Gas Exchange and Transport

Gas Exchange and Transport

Christopher A. Hirsch

Respiration is the process of getting oxygen (O2) into the body for tissue use and removing carbon dioxide (CO2) into the atmosphere. This complex process involves both gas exchange (at the lungs and at the cellular level) and transport of the gases. O2 must be moved into the lungs, where it diffuses into the pulmonary circulation and is transported in the blood to the tissues. CO2 builds up in the tissues because of metabolism and diffuses into the capillary blood before being carried to the lung for exchange with alveolar gases. Normally, these processes are well integrated. However, in disease states, impaired gas exchange or transport can cause physiologic imbalances, which can alter function or threaten survival. At such times, respiratory care intervention may be the only way to maintain or restore a level of function consistent with life. This chapter provides the background knowledge that respiratory therapists (RTs) need to understand and treat patients with diseases that affect gas exchange.


Whole-Body Diffusion Gradients

Gas movement between the lungs and tissues occurs via simple diffusion (see Chapters 6 and 8). Figure 11-1 shows the normal diffusion gradients for O2 and CO2. For O2, there is a stepwise downward “cascade” of partial pressures from the normal atmospheric inspired partial pressure of O2 (PiO2) of 159 mm Hg to a low point of 40 mm Hg or less in the capillaries. The intracellular PO2 (approximately 5 mm Hg) provides the final gradient for O2 diffusion into the cell.

The diffusion gradient for CO2 is the opposite of the diffusion gradient for O2. The partial pressure of CO2 (PCO2) is highest in the cells (approximately 60 mm Hg) and lowest in room air (1 mm Hg). This reverse cascade causes CO2 movement from the tissues into the venous blood, which is transported to the lungs and—with the aid of ventilation—out to the atmosphere.

Determinants of Alveolar Gas Tensions

Alveolar Carbon Dioxide

The alveolar partial pressure of CO2 (PACO2) varies directly with the body’s production of CO2 (image) and inversely with alveolar ventilation (image). The relationship is expressed by the following formula:




Because image is expressed as a flow of dry gas at 0° C and 760 mm Hg, and image is reported as saturated gas at body temperature and ambient pressure, the factor 863 is employed to correct the measurement for comparison under the same conditions. It confers the units of pressure to the resulting dimensionless ratio of flow rates.

As an example, given image of 200 ml/min and alveolar ventilation of 4315 ml/min, application of this formula yields a PACO2 of approximately 40 mm Hg:

PACO2=(863mm Hg×200ml/min)÷4315ml/min=40mm Hg


PACO2 increases above this level if CO2 production increases while alveolar ventilation remains constant or if alveolar ventilation decreases while image remains constant. An increase in dead space, the portion of inspired air that is exhaled without being exposed to perfused alveoli, can also lead to an increased PACO2:




Likewise, PACO2 decreases if CO2 production decreases or alveolar ventilation increases. Normally, complex respiratory control mechanisms maintain PACO2 within a range of 35 to 45 mm Hg under various conditions (see Chapter 14). If CO2 production increases, as with exercise or fever, ventilation automatically increases to maintain PACO2 within normal range.

Alveolar Oxygen Tensions

Many factors determine the alveolar partial pressure of O2 (PAO2). Most important is PiO2. In addition, when O2 is in the lungs, it is diluted by both water vapor and CO2. To account for all these factors, the following alveolar air equation is applied:




The equation component FiO2 × (PB − 47) is a simple application of Dalton’s law:

Partial pressure=Fractional concentration×Total pressure


However, under BTPS conditions in the lungs, the total pressure available for O2 is reduced by an amount equal to the saturated water vapor pressure at 37° C, or 47 mm Hg.

The equation component (PaCO2 ÷ 0.8) accounts for the alveolar CO2. However, PaCO2 cannot simply be subtracted, as was done for water vapor. Instead, the equation must be corrected for the difference between O2 and CO2 movement into and out of the alveoli, which is done by dividing the PACO2 by R. R is the ratio of CO2 excretion to O2 uptake, which normally averages 0.8 throughout the lung. In addition, because PaCO2 nearly equals PACO2, PaCO2 can be substituted for PACO2. For example, if FiO2 is 0.21, PB is 760 mm Hg, and PaCO2 is 40 mm Hg, the normal alveolar partial pressure of O2 can be estimated as follows:

PAO2=0.21×(760mm Hg47)(40mm Hg÷0.8)=99.73mm Hg


In clinical practice, if a patient is breathing 60% or more O2 (FiO2 ≥ 0.60), the correction for R can be dropped because the magnitude of the correction to PaCO2 falls below significance relative to the much larger calculated FiO2 (PB − 47). This yields the following simplified form of the alveolar air equation:



The accompanying Mini Clini provides an example of how to use the alveolar air equation.

Mini Clini

Alveolar-Arterial PO2 Difference and a/A Ratio

Not all of the O2 from the alveoli gets into the blood. Why this occurs is discussed later in this chapter. This Mini Clini considers how the efficiency of O2 transfer from the alveoli to the blood can be computed.

Several bedside computations can be used to estimate the efficiency of pulmonary O2 transfer. The most common computation is the difference between the alveolar and arterial PO2, called the A-a gradient (P[A−a]O2). Normally, this difference is small—only 5 to 10 mm Hg when air is breathed and no more than 65 mm Hg when 100% O2 is breathed.

Another common bedside computation is the ratio of arterial to alveolar PO2, called the a/A ratio. The a/A ratio should be thought of as the proportion of O2 getting from the alveoli to the blood. Normally, this proportion is at least 90% (a ratio of 0.9).

Changes in Alveolar Gas Partial Tensions

In addition to CO2, O2, and water vapor, alveoli normally contain nitrogen. Nitrogen is inert and plays no role in gas exchange; however, it occupies space and exerts pressure. According to Dalton’s law, the partial pressure of alveolar nitrogen (PAN2) must equal the pressure it would exert if it alone were present. To compute PAN2, subtract the pressures exerted by all the other alveolar gases, as follows:



PAN2=760mm Hg(100mm Hg+40mm Hg+47mm Hg)


PAN2=760mm Hg187mm Hg


PAN2=573mm Hg


Because both water vapor tension and PAN2 remain constant, the only partial pressures that change in the alveolus are O2 and CO2. Based on the alveolar air equation, if FiO2 remains constant, PAO2 must vary inversely with PACO2.2-4

PACO2 itself varies inversely with the level of alveolar ventilation. For a constant CO2 production, a decrease in image simultaneously increases PACO2 and decreases PAO2, whereas an increase in image has the opposite effect (Figure 11-2). However, ventilation can be increased only so much. Neural control mechanisms and the increased work of breathing prevent decreases in PACO2 much below 15 to 20 mm Hg. Whenever a patient is breathing room air at sea level, the RT should not expect to see a PaO2 greater than 120 mm Hg during hyperventilation. PaO2 values greater than 120 mm Hg indicate that the patient is breathing supplemental O2. The accompanying Mini Clini presents a clinical application of these principles.

Mechanism of Diffusion

As described in Chapter 6, diffusion is the process whereby gas molecules move from an area of high partial pressure to an area of low partial pressure. To diffuse into and out of the lung and tissues, O2 and CO2 must move through significant barriers.

Pulmonary Diffusion Gradients

For gas exchange to occur between the alveoli and pulmonary capillaries, a difference in partial pressures (P1 − P2) must exist. Figure 11-3 shows the size and direction of these gradients for O2 and CO2. In the normal lung, the alveolar PO2 averages approximately 100 mm Hg, whereas the mean PCO2 is approximately 40 mm Hg. Venous blood returning to the lungs has a lower PO2 (40 mm Hg) than alveolar gas. The pressure gradient for O2 diffusion into the blood is approximately 60 mm Hg (100 mm Hg − 40 mm Hg). As blood flows past the alveolus, it takes up O2 and moves to the left atrium with a PO2 close to 100 mm Hg in healthy people.

Because venous blood has higher PCO2 than alveolar gas (46 mm Hg vs. 40 mm Hg), the pressure gradient for CO2 causes it to diffuse in the opposite direction, from the blood into the alveolus. This diffusion continues until capillary PCO2 equilibrates with the alveolar level, at approximately 40 mm Hg.

Although the pressure gradient for CO2 is approximately one-tenth of the pressure gradient for O2, CO2 has little difficulty diffusing across the alveolar-capillary membrane. CO2 diffuses approximately 20 times faster across the alveolar-capillary membrane than O2 because of its much higher solubility in plasma. Disorders that impair the diffusion capacity of the lung (DL) can affect O2 movement into the blood, especially when blood flow through the lung is rapid because the time the RBCs are in contact with the alveoli is reduced.

Time Limits to Diffusion

For blood leaving the pulmonary capillary to be adequately oxygenated, it must spend sufficient time in contact with the alveolus to allow equilibration.5,8 If the time available for diffusion is inadequate, blood leaving the lungs may not be fully oxygenated. The diffusion time in the lung depends on the rate of pulmonary blood flow. As depicted in Figure 11-4, blood normally takes approximately 0.75 second to pass through the pulmonary capillary. This time is more than enough to ensure complete diffusion of O2 across the alveolar-capillary membrane normally.

If blood flow increases, such as during heavy exercise, capillary transit time can decrease to 0.25 second. This short time frame is adequate to ensure that equilibration occurs as long as no other factors impair diffusion. However, in the presence of a diffusion limitation, rapid blood flow through the pulmonary circulation can result in inadequate oxygenation. High fever and septic shock, which often cause increased cardiac output, are good examples of conditions that limit diffusion time because of increased blood flow.

In clinical practice, knowledge of DL can be helpful in evaluating certain diseases. DL is the bulk flow of gas (ml/min) that diffuses into the blood for each 1-mm Hg difference in the pressure gradient. Although O2 can be used to measure DL, low concentrations (0.1% to 0.3%) of carbon monoxide are used more commonly. Chapter 19 provides details on the technique for measuring DL and its diagnostic use.

Normal Variations from Ideal Gas Exchange

This chapter has focused so far almost entirely on gas pressures in a perfect alveolus (i.e., one with ideal ventilation and blood flow). In reality, the normal lung is an imperfect organ of gas exchange. Clinically, this imperfection becomes clear, PaO2 is measured in the average individual. Rather than equaling PAO2 of 100 mm Hg, PaO2 of healthy individuals breathing air at sea level is approximately 5 to 10 mm Hg less than the calculated PaO2. Two factors account for this difference: (1) right-to-left shunts in the pulmonary and cardiac circulation and (2) regional differences in pulmonary ventilation and blood flow.

Anatomic Shunts

A shunt is the portion of the cardiac output that returns to the left heart without being oxygenated by exposure to ventilated alveoli. Two right-to-left anatomic shunts exist in normal humans: (1) bronchial venous drainage and (2) thebesian venous drainage (see Chapters 8 and 9). A right-to-left shunt causes poorly oxygenated venous blood to move directly into the arterial circulation (venous admixture), reducing the O2 content of arterial blood. Together, these normal shunts account for approximately three-fourths of the normal difference between PAO2 and PaO2. The remaining difference is a result of normal inequalities in pulmonary ventilation and perfusion.5

Regional Inequalities in Ventilation and Perfusion

The normal respiratory exchange ratio of 0.8 assumes that ventilation and perfusion in the lung are in balance, with every liter of alveolar ventilation (image) matched by approximately 1 L of pulmonary capillary blood flow (image). Any variation from this perfect balance alters gas tensions in the affected alveoli. As previously discussed, changes in image affect PACO2, which alters PAO2. Changes in blood flow also alter alveolar gas pressures. If blood flow to an area of the lung increases, CO2 coming from the tissues is delivered faster, causing an increase in PACO2 if minute ventilation remains the same. At the same time, O2 is taken up by the capillaries faster than restored by ventilation, causing a decrease in alveolar PAO2. Decrease in pulmonary capillary blood flow has the opposite effect (i.e., decrease in PACO2 and increase in PAO2) assuming minute ventilation remains the same.5,7,8

Effect of Alterations in Ventilation/Perfusion Ratio

Figure 11-5 shows graphs of the effect of image changes on the respiratory exchange ratio (R), plotting all possible values of PAO2 and PACO2. When ventilation and perfusion are in perfect balance (image = 0.99), R equals 0.8. At this point, PAO2 and PACO2 values equal the ideal values of 100 mm Hg and 40 mm Hg.

As the image increases above 1.0 (following the curve to the right), R increases. The result is a higher PAO2 and lower PACO2. At the extreme right of the graph, perfusion is zero (image = ∞). Areas with ventilation but no blood flow represent alveolar dead space (see Chapter 10). The makeup of gases in these areas is similar to that of inspired air (PO2 = 150 mm Hg; PCO2 = 0 mm Hg).

As the image decreases below 1.0 (following the curve to the left), R decreases. The result is a lower PAO2 and higher PACO2. At the extreme left of the graph, there is perfusion but no ventilation (image = 0). With no ventilation to remove CO2 and restore fresh O2, the makeup of gases in these areas is similar to mixed venous blood (image = 40 mm Hg; image = 46 mm Hg).

Venous blood entering areas with image values of zero cannot pick up O2 or unload CO2 and leave the lungs unchanged. As this venous blood returns to the left side of the heart, it mixes with well-oxygenated arterial blood, diluting its O2 contents in a manner similar to that described for a right-to-left anatomic shunt. To distinguish such areas from true anatomic shunts, exchange units with image values of zero are called alveolar shunts. Although small anatomic shunts are normal, alveolar shunts are not.

Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Gas Exchange and Transport

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