2 will be most helpful if the person’s predominant V/Q defect is

(A) dead space 
(B) shunt 
(C) high V/Q 
(D) low V/Q 
(E) V/Q = 0 
(F) V/Q = ×

Answer 25

D. Supplemental O2 (breathing inspired air with a high PO2) is most helpful in treating hypoxemia associated with a ventilation/perfusion (V/Q) defect if the predominant defect is low  V/Q. Regions of low  V/Q have the highest blood flow.  Thus, breathing high PO2 air will raise the PO2 of a large volume of blood and have the greatest influence on the total blood flow leaving the lungs (which becomes systemic arterial blood). 
Dead space (i.e.,  V/Q =  ∞ has no blood flow, so supplemental O2 has no effect on these regions. 
Shunt (i.e.,  V/Q = 0) has no ventilation, so supplemental O2 has no effect. 
Regions of high  V/Q have little blood flow, thus raising the PO2 of a small volume of blood will have little overall effect on systemic arterial blood.

Question 26

29. Which person would be expected to have the largest A–a gradient?

(A) Person with pulmonary fibrosis
(B) Person who is hypoventilating due to morphine overdose
(C) Person at 12,000 feet above sea level
(D) Person with normal lungs breathing 50% O2
(E) Person with normal lungs breathing 100% O2

Answer 26

A. Increased A–a gradient signifies lack of O2 equilibration between alveolar gas (A) and systemic arterial blood (a).
In pulmonary fibrosis, there is thickening of the alveolar/pulmonary capillary barrier and increased diffusion distance for O2, which results in lack of equilibration of O2, hypoxemia, and increased A–a gradient.
Hypoventilation and ascent to 12,000 feet also cause hypoxemia, because systemic arterial blood is equilibrated with a lower alveolar PO2 (normal A–a gradient).
Persons breathing 50% or 100% O2 will have elevated alveolar PO2, and their arterial PO2 will equilibrate with this higher value (normal A–a gradient).