Alveolar, Arterial, & Venous Gas Tensions

ALVEOLAR, ARTERIAL, & VENOUS GAS TENSIONS

When dealing with gas mixtures, each gas is considered to contribute separately to total gas pressure, and its partial pressure is directly pro-portional to its concentration. Air has an O₂ con-centration of approximately 21%; therefore, if the barometric pressure is 760 mm Hg (sea level), the partial pressure of O₂ (Po₂) in air is normally 159.6 mm Hg: 760 mm Hg × 0.21 = 159.6 mm Hg

In its general form, the equation may be written as follows:

Pio₂= Pb × Fio₂

where Pb = barometric pressure and Fio₂= the frac-tion of inspired O ₂.

Two general rules can also be used:

·        Partial pressure in millimeters of mercury approximates the percentage × 7

·        Partial pressure in kilopascals is approximately the same as the percentage.

Oxygen

Alveolar Oxygen Tension

With every breath, the inspired gas mixture is humidified at 37°C in the upper airway. The inspired tension of O₂ (Pio₂) is therefore reduced by the added water vapor. Water vapor pressure is depen-dent only upon temperature and is 47 mm Hg at 37°C. In humidified air, the normal partial pressure of O₂ at sea level is 149.7 mm Hg:

(760 − 47) × 0.21 = 149.1 mm Hg

The general equation is

Pio₂= (Pb − Ph₂o) × Fio₂

where Ph₂o = the vapor pressure of water at body temperature.

In alveoli, the inspired gases are mixed with residual alveolar gas from previous breaths, O₂ is taken up, and CO₂ is added. The final alveolar O₂ tension (Pao₂) is therefore dependent on all of these factors and can be estimated by the following equation:

where Paco₂= arterial CO₂ tension and Rq = respiratory quotient.

Rq is usually not measured. Note that large

increases in Paco₂ (>75 mm Hg) readily pro-duce hypoxia (Pao₂< 60 mm Hg) at room air, but not at high inspired O ₂ concentrations.

A yet simpler method of approximating Pao₂ in millimeters of mercury is to multiply the percentage of inspired O ₂ concentration by 6. Thus, at 40%, Pao₂ is 6 × 40, or 240 mm Hg.

Pulmonary End-Capillary Oxygen Tension

For all practical purposes, pulmonary end-capillary O₂ tension (Pc′o₂) may be considered identical to Pao₂; the Pao₂–Pc′o₂ gradient is normally minute. Pc′o₂ is dependent on the rate of O₂ diffusion across the alveolar–capillary membrane, as well as on pul-monary capillary blood volume and transit time. The large capillary surface area in alveoli and the 0.4–0.5 µm thickness of the alveolar–capillary mem-brane greatly facilitate O₂ diffusion. Enhanced O ₂ binding to hemoglobin at saturations above 80% also augments O ₂ diffusion . Capillary transit time can be estimated by dividing pulmonary capillary blood volume by cardiac output (pulmo-nary blood flow); thus, normal capillary transit time is 70 mL ÷ 5000 mL/min (0.8 s). Maximum Pc′o₂ is usually attained after only 0.3 sec, providing a large safety margin.The binding of O₂ to hemoglobin seems to be the principal rate-limiting factor in the transferof O₂ from alveolar gas to blood. Therefore, pulmo-nary diffusing capacity reflects not only the capacity and permeability of the alveolar–capillary mem-brane, but also pulmonary blood flow. Moreover, O₂ uptake is normally limited by pulmonary blood flow, not O₂ diffusion across the alveolar–capillary membrane; the latter may become significant dur-ing exercise in normal individuals at high altitudes and in patients with extensive destruction of the alveolar–capillary membrane.

O₂ transfer across the alveolar–capillary mem-brane is expressed as O₂ diffusing capacity (Dlo₂):

Because Pc′o₂ cannot be measured accurately, measurement of carbon monoxide diffusion capacity (Dlco) is used instead to assess gas transfer across the alveolar–capillary membrane. Because carbon monoxide has a very high affinity for hemoglobin, there is little or no CO in pulmonary capillary blood, so that even when it is administered at low concen-tration, Pc′co can be considered zero. Therefore,

Reductions in Dlco imply an impediment in gas transfer across the alveolar–capillary membrane Such impediments may be due to abnormal V/Q ratios, extensive destruction of the gas alveolar– capillary membrane, or very short capillary transit times. Abnormalities are accentuated by increases in O₂ consumption and cardiac output, such as occurs during exercise.

Arterial Oxygen Tension

Pao₂ cannot be calculated like Pao₂ but must be measured at room air. T he alveolar-to-arterial O ₂ partial pressure gradient (A–a gradient) is normally less than 15 mm Hg, but progressively increases with age up to 20–30 mm Hg. Arterial O ₂ tension can be approximated by the following formula (in mm Hg):

The range is 60–100 mm Hg (8–13 kPa). Decreases are probably the result of a progressive increase in closing capacity relative to FRC (see above). Table 23–4 lists the mechanisms of hypox-emia (Pao₂<60 mm Hg).

The most common mechanism for hypoxemia is an increased alveolar–arterial gradient. The A–agradient for Odepends on the amount of right to-left shunting, the amount of V/Q scatter, and the mixed venous O₂ tension . The last depends on cardiac output, O₂ consumption, and hemoglobin concentration.

The A–a gradient for O₂ is directly proportional to shunt, but inversely proportional to mixed venous O₂ tension. The effect of each variable on Pao₂ (and consequently the A–a gradient) can be determined only when the other variables are held constant. Figure 23–19 shows the effect of different degrees of shunting on Pao₂. It should also be noted that the greater the shunt, the less likely the possibility that an increase in Fio₂ will prevent hypoxemia. Moreover, isoshunt lines seem to be most useful for O₂ concentrations between 35% and 100%. Lower O₂ concentrations require modification of isoshunt lines to account for the effect of V/Q scatter.

The effect of cardiac output on the A–a gradi-ent (Figure 23–20) is due not only to its second-ary effects on mixed venous O₂ tension but also to a direct relationship between cardiac output and intrapulmonary shunting. As can be seen, a low car-diac output tends to accentuate the effect of shunt on Pao₂. A reduction in venous admixture may be observed with low-normal cardiac outputs second-ary to accentuated pulmonary vasoconstriction from a lower mixed venous O₂ tension. On the other hand, high cardiac outputs can increase venous admixture by elevating mixed venous O₂ tension, which in turn inhibits hypoxic pulmonary vasoconstriction.

O₂ consumption and hemoglobin concentra-tion can also affect Pao₂ through their secondary effects on mixed venous O₂ tension (below). High O₂

consumption rates and low hemoglobin concentra-tions can increase the A–a gradient and depress Pao₂.

Mixed Venous Oxygen Tension

Normal mixed venous O₂ tension (Pvo₂₎ is about 40 mm Hg and represents the overall balance betweenO₂consumptionandOdelivery (Table 23–5). A true mixed venous blood sample contains venous drainage from the superior vena cava, the inferior vena cava, and the heart; it must therefore be obtained from a pulmonary artery catheter.

2. Carbon Dioxide

Carbon dioxide is a by-product of aerobic metabo-lism in mitochondria. There are therefore small con-tinuous gradients for CO₂ tension from mitochondria to cell cytoplasm, extracellular fluid, venous blood, and alveoli, where the CO₂ is finally eliminated.

Mixed Venous Carbon Dioxide Tension

Normal mixed venous CO₂ tension (Pvco₂ ) is about 46 mm Hg and is the end result of mixing of blood from tissues of varying metabolic activity. Venous CO₂ tension is lower in tissues with low metabolic activity (eg, skin), but higher in blood from those with relatively high activity (eg, heart).

Alveolar Carbon Dioxide Tension

Alveolar CO₂ tension (Paco₂) is generally considered to represent the balance between total CO production (Vco₂) and alveolar ventilation (elimination):

where Va is alveolar ventilation ( Figure 23–21). In reality, Paco₂ is related to CO₂ elimination rather than production. Although the two are equal in a steady state, an imbalance occurs during periods

of acute hypoventilation or hypoperfusion, and the excess CO₂ increases total body CO₂ content.Clinically Pacois moredependentonalveolarventilation than is Vco₂, because CO₂ output does not vary appreciably under most circumstances. Moreover, the body’s large capacity to store CO  buffers acute changes in Vco₂.

Pulmonary End-Capillary Carbon Dioxide Tension

Pulmonary end-capillary CO ₂ tension (Pc′co₂) is virtually identical to Paco₂ for the same reasons as those discussed in the section about O₂. In addition, the diffusion rate for CO₂ across the alveolar–capil-lary membrane is 20 times that of O₂.

Arterial Carbon Dioxide Tension

Arterial CO₂ tension (Paco₂), which is readily mea-surable, is identical to Pc′co_2, and, necessarily, Paco₂. Normal Paco₂ is 38 ± 4 mm Hg (5.1 ± 0.5 kPa); in practice, 40 mm Hg is usually considered normal.Although low V/Q  ratios tend to increase•Paco2,whereas high V/Q ratios tend to decrease it (in contrast to the case for O2 [see above]), significant arterial-to-alveolar gradients for CO develop only in the presence of marked V/Q abnormalities (>30% venous admixture); even then the gradient is rela-tively small (2–3 mm Hg). Moreover, small increasesin the gradient appreciably increase COoutput into alveoli with relatively normal V/Q. Even moderate to severe disturbances usually fail to appreciably alter arterial CO ₂ because of a reflex increase in ven-tilation from concomitant hypoxemia.

End-Tidal Carbon Dioxide Tension

Because end-tidal gas is primarily alveolar gas and Paco₂ is virtually identical to Paco₂, end-tidal CO ₂ tension (Petco₂) is used clinically as an estimate of Paco₂. The Paco₂–Petco₂ gradient is normally less than 5 mm Hg and represents dilution of alveolar gas with CO₂-free gas from nonperfused alveoli (alveolar dead space).