Anesthesiology.Respiratory Physiology

1. The normal FEV₁/FVC ratio is

0.95

0.80

0.60

0.50

0.40

The forced expiratory volume in one second (FEV1) is the total volume
of air that can be exhaled in the first second. Healthy adults can exhale
approximately 75% to 80% of their forced vital capacity (FVC) in the
first second. Therefore, the normal FEV1/FVC ratio is ≥ 0.80. In the
presence of obstructive airway disease, the FEV1/FVC ratio is This ratio can be used to determine the severity of obstructive airway
disease and to monitor the efficacy of bronchodilator therapy.

Explanation

The forced expiratory volume in one second (FEV1) is the total volume
of air that can be exhaled in the first second. Healthy adults can exhale
approximately 75% to 80% of their forced vital capacity (FVC) in the
first second. Therefore, the normal FEV1/FVC ratio is ≥ 0.80. In the
presence of obstructive airway disease, the FEV1/FVC ratio is This ratio can be used to determine the severity of obstructive airway
disease and to monitor the efficacy of bronchodilator therapy.

2. The most important buffering system in the body is

Hemoglobin

Plasma proteins

Bone

HCO3-

Phosphate

Buffer systems represent the first line of defense against adverse changes in pH. The HC03- buffer system is the most important system and represents > 50% of the total buffering capacity of the body. Other important buffer systems include hemoglobin, which is responsible for approximately 35% of the buffering capacity of blood, phosphates, plasma proteins, and bone.

Explanation

Buffer systems represent the first line of defense against adverse changes in pH. The HC03- buffer system is the most important system and represents > 50% of the total buffering capacity of the body. Other important buffer systems include hemoglobin, which is responsible for approximately 35% of the buffering capacity of blood, phosphates, plasma proteins, and bone.

3. The functional residual capacity is composed of the

Expiratory reserve volume and residual volume

Inspiratory reserve volume and residual volume

Inspiratory capacity and vital capacity

Expiratory capacity and tidal volume

Expiratory reserve volume and tidal volume

A comprehensive understanding of respiratory physiology is important for understanding the effects of both regional and general anesthesia on respiratory mechanics and pulmonary gas exchange. The volume of gas remaining in the lungs after a normal expiration is called the functional residual capacity. The volume of gas remaining in the lungs after a maximal expiration is called the residual volume. The difference between these two volumes is called the expiratory reserve volume. Therefore, the functional residual capacity is composed of the expiratory reserve volume and residual volume.

Explanation

A comprehensive understanding of respiratory physiology is important for understanding the effects of both regional and general anesthesia on respiratory mechanics and pulmonary gas exchange. The volume of gas remaining in the lungs after a normal expiration is called the functional residual capacity. The volume of gas remaining in the lungs after a maximal expiration is called the residual volume. The difference between these two volumes is called the expiratory reserve volume. Therefore, the functional residual capacity is composed of the expiratory reserve volume and residual volume.

4. The normal vital capacity for a 70-kg man is

1 L

2 L

5 L

7 L

9 L

The volume of gas exhaled during a maximum expiration is the vital ca¬pacity. In a healthy adult, the vital capacity is 60-70 mL/kg. In a 70-kg patient, the vital capacity is approximately 5 L.

Explanation

The volume of gas exhaled during a maximum expiration is the vital ca¬pacity. In a healthy adult, the vital capacity is 60-70 mL/kg. In a 70-kg patient, the vital capacity is approximately 5 L.

5. Reynold's number is an important factor in the determination of

O2 transport

Surface tension

Turbulent vs. laminar flow

Physiologic dead-space ventilation

Functional residual capacity

. Reynold's number is a calculated value that represents the overall ratio of inertial forces to viscous forces during flow. Reynold's number is directly proportional to the density of the substance, the flow velocity of the substance, and the radius of the container through which the substance is flowing, and is inversely proportional to the viscosity of the substance. In general, flow through a long, straight, smooth-walled container becomes turbulent when the Reynold's number is greater than 2,300.

Explanation

. Reynold's number is a calculated value that represents the overall ratio of inertial forces to viscous forces during flow. Reynold's number is directly proportional to the density of the substance, the flow velocity of the substance, and the radius of the container through which the substance is flowing, and is inversely proportional to the viscosity of the substance. In general, flow through a long, straight, smooth-walled container becomes turbulent when the Reynold's number is greater than 2,300.

6. The anatomic dead space in a 70-kg male is

50 mL

150 mL

250 mL

500 mL

700 to 1000 mL

The conducting airways (trachea, right and left mainstem bronchi, and lobar and segmental bronchi) do not contain alveoli and therefore do not take part in pulmonary gas exchange. These structures constitute the anatomic dead space. In the adult, the anatomic dead space is approximately 1 mL/lb or 2 mL/kg. The anatomic dead space increases during inspiration because of the traction exerted on the conducting airways by the surrounding lung parenchyma. In addition, the anatomic dead space depends on the size and posture of the subject.

Explanation

The conducting airways (trachea, right and left mainstem bronchi, and lobar and segmental bronchi) do not contain alveoli and therefore do not take part in pulmonary gas exchange. These structures constitute the anatomic dead space. In the adult, the anatomic dead space is approximately 1 mL/lb or 2 mL/kg. The anatomic dead space increases during inspiration because of the traction exerted on the conducting airways by the surrounding lung parenchyma. In addition, the anatomic dead space depends on the size and posture of the subject.

7. The P₅₀ for normal adult hemoglobin is

15

25

35

45

50

P50 is the PaO2 required to produce 50% saturation of hemoglobin. The P50 for adult hemoglobin is 26 mm Hg

Explanation

P50 is the PaO2 required to produce 50% saturation of hemoglobin. The P50 for adult hemoglobin is 26 mm Hg

8. Each of the following will cause erroneous readings by dual-wavelength pulse oximeters EXCEPT

Carboxyhemoglobin

Methylene blue

Fetal hemoglobin

Methemoglobin

Nail polish

The presence of hemoglobin species other than oxyhemoglobin can cause erroneous readings by dual-wavelength pulse oximeters. Hemoglobin species such as carboxyhemoglobin and methemoglobin, dyes such as methylene blue and indocyanine green, and nail polish will cause erroneous readings. Since the absorption spectrum of fetal hemoglobin is similar to that of adult oxyhemoglobin, fetal hemoglobin does not significantly affect the accuracy of these types of pulse oximeters. High levels of bilirubin have no significant effect on the accuracy of dual-wavelength pulse oximeters, but may cause falsely low readings by nonpulsatile oximeters.

Explanation

The presence of hemoglobin species other than oxyhemoglobin can cause erroneous readings by dual-wavelength pulse oximeters. Hemoglobin species such as carboxyhemoglobin and methemoglobin, dyes such as methylene blue and indocyanine green, and nail polish will cause erroneous readings. Since the absorption spectrum of fetal hemoglobin is similar to that of adult oxyhemoglobin, fetal hemoglobin does not significantly affect the accuracy of these types of pulse oximeters. High levels of bilirubin have no significant effect on the accuracy of dual-wavelength pulse oximeters, but may cause falsely low readings by nonpulsatile oximeters.

9. O₂ requirement for a 70-kg adult under general anesthesia is

150 mL/min

250 mL/min

350 mL/min

450 mL/min

550 mL/min

The O2 requirement for an adult under general anesthesia is 3 to 4 mL/kg/min. The O2 requirement for a newborn under general anesthesia is 7 to 9 mL/kg/min. Alveolar ventilation (VA) in neonates is double that of adults to help meet their increased O2 requirements. This increase in VA is achieved primarily by an increase in respiratory rate as tidal volume (VT) is similar to that of adults. Although CO2 production is also increased in neonates, the elevated VA maintains the PaCO2 hear 38 to 40 mm Hg.

Explanation

The O2 requirement for an adult under general anesthesia is 3 to 4 mL/kg/min. The O2 requirement for a newborn under general anesthesia is 7 to 9 mL/kg/min. Alveolar ventilation (VA) in neonates is double that of adults to help meet their increased O2 requirements. This increase in VA is achieved primarily by an increase in respiratory rate as tidal volume (VT) is similar to that of adults. Although CO2 production is also increased in neonates, the elevated VA maintains the PaCO2 hear 38 to 40 mm Hg.

10. What is the O₂ content of whole blood if the hemoglobin concentration is 10 mg/dL, the PaO₂ is 60 mm Hg, and the SaO₂ is 90%?

10 mL/dL

13 mL/dL

15 mL/dL

18 mL/dL

21 mL/dL

The amount of O2 in blood (O2 content) is the sum of the amount of O2 dissolved in plasma and the amount of O2 combined with hemoglo¬bin. The amount of O2 dissolved in plasma is directly proportional to the product of the blood:gas solubility coefficient of O2 (0.003) and PaO2. The amount of O2 bound to hemoglobin is directly related to the fraction of hemoglobin that is saturated. One gram of hemoglobin can bind 1.39 ml of O2. The mathematical expression of O2 content is as follows:
O2 content = 1.39 * [Hgb] * SaO2 + 0.003 * (PaO2), where [Hgb] is the hemoglobin concentration (mg/dL), SaO2 is the fraction of hemoglobin saturated with O2, and 0.003 (PaO2) is the amount of O2 dissolved in plasma. The O2 content of blood in this patient is approximately 13 mL/dL.

Explanation

The amount of O2 in blood (O2 content) is the sum of the amount of O2 dissolved in plasma and the amount of O2 combined with hemoglo¬bin. The amount of O2 dissolved in plasma is directly proportional to the product of the blood:gas solubility coefficient of O2 (0.003) and PaO2. The amount of O2 bound to hemoglobin is directly related to the fraction of hemoglobin that is saturated. One gram of hemoglobin can bind 1.39 ml of O2. The mathematical expression of O2 content is as follows:
O2 content = 1.39 * [Hgb] * SaO2 + 0.003 * (PaO2), where [Hgb] is the hemoglobin concentration (mg/dL), SaO2 is the fraction of hemoglobin saturated with O2, and 0.003 (PaO2) is the amount of O2 dissolved in plasma. The O2 content of blood in this patient is approximately 13 mL/dL.

11. Which of the following is the correct mathematical expression of Fick's law of diffusion of a gas through a lipid membrane (V = rate of diffusion, D = diffusion coefficient of the gas, A = area of the membrane, P₁ - P₂ = transmembrane partial pressure gradient of the gas, T = thickness of the membrane)?

V=D*A*T/(P1-P2)

V=A*T/D*(P1-P2)

V=D*A*(P1-P2)/T

V=D*T*(P1-P2)/A

V=D*T*A/(P1-P2)

The rate that a gas diffuses through a lipid membrane is directly proportional to the area of the membrane, the transmembrane partial pres¬sure gradient of the gas, and the diffusion constant of the gas, and is inversely proportional to the thickness of the membrane. The diffusion constant is directly proportional to the square root of gas solubility and is inversely proportional to the square root of the molecular weight of the gas. This is known as Fick's law of diffusion.

Explanation

The rate that a gas diffuses through a lipid membrane is directly proportional to the area of the membrane, the transmembrane partial pres¬sure gradient of the gas, and the diffusion constant of the gas, and is inversely proportional to the thickness of the membrane. The diffusion constant is directly proportional to the square root of gas solubility and is inversely proportional to the square root of the molecular weight of the gas. This is known as Fick's law of diffusion.

12. During the first minute of apnea, the PaCO₂ will rise

2 mm Hg/min

4 mm Hg/min

6 mm Hg/min

8 mm Hg/min

10 mm Hg/min

During apnea, the PaCO2 will increase approximately 6 mm Hg during
the first minute and then 3 to 4 mm Hg each minute thereafter

Explanation

During apnea, the PaCO2 will increase approximately 6 mm Hg during
the first minute and then 3 to 4 mm Hg each minute thereafter

13. Which of the following statements correctly defines the relationship between minute ventilation (Ve), dead space ventilation (Vd), and PaCO₂?

If VE is constant and VD increases, then PaCO2 will increase

If VE is constant and VD increases, then PaCO2 will decrease

If VD is constant and VE increases, then PaCO2 will increase

If VD is constant and VE increases, then PaCO2 will decrease

None of the above

The volume of gas in the conducting airways of the lungs (and not available for gas exchange) is called the anatomic dead space. The volume of gas in ventilated alveoli that are unperfused (and also not available for gas exchange) is called the functional dead space. The anatomic dead space together with the functional dead space is called the physiologic dead space. Physiologic dead-space ventilation can be calculated by the Bohr dead-space equation, which is mathematically expressed as follows:
VD/VT = (PaCO2 — PeCO2)/PaCO2,
where VD/VT is the ratio of physiologic dead-space ventilation (VD) to VT, and the a and e represent arterial and mixed expired, respectively. Of the choices given, only the first is correct. A large increase in physiologic dead-space ventilation will result in an increase in PaCO2

Explanation

The volume of gas in the conducting airways of the lungs (and not available for gas exchange) is called the anatomic dead space. The volume of gas in ventilated alveoli that are unperfused (and also not available for gas exchange) is called the functional dead space. The anatomic dead space together with the functional dead space is called the physiologic dead space. Physiologic dead-space ventilation can be calculated by the Bohr dead-space equation, which is mathematically expressed as follows:
VD/VT = (PaCO2 — PeCO2)/PaCO2,
where VD/VT is the ratio of physiologic dead-space ventilation (VD) to VT, and the a and e represent arterial and mixed expired, respectively. Of the choices given, only the first is correct. A large increase in physiologic dead-space ventilation will result in an increase in PaCO2

14. Calculate the Vd/Vt ratio (physiologic dead-space ventilation) based on the following data: PaCO₂ 45 mm Hg, mixed expired CO₂ tension (PeCO₂) 30 mm Hg.

0.1

0.2

0.3

0.4

0.5

Physiologic dead-space ventilation can be estimated using the Bohr equation
Vd/Vt= (45mm Hg - 30 mm Hg)/45 mm Hg= 0.33

Explanation

Physiologic dead-space ventilation can be estimated using the Bohr equation
Vd/Vt= (45mm Hg - 30 mm Hg)/45 mm Hg= 0.33

15. The shift of the CO₂-hemoglobin dissociation curve which occurs in response to changes in PaO₂ is known as the

Fick principle

Bohr effect

Haldane effect

Law of Laplace

Le Chatelier principle

The shift of the CO2-hemoglobin dissociation curve that occurs in response to changes in PaO2 is known as the Haldane effect. Because of this effect, deoxygenated hemoglobin (in peripheral tissues) has a greater affinity for CO2 than does oxygenated hemoglobin.

Explanation

The shift of the CO2-hemoglobin dissociation curve that occurs in response to changes in PaO2 is known as the Haldane effect. Because of this effect, deoxygenated hemoglobin (in peripheral tissues) has a greater affinity for CO2 than does oxygenated hemoglobin.

16. The leftward shift of the oxyhemoglobin dissociation curve caused by hypocarbia is known as the

Fick principle

Bohr effect

Haldane effect

Law of Laplace

None of the above

The effects of PaCO2 and pH on the position of the oxyhemoglobin dissociation curve is known as the Bohr effect. Hypercarbia and acidosis shift the curve to the right, and hypocarbia and alkalosis shift the curve to the left. The Bohr effect is attributed primarily to the action of CO2 and pH on erythrocyte 2,3-DPG metabolism.

Explanation

The effects of PaCO2 and pH on the position of the oxyhemoglobin dissociation curve is known as the Bohr effect. Hypercarbia and acidosis shift the curve to the right, and hypocarbia and alkalosis shift the curve to the left. The Bohr effect is attributed primarily to the action of CO2 and pH on erythrocyte 2,3-DPG metabolism.

17. Each of the following is decreased in elderly patients compared with their younger counterparts EXCEPT

PaO2

FEV1

Ventilatory response to hypercarbia

Vital capacity

Closing volume

In general, aging is associated with reduced ventilatory volumes and capacities, and decreased efficiency of pulmonary gas exchange. These changes are caused by progressive stiffening of cartilage and replacement of elastic tissue in the intercostal and intervertebral areas, which decreases compliance of the thoracic cage. In addition, progressive kyphosis or scoliosis produces upward and anterior rotation of the ribs and sternum, which further restricts chest wall expansion during inspiration. With aging, the functional residual capacity, residual volume, and closing volume are increased, while the vital capacity, total lung capacity, maximum breathing capacity, FEV1, and ventilatory response to hypercarbia and hypoxemia are reduced. In addition, age-related changes in lung parenchyma, alveolar surface area, and diminished pulmonary capillary bed density cause ventilation/perfusion mismatch, which decreases resting PaO2.

Explanation

In general, aging is associated with reduced ventilatory volumes and capacities, and decreased efficiency of pulmonary gas exchange. These changes are caused by progressive stiffening of cartilage and replacement of elastic tissue in the intercostal and intervertebral areas, which decreases compliance of the thoracic cage. In addition, progressive kyphosis or scoliosis produces upward and anterior rotation of the ribs and sternum, which further restricts chest wall expansion during inspiration. With aging, the functional residual capacity, residual volume, and closing volume are increased, while the vital capacity, total lung capacity, maximum breathing capacity, FEV1, and ventilatory response to hypercarbia and hypoxemia are reduced. In addition, age-related changes in lung parenchyma, alveolar surface area, and diminished pulmonary capillary bed density cause ventilation/perfusion mismatch, which decreases resting PaO2.

18. The degree of transpulmonary shunt can be estimated to equal 1% of the cardiac output for each

10 mm Hg increase in the alveolar-to-arterial difference in O2 tension P(A - a)O2

20 mm Hg increase in the P(A - a)O2

30 mm Hg increase in the P(A - a)O2

40 mm Hg increase in the P(A - a)O2

50 mm Hg increase in the P(A - a)O2

The fraction of the cardiac output shunted through the lungs without exposure to ventilated alveoli (i.e., transpulmonary shunt) can be estimated using the general rule that for every increase in the alveolar-to-arterial difference in O2 tension P(A-a)O2 of 20 mm Hg, there is a shunt fraction of approximately 1% of the cardiac output (i.e., Qs/Qt = P(A-a)O2/20, where Qs/Qt is the shunt fraction)

Explanation

The fraction of the cardiac output shunted through the lungs without exposure to ventilated alveoli (i.e., transpulmonary shunt) can be estimated using the general rule that for every increase in the alveolar-to-arterial difference in O2 tension P(A-a)O2 of 20 mm Hg, there is a shunt fraction of approximately 1% of the cardiac output (i.e., Qs/Qt = P(A-a)O2/20, where Qs/Qt is the shunt fraction)

19. What is the maximum compensatory increase in serum bicarbonate concentration ([HC0₃^-]) for every 10 mm Hg increase in PaCO₂ with chronic respiratory acidosis?

1 mEq/L

3 mEq/L

7 mEq/L

10 mEq/L

15 mEq/L

The kidneys respond to chronic respiratory acidosis by conserving bicarbonate (HCO3-) and secreting hydrogen (H+). In respiratory acidosis, there is an immediate hydration of CO2 in plasma to produce HCO3-. This acute process produces approximately 1 mEq/L of HCO3- for every 10 mm Hg increase in PaCO2. Hydration of CO2 in the proximal and distal renal tubules stimulates the secretion of H+ into the urine. This compensatory response requires 12 to 48 hours. The compensatory response to chronic respiratory acidosis is rarely complete such that the pH does not fully return to 7.4. The maximum compensatory increase in serum bicarbonate concentration ([HCO3-]) in response to chronic respiratory acidosis is 3 mEq/L.

Explanation

The kidneys respond to chronic respiratory acidosis by conserving bicarbonate (HCO3-) and secreting hydrogen (H+). In respiratory acidosis, there is an immediate hydration of CO2 in plasma to produce HCO3-. This acute process produces approximately 1 mEq/L of HCO3- for every 10 mm Hg increase in PaCO2. Hydration of CO2 in the proximal and distal renal tubules stimulates the secretion of H+ into the urine. This compensatory response requires 12 to 48 hours. The compensatory response to chronic respiratory acidosis is rarely complete such that the pH does not fully return to 7.4. The maximum compensatory increase in serum bicarbonate concentration ([HCO3-]) in response to chronic respiratory acidosis is 3 mEq/L.

20. The predominant stimulus for activation of hypoxic pulmonary vasoconstriction is

Increased PaCO2

Decreased PaCO2

Increased PaO2

Decreased PAO2

None of the above

Hypoxic pulmonary vasoconstriction is a reflex within the lungs that causes regional vasoconstriction of the pulmonary vasculature to reduce blood flow to hypoxic alveoli. This is an important compensatory mechanism for minimizing transpulmonary shunt. The most important stimulus for this reflex is PAO2.

Explanation

Hypoxic pulmonary vasoconstriction is a reflex within the lungs that causes regional vasoconstriction of the pulmonary vasculature to reduce blood flow to hypoxic alveoli. This is an important compensatory mechanism for minimizing transpulmonary shunt. The most important stimulus for this reflex is PAO2.

21. Inhalation of CO₂ increases Ve by

0.5 L/min/mm Hg increase in PaCO2

1 to 3 L/min/mm Hg increase in PaCO2

3 to 5 L/min/mm Hg increase in PaCO2

5 to 10 L/min/mm Hg increase in PaCO2

10 to 20 L/min/mm Hg increase in PaCO2

The degree of ventilatory depression caused by volatile anesthetics can be assessed by measuring resting PaCO2, the ventilatory response to hypercarbia and the ventilatory response to hypoxemia. Of these techniques, the resting PaCO2 is the most frequently used index. How¬ever, measuring the effects of increased PaCO2 on ventilation is the most sensitive method of quantifying the effects of drugs on ventilation. In awake, unanesthetized humans, inhalation of CO2 increases minute ventilation (VE) by approximately 1 to 3 L/min/mm Hg increase in PaCO2. Using this technique, halothane, isoflurane, enflurane, and N2O cause a dose-dependent depression of the ventilation.

Explanation

The degree of ventilatory depression caused by volatile anesthetics can be assessed by measuring resting PaCO2, the ventilatory response to hypercarbia and the ventilatory response to hypoxemia. Of these techniques, the resting PaCO2 is the most frequently used index. How¬ever, measuring the effects of increased PaCO2 on ventilation is the most sensitive method of quantifying the effects of drugs on ventilation. In awake, unanesthetized humans, inhalation of CO2 increases minute ventilation (VE) by approximately 1 to 3 L/min/mm Hg increase in PaCO2. Using this technique, halothane, isoflurane, enflurane, and N2O cause a dose-dependent depression of the ventilation.

22. The most important mechanism for the transport of CO₂ from peripheral tissues to the lungs is

CO2 dissolved in plasma

Carbonic acid

Carbaminohemogiobin

HC03-

(CO3)-2

CO2 is transported from the peripheral tissues to the lungs, primarily in the form of HCO3-; there it is eliminated from the body. The conversion of CO2 to HCO3- occurs within erythrocytes and is catalyzed by the enzyme carbonic anhydrase. HCO3- then diffuses out of the cell in exchange for a chloride ion (Cl-) to maintain electrical neutrality. This exchange is called the chloride shift. CO2 is also transported dissolved in blood and bound to proteins as carbamino compounds. Carbamino compounds are formed by the combination of CO2 with terminal amine groups on blood proteins, primarily hemoglobin. This reaction occurs very rapidly without enzymatic catalysts. Approximately 60% of CO2 is transported from peripheral tissues to the lungs in the form of HC03-, 30% in the form of carbaminohemoglobin, and 10% dissolved in plasma.

Explanation

CO2 is transported from the peripheral tissues to the lungs, primarily in the form of HCO3-; there it is eliminated from the body. The conversion of CO2 to HCO3- occurs within erythrocytes and is catalyzed by the enzyme carbonic anhydrase. HCO3- then diffuses out of the cell in exchange for a chloride ion (Cl-) to maintain electrical neutrality. This exchange is called the chloride shift. CO2 is also transported dissolved in blood and bound to proteins as carbamino compounds. Carbamino compounds are formed by the combination of CO2 with terminal amine groups on blood proteins, primarily hemoglobin. This reaction occurs very rapidly without enzymatic catalysts. Approximately 60% of CO2 is transported from peripheral tissues to the lungs in the form of HC03-, 30% in the form of carbaminohemoglobin, and 10% dissolved in plasma.

23. Each of the following will alter the position or slope of the CO₂-ventilatory response curve EXCEPT

Hypoxemia

Fentanyl

N2O

Volatile anesthetics

Ketamine

Measuring the ventilatory response to increased PaCO2 is a sensitive method for quantifying the effects of drugs on ventilation. In general, all volatile anesthetics (including N2O), narcotics, benzodiazepines, and barbiturates depress the CO2-ventilatory response curve in a dose-dependent manner. The magnitude of ventilatory depression by volatile anesthetics is greater in patients with chronic obstructive pulmonary disease (COPD) than in healthy patients. Thus, it is recommended that arterial blood gases are monitored during recovery from general anesthesia in patients with COPD. Ketamine causes minimal respiratory depression. Typically, respiratory rate is decreased only 2 to 3 breaths/min and the ventilatory response to changes in PaCO2 is maintained during ketamine anesthesia.

Explanation

Measuring the ventilatory response to increased PaCO2 is a sensitive method for quantifying the effects of drugs on ventilation. In general, all volatile anesthetics (including N2O), narcotics, benzodiazepines, and barbiturates depress the CO2-ventilatory response curve in a dose-dependent manner. The magnitude of ventilatory depression by volatile anesthetics is greater in patients with chronic obstructive pulmonary disease (COPD) than in healthy patients. Thus, it is recommended that arterial blood gases are monitored during recovery from general anesthesia in patients with COPD. Ketamine causes minimal respiratory depression. Typically, respiratory rate is decreased only 2 to 3 breaths/min and the ventilatory response to changes in PaCO2 is maintained during ketamine anesthesia.

24. Which of the following pulmonary function tests is least dependent on patient effort?

FEV1

FVC

FEF800-1200

FEF25-75

MVV

Pulmonary function tests can be divided into those that assess ventilatory capacity and into those that assess pulmonary gas exchange. The simplest test to assess ventilatory capacity is the FEV1/FVC ratio. Other tests to assess ventilatory capacity include the maximum midexpiratory flow (FEF25-75), maximum voluntary ventilation (MVV), and flow-volume curves. The most significant disadvantage of these tests is that they are dependent on patient effort; however, since the FEF25-75 is obtained from the midexpiratory portion of the flow-volume loop, it is least dependent on patient effort.

Explanation

Pulmonary function tests can be divided into those that assess ventilatory capacity and into those that assess pulmonary gas exchange. The simplest test to assess ventilatory capacity is the FEV1/FVC ratio. Other tests to assess ventilatory capacity include the maximum midexpiratory flow (FEF25-75), maximum voluntary ventilation (MVV), and flow-volume curves. The most significant disadvantage of these tests is that they are dependent on patient effort; however, since the FEF25-75 is obtained from the midexpiratory portion of the flow-volume loop, it is least dependent on patient effort.

25. Which of the following statements concerning the distribution of alveolar ventilation (Va) in the upright lungs is true?

The distribution of VA is not affected by body posture

Alveoli at the apex of the lungs (nondependent alveoli) are better ventilated than those at the base

All areas of the lungs are ventilated equally

Alveoli at the base of the lungs (dependent alveoli) are betterventilated than those at the apex

Alveoli at the central regions of the lungs are better ventilatedthan those at the base or apex

The orientation of the lungs relative to gravity has a profound effect on efficiency or pulmonary gas exchange. Because alveoli in dependent regions of the lungs expand more per unit change in transpulmonary pressure (i.e., are more compliant) than alveoli in nondependent regions of the lungs, Va increases from the top to the bottom of the lungs. Because pulmonary blood flow increases more from the top to the bottom of the lungs than does Va, the ventilation/perfusion ratio is high in nondependent regions of the lungs and is low in dependent regions of the lungs. Therefore, in the upright lungs, the PO2 and pH are greater at the apex, while the PCO2 is greater at the base.

Explanation

The orientation of the lungs relative to gravity has a profound effect on efficiency or pulmonary gas exchange. Because alveoli in dependent regions of the lungs expand more per unit change in transpulmonary pressure (i.e., are more compliant) than alveoli in nondependent regions of the lungs, Va increases from the top to the bottom of the lungs. Because pulmonary blood flow increases more from the top to the bottom of the lungs than does Va, the ventilation/perfusion ratio is high in nondependent regions of the lungs and is low in dependent regions of the lungs. Therefore, in the upright lungs, the PO2 and pH are greater at the apex, while the PCO2 is greater at the base.

26. Which of the following statements concerning the distribution of O₂ and CO₂ in the upright lungs is true?

PAO2 is greater at the apex than at the base

PACO2 is greater at the apex than at the base

Both PAO2 and PACO2 are greater at the apex than at the base

Both PAO2 and PACO2 are greater at the base than at the apex

The PACO2 is equal throughout the lung

The ventilation/perfusion ratio is greater at the apex of the lungs than at the base of the lungs. Thus, dependent regions of the lungs are hypoxic and hypercarbic compared to the nondependent regions.

Explanation

The ventilation/perfusion ratio is greater at the apex of the lungs than at the base of the lungs. Thus, dependent regions of the lungs are hypoxic and hypercarbic compared to the nondependent regions.

27. The vital capacity is composed of the

Expiratory reserve volume

Inspiratory reserve volume

Tidal volume

Functional residual capacity

The vital capacity is the volume of gas that can be exhaled during a maximal expiration. It is composed of the inspiratory and expiratory reserve volumes, and the Vt.

Explanation

The vital capacity is the volume of gas that can be exhaled during a maximal expiration. It is composed of the inspiratory and expiratory reserve volumes, and the Vt.

Submit

28. An acute increase in PaCO₂ of 10 mm Hg will result in an immediate compensatory increase in [HCO₃^-] of

1 mEq/L

2 mEq/L

4 mEq/L

5 mEq/L

7 mEq/L

A prolonged increase in PaCO2 of 10 mm Hg will result in a maximum compensatory increase in [HC03-] of 3 mEq/L. An acute increase in PaCO2 of 10 mm Hg results in an immediate compensatory increase in [HCO3-] of 1 mEq/L. This immediate compensatory increase in [HC03-] is caused by the hydration of CO2 in plasma to produce HCO3-. An acute decrease in PaCO2 of 10 mm Hg will cause an immediate compensatory decrease in [HCO3-] of 2 mEq/L, and a chronic decrease in PaCO2 of 10 mm Hg will cause a maximum compensatory decrease in [HCO3-] of 5 mEq/L.

Explanation

A prolonged increase in PaCO2 of 10 mm Hg will result in a maximum compensatory increase in [HC03-] of 3 mEq/L. An acute increase in PaCO2 of 10 mm Hg results in an immediate compensatory increase in [HCO3-] of 1 mEq/L. This immediate compensatory increase in [HC03-] is caused by the hydration of CO2 in plasma to produce HCO3-. An acute decrease in PaCO2 of 10 mm Hg will cause an immediate compensatory decrease in [HCO3-] of 2 mEq/L, and a chronic decrease in PaCO2 of 10 mm Hg will cause a maximum compensatory decrease in [HCO3-] of 5 mEq/L.

29. Which of the following acid-base disturbances is the least well compensated?

Metabolic alkalosis

Respiratory alkalosis

Increased anion gap metabolic acidosis

Normal anion gap metabolic acidosis

Respiratory acidosis

The degree to which a person can hypoventilate to compensate for metabolic alkalosis is limited and hence, this is the least well compensated acid-base disturbance. Respiratory compensation for metabolic alkalosis is rarely more than 75% complete. Hypoventilation to a PaCO2 > 55 mm Hg is the maximum respiratory compensation for metabolic alkalosis. A PaCO2 > 55 mm Hg most likely reflects concomitant respiratory acidosis.

Explanation

The degree to which a person can hypoventilate to compensate for metabolic alkalosis is limited and hence, this is the least well compensated acid-base disturbance. Respiratory compensation for metabolic alkalosis is rarely more than 75% complete. Hypoventilation to a PaCO2 > 55 mm Hg is the maximum respiratory compensation for metabolic alkalosis. A PaCO2 > 55 mm Hg most likely reflects concomitant respiratory acidosis.

30. Correct mathematical expressions of static lung capacities and volumes include which of the following?

Total lung capacity = vital capacity + residual volume

Functional residual capacity = expiratory reserve volume + residual volume

Inspiratory capacity = inspiratory reserve volume + tidal volume

Closing capacity = residual volume + closing volume

The maximum volume of gas that can be inhaled is called the inspiratory capacity. The volume of gas that can be inhaled from the end of a normal inspiration is called the inspiratory reserve volume. Thus, the inspiratory capacity is corn-posed of the VT and inspiratory reserve volume.

Explanation

The maximum volume of gas that can be inhaled is called the inspiratory capacity. The volume of gas that can be inhaled from the end of a normal inspiration is called the inspiratory reserve volume. Thus, the inspiratory capacity is corn-posed of the VT and inspiratory reserve volume.

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31. An increase in PaCO₂ of 10 mm Hg will result in a decrease in pH of

0.01 pH units

0.02 pH units

0.04 pH units

0.08 pH units

None of above

Respiratory acidosis is present when the PaCO2 exceeds 44 mm Hg. Respiratory acidosis is caused by decreased elimination of CO2 by the lungs (i.e., hypoventila¬tion) or increased metabolic production of CO2. An acute increase in PaCO2 of 10 mm Hg will result in a decrease in pH of approximately 0.08 pH units. The acidosis of arterial blood will stimulate ventilation via the carotid bodies and the acidosis of cerebrospinal fluid will stimulate ventilation via the medullary chemoreceptors located in the fourth cerebral ventricle. Volatile anesthetics greatly attenuate the carotid body-mediated and aortic body-mediated ventilatory responses to arterial acidosis, but have little effect on the medullary chemoreceptor-mediated ventilatory response to cerebrospinal fluid acidosis.

Explanation

Respiratory acidosis is present when the PaCO2 exceeds 44 mm Hg. Respiratory acidosis is caused by decreased elimination of CO2 by the lungs (i.e., hypoventila¬tion) or increased metabolic production of CO2. An acute increase in PaCO2 of 10 mm Hg will result in a decrease in pH of approximately 0.08 pH units. The acidosis of arterial blood will stimulate ventilation via the carotid bodies and the acidosis of cerebrospinal fluid will stimulate ventilation via the medullary chemoreceptors located in the fourth cerebral ventricle. Volatile anesthetics greatly attenuate the carotid body-mediated and aortic body-mediated ventilatory responses to arterial acidosis, but have little effect on the medullary chemoreceptor-mediated ventilatory response to cerebrospinal fluid acidosis.

32. The normal arterial-to-alveolar ratio (a/A) is greater than

0.10

0.65

0.75

0.50

0.25

Arterial hypoxemia is defined as a decrease in PaO2 below 60 mm Hg. Arterial hypoxemia can be caused by low PO2, hypoventilation, or shunt. Shunt can be caused by a right-to-left transpulmonary or intracardiac shunt, or mismatching of ventilation to perfusion. Diffusion limitation to the passage of O2 from the alveoli to blood has not been documented as a cause of arterial hypoxemia in humans. The degree of shunt can be estimated by calculating the P(A-a)O2 or arterial-to-alveolar (a/A) ratio. It is easier to use the a/A ratio to calculate shunt fraction because the normal range for the P(A-a)O2 changes with the PO2 of inspired gas. The normal a/A ratio should be greater than 0.75.

Explanation

Arterial hypoxemia is defined as a decrease in PaO2 below 60 mm Hg. Arterial hypoxemia can be caused by low PO2, hypoventilation, or shunt. Shunt can be caused by a right-to-left transpulmonary or intracardiac shunt, or mismatching of ventilation to perfusion. Diffusion limitation to the passage of O2 from the alveoli to blood has not been documented as a cause of arterial hypoxemia in humans. The degree of shunt can be estimated by calculating the P(A-a)O2 or arterial-to-alveolar (a/A) ratio. It is easier to use the a/A ratio to calculate shunt fraction because the normal range for the P(A-a)O2 changes with the PO2 of inspired gas. The normal a/A ratio should be greater than 0.75.

33. Which of the following muscles or muscle groups of respiration is not used for inspiration?

Diaphragm

Internal intercostal muscles

External intercostal muscles

Scalene muscles

Sternomastoids

The muscles of expiration are those of the abdominal wall and the internal intercostal muscles. The internal intercostal muscles function to pull the ribs downward and inward, which decreases the volume of the thoracic cavity

Explanation

The muscles of expiration are those of the abdominal wall and the internal intercostal muscles. The internal intercostal muscles function to pull the ribs downward and inward, which decreases the volume of the thoracic cavity

34. The mechanism for the compensatory shift of the oxyhemoglobin dissociation curve toward normal in response to chronic (>24 hours) respiratory alkalosis is

Increased renal excretion of HCO3-

An influx of potassium into red blood cells

Altered erythrocyte 2,3-diphosphoglycerate (2,3-DPG) metabolism

Decreased sensitivity of the central nervous system to changes inPaCO2

None of the above

The compensatory shift of the oxyhemoglobin dissociation curve toward normal in response to chronic acid-base abnormalities is a result of altered erythrocyte 2,3-diphosphoglycerate (2,3-DPG) metabolism.

Explanation

The compensatory shift of the oxyhemoglobin dissociation curve toward normal in response to chronic acid-base abnormalities is a result of altered erythrocyte 2,3-diphosphoglycerate (2,3-DPG) metabolism.

35. What is the PaO₂ of air in a patient in Denver, Colorado (assume a barometric pressure of 630 mm Hg, respiratory quotient of 0.8, and PaCO₂ of 34 mm Hg)?

40 mm Hg

50 mm Hg

60 mm Hg

70 mm Hg

80 mm Hg

PAO2 can be estimated using the alveolar gas equation which is as follows:
PAO2 = (Pb-47)*FiO2-PaCO2/R, where Pb is the barometric pressure (mm Hg), Fi02 is the fraction of inspired 02, PaCO2 is the arterial CO2 tension (mm Hg), and R is the respiratory quotient.

Explanation

PAO2 can be estimated using the alveolar gas equation which is as follows:
PAO2 = (Pb-47)*FiO2-PaCO2/R, where Pb is the barometric pressure (mm Hg), Fi02 is the fraction of inspired 02, PaCO2 is the arterial CO2 tension (mm Hg), and R is the respiratory quotient.

36. The half-life of carboxyhemoglobin in a patient breathing 100% 0₂ is

5 minutes

1 hour

2 hours

4 hours

12 hours

The most frequent immediate cause of death from fires is carbon monoxide toxicity. Carbon monoxide is a colorless, odorless gas that exerts its adverse effects by decreasing O2 delivery to peripheral tissues. This is accomplished by two mechanisms. First, because the affinity of carbon monoxide for the O2 binding sites on hemoglobin is 240 times that of O2, O2 is readily displaced from hemoglobin. Thus, O2 content is reduced. Second, carbon monoxide causes a leftward shift of the oxyhemoglobin dissociation curve, which increases the affinity of hemoglobin for O2 at peripheral tissues. Treatment of carbon monoxide toxicity is administration of 100% O2. Breathing 100% O2 decreases the half-life of carboxyhemoglobin from 250 minutes to approximately 50 minutes.

Explanation

The most frequent immediate cause of death from fires is carbon monoxide toxicity. Carbon monoxide is a colorless, odorless gas that exerts its adverse effects by decreasing O2 delivery to peripheral tissues. This is accomplished by two mechanisms. First, because the affinity of carbon monoxide for the O2 binding sites on hemoglobin is 240 times that of O2, O2 is readily displaced from hemoglobin. Thus, O2 content is reduced. Second, carbon monoxide causes a leftward shift of the oxyhemoglobin dissociation curve, which increases the affinity of hemoglobin for O2 at peripheral tissues. Treatment of carbon monoxide toxicity is administration of 100% O2. Breathing 100% O2 decreases the half-life of carboxyhemoglobin from 250 minutes to approximately 50 minutes.

37. Which of the following respiratory variables can be measured by simple spirometry?

Vital capacity

Expiratory reserve volume

Inspiratory capacity

Residual volume

Static lung volumes can be divided into those that can be measured by simple spirometry and into those that cannot. The functional residual capacity and residual volume cannot be measured by simple spirometry; however, these two variables can be measured using gas-dilution techniques or body plethysmography

Explanation

Static lung volumes can be divided into those that can be measured by simple spirometry and into those that cannot. The functional residual capacity and residual volume cannot be measured by simple spirometry; however, these two variables can be measured using gas-dilution techniques or body plethysmography

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38. During a normal Vt (500 mL) breath, the transpulmonary pressure increases from 0 to 5 cm H₂O). The product of transpulmonary pressure and Vt is 2,500 cmH₂O-ml. This expression of the pressure-volume relationship during breathing determines what variable of respiratory mechanics?

Lung compliance

Airway resistance

Pulmonary elastance

Work of breathing

Closing capacity

The work of breathing is defined as the product of transpulmonary pres¬sure and VT. The work of breathing is related to two factors: the work required to overcome the elastic forces of the lungs and the work required to overcome airflow or frictional resistances of the airways. Volatile anesthetics cause a marked increase in the elastic component of the work of breathing .

Explanation

The work of breathing is defined as the product of transpulmonary pres¬sure and VT. The work of breathing is related to two factors: the work required to overcome the elastic forces of the lungs and the work required to overcome airflow or frictional resistances of the airways. Volatile anesthetics cause a marked increase in the elastic component of the work of breathing .

39. The P₅₀ of sickle cell hemoglobin is

19

26

31

35

40

A P50 less than 26 mm Hg defines a leftward shift of the oxyhemoglobin dissociation curve, which means that at any given PaO2, hemoglobin has a higher affinity for O2. A P50 greater than 26 mm Hg describes a rightward shift of the oxyhemoglobin dissociation curve, which means that at any given Pao2, hemoglobin has a lower affinity for O2. Conditions that cause a rightward shift of the oxyhemoglobin dissociation curve are metabolic and respiratory acidosis, hyperthermia, increased erythrocyte 2,3-DPG content, pregnancy, and abnormal hemoglobins, such as sickle cell hemoglobin or thalassemia. Alkalosis, hypothermia, fetal hemoglobin, abnormal hemoglobin species, such as carboxyhemoglobin, methemoglobin, and sulfhemoglobin, and decreased erythrocyte 2,3-DPG content will cause a leftward shift of the oxyhemoglobin dissociation curve.

Explanation

A P50 less than 26 mm Hg defines a leftward shift of the oxyhemoglobin dissociation curve, which means that at any given PaO2, hemoglobin has a higher affinity for O2. A P50 greater than 26 mm Hg describes a rightward shift of the oxyhemoglobin dissociation curve, which means that at any given Pao2, hemoglobin has a lower affinity for O2. Conditions that cause a rightward shift of the oxyhemoglobin dissociation curve are metabolic and respiratory acidosis, hyperthermia, increased erythrocyte 2,3-DPG content, pregnancy, and abnormal hemoglobins, such as sickle cell hemoglobin or thalassemia. Alkalosis, hypothermia, fetal hemoglobin, abnormal hemoglobin species, such as carboxyhemoglobin, methemoglobin, and sulfhemoglobin, and decreased erythrocyte 2,3-DPG content will cause a leftward shift of the oxyhemoglobin dissociation curve.

40. The P(A - a)O₂ of a patient breathing 100% O₂ is 240 mm Hg. The estimated fraction of the cardiac output shunted past the lungs without exposure to ventilated alveoli (i.e., transpulmonary shunt) is

5%

12%

17%

20%

34%

Qs/Qt=P(A-a)O2/20, where Qs is the cardiac output that is shunted past the lungs without exposure to ventilated alveoli, Qt is the total cardiac output, and P(A-a)O2 is the alveolar-to-arterial difference in O2 tension.

Explanation

Qs/Qt=P(A-a)O2/20, where Qs is the cardiac output that is shunted past the lungs without exposure to ventilated alveoli, Qt is the total cardiac output, and P(A-a)O2 is the alveolar-to-arterial difference in O2 tension.

41. Factors that determine the diffusing capacity of the lungs for carbon monoxide (DLco) include the

Area of the alveolar membrane

Blood volume of the pulmonary vasculature

Thickness of the alveolar membrane

Red blood cell hemoglobin concentration

The diffusing capacity of the lungs is determined by several processes: 1) diffusion of a gas through the alveolar walls and 2) the rate of reaction of the gas with hemoglobin. The mathematical expression of the diffusing capacity of the lungs is as follows: DL = DM + ( Θ • Vc),
where DL is the diffusing capacity of the lungs, DM is the diffusing capacity of the alveolar membrane, Θ is the rate (in mL/min) a gas can combine with 1 mL of blood/mm Hg partial pressure of the gas in the blood, and Vc is the volume of blood in the pulmonary capillaries. Thus, DL is determined by the area and thickness of the alveolar membrane, the blood:gas solubility and molecular weight of the gas, the transmembrane partial pressure difference of the gas, pulmonary blood volume, and hemoglobin concentration.

Explanation

The diffusing capacity of the lungs is determined by several processes: 1) diffusion of a gas through the alveolar walls and 2) the rate of reaction of the gas with hemoglobin. The mathematical expression of the diffusing capacity of the lungs is as follows: DL = DM + ( Θ • Vc),
where DL is the diffusing capacity of the lungs, DM is the diffusing capacity of the alveolar membrane, Θ is the rate (in mL/min) a gas can combine with 1 mL of blood/mm Hg partial pressure of the gas in the blood, and Vc is the volume of blood in the pulmonary capillaries. Thus, DL is determined by the area and thickness of the alveolar membrane, the blood:gas solubility and molecular weight of the gas, the transmembrane partial pressure difference of the gas, pulmonary blood volume, and hemoglobin concentration.

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42. Which of the following will increase the closing capacity?

Smoking

Obesity

Supine position

Aging

The closing capacity is the product of residual volume and the volume remaining in the lung when airway closure occurs (i.e., closing volume). Measurement of the closing capacity is a sensitive test of early small-airway diseases, such as emphysema, asthma, bronchitis, and pulmonary interstitial edema. Smoking tobacco, obesity, aging, and the supine position increase the closing capacity.

Explanation

The closing capacity is the product of residual volume and the volume remaining in the lung when airway closure occurs (i.e., closing volume). Measurement of the closing capacity is a sensitive test of early small-airway diseases, such as emphysema, asthma, bronchitis, and pulmonary interstitial edema. Smoking tobacco, obesity, aging, and the supine position increase the closing capacity.

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43. A decrease in PaCO₂ of 10 mm Hg will result in

A decrease in serum potassium concentration ([K+]) of 0.5mEq/L

A decrease in [K+] of 1.0 mEq/L

No change in [K+] under normal circumstances

An increase in [K+] of 0.5 mEq/L

An increase in [K+] of 1.0 mEq/L

Cardiac dysrhythmias are a common complication associated with acid-base abnormalities. The etiology of these dysrhythmias is related partly to the effects of pH on myocardial potassium homeostasis. As a general rule, there is an inverse relationship between [K+] and pH. For every 0.08 unit change in pH, there is a reciprocal change in [K+] of approximately 0.5 mEq/L.

Explanation

Cardiac dysrhythmias are a common complication associated with acid-base abnormalities. The etiology of these dysrhythmias is related partly to the effects of pH on myocardial potassium homeostasis. As a general rule, there is an inverse relationship between [K+] and pH. For every 0.08 unit change in pH, there is a reciprocal change in [K+] of approximately 0.5 mEq/L.

44. An increase in [HCO₃^-] of 10 mEq/L will result in an increase in pH of

0.10 pH units

0.15 pH units

0.20 pH units

0.25 pH units

None of the above

There are several guidelines that can be used in the initial interpretation of arterial blood gases that will permit rapid recognition of the type of acid-base disturbance. These guidelines are as follows: 1) a 1 mm Hg change in PaCO2 above or below 40 mm Hg results in a 0.008-unit change in the pH in the opposite direction; 2) the PaCO2 will decrease by about 1 mm Hg for every 1 mEq/L reduction in [HCO3-] below 24 mEq/L; 3) a change in [HCO3-] of 10 mEq/L from 24 mEq/L will result in a change in pH of approximately 0.15 pH units in the same direction.

Explanation

There are several guidelines that can be used in the initial interpretation of arterial blood gases that will permit rapid recognition of the type of acid-base disturbance. These guidelines are as follows: 1) a 1 mm Hg change in PaCO2 above or below 40 mm Hg results in a 0.008-unit change in the pH in the opposite direction; 2) the PaCO2 will decrease by about 1 mm Hg for every 1 mEq/L reduction in [HCO3-] below 24 mEq/L; 3) a change in [HCO3-] of 10 mEq/L from 24 mEq/L will result in a change in pH of approximately 0.15 pH units in the same direction.

45. In the resting adult, what percent of total body O₂ consumption is spent doing the work of breathing?

2%

5%

10%

20%

50%

The work required to overcome the elastic recoil of the lungs and thorax, along with airflow or frictional resistances of the airways, contributes to the work of breathing. When the respiratory rate or airway resistance is high, or pulmonary or chest wall compliance is reduced, a large amount of energy is spent in overcoming the work of breathing. In the healthy, resting adult, only 1% to 2% of total O2 consumption is used for the work of breathing.

Explanation

The work required to overcome the elastic recoil of the lungs and thorax, along with airflow or frictional resistances of the airways, contributes to the work of breathing. When the respiratory rate or airway resistance is high, or pulmonary or chest wall compliance is reduced, a large amount of energy is spent in overcoming the work of breathing. In the healthy, resting adult, only 1% to 2% of total O2 consumption is used for the work of breathing.

46. What is the rate of O₂ transported to peripheral tissues in a healthy 70-kg patient with a hemoglobin concentration of 10 mg/dL, a PaO₂ of 60 mm Hg, an SaO₂ of 90%, and a cardiac output of 5 L/min?

300 mL/min

400 mL/min

500 mL/min

600 mL/min

700 mL/min

The amount of O2 transported from the lungs to peripheral tissues is determined by the O2 content and the cardiac output. The mathematical expression of O2 transport is as follows:
02 transport = CO • 02 content, where CO is the cardiac output (mL/min).
In this patient, O2 transport is approximately 600 mL/min

Explanation

The amount of O2 transported from the lungs to peripheral tissues is determined by the O2 content and the cardiac output. The mathematical expression of O2 transport is as follows:
02 transport = CO • 02 content, where CO is the cardiac output (mL/min).
In this patient, O2 transport is approximately 600 mL/min

47. A venous blood sample from which of the following sites would correlate most reliably with PaO₂ and PaCO₂?

Jugular vein

Subclavian vein

Antecubital vein

Femoral vein

Vein on posterior surface of a warmed hand

When arterial sampling is not possible, "arterialized" venous blood can be used to determine arterial blood gas tensions. Because blood in the veins on the back of the hands have very little O2 extracted, the O2 content in this blood best approximates the O2 content in a sample of blood obtained from an artery.

Explanation

When arterial sampling is not possible, "arterialized" venous blood can be used to determine arterial blood gas tensions. Because blood in the veins on the back of the hands have very little O2 extracted, the O2 content in this blood best approximates the O2 content in a sample of blood obtained from an artery.

48. Each of the following will shift the oxyhemoglobin dissociation curve to the right EXCEPT

Volatile anesthetics

Decreased PaO2

Decreased pH

Increased temperature

Increased red blood cell (RBC) 2,3-DPG content

In addition to the items listed in this question, other factors that shift the oxyhemoglobin dissociation curve to the right include pregnancy and all abnormal hemoglobins such as hemoglobin S (sickle cell hemoglobin). For reasons unknown, volatile anesthetics increase the P50 of adult hemoglobin by 2 to 3.5 mm Hg. A rightward shift of the oxyhemoglobin dissociation curve will decrease the transfer from O2 from alveoli to hemoglobin and improve release of O2 from hemoglobin to peripheral tissues.

Explanation

In addition to the items listed in this question, other factors that shift the oxyhemoglobin dissociation curve to the right include pregnancy and all abnormal hemoglobins such as hemoglobin S (sickle cell hemoglobin). For reasons unknown, volatile anesthetics increase the P50 of adult hemoglobin by 2 to 3.5 mm Hg. A rightward shift of the oxyhemoglobin dissociation curve will decrease the transfer from O2 from alveoli to hemoglobin and improve release of O2 from hemoglobin to peripheral tissues.

49. Which of the following can cause a rightward shift of the oxyhemoglobin dissociation curve?

Methemoglobinemia

Carboxyhemoglobinemia

Rapid transfusion of large amounts of citrate-preserved packed erythrocytes

Pregnancy

During pregnancy, there is an increased production of 2,3-bisphosphoglycerate (2,3-BPG) in red blood cells. 2,3-BPG binds to hemoglobin and reduces its affinity for oxygen, causing a rightward shift of the oxyhemoglobin dissociation curve. This shift allows for increased release of oxygen to the tissues, compensating for the increased oxygen demand during pregnancy. Methemoglobinemia and carboxyhemoglobinemia cause a leftward shift of the curve, while rapid transfusion of citrate-preserved packed erythrocytes does not have a significant effect on the curve.

Explanation

During pregnancy, there is an increased production of 2,3-bisphosphoglycerate (2,3-BPG) in red blood cells. 2,3-BPG binds to hemoglobin and reduces its affinity for oxygen, causing a rightward shift of the oxyhemoglobin dissociation curve. This shift allows for increased release of oxygen to the tissues, compensating for the increased oxygen demand during pregnancy. Methemoglobinemia and carboxyhemoglobinemia cause a leftward shift of the curve, while rapid transfusion of citrate-preserved packed erythrocytes does not have a significant effect on the curve.

50. 20-year-old, 80-kg patient with a history of insulin-dependent diabetes mellitus arrives in the emergency room in diabetic ketoacidosis. The arterial blood gases (on room air) are as follows: pH 6.95, PaCO₂ 30 mm Hg, PaO₂ 98 mm Hg, [HC0₃^-] 6 mEq/L, What is the total body deficit of HCO₃^- in this patient?

500 mEq

400 mEq

300 mEq

200 mEq

100 mEq

Metabolic acidosis occurs when the pH is less than 7.36 and [HCO3-] is below 24 mEq/L. A decrease in [HCO3-] is caused by decreased elimination of H+ by the renal tubules (e.g., renal tubule acidosis) or increase metabolic production of H+ relative to HCO3- (e.g., lactic acidosis, ketoacidosis, or uremia). Total body deficit in HCO3- can be estimated using the following formula:
Total body deficit (mEq) = Total body weight (kg) * Deviation of HCO3- from 24 mEq/L * Extracellular fluid volume as a fraction of body mass (L)
The total body deficit in HCO3- in this patient is: 80 • (24 - 6) • 0.2 = 288 mEq

Explanation

Metabolic acidosis occurs when the pH is less than 7.36 and [HCO3-] is below 24 mEq/L. A decrease in [HCO3-] is caused by decreased elimination of H+ by the renal tubules (e.g., renal tubule acidosis) or increase metabolic production of H+ relative to HCO3- (e.g., lactic acidosis, ketoacidosis, or uremia). Total body deficit in HCO3- can be estimated using the following formula:
Total body deficit (mEq) = Total body weight (kg) * Deviation of HCO3- from 24 mEq/L * Extracellular fluid volume as a fraction of body mass (L)
The total body deficit in HCO3- in this patient is: 80 • (24 - 6) • 0.2 = 288 mEq

51. Adverse effects of respiratory or metabolic acidosis include

Increased incidence of cardiac dysrhythmias

Hypovolemia

Increased serum potassium concentration

Increased pulmonary vascular resistance

Adverse physiologic effects of respiratory or metabolic acidosis include central nervous system depression, cardiovascular system depression (which is a result of the direct depressant effects of the acidosis on the vasomotor center, arteriolar smooth muscle, and myocardial contractility), increased incidence of cardiac dysrhythmias, hypovolemia (which is a result of decreased precapillary and increased postcapillary sphincter tone), pulmonary hypertension, and hyperkalemia. Depression of the cardiovascular system is partially offset until severe acidosis occurs by increased secretion of catecholamines and elevated [Ca2+] .

Explanation

Adverse physiologic effects of respiratory or metabolic acidosis include central nervous system depression, cardiovascular system depression (which is a result of the direct depressant effects of the acidosis on the vasomotor center, arteriolar smooth muscle, and myocardial contractility), increased incidence of cardiac dysrhythmias, hypovolemia (which is a result of decreased precapillary and increased postcapillary sphincter tone), pulmonary hypertension, and hyperkalemia. Depression of the cardiovascular system is partially offset until severe acidosis occurs by increased secretion of catecholamines and elevated [Ca2+] .

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52. Which of the following can cause metabolic acidosis?

Chronic renal failure

Pancreatic-duodenal fistula

Excessive diarrhea

Cirrhotic liver disease

The causes of metabolic acidosis can be grouped into those associated with an increased anion gap and those associated with a normal anion gap. The anion gap is defined by the following equation:
Anion gap = [Na + ] - ([CI'] + [HC03-])
The anion gap is composed of unmeasured anions, such as sulfates, phosphates, plasma proteins, and organic acids. A normal anion gap is approximately 5 to 12 mEq/L. Causes of normal anion gap metabolic acidosis include pancreatic-duodenal fistula, ureteral-enteric fistula, renal tubule acidosis, hyperchloremia (e.g., hyperalimentation), excessive diarrhea, and drugs that produce a HC03~ diuresis, such as acetazolamide, Causes of increased anion gap metabolic acidosis include excessive, lactate production (e.g., shock), cirrhosis of the liver, uremia (e.g. renal failure), diabetic ketoacidosis, and ingestion of excessive amounts of salicylates, methanol, ethylene glycol, oral hypoglycemic agents (e.g., phenformin), and ethanol.

Explanation

The causes of metabolic acidosis can be grouped into those associated with an increased anion gap and those associated with a normal anion gap. The anion gap is defined by the following equation:
Anion gap = [Na + ] - ([CI'] + [HC03-])
The anion gap is composed of unmeasured anions, such as sulfates, phosphates, plasma proteins, and organic acids. A normal anion gap is approximately 5 to 12 mEq/L. Causes of normal anion gap metabolic acidosis include pancreatic-duodenal fistula, ureteral-enteric fistula, renal tubule acidosis, hyperchloremia (e.g., hyperalimentation), excessive diarrhea, and drugs that produce a HC03~ diuresis, such as acetazolamide, Causes of increased anion gap metabolic acidosis include excessive, lactate production (e.g., shock), cirrhosis of the liver, uremia (e.g. renal failure), diabetic ketoacidosis, and ingestion of excessive amounts of salicylates, methanol, ethylene glycol, oral hypoglycemic agents (e.g., phenformin), and ethanol.

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53. Pulmonary surfactant is decreased in which of the following situations

After cardiopulmonary bypass

With pulmonary embolism

Prolonged inhalation of 100% O2

Administration of corticosteroids to parturients

Pulmonary surfactant is lipophilic material that is composed primarily of dipalmitoyl phosphatidyl choline. This substance is produced by type 2 alveolar cells from fatty acids that are extracted from the blood, which are themselves synthesized by the lungs. This process is efficient with very rapid turnover. If blood flow to a region of the lungs is markedly reduced or abolished (e.g., pulmonary embolism or cardiopulmonary bypass) or the type 2 alveolar cells are destroyed (e.g., O2 toxicity or gastric acid aspiration), surfactant will be depleted causing atelectasis. Administration of corticosteroids during pregnancy has been demonstrated to increase the production of pulmonary surfactant in the fetus.

Explanation

Pulmonary surfactant is lipophilic material that is composed primarily of dipalmitoyl phosphatidyl choline. This substance is produced by type 2 alveolar cells from fatty acids that are extracted from the blood, which are themselves synthesized by the lungs. This process is efficient with very rapid turnover. If blood flow to a region of the lungs is markedly reduced or abolished (e.g., pulmonary embolism or cardiopulmonary bypass) or the type 2 alveolar cells are destroyed (e.g., O2 toxicity or gastric acid aspiration), surfactant will be depleted causing atelectasis. Administration of corticosteroids during pregnancy has been demonstrated to increase the production of pulmonary surfactant in the fetus.

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54. A 44-year-old patient is hyperventilated to a PaCO₂ of 24 mm Hg for 24 hours. What [HC0₃^-] would you expect (normal [HCO₃^-] is 24 mEq/L)?

10 mEq/L

12 mEq/L

14 mEq/L

16 mEq/L

18 mEq/L

Respiratory alkalosis is present when the PaCO2 is less than 36 mm Hg. There are three compensatory mechanisms responsible for attenuating the increase in pH that accompanies respiratory alkalosis. First, there is an immediate shift in the equilibrium of the HCO3- buffer system, which results, in the production of CO2. Second, alkalosis stimulates the activity of phosphofructokinase, which increases glycolysis and the production of pyruvate and lactic acid. Third, there is a decrease in reabsorption of HCO3- by the proximal and distal renal tubules. These three compensatory mechanisms result in a maximum decrease in [HCO3-] of approximately 5 mEq/L for every 10 mm Hg decrease in PaCO2 below 40 mm Hg.

Explanation

Respiratory alkalosis is present when the PaCO2 is less than 36 mm Hg. There are three compensatory mechanisms responsible for attenuating the increase in pH that accompanies respiratory alkalosis. First, there is an immediate shift in the equilibrium of the HCO3- buffer system, which results, in the production of CO2. Second, alkalosis stimulates the activity of phosphofructokinase, which increases glycolysis and the production of pyruvate and lactic acid. Third, there is a decrease in reabsorption of HCO3- by the proximal and distal renal tubules. These three compensatory mechanisms result in a maximum decrease in [HCO3-] of approximately 5 mEq/L for every 10 mm Hg decrease in PaCO2 below 40 mm Hg.

55. The respiratory quotient

Describes the relationship between the rate of C02 production and the rate of O2 utilization

Is not dependent on diet

Is increased when the diet consists predominately of carbohydrates

Is increased when the diet consists predominately of fats

The respiratory quotient is the ratio of the rate of CO2 production to the rate of O2 consumption. Metabolic substrate is an important determinant of the rate of CO2 production and thus affects the respiratory quotient

Explanation

The respiratory quotient is the ratio of the rate of CO2 production to the rate of O2 consumption. Metabolic substrate is an important determinant of the rate of CO2 production and thus affects the respiratory quotient

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56. Which of the following vasoactive substances is inactivated by the lungs?

Epinephrine

Prostaglandin A1

Angiotensin II

Serotonin

Vasopressin

Although the primary function of the lungs is gas exchange, the lungs also have important metabolic functions. These include the synthesis of phospholipids such as dipalmitoyl phosphatidyl choline, an important component of pulmonary surfactant; proteins, such as collagen and elastin, which form the structural framework of the lungs; and complex mucopolysaccharides. In addition, a number of vasoactive substances arc metabolized by the lungs. These substances include bradykinin (which is enzymatically metabolized by angiotensin-converting enzyme), serotonin (which is taken up by and stored in alveolar cells), prostaglandins (except prostaglandins A1 and A2), and norepinephrine. Epinephrine, angiotensin II, and vasopressin pass through the lungs without being metabolized. There is evidence that histamine may be metabolized by lung slices in vitro. Patients with intestinal carcinoid do not develop left-sided cardiac valve lesions, because serotonin is taken up by the lungs.

Explanation

Although the primary function of the lungs is gas exchange, the lungs also have important metabolic functions. These include the synthesis of phospholipids such as dipalmitoyl phosphatidyl choline, an important component of pulmonary surfactant; proteins, such as collagen and elastin, which form the structural framework of the lungs; and complex mucopolysaccharides. In addition, a number of vasoactive substances arc metabolized by the lungs. These substances include bradykinin (which is enzymatically metabolized by angiotensin-converting enzyme), serotonin (which is taken up by and stored in alveolar cells), prostaglandins (except prostaglandins A1 and A2), and norepinephrine. Epinephrine, angiotensin II, and vasopressin pass through the lungs without being metabolized. There is evidence that histamine may be metabolized by lung slices in vitro. Patients with intestinal carcinoid do not develop left-sided cardiac valve lesions, because serotonin is taken up by the lungs.

57. Structures that contribute to physiologic shunt include

Thebesian veins

Bronchial veins

Pleural veins

Nonperfused alveoli

Physiologic shunt is that portion of the cardiac output that perfuses areas of the lungs that are not ventilated. In the normal patient, physiologic shunt accounts for approximately 5% to 10% of the cardiac
output. There are several anatomic sources for physiologic shunt. These include bronchial vessels, which supply blood and O2 to the main conducting airways of the lungs, the Thebesian veins, which drain blood from the coronary vessels that supply the myocardium, and pleural veins, which drain blood that has supplied 02 to the pleura. Alveoli that are poorly perfused but are adequately ventilated contribute to physiologic dead-space ventilation.

Explanation

Physiologic shunt is that portion of the cardiac output that perfuses areas of the lungs that are not ventilated. In the normal patient, physiologic shunt accounts for approximately 5% to 10% of the cardiac
output. There are several anatomic sources for physiologic shunt. These include bronchial vessels, which supply blood and O2 to the main conducting airways of the lungs, the Thebesian veins, which drain blood from the coronary vessels that supply the myocardium, and pleural veins, which drain blood that has supplied 02 to the pleura. Alveoli that are poorly perfused but are adequately ventilated contribute to physiologic dead-space ventilation.

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58. Compensatory mechanisms for metabolic acidosis include which of the following

Secretion of H+ and absorption of HC03- by the renal tubules

Increased Va caused by direct stimulation of the carotid bodies by H+

Buffering of nonvolatile acids by bone

Buffering of nonvolatile acids by hemoglobin

The compensatory mechanisms for metabolic acidosis can be divided into two groups: acute compensatory responses and chronic compensatory responses. The acute compensatory responses include increased Va, which is caused primarily by stimulation of the carotid bodies by H+, and the buffering of H+ by HC03-, hemoglobin, phosphates, and proteins. The chronic compensatory responses include secretion of H+ and the reabsorption of HC03- by the proximal and distal renal tubules, and the buffering of H+ by bone.

Explanation

The compensatory mechanisms for metabolic acidosis can be divided into two groups: acute compensatory responses and chronic compensatory responses. The acute compensatory responses include increased Va, which is caused primarily by stimulation of the carotid bodies by H+, and the buffering of H+ by HC03-, hemoglobin, phosphates, and proteins. The chronic compensatory responses include secretion of H+ and the reabsorption of HC03- by the proximal and distal renal tubules, and the buffering of H+ by bone.

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59. A 28-year-old woman (70 kg) with ulcerative colitis is undergoing general anesthesia for colon resection and ileostomy. Current medications include sulfasalazine and corticosteroids. Induction of anesthesia and tracheal intubation are uneventful. Anesthesia is maintained with isoflurane, N₂O and 50% O₂, and fentanyl, and the patient is paralyzed with atracurium. The patient's lungs are mechanically ventilated using the following parameters: Ve 5,000 mL, respiratory rate 10 breaths/min. How would Va change if the respiratory rate were increased from 10 to 20 breaths/min?

Increase by 500 mL

Increase by 1,000 mL

No change

Decrease by 750 mL

Decrease by 1,500 mL

A patient with a Vd of 150 mL and a Va of 350 mL (assuming a normal Vt of 500 mL) will have a Vd minute ventilation (Vd) of 1,500 mL and a Va minute ventilation (Va) of 3,500 mL (a Ve of 5,000 mL) at a respiratory rate of 10 breaths/min. If the respiratory rate is doubled but Ve remains unchanged, then the Vd would double to 3,000 mL, an increase in Vd of 1,500 mL and decrease in Va of 1,500 mL.

Explanation

A patient with a Vd of 150 mL and a Va of 350 mL (assuming a normal Vt of 500 mL) will have a Vd minute ventilation (Vd) of 1,500 mL and a Va minute ventilation (Va) of 3,500 mL (a Ve of 5,000 mL) at a respiratory rate of 10 breaths/min. If the respiratory rate is doubled but Ve remains unchanged, then the Vd would double to 3,000 mL, an increase in Vd of 1,500 mL and decrease in Va of 1,500 mL.

60. Effects of carboxyhemoglobin include

A leftward shift of the oxyhemoglobin dissociation curve

Overestimation of SaO2 by pulse oximeters

Negative inotropic effect on the heart

Increased incidence of deep vein thrombosis

Patients who smoke cigarettes have a higher incidence of postoperative pulmonary complications than those who do not smoke cigarettes. It is thought that part of the morbidity associated with cigarette smoking is associated with the adverse effects of carbon monoxide on the O2-carrying capacity of hemoglobin. Carbon monoxide combines with hemoglobin to produce carboxyhemoglobin causing a leftward shift of the oxyhemoglobin dissociation curve, which increases the affinity of hemoglobin for O2. In addition, carbon monoxide has a negative inotropic effect on myocardial contractility. Although the effects of carbon monoxide on the cardiovascular system are short-lived and readily reversible with cessation of smoking, short-term abstinence from cigarettes prior to elective surgery has not been shown to decrease the incidence of postoperative pulmonary complications. Carboxyhemoglobin will cause dual-wavelength pulse oximeters to display falsely elevated arterial O2 saturations. There is no evidence. that, carboxyhemoglobin associated with cigarette smoking will increase the incidence of deep vein thrombosis in the postoperative period.

Explanation

Patients who smoke cigarettes have a higher incidence of postoperative pulmonary complications than those who do not smoke cigarettes. It is thought that part of the morbidity associated with cigarette smoking is associated with the adverse effects of carbon monoxide on the O2-carrying capacity of hemoglobin. Carbon monoxide combines with hemoglobin to produce carboxyhemoglobin causing a leftward shift of the oxyhemoglobin dissociation curve, which increases the affinity of hemoglobin for O2. In addition, carbon monoxide has a negative inotropic effect on myocardial contractility. Although the effects of carbon monoxide on the cardiovascular system are short-lived and readily reversible with cessation of smoking, short-term abstinence from cigarettes prior to elective surgery has not been shown to decrease the incidence of postoperative pulmonary complications. Carboxyhemoglobin will cause dual-wavelength pulse oximeters to display falsely elevated arterial O2 saturations. There is no evidence. that, carboxyhemoglobin associated with cigarette smoking will increase the incidence of deep vein thrombosis in the postoperative period.

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61. Anatomic dead space is

Dependent on lung size

Approximately 1 mL/kg body weight

Affected by anesthesia equipment

Of less importance in the newborn than in the adult

Anatomic dead space consists of the conducting airways that contain no alveoli and therefore take no part in gas exchange. Anatomic dead space is approximately 1 mL/lb of body weight

Explanation

Anatomic dead space consists of the conducting airways that contain no alveoli and therefore take no part in gas exchange. Anatomic dead space is approximately 1 mL/lb of body weight

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62. Normal metabolic functions of the lungs include which of the following?

Synthesis of dipalmitoyl phosphatidyl choline

Synthesis of angiotensin-converting enzyme

Inactivation of prostaglandins

Inactivation of vasopressin (ADH)

In addition to the primary function of gas exchange, the lungs also have important metabolic functions. One of the most important is the synthesis of dipalmitoyl phosphatidyl choline, a component of pulmonary surfactant. Other important metabolic functions include the synthesis of collagen, elastin, and angiotensin-converting enzyme, and inactivation of numerous vasoactive substances including bradykinin, serotonin, prostaglandins, and norepinephrine. Epinephrine, angiotensin II, histamine, and vasopressin are not significantly metabolized by the lungs.

Explanation

In addition to the primary function of gas exchange, the lungs also have important metabolic functions. One of the most important is the synthesis of dipalmitoyl phosphatidyl choline, a component of pulmonary surfactant. Other important metabolic functions include the synthesis of collagen, elastin, and angiotensin-converting enzyme, and inactivation of numerous vasoactive substances including bradykinin, serotonin, prostaglandins, and norepinephrine. Epinephrine, angiotensin II, histamine, and vasopressin are not significantly metabolized by the lungs.

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63. The cilia of the respiratory tract

Are not affected by the temperature and humidity of inspired gases

Are inhibited by the presence of a cuffed endotracheal tube

Are part of goblet cells

Are a protective mechanism for removing particles from conducting airways

The cilia of the respiratory tract extend from the columnar cells lining the conducting airways. They propel a double layer of mucus up to the epiglottis, an important mechanism for removing small particles from the conducting airways. The rhythmic motion of cilia is altered by changes in gas temperature and humidity.
167. (B) Also see explanation to qu

Explanation

The cilia of the respiratory tract extend from the columnar cells lining the conducting airways. They propel a double layer of mucus up to the epiglottis, an important mechanism for removing small particles from the conducting airways. The rhythmic motion of cilia is altered by changes in gas temperature and humidity.
167. (B) Also see explanation to qu

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64. Which of the following can increase physiologic dead-space ventilation?

PEEP

Venous air embolism

Hypotension

Pregnancy

Physiologic dead-space ventilation is the ventilation of areas of the lungs that are poorly perfused. Except for pregnancy, all of the choices will increase physiologic dead-space ventilation.

Explanation

Physiologic dead-space ventilation is the ventilation of areas of the lungs that are poorly perfused. Except for pregnancy, all of the choices will increase physiologic dead-space ventilation.

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65. Which of the following can cause methemoglobinemia?

O-toluidine

Nitroglycerin

Sodium nitroprusside

Phencyclidines

Methemoglobin is oxidized adult hemoglobin (i.e., the iron is oxidized from the ferrous to the ferric form). Because methemoglobin is not able to bind O2, it causes cyanosis despite an adequate PaO2. Causes of methemoglobinemia include congenital absence of methemoglobin reductase, the enzyme that reduces methemoglobin to normal hemoglobin, and nitrate-containing compounds. O-toluidine, a metabolite of the local anesthetic prilocaine, oxidizes adult hemoglobin to methemoglobin. Sodium nitroprusside and nitroglycerin are metabolized within erythrocytes by a nonenzymatic reaction which requires the oxidation of oxyhemoglobin to methemoglobin.

Explanation

Methemoglobin is oxidized adult hemoglobin (i.e., the iron is oxidized from the ferrous to the ferric form). Because methemoglobin is not able to bind O2, it causes cyanosis despite an adequate PaO2. Causes of methemoglobinemia include congenital absence of methemoglobin reductase, the enzyme that reduces methemoglobin to normal hemoglobin, and nitrate-containing compounds. O-toluidine, a metabolite of the local anesthetic prilocaine, oxidizes adult hemoglobin to methemoglobin. Sodium nitroprusside and nitroglycerin are metabolized within erythrocytes by a nonenzymatic reaction which requires the oxidation of oxyhemoglobin to methemoglobin.

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66. A 22-year-old black man comes to the emergency room diaphoretic and short of breath. The patient is given 100% 0₂ by nonrebreathing face mask. Arterial blood gas levels are as follows: PaO₂ 309 mm Hg, PaCO₂ 24 mm Hg, pH 7.57, and SaO₂ 89%. Causes of these findings could include the presence of

Methemoglobin

Carboxyhemoglobin

Sulfhemoglobin

Sickle cell hemoglobin

Abnormal hemoglobin species, such as methemoglobin, sulfhemoglobin, and carboxyhemoglobin, bind O2 less avidly than does normal hemoglobin, which greatly reduces the O2 carrying capacity of blood, The presence of these abnormal hemoglobin species is suggested by a low SaO2 in the presence of a normal PaO2. The diagnosis of these abnormal hemoglobin species is confirmed by direct measurement in plasma.

Explanation

Abnormal hemoglobin species, such as methemoglobin, sulfhemoglobin, and carboxyhemoglobin, bind O2 less avidly than does normal hemoglobin, which greatly reduces the O2 carrying capacity of blood, The presence of these abnormal hemoglobin species is suggested by a low SaO2 in the presence of a normal PaO2. The diagnosis of these abnormal hemoglobin species is confirmed by direct measurement in plasma.

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67. 'True statements concerning pulmonary vascular resistance (PVR) include which of the following?

PVR increases with increasing lung volume from functional residual capacity

PVR increases with decreasing lung volume from functional residual capacity

PVR decreases with increasing cardiac output

PVR increases with decreasing PaO2.

Changes in pulmonary vascular resistance (PVR) may have significant effects on pulmonary gas exchange. Many factors, including vasoactive peptides and hormones, cardiac output, and mechanical forces, interact in a complex manner to determine PVR. Lung volume has a significant effect on PVR, in the normal lung, PVR increases with an increase or decrease in lung volume from functional residual capacity. The effect of lung volume on PVR is related to the direct effects of tissue expansion and collapse on the caliber of the extra-alveolar vessels and alveolar capillaries. At low lung volumes, PVR is elevated because the extra-alveolar vessels are compressed. At high lung volumes, PVR is elevated because the alveolar capillaries are compressed. Cardiac output also has a significant effect on PVR. PVR is directly proportional to the mean pulmonary perfusion pressure and is inversely proportional to cardiac output. As cardiac output increases, PVR decreases. The mechanisms responsible for this inverse relationship between cardiac output and PVR are the processes of recruitment and distention of pulmonary vessels. Recruitment of previously closed capillaries in nondependent regions of the lungs is the predominant mechanism for the fall in PVR as cardiac output and pulmonary artery pressure increases from low levels. However, distention of pulmonary vessels is the predominant mechanism for the fall in PVR at relatively high cardiac outputs and pulmonary vascular pressures.

Explanation

Changes in pulmonary vascular resistance (PVR) may have significant effects on pulmonary gas exchange. Many factors, including vasoactive peptides and hormones, cardiac output, and mechanical forces, interact in a complex manner to determine PVR. Lung volume has a significant effect on PVR, in the normal lung, PVR increases with an increase or decrease in lung volume from functional residual capacity. The effect of lung volume on PVR is related to the direct effects of tissue expansion and collapse on the caliber of the extra-alveolar vessels and alveolar capillaries. At low lung volumes, PVR is elevated because the extra-alveolar vessels are compressed. At high lung volumes, PVR is elevated because the alveolar capillaries are compressed. Cardiac output also has a significant effect on PVR. PVR is directly proportional to the mean pulmonary perfusion pressure and is inversely proportional to cardiac output. As cardiac output increases, PVR decreases. The mechanisms responsible for this inverse relationship between cardiac output and PVR are the processes of recruitment and distention of pulmonary vessels. Recruitment of previously closed capillaries in nondependent regions of the lungs is the predominant mechanism for the fall in PVR as cardiac output and pulmonary artery pressure increases from low levels. However, distention of pulmonary vessels is the predominant mechanism for the fall in PVR at relatively high cardiac outputs and pulmonary vascular pressures.

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68. Which of the following is associated with a decreased DLco?

Emphysema

Severe anemia

Pulmonary hypertension

Asthma

The DLco is determined in part by the volume of blood (hemoglobin concentration) within the pulmonary capillaries. Thus, diseases associated with a reduction in pulmonary blood volume, such as anemia, emphysema, dehydration, and pulmonary hypertension, will result in a decrease in DLco. Although the mechanism is not known, acute asthma is associated with an increase in DLco.

Explanation

The DLco is determined in part by the volume of blood (hemoglobin concentration) within the pulmonary capillaries. Thus, diseases associated with a reduction in pulmonary blood volume, such as anemia, emphysema, dehydration, and pulmonary hypertension, will result in a decrease in DLco. Although the mechanism is not known, acute asthma is associated with an increase in DLco.

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69. Adverse effects of respiratory or metabolic alkalosis include

Decreased plasma ionized calcium concentration ([Ca2+])

Coronary artery vasoconstriction

Bronchial smooth muscle constriction

Increased right-to-left transpulmonary shunting

Maintenance of acid-base equilibrium is necessary to ensure optimal function of enzymes and of the cardiovascular, pulmonary, and neurologic systems. In addition, the acid-base status has direct influence on SaO2 and the distribution of electrolytes within the intracellular and extracellular fluid spaces. Adverse physiologic effects of alkalosis include coronary artery vasoconstriction, increased cardiac dysrhythmias and airway resistance, decreased cerebral blood flow, central nervous system excitation, decreased [K+] and ionized calcium concentrations ([Ca2+]), and a leftward shift of the oxyhemoglobin dissociation curve, which decreases availability of O2 to tissues.

Explanation

Maintenance of acid-base equilibrium is necessary to ensure optimal function of enzymes and of the cardiovascular, pulmonary, and neurologic systems. In addition, the acid-base status has direct influence on SaO2 and the distribution of electrolytes within the intracellular and extracellular fluid spaces. Adverse physiologic effects of alkalosis include coronary artery vasoconstriction, increased cardiac dysrhythmias and airway resistance, decreased cerebral blood flow, central nervous system excitation, decreased [K+] and ionized calcium concentrations ([Ca2+]), and a leftward shift of the oxyhemoglobin dissociation curve, which decreases availability of O2 to tissues.

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70. The factors that influence the rate of diffusion of molecules through a lipid membrane are described in

Laplace's law

Graham's law

Boyle's law

Fick's law

The rate of simple diffusion of molecules through a lipid membrane is influenced by factors described in both Graham's law and Fick's law. Graham's law states that rate of diffusion of a gas through a lipid membrane is directly proportional to the solubility of the gas and is inversely proportional to the square root of the molecular weight of the gas. Fick's law states that the rate of diffusion of a gas through a lipid membrane is directly proportional to the pressure gradient of the gas across the membrane and the area of the membrane, and is inversely proportional to the thickness of the membrane.

Explanation

The rate of simple diffusion of molecules through a lipid membrane is influenced by factors described in both Graham's law and Fick's law. Graham's law states that rate of diffusion of a gas through a lipid membrane is directly proportional to the solubility of the gas and is inversely proportional to the square root of the molecular weight of the gas. Fick's law states that the rate of diffusion of a gas through a lipid membrane is directly proportional to the pressure gradient of the gas across the membrane and the area of the membrane, and is inversely proportional to the thickness of the membrane.

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71. Mechanisms responsible for the compensatory decrease in [HC0₃^_] in response to respiratory alkalosis include

Production of CO2 by the bicarbonate buffer system

Generation of lactic acid by glycolysis

Decreased absorption of HCO3- by the proximal convoluted renal tubules

Hydration of CO2

There are three compensatory mechanisms for respiratory alkalosis. First, HC03- is oxidized to produce water and CO2. Second, the alkalosis stimulates the activity of phosphofructokinase, which increases glycolysis and lactic acid production. Finally, reabsorption of HC03- by the proximal convoluted renal tubules is reduced. Hydration of CO2 in erythrocytes increases [HC03-], which will exacerbate the alkalosis.

Explanation

There are three compensatory mechanisms for respiratory alkalosis. First, HC03- is oxidized to produce water and CO2. Second, the alkalosis stimulates the activity of phosphofructokinase, which increases glycolysis and lactic acid production. Finally, reabsorption of HC03- by the proximal convoluted renal tubules is reduced. Hydration of CO2 in erythrocytes increases [HC03-], which will exacerbate the alkalosis.

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72. PVR is increased by which of the following?

Hypocarbia

Vasopressin

Hyperthermia

Metabolic acidosis

Factors that increase pulmonary vascular resistance include acidosis, hypoxia, hypercarbia, sympathetic stimulation, atelectasis, and high hematocrit. Hypocarbia causes alkalosis, which decreases pulmonary vascular resistance.

Explanation

Factors that increase pulmonary vascular resistance include acidosis, hypoxia, hypercarbia, sympathetic stimulation, atelectasis, and high hematocrit. Hypocarbia causes alkalosis, which decreases pulmonary vascular resistance.

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