Respi
Respi
Respi
chapter
4 Respiratory Physiology
PA CO ⴚ PECO
VD ⴝ VT ⴛ 2 2
PA CO
2
where:
VD = physiologic dead space (mL)
VT = tidal volume (mL)
PACO = PCO2 of alveolar gas (mm Hg) = PCO2 of arterial blood
2
PECO = PCO2 of expired air (mm Hg)
2
113
98761_Ch04_Chapter 04 5/7/10 6:35 PM Page 114
Inspiratory reserve
volume Vital
Inspiratory capacity capacity
■ In words, the equation states that physiologic dead space is tidal volume multiplied
by a fraction. The fraction represents the dilution of alveolar PCO2 by dead-space air,
which does not participate in gas exchange and does not therefore contribute CO2
to expired air.
6. Ventilation rate
a. Minute ventilation is expressed as follows:
■ Sample problem: A person with a tidal volume (VT) of 0.5 L is breathing at a rate of 15
breaths/min. The PCO2 of his arterial blood is 40 mm Hg, and the PCO2 of his expired
air is 36 mm Hg. What is his rate of alveolar ventilation?
PA CO − PECO
Dead space = VT ×
2 2
PA CO
2
40 mm Hg − 36 mm Hg
= 0.5 L ×
40 mm Hg
= 0.05 L
)
Alveolar ventilation = ( Tidal volume − Dead space × Breaths min
)
= ( 0.5 L − 0.05 L × 15 Breaths min
= 6.75 L min
7 7 7
6 6 FEV1 6
FVC FEV1 FVC
Volume (L)
5 FEV1 5 5
FVC
4 4 4
3 3 3
2 2 2
1 1 1
0 1 2 3 0 1 2 3 0 1 2 3
Time (sec) Time (sec) Time (sec)
A Normal B Asthma C Fibrosis
FIGURE 4-2 Forced vital capacity (FVC) and FEV1 in normal subjects and in patients with lung disease. FEV1 = volume
expired in first second of forced maximal expiration.
■ In obstructive lung disease, such as asthma, FEV1 is reduced more than FVC so that
FEV1/FVC is decreased.
■ In restrictive lung disease, such as fibrosis, both FEV1 and FVC are reduced and FEV1/FVC
is either normal or is increased.
B. Muscles of expiration
■ Expiration is normally passive.
98761_Ch04_Chapter 04 5/7/10 6:35 PM Page 116
■ Because the lung–chest wall system is elastic, it returns to its resting position after
inspiration.
■ Expiratory muscles are used during exercise or when airway resistance is increased
because of disease (e.g., asthma).
1. Abdominal muscles
■ compress the abdominal cavity, push the diaphragm up, and push air out of the lungs.
2. Internal intercostal muscles
■ pull the ribs downward and inward.
Cⴝ VP
where:
C = compliance (mL/mm Hg)
V = volume (mL)
P = pressure (mm Hg)
■ describes the distensibility of the lungs and chest wall.
■ is inversely related to elastance, which depends on the amount of elastic tissue.
■ is inversely related to stiffness.
■ is the slope of the pressure–volume curve.
■ is the change in volume for a given change in pressure. Pressure refers to transmural, or
transpulmonary, pressure (i.e., the pressure difference across pulmonary structures).
1. Compliance of the lungs (Figure 4-3)
■ Transmural pressure is alveolar pressure minus intrapleural pressure.
■ When the pressure outside of the lungs (i.e., intrapleural pressure) is negative, the
lungs expand and lung volume increases.
■ When the pressure outside of the lungs is positive, the lungs collapse and lung volume
decreases.
■ Inflation of the lungs (inspiration) follows a different curve than deflation of the lungs
(expiration); this difference is called hysteresis.
■ In the middle range of pressures, compliance is greatest and the lungs are most
distensible.
■ At high expanding pressures, compliance is lowest, the lungs are least distensible, and
the curve flattens.
n
tio
ira
p
Ex
Volume
Inspiration
Combined lung
and chest wall
Chest
wall
Volume
only
FRC
Lung only
P = 2T
r
r r Same r
P P T causes P
■ creates a collapsing pressure that is directly proportional to surface tension and inverse-
ly proportional to alveolar radius (Laplace’s law), as shown in the following equation:
2T
Pⴝ
r
where:
P = collapsing pressure on alveolus (or pressure required to
keep alveolus open) [dynes/cm2]
T = surface tension (dynes/cm)
r = radius of alveolus (cm)
a. Large alveoli (large radii) have low collapsing pressures and are easy to keep open.
b. Small alveoli (small radii) have high collapsing pressures and are more difficult to keep
open.
■ In the absence of surfactant, the small alveoli have a tendency to collapse (atelectasis).
2. Surfactant (see Figure 4-5)
■ lines the alveoli.
■ reduces surface tension by disrupting the intermolecular forces between liquid mole-
cules. This reduction in surface tension prevents small alveoli from collapsing and
increases compliance.
■ is synthesized by type II alveolar cells and consists primarily of the phospholipid
dipalmitoyl phosphatidylcholine (DPPC).
■ In the fetus, surfactant synthesis is variable. Surfactant may be present as early as ges-
tational week 24 and is almost always present by gestational week 35.
■ Generally, a lecithin:sphingomyelin ratio greater than 2:1 in amniotic fluid reflects
mature levels of surfactant.
■ Neonatal respiratory distress syndrome can occur in premature infants because of the
lack of surfactant. The infant exhibits atelectasis (lungs collapse), difficulty reinflating
the lungs (as a result of decreased compliance), and hypoxemia (as a result of
decreased V/Q).
■ is inversely proportional to airway resistance; thus, the higher the airway resistance, the
lower the airflow. This inverse relationship is shown in the following equation:
⌬P
Q ⴝ
R
where:
Q = airflow (mL/min or L/min)
ΔP = pressure gradient (cm H2O)
R = airway resistance (cm H2O/L/min)
2. Resistance of the airways
■ is described by Poiseuille’s law, as shown in the following equation:
8 l
R ⴝ
o r4
where:
R = resistance
η = viscosity of the inspired gas
l = length of the airway
r = radius of the airway
■ Notice the powerful inverse fourth-power relationship between resistance and the
size (radius) of the airway.
■ For example, if airway radius decreases by a factor of 4, then resistance will increase by
a factor of 256 (44), and airflow will decrease by a factor of 256.
3. Factors that change airway resistance
■ The major site of airway resistance is the medium-sized bronchi.
■ The smallest airways would seem to offer the highest resistance, but they do not
because of their parallel arrangement.
a. Contraction or relaxation of bronchial smooth muscle
■ changes airway resistance by altering the radius of the airways.
(1) Parasympathetic stimulation, irritants, and the slow-reacting substance of ana-
phylaxis (asthma) constrict the airways, decrease the radius, and increase the
resistance to airflow.
(2) Sympathetic stimulation and sympathetic agonists (isoproterenol) dilate the
airways via a2 receptors, increase the radius, and decrease the resistance to
airflow.
b. Lung volume
■ alters airway resistance because of the radial traction exerted on the airways by
surrounding lung tissue.
(1) High lung volumes are associated with greater traction and decreased airway
resistance. Patients with increased airway resistance (e.g., asthma) “learn” to
breathe at higher lung volumes to offset the high airway resistance associated
with their disease.
(2) Low lung volumes are associated with less traction and increased airway resist-
ance, even to the point of airway collapse.
c. Viscosity or density of inspired gas
■ changes the resistance to airflow.
■ During a deep-sea dive, both air density and resistance to airflow are increased.
■ Breathing a low-density gas, such as helium, reduces the resistance to airflow.
98761_Ch04_Chapter 04 5/7/10 6:35 PM Page 120
Inspiration Expiration
Rest Rest
Volume of
breath (L)
–3
Intrapleural
pressure
(cm H2O)
–6
+
Alveolar
pressure 0
(cm H2O)
–
FIGURE 4-6 Volumes and pressures dur-
ing the breathing cycle.
Asthma ↓↓ ↓ ↓ ↑
COPD ↓↓ ↓ ↓ ↑
Fibrosis ↓ ↓↓ ↑ (or normal) ↓
COPD = chronic obstructive pulmonary disease; FEV1 = volume expired in first second of forced expiration; FRC = func-
tional residual capacity; FVC = forced vital capacity.
98761_Ch04_Chapter 04 5/7/10 6:35 PM Page 122
1. In dry inspired air, the partial pressure of O2 can be calculated as follows. Assume that
total pressure is atmospheric and the fractional concentration of O2 is 0.21.
PO = 760 mm Hg × 0.21
2
= 160 mm Hg
2. In humidified tracheal air at 37°C, the calculation is modified to correct for the partial
pressure of H2O, which is 47 mm Hg.
PTotal = 760 mm Hg − 47 mm Hg
= 713 mm Hg
PO = 713 mm Hg × 0.2 21
2
= 150 mm Hg
B. Partial pressures of O2 and CO2 in inspired air, alveolar air, and blood (Table 4-2)
■ Approximately 2% of the systemic cardiac output bypasses the pulmonary circulation
(“physiologic shunt”). The resulting admixture of venous blood with oxygenated arterial
blood makes the PO2 of arterial blood slightly lower than that of alveolar air.
C. Dissolved gases
■ The amount of gas dissolved in a solution (such as blood) is proportional to its partial
pressure. The units of concentration for a dissolved gas are mL gas/100 mL blood.
■ The following calculation uses O2 in arterial blood as an example:
ⴝ 100 mm Hg ⴛ 0.03 mL O2 L mm Hg
ⴝ 0.3 mL O2 100 mL blood
where:
[O2] = O2 concentration in blood
PO2 = Partial pressure of O2 in blood
0.03 mL O2/L/mm Hg = Solubility of O2 in blood
■ In perfusion-limited exchange, the gas equilibrates early along the length of the pul-
monary capillary. The partial pressure of the gas in arterial blood becomes equal to the
partial pressure in alveolar air.
■ Thus, for a perfusion-limited process, diffusion of the gas can be increased only if
blood flow increases.
2. Diffusion-limited exchange
■ is illustrated by CO and by O2 during strenuous exercise.
■ is also illustrated in disease states. In fibrosis, the diffusion of O2 is restricted because
thickening of the alveolar membrane increases diffusion distance. In emphysema, the
diffusion of O2 is decreased because the surface area for diffusion of gases is decreased.
■ In diffusion-limited exchange, the gas does not equilibrate by the time blood reaches the
end of the pulmonary capillary. The partial pressure difference of the gas between
alveolar air and pulmonary capillary blood is maintained. Diffusion continues as long
as the partial pressure gradient is maintained.
A. Hemoglobin
1. Characteristics—globular protein of four subunits
■ Each subunit contains a heme moiety, which is iron-containing porphyrin.
■ The iron is in the ferrous state (Fe2+), which binds O2.