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Lung Volumes and Capacities
Measurable by Spirometry
Respiratory Physiology MCQ (Respiratory)
Questions with Answers and Explanations 2023/
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: (E) Vital capacity (VC) Explanation: 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.
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: (B) Collapse of the small alveoli Explanation: Neonatal respiratory distress syndrome is characterized by the lack of surfactant, which leads to the collapse of small alveoli (atelectasis). This results in decreased lung compliance, hypoxemia, and increased work of breathing. The other options are not typical findings in neonatal respiratory distress syndrome.
In which vascular bed does hypoxia cause vasoconstriction? (A) Coronary (B) Pulmonary (C) Cerebral (D) Muscle (E) Skin
Answer: (B) Pulmonary Explanation: Hypoxia causes vasoconstriction in the pulmonary vascular bed, which is a unique response compared to the vasodilation seen in other vascular beds (coronary, cerebral, muscle, and skin) in response to hypoxia.
Questions 4 and 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.
Which of the following statements about this patient is most likely to be true? (A) Forced expiratory volume1/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: (D) His arterial PCO2 is lower than normal because hypoxemia is causing him to hyperventilate Explanation: During an asthmatic attack, the airways become constricted, leading to ventilation- perfusion (V/Q) mismatch and hypoxemia. The hypoxemia stimulates the respiratory center, causing the patient to hyperventilate, which leads to a lower-than-normal arterial PCO2.
To treat this patient, the physician should administer (A) an Ī±1- adrenergic antagonist (B) a Ī²1-adrenergic antagonist (C) a Ī²2- adrenergic agonist (D) a muscarinic agonist (E) a nicotinic agonist
Answer: (C) a Ī²2-adrenergic agonist Explanation: The appropriate treatment for an acute asthmatic attack is the administration of a Ī²2- adrenergic agonist, which helps to relax the bronchial smooth muscle and improve airflow.
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: (E) Intrapleural pressure is more negative than it is during expiration Explanation: During inspiration, the diaphragm and intercostal muscles contract, causing the intrapleural pressure to become more negative, which in turn leads to an increase in lung volume and a decrease in alveolar pressure below atmospheric pressure.
Which volume remains in the lungs after a tidal volume (VT) is expired? (A) Tidal volume (VT) (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: (D) Residual volume (RV) Explanation: After a tidal volume (VT) is expired, the residual volume (RV) remains in the lungs. RV is the volume of air that remains in the lungs after a maximal expiration.
A 35-year-old man has a vital capacity (VC) of 5 L, a tidal volume (VT) 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: (D) 3.0 L Explanation: Expiratory reserve volume (ERV) can be calculated as the difference between the vital capacity (VC) and the sum of
affected lung. This will lead to a decrease in the overall systemic arterial PO2.
Questions 13 and 14:
In the hemoglobināO2 dissociation curves shown above, the shift from curve A to curve B could be caused by (A) increased pH (B) decreased 2,3-diphosphoglycerate (DPG) concentration (C) strenuous exercise (D) fetal hemoglobin (HbF) (E) carbon monoxide (CO) poisoning
Answer: (B) decreased 2,3-diphosphoglycerate (DPG) concentration Explanation: A shift from curve A to curve B represents an increase in the affinity of hemoglobin for oxygen, which can be caused by a decrease in 2,3-diphosphoglycerate (DPG) concentration.
The shift from curve A to curve B is associated with (A) increased P50 (B) increased affinity of hemoglobin for O2 (C) impaired ability to unload O2 in the tissues (D) increased O2-carrying capacity of hemoglobin (E) decreased O2-carrying capacity of hemoglobin
Answer: (C) impaired ability to unload O2 in the tissues Explanation: The shift from curve A to curve B represents an increase in the affinity of hemoglobin for oxygen, which results in a decreased ability to unload oxygen in the tissues.
Which volume remains in the lungs after a maximal expiration? (A) Tidal volume (VT) (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: (D) Residual volume (RV) Explanation: After a maximal expiration, the residual volume (RV) remains in the lungs. RV is the volume of air that remains in the lungs after a maximal expiration.
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: (B) lower resistance Explanation: The pulmonary circulation has a lower resistance compared to the systemic circulation, which allows for a lower arterial pressure and lower capillary pressure in the pulmonary circulation.
A healthy 65-year-old man with a tidal volume (VT) 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: (D) 6.14 L/min Explanation: Alveolar ventilation can be calculated using the formula: Alveolar ventilation = (VT Ć Breathing
frequency) Ć (PaCO2 - PECO2) / PaCO2, where PECO2 is the PCO2 of the expired air. Plugging in the given values, the alveolar ventilation is calculated to be 6.14 L/min.
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: (C) a higher ventilation/perfusion (V/Q) ratio Explanation: Due to the effects of gravity, the base of the lung has a higher blood flow (perfusion) compared to the apex, while the ventilation remains relatively constant. This results in a higher ventilation/perfusion (V/Q) ratio at the base of the lung.
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: (E) carotid and aortic body chemoreceptors Explanation: Hypoxemia is detected by the carotid and aortic body chemoreceptors, which then stimulate the respiratory center in the medulla to increase ventilation, leading to hyperventilation.
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: (A) Ventilation rate and O2 consumption increase to the same extent Explanation: During strenuous exercise, the ventilation rate and oxygen consumption increase proportionally to meet the increased metabolic demands of the working muscles.
If an area of the lung is not ventilated because of bronchial obstruction, the pulmonary 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 PO
Answer: (B) equal to mixed venous PO2 Explanation: In an area of the lung that is not ventilated due to bronchial obstruction, the pulmonary capillary blood will have a PO2 equal to the mixed venous PO2, as there is no gas exchange occurring in that region.
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 HCO3ā in the red blood cells (RBCs) (B) Buff
Bronchiolar Constriction and Asthma
A cause of airway obstruction in asthma is bronchiolar constriction. Ī²2-adrenergic stimulation (Ī²2-adrenergic agonists) produces relaxation of the bronchioles.
Lung Volumes and Pressures
Inspiration and Expiration
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 (VT).
Lung Volumes and Capacities
During normal breathing, the volume inspired and then expired is a tidal volume (VT). The volume remaining in the lungs after expiration of a VT is the functional residual capacity (FRC). Expiratory reserve volume (ERV) equals vital capacity (VC) minus inspiratory capacity [inspiratory capacity includes tidal volume (VT) and inspiratory reserve volume (IRV)].
Gravitational Effects on Pulmonary Blood
Flow
The distribution of blood flow in the lungs is affected by gravitational effects on arterial hydrostatic pressure. Blood flow is highest at the base, where arterial hydrostatic pressure is greatest and the difference between arterial and venous pressure is also greatest, driving the blood flow.
Lung Compliance and Airway Pressure
By convention, when airway pressure is equal to atmospheric pressure, it is designated as zero pressure. Under equilibrium conditions, there is no airflow because there is no pressure gradient between the atmosphere and the alveoli, and the volume in the lungs is the functional residual capacity (FRC). The compliance of the lungs alone or the chest wall alone is greater than that of the combined lungāchest wall system (the slopes of the
individual curves are steeper than the slope of the combined curve, which means higher compliance). When airway pressure is zero (equilibrium conditions), intrapleural pressure is negative because of the opposing tendencies of the chest wall to spring out and the lungs to collapse.
Airway Resistance
The medium-sized bronchi actually constitute the site of highest resistance along the bronchial tree. Early changes in resistance in the small airways may be "silent" and go undetected because of their small overall contribution to resistance.
Unilateral Lung Collapse
Alveolar PO2 in the left lung will equal the PO2 in inspired air because there is no blood flow to the left lung, and there can be no gas exchange between the alveolar air and the pulmonary 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 be decreased because the left lung has no gas exchange, but alveolar PO2 in the right lung is unaffected.
Hemoglobin-Oxygen Dissociation Curve
Factors Affecting the Curve
Strenuous exercise increases the temperature and decreases the pH of skeletal muscle, both of which cause the hemoglobināO2 dissociation curve to shift to the right, making it easier to unload O2 in the tissues. 2,3-Diphosphoglycerate (DPG) binds to the Ī² chains of adult hemoglobin and reduces its affinity for O2, shifting the curve to the right. In fetal hemoglobin, the Ī² chains are replaced by Ī³ chains, which do not bind 2,3-DPG, so the curve is shifted to the left. Carbon monoxide (CO) increases the affinity of the remaining binding sites for O2, shifting the curve to the left.
Interpreting the Curve
A shift to the right of the hemoglobināO2 dissociation curve represents decreased affinity of hemoglobin for O2, facilitating the unloading of O in the tissues. The O2-carrying capacity of hemoglobin is unaffected by the shift from curve A to curve B.
Venous PCO2 increases because extra CO2 is being produced by the exercising muscle, but it is blown off by the hyperventilating lungs, so it does not increase the arterial PCO2. Pulmonary blood flow (cardiac output) increases manifold during strenuous exercise.
Ventilation/Perfusion Mismatch and Hypoxia
If an area of lung is not ventilated, there can be no gas exchange in that region, and the pulmonary capillary blood serving that region will have a PO2 equal to that of mixed venous blood.
Carbon Dioxide Transport
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).
Causes of Hypoxia
Hypoxia is defined as decreased O2 delivery to the tissues and can be caused by decreased blood flow or decreased O2 content of the blood. Decreased O2 content of the blood can be due to 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, but only right-to-left shunt is associated with an increased Aāa gradient.
Respiratory Alkalosis and Hypoxemia
The patient's arterial blood gases show increased pH, decreased PaO2, and decreased PaCO2, indicating respiratory alkalosis. The decreased PaO2 causes hyperventilation (stimulates breathing) via the peripheral chemoreceptors, but the decreased PaCO2 inhibits breathing via the peripheral and central chemoreceptors.
High-Altitude Adaptation
At high altitudes, the PO2 of alveolar air is decreased due to decreased barometric pressure, leading to decreased arterial PO2 and hypoxemia, which causes hyperventilation via an effect on peripheral chemoreceptors.
2,3-Diphosphoglycerate (DPG) levels increase adaptively, causing the hemoglobināO2 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.
Carbon Dioxide Transport (Continued)
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 that the pH of venous blood is only slightly more acid than the pH of arterial blood.
Lung Volumes and Capacities (Continued)
The volume expired in a forced maximal expiration is forced vital capacity, or vital capacity (VC).
Supplemental Oxygen and Ventilation/
Perfusion Defects
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.
Oxygen Diffusion and Ventilation-Perfusion
Mismatch
Regions of Low Ventilation-Perfusion Ratio (V/Q)
Regions of low V/Q have the highest blood flow. 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 and Shunt
Dead space (V/Q = ā) has no blood flow, so supplemental O2 has no effect on these regions. Shunt (V/Q = 0) has no ventilation, so supplemental O2 has no effect.
Regions of High Ventilation-Perfusion Ratio (V/Q)
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.
