• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/27

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

27 Cards in this Set

  • Front
  • Back
An infant born prematurely in gestational week 25 has neonatal respiratory distress syndrome. Which of the following would be expected in this infants?
a. Arterial PO2 of 100 mmHg
b. Collapse of the small alveoli
c. Increase lung compliance
d. Normal breathing rate
e. Lecithin:spingomyelin ratio of greater than 2:1 in amniotic fluid
B: Neonatal respiratory syndrome is caused by lack of adequate surfactant in the immature lung. Surfactant appears between the 24th and 35th gestational week. In the absence of surfactant, the surface tension of small alveoli is too high. When the pressure on the small alveoli is too high, the small alveoli collapse into larger alveoli. There is decrease gas exchange and 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. Generally L:S ratio greater than 2:1 signify mature levels of surfactant
Which of the following lung volumes or capacities can be measured by spirometry?
a. FRC
b. Physiological dead space
c. Residual volume
d. TLC
e. Vital capacity
E: Residual volume cannot be measured by spirometry. Therefore, any lung volume or capacity that include the RV cannot be measured by spirometry. Measurements that include RV are FRC and TLC. Vital capacity does not include RV and is , therefore, measurable by spirometry. Physiological dead space is not measurable by spirometry and requires sampling of arterial PCO2 and expired CO2
In which vascular bed does hypoxia cause vasoconstriction?
a. Coronary
b. Pulmonary
c. Cerebral
d. Muscle
e. Skin
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, hypoxia causes vasodilation. The cerebral , muscle and skin circulation are not controlled directly by PO2
A 12-year-old boy has a severe asthmatic attack with wheezing. He experiences rapid breathing and becomes cyanotic. His arterial PO2 is 60 mmHg and his PCO2 is 30 mmHg. Which of the following statements about this patient is most likely to be true?
a. FEV1/FVC ratio is increased
b. V/Q ratio is increased in the affected areas of his lungs
c. His arterial PCO2 is higher than normal because of
d. inadequate gas exchange
e. His arterial PCO2 is lower than normal because hypoxemia is causing him to hyperventilate
His residual volume is decreased
D: The patient’s arterial PCO2 is lower than normal value of 40 mmHg 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 FEV1 and FVC are decreased, with the larger decrease occurring in FEV1. Therefore, FEV1/FVC ratio is decreased. Poor ventilation of the affected areas decreases the V/Q ratio and causes hypoxemia. The patient’s residual volume is increased because he is breathing at a higher lung volume to offset the increased resistance of his airways.
To treat this patient (asthma attack), the physician should administer
a. An alpha- adrenergic antagonist
b. A beta 1- adrenergic antagonist
c. A beta 2- adrenergic agonist
d. A muscarinic agonist
e. A nicotinic agonist
C: The cause of airway obstruction in asthma is bronchiolar constriction. beta 2- adrenergic stimulation (beta 2- adrenergic agonist) produces relaxation of the bronchioles.
Which of the following is true during inspiration?
a. Intrapleural pressure is positive
b. The volume in the lungs is less than the FRC
c. Alveolar pressure equals atmospheric pressure
d. Alveolar pressure is higher than atmospheric pressure
e. Intrapleural pressure is more negative that is during expiration
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 flow 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 of lungs during inspiration is the FRC plus one TV
A person has a VC of 5L, a TV of 0.5L , an inspiratory capacity of 3.5L, FRC of 2.5L, and a residual volume of 1.0 L. What is his expiratory reserve volume?
a. 4.5L
b. 3.9L
c. 3.6L
d. 3.0L
e. 2.5L
f. 2.0L
g. 1.5L
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
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. The pressure difference drives the blood flow
Which of the following is illustrated in the graph showing volume versus pressure in the lung-chest wall system?
a. The slop of each curve is resistance
b. The compliance of the lungs alone is less than the compliance of the lungs plus chest wall
c. The compliance of the chest wall alone is less than the compliance of the lungs plus chest wall
d. When airway pressure is zero (atmospheric), the volume in the lungs plus chest wall is FRC
e. When airway pressure is zero (atmospheric), intrapleural pressure is zero
D: By convention, when airway pressure is equal to atmospheric pressure, it is designated as zero pressure. Under these condition, there is no airflow because there is no pressure gradient between the atmosphere and alveoli, and the volume in the lungs is the FRC. The slop of each curve is compliance, not resistance; the steeper the slop, the greater the volume change for a given pressure change, or the greater compliance. The compliance of the lungs alone or the chest wall alone is greater than that of the combined lung-chest 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 condition ), intrapleural pressure is negative because of the opposing tendencies of the chest wall to spring out and lungs to collapse
Which of the following is the highest airways resistance?
a. Trachea
b. Largest bronchi
c. Medium-sized bronchi
d. Smallest bronchi
e. Alveoli
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.
If flow of the left lung is completely blocked by an embolism in the pulmonary artery, which of the following will occur?
a. 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 equals to the PO2 in inspired air
e. Alveolar PO2 in the right lung will be approximately equal to the PO2 in venous blood
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 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
In the Hb-O2 dissociation curves shown, the shift from normal to right could be caused by
a. Increased pH
b. Decreased 2,3-DPG
c. Strenuous exercise
d. Fetal hemoglobin
e. Carbon monoxide
c: Strenuous exercise increases the temperature and decreases the pH of skeletal muscle; both effects would cause the Hb-O2 dissociation curve to shift to the right, making it easier to unload O2 in the tissue to meet the high demand of the exercising muscle. 2, 3 DPG binds to the beta-chain of adult Hb and reduces its affinity for O2, shifting the curve to the right. In fetal Hb, the beta-chain are replaced by gamma chain, which do not bind 2,3 DPG, so the curve is shifted to left. Because CO increases the affinity of the remaining binding sites for O2, the curve is shifted to the left.
The shift from normal to curve X is associated with
a. Decreased P50
b. Decreased affinity of Hb for O2
c. Impaired ability to unload O2 in the tissues
d. Increased O2-carrying capacity of Hb
e. Decreased O2-carring capacity of Hb
B: A shift to the right of the Hb-O2 dissociation curve represents decreased affinity of Hb for O2. At any given PO2, the percent saturation is decreased, the P50 is increased (read the PO2 from the graph at 50% Hb saturation), and unloading of O2 in the tissue is facilitated. The O2-carrying capacity of Hb is determined by the Hb concentration and is unaffected by the shift from normal to curve X.
The pH of venous blood is only slightly more acid 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
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 out put
B: Blood flow ( or cardiac out put) in the systemic and pulmonary circulation 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 flow through the two circulation are approximately equal (flow =pressure / resistance).
A person with TV of 0.45L has a breathing frequency of 16. His arterial PCO2 is 41 mmHg, and the PCO2 of his expired air is 35 mmHg. 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
Alveolar ventilation = (TV –DS) x RR
First calculate the dead space;
Dead space = 0.45 x (41-35/41) = 0.066L
Alveolar ventilation= (0.45- 0.066) x 16 =6.14L/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 V/Q ratio
d. The same V/Q ratio
Hypoxemia produces hyperventilation by direct effect on the
a. Phrenic nerve
b. J receptor
c. Lung stretch receptor
d. Medullary chemoreceptors
e. Carotid and aortic body chemoreceptors
E: Hypoxemia stimulates breathing by a direct effect on the peripheral chemoreceptors in the carotid and aortic bodies. Central 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
Which of the following changes occurs during strenuous exercise ?
a. Ventilation rate and O2 consumption increase at the same extent
b. Systemic arterial PO2 decreases to about 70 mmHg
c. Systemic arterial PCO2 increases to about 60 mmHg
d. Systemic venous PCO2 decreases to about 20 mmHg
e. Pulmonary blood flow decreases
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 muscles. Because this CO2 will be blown off by the hyperventilating lungs, it does not increase the arterial PCO2. Pulmonary blood flow (cardiac output) increases many folds during strenuous exercise.
If an area of lung is not ventilated because of bronchial obstruction, the pulmonary capillary blood serving that
a. area will have a PO2 that is
b. Equals to atmospheric PO2
c. Equals to mixed venous PO2
d. Equals to normal systemic arterial PO2
e. Higher than inspired PO2
f. Lower than mixed venous PO2
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
In the transport of CO2 from the tissue to the lungs, which of the following occurs in venous blood?
a. Conversion of CO2 and H2O to H+ and HCO3- in the 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 Hb
e. Alkalinization of RBCs
A: CO2 generated in the tissues is hydrated to form H+ and HCO3- in 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 Hb (carbaminohemoglobin)
Volume remaining in the lungs after TV is expired
a. TV
b. VC
c. ERV
d. RV
e. FRC
E: During normal breathing, the volume inspired and then expired is a tidal volume. The volume remaining in the lungs after expiration of a TV is the FRC
Volume remaining in the lungs after a maximal expiration
a. TV
b. VC
c. ERV
d. RV
e. FRC
D: During a forced expiration , the volume expired is a tidal volume plus the expiratory reserve volume. The volume remaining in the lungs is the residual volume (RV)
Which of the following causes of hypoxia is characterized by a decrease arterial PO2 and an increase A-a gradient?
a. Hypoventilation
b. Right-to-left cardiac shunt
c. Anemia
d. CO poisoning
e. Ascent to high altitude
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 blood is caused by decreased Hb conc. (anemia), decreased O2 binding capacity of Hb (CO poisoning) or decreased arterial PO2 (hypoxemia). Hypoventilation, right to left shunt and ascent to high altitude all cause hypoxia by decreasing arterial PO2. Of these , only right-to-left cardiac shunt is associated with and increased A-a gradient, reflecting a lack of O2 equilibrium 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 lung and thereby “dilute” 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
A patient with severe pulmonary fibrosis is evaluated by her physician and has the following ABGs: pH= 7.48, PaO2=55 , PaCO2= 32. Which statement best explains the observed value of PaO2?
a. The increase pH stimulates breathing via peripheral chemoreceptor
b. The increased pH stimulates breathing via central chemoreceptor
c. The decrease PO2 inhibits breathing via peripheral chemoreceptors
d. The decrease PO2 stimulates breathing via peripheral chemoreceptor
e. The decreased PO2 stimulates breathing via central chemoreceptors
D: The patient’s ABGs shows increased pH, decreased PaO2, and decreased PCO2. The decreased PO2 causes hyperventilation via peripheral chemoreceptor, but not via central chemoreceptor. The decreased PaCO2 results from hyperventilation and causes increased pH which inhibits breathing via the peripheral and central chemoreceptor
Which of the following will occur as a result of residing at high altitude?
a. Hypoventilation
b. Atrial PO2 greater than 100 mmHg
c. Decrease 2,3 DPG
d. Shift to right of oxy-Hb curve
e. Pulmonary vasodilation
f. Hypertrophy of left ventricle
g. Respiratory acidosis
D: At high altitude, the PO2 of alveolar air is decreased because barometric pressure is decreased. As a result, arterial PO2 is decreased (<100 mmHg), and hypoxemia occurs and causes hyperventilation by an effect on peripheral chemoreceptors. Hyperventilation leads to respiratory alkalosis. 2,3 DPG levels increase adaptively; 2,3 DPG binds to Hb and causes the oxy-Hb curve shift to right to improve unloading of O2 in the tissue. The pulmonary vascular vasoconstriction in response to alveolar hypoxia, resulting in increased in increase pulmonary arterial pressure and hypertrophy of right ventricle (not the left ventricle)
A person with a 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 =infinity
D: Supplemental O2 is most helpful in treating hypoxemia associated with a V/Q ratio 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 rising the PO2 of a small volume of blood will have little overall effect on systemic arterial blood.