GAS EXCHANGE

The major function of the lung is gas exchange: the addition of O₂ to blood and the elimination of CO₂ from blood. Because of the close relationship between the partial pressure of CO₂ in blood (PCO₂ ) and arterial (and hence tissue) pH, the goal is maintenance of arterial CO₂ within an appropriate physiologic range. Adequate O₂ delivery must also be maintained. Figure 36-1 shows the O₂ cascade from atmospheric gas to the intracellular site of use. Assessment of the adequacy of this delivery system may be made at any step of the cascade. For example, common clinical practice dictates that arterial O₂ content (PaO₂ ) should be sufficient. It is common practice to attempt to maintain arterial hemoglobin (Hb) O₂ saturation (SaO₂ ) level above 90%, a reasonable and practical goal for two reasons. First, clinical experience supports the notion that maintenance of hemoglobin at 90% saturation with O₂ in the presence of adequate cardiac output can provide sufficient O₂ delivery to the tissues. Second, because the Hb-O₂ dissociation curve becomes abruptly steeper at O₂ saturation levels below 90% (typical PO₂ of 55 to 60 mm Hg), further decreases in PaO₂ may result in sharp diminution of arterial O₂ content.

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In addition to SaO₂ , O₂ delivery is a function of blood flow and hemoglobin concentration. A target value for SaO₂ of 90% or greater should therefore not become a sacrosanct standard for all conditions. Acute altitude hypoxia with SaO₂ values between 50% and 70% is well tolerated by normal individuals,^{[5] [6]} even during exercise, for periods of several hours or days, with no loss of consciousness, preservation of cardiac function, and minimal or no evidence of permanent sequelae.^{[7] [8] [9] [10] [11]} Individuals with acute anemia may tolerate hypoxia less well because of the enhanced reduction in arterial O₂ content.

Alveolar Gases

The lung consists of a heterogeneous collection of gas exchange units (alveoli), with a range of O₂ and CO₂ gas tensions. It is therefore erroneous to speak of "the" alveolar PO₂ or PCO₂ . However, the concept of a homogeneous lung, in which all alveoli have the same gas tensions, is a useful one. The alveolar partial pressures calculated by using such a model may be thought of as averages for the O₂ and CO₂ partial pressures in the real (nonhomogeneous) lung. Equations for alveolar PO₂ and PCO₂ (PAO₂ and PACO₂ ), or alveolar gas equations, are as follows:









In these equations, V̇CO₂ is the CO₂ production rate, V̇O₂ is the O₂ consumption rate, V̇A is the alveolar ventilation rate, k is a constant, FIO₂ is the fractional inspired O₂ concentration, PIO₂ is the inspired PO₂ after humidification or (P_barometric − P_H2O ) · FIO₂ , and R is the respiratory exchange ratio or V̇CO₂ /V̇O₂ (typically about 0.8).

An approximation to the O₂ alveolar gas equation follows:

PAO₂ PIO₂ − 1.2 × PCO₂ (3)

Unlike the alveolar equation for O₂ , the equation for PACO₂ is a function of only two variables. Because in clinical medicine V̇CO₂ is relatively constant, PACO₂ is therefore mainly a function of alveolar ventilation V̇A, to which it is inversely proportional.

V̇A = V̇E − V̇D (4)

In Equation 4, V̇E is the respiratory minute ventilation, and V̇D is dead space ventilation. Because alveolar ventilation is usually a constant fraction of minute ventilation, the following relationship applies:

V̇A = k' · V̇E (5)

The alveolar gas equation for CO₂ may be rewritten as follows:





In this form of the equation, c is a constant derived from constants k and k'.

This approximation may not hold if CO₂ production is substantially elevated, such as during a major motor seizure, shivering, or fever. CO₂ production may decrease as a result of general anesthesia or hypothermia. It is altered by approximately 7% for each 1°C change in body temperature. In young individuals, it has been observed to increase by 100% to 300% during violent shivering,^[12] although in elderly patients (>60 years), the observed increase is only about 38%.^[13]

The alveolar gas equation for O₂ (Equation 2) can be used to delineate the factors that result in low PAO₂ . Several major factors apply:

1. Low PIO₂ caused by decreased barometric pressure (altitude) or breathing a gas mixture with inspired O₂ fraction (FIO₂ ) less than 0.21
2. Elevated PACO₂ caused by hypoventilation or increased CO₂ production
3. Reduced respiratory exchange ratio (R), which is usually a minor effect because the physiologic range of R is on the order of 0.7 to 1.2, with the latter value seen during acute metabolic acidosis or excessive feeding.