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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.
PaO2 60 mm Hg
PaCO2 30 mm Hg
Hemoglobin 14 g/dl blood
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 SaO2 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).
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 O2 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 PAO2 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 PaO2 and SaO2. Arterial oxygen content is provided by the following formula:
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 PaO2 (see the next two questions).
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
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; anydisproportionat e 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:
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 CO2 production (as during modest exercise), VA will normally rise a proportionate amount and thereby maintain a normal PaCO2. If VA does not rise along with VCO2, or if VA falls while VCO2 does not or if VA falls more than VCO2, 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 ishyperventilati on, 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 CO2 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.)
From the alveolar gas equation, PAO2 = 114 mm Hg. This patient is hyperventilating. Hence alveolar PO2 is increased. (The alveolar gas equation shows that PAO2 always increases if PaCO2 decreases, other factors remaining unchanged.)
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