1. What is the functional residual capacity? What factors affect it?
The functional residual capacity (FRC) is the volume in the lungs at the end of passive
expiration. It is determined by opposing forces of the expanding chest wall and the elastic
recoil of the lung. A normal FRC ¼ 1.7 to 3.5 L. FRC is increased by:
n Body size (FRC increases with height)
n Age (FRC increases slightly with age)
n Certain lung diseases, including asthma and chronic obstructive pulmonary disease (COPD).
FRC is decreased by:
n Sex (woman have a 10% decrease in FRC when compared to men)
n Diaphragmatic muscle tone (individuals with paralyzed diaphragms have less FRC when
compared to normal individuals)
n Posture (FRC greatest standing > sitting > prone > lateral > supine)
n Certain lung diseases in which elastic recoil is diminished (e.g., interstitial lung disease,
thoracic burns, and kyphoscoliosis)
n Increased abdominal pressure (e.g., obesity, ascites)
2. What is closing capacity? What factors affect the closing capacity? What is the
relationship between closing capacity and functional residual capacity?
Closing capacity is the point during expiration when small airways begin to close. In young
individuals with average body mass index, closing capacity is approximately half the FRC when
upright and approximately two thirds of the FRC when supine.
Closing capacity increases with age and is equal to FRC in the supine individual at
approximately 44 years and in the upright individual at approximately 66 years. The FRC
depends on position; the closing capacity is independent of position. Closing capacity
increases with increasing intraabdominal pressure, age, decreased pulmonary blood flow, and
pulmonary parenchymal disease, which decreases compliance.
3. What muscles are responsible for inspiration and expiration?
The respiratory muscles include the diaphragm, internal and external intercostals, abdominal
musculature, cervical strapmuscles, sternocleidomastoidmuscle, and large back and intervertebral
muscles of the shoulder girdle. During normal breathing inspiration requires work, whereas
expiration is passive. The diaphragm, scalene muscles, and external intercostal muscles provide
most of the work during normal breathing. However, as the work of breathing increases, abdominal
musculature and internal intercostal muscles become active during expiration, and the scalene and
sternocleidomastoid muscles become increasingly important for inspiration.
4. What is the physiologic work of breathing?
The physiologic work of breathing involves the work of overcoming the elastic recoil of the
lung (compliance and tissue resistance work) and the resistance to gas flow. The elastic recoil
is altered in certain pathologic states, including pulmonary edema, pulmonary fibrosis, thoracic
burns, and COPD. The resistance to gas flow is increased dramatically during labored
breathing. In addition to the physiologic work of breathing, a patient on a ventilator must also
overcome the resistance of the endotracheal tube.
17
5. Discuss the factors that affect the resistance to gas flow. What is laminar and
turbulent gas flow?
The resistance to flow can be separated into the properties of the tube and the properties of
the gas. At low flow, or laminar flow (nonobstructed breathing), the viscosity is the major
property of the gas that affects flow. Clearly the major determining factor is the radius of the
tube. This can be shown by the Hagen-Poiseuille relationship:
R ¼ ð8 L mÞ=ðp r4Þ
where R is resistance, L is the length of the tube, m is the viscosity, and r is the radius of the
tube. At higher flow rate (in obstructed airways and heavy breathing), the flow is turbulent.
At these flows the major determinants of resistance to flow are the density of the gas (r) and
the radius of the tube, r.
Ra r=r5
6. Suppose a patient has an indwelling 7-mm endotracheal tube and cannot be
weaned because of the increased work of breathing. What would be of greater
benefit, cutting off 4 cm of endotracheal tube or replacing the tube with one of
greater internal diameter?
According to the Hagen-Poiseuille relationship discussed previously, if the radius is
halved, the resistance within the tube increases to sixteenfold; but if the length of the tube is
doubled, the resistance is only doubled. Cutting the length of the tube minimally
affects resistance, but increasing the tube diameter dramatically decreases resistance.
Therefore, to reduce the work of breathing the endotracheal tube should be changed to a
larger size.
7. Why might helium be of benefit to a stridorous patient?
When flow is turbulent, as is the case in a stridorous patient, driving pressure is mostly
related to gas density. Use of low-density gas mixtures containing helium and oxygen lowers
the driving pressure needed to move gas in and out of the area, decreasing the work of
breathing.
8. Discuss dynamic and static compliance.
Compliance describes the elastic properties of the lung. It is a measure of the change in
volume of the lung when pressure is applied. The lung is an elastic body that exhibits elastic
hysteresis. When the lung is rapidly inflated and held at a given volume, the pressure
peaks and then exponentially falls to a plateau pressure. The volume change of the lung per the
initial peak pressure change is the dynamic compliance. The volume change per the plateau
pressure represents the static compliance of the lung.
9. How does surface tension affect the forces in the small airways and alveoli?
Laplace’s law describes the relationship between pressure (P), tension (T), and the radius
(R) of a bubble and can be applied to the alveoli.
P ¼ 2T=R
As the radius decreases, the pressure increases. In a lung without surfactant present, as
the alveoli decrease in size, the pressure is higher in small alveoli, causing gas to move from
the small to larger airways, collapsing in the process. Surfactant, a phospholipid substance
produced in the lung by type II alveolar epithelium, reduces the surface tension of the small
airways, thus decreasing the pressure as the airways decrease in size. This important
substance helps keep the small airways open during expiration.
18 CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY
10. Review the different zones (of West) in the lung with regard to perfusion and
ventilation.
West described three areas of perfusion in an upright lung, and a fourth was later added.
Beginning at the apices, they are:
n Zone 1: Alveolar pressure (PAlv) exceeds pulmonary artery pressure (Ppa) and pulmonary
venous pressure (Ppv), leading to ventilation without perfusion (alveolar dead space) (PAlv
> Ppa > Ppv).
n Zone 2: Pulmonary arterial pressure exceeds alveolar pressure, but alveolar pressure still
exceeds venous pressure (Ppa > PAlv > Ppv). Blood flow in zone 2 is determined by
arterial-alveolar pressure difference.
n Zone 3: Pulmonary venous pressure exceeds alveolar pressure, and flow is determined
by the arterial-venous pressure difference (Ppa > Ppv >PAlv).
n Zone 4: Interstitial pressure (Pinterstitium) is greater than venous and alveolar pressures;
thus flow is determined by the arterial-interstitial pressure difference (Ppa > Pinterstitium >
Ppv > PAlv). Zone 4 should be minimal in a healthy patient.
A change from upright to supine position increases pulmonary blood volume by 25% to
30%, thus increasing the size of larger-numbered West zones.
11. What are the alveolar gas equation and the normal alveolar pressure at sea
level on room air?
The alveolar gas equation is used to calculate the alveolar oxygen partial pressure:
PAO2 ¼ FiO2 ðPB PH2OÞ PaCO2=RQ
where PAO2 is the alveolar oxygen partial pressure, FiO2 is the fraction of inspired oxygen,
Pb is the barometric pressure, PH2O is the partial pressure of water (47mmHg), PaCO2 is the partial
pressure of carbon dioxide, and RQ is the respiratory quotient, dependent on metabolic activity and
diet and is considered to be about 0.825. At sea level the alveolar partial pressure (PAO2) is:
PaO2 ¼ 0:21ð760 47Þ 40=0:8 ¼ 99:7
Knowing the PaO2 allows us to calculate the alveolar-arterial O2 gradient (A-a gradient).
Furthermore, by understanding the alveolar gas equation we can see how hypoventilation
(resulting in hypercapnia) lowers PaO2, and therefore PaO2.
12. What is the A-a gradient and what is a normal value for this gradient?
The alveolar-arterial O2 gradient is known as the A-a gradient. It is the difference in partial
pressure of O2 in the alveolus (PaO2), calculated by the alveolar gas equation, and the partial
pressure of O2 measured in the blood (PaO2):
A-a gradient = PaO2 PaO2
A normal A-a gradient is estimated as follows:
A-a gradient = (age/4) þ 4.
13. What is the practical significance of estimating A-a gradient?
The A-a gradient, together with the PaO2 and PaCO2, allows systematic evaluation of
hypoxemia, leading to a concise differential diagnosis. As previously stated, the ABG provides
an initial assessment of oxygenation by measuring the PaO2. The A-a gradient is an extension
of this, for by calculating the difference between the PaO2 and the PaO2 we are assessing
the efficiency of gas exchange at the alveolar-capillary membrane.
14. What are the causes of hypoxemia?
n Low inspired oxygen concentration (FiO2): To prevent delivery of hypoxic gas mixtures
during an anesthetic, oxygen alarms are present on the anesthesia machine.
CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY 19
n Hypoventilation: Patients under general anesthesia may be incapable of maintaining an
adequate minute ventilation because of muscle relaxants or the ventilatory depressant
effects of anesthetic agents. Hypoventilation is a common problem after surgery.
n Shunt: Sepsis, liver failure, arteriovenous malformations, pulmonary emboli, and right-toleft
cardiac shunts may create sufficient shunting to result in hypoxemia. Since shunted
blood is not exposed to alveoli, hypoxemia caused by a shunt cannot be overcome by
increasing FiO2.
n Ventilation-perfusion (V/Q) mismatch: Ventilation and perfusion of the alveoli in the lung
ideally have close to a one-to-one relationship, promoting efficient oxygen exchange
between alveoli and blood. When alveolar ventilation and perfusion to the lungs are unequal
(V/Q mismatching), hypoxemia results. Causes of V/Q mismatching include atelectasis,
lateral decubitus positioning, bronchial intubation, bronchospasm, pneumonia, mucous
plugging, pulmonary contusion, and adult respiratory distress syndrome. Hypoxemia
caused by V/Q mismatching can usually be overcome by increasing FiO2.
n Diffusion defects: Efficient O2 exchange depends on a healthy interface between the alveoli
and the bloodstream. Advanced pulmonary disease and pulmonary edema may have
associated diffusion impairment.
KEY POINTS: CAUSES OF HYPOXEMIA
1. Low inspired oxygen tension
2. Alveolar hypoventilation
3. Right-Left shunting
4. V/Q mismatch
5. Diffusion abnormality
15. What are the A-a gradients for the different causes of hypoxemia:
n Low fractional concentration of inspired O2: normal A-a gradient
n Alveolar hypoventilation: normal A-a gradient
n Right-to-left shunting: elevated A-a gradient
n Ventilation/perfusion mismatch: elevated A-a gradient
n Diffusion abnormality: elevated A-a gradient
16. Discuss V/Q mismatch. How can general anesthesia worsen V/Q mismatch?
V/Q mismatch ranges from shunt at one end of the spectrum to dead space at the other end.
In the normal individual alveolar ventilation (V) and perfusion (Q) vary throughout the lung
anatomy. In the ideal situation V and Q are equal, and V/Q ¼ 1. In shunted lung the perfusion is
greater than the ventilation, creating areas of lung where blood flow is high but little gas
exchange occurs. In dead-space lung, ventilation is far greater than perfusion, creating areas of
lung where gas is delivered but little blood flow and gas exchange occur. Both situations
can cause hypoxemia. In the case of dead space, increasing the FiO2 will potentially increase
the hemoglobin oxygen saturation, whereas in cases of shunt it will not. In many pathologic
situations both extremes coexist within the lung.
Under general anesthesia FRC is reduced by approximately 400 ml in an adult. The supine
position decreases FRC another 800 ml. A large enough decrease in FRC may bring end-expiratory
volumes or even the entire tidal volume to levels below the closing volume (the volume at which
small airways close). When small airways begin to close, atelectasis and low V/Q areas develop.
20 CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY
17. Define anatomic, alveolar, and physiologic dead space.
Physiologic dead space (VD) is the sum of anatomic and alveolar dead space. Anatomic dead
space is the volume of lung that does not exchange gas. This includes the nose, pharynx,
trachea, and bronchi. This is about 2 ml/kg in the spontaneously breathing individual and is
the majority of physiologic dead space. Endotracheal intubation will decrease the total
anatomic dead space. Alveolar dead space is the volume of gas that reaches the alveoli but
does not take part in gas exchange because the alveoli are not perfused. In healthy patients
alveolar dead space is negligible.
18. How is VD/VT calculated?
VD/VT is the ratio of the physiologic dead space to the tidal volume (VT), is usually about 33%,
and is determined by the following formula:
VD=VT ¼ ½ðalveolar PCO2 expired PCO2Þ =alveolar PCO2
Alveolar PCO2 is calculated using the alveolar gas equation, and expired PCO2 is the average
PCO2 in an expired gas sample (not the same as end-tidal PCO2).
19. Define absolute shunt. How is the shunt fraction calculated?
Absolute shunt is defined as blood that reaches the arterial system without passing
through ventilated regions of the lung. The fraction of cardiac output that passes through a
shunt is determined by the following equation:
Qs=Qt ¼ ðCiO2 CaO2Þ=ðCiO2 CvO2Þ
where Qs is the physiologic shunt blood flow per minute, Qt is the cardiac output per minute,
CiO2 is the ideal arterial oxygen concentration when V/Q ¼ 1, CaO2 is arterial oxygen
content, and CvO2 is mixed venous oxygen content. It is estimated that 2% to 5% of cardiac
output is normally shunted through postpulmonary shunts, thus accounting for the normal
alveolar-arterial oxygen gradient (A-a gradient). Postpulmonary shunts include the thebesian,
bronchial, mediastinal, and pleural veins.
20. What is hypoxic pulmonary vasoconstriction?
Hypoxic pulmonary vasoconstriction (HPV) is a local response of pulmonary arterial
smooth muscle that decreases blood flow in the presence of low alveolar oxygen pressure,
helping to maintain normal V/Q relationships by diverting blood from under ventilated areas. HPV
is inhibited by volatile anesthetics and vasodilators but is not affected by intravenous anesthesia.
21. Calculate arterial and venous oxygen content (CaO2 and CvO2).
Oxygen content (milliliters of O2/dl) is calculated by summing the oxygen bound to hemoglobin
(Hgb) and the dissolved oxygen of blood:
Oxygen content ¼ 1:34 ½Hgb SaO2 þ ðPaO2 0:003Þ
where 1.34 is the O2 content per gram hemoglobin, SaO2 is the hemoglobin saturation, [Hgb]
is the hemoglobin concentration, and PaO2 is the arterial oxygen concentration.
If [Hgb] ¼ 15 g/dl, arterial saturation ¼ 96%, and PaO2 ¼ 90 mm Hg, mixed venous
saturation ¼ 75%, and PvO2 ¼ 40 mm Hg, then:
CaO2 ¼ ð1:34 ml O2=g Hgb 15 g Hgb=dl 0:96Þ þ ð90 0:003Þ ¼ 19:6 ml O2=dl
and
CvO2 ¼ ð1:34 ml O2=g Hgb 15 g Hgb=dl 0:75Þ þ ð40 0:003Þ ¼ 15:2 ml O2=dl
22. How is CO2 transported in the blood?
CO2 exists in three forms in blood: dissolved CO2 (7%), bicarbonate ions (HCO3
) (70%), and
combined with hemoglobin (23%).
CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY 21
23. How is PCO2 related to alveolar ventilation?
The partial pressure of CO2 (PCO2) is inversely related to the alveolar ventilation and is
described by the equation:
PCO2 ¼ ðVCO2=ValveolarÞ
where VCO2 is total CO2 production and Valveolar is the alveolar ventilation (minute
ventilation less the dead space ventilation). In general, minute ventilation and PCO2 are
inversely related.
KEY POINTS: USEFUL PULMONARY EQUATIONS
1. Alveolar gas partial pressure: PAO2 ¼ FiO2 (PB PH2O) PaCO2/Q
2. Oxygen content of blood: CaO2 ¼ 1.34 [Hgb] SaO2 þ (PaO2 0.003)
3. Resistance of laminar flow through a tube: R ¼ (8 L μ)/(p r4)
4. Resistance of turbulent flow through a tube: R a r/r5
5. Calculation of shunt fraction: Qs/Qt ¼ (CiO2 CaO2)/(CiO2 CvO2)
24. What factors alter oxygen consumption?
Factors increasing oxygen consumption include hyperthermia (including malignant
hyperthermia), hypothermia with shivering, hyperthyroidism, pregnancy, sepsis, burns, pain,
and pheochromocytoma. Factors decreasing oxygen consumption include hypothermia
without shivering, hypothyroidism, neuromuscular blockade, and general anesthesia.
25. Where is the respiration center located in the brain?
The respiratory center is located bilaterally in the medulla and pons. Three major centers contribute
to respiratory regulation. The dorsal respiratory center is mainly responsible for inspiration, the
ventral respiratory center is responsible for both expiration and inspiration, and the pneumotaxic
center helps control the breathing rate and pattern. The dorsal respiratory center is the most
important. It is located within the nucleus solitarius where vagal and glossopharyngeal nerve fibers
terminate and carry signals from peripheral chemoreceptors and baroreceptors (including the
carotid and aortic bodies) and several lung receptors. A chemosensitive area also exists in the
brainstem just beneath the ventral respiratory center. This area responds to changes in
cerebrospinal fluid (CSF) pH, sending corresponding signals to the respiratory centers. Anesthetics
cause repression of the respiratory centers of the brainstem.
26. How do carbon dioxide and oxygen act to stimulate and repress breathing?
Carbon dioxide (indirectly) or hydrogen ions (directly) work on the chemosensitive area in the
brainstem. Oxygen interacts with the peripheral chemoreceptors located in the carotid and
aortic bodies. During hypercapnic and hypoxic states the brainstem is stimulated to increase
minute ventilation, whereas the opposite is true for hypocapnia and normoxia. Carbon
dioxide is by far more influential in regulating respiration than is oxygen.
27. What are the causes of hypercarbia?
n Hypoventilation: Decreasing the minute ventilation ultimately decreases alveolar
ventilation, increasing PCO2. Some common causes of hypoventilation include muscle
paralysis, inadequate mechanical ventilation, inhalational anesthetics, and opiates.
n Increased CO2 production: Although CO2 production is assumed to be constant,
there are certain situations in which metabolism and CO2 production are increased.
22 CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY
Malignant hyperthermia, fever, thyrotoxicosis, and other hypercatabolic states are
some examples.
n Iatrogenic: The anesthesiologist can administer certain drugs to increase CO2. The most
common is sodium bicarbonate, which is metabolized by the enzyme carbonic anhydrase
to form CO2. CO2 is absorbed into the bloodstream during laparoscopic procedures.
Rarely CO2-enriched gases can be administered. Carbon dioxide insufflation for
laparoscopy is a cause. Exhaustion of the CO2 absorbent in the anesthesia breathing
circuit can result in rebreathing of exhaled gases and may also result in hypercarbia.
28. What are the signs and symptoms of hypercarbia?
Hypercarbia acts as a direct vasodilator in the systemic circulation and as a direct
vasoconstrictor in the pulmonary circulation. It is also a direct cardiac depressant. Cerebral
blood flow increases in proportion to arterial CO2. An increase in catecholamines is
responsible for most of the clinical signs and symptoms of hypercarbia. Hypercarbia
causes an increase in heart rate, myocardial contractility, and respiratory rate along with a
decrease in systemic vascular resistance. Higher systolic blood pressure, wider pulse
pressure, tachycardia, greater cardiac output, higher pulmonary pressures, and tachypnea
are common clinical findings. In awake patients symptoms include headache, anxiety/
restlessness, and even hallucinations. Extreme hypercapnia produces hypoxemia as CO2
displaces O2 in alveoli.
The functional residual capacity (FRC) is the volume in the lungs at the end of passive
expiration. It is determined by opposing forces of the expanding chest wall and the elastic
recoil of the lung. A normal FRC ¼ 1.7 to 3.5 L. FRC is increased by:
n Body size (FRC increases with height)
n Age (FRC increases slightly with age)
n Certain lung diseases, including asthma and chronic obstructive pulmonary disease (COPD).
FRC is decreased by:
n Sex (woman have a 10% decrease in FRC when compared to men)
n Diaphragmatic muscle tone (individuals with paralyzed diaphragms have less FRC when
compared to normal individuals)
n Posture (FRC greatest standing > sitting > prone > lateral > supine)
n Certain lung diseases in which elastic recoil is diminished (e.g., interstitial lung disease,
thoracic burns, and kyphoscoliosis)
n Increased abdominal pressure (e.g., obesity, ascites)
2. What is closing capacity? What factors affect the closing capacity? What is the
relationship between closing capacity and functional residual capacity?
Closing capacity is the point during expiration when small airways begin to close. In young
individuals with average body mass index, closing capacity is approximately half the FRC when
upright and approximately two thirds of the FRC when supine.
Closing capacity increases with age and is equal to FRC in the supine individual at
approximately 44 years and in the upright individual at approximately 66 years. The FRC
depends on position; the closing capacity is independent of position. Closing capacity
increases with increasing intraabdominal pressure, age, decreased pulmonary blood flow, and
pulmonary parenchymal disease, which decreases compliance.
3. What muscles are responsible for inspiration and expiration?
The respiratory muscles include the diaphragm, internal and external intercostals, abdominal
musculature, cervical strapmuscles, sternocleidomastoidmuscle, and large back and intervertebral
muscles of the shoulder girdle. During normal breathing inspiration requires work, whereas
expiration is passive. The diaphragm, scalene muscles, and external intercostal muscles provide
most of the work during normal breathing. However, as the work of breathing increases, abdominal
musculature and internal intercostal muscles become active during expiration, and the scalene and
sternocleidomastoid muscles become increasingly important for inspiration.
4. What is the physiologic work of breathing?
The physiologic work of breathing involves the work of overcoming the elastic recoil of the
lung (compliance and tissue resistance work) and the resistance to gas flow. The elastic recoil
is altered in certain pathologic states, including pulmonary edema, pulmonary fibrosis, thoracic
burns, and COPD. The resistance to gas flow is increased dramatically during labored
breathing. In addition to the physiologic work of breathing, a patient on a ventilator must also
overcome the resistance of the endotracheal tube.
17
5. Discuss the factors that affect the resistance to gas flow. What is laminar and
turbulent gas flow?
The resistance to flow can be separated into the properties of the tube and the properties of
the gas. At low flow, or laminar flow (nonobstructed breathing), the viscosity is the major
property of the gas that affects flow. Clearly the major determining factor is the radius of the
tube. This can be shown by the Hagen-Poiseuille relationship:
R ¼ ð8 L mÞ=ðp r4Þ
where R is resistance, L is the length of the tube, m is the viscosity, and r is the radius of the
tube. At higher flow rate (in obstructed airways and heavy breathing), the flow is turbulent.
At these flows the major determinants of resistance to flow are the density of the gas (r) and
the radius of the tube, r.
Ra r=r5
6. Suppose a patient has an indwelling 7-mm endotracheal tube and cannot be
weaned because of the increased work of breathing. What would be of greater
benefit, cutting off 4 cm of endotracheal tube or replacing the tube with one of
greater internal diameter?
According to the Hagen-Poiseuille relationship discussed previously, if the radius is
halved, the resistance within the tube increases to sixteenfold; but if the length of the tube is
doubled, the resistance is only doubled. Cutting the length of the tube minimally
affects resistance, but increasing the tube diameter dramatically decreases resistance.
Therefore, to reduce the work of breathing the endotracheal tube should be changed to a
larger size.
7. Why might helium be of benefit to a stridorous patient?
When flow is turbulent, as is the case in a stridorous patient, driving pressure is mostly
related to gas density. Use of low-density gas mixtures containing helium and oxygen lowers
the driving pressure needed to move gas in and out of the area, decreasing the work of
breathing.
8. Discuss dynamic and static compliance.
Compliance describes the elastic properties of the lung. It is a measure of the change in
volume of the lung when pressure is applied. The lung is an elastic body that exhibits elastic
hysteresis. When the lung is rapidly inflated and held at a given volume, the pressure
peaks and then exponentially falls to a plateau pressure. The volume change of the lung per the
initial peak pressure change is the dynamic compliance. The volume change per the plateau
pressure represents the static compliance of the lung.
9. How does surface tension affect the forces in the small airways and alveoli?
Laplace’s law describes the relationship between pressure (P), tension (T), and the radius
(R) of a bubble and can be applied to the alveoli.
P ¼ 2T=R
As the radius decreases, the pressure increases. In a lung without surfactant present, as
the alveoli decrease in size, the pressure is higher in small alveoli, causing gas to move from
the small to larger airways, collapsing in the process. Surfactant, a phospholipid substance
produced in the lung by type II alveolar epithelium, reduces the surface tension of the small
airways, thus decreasing the pressure as the airways decrease in size. This important
substance helps keep the small airways open during expiration.
18 CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY
10. Review the different zones (of West) in the lung with regard to perfusion and
ventilation.
West described three areas of perfusion in an upright lung, and a fourth was later added.
Beginning at the apices, they are:
n Zone 1: Alveolar pressure (PAlv) exceeds pulmonary artery pressure (Ppa) and pulmonary
venous pressure (Ppv), leading to ventilation without perfusion (alveolar dead space) (PAlv
> Ppa > Ppv).
n Zone 2: Pulmonary arterial pressure exceeds alveolar pressure, but alveolar pressure still
exceeds venous pressure (Ppa > PAlv > Ppv). Blood flow in zone 2 is determined by
arterial-alveolar pressure difference.
n Zone 3: Pulmonary venous pressure exceeds alveolar pressure, and flow is determined
by the arterial-venous pressure difference (Ppa > Ppv >PAlv).
n Zone 4: Interstitial pressure (Pinterstitium) is greater than venous and alveolar pressures;
thus flow is determined by the arterial-interstitial pressure difference (Ppa > Pinterstitium >
Ppv > PAlv). Zone 4 should be minimal in a healthy patient.
A change from upright to supine position increases pulmonary blood volume by 25% to
30%, thus increasing the size of larger-numbered West zones.
11. What are the alveolar gas equation and the normal alveolar pressure at sea
level on room air?
The alveolar gas equation is used to calculate the alveolar oxygen partial pressure:
PAO2 ¼ FiO2 ðPB PH2OÞ PaCO2=RQ
where PAO2 is the alveolar oxygen partial pressure, FiO2 is the fraction of inspired oxygen,
Pb is the barometric pressure, PH2O is the partial pressure of water (47mmHg), PaCO2 is the partial
pressure of carbon dioxide, and RQ is the respiratory quotient, dependent on metabolic activity and
diet and is considered to be about 0.825. At sea level the alveolar partial pressure (PAO2) is:
PaO2 ¼ 0:21ð760 47Þ 40=0:8 ¼ 99:7
Knowing the PaO2 allows us to calculate the alveolar-arterial O2 gradient (A-a gradient).
Furthermore, by understanding the alveolar gas equation we can see how hypoventilation
(resulting in hypercapnia) lowers PaO2, and therefore PaO2.
12. What is the A-a gradient and what is a normal value for this gradient?
The alveolar-arterial O2 gradient is known as the A-a gradient. It is the difference in partial
pressure of O2 in the alveolus (PaO2), calculated by the alveolar gas equation, and the partial
pressure of O2 measured in the blood (PaO2):
A-a gradient = PaO2 PaO2
A normal A-a gradient is estimated as follows:
A-a gradient = (age/4) þ 4.
13. What is the practical significance of estimating A-a gradient?
The A-a gradient, together with the PaO2 and PaCO2, allows systematic evaluation of
hypoxemia, leading to a concise differential diagnosis. As previously stated, the ABG provides
an initial assessment of oxygenation by measuring the PaO2. The A-a gradient is an extension
of this, for by calculating the difference between the PaO2 and the PaO2 we are assessing
the efficiency of gas exchange at the alveolar-capillary membrane.
14. What are the causes of hypoxemia?
n Low inspired oxygen concentration (FiO2): To prevent delivery of hypoxic gas mixtures
during an anesthetic, oxygen alarms are present on the anesthesia machine.
CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY 19
n Hypoventilation: Patients under general anesthesia may be incapable of maintaining an
adequate minute ventilation because of muscle relaxants or the ventilatory depressant
effects of anesthetic agents. Hypoventilation is a common problem after surgery.
n Shunt: Sepsis, liver failure, arteriovenous malformations, pulmonary emboli, and right-toleft
cardiac shunts may create sufficient shunting to result in hypoxemia. Since shunted
blood is not exposed to alveoli, hypoxemia caused by a shunt cannot be overcome by
increasing FiO2.
n Ventilation-perfusion (V/Q) mismatch: Ventilation and perfusion of the alveoli in the lung
ideally have close to a one-to-one relationship, promoting efficient oxygen exchange
between alveoli and blood. When alveolar ventilation and perfusion to the lungs are unequal
(V/Q mismatching), hypoxemia results. Causes of V/Q mismatching include atelectasis,
lateral decubitus positioning, bronchial intubation, bronchospasm, pneumonia, mucous
plugging, pulmonary contusion, and adult respiratory distress syndrome. Hypoxemia
caused by V/Q mismatching can usually be overcome by increasing FiO2.
n Diffusion defects: Efficient O2 exchange depends on a healthy interface between the alveoli
and the bloodstream. Advanced pulmonary disease and pulmonary edema may have
associated diffusion impairment.
KEY POINTS: CAUSES OF HYPOXEMIA
1. Low inspired oxygen tension
2. Alveolar hypoventilation
3. Right-Left shunting
4. V/Q mismatch
5. Diffusion abnormality
15. What are the A-a gradients for the different causes of hypoxemia:
n Low fractional concentration of inspired O2: normal A-a gradient
n Alveolar hypoventilation: normal A-a gradient
n Right-to-left shunting: elevated A-a gradient
n Ventilation/perfusion mismatch: elevated A-a gradient
n Diffusion abnormality: elevated A-a gradient
16. Discuss V/Q mismatch. How can general anesthesia worsen V/Q mismatch?
V/Q mismatch ranges from shunt at one end of the spectrum to dead space at the other end.
In the normal individual alveolar ventilation (V) and perfusion (Q) vary throughout the lung
anatomy. In the ideal situation V and Q are equal, and V/Q ¼ 1. In shunted lung the perfusion is
greater than the ventilation, creating areas of lung where blood flow is high but little gas
exchange occurs. In dead-space lung, ventilation is far greater than perfusion, creating areas of
lung where gas is delivered but little blood flow and gas exchange occur. Both situations
can cause hypoxemia. In the case of dead space, increasing the FiO2 will potentially increase
the hemoglobin oxygen saturation, whereas in cases of shunt it will not. In many pathologic
situations both extremes coexist within the lung.
Under general anesthesia FRC is reduced by approximately 400 ml in an adult. The supine
position decreases FRC another 800 ml. A large enough decrease in FRC may bring end-expiratory
volumes or even the entire tidal volume to levels below the closing volume (the volume at which
small airways close). When small airways begin to close, atelectasis and low V/Q areas develop.
20 CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY
17. Define anatomic, alveolar, and physiologic dead space.
Physiologic dead space (VD) is the sum of anatomic and alveolar dead space. Anatomic dead
space is the volume of lung that does not exchange gas. This includes the nose, pharynx,
trachea, and bronchi. This is about 2 ml/kg in the spontaneously breathing individual and is
the majority of physiologic dead space. Endotracheal intubation will decrease the total
anatomic dead space. Alveolar dead space is the volume of gas that reaches the alveoli but
does not take part in gas exchange because the alveoli are not perfused. In healthy patients
alveolar dead space is negligible.
18. How is VD/VT calculated?
VD/VT is the ratio of the physiologic dead space to the tidal volume (VT), is usually about 33%,
and is determined by the following formula:
VD=VT ¼ ½ðalveolar PCO2 expired PCO2Þ =alveolar PCO2
Alveolar PCO2 is calculated using the alveolar gas equation, and expired PCO2 is the average
PCO2 in an expired gas sample (not the same as end-tidal PCO2).
19. Define absolute shunt. How is the shunt fraction calculated?
Absolute shunt is defined as blood that reaches the arterial system without passing
through ventilated regions of the lung. The fraction of cardiac output that passes through a
shunt is determined by the following equation:
Qs=Qt ¼ ðCiO2 CaO2Þ=ðCiO2 CvO2Þ
where Qs is the physiologic shunt blood flow per minute, Qt is the cardiac output per minute,
CiO2 is the ideal arterial oxygen concentration when V/Q ¼ 1, CaO2 is arterial oxygen
content, and CvO2 is mixed venous oxygen content. It is estimated that 2% to 5% of cardiac
output is normally shunted through postpulmonary shunts, thus accounting for the normal
alveolar-arterial oxygen gradient (A-a gradient). Postpulmonary shunts include the thebesian,
bronchial, mediastinal, and pleural veins.
20. What is hypoxic pulmonary vasoconstriction?
Hypoxic pulmonary vasoconstriction (HPV) is a local response of pulmonary arterial
smooth muscle that decreases blood flow in the presence of low alveolar oxygen pressure,
helping to maintain normal V/Q relationships by diverting blood from under ventilated areas. HPV
is inhibited by volatile anesthetics and vasodilators but is not affected by intravenous anesthesia.
21. Calculate arterial and venous oxygen content (CaO2 and CvO2).
Oxygen content (milliliters of O2/dl) is calculated by summing the oxygen bound to hemoglobin
(Hgb) and the dissolved oxygen of blood:
Oxygen content ¼ 1:34 ½Hgb SaO2 þ ðPaO2 0:003Þ
where 1.34 is the O2 content per gram hemoglobin, SaO2 is the hemoglobin saturation, [Hgb]
is the hemoglobin concentration, and PaO2 is the arterial oxygen concentration.
If [Hgb] ¼ 15 g/dl, arterial saturation ¼ 96%, and PaO2 ¼ 90 mm Hg, mixed venous
saturation ¼ 75%, and PvO2 ¼ 40 mm Hg, then:
CaO2 ¼ ð1:34 ml O2=g Hgb 15 g Hgb=dl 0:96Þ þ ð90 0:003Þ ¼ 19:6 ml O2=dl
and
CvO2 ¼ ð1:34 ml O2=g Hgb 15 g Hgb=dl 0:75Þ þ ð40 0:003Þ ¼ 15:2 ml O2=dl
22. How is CO2 transported in the blood?
CO2 exists in three forms in blood: dissolved CO2 (7%), bicarbonate ions (HCO3
) (70%), and
combined with hemoglobin (23%).
CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY 21
23. How is PCO2 related to alveolar ventilation?
The partial pressure of CO2 (PCO2) is inversely related to the alveolar ventilation and is
described by the equation:
PCO2 ¼ ðVCO2=ValveolarÞ
where VCO2 is total CO2 production and Valveolar is the alveolar ventilation (minute
ventilation less the dead space ventilation). In general, minute ventilation and PCO2 are
inversely related.
KEY POINTS: USEFUL PULMONARY EQUATIONS
1. Alveolar gas partial pressure: PAO2 ¼ FiO2 (PB PH2O) PaCO2/Q
2. Oxygen content of blood: CaO2 ¼ 1.34 [Hgb] SaO2 þ (PaO2 0.003)
3. Resistance of laminar flow through a tube: R ¼ (8 L μ)/(p r4)
4. Resistance of turbulent flow through a tube: R a r/r5
5. Calculation of shunt fraction: Qs/Qt ¼ (CiO2 CaO2)/(CiO2 CvO2)
24. What factors alter oxygen consumption?
Factors increasing oxygen consumption include hyperthermia (including malignant
hyperthermia), hypothermia with shivering, hyperthyroidism, pregnancy, sepsis, burns, pain,
and pheochromocytoma. Factors decreasing oxygen consumption include hypothermia
without shivering, hypothyroidism, neuromuscular blockade, and general anesthesia.
25. Where is the respiration center located in the brain?
The respiratory center is located bilaterally in the medulla and pons. Three major centers contribute
to respiratory regulation. The dorsal respiratory center is mainly responsible for inspiration, the
ventral respiratory center is responsible for both expiration and inspiration, and the pneumotaxic
center helps control the breathing rate and pattern. The dorsal respiratory center is the most
important. It is located within the nucleus solitarius where vagal and glossopharyngeal nerve fibers
terminate and carry signals from peripheral chemoreceptors and baroreceptors (including the
carotid and aortic bodies) and several lung receptors. A chemosensitive area also exists in the
brainstem just beneath the ventral respiratory center. This area responds to changes in
cerebrospinal fluid (CSF) pH, sending corresponding signals to the respiratory centers. Anesthetics
cause repression of the respiratory centers of the brainstem.
26. How do carbon dioxide and oxygen act to stimulate and repress breathing?
Carbon dioxide (indirectly) or hydrogen ions (directly) work on the chemosensitive area in the
brainstem. Oxygen interacts with the peripheral chemoreceptors located in the carotid and
aortic bodies. During hypercapnic and hypoxic states the brainstem is stimulated to increase
minute ventilation, whereas the opposite is true for hypocapnia and normoxia. Carbon
dioxide is by far more influential in regulating respiration than is oxygen.
27. What are the causes of hypercarbia?
n Hypoventilation: Decreasing the minute ventilation ultimately decreases alveolar
ventilation, increasing PCO2. Some common causes of hypoventilation include muscle
paralysis, inadequate mechanical ventilation, inhalational anesthetics, and opiates.
n Increased CO2 production: Although CO2 production is assumed to be constant,
there are certain situations in which metabolism and CO2 production are increased.
22 CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY
Malignant hyperthermia, fever, thyrotoxicosis, and other hypercatabolic states are
some examples.
n Iatrogenic: The anesthesiologist can administer certain drugs to increase CO2. The most
common is sodium bicarbonate, which is metabolized by the enzyme carbonic anhydrase
to form CO2. CO2 is absorbed into the bloodstream during laparoscopic procedures.
Rarely CO2-enriched gases can be administered. Carbon dioxide insufflation for
laparoscopy is a cause. Exhaustion of the CO2 absorbent in the anesthesia breathing
circuit can result in rebreathing of exhaled gases and may also result in hypercarbia.
28. What are the signs and symptoms of hypercarbia?
Hypercarbia acts as a direct vasodilator in the systemic circulation and as a direct
vasoconstrictor in the pulmonary circulation. It is also a direct cardiac depressant. Cerebral
blood flow increases in proportion to arterial CO2. An increase in catecholamines is
responsible for most of the clinical signs and symptoms of hypercarbia. Hypercarbia
causes an increase in heart rate, myocardial contractility, and respiratory rate along with a
decrease in systemic vascular resistance. Higher systolic blood pressure, wider pulse
pressure, tachycardia, greater cardiac output, higher pulmonary pressures, and tachypnea
are common clinical findings. In awake patients symptoms include headache, anxiety/
restlessness, and even hallucinations. Extreme hypercapnia produces hypoxemia as CO2
displaces O2 in alveoli.
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