CLINICAL CARDIAC AND PULMONARY PHYSIOLOGY

Question 1

1. What is mean arterial pressure (MAP)?

Answer 1

1. Mean arterial pressure (MAP) is the average blood pressure. On modern monitors,MAP is calculated from integrating the arterial waveform over time. MAP can often be estimated by adding one third of the pulse pressure to the diastolic blood
   pressure. (50)

Question 2

2. What is the relationship of MAP to cardiac output and systemic vascular resistance?

Answer 2

2. MAP is the product of cardiac output (CO) and SVR, or MAP ¼ CO SVR. This
   is similar to electricity where voltage ¼ current resistance. (If we were to be
   exactly correct, we would use the pressure drop across the systemic vascular system,
   or MAP – CVP.)

Question 3

3. What is the “pulse pressure”?

Answer 3

3. Pulse pressure is the difference between systolic and diastolic blood pressure. (50)

Question 4

4. What factors affect pulse pressure?

Answer 4

4. Pulse pressure is produced from the stroke volume being pushed into the aorta.
   The compliance features of the aorta therefore have a very significant effect
   on pulse pressure so that a stiff aorta results in a higher pulse pressure, a common
   feature of aging. A lower diastolic pressure can reduce pulse pressure by moving to a
   more compliant part of the aortic compliance curve. A higher stroke volume
   generally increases pulse pressure. Lower SVR can decrease pulse pressure because
   part of the stroke volume “runs off” rapidly during ejection. Aortic insufficiency
   can increase pulse pressure as the diastolic pressure drops significantly during
   backward flow into the left ventricle. (50-5

Question 5

5. What pathologic factors may decrease systemic vascular resistance?

Answer 5

5. Classic pathologic causes of low SVR include sepsis, anaphylactic and
   anaphylactoid reactions, and reperfusion of ischemic organs. Many anesthetic
   drugs and neuraxial anesthesia also lower SVR.

Question 6

6. How is systemic vascular resistance calculated?

Answer 6

6. SVR ¼ 80 ðMAP CVPÞ
   CO , where MAP is mean arterial pressure, SVR is systemic
   vascular resistant, CVP is central venous pressure, and CO is cardiac output. The
   factor “80” converts the SVR to the proper units. (51)

Question 7

7. Where is most of the resistance in the vascular system?

Answer 7

7. Most of the resistance in the vascular system is in the arterioles. Despite having
   smaller diameters, there are large numbers of capillaries in parallel, resulting
   in overall lower resistance at this level of the vascular tree. (51)

Question 8

8. How is resistance related to the radius of the blood vessel?

Answer 8

8. Resistance is inversely proportional to the fourth power of the radius of the
   vessel. (51)

Question 9

9. Which monitors allow calculation of cardiac output?

Answer 9

9. Cardiac output can be determined by thermodilution with a PA catheter. In addition,
   transesophageal echocardiography (TEE) may be used to estimate cardiac output.
   A variety of other noninvasive monitors are available and being developed that
   estimate cardiac output, including Doppler of the ascending aorta and arterial
   pressure waveform analysis. Thermodilution is still the dominant technique. The
   Fick equation can also be used to calculate cardiac output from the oxygen
   consumption, and arterial and mixed venous oxygen content. (51)

Question 10

10. How is stroke volume calculated?

Answer 10

10. Stroke volume is the cardiac output divided by heart rate. It is important to calculate
    stroke volume, because a high heart rate may make cardiac output appear normal
    despite inadequate stroke volume. (51)

Question 11

11. What is the cardiac index?

Answer 11

11. Because the appropriate cardiac output changes with body size, the cardiac “index” is
    used to normalize for body size by dividing cardiac output by body surface area. (51)

Question 12

12. How might changes in heart rate affect stroke volume?

Answer 12

12. An excessively rapid heart rate might not leave sufficient time to fill the ventricle.
    Loss of a “p” wave with certain rhythms will also lead to inadequate ventricular
    filling from loss of atrial contraction. (5

Question 13

13. What is the definition of ejection fraction and what is a normal value?

Answer 13

13. Ejection fraction is the percentage of ventricular blood volume that is pumped
    during a single contraction or SV/end-diastolic volume. Unlike stroke volume,
    ejection fraction does not change with body size. A normal ejection fraction is 60%
    to 70%. (51, Figure 6-3)

Question 14

14. How can “preload” be measured clinically?

Answer 14

14. The volume of the heart at end-diastole can be directly measured by
    transesophageal echocardiography (TEE). Ventricular filling pressures can be
    measured on the right side of the heart with central venous pressure and on the left
    side of the heart by pulmonary capillary wedge pressure. A complete picture of
    preload would still require both pressure and volume information to more fully
    understand the compliance of the heart. Systolic pressure variation may also be an
    important indicator of low preload. (51-52, Figure 6-1)

Question 15

15. When will central venous pressure (CVP) poorly reflect filling pressures in the left
    heart?

Answer 15

15. CVP will poorly reflect filling of the left ventricle in a number of pathologic
    conditions. With pulmonary disease and elevated PVR, right heart failure maydevelop with elevated CVP despite poor filling of the left ventricle. With left
    ventricular failure, CVP may be normal despite elevated left heart filling pressures
    as long as right ventricular function is preserved. (51)

Question 16

16. What is the Frank-Starling mechanism?

Answer 16

16. The Frank-Starling mechanism describes how the heart responds to increased
    filling by increasing contraction and stroke volume. This can be described by the
    cardiac function curves in Figure 6-2. (51)

Question 17

17. What are common causes of low preload?

Answer 17

17. “Hypovolemia” or low circulating blood volume is a key cause of low preload. Blood
    loss and fluid loss from other sources are commonly faced during surgery. Low
    preload can also occur with venodilation from an anesthetic agent and neuraxial
    anesthesia. Pathologic problems such as pericardial tamponade and tension
    pneumothorax may result in low preload (inadequate filling of the heart) despite
    normal blood volume and high CVP. (52)

Question 18

18. What is systolic pressure variation and how might it be useful in analyzing
    hypotension?

Answer 18

18. Systolic pressure variation describes the regular changes in systolic pressure
    that occur with ventilation. During mechanical ventilation, significant systolic
    pressure variation reflects low preload. Systolic pressure variation may
    be more useful than other monitors in determining which patients will
    appropriately respond to fluid administration. In cases of hypotension, SPV
    may indicate low preload. Extreme SPV may indicate other important causes
    of hypotension, such as pericardial tamponade or tension pneumothorax.
    Pulse pressure variation, which is closely related, requires a computer to evaluate;
    systolic pressure variation can be measured with a standard arterial line and
    monitor. (52)

Question 19

19. What is “contractility”?

Answer 19

19. Contractility, or inotropic state, describes the force of contraction independent
    of preload and afterload. It is reflected in the rate of rise of pressure over
    time. Graphically, it is reflected in the systolic pressure volume relationship.
    (52, Figure 6-3)

Question 20

20. What are some important clinical causes of low contractility?

Answer 20

20. Important causes of poor contractility that may be associated with hypotension
    include myocardial ischemia, previous myocardial infarction, cardiomyopathy, and
    myocardial depression from a number of different drugs. In addition, when
    considering a differential diagnosis of hypotension, valvular heart disease would be
    considered as low contractility. (52, Table 6-1)

Question 21

21. What does low systemic vascular resistance (SVR) or afterload do to ejection
    fraction?

Answer 21

21. Low SVR or afterload increases ejection fraction, which can approach 75% or
    even 80% in low SVR states. This is a classic feature of low SVR conditions such as
    liver failure. (52-53, Figure 6-4)

Question 22

22. What does low SVR or afterload do to cardiac filling pressures?

Answer 22

22. Low SVR or afterload lowers cardiac filling pressure (central venous pressure
    or pulmonary capillary wedge pressure) via the Frank-Starling mechanism.
    Vasodilation can therefore cause relative hypovolemia and a volume-responsive
    condition. Likewise high SVR or afterload increases cardiac filling pressure.

Question 23

23. What does low SVR or afterload do to end-systolic volume and how might this best
    be detected by monitoring?

Answer 23

23. Low SVR or afterload leads to low end-systolic left ventricular volume. This is a
    pathognomonic sign of low SVR on TEE. (52-53, Figure 6-4)

Question 24

24. What are the physiologic effects of the sympathetic and parasympathetic nerves on
    the cardiovascular system?

Answer 24

24. The parasympathetic nervous system primarily affects the cardiovascular system by
    decreasing heart rate through vagal innervation of the sinoatrial node. Mild
    negative effects on contractility are probably less important. The sympathetic
    nervous system can increase heart rate and contractility, but it also causes
    peripheral vasoconstriction

Question 25

25. What are the baroreceptors and where are they located?

Answer 25

25. Baroreceptors are present in the carotid sinus and aortic arch. Increased blood
    pressure will stimulate baroreceptors, leading to parasympathetic stimulation and a
    decrease in sympathetic stimulation

Question 26

26. What is the Bainbridge reflex?

Answer 26

26. The Bainbridge reflex describes the increase in heart rate from atrial stretch.
    This helps increase cardiac output in response to increased venous return.

Question 27

27. What effects do anesthetic agents have on cardiac reflexes?

Answer 27

27. Anesthetic agents decrease cardiac reflex responsiveness. This increases the
    likelihood of hypotension under anesthesia.

Question 28

28. What is the usual myocardial oxygen extraction and how does this compare to the
    body as a whole?

Answer 28

28. What is the usual myocardial oxygen extraction and how does this compare to the
    body as a whole?

Question 29

29. When is the subendocardium perfused?

Answer 29

29. Intramural pressure of the myocardium during systole stops blood flow to the
    subendocardium. Therefore, blood flow to the subendocardium occurs
    predominantly during diastole.

Question 30

30. What are normal pulmonary artery (PA) pressures?

Answer 30

30. The pulmonary circulation has much lower pressures than the system
    circulation. This is due to lower PVR compared to the systemic vascular
    resistance, since both systems accept the entire cardiac output. Since these pressures
    can be measured clinically with a PA catheter, the anesthesiologist should be
    familiar with normal and pathologic values, which are shown in Table 6-2.

Question 31

31. How does pulmonary vascular resistance (PVR) respond to increased cardiac
    output?

Answer 31

32. Both high and low lung volumes increase PVR. At high lung volumes,
    intraalveolar vessels are compressed. At low lung volumes, extraalveolar vessels are
    compressed. Increased PVR at low lung volumes may be physiologically helpful
    in diverting blood flow from a collapsed lung. (55)

Question 32

32. How does lung volume affect PVR?

Answer 32

32. Both high and low lung volumes increase PVR. At high lung volumes,
    intraalveolar vessels are compressed. At low lung volumes, extraalveolar vessels are
    compressed. Increased PVR at low lung volumes may be physiologically helpful
    in diverting blood flow from a collapsed lung. (55)

Question 33

33. What drugs modify PVR?

Answer 33

33. Elevated PVR can be very difficult to treat. Inhaled nitric oxide, prostaglandins, and
    phosphodiesterase inhibitors may lower PVR, but cannot always completely
    reverse elevated PA pressure. (55

Question 34

34. What is the effect of hypoxia on PVR?

Answer 34

34. Hypoxia increases PVR through “hypoxic pulmonary vasoconstriction” (HPV). This
    process may significantly improve gas exchange by lowering blood flow to areas
    of poor ventilation. However, global hypoxia, such as occurs at high altitude,
    can result in increased PA pressure through HPV. (55)

Question 35

35. What are some pathologic causes of elevated PVR?

Answer 35

35. Pathologic elevation in PVR may occur with pulmonary emboli. In addition,
    arteriolar hyperplasia may occur with certain congenital cardiac diseases
    (Eisenmenger syndrome), idiopathically (primary pulmonary hypertension), and
    associated with cirrhosis (portopulmonary hypertension). Intrinsic lung disease
    from a variety of causes can also increase PVR. (55)

Question 36

36. How does gravity affect pulmonary blood flow?

Answer 36

36. Because the hydrostatic changes due to gravity are of a similar order of magnitude
    as PA pressure, gravity can have significant effects on pulmonary blood flow.
    Notable effects are in zone 1, where airway pressure is higher than pulmonary artery
    pressure, leading to no perfusion and therefore dead space. If areas of poor gasexchange are in an elevated position, lower perfusion can result, improving gas
    exchange. In lung surgery, the lower PA pressure in the nondependent collapsed
    lung helps gas exchange. (55)

Question 37

37. What are the two types of pulmonary edema?

Answer 37

Pulmonary Edema
37. Hydrostatic leak can occur in the lung when pulmonary capillary pressure is
elevated. Pulmonary edema (hydrostatic) results when lymphatic system removal of
fluid is overwhelmed. The risk of pulmonary edema increases as pulmonary
capillary wedge pressure exceeds 20 mm Hg. Capillary leak can also occur with
pulmonary injury from a variety of causes, such as aspiration or sepsis. The adult
respiratory distress syndrome (ARDS) represents very significant lung injury
with a high risk of mortality. (56

Question 38

38. How is blood oxygen measured?

Answer 38

38. Three measurements of blood oxygen are used clinically: partial pressure (in mm Hg),
    oxygen saturation (in %), and oxygen content (in mL O2/dL). The oxyhemoglobin
    dissociation curve (Figure 6-5) relates oxygen partial pressure and saturation.
    “Content,” really a concentration, is the sum of the amount of oxygen in hemoglobin
    (1.39 mL O2/dL/g hemoglobin) and in the dissolved (0.003 mL O2/mm Hg). (56)

Question 39

39. What is the “P50”? What is a normal value?

Answer 39

39. The “P50” is the partial pressure at which hemoglobin is 50% saturated, normally
    26.8 mm Hg. Sigmoidal curves are usually defined by such midpoints. This is
    shown graphically in Figure 6-5. (56, Figure 6-5)

Question 40

40. What are common clinical factors that shift the oxyhemoglobin dissociation curve
    left and right?

Answer 40

40. The most important factors shifting the oxyhemoglobin dissociation curve to the
    right are metabolic acidosis and hypercapnia. Metabolic alkalosis and hypocapnia
    shift the curve to the left. Lower 2-3 DPG in stored blood leads to a significant left
    shift. (56, Table 6-3)

Question 41

41. What are the benefits of a rightward shift in the oxyhemoglobin dissociation curve?

Answer 41

41. Right shifts of the oxyhemoglobin dissociation curve improve unloading of oxygen
    in the tissues. For the same tissue PO2 more oxygen will be unloaded because
    of a right shift. Because of the sigmoidal shape of the curve, little change in loading
    of oxygen in the lungs will occur because of the rightward shift. (56)

Question 42

42. What is the equation describing the effect of ventilation on oxygenation?

Answer 42

42. The “alveolar gas equation” is used most to determine the effect of ventilation on
    oxygenation. The equation describes the transfer of oxygen from the environment
    to the alveoli, and therefore contains all the determinants of alveolar oxygen:
    barometric pressure, FIO2, and ventilation. (57)

Question 43

43. How does increased FIO2 improve oxygenation during hypercapnia?

Answer 43

43. FIO2 is another determinant of alveolar oxygen, and it can overcome the effect of
    higher CO2 on alveolar oxygen. The effect of hypoventilation with and without
    supplemental oxygen is shown in Figure 6-8. (57-58)

Question 44

44. Is it possible to deliver hypoxic gas mixtures with a modern anesthesia machine?

Answer 44

44. Modern anesthesia machines can effectively prevent delivery of hypoxic gas
    mixtures. Multiple features are necessary, including pin indexing of tanks and gas
    hoses, shut-off valves for nitrous oxide, and use of oxygen to drive the bellows. These
    safety mechanisms might be overcome if a gas other than oxygen were delivered
    through the oxygen piping, which has occurred because of construction mishaps.
    A monitor measuring FIO2 is therefore still critical. Hypoxemia still occurs because of
    unintentional delivery of room air in patients requiring supplemental oxygen. (58)

Question 45

45. What does an A-a gradient mean with respect to a problem in oxygenation?

Answer 45

45. Calculation of an A-a gradient divides the potential causes of hypoxemia into two
    groups of causes. Figure 6-7 illustrates this division. The first group of causes includes
    all the factors that determine alveolar oxygen: FIO2, barometric pressure (altitude),
    and ventilation. A normal A-a gradient would indicate that this first group is theproblem. An abnormal A-a gradient indicates a gas exchange issue, usually V/Q • •
    mismatch or shunt. (58)

Question 46

46. What is intrapulmonary shunt?

Question 47

47. What is the shunt equation?

Question 48

48. Is diffusion limitation a significant clinical cause of hypoxemia?

Answer 48

48. Diffusion impairment or limitation is not a major clinical cause of hypoxemia.
    However, diffusion limitation is often misunderstood. If an alveolus is filled
    with fluid, such that no diffusion of oxygen occurs, this is shunt, not diffusion
    limitation. Diffusion limitation occurs when a partial pressure gradient still
    exists between the alveolus and the capillary blood after the blood has passed
    through. Sufficient time for diffusion usually occurs, such that equilibration
    occurs early in the process. Even alveolar thickening, which may slow diffusion,
    does not usually result in diffusion limitation because equilibration of PO2
    between the alveolus and capillary blood does occur. Diffusion limitation
    may be a clinically significant physiologic problem at extreme altitude during
    exercise. (59)

Question 49

49. Which causes of hypoxemia are very responsive to supplemental oxygen and
    therefore easily treated with higher FIO2?

Answer 49

48. Diffusion impairment or limitation is not a major clinical cause of hypoxemia.
    However, diffusion limitation is often misunderstood. If an alveolus is filled
    with fluid, such that no diffusion of oxygen occurs, this is shunt, not diffusion
    limitation. Diffusion limitation occurs when a partial pressure gradient still
    exists between the alveolus and the capillary blood after the blood has passed
    through. Sufficient time for diffusion usually occurs, such that equilibration
    occurs early in the process. Even alveolar thickening, which may slow diffusion,
    does not usually result in diffusion limitation because equilibration of PO2
    between the alveolus and capillary blood does occur. Diffusion limitation
    may be a clinically significant physiologic problem at extreme altitude during
    exercise. (59)49. Hypoventilation, diffusion impairment, and V/Q • • mismatch are all very responsive to
    supplemental oxygen. High FIO2 can effectively eliminate hypoxemia from these
    causes. Shunt is much more resistant to supplemental oxygen. At shunt fractions
    over 30%, hypoxemia may remain despite administration of 100% oxygen. Higher
    FIO2 does improve oxygenation with pure shunt, although there is an incorrect
    impression that this impact is minimal. The effect of FIO2 is difficult to calculate and
    is not linear, so it is best graphically illustrated as in Figure 6-9. (59)

Question 50

50. How does low mixed venous oxygen saturation affect arterial oxygenation?

Answer 50

50. Low mixed venous oxygen levels may affect PaO2, but only in the presence of
    intrapulmonary shunt. For the same shunt, lower mixed venous oxygen results in
    a lower PaO2. (59)

Question 51

51. What are the three forms in which carbon dioxide is carried in the blood?

Answer 51

51. In the blood, CO2 is carried as dissolved gas, as bicarbonate, and bound to
    hemoglobin as carbaminohemoglobin. The greatest total quantity of CO2 is as
    bicarbonate, which is in fairly rapid equilibrium with CO2 through carbonic acid.
    Despite being the smallest total, the CO2 from carbaminohemoglobin represents
    about one third of the arterial to venous CO2 movement. (59)

Question 52

52. Why is hypercapnia a problem clinically?

Answer 52

52. Hypercapnia can be well tolerated, although at higher levels, probably approaching
    80 mm Hg or greater, hypercapnia can cause CO2 narcosis. The most significant
    problem is what hypercapnia represents. A major cause of hypercapnia is
    oversedation or narcotization. This could progress to apnea and anoxia.
    Hypercapnia may also represent impending respiratory failure from a variety
    of causes. (59-60)

Question 53

53. What are the four physiologic causes of hypercapnia?

Answer 53

53. Physiologically, hypercapnia can be caused by (1) rebreathing (elevated inspired
    CO2), (2) hypoventilation, (3) elevated CO2 production, and (4) elevated dead space.
    (60-61)

Question 54

54. What are significant causes of increased CO2 production under anesthesia?

Answer 54

54. The most concerning cause of significant CO2 production under general anesthesia
    is malignant hyperthermia (MH). While fever alone will increase CO2 production, the
    increase is not dramatic. MH may increase CO2 production several fold. Thyroid
    storm may increase CO2 production. Absorption of CO2 introduced during
    laparoscopy may be quite significant for certain procedures, particularly if

Question 55

55. What are the various types of dead space?

Answer 55

55. Dead space is described as anatomic, alveolar, or physiologic (total). Anatomic dead
    space consists of the conducting airways, which are not involved in gas exchange,
    plus the larynx and pharynx. Alveolar dead space consists of alveoli that are
    not involved in gas exchange, usually from lack of blood flow. Physiologic or total
    dead space consists of all dead space, and is the easiest to measure. “Equipment”
    dead space may be produced by the addition of tubing beyond the y-connector
    of the anesthesia circuit. (60-

Question 56

56. What pathologic conditions may increase dead space?

Answer 56

56. Many forms of end-stage lung disease, such as emphysema, are characterized by
    elevated dead space. Pulmonary emboli of any source increase dead space.
    Hypovolemic shock increases dead space, since very low PA pressures result in more
    zone 1 of the lung, where alveoli are not perfused and therefore represent dead
    space. (60-61)

Question 57

57. What is a normal value for physiologic dead space?

Answer 57

57. Normal dead space is 25% to 30% and consists almost entirely of anatomic dead
    space. (60-61)

Question 58

58. What is the Bohr equation?

Answer 58

58. The Bohr equation is used to calculate dead space, Vd/Vt. It requires measuring
    PaCO2 and mixed-expired CO2 by collecting exhaled gas. The gradient from
    PaCO2 to end-tidal PaCO2 is a reflection of alveolar dead space and is a simple
    semiquantitative way of evaluating dead space under general anesthesia. (61)

Question 59

59. How quickly can apnea increase PaCO2?

Answer 59

59. CO2 jumps up fairly rapidly during the first 30 seconds to one minute of apnea. This
    jump is due to rapid transition to mixed venous CO2 levels, which usually means
    an increase of about 6 mm Hg. This occurs because the lungs do not continue to
    store CO2, so once equilibration of CO2 occurs across the alveoli, PaCO2 will jump
    to mixed venous levels. Thereafter, CO2 increases due to metabolism at a slower
    rate of about 2 to 3 mm Hg/min. (61)

Question 60

60. What are pulmonary mechanics?

Answer 60

60. Pulmonary mechanics describes the pressure, volume, and flow relationships of gas
    within the lungs and the tracheobronchial tree. (61)

Question 61

61. What factors contribute to the static pressure in the lung?

Answer 61

62. Without surfactant, surface tension would make the lungs much stiffer.
    Additionally, alveoli would be less stable and would tend to collapse. (61-62)

Question 62

62. How is surface tension reduced in the lungs?

Answer 62

62. Without surfactant, surface tension would make the lungs much stiffer.
    Additionally, alveoli would be less stable and would tend to collapse. (61-62)

Question 63

63. What is the definition of static compliance?

Answer 63

63. Static compliance is the change in volume divided by the change in pressure. By
    static, this means that the pressure and volume measurements are made at a point
    of no gas flow, which would contribute a resistive pressure component. Low or
    poor compliance would indicate that more pressure is needed to inflate the lungs.
    (62-63, Figures 6-12 and 6-13)

Question 64

64. What is functional residual capacity (FRC) with respect to the static mechanical
    properties of the lung and chest wall?

Answer 64

64. The FRC is simply the balance point between the lungs collapsing and the chest wall
    expanding. Stiffer lungs will produce a lower FRC, because this balance point
    will occur at a lower lung volume. On the other hand a disease such as emphysema,
    with loss of elastic recoil, results in a higher FRC. (62)

Question 65

65. What determines airway resistance?

Answer 65

65. Similar to the vascular system, resistance is largely determined by airway diameter.
    However, turbulent gas flow can add a significant resistance component, which
    can happen at airway narrowing. (62)

Question 66

66. How can one distinguish clinically between elevated airway pressure produced from
    resistance or static compliance?

Answer 66

66. Pressure from resistance only occurs during gas flow. By ceasing gas flow with
    aninspiratory pause, one can determine the static or plateau pressure. (62, Figure 6-12)

Question 67

67. What are important clinical causes of elevated airway resistance?

Answer 67

67. High airway resistance can be caused by a number of common clinical
    conditions. A useful differential might trace the potential resistance anatomically,
    starting with airway equipment, including the endotracheal tube. Cause of
    resistance in the upper airways can include compression, foreign bodies, and
    secretions. In the lower airway, bronchoconstriction becomes the dominant cause.
    (62-63, Table 6-5

Question 68

68. Where are the central chemoreceptors located?

Answer 68

68. The central chemoreceptors are located on the ventral surface of the brainstem. (6

Question 69

69. What is the main stimulus for the central chemoreceptors?

Answer 69

69. Carbon dioxide is the main stimulus for the central chemoreceptors. While the
    signal transduction may be through protons, the mechanisms are not completely
    understood. Because CO2 crosses the blood-brain barrier, for clinical purposes, we
    consider that CO2 is the primary stimulus. (62-63

Question 70

70. How would the central chemoreceptors respond to lactic acidosis?

Answer 70

70. The central chemoreceptors are protected from metabolic acid by the blood-brain
    barrier. Cerebrospinal fluid pH will change in response to peripheral blood pH
    changes, but this may take days. An acute lactic acidosis will therefore have no
    effect on central chemoreceptors, except due to decreases in PaCO2 that may occur
    from the ventilatory response to the peripheral acidosis. (63

Question 71

71. What are the primary peripheral chemoreceptors?

Answer 71

71. The carotid bodies are the primary peripheral chemoreceptors in humans. Aortic
    bodies do not appear to have a significant clinical effect (which was studied in
    humans who had aortic body denervation). (63)

Question 72

72. What factors stimulate the peripheral chemoreceptors?

Answer 72

72. The peripheral chemoreceptors are stimulated by low pH, high PaCO2, and low PaO2.
    Unlike the central chemoreceptors, the peripheral chemoreceptors are not protected
    from an acute metabolic acidosis, which will cause stimulation and
    hyperventilation (the lower PaCO2 from this hyperventilation will affect the central
    chemoreceptors). (6

Question 73

73. Why do peripheral chemoreceptors effectively sense arterial, not venous, blood
    values?

Answer 73

73. High blood flow relative to metabolic rate creates a tissue with hardly any arterial to
    venous PO2 difference. This allows the carotid bodies to effectively sense arterial
    values. (63

Question 74

74. How is the hypercapnic ventilatory response measured?

Answer 74

74. While a variety of techniques are used to obtain ventilatory data, the slope of CO2 versus
    minute ventilation is the primary measure of hypercapnic ventilatory responsiveness.
    The slope is the change in minute ventilation divided by the change in CO2 (usually end-
    tidal PCO2 since a noninvasive measurement can be preferable). (63-64, Figure 6-14)

Question 75

75. What receptors drive the hypercapnic response?

Answer 75

75. The central chemoreceptors are the major receptor system responsible for hypercapnic
    drive. However, in room air, approximately one third of the CO2 response is from
    peripheral chemoreceptor drive. Usually hypercapnic drive is measured at higher FIO2
    where the majority of the response will then be from central chemoreceptors. (63-64)

Question 76

76. What is an “apneic threshold”?

Answer 76

76. Below a certain value of PaCO2, ventilation usually ceases. In an awake person, this
    can be difficult to measure due to an awake drive to breath. Under general

Question 77

77. How quickly does a CO2 response develop?

Answer 77

77. CO2 ventilatory drive is a slow response, with a time constant of approximately
    2 minutes. This is rarely appreciated, although it is easy to observe that ventilation
    takes noticeable time to stabilize as CO2 rises to a patient’s set point. (64)

Question 78

78. How is hypoxic ventilatory drive measured?

Answer 78

78. Hypoxic ventilatory drive can be measured from a plot of PO2 versus minute
    ventilation or SaO2 versus minute ventilation. Because the relationship of PO2 to
    minute ventilation is nonlinear, more complex parameters would be needed to
    describe the relationship, which then are not very clinically useful. A plot of SaO2
    (SpO2 is conveniently and noninvasively measured by pulse oximetry) versus
    minute ventilation is quite linear. Hypoxic responsiveness can then be measured by
    a simple slope (which will be negative), the change in minute ventilation divided by
    the change in SpO2. (64, Figure 6-15)

Question 79

79. What receptors are responsible for hypoxic stimulation of ventilation?

Answer 79

79. Hypoxic ventilatory stimulation is from the carotid bodies. (64)

Question 80

80. How does hypoxia depress ventilation?

Answer 80

80. Central nervous effects of hypoxia lead to a slower development of ventilatory
    depression known as hypoxic ventilatory decline. The carotid bodies initially lead to
    increased minute ventilation, but if hypoxia is prolonged, ventilation drops to a
    level lower than peak ventilation, but still above baseline. This central response is a
    regulated response probably involving several inhibitory neurotransmitters. (64)

Question 81

81. How quickly does the hypoxic response develop?

Answer 81

81. Hypoxic drive from the peripheral chemoreceptors develops extremely rapidly.
    The time constant is 10 to 20 seconds. Peak ventilation will therefore usually occur
    within 1 minute. The response is rapid enough that carotid body output will actually
    vary in response to the small oscillations of PO2 and PCO2 that occur with tidal
    breathing. (64)

Question 82

82. What is the effect of higher PCO2 on hypoxic drive?

Answer 82

82. The hypoxic drive is significantly higher with a higher PCO2. This synergistic
    response between PO2 and PCO2 will be most noticeable during apnea. (64)

Question 83

83. Do opioids depress hypercapnic ventilatory drive, hypoxic ventilatory drive, or both?

Answer 83

83. Opioids and most ventilatory depressants work on neurons in the integratory
    area of the brainstem. They do not affect detection of hypoxia or hypercapnia
    per se. The clinically observed respiratory depression therefore affects both
    hypercapnic and hypoxic ventilatory drive equally. (64)

Question 84

84. What ventilatory problems are premature infants of low postconceptual age at
    risk for?

Answer 84

84. Premature infants less than 60 weeks of postconceptual age can be at risk of apnea
    following general anesthesia. (64)

Question 85

85. What is Ondine curse?

Answer 85

85. Originally described following surgery near the high cervical spinal cord,
    Ondine curse describes patients with a nearly absent drive to breath. While
    awake, they may breathe fairly normally. But asleep, or under general anesthesia,
    breathing can be significantly depressed. This is due to abnormalities in the
    central integratory system that seem to blunt the hypoxic and hypercapnic
    ventilatory responses. Idiopathic forms of Ondine curse, which can be seen in
    children, are usually referred to as primary central alveolar hypoventilation
    syndrome. (64)

Question 86

86. When is periodic breathing most likely to occur?

Answer 86

86. Periodic breathing, most commonly Cheyne-Stokes breathing, occurs frequently
    when some degree of hypoxia is present. The stimulation of the carotid bodies
    can lead to overshoots and undershoots of ventilation. Periodic breathing can often
    be observed on sedated patients with some degree of hypoxia during sleep. This is

Question 87

87. What is the Fick equation?

Answer 87

87. The Fick equation describes the relationship between cardiac output, oxygen
    consumption, and oxygen about (arterial to venous content difference). (64)

Question 88

88. What is oxygen delivery?

Answer 88

88. Oxygen delivery (DO2) is defined as the product of cardiac output (CO) and arterial
    oxygen content (CaO2), DO2 ¼ CO • CaO2. (65)

Question 89

89. Why is examining oxygen extraction clinically useful?

Answer 89

89. Examining oxygen extraction provides a better global indication of whether cardiac
    output is matched to the body’s oxygen needs. Oxygen extraction may provide
    clinically and diagnostically useful clues as to disease state. In cardiogenic shock,
    oxygen extraction is high because cardiac output is insufficient. In sepsis and liver
    failure, oxygen extraction may be very low. (65)

Question 90

90. What is normal mixed venous oxygen saturation?

Answer 90

90. Normal whole body mixed venous oxygen saturation is about 75%. Individual
    organs and tissues can differ significantly. (65)

Question 91

91. How would the arterial to venous oxygen content difference change with higher FIO2?

Answer 91

91. Arterial to venous oxygen content difference (CaO2 – CvO2) is independent of FIO2,
    whereas the mixed venous oxygen saturation (SvO2) can increase significantly with
    higher PaO2. (65)

Question 92

92. Why is the oxygen extraction ratio useful?

Answer 92

92. Oxygen extraction ratio is probably the most reliable index. It is the oxygen
    extraction value most independent of FIO2 and hemoglobin level. (65)

Question 93

93. How can the body respond physiologically to anemia or increased metabolic
    demand (oxygen consumption)?

Answer 93

93. The two major compensatory mechanisms for increased demand or less availability
    of oxygen is (1) increased cardiac output and (2) increased extraction. This is readily
    apparent by examining the Fick equation. In anemia without general anesthesia,
    the primary compensation is increased cardiac output. Increased extraction occurs
    with more severe anemia. Under anesthesia, the cardiac output compensation
    may be blunted, and oxygen extraction is more important. In exercise, both
    increased cardiac output and increased extraction are utilized. (65)