Zanki Respiratory Physiology

1. The large airways of the conducting zone of the lung consists of the nose pharynx larynx trachea and bronchi
2. The small airways of the conducting zone of the lung consist of bronchioles that further divide into terminal bronchioles
3. The conducting zone of the lung is responsible for warming humidifying and filtering the air
4. Does the conducting zone of the lung participate in gas exchange? No
5. The volume of the conducting zone of the lung comprises the "anatomic dead space"
6. The volume of the conducting zone of the lung comprises the "anatomic dead space"
7. Cartilage and goblet cells extend to the end of the bronchi of the conducting zone
8. Cartilage and goblet cells extend to the end of the bronchi of the conducting zone
9. Cartilage and goblet cells extend to the end of the bronchi of the conducting zone
10. The cilia lining the epithelium of the respiratory tract help clear mucus and debris from the lungs via the mucociliary escalator
11. The cilia lining the epithelium of the respiratory tract help clear mucus and debris from the lungs via the mucociliary escalator
12. Airway smooth muscle cells extend to the terminal bronchioles of the conducting zone (sparse beyond this point)
13. The smooth muscle of the conducting airways of the lung relaxes in response to sympathetic activation of the Œ≤2 adrenergic receptors
14. The smooth muscle of the conducting airways of the lung relaxes in response to sympathetic activation of the Œ≤2 adrenergic receptors
15. The smooth muscle of the conducting airways of the lung constrict in response to parasympathetic activation of muscarinic receptors
16. The smooth muscle of the conducting airways of the lung constrict in response to parasympathetic activation of muscarinic receptors
17. What is the effect of sympathetic innervation on the smooth muscle of the conducting airways of the lung? Relaxation
18. What is the effect of parasympathetic innervation on the smooth muscle of the conducting airways of the lung? Constriction
19. The respiratory zone of the lung consists of the respiratory bronchioles alveolar ducts and alveolar sacs
20. Does the respiratory zone of the lung participate in gas exchange? Yes
21. Which part of the respiratory zone still contains some smooth muscle? Respiratory bronchioles
22. Where in the respiratory tract do cilia terminate? Respiratory bronchioles
23. Do the alveolar ducts and/or sacs have cilia? No
24. The alveolar walls are lined with epithelial cells called type I and type II pneumocytes
25. Type II pneumocytes are responsible for synthesis of pulmonary surfactant
26. Type II pneumocytes are responsible for synthesis of pulmonary surfactant
27. Type II pneumocytes have regenerative capacity for both type I and type II pneumocytes
28. The alveoli contain phagocytic cells called alveolar macrophages which clear debris and participate in the immune response
29. Pulmonary blood flow is equal to the cardiac output of the right heart
30. When a person is standing pulmonary blood flow is lowest at the apex (top) of the lungs
31. When a person is standing pulmonary blood flow is highest at the base (bottom) of the lungs
32. The volume that moves into the lung with each quiet inspiration is the tidal volume
33. What is the typical normal value for tidal volume (mL)? 500 mL
34. The additional volume that can be inspired above tidal volume is the inspiratory reserve volume
35. The additional volume that can be expired below tidal volume is the expiratory reserve volume
36. The volume that remains in the lungs after maximal forced expiration is the residual volume
37. Which lung volume cannot be measured on spirometry? Residual volume
38. The sum of the tidal volume plus the inspiratory reserve volume is known as inspiratory capacity
39. The sum of the residual volume plus the expiratory reserve volume is known as functional residual capacity
40. The volume of gas remaining in the lungs after normal exhalation is the functional residual capacity
41. The sum of the tidal volume inspiratory reserve volume and expiratory reserve volume is known as the vital capacity
42. The maximum volume of gas that can be expired after maximal inspiration is known as the (forced) vital capacity
43. The sum of the tidal volume inspiratory reserve volume expiratory reserve volume and residual volume is known as the total lung capacity
44. The volume of gas present in the lungs after a maximal inspiration is known as the total lung capacity
45. Which lung capacities (2) cannot be measured on spirometry? Functional residual capacity Total lung capacity
46. Functional residual capacity may be measured using helium dilution or body plethysmograph
47. Functional residual capacity may be measured using helium dilution or body plethysmograph
48. What is the typical normal value for anatomic dead space (mL)? 150 mL
49. The volume of the anatomic dead space plus the alveolar dead space comprises the "physiologic dead space"
50. The volume of the anatomic dead space plus the alveolar dead space comprises the "physiologic dead space"
51. The apex of a healthy lung is the largest contributor of alveolar dead space
52. Physiologic dead space is the total volume of the lungs that does not participate in gas exchange
53. In healthy lungs the physiologic dead space is approximately equal to the anatomic dead space
54. In certain pathologic situations the physiologic dead space may become greater than the anatomic dead space suggesting a ventilation/perfusion (V/Q) defect
55. Pathologic dead space is when part of the respiratory zone is ventilated but not perfused (perfused ventilated)
56. Minute ventilation is the total volume of gas that enters the lungs per unit time
57. Alveolar ventilation is the volume of gas per unit time that reaches the alveoli (accounts for physiologic dead space)
58. What equation may be used to calculate minute ventilation? Minute Ventilation (VE) = VT * Respiratory Rate
59. What equation may be used to calculate alveolar ventilation? Alveolar Ventilation (VA) = (VT - VD) * Respiratory Rate
60. What is the normal range of respiratory rates for a healthy adult (breaths/min)? 12-20 breaths/min
61. If CO2 production is constant then the arterial and alveolar Pco2 is determined by alveolar ventilation
62. If CO2 production is constant then the arterial and alveolar Pco2 is determined by alveolar ventilation
63. What is the effect of increased alveolar ventilation on arteriolar (and alveolar) Pco2? Decreased Pco2
64. What is the effect of decreased alveolar ventilation on arteriolar (and alveolar) Pco2? Increased Pco2
65. In the steady state the respiratory quotient R is normally equal to 0.8
66. Under normal conditions PO2 of humidified inspired air is 150 mmHg
67. Under normal conditions PO2 of humidified inspired air is 150 mmHg
68. The gradient between PAo2 - PaO2 is known as the A-a gradient and is normally 10 - 15 mmHg
69. The gradient between PAo2 - PaO2 is known as the A-a gradient and is normally 10 - 15 mmHg
70. The total volume of air that can be forcibly expired after a maximal inhalation is known as the forced vital capacity (FVC)
71. The volume of air that can be forcibly expired after a maximal inspiration in one second is known as the FEV1
72. The normal value for the ratio of FEV1/FVC is approximately 0.8
73. In obstructive lung disease the FEV1/FVC is decreased
74. In obstructive lung disease the FEV1/FVC is decreased
75. In restrictive lung disease the FEV1/FVC is normal or increased
76. In restrictive lung disease the FEV1/FVC is normal or increased
77. The diaphragm is the most important muscle for inspiration
78. When the diaphragm contracts the abdominal contents are pushed downwards
79. During exercise or respiratory distress the external intercostal muscles and accessory muscles may be used for vigorous inspiration
80. During exercise or respiratory distress the external intercostal muscles and accessory muscles may be used for vigorous inspiration
81. During exercise or respiratory distress the external intercostal muscles and accessory muscles may be used for vigorous inspiration
82. What muscles are normally used for expiration at rest? none :) (normally passive)
83. During exercise or in diseases with increased airway resistance (e.g. asthma) abdominal muscles and internal intercostal muscles may be used to aid expiration
84. During exercise or in diseases with increased airway resistance (e.g. asthma) abdominal muscles and internal intercostal muscles may be used to aid expiration
85. During exercise or in diseases with increased airway resistance (e.g. asthma) abdominal muscles and internal intercostal muscles may be used to aid expiration
86. Lung compliance describes the change in lung volume for a given change in lung pressure
87. Lung compliance may be calculated by the equation C = ŒîV/ŒîP
88. The compliance of the lungs and chest wall is inversely proportional to their elastance
89. The compliance of the lungs and chest wall is inversely proportional to the wall stiffness
90. Elastic recoil is the force generated due to the tendency for the lungs to collapse inward and the chest wall to spring outward
91. Elastic recoil is inversely proportional to compliance and directly proportional to elastance
92. A lung with high compliance is easier to fill
93. A lung with low compliance is harder to fill
94. The slope of a respiratory system pressure-volume curve represents lung compliance
95. The slope of a respiratory system pressure-volume curve represents lung compliance
96. The slope (compliance) of the pressure-volume loop curves for inspiration and expiration are different due to a phenomenom known as hysteresis
97. Hysteresis occurs because the lung must overcome surface tension during lung inhalation (inspiration)
98. Hysteresis occurs because the lung must overcome surface tension during lung inhalation (inspiration)
99. Are the lungs generally more compliant during inspiration or expiration? Expiration (due to hysteresis)
100.The intermolecular forces between liquid molecules lining the lung are much stronger than the forces between liquid and air
101.During initial inspiration liquid molecules are close together and intermolecular forces are high
102.During expiration the slope of the pressure-volume loop increases as the density of surfactant molecules rapidly increases
103.At FRC the intrapleural space normally has a negative pressure relative to the atmosphere At FRC the intrapleural pressure is normally -5cmH2O
104.At FRC the intrapleural space normally has a negative pressure relative to the atmosphere At FRC the intrapleural pressure is normally -5cmH2O
105.The inward pull of the lung is balanced by the outward pull of the chest at the functional residual capacity
106.The inward pull of the lung is balanced by the outward pull of the chest at the functional residual capacity
107.The inward pull of the lung is balanced by the outward pull of the chest at the functional residual capacity
108.If a sharp object punctures the intrapleural space (pneumothorax) the intrapleural pressure becomes equal to atmospheric pressure
109.If a sharp object punctures the intrapleural space (pneumothorax) the intrapleural pressure becomes equal to atmospheric pressure
110.The compliance of the lung-chest wall system is less than that of the lungs or chest wall alone
111.At FRC airway and alveolar pressures are equal to 0 (atmospheric pressure)
112.When lung volume is less than FRC there is a net expanding force on the lung-chest wall system
113.When lung volume is less than FRC there is a net expanding force on the lung-chest wall system
114.When lung volume is greater than FRC there is a net collapsing force on the lung-chest wall system
115.When lung volume is greater than FRC there is a net collapsing force on the lung-chest wall system
116.At highest lung volumes both the lungs and the chest wall contribute to collapsing forces on the lung-chest wall system
117.What is the effect of emphysema on lung compliance? Increased compliance
118.At the original FRC the tendency of the lung to collapse in a patient with emphysema is less than the tendency of the chest wall to expand In emphysema FRC increases
because the the collapsing force of the lungs decreases.
119.How does emphysema affect functional residual capacity (FRC)? Increased FRC
120.A patient with emphysema breathes at a higher lung volume and will thus have a barrel-shaped chest (increased anterior-posterior diameter)
121.A patient with emphysema breathes at a higher lung volume and will thus have a barrel-shaped chest (increased anterior-posterior diameter)
122.What is the effect of normal aging on lung compliance? Increased compliance
123.What is the effect of pulmonary fibrosis on lung compliance? Decreased compliance
124.At the original FRC the tendency of the lung to collapse in a patient with pulmonary fibrosis is greater than the tendency of the chest wall to expand
125.At the original FRC the tendency of the lung to collapse in a patient with pulmonary fibrosis is greater than the tendency of the chest wall to expand
126.What is the effect of pulmonary fibrosis on functional residual capacity (FRC)? Decreased FRC
127.What is the effect of pulmonary edema on lung compliance? Decreased compliance
128.What is the effect of pneumonia on lung compliance? Decreased compliance
129.What is the effect of surfactant on lung compliance? Increased compliance
130.The law of Laplace states that the collapsing pressure of an alveoli P is equal to 2T / r
131.According to the law of Laplace a large alveolus will have a low collapsing pressure
132.According to the law of Laplace a small alveolus will have a high collapsing pressure
133.Surfactant is a mixture of phospholipids that line the alveoli and reduce their surface tension
134.Surfactant reduces surface tension by disrupting the intermolecular forces between liquid molecules
135.Without surfactant small alveoli are more likely to collapse which is termed atelectasis
136.Pulmonary surfactant is a mix of lecithins the most important of which is dipalmitoyl phosphatidylcholine (DPCC)
137.In the developing fetus surfactant synthesis begins as early as gestastional week 20
138.In the developing fetus mature levels of surfactant are not achieved until around week 35
139.Alveoli have increased tendency to collapse on exhalation (inhalation/exhalation)
140.Alveoli have increased tendency to collapse on exhalation (inhalation/exhalation)
141.What equation may be used to calculate the airflow (Q) given the pressure and resistance of the airway? Q = ŒîP/R
142.Airflow is inversely proportional to airway resistance
143.Airflow is directly proportional to the pressure gradient
144.Airway resistance is inversely proportional to the fourth power of the radius of the airway
145.Airway resistance is inversely proportional to the fourth power of the radius of the airway
146.Airway resistance is inversely proportional to the fourth power of the radius of the airway
147.The major site of airway resistance is the medium-sized bronchi
148.What is the effect of parasympathetic innervation on airway resistance? Increased resistance
149.What is the effect of sympathetic innervation on airway resistance? Decreased resistance
150.What is the effect of high lung volumes on airway resistance? Decreased resistance
151.What is the effect of low lung volumes on airway resistance? Increased resistance
152.What is the effect of increased viscosity (e.g. deep-sea diving) on airway resistance? Increased resistance
153.What is the effect of decreased viscosity (e.g. helium inhalation) on airway resistance? Decreased resistance
154.What equation may be used to calculate the pulmonary vascular resistance (PVR)? PVR = (Ppulm artery - PL atrium) / cardiac output
155.The transpulmonary pressure across the lungs is calculated as alveolar pressure minus intrapleural pressure
156.The transpulmonary pressure across the lungs is calculated as alveolar pressure minus intrapleural pressure
157.How does the volume of breath change during inspiration? Increased
158.How does the intrapleural pressure change during inspiration (relative to atmosphere)? More negative relative to atmosphere
159.How does the alveolar pressure change during mid-inspiration (relative to atmosphere)? More negative relative to atmosphere
160.As the alveolar pressure becomes negative relative to the atmosphere (mid-inspiration) air flows inwards
161.How does the volume of breath change during expiration? Decreased
162.How does the intrapleural pressure change during expiration (relative to atmosphere)? Less negative relative to atmosphere
163.How does the alveolar pressure change during mid-expiration (relative to atmosphere)? More positive relative to atmosphere
164.As the alveolar pressure becomes positive relative to the atmosphere (mid-expiration) air flows outwards
165.In what normal scenario may intrapleural pressure be positive (relative to the atmosphere)? Forced expiration
166.Transfer of gases across cell membranes or capillary walls occurs by simple diffusion
167.The diffusion coefficient (DK) for CO2 is approximately 20x higher than that of O2
168.The lung diffusing capacity (DL) represents the permeability of the alveolar-pulmonary capillary barrier
169.The lung diffusing capacity (DL) can be measured with carbon monoxide (CO) because it is exclusively diffusion-limited
170.DLCO may be used to estimate the extent to which oxygen passes from the air sacs of lungs into blood
171.The lung diffusing capacity DL is directly proportional to the surface area available for diffusion
172.The lung diffusing capacity DL is directly proportional to the diffusion coefficient of the gas
173.The lung diffusing capacity DL is inversely proportional to the alveolar wall thickness
174.The lung diffusing capacity DL decreases in emphysema due to decreased surface area (A)
175.The lung diffusing capacity DL decreases in emphysema due to decreased surface area (A)
176.The lung diffusing capacity DL decreases in pulmonary fibrosis due to increased wall thickness (Œîx)
177.The lung diffusing capacity DL decreases in pulmonary fibrosis due to increased wall thickness (Œîx)
178.The lung diffusing capacity DL increases during exercise due to increased surface area (A)
179.The lung diffusing capacity DL increases during exercise due to increased surface area (A)
180.The Po2 in dry inspired air is normally approximately 160 mmHg
181.The Po2 in humidified tracheal air is normally approximately 150 mmHg
182.The partial pressure of oxygen in the alveolar air (PAO2) and arterial blood (PaO2) is normally approximately 100 mmHg
183.The partial pressure of CO2 in the alveolar air (PACO2) and arterial blood (PaCO2) is normally approximately 40 mmHg Normal value of PACO2 and PaCO2 is:
184.The partial pressure of oxygen in the venous blood (PvO2) is normally approximately 40 mmHg
185.The partial pressure of carbon dioxide in mixed venous blood (PvCO2) is normally approximately 46 mmHg
186.The partial pressure of O2 in arteriolar blood is slightly lower than alveolar air due to the "physiologic shunt"
187.The partial pressure of O2 in arteriolar blood is slightly lower than alveolar air due to the "physiologic shunt"
188.The two sources of the physiologic shunt are: bronchial blood flow & a small portion of coronary venous blood (drains into the left ventricle via the thebesian vein) What are
the two sources of physiologic bood flow?
189.The two sources of the physiologic shunt are: bronchial blood flow & a small portion of coronary venous blood (drains into the left ventricle via the thebesian vein) What are
the two sources of physiologic bood flow?
190.The partial pressure gradient is the driving force for the diffusion of a gas
191.The partial pressure of a gas is determined only by the free dissolved gas in solution
192.If gas does not equilibrate by the end of the capillary gas exchange is diffusion-limited
193.In perfusion-limited gas exchange the gas equilibrates early along the length of the capillary
194.In perfusion-limited gas exchange diffusion can be increased only if blood flow increases
195.In perfusion-limited gas exchange diffusion can be increased only if blood flow increases
196.In a healthy person O2 exhibits perfusion-limited gas exchange
197.CO2 exhibits perfusion-limited gas exchange
198.N2O exhibits perfusion-limited gas exchange
199.CO exhibits diffusion-limited gas exchange
200.When patients have diseased lung tissue (e.g. fibrosis/emphysema) O2 transfer becomes diffusion-limited
201.At high altitude the partial pressure gradient of O2 is lower and thus equilibration takes longer
202.At high altitude the partial pressure gradient of O2 is lower and thus equilibration takes longer
203.O2 is carried in blood in two forms: dissolved (2%) or bound to hemoglobin (98%)
204.O2 is carried in blood in two forms: dissolved (2%) or bound to hemoglobin (98%)
205.Hemoglobin is a globular protein consisting of four subunits
206.Each subunit of hemoglobin contains a heme moiety which is an iron-binding porphyrin and a polypeptide chain
207.Each subunit of hemoglobin contains a heme moiety which is an iron-binding porphyrin and a polypeptide chain
208.Iron in hemoglobin is normally in the ferrous (Fe2+) state
209.If the iron in hemoglobin is in the ferric (Fe3+) state it is called methemoglobin
210.If the iron in hemoglobin is in the ferric (Fe3+) state it is called methemoglobin
211.Methemoglobin (Fe3+) binds O2 much less readily than hemoglobin (Fe2+)
212.Methemoglobin has an increased affinity for cyanide relative to hemoglobin
213.Methemoglobin has an increased affinity for cyanide relative to hemoglobin
214.Methemoglobinemia may present with cyanosis and chocolate-colored blood
215.Methemoglobinemia may present with cyanosis and chocolate-colored blood
216.Methemoglobinemia may present with cyanosis and chocolate-colored blood
217.Induced-methemoglobinemia (i.e. nitrites followed by thiosulfate) may be used to treat cyanide poisoning
218.Induced-methemoglobinemia (i.e. nitrites followed by thiosulfate) may be used to treat cyanide poisoning
219.Induced-methemoglobinemia (i.e. nitrites followed by thiosulfate) may be used to treat cyanide poisoning
220.Methemoglobinemia can be treated with methylene blue or vitamin C
221.Methemoglobinemia can be treated with methylene blue or vitamin C
222.What two drug classes are associated with methemoglobinemia? Nitrates (and nitrites) Sulfa drugs
223.Polluted/high altitude H2O may contain nitrites which can cause methemoglobinemia
224.Polluted/high altitude H2O may contain nitrites which can cause methemoglobinemia
225.Benzocaine is a local anesthetic that may cause methemoglobinemia in toxic doses
226.Methemoglobinemia is associated with decreased SaO2 decreased O2 content and normal PaO2
227.Most adult hemoglobin is composed of 2 Œ± and 2 Œ≤ subunits; known as HbA
228.Most adult hemoglobin is composed of 2 Œ± and 2 Œ≤ subunits; known as HbA
229.Fetal hemoglobin known as HbF is composed of 2 alpha and 2 gamma subunits
230.Fetal hemoglobin known as HbF is composed of 2 alpha and 2 gamma subunits
231.Fetal hemoglobin (HbF) has a much higher binding affinity for O2 than adult hemoglobin (HbA)
232.Why must fetal hemoglobin have a much higher O2 binding affinity than HbA? Drives O2 diffusion across placenta from mother to fetus
233.The increased O2 binding affinity of fetal hemoglobin results from decreased affinity of HbF for 2 3-BPG
234.The increased O2 binding affinity of fetal hemoglobin results from decreased affinity of HbF for 2 3-BPG
235.Hemoglobin exists in two forms: taut (deoxygenated) and relaxed (oxygenated)
236.The taut form of hemoglobin has a low affinity for O2
237.The taut form of hemoglobin has a low affinity for O2
238.The relaxed form of hemoglobin has a high affinity for O2
239.The relaxed form of hemoglobin has a high affinity for O2
240.The taut form of hemoglobin is found in most tissues
241.The relaxed form of hemoglobin is found in the respiratory tract
242.Normally 1g of hemoglobin can bind 1.34 mL of O2
243.Normally there is ~15 g/dL of hemoglobin in blood
244.The O2-binding capacity of blood is 20.1 mL O2/ 100 mL blood
245.Decreased hemoglobin (e.g. anemia) is associated with normal SaO2 decreased O2 content and normal PaO2
246.The sigmoidal shape of the oxygen-hemoglobin dissociation curve is due to positive cooperativity (increased affinity for each sucessive O2 bound)
247.The sigmoidal shape of the oxygen-hemoglobin dissociation curve is due to positive cooperativity (increased affinity for each sucessive O2 bound)
248.A hemo-globin molecule has the potential to bind 4 O2 molecule(s)
249.A hemo-globin molecule has the potential to bind 4 O2 molecule(s)
250.A myo-globin molecule has the potential to bind 1 O2 molecule(s)
251.A myo-globin molecule has the potential to bind 1 O2 molecule(s)
252.The P50 of the oxygen-Hb dissociation curve is the Po2 at which hemoglobin is 50% saturated
253.The oxygen-Hb dissociation curve is roughly flat when the Po2 is between 60 and 100 mmHg
254.Does the oxygen-myoglobin dissociation curve have a sigmoidal shape? Why? No myoglobin is monomeric (no positive cooperativity)
255.Shifts of the O2-Hb dissociation curve to the right occur when there is decreased affinity of hemoglobin for O2
256.Shifts of the O2-Hb dissociation curve to the right occur when there is decreased affinity of hemoglobin for O2
257.Shifts of the O2-Hb dissociation curve to the right cause increased unloading of O2 at tissues
258.Shifts of the O2-Hb dissociation curve to the right cause increased unloading of O2 at tissues
259.Increased pCO2 and resulting decrease of pH enhancing the release of O2 from hemoglobin is called the Bohr effect
260.Increases in Pco2 cause the O2-hemoglobin dissociation curve to shift to the right
261.Increases in Pco2 cause the O2-hemoglobin dissociation curve to shift to the right
262.Decreases in pH cause the O2-hemoglobin dissociation curve to shift to the right
263.Decreases in pH cause the O2-hemoglobin dissociation curve to shift to the right
264.Increases in temperature cause the O2-hemoglobin dissociation curve to shift to the right
265.Increases in temperature cause the O2-hemoglobin dissociation curve to shift to the right
266.Increases in 2 3-BPG cause the O2-hemoglobin dissociation curve to shift to the right
267.Increases in 2 3-BPG cause the O2-hemoglobin dissociation curve to shift to the right
268.2 3-BPG decreases the affinity of hemoglobin for O2 by binding to hemoglobin Œ≤ chains
269.2 3-BPG decreases the affinity of hemoglobin for O2 by binding to hemoglobin Œ≤ chains
270.How do levels of 2 3-BPG change at high altitudes? Increased
271.2 3-BPG increases under hypoxic conditions (e.g. high altitude)
272.High altitudes indirectly cause the O2-hemoglobin dissociation curve to shift to the right
273.Factors that shift the O2-Hb dissociation curve to the right favor the taut form of hemoglobin
274.Factors that shift the O2-Hb dissociation curve to the right favor the taut form of hemoglobin
275.Shifts of the O2-Hb dissociation curve to the left occur when there is increased affinity of hemoglobin for O2
276.Shifts of the O2-Hb dissociation curve to the left occur when there is increased affinity of hemoglobin for O2
277.Shifts of the O2-Hb dissociation curve to the left cause decreased unloading of O2 at tissues
278.Shifts of the O2-Hb dissociation curve to the left cause decreased unloading of O2 at tissues
279.Decreases in Pco2 cause the O2-hemoglobin dissociation curve to shift to the left
280.Decreases in Pco2 cause the O2-hemoglobin dissociation curve to shift to the left
281.Increases in pH cause the O2-hemoglobin dissociation curve to shift to the left
282.Increases in pH cause the O2-hemoglobin dissociation curve to shift to the left
283.Decreases in temperature cause the O2-hemoglobin dissociation curve to shift to the left
284.Decreases in temperature cause the O2-hemoglobin dissociation curve to shift to the left
285.Decreases in 2 3-BPG cause the O2-hemoglobin dissociation curve to shift to the left
286.Decreases in 2 3-BPG cause the O2-hemoglobin dissociation curve to shift to the left
287.Œ≥ chains in hemoglobin F cause the O2-hemoglobin dissociation curve to shift to the left
288.Œ≥ chains in hemoglobin F cause the O2-hemoglobin dissociation curve to shift to the left
289.Carboxyhemoglobin is a form of hemoglobin bound to CO in place of O2
290.Carboxyhemoglobin is a form of hemoglobin bound to CO in place of O2
291.Carbon monoxide binds competitively to Hb and with 200-250x greater affinity than O2
292.Carboxyhemoglobin causes the O2-hemoglobin dissociation curve to shift to the left
293.Carboxyhemoglobin heme groups not bound by CO have a(n) increased affinity for O2
294.Carboxyhemoglobin causes decreased unloading of O2 at tissues
295.Carboxyhemoglobin causes decreased O2-binding capacity
296.Carboxyhemoglobinemia (CO poisoning) may be treated with 100% O2 and hyperbaric O2
297.Carboxyhemoglobinemia (CO poisoning) may be treated with 100% O2 and hyperbaric O2
298.Carboxyhemoglobinemia is associated with decreased SaO2 decreased O2 content and normal PaO2
299.What is the hemoglobin concentration in carboxyhemoglobinemia? Normal
300.Anemia is associated with normal SaO2 decreased O2 content and normal PaO2
301.How does the hemoglobin concentration change in anemia? Decreased
302.Polycythemia is associated with normal SaO2 increased O2 content and normal PaO2
303.How does the hemoglobin concentration change in polycythemia? Increased
304.Erythropoietin (EPO) is a hormone synthesized in the kidneys in response to hypoxia
305.Erythropoietin (EPO) is a hormone synthesized in the kidneys in response to hypoxia
306.Decreased O2 delivery to the kidneys due to hypoxia causes increased production of hypoxia-inducible factor 1Œ± which then stimulates synthesis of EPO
307.Hypoxia-inducible factor 1Œ± acts on renal fibroblasts to cause synthesis of the mRNA for erythropoietin
308.Hypoxia-inducible factor 1Œ± acts on renal fibroblasts to cause synthesis of the mRNA for erythropoietin
309.Erythropoietin (EPO) causes differentiation of proerythroblasts which undergo further development to form mature erythrocytes
310.Hemoglobin may act as a buffer for H+ ions
311.Hemoglobin may act as a buffer for H+ ions
312.One way in which CO2 is carried in the blood is as dissolved CO2 (5%)
313.One way in which CO2 is carried in the blood is bound to hemoglobin known as carbaminohemoglobin (HbCO2) (5%)
314.The majority of CO2 transported in blood is in the form of HCO3- (bicarbonate) (90%)
315.CO2 binding to hemoglobin favors the taut form thus reducing Hb affinity for O2
316.CO2 binds to hemoglobin at the N-terminus of globin (heme or globin)
317.Haldane Effect Decreased O2 binding to hemoglobin causes increased affinity for CO2 and H+ (Haldane effect)
318.Haldane Effect Decreased O2 binding to hemoglobin causes increased affinity for CO2 and H+ (Haldane effect)
319.Increased O2 binding to hemoglobin causes decreased affinity for CO2 (Haldane effect)
320.Increased O2 binding to hemoglobin causes decreased affinity for CO2 (Haldane effect)
321.Increased O2 binding to hemoglobin causes decreased affinity for CO2 (Haldane effect)
322.In red blood cells CO2 is combined with H2O via the enzyme carbonic anhydrase forming H2CO3
323.In red blood cells CO2 is combined with H2O via the enzyme carbonic anhydrase forming H2CO3
324.In red blood cells CO2 is combined with H2O via the enzyme carbonic anhydrase forming H2CO3
325.In red blood cells CO2 is combined with H2O via the enzyme carbonic anhydrase forming H2CO3
326.H2CO3 formed from CO2 and H2O in red blood cells dissociates into H+ and HCO3-
327.The H+ in red blood cells (from H2CO3) is buffered by deoxyhemoglobin
328.The H+ in red blood cells (from H2CO3) is buffered by deoxyhemoglobin
329.The HCO3- in red blood cells (from H2CO3) is transported out to the plasma in exchange for Cl-
330.The HCO3- in red blood cells (from H2CO3) is transported out to the plasma in exchange for Cl-
331.The HCO3- transported out of RBCs is carried to the lungs in the plasma of venous blood
332.In the lungs oxygenation of hemoglobin promotes H+ release from its buffering sites
333.In the lungs oxygenation of hemoglobin promotes H+ release from its buffering sites
334.In the lungs HCO3- enters the red blood cells in exchange for Cl-
335.In the lungs HCO3- enters the red blood cells in exchange for Cl-
336.In the lungs H2CO3 in the red blood cell is reconverted to CO2 and H2O and expired
337.In the lungs H2CO3 in the red blood cell is reconverted to CO2 and H2O and expired
338.The Cl--HCO3- exchange that occurs across the RBC membrane is accomplished by an anion exchange protein called band three protein
339.The pulmonary circulation is normally characterized as a low resistance high compliance system (low or high)
340.A decrease in PAO2 causes a hypoxic vasoconstriction that shunts blood away from poorly ventilated regions of the lung
341.Fetal pulmonary vascular resistance is very high because of generalized hypoxic vaso-constriction
342.In the pulmonary circulation decreased Po2 (hypoxia) causes vaso-constriction
343.Increased Pco2 (hypercapnia) in the pulmonary circulation causes vaso-constriction
344.Decreased Po2 (hypoxia) causes vaso-dilation in the systemic circulation
345.Increased Pco2 (hypercapnia) causes vaso-dilation in the systemic circulation
346.In zone 1 (apex) of the lung blood flow (Q) is lowest
347.In zone 1 (apex) of the lung blood flow (Q) is lowest
348.In zone 3 (base) of the lung blood flow (Q) is highest
349.In zone 3 (base) of the lung blood flow (Q) is highest
350.Rank the following variables for zone 1 of the lung: PA Pa and Pv PA > Pa > Pv
351.Rank the following variables for zone 2 of the lung: PA Pa and Pv Pa > PA > Pv
352.Rank the following variables for zone 3 of the lung: PA Pa and Pv Pa > Pv > PA
353.In zone 1 of the lung high alveolar pressure may compress the capillaries and reduce blood flow in this zone
354.In zone 2 of the lung blood flow is driven by the difference between arteriolar and alveolar pressure
355.In zone 3 of the lung blood flow is driven by the difference between arteriolar and venous pressure
356.In right-to-left shunts hypoxemia always occurs because a significant fraction of the cardiac output is not delivered to the lungs
357.In right-to-left shunts hypoxemia always occurs because a significant fraction of the cardiac output is not delivered to the lungs
358.A defining characteristic of hypoxemia caused by a right-to-left shunt is that it cannot be corrected with high O2 gas
359.Do left-to-right shunts result in hypoxemia? No
360.A consequence of pulmonary hypertension is right ventricular hypertrophy with eventual cor pulmonale
361.The ventilation/perfusion (V/Q) ratio is the ratio of alveolar ventilation to pulmonary blood flow
362.The normal average value for V/Q is 0.8
363.In zone 1 (apex) of the lung alveolar ventilation (V) is lowest
364.In zone 1 (apex) of the lung alveolar ventilation (V) is lowest
365.In zone 3 (base) of the lung alveolar ventilation (V) is highest
366.In zone 3 (base) of the lung alveolar ventilation (V) is highest
367.Both ventilation and perfusion are greater at the base of the lung than at the apex of the lung
368.The V/Q ratio is highest in zone 1 (apex) of the lung
369.The V/Q ratio is highest in zone 1 (apex) of the lung
370.The V/Q ratio is lowest in zone 3 (base) of the lung
371.The V/Q ratio is lowest in zone 3 (base) of the lung
372.The V/Q ratio at the apex of the lung is normally 3 indicating wasted ventilation
373.The V/Q ratio at the apex of the lung is normally 3 indicating wasted ventilation
374.The V/Q ratio at the base of the lung is normally 0.6 indicating wasted perfusion
375.The V/Q ratio at the base of the lung is normally 0.6 indicating wasted perfusion
376.What is the ideal V/Q ratio for adequate gas exchange? 1 (ventilation matches perfusion)
377.If there is a(n) blood flow obstruction the V/Q ratio = ‚àû (dead space)
378.If there is a(n) blood flow obstruction the V/Q ratio = ‚àû (dead space)
379.Dead space is ventilation of lung regions that are not perfused (V/Q = ‚àû)
380.If there is a(n) airway obstruction the V/Q ratio = 0 (shunt)
381.If there is a(n) airway obstruction the V/Q ratio = 0 (shunt)
382.Shunt is perfusion of lung regions that are not ventilated (V/Q = 0)
383.What type of V/Q mismatch occurs due to pulmonary embolus? Dead space (ventilation but no perfusion)
384.What type of V/Q mismatch occurs due to airway obstruction? Shunt (perfusion but no ventilation)
385.Does 100% O2 improve PaO2 in V/Q mismatch due to physiologic dead space? Yes assuming < 100% dead space
386.Does 100% O2 improve PaO2 in V/Q mismatch due to shunt? No
387.Certain organisms that thrive in high O2 (e.g. TB) flourish in the apex of the lung
388.With exercise (increased cardiac output) there is vasodilation of apical capillaries in the lung which causes the V/Q ratio to approach a value of 1
389.With exercise (increased cardiac output) there is vasodilation of apical capillaries in the lung which causes the V/Q ratio to approach a value of 1
390.Breathing as an involuntary process is controlled by the medulla and pons of the brain stem
391.Breathing as an involuntary process is controlled by the medulla and pons of the brain stem
392.The medullary respiratory center is located in the reticular formation and contains an inspiratory and expiratory center
393.The dorsal and ventral respiratory groups are located in the medulla of the brain stem
394.The dorsal respiratory group is primarily responsible for inspiration and generates the basic rhythm for breathing
395.The dorsal respiratory group is primarily responsible for inspiration and generates the basic rhythm for breathing
396.The dorsal respiratory group receives sensory input from peripheral chemoreceptors via the glossopharyngeal (CN IX) and vagus (CN X)nerves
397.The dorsal respiratory group receives sensory input from lung stretch receptors via the vagus (CN X) nerve
398.The dorsal respiratory group sends its motor output to the diaphragm via the phrenic nerve
399.The ventral respiratory group is primarily responsible for expiration and is not active during normal quiet breathing
400.The ventral respiratory group is primarily responsible for expiration and is not active during normal quiet breathing
401.The apneustic center is located in the lower pons and stimulates inspiration
402.The apneustic center is located in the lower pons and stimulates inspiration
403.The pneumotaxic center is located in the upper pons and inhibits inspiration
404.The pneumotaxic center is located in the upper pons and inhibits inspiration
405.Commands from the cerebral cortex can temporarily override the automatic respiratory brain stem centers
406.Where are the central chemoreceptors located? Medulla
407.Central chemoreceptors are especially sensitive to the pH of the cerebrospinal fluid
408.Central chemoreceptors are especially sensitive to the pH of the cerebrospinal fluid
409.In response to decreased pH sensed by chemoreceptors the breathing rate increases (hyperventilation)
410.In response to decreased pH sensed by chemoreceptors the breathing rate increases (hyperventilation)
411.Central chemoreceptors respond indirectly to increased Pco2 and directly to decreased pH
412.Where are the peripheral chemoreceptors located (2)? carotid bodies and aortic bodies
413.Peripheral chemoreceptors respond to decreases in Pao2 and pH
414.Peripheral chemoreceptors respond to increases in Pco2
415.Peripheral chemoreceptors respond to decreased Po2 when the arterial Po2 is less than 60 mmHg
416.Increases in arterial H+ stimulate the carotid body peripheral chemoreceptors only independent of changes in Pco2
417.Lung stretch receptors are mechanoreceptors located in the smooth muscle of the airways
418.Lung stretch receptors cause a(n) decreased breathing frequency in response to distention of the lungs (Hering-Breuer reflex)
419.Irritant receptors are located between the airway epithelial cells and are stimulated by noxious substances
420.Joint and muscle receptors are activated during movement of the limbs and stimulate breathing early during exercise
421.Juxtacapillary (J) receptors are located in the alveolar walls and cause rapid shallow breathing in response to pulmonary capillary engorgement (e.g. left heart failure)
422.In response to exercise there is increased CO2 production
423.In response to exercise there is increased O2 consumption
424.In response to exercise there is increased ventilation rate to meet O2 demand
425.In response to exercise the V/Q ratio from apex to base becomes more even (even or uneven)
426.In response to exercise there is increased pulmonary blood flow due to increased cardiac output
427.In response to exercise there is increased pulmonary blood flow due to increased cardiac output
428.There is a(n) decrease in pulmonary resistance associated with increased perfusion of pulmonary capillary beds
429.In response to strenuous exercise there is decreased pH secondary to lactic acidosis
430.How does Paco2 change in response to exercise? no change
431.In response to exercise there is increased venous CO2 content
432.In response to exercise there is decreased venous O2 content
433.In response to decreased atmospheric oxygen (e.g. high altitude) there is a decreased Pao2
434.In response to decreased Pao2 (e.g. high altitude) there is increased ventilation
435.Increased ventilation (e.g. high altitude) causes decreased Paco2
436.High altitude initially causes respiratory alkalosis and hypoxia which may cause acute altitude sickness
437.High altitude initially causes respiratory alkalosis and hypoxia which may cause acute altitude sickness
438.High altitude initially causes respiratory alkalosis and hypoxia which may cause acute altitude sickness
439.In response to high altitude there is a chronic increase in ventilation
440.The respiratory alkalosis that occurs as a result of ascent to high altitude may be treated with carbonic anhydrase inhibitors
441.Living at high altitude chronically causes hypoxia which increases the synthesis of erythropoietin causing polycythemia
442.In response to high altitude there is an increase in 2 3-BPG
443.In response to high altitude there are cellular changes such as increased mitochondria
444.In response to respiratory alkalosis (e.g. due to high altitude) there is increased renal excretion of HCO3-
445.In response to high altitude there is chronic hypoxic pulmonary vasoconstriction which results in pulmonary hypertension and RV hypertrophy
446.In response to high altitude there is chronic hypoxic pulmonary vasoconstriction which results in pulmonary hypertension and RV hypertrophy
447.Hypoxemia is defined as a decrease in Pao2
448.Hypoxemia is defined as a decrease in Pao2
449.Is the A - a gradient normal increased or decreased in response to high altitude? Normal
450.Is the A - a gradient normal increased or decreased in response to hypoventilation (e.g. opioid use obesity hypoventilation syndrome)? Normal
451.Is the A - a gradient normal increased or decreased in response to diffusion defects (e.g. fibrosis pulmonary edema)? Increased
452.Is the A - a gradient normal increased or decreased in response to V/Q mismatch? Increased
453.Is the A - a gradient normal increased or decreased in response to right-to-left shunts? Increased
454.What cause of hypoxemia is not greatly helped by supplemental O2? Right-to-left shunt
455.Hypoxia is defined as a decrease of O2 delivery to tissues
456.Hypoxia is defined as a decrease of O2 delivery to tissues
457.Hypoxia may be caused by a decreased cardiac output
458.Hypoxia may be caused by hypoxemia (hypoxia or hypoxemia)
459.Hypoxia may be caused by anemia due to decreased levels of hematocrit and Hb
460.Hypoxia may be caused by carbon monoxide poisoning which decrease the O2 content of blood
461.Ischemia is a cause of O2 deprivation due to a loss of blood flow (e.g. impeded arterial flow decreased venous drainage)
462.Which zone of the lung has the highest Pao2? Zone 1
463.Lung development begins with development of a lung bud from the distal end of the respiratory diverticulum
464.What week does lung development begin? Week 4
465.The embryonic lung bud divides into two bronchial buds that branch off into bronchi
466.The embryonic lung bud divides into two bronchial buds that branch off into bronchi
467.The embryonic period of lung development occurs from weeks 4 to 7
468.The embryonic period of lung development occurs from weeks 4 to 7
469.Errors at what stage of lung development can lead to the formation of a Tracheoesophageal Fistula? Embryonic Period (Weeks 4-7)
470.The pseudoglandular period of lung development occurs from weeks 5 to 16
471.The pseudoglandular period of lung development occurs from weeks 5 to 16
472.During the pseudoglandular period (lung development) the endodermal tubules form the terminal bronchioles
473.During the pseudoglandular period (lung development) the endodermal tubules form the terminal bronchioles
474.During the pseudoglandular period (lung development) the endodermal tubules form the terminal bronchioles
475.During the pseudoglandular period of lung development the bronchioles are surrounded by a modest capillary network
476.Is respiration possible during the pseudoglandular period of lung development? No; incompatible with life
477.The canalicular period of lung development occurs from weeks 16 to 26
478.The canalicular period of lung development occurs from weeks 16 to 26
479.During the canalicular period (lung development) the terminal bronchioles form the respiratory bronchioles which then form the alveolar ducts
480.During the canalicular period (lung development) the terminal bronchioles form the respiratory bronchioles which then form the alveolar ducts
481.During the canalicular period (lung development) the terminal bronchioles form the respiratory bronchioles which then form the alveolar ducts
482.During the canalicular period (lung development) the terminal bronchioles form the respiratory bronchioles which then form the alveolar ducts
483.During the canalicular period of lung development the bronchioles are surrounded by a prominent capillary network
484.During the canalicular period of lung development airways increase in diameter
485.Respiration may be possible at week 25 (canalicular period)
486.The saccular period of lung development occurs from weeks 26 to birth
487.The saccular period of lung development occurs from weeks 26 to birth
488.During the saccular period (lung development) the alveolar ducts form the terminal sacs
489.During the saccular period (lung development) the alveolar ducts form the terminal sacs
490.During the saccular period (lung development) the alveolar ducts form the terminal sacs
491.During the saccular period (lung development) terminal sacs are separated by primary septae
492.In which period of lung development do pneumocytes develop? Canalicular period (weeks 16 - 25)
493.The alveolar period of lung development occurs from weeks 32 to 8 years
494.The alveolar period of lung development occurs from weeks 32 to 8 years
495.During the alveolar period (lung development) the terminal sacs form the adult alveoli
496.During the alveolar period (lung development) the terminal sacs form the adult alveoli
497.During the alveolar period (lung development) the terminal sacs form the adult alveoli
498.Terminal sacs form into adult alveoli due to secondary septation
499.In utero production and expulsion of fetal lung fluid causes increased pulmonary vascular resistance through gestation
500.In utero production and expulsion of fetal lung fluid causes increased pulmonary vascular resistance through gestation
501.Pulmonary hypoplasia is characterized by a poorly-developed bronchial tree with abnormal histology
502.Pulmonary hypoplasia is associated with bilateral renal agenesis (Potter sequence) and congenital diaphragmatic hernia
503.Pulmonary hypoplasia is associated with bilateral renal agenesis (Potter sequence) and congenital diaphragmatic hernia
504.Congenital bronchogenic cysts are caused by abnormal budding of the foregut and dilation of terminal or large bronchi
505.Congenital bronchogenic cysts are caused by abnormal budding of the foregut and dilation of terminal or large bronchi
506.Bronchogenic cyst is a congenital lung malformation that presents as discrete round sharply defined and air-filled densities on CXR
507.Type I pneumocytes line the alveoli (97% of alveolar surfaces)
508.Type I pneumocytes are squamous cells; thin for optimal gas diffusion
509.Type I pneumocytes are squamous cells; thin for optimal gas diffusion
510.Type II pneumocytes are clustered cuboidal (shape) cells
511.Type II pneumocytes are clustered cuboidal (shape) cells
512.Type II pneumocytes proliferate during lung damage
513.Club (Clara) cells are non-ciliated low columnar/cuboidal cells with secretory granules in the lung
514.Club (clara) cells of the lung secrete a component of surfactant and act as reserve cells
515.Club (clara) cells of the lung may degrade toxins
516.The right lung has three lobes
517.The left lung has two lobes
518.Which lung (right or left) has a lingula? Left
519.The right lung is the more common site for inhaled foreign bodies because it has a wider and more verticle bronchus
520.In the right lung the pulmonary artery is anterior to the bronchus
521.In the left lung the pulmonary artery is superior to the bronchus
522.The IVC perforates the diaphragm at the level of T8
523.The IVC perforates the diaphragm at the level of T8
524.The esophagus and vagus nerve perforate the diaphragm at the level of T10
525.The esophagus and vagus nerve perforate the diaphragm at the level of T10
526.The esophagus and vagus nerve perforate the diaphragm at the level of T10
527.The aorta thoracic duct and azygos vein perforate the diaphragm at the level of T12
528.The aorta thoracic duct and azygos vein perforate the diaphragm at the level of T12
529.The aorta thoracic duct and azygos vein perforate the diaphragm at the level of T12
530.The aorta thoracic duct and azygos vein perforate the diaphragm at the level of T12
531.The diaphragm is innervated by the phrenic nerve
532.What are the roots of the phrenic nerve? C3 C4 C5
533.Pain from diaphragm irritation can be referred to the shoulder (C5) or trapezius ridge (C3 4)
534.Pain from diaphragm irritation can be referred to the shoulder (C5) or trapezius ridge (C3 4)
535.The trachea bifurcates at the level of T4
536.The common carotid artery bifurcates at the level of C4
537.During the Canalicular phase of lung development pneumocytes develop starting at 20 weeks
538.Club cells are located in the bronchioles
539.Corticosteroids are important for fetal surfactant production and overall lung development
540.What is the effect of normal aging on chest wall compliance? Decreased compliance
541.What is the effect of normal aging on residual volume? Increased RV
542.What is the effect of normal aging on FVC? Decreased
543.What is the effect of normal aging on FEV1? Decreased
544.What is the effect of normal aging on total lung capacity? No change
545.Can normal aging cause a ventilation/perfusion mismatch? Yes
546.How does normal aging change the A-a gradient? Increased A-a gradient
547.How does normal aging change respiratory muscle strength? Decreased
548.Cyanide poisoning is usually due to inhalation injury
549.Cyanide inhibits aerobic metabolism resulting in hypoxia unresponsive to supplemental O2
550.Cyanide inhibits aerobic metabolism resulting in hypoxia unresponsive to supplemental O2
551.Patients with cyanide poisoning present with an "almond" breath odor and reddish skin discoloration
552.In exercise O2 exhibits mixed-limited gas exchange
553.In exercise blood is flowing faster through the pulmonary capillaries resulting it taking a longer::shorter or longer time for capillary O2 concentration to maximize
554.In a healthy patient can exercise alone make patients hypoxemic? No
555.Infections in the sphenoid or ethmoid sinus may extend to the cavernous sinus and cause complications
556.Because the facial vein is valveless infections of the face can spread to the cavernous sinus
557.Patients with cyanide poisoning have a narrowing of the venous-arterial PO2 gradient
558.Photoaging results in gradual thinning of the epidermis allowing the stratum corneum to become dessicated
559.Irritation of the phrenic nerve can refer pain to the C3-C5::dermatomes shoulder region (Kehr sign) and cause hiccups
560.Irritation of the phrenic nerve can refer pain to the C3-C5::dermatomes shoulder region (Kehr sign) and cause hiccups
561.Dissolved gas + Bound gas + Chemically modified gas = Total gas concentration
562.Dissolved gas + Bound gas + Chemically modified gas = Total gas concentration
563.Dissolved gas + Bound gas + Chemically modified gas = Total gas concentration
564.Bronchoconstriction occurs when the parasympathetic system activates muscarinic receptors
565.At FRC the intrapleural space normally has a negative pressure relative to the atmosphere At FRC the intrapleural pressure is normally -5cmH2O