Chapter 5. Ventilation-Perfusion Relationships

Objectives

The reader understands the importance of matching of ventilation and perfusion in the lung.

Predicts the consequences of mismatched ventilation and perfusion.
Describes the methods used to assess the matching of ventilation and perfusion.
Describes the methods used to determine the uniformity of the distribution of the inspired gas and pulmonary blood flow.
Explains the regional differences in the matching of ventilation and perfusion of the normal upright lung.
Predicts the consequences of the regional differences in the ventilation and perfusion of the normal upright lung.

Ventilation-Perfusion Relationships: Introduction

Gas exchange between the alveoli and the pulmonary capillary blood occurs by diffusion, as will be discussed in the next chapter. Diffusion of oxygen and carbon dioxide occurs passively, according to their concentration differences across the alveolar-capillary barrier. These concentration differences must be maintained by ventilation of the alveoli and perfusion of the pulmonary capillaries.

The Concept of Matching Ventilation and Perfusion

Listen

Alveolar ventilation brings oxygen into the lung and removes carbon dioxide from it. Similarly, the mixed venous blood brings carbon dioxide into the lung and takes up alveolar oxygen. The alveolar

and

are thus determined by the relationship between alveolar ventilation and pulmonary capillary perfusion. Alterations in the ratio of ventilation to perfusion, called the

, will result in changes in the alveolar

and

, as well as in gas delivery to or removal from the lung.

Alveolar ventilation is normally about 4 to 6 L/min and pulmonary blood flow (which is equal to cardiac output) has a similar range, and so the

for the whole lung is in the range of 0.8 to 1.2.

However, ventilation and perfusion must be matched on the alveolar-capillary level, and the

for the whole lung is really of interest only as an approximation of the situation in all the alveolar-capillary units of the lung. For instance, suppose that all 5 L/min of the cardiac output went to the left lung and all 5 L/min of alveolar ventilation went to the right lung. The whole lung

would be 1.0, but there would be no gas exchange because there could be no gas diffusion between the ventilated alveoli and the perfused pulmonary capillaries.

Consequences of High and Low Ventilation-Perfusion Ratio

Listen

Oxygen is delivered to the alveolus by alveolar ventilation, is removed from the alveolus as it diffuses into the pulmonary capillary blood, and is carried away by blood flow. Similarly, carbon dioxide is delivered to the alveolus in the mixed venous blood and diffuses into the alveolus in the pulmonary capillary. The carbon dioxide is removed from the alveolus by alveolar ventilation. As will be discussed in Chapter 6, at resting cardiac outputs the diffusion of both oxygen and carbon dioxide is normally limited by pulmonary perfusion. Thus, the alveolar partial pressures of both oxygen and carbon dioxide are determined by the

If the

in an alveolar-capillary unit increases, the delivery of oxygen relative to its removal will increase, as will the removal of carbon dioxide relative to its delivery. Alveolar

will therefore rise, and alveolar

will fall. If the

in an alveolar-capillary unit decreases, the removal of oxygen relative to its delivery will increase and the delivery of carbon dioxide relative to its removal will increase. Alveolar

will therefore fall, and alveolar

will rise.

Figure 5–1 shows the consequences of alterations in the relationship of ventilation and perfusion on hypothetical alveolar-capillary units. Unit A has a normal

. Inspired air enters the alveolus with a

of about 150 mm Hg and a

of nearly 0 mm Hg. Mixed venous blood enters the pulmonary capillary with a

of about 40 mm Hg and a

of about 45 mm Hg. This results in an alveolar

of about 100 mm Hg and an alveolar

of 40 mm Hg (see Chapter 3). The partial pressure difference for oxygen diffusion from alveolus to pulmonary capillary is thus about 100 to 40 mm Hg, or 60 mm Hg; the partial pressure gradient for CO2 diffusion from pulmonary capillary to alveolus is only about 45 to 40, or 5 mm Hg.

Figure 5–1.

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The effect of changes in the ventilation-perfusion ratio on the alveolar

and

A: Normal

; B:

= 0; C:

is infinite. (Reproduced with permission from West, 1977, 1990.)

The airway supplying unit B has become completely occluded. Its

is zero. As time goes on, the air trapped in the alveolus equilibrates by diffusion with the gas dissolved in the mixed venous blood entering the alveolar-capillary unit. (If the occlusion persists, the alveolus is likely to collapse.) No gas exchange can occur, and any blood perfusing this alveolus will leave it exactly as it entered it. Unit B is therefore acting as a right-to-left shunt.

The blood flow to unit C is blocked by a pulmonary embolus, and unit C is therefore completely unperfused. It has an infinite

. Because no oxygen can diffuse from the alveolus into pulmonary capillary blood and because no carbon dioxide can enter the alveolus from the blood, the

of the alveolus is approximately 150 mm Hg and its

is approximately zero. That is, the gas composition of this unperfused alveolus is the same as that of inspired air. Unit C is alveolar dead space. If unit C were unperfused because its alveolar pressure exceeded its pre-capillary pressure (rather than because of an embolus), then it would also correspond to part of zone 1.

Units B and C represent the 2 extremes of a continuum of ventilation-perfusion ratios. The

ratio of a particular alveolar-capillary unit can fall anywhere along this continuum, as shown at the bottom of Figure 5–1. The alveolar

and

of such units will therefore fall between the two extremes shown in the figure: Units with low

ratios will have relatively low

and high

; units with high

ratios will have relatively high

and low

. This is demonstrated graphically in an O2-CO2 diagram such as that seen in Figure 5–2.

The diagram shows the results of mathematical calculations of alveolar

and

for

ratios between zero (for mixed venous blood) and infinity (for inspired air). The resulting curve is known as the ventilation-perfusion ratio line. This simple O2-CO2 diagram can be modified to include correction lines for other factors, such as the respiratory exchange ratios of the alveoli and the blood or the dead space. The position of the

ratio line is altered if the partial pressures of the inspired gas or mixed venous blood are altered.

Figure 5–2.

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The ventilation-perfusion ratio line on an O2-CO2 diagram. Unit with a

of zero has the

and

of mixed venous blood; a unit with an infinite

has the

and

of inspired air. (Reproduced with permission from West 1977, 1990.)

Testing for Nonuniform Distribution of Inspired Gas and Pulmonary Blood Flow

Listen

Nonuniform ventilation of the alveoli can be caused by uneven resistance to airflow or nonuniform compliance in different parts of the lung. Uneven resistance to airflow may be a result of collapse of airways, as seen in emphysema; bronchoconstriction, as in asthma; decreased lumen diameter due to inflammation, as in bronchitis; obstruction by mucus, as in asthma or chronic bronchitis; or compression by tumors or edema. Uneven compliance may be a result of fibrosis, regional variations in surfactant production, pulmonary vascular congestion or edema, emphysema, diffuse or regional atelectasis, pneumothorax, or compression by tumors or cysts.

Nonuniform perfusion of the lung can be caused by embolization or thrombosis; compression of pulmonary vessels by high alveolar pressures, tumors, exudates, edema, pneumothorax, or hydrothorax; destruction or occlusion of pulmonary vessels by various disease processes; pulmonary vascular hypotension; or collapse or overexpansion of alveoli.

As already noted in Chapters 3 and 4, gravity, local factors, and regional differences in intrapleural pressure cause a degree of nonuniformity in the distribution of ventilation and perfusion in normal lungs. This will be discussed in detail later in this chapter.

The methods used for testing for nonuniform ventilation, nonuniform perfusion, and ventilation-perfusion mismatch are summarized in Table 5–1.

Table 5–1. Testing for

Mismatch

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Table 5–1. Testing for

Mismatch

I. Nonuniform gas distribution
II. Nonuniform pulmonary blood flow
III. Mismatched

= ventilation-perfusion ratio: (A-a)

= alveolar-arterial oxygen difference.

Testing for Nonuniform Distribution of Inspired Gas

Several methods can be used to demonstrate an abnormal distribution of ventilation in a patient.

Single‐Breath‐of-Oxygen Test

A rising expired nitrogen concentration in phase III (the “alveolar plateau”) of the single-breath-of-oxygen test shown in Figure 3–14 indicates the possibility of a maldistribution of ventilation (see “The Closing Volume” section of Chapter 3).

Nitrogen-Washout Test

The same equipment used in the single-breath-of-oxygen test mentioned above can be used in another test for nonuniform ventilation of the lungs. In this test, the subject breathes normally through a 1-way valve from a bag of 100% oxygen, and the expired nitrogen concentration is monitored over a number of breaths. With each successive inspiration of 100% oxygen and subsequent expiration, the expired end-tidal nitrogen concentration falls as nitrogen is washed out of the lung (Figure 5–3).

Figure 5–3.

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Illustration of a nitrogen-washout curve.

The rate of decrease of the expired end-tidal nitrogen concentration depends on several factors. A high functional residual capacity (FRC), a low tidal volume, a large dead space, or a low breathing frequency could each contribute to a slower washout of alveolar nitrogen. Nonetheless, subjects with a normal distribution of airways resistance will reduce their expired end-tidal nitrogen concentration to less than 2.5% within 7 minutes. Subjects breathing normally who take more than 7 minutes to reach an alveolar nitrogen concentration of less than 2.5% have high-resistance pathways, or “slow alveoli” (see section “Dynamic Compliance” in Chapter 2).

If the logarithms of the end-tidal nitrogen concentrations are plotted against the number of breaths taken (for a subject breathing regularly), a straight line results (Figure 5–4A). On the other hand, the log [N2] plotted for a patient with a maldistribution of airways resistance, such as that produced experimentally by inhaling a histamine aerosol (Figure 5–4B), displays a more complex curve. After a short period of relatively rapid nitrogen washout, a long period of extremely slow nitrogen washout occurs, indicating a population of poorly ventilated “slow alveoli.”

Figure 5–4.

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Expired nitrogen concentration versus number of breaths during a nitrogen washout. Note the logarithmic scale for the nitrogen concentration. A: Curve from a normal subject. B: Curve from a normal subject after inhalation of a histamine aerosol, which produces a marked nonuniformity of ventilation. (Reproduced with permission from Bouhuys A, Jonsson R, Lichtneckert S, et al. Effects of histamine on pulmonary ventilation in man. Clin Sci. 1960;19:79–94. © the Biochemical Society and the Medical Research Society.)

Trapped Gas

Differences between the FRC determined by the helium-dilution technique and the FRC determined using a body plethysmograph may indicate gas trapped in the alveoli because of airway closure (see Chapter 3). Furthermore, if a number of high-resistance pathways are present in the lung of the patient being tested, it may take an exceptionally long time for the patient’s expired end-tidal helium concentration to equilibrate with the helium concentration in the spirometer. The closing volume determination, discussed at the end of Chapter 3, can also demonstrate airway closure in the lung.

Radioactive Markers

The methods described thus far can indicate the presence of poorly ventilated regions of the lung but not their location. Images of the whole lung taken with a scintillation counter, after the subject has taken a breath of a radioactive gas mixture such as 133Xe or 99mTc DTPA (technetium-labeled diethylene triamine pentaacetic acid) and oxygen, can indicate which regions of the lung are poorly ventilated.

Testing for Nonuniform Distribution of Pulmonary Blood Flow

These methods were all discussed briefly in Chapter 4. They include angiograms, lung scans after intravenous injection of radiolabeled (with radioactive iodine or technetium) macroaggregates of albumin, and lung scans after intravenous administration of dissolved 133Xe. Each of these methods can indicate the locations of relatively large regions of poor perfusion.

Testing for Mismatched Ventilation and Perfusion

Several methods can demonstrate the presence or location of areas of the lung with mismatched ventilation and perfusion. These methods include calculations of the physiologic shunt, the physiologic dead space, differences between the alveolar and arterial

and between arterial and end-tidal (“alveolar”)

, which can indicate the presence or quantity of ventilation-perfusion mismatch; and lung scans after inhaled and intravenously administered 133Xe or 99mTc, which can indicate the location of ventilation-perfusion mismatch.

Physiologic Shunts and the Shunt Equation

A right-to-left shunt is the mixing of venous blood that has not been oxygenated (or not fully oxygenated) into the arterial blood. The physiologic shunt, which corresponds to the physiologic dead space, consists of the anatomic shunts plus the intrapulmonary shunts. The intrapulmonary shunts can be absolute shunts, or they can be “shuntlike states,” that is, areas of low ventilation-perfusion ratios in which alveoli are underventilated and/or overperfused.

Anatomic Shunts

Anatomic shunts consist of systemic venous blood entering the left ventricle without having entered the pulmonary vasculature. In a normal healthy adult, about 2% to 5% of the cardiac output, including venous blood from the bronchial veins, the thebesian veins, and the pleural veins, enters the left side of the circulation directly without passing through the pulmonary capillaries. Therefore, the output of the left ventricle is normally greater than that of the right ventricle in adults. (This normal anatomic shunt is also occasionally referred to as the physiologic shunt because it does not represent a pathologic condition.) Pathologic anatomic shunts such as right-to-left intracardiac shunts can also occur, as in tetralogy of Fallot.

Absolute Intrapulmonary Shunts

Mixed venous blood perfusing pulmonary capillaries associated with totally unventilated or collapsed alveoli constitutes an absolute shunt (like the anatomic shunts) because no gas exchange occurs as the blood passes through the lung. Absolute shunts are sometimes also referred to as true shunts.

Shuntlike States

Alveolar-capillary units with low

also act to lower the arterial oxygen content because blood draining these units has a lower

than blood from units with well-matched ventilation and perfusion.

The Shunt Equation

The shunt equation conceptually divides all alveolar-capillary units into two groups: those with well-matched ventilation and perfusion and those with ventilation-perfusion ratios of zero. Thus, the shunt equation combines the areas of absolute shunt (including the anatomic shunts) and the shuntlike areas into a single conceptual group. The resulting ratio of shunt flow to the cardiac output, often referred to as the venous admixture, is the part of the cardiac output that would have to be perfusing absolutely unventilated alveoli to cause the systemic arterial oxygen content obtained from a patient. A much larger portion of the cardiac output could be overperfusing poorly ventilated alveoli and yield the same ratio.

The shunt equation can be derived as follows: Let

represent the total pulmonary blood flow per minute (ie, the cardiac output), and let

represent the amount of blood flow per minute entering the systemic arterial blood without receiving any oxygen (the “shunt flow”). The volume of blood per minute that perfuses alveolar-capillary units with well-matched ventilation and perfusion then equals

The total volume of oxygen per time entering the systemic arteries is therefore

where

equals oxygen content of arterial blood in milliliters of oxygen per 100 mL of blood. This total amount of oxygen per time entering the systemic arteries is composed of the oxygen coming from the well-ventilated and well-perfused alveolar-capillary units:

where

equals the oxygen content of the blood at the end of the ventilated and perfused pulmonary capillaries, plus the oxygen in the unaltered mixed venous blood coming from the shunt,

(where

is equal to the oxygen content of the mixed venous blood). As will be discussed in Chapter 7, there is normally a substantial amount of oxygen in the mixed venous blood.

That is,

The shunt fraction

is usually multiplied by 100% so that the shunt flow is expressed as a percentage of the cardiac output.

The arterial and mixed venous oxygen contents can be determined if blood samples are obtained from a systemic artery and from the pulmonary artery (for mixed venous blood), but the oxygen content of the blood at the end of the pulmonary capillaries with well-matched ventilation and perfusion is, of course, impossible to measure directly. This must be calculated from the alveolar air equation, discussed in Chapter 3, and the patient’s hemoglobin concentration, which will be discussed in Chapter 7.

The relative contributions of the true intrapulmonary shunts and the shuntlike states to the calculated shunt flow can be estimated by repeating the measurements and calculations with the patient on a normal or slightly elevated inspired concentration of oxygen and then on a very high inspired oxygen concentration (

of 0.95 to 1.00). At the lower inspired oxygen concentrations, the calculated

will include both the true shunts and the alveolar-capillary units with low

ratios. After a patient has inspired nearly 100% oxygen for 20 to 30 minutes, even alveoli with very low

s will have high enough alveolar

to completely saturate the hemoglobin in the blood perfusing them. These units will therefore no longer contribute to the calculated

, and the new calculated shunt should include only areas of absolute shunt. Unfortunately, very high inspired oxygen concentrations may lead to absorption atelectasis of very poorly ventilated alveoli that remain perfused, and so this test may alter what it is trying to measure when high levels of

are used.

Physiologic Dead Space

The use of the Bohr equation to determine the physiologic dead space was discussed in detail in Chapter 3. If the anatomic dead space is subtracted from the physiologic dead space, the result (if there is a difference) is alveolar dead space, or areas of infinite

. Alveolar dead space also results in an arterial-alveolar CO2 difference; that is, the end-tidal

is normally equal to the arterial

. End-tidal

is used as an estimate of the mean

of all ventilated alveoli. An arterial

greater than the end-tidal

usually indicates the presence of alveolar dead space.

Alveolar-Arterial Oxygen Difference

Throughout most of this book, the alveolar and arterial

are treated as though they are equal. However, the arterial

is normally a few mm Hg less than the alveolar

. This normal alveolar-arterial oxygen difference, the (A-a)

, is caused by the normal anatomic shunt, some degree of ventilation-perfusion mismatch (see later in this chapter), and diffusion limitation (see Chapter 6) in some parts of the lung. Of these,

mismatch is usually the most important, with a small contribution from shunts and very little from diffusion limitation. Larger-than-normal differences between the alveolar and arterial

may indicate significant ventilation-perfusion mismatch; however, increased alveolar-arterial oxygen differences (Table 5–2) can also be caused by anatomic or intrapulmonary shunts, diffusion block, low mixed venous s

, breathing higher than normal oxygen concentrations, or shifts of the oxyhemoglobin dissociation curve (also see Table 8–6).

Table 5–2. Causes of Increased Alveolar-Arterial Oxygen Difference

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Table 5–2. Causes of Increased Alveolar-Arterial Oxygen Difference

Increased right-to-left shunt
- Anatomic
- Intrapulmonary
Increased ventilation-perfusion mismatch
Impaired diffusion
Increased inspired partial pressure of oxygen
Decreased mixed venous partial pressure of oxygen
Shift of oxyhemoglobin dissociation curve

Reproduced with permission from Marshall and Wyche (1972).

The alveolar-arterial

difference is normally about 5 to 15 mm Hg in a young healthy person breathing room air at sea level. It increases with age because of the progressive decrease in arterial

that occurs with aging for the reasons discussed at the end of Chapter 3. The normal alveolar-arterial

difference increases by about 20 mm Hg between the ages of 20 and 70. A person’s age/4 +4 mm Hg is a good clinical estimate of the normal alveolar-arterial

difference.

Note that the “alveolar”

used in determining the alveolar-arterial oxygen difference is the

calculated using the alveolar air equation. As noted in Chapter 3, it is an idealized average alveolar

that represents what alveolar

should be, not necessarily what it is.

Another useful clinical index in addition to the alveolar-arterial oxygen difference is the ratio of arterial

to the fractional concentration of oxygen in the inspired air. The

should be greater than or equal to 200; a

less than 200 is seen in acute respiratory distress syndrome.

Single-Breath Carbon Dioxide Test

The expired concentration of carbon dioxide can be monitored by a rapid-response carbon dioxide meter in a manner similar to that used in the single-breath tests utilizing a nitrogen meter, as described in Chapter 3 (see Figure 3–9). The alveolar plateau phase of the expired carbon dioxide concentration may show signs of poorly matched ventilation and perfusion if such regions empty asynchronously with other regions of the lung.

Lung Scans after Inhaled and Infused Markers

Lung scans after both inhaled and injected markers can be used to inspect the location and amount of ventilation and perfusion to the various regions of the lung (see Chapters 3 and 4).

Multiple Inert Gas Elimination Technique

A more specific graphic method for assessing ventilation-perfusion relationships in human subjects is called the multiple inert gas elimination technique. This technique uses the concept that the elimination via the lungs of different gases dissolved in the mixed venous blood is affected differently by variations in the ventilation-perfusion ratios of alveolar-capillary units, according to the solubility of each gas in the blood. At a ventilation-perfusion ratio of 1.0, a greater volume of a relatively soluble gas would be retained in the blood than would be the case with a relatively insoluble gas. Thus, the retention of any particular gas by a single alveolar-capillary unit is dependent on the blood-gas partition coefficient of the gas and the ventilation-perfusion ratio of the unit. Gases with very low solubilities in the blood would be retained in the blood only by units with very low (or zero)

. Gases with very high solubilities in the blood would be eliminated mainly in the expired air of units with very high

In the standard multiple inert gas elimination technique for assessing

relationships, a mixture of 6 gases dissolved in saline is infused into a peripheral arm vein at a constant rate of 2 to 5 mL/min until a steady state of gas exchange is established. This usually takes about 20 minutes. The 6 gases—sulfur hexafluoride, ethane, cyclopropane, halothane, diethyl ether, and acetone—were chosen to represent a wide range of solubilities in blood, with acetone the most soluble and sulfur hexafluoride the least soluble. Samples of expired air and arterial blood are analyzed by gas chromatography to determine the concentrations of each of the 6 gases. Other data usually obtained include cardiac output by indicator dilution, minute ventilation, and arterial and mixed venous blood gases.

Graphs plotting the blood-gas partition coefficients for each of the 6 gases versus their retentions and excretions are constructed. A computer is then used to convert these data into graphs like the one shown in Figure 5–5A. The graph, which shows the distribution of ventilation-perfusion ratios in a young healthy male subject, can be read as a frequency histogram. The x-axis is the spectrum of ventilation-perfusion ratios from 0 to 100, displayed as a logarithmic scale. The y-axis shows the amount of ventilation or blood flow going to alveolar-capillary units with the

ratio on the x-axis. The figure demonstrates that in this young, healthy subject almost all the blood flow and ventilation go to alveolar-capillary units with

ratios near 1. There is no ventilation or perfusion of units with ratios below 0.3 or above 3.0. Figure 5–5B shows the distribution of ventilation and perfusion in a healthy middle-aged subject. Note the wider dispersion of ventilation and perfusion, with more perfusion going to units with ratios above 3.0 and much more going to units with ratios below 0.3. Similarly, the ventilation is also more widely distributed. Note that there was no true intrapulmonary shunt in either subject, that is, no blood flow to alveolar-capillary units with

of zero.

Figure 5–5.

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Examples of distributions of ventilation-perfusion ratios in normal subjects. A: The results in a young subject. B: The results in an older man. Reproduced from Wagner PD, Laravuso RB, Uhl RR, West JB. Continuous distributions of ventilation-perfusion ratios in normal subjects breathing air and 100% O2. J Clin Invest. 1974;54:54–68 by copyright permission of The American Society for Clinical Investigation.

Regional Ventilation-Perfusion Ratio Differences and Their Consequences in the Lung

Listen

The regional variations in ventilation in the normal upright lung were discussed in Chapter 3. As summarized on the left side of Figure 5–6, gravity-dependent regions of the lung receive more ventilation per unit volume than do upper regions of the lung when one is breathing near the FRC. The reason for this regional difference in ventilation is that there is a gradient of pleural surface pressure, which is probably caused by gravity and the mechanical interaction of the lung and the chest wall. The pleural surface pressure is more negative in nondependent regions of the lung, and so the alveoli in these areas are subjected to greater transpulmonary pressures. As a result, these alveoli have larger volumes than do alveoli in more dependent regions of the lung and are therefore on a less steep portion of their pressure-volume curves. These less-compliant alveoli change their volume less with each breath than do those in more dependent regions.

Figure 5–6.

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Summary of regional differences in ventilation (left) and perfusion (right) in the normal upright lung.

The right side of Figure 5–6 shows that the more gravity-dependent regions of the lung also receive more blood flow per unit volume than do the upper regions of the lung, as discussed in Chapter 4. The reason for this is that the intravascular pressure in the lower regions of the lung is greater because of hydrostatic effects. Blood vessels in more dependent regions of the lung are therefore more distended, or more vessels are perfused because of recruitment so there is less resistance to blood flow in lower regions of the lung.

Regional Differences in the Ventilation-Perfusion Ratios in the Upright Lung

Simplified graphs of the differences of ventilation and perfusion from the bottom to the top of normal upright dog lungs are shown plotted on the same axis in Figure 5–7. The ventilation-perfusion ratio was then calculated for several locations.

Figure 5–7.

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Distribution of ventilation and perfusion and ventilation-perfusion ratio down the upright dog lung. (Reproduced with permission from West, 1977, 1990.)

Figure 5–7 shows that the difference of perfusion from the bottom of the lung to the top is greater than the difference of ventilation. Because of this, the ventilation-perfusion ratio is relatively low in more gravity-dependent regions of the lung and greater in upper regions of the lung. If pulmonary perfusion pressure is low, for example, because of hemorrhage, or if alveolar pressure is high because of positive-pressure ventilation with positive end-expiratory pressure, or if both factors are present, then there may be areas of zone 1 with infinite ventilation-perfusion ratios in the upper parts of the lung.

The Consequences of Regional Ventilation-Perfusion Differences in the Normal Upright Lung

The effects of the regional differences in

on the alveolar

and

can be seen in Figure 5–8. The lung was arbitrarily divided into 9 imaginary horizontal sections, and the

was calculated for each section. These sections were then positioned on the ventilation-perfusion line of the O2-CO2 diagram, and the

and

of the alveoli in each section could be estimated. Under normal circumstances the blood in the pulmonary capillaries equilibrates with the alveolar

and

as it travels through the lung, and so the effects of regional differences in

on the regional gas exchange could be predicted. As can be seen from the figure, the upper sections have relatively high

and low

; the lower sections have relatively low

and high

Figure 5–8.

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The

for each of 9 imaginary sections of a vertical lung on the ventilation-perfusion line of an O2-CO2 diagram. Upper sections have higher

with higher

, and lower

, and lower sections have lower

with lower

and higher

. (Reproduced with permission from West JB. Respiratory Physiology–The Essentials. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1990.)

Figures 5–7 and 5–8 demonstrate that the lower regions of the lung receive both better ventilation and better perfusion than do the upper portions of the lung. However, the perfusion difference is much steeper than the ventilation difference, and so the ventilation-perfusion ratio is higher in the apical regions than it is in the basal regions.

As a result, the alveolar

is greater and the alveolar

is less in upper portions of the lung than they are in lower regions. This means that the oxygen content of the blood draining the upper regions is greater and the carbon dioxide content is less than that of the blood draining the lower regions. However, these contents are based on milliliters of blood (see Chapter 7), and there is much less blood flow to the uppermost sections than there is to the bottom sections. Therefore, even though the uppermost sections have the greatest

and

and the lowest

, there is more gas exchange in the more basal sections.

Key Concepts

Listen

Ventilation and perfusion must be matched on the alveolar-capillary level for optimal gas exchange.

Ventilation-perfusion ratios close to 1.0 result in alveolar

of approximately 100 mm Hg and

close to 40 mm Hg; ventilation-perfusion ratios greater than 1.0 increase the

and decrease the

; ventilation-perfusion ratios less than 1.0 decrease the

and increase the

Alveolar dead space and intrapulmonary shunt represent the 2 extremes of ventilation-perfusion ratios, infinite and zero, respectively.

The ventilation-perfusion ratios in lower regions of the normal upright lung are less than 1.0, resulting in lower

and higher

; the ventilation-perfusion ratios in upper parts of the lung are greater than 1.0, resulting in higher

and lower

; nonetheless, there is normally more gas exchange in lower regions of the lung because they receive more blood flow.

Clinical Correlation

Listen

From Raff H, Levitzky MG, eds. Medical Physiology: A Systems Approach. New York: McGraw-Hill; 2011:360–361.

A 40-year-old man with a broken leg in a cast because of a skiing injury and no history of respiratory problems suddenly has difficulty in breathing and complains of chest pain. He is brought to the hospital. In the Emergency Department, his breathing is observed to be rapid and shallow. His heart rate is 120/min, and his arterial blood pressure is 80/60 mm Hg. His respiratory rate is 25/min. A chest x-ray and an electrocardiogram (ECG) are performed on the patient to help determine the cause of his chest pain and dyspnea. The ECG shows no abnormalities indicative of myocardial ischemia (insufficient blood flow to the heart muscle) or myocardial infarction (injury of the heart muscle) such as ST-segment or T-wave abnormalities. The chest x-ray shows no abnormalities indicative of pneumonia, atelectasis (collapsed alveoli), or pneumothorax (air between the inside of the chest wall and the outside of the lung). An arterial blood sample is obtained from the patient while he was breathing room air to determine his arterial blood gases (arterial

, arterial

, and arterial pH). His arterial

was 70 mm Hg (normal >90), his arterial

was 30 mm Hg (normal range is 35–45), and his pH was 7.50 (normal range is 7.35–7.45); his calculated bicarbonate concentration was 22 mmol/L (normal range is 22–26).

The patient has a pulmonary embolus, most likely as a result of blood clotting in his immobilized leg. Flow of venous blood in the broken leg is impaired by the cast and the lack of muscle contraction to enhance venous return from his leg to his heart. Stasis (low or absent flow) of blood often leads to clotting (thrombosis). When thrombosis occurs in nonsuperfical veins such as those in the leg, it is called deep venous thrombosis (DVT). The thrombus can break loose and be carried to the right side of the heart and enter the pulmonary arterial tree, where it can block blood flow to part of the lung. This is called a pulmonary embolus, in this case, a thromboembolus. Pulmonary emboli can be life threatening if they occlude a significant fraction of the pulmonary vascular bed. The region of the lung with occluded blood flow creates alveolar dead space (ventilated but not perfused) that contributes nothing to gas exchange. The patient’s end-tidal

decreases because it contains air coming from unperfused alveoli, which contribute no carbon dioxide to the exhaled air. The arterial

is therefore greater than the end-tidal (“alveolar”)

. The diffusing capacity of the patient is decreased because of decreased surface area for gas exchange. Occlusion of pulmonary vessels is likely to increase pulmonary vascular resistance, increase pulmonary artery pressure, and increase right ventricular work. Blood flow to the left side of the patient’s heart decreases, which explains his low systemic blood pressure. His tachycardia is likely a result of the response of his baroreceptor reflex to his low blood pressure, and the pain and anxiety he is experiencing. His tachypnea is explained by the influence of receptors in his lungs (the J receptors, which will be described in Chapter 9) and the pain and anxiety. The tachypnea resulted in hyperventilation causing his arterial

to fall below the normal range and his arterial pH to exceed the normal range (see discussion of uncompensated respiratory alkalosis in Chapter 8). His low arterial

is a result of the occlusion of pulmonary vessels forcing blood flow to poorly ventilated alveoli.

Treatment of patients with pulmonary emboli (sometimes called pulmonary embolism) depends on the severity of the disorder. Anticoagulants are used to prevent further clotting, thrombolytic drugs are used to break clots down, intravenous catheters with deployable filters can be used to remove the emboli, and large life-threatening emboli may be removed surgically (embolectomy).

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Figure 5–1.

Figure 5–2.

Testing for Nonuniform Distribution of Inspired Gas

Single‐Breath‐of-Oxygen Test

Nitrogen-Washout Test

Figure 5–3.

Figure 5–4.

Trapped Gas

Radioactive Markers

Testing for Nonuniform Distribution of Pulmonary Blood Flow

Testing for Mismatched Ventilation and Perfusion

Physiologic Shunts and the Shunt Equation

Anatomic Shunts

Absolute Intrapulmonary Shunts

Shuntlike States

The Shunt Equation

Physiologic Dead Space

Alveolar-Arterial Oxygen Difference

Single-Breath Carbon Dioxide Test

Lung Scans after Inhaled and Infused Markers

Multiple Inert Gas Elimination Technique

Figure 5–5.

Figure 5–6.

Regional Differences in the Ventilation-Perfusion Ratios in the Upright Lung

Figure 5–7.

The Consequences of Regional Ventilation-Perfusion Differences in the Normal Upright Lung

Figure 5–8.

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