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Obstructive Airway Disease

A 50-year-old man comes to the pulmonary laboratory for evaluation of chronic shortness of breath. He has
smoked one pack of cigarettes a day for 30 years. His arterial blood is analyzed for pH, partial pressure of
oxygen (PaO2), partial pressure of carbon dioxide (PaCO2), percentage saturation of hemoglobin with oxygen
(SaO2), and hemoglobin content; the results are shown below. The patient is at sea level and breathing
ambient air (21% oxygen). His respiratory rate is 25 respirations per minute, and tidal volume is 400 ml.

pH 7.47
PaO2 60 mm Hg
SaO2 90%
PaCO2 30 mm Hg
Hemoglobin 14 g/dl blood

1. What do PaO2 and SAO2 signify, and how are they related?

PaO2 is the partial pressure of oxygen in arterial blood and is expressed in mm Hg. This pressure is
exerted by oxygen molecules in their gas phase (dissolved in the plasma component of blood, as
opposed to chemically combined with hemoglobin). Note that once oxygen is chemically bound with
hemoglobin, it no longer exerts a pressure. Note also that PO2 (without the a) is the generic term for
partial pressure of oxygen in any gas or liquid, and it should not be used without reference to the site
(e.g., inspired air, alveolar air, pulmonary veins, etc.).

SaO2 is the saturation of hemoglobin with oxygen in arterial blood, and it is expressed as a percentage
of total binding sites that are combined with oxygen. Thus if 95 of every 100 hemoglobin binding sites
are combined with oxygen, the blood has an SaO 2 of 95%. A major, but not the only, determinant of
SaO2 is the PaO2.

The relation between PaO2 and SaO2 is illustrated by the oxygen-hemoglobin equilibrium (dissociation)
curve, the exact shape and position of which depend on several factors (pH; 2,3-diphosphoglycerate;
PaCO2; and body temperature).

2. What is the total oxygen content in the patient's arterial blood? Do you need to use a hemoglobin-
oxygen equilibrium curve to answer this question?

Oxygen content is a measurement of quantity. Unlike PAO2 and SaO2, oxygen content directly reflects
the number of oxygen molecules in the blood; the units are ml O 2 per 100 ml, or per liter, of blood
(both per dl and per L will be found in various texts and also in hospital laboratories). Neither PAO 2 nor
SaO2 gives information on the content of oxygen in the blood; they only provide a pressure and

percentage of saturation, respectively. PAO2 and the shape and position of the oxygen equilibrium curve
determine the SaO2. The SaO2 and the hemoglobin (Hb) content determine the oxygen content (along
with a small contribution from dissolved PaO2). Clearly, without knowledge of the hemoglobin content
there is no way to know how much oxygen is in the blood. Anemia does not affect PaO2 or SaO2. Hence
a severely anemic patient could have a low oxygen content and a normal PaO 2 and SaO2. Arterial
oxygen content is provided by the following formula:

(Amount O2 bound to hemoglobin) (Amount O2 dissolved in blood)

SaO2 x Hb (g/dl) x 1.34 ml O2/g Hb + 0.003 ml O2/mm Hg PaO2/dl

Because SaO2 is provided in the data given, there is no need to use the hemoglobin-oxygen equilibrium
curve to answer this question. Based on these data, the patient's arterial O2 content is

0.90 x 14 g Hb/dl x 1.34 ml O2/g Hb + 0.003 ml O2 (60 mm Hg)/dl

= 16.9 ml O2/dl + 0.18 ml O2 = 17.1 ml O2/dl blood*

*Or 171 ml O2/L blood

3. Is there sufficient information to calculate minute ventilation, dead space ventilation, and alveolar
ventilation? If so, make the calculation; if not, state why not. Can you discern from the respiratory rate
and/or tidal volume if he is hyperventilating?

Minute ventilation = respiratory rate x tidal volume = 25 breaths/min x 400 ml = 10 L/min; this value
is higher than the typical resting minute ventilation of 6 L/min. Because neither dead space volume nor
alveolar volume is given, we cannot calculate dead space ventilation or alveolar ventilation. Even
though his respiratory rate and minute ventilation are increased, we should not state that he is
hyperventilating (for the reasons explained in the next question). However, we can answer this question
and assess overall adequacy of alveolar ventilation from the measured PaO 2 (see the next two

4. From the alveolar ventilation equation below, state what determines the alveolar PCO2 and under what
circumstances it might change.

PaCO2 = (VCO2 x 0.863)/VA

The alveolar ventilation equation is called "the central equation of pulmonary physiology." In fact, this
equation is crucial to understanding many physiologic derangements in patients with respiratory tract
problems. Rearranging the equation we obtain

PACO2 = (VCO2 x 0.863)/VA

Thus alveolar PCO2 is directly proportional to the CO2 production (VCO2) and inversely proportional
to alveolar ventilation (VA). Any proportionate changes in the VCO2 and VA will not change PACO2;
any disproportionate changes will affect PACO2 predictably, depending on whether the greater
change is in the numerator or denominator. For example, a 40% rise in VA and a 10% rise in VCO2
will lower PaCO2.

5. Is this patient's alveolar ventilation, relative to CO2 production, more or less than normal? How is the
answer to this question used to determine if a patient is hyperventilating or hypoventilating? What is
the clinical significance of this information?

Alveolar PCO2 in the alveolar ventilation and alveolar gas equations can be replaced by the measured
arterial PCO2; this is true because there is no "gradient" between the two values, as there is between
alveolar and arterial PO2. Substituting PaCO2 in the alveolar ventilation equation, we see that PaCO2 is
determined by the ratio of CO2 production to alveolar ventilation:

PACO2 = (VCO2 x 0.863)/VA

Normally, the amount of VA is sufficient to excrete the produced CO2 and thereby keep PaCO2 in the
normal range (36 to 44 mm Hg). With increases in CO 2 production (as during modest exercise), VA will
normally rise a proportionate amount and thereby maintain a normal PaCO 2. If VA does not rise along
with VCO2, or if VA falls while VCO2 does not or if VA falls more than VCO 2, VA will be reduced out of
proportion for the VCO2; this situation represents hypoventilation, which raises PaCO2. Conversely,
when VA is elevated out of proportion to the VCO2 there is hyperventilation, which reduces PaCO2. By
definition, then, hyperventilation and hypoventilation refer only to a specific PaCO2 value, which in turn
reflects the state of alveolar ventilation relative to CO 2 production. Note that hyperventilation and
hypoventilation do not refer to rate or depth of breathing, or a patient's respiratory effort. This is why
you cannot say, from observation alone, that a patient is "hyperventilating." Irrespective of rate or
depth of breathing, a patient with lung disease may in fact be hyper-, hypo-, or normally ventilating
relative to CO2 production.

6. What is his calculated PACO2? (Use the alvolar gas equation below. As is customary, assume that PCO2
measured in arterial blood [PaCO2] equals mean alveolar PCO2 [PACO2]. Also, assume his respiratory
quotient is 0.8.)

PAO2 = PIO2 - PaCO2 [FIO2 + (1-FIO2)/R]

Where PIO2 = FIO2 (barometric pressure - 47 mm Hg)

From the alveolar gas equation, PAO2 = 114 mm Hg. This patient is hyperventilating. Hence alveolar
PO2 is increased. (The alveolar gas equation shows that PAO 2 always increases if PaCO2 decreases,
other factors remaining unchanged.)

7. Subtract PaO2 from the calculated PAO2. Is the value for (PAO2 - PaO2) abnormally increased? What is
the significance of an increased (PAO2 ¨C PaO2)?

PAO2 ¨C PaO2 = 114 - 60 = 54 mm Hg and is definitely abnormal; normal (PAO2 ¨C PaO2) for a man
this age, breathing ambient air, is about 10 to 15 mm Hg. For someone who is breathing room air at
sea level and who has a PaCO2 of 40 mm Hg, PAO 2 = 102 mm Hg. Under the same conditions, the
normal PaO2 for a man this age should be about 90 mm Hg; (PAO 2 ¨C PaO2) would then be 102 - 90 =
12 mm Hg. Although this patient's PaO2 is slightly elevated because of hyperventilation, his PaO2 is
reduced (their difference is 54 mm Hg). This large difference between PAO 2 and PaO2 indicates a
significant defect in getting oxygen from the alveoli into the pulmonary circulation.

8. What is your overall interpretation of the blood gas data, in terms of the patient's oxygenation and
The patient next undergoes tests of mechanical lung function. The following lung volumes and
capacities are measured. (Percentages of predicted values are shown; any lung volume or capacity
between 80% to 120% of predicted is considered in the normal range.)

Forced vital capacity (FVC) = 3 L = 75% of predicted

Forced expiratory volume in one second (FEV-l) = 1.6 L = 55% of predicted
Total lung capacity = 7.8 L = 130% of predicted
Residual volume = 2.8 L = 140% of predicted

Ventilation: The patient is hyperventilating; in other words, his level of alveolar ventilation is more than
needed to excrete his metabolic production CO2 and to keep PaCO2 in the normal range. Oxygenation:
First, the transfer of oxygen from alveoli into the pulmonary capillaries is impaired; this is evident
because (PAO2 ¨C PaO2) is greater than normal. Second, hemoglobin content is normal, but oxygen
saturation is reduced slightly at 90%; therefore his oxygen content is also reduced.

9. What is the difference between a lung volume and a lung capacity?

A lung volume is a quantity of air not subdivided further (e.g., tidal volume, residual volume). A lung
capacity is a quantity that includes two or more lung volumes (e.g., total lung capacity, functional
residual capacity).

10. How do you interpret the lung volume and capacity information? What do you think is the nature of his
clinical problem?

The forced vital capacity (FVC) is slightly reduced below the lower normal limit of 80%, and the FEV-1
is reduced even more. When the FEV-1 is reduced more than FVC, there is some air flow obstruction
(the patient cannot exhale forcefully at a normal rate). At the same time, the total lung capacity and
residual volume are above normal; this finding suggests some air trapping. Overall, these changes are
typical of obstructive airway disease commonly seen in long-term smokers. If air flow remains

obstructed despite treatment, the patient is said to have chronic obstructive pulmonary disease

11. Which of the lung volume and lung capacity measurements cannot be determined by spirometry alone,
but requires an additional technique (such as inert gas dilution)?

Total lung capacity and residual volume cannot be determined by spirometry alone.