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Respiratory: An Integrated Approach to Disease >

Chapter 9: Alveolar O2 and CO2 Exchange,

Physiological Shunt, and Acid-Base Balance
Andrew J. Lechner

INTRODUCTION TO ALVEOLAR GAS DIFFUSION

Learning Objectives

The student will be able to define the terms governing alveolar O2 di usion, and the circumstances when O2 uptake is limited
by perfusion or di usion.

The student will be able to calculate the percentage of Q̇ comprising physiological shunt by using appropriate patient data
and knowledge of HbO2 interactions in blood.

The student will be able to summarize processes in CO2 excretion and the manner by which blood CO2 acts to maintain
normal blood pH.

The student will be able to use patient data to distinguish among respiratory acidosis, metabolic acidosis, respiratory
alkalosis, and metabolic alkalosis.

Once gases reach the alveolar parenchyma by ventilation, absorption into the blood or excretion from it occurs not by
convection, but by molecular di usion according to a physiological restatement of Ohm’s law (Fig. 9.1). Di usion of any gas
through the septal barrier and into the blood is proportional to the alveolar epithelial surface area (SA) and the alveolar
capillary endothelial surface area (SC) comprising the membrane available for such exchange. Quantitative measurements on

electron photomicrographs of normal lung have estimated SA and SC to each be 50-70 m2. This symmetry of SA and SC
dimensions is perhaps not surprising, given the importance placed earlier on good V̇A/Q̇ matching. Alveolar di usion of any
gas is inversely proportional to septal barrier thickness, estimated as its harmonic mean (τS) to emphasize statistically the
thinnest regions where di usion is presumably favored.

FIGURE 9.1
Alveolar di usion as described by a physiological version of Ohm’s law: Flow = (P1 − P2)/R, where P1 and P2 are the "source"
and "sink" gas partial pressures in two adjacent compartments. Conductance (C) is the inverse of resistance R, and thus Flow
= C • (P1 − P2). C is proportional to the average of all alveolar and capillary surface areas [(SA + SC)/2] in the septa available for
di usion, and inversely proportional to the harmonic mean thickness of those septal barriers (τs). C is also proportional to
Krogh’s coe icient of di usivity (D) for each gas, which is in turn the ratio of its solubility in saline divided by the molecular
weight (MW) of each gas.

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Given these lung anatomical features that a ect all gases, other factors will determine whether di usional equilibrium is
achieved between an alveolar airspace and the blood flowing through its capillaries. Again by analogy to Ohm’s law, each gas
di uses proportionally to the pressure gradient between its "source" (P1, the higher value) and its "sink" (P2, the lower value).
For O2, P1 = PAo2 (Chap. 8) and P2 = PV̄o2 as measured by a pulmonary artery catheter, yielding a normal inwardly directed
gradient of ~60 mm Hg on room air. That gradient is dramatically a ected by both FIo2 and PB insofar as those a ect PIo2 and
thus PAo2. For CO2, P1 = PV̄co2, and P2 = PAco2 (= Paco2), for a normal outwardly directed gradient of 5-6 mm Hg and one that
is less sensitive to FIo2 or PB than that for Po2. Indeed, data in Table 3.2 were used to make this point earlier of a tenfold larger
gradient for O2 despite that the flow of CO2 outward and O2 inward are nearly the same. How can this occur? Gases will
di use at di erent rates, despite equal values for SA, SC, τS, and (P1-P2), because of di ering coe icients of di usivity (D),
defined as the solubility of a gas in aqueous media divided by its mass-dependent rate of gaseous-free di usion. The value of
D for CO2 is ~20 times that of O2 in biological systems, implying that lung disorders will present more o en with hypoxemia
(low blood O2 content) than with hypercarbia (high blood CO2 content). One can also appreciate that alveolar di usion of all
gases will diminish in a disease like emphysema where SA and SC are decreased (Fig. 9.2). Likewise, alveolar di usion
decreases in those diseases for which τS is increased, for example during the edema of acute lung injury (Chap. 28) or a er
the development of fibrosis in some interstitial lung diseases that show a restrictive pattern by pulmonary function test (PFT)
(Chap. 24).

FIGURE 9.2
SA is a key determinant of di usion, and any decrease reduces maximal O2 uptake and CO2 excretion. Three images of lung
tissue (all at the same magnification) are shown with their Emphysema Severity Scores assigned by the American Thoracic
Society. A score of 0-2 would be normal for urban adults. From Nagai et al. Am Rev Respir Dis. 1989;139:313-319.

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DISTINGUISHING DIFFUSIONAL AND PERFUSIONAL LIMITS TO GAS EXCHANGE

Given this discussion, what time constraints exist on gas di usion in the lung? This question can be answered by considering
capillary transit times of erythrocytes in the lung in relation to the equilibration rate of alveolar gases with the interiors of
those red blood cells (RBCs) (Fig. 9.3). An RBC spends ~0.8 seconds in an alveolar capillary at a resting Q̇ but less than 0.3
seconds when Q̇ approaches maximal values. The long RBC transit time at low Q̇ is usually su icient for N2O (an anesthetic
gas), CO, CO2, and O2 to equilibrate across the alveolar-capillary barrier, that is, P1 ≅ P2 for these gases near the venular end
of alveolar capillaries. By example, N2O is very soluble in blood but does not bind to Hb. Thus, it equilibrates across the
barrier regardless of the original (PAn2o-Pc’n2o) or transit time, so that its absorption is perfusion limited only by Q̇. If Q̇
increases, then N2O uptake increases because more RBCs pass through the alveolar capillaries in the same interval of time. In
contrast, CO binds to Hb in such large amounts that no RBC spends enough time in an alveolar capillary to equilibrate PAco
with Pc’co. Thus, the absorption of CO is di usion limited, and simply increasing Q̇ will not necessarily increase CO uptake.
Rather, the alveolar uptake of CO and other di usion limited gases will more likely increase if SA and SC increase, or if τs
decreases.

FIGURE 9.3
Equilibration rates of CO, nitrous oxide (N2O), and O2 along the alveolar capillary. Pcn2o equilibrates rapidly with alveolar
PAN2O, well before the capillary ends, and so N2O is perfusion limited. In contrast, PĆco in capillary blood is nearly unchanged
during one capillary transit, and thus CO transfer is di usion limited. O2 transfer into alveolar blood can be perfusion limited
or di usion limited, depending upon conditions. From West, Respiratory Physiology; 2005.

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Normally O2 has an intermediate equilibration rate to those of N2O or CO. In healthy individuals, O2 is a perfusion-limited gas
over a wide range of Q̇ (Fig. 9.3), and at sea level alveolar O2 uptake usually is not considered to be the rate-limiting step to
maximal O2 consumption, V̇o2max (Chap. 12). However, in diseased lungs with destroyed or fibrotic alveolar septa, O2
becomes di usion limited during moderate exercise, and potentially at rest despite long RBC transit times. Even in healthy
individuals, O2 becomes a di usion-limited gas when PAo2 is reduced by a low FIo2 or by the reduced PB at high altitude
(Chap. 13).

Based on its greater aqueous solubility, CO2 di uses into and out of tissues ~20 times faster than O2 per mm Hg of pressure
gradient. Consequently, there is usually ample capillary transit time for CO2 to achieve equilibrium despite its much smaller
partial pressure gradient versus O2. However, under conditions of reduced RBC transit time or with thickening of the alveolar
septal membranes, CO2 transfer may be incomplete and result in hypercarbia.

ESTIMATING MAXIMAL PULMONARY DIFFUSING CAPACITY

The long equilibration time of inhaled CO is used clinically to estimate the single-breath lung di using capacity for CO (DLCO).
As detailed in Chap. 16, this pulmonary function test is most o en conducted on patients who are suspected of having
reduced SA or SC, or increased τs. Subjects begin the maneuver at their RV and inhale gas with a low FIco (usually ~0.003) up to
their TLC. Once at TLC, the breath is held for 10 seconds and then exhaled completely. Concentrations of CO in the exhaled
gas are measured to establish FĒco and FÉco (= FAco), and thus PAco by Dalton’s law. These data yield the CO uptake rate (V̇co)
plus the "P1" from the equation in Fig. 9.1 that drove its absorption. "P2" in that same equation, being the subject’s PĆco, is
considered zero since inhaled CO never equilibrates with blood in the capillaries. The di usivity coe icient DCO is constant
because the aqueous solubility and mass of CO are known. DLCO is computed then as:

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where carbon monoxide conductance, CCO = [DCO · (SA + SC)]/(2 · τs). Thus, the working equation for the DLCO test becomes:

(SA + SC)]/(2 · τs) = [V̇co/(PAco − PĆco)]/DCO

Since all terms on the right side of this equation are measured by the single-breath DLCO procedure, the test yields a robust
"lump sum" or aggregate estimate of a subject’s alveolar and capillary surface areas available for di usion, as well as their
alveolar barrier’s thickness as an impediment to that di usion. The subject’s measured value for DLCO then can be compared
with expected normative values like other spirometric data to assess the severity of emphysema, edema, interstitial fibrosis,
or other disease processes that impact SA, SC, or τS.

It should be emphasized that despite crossing the alveolar-capillary membrane, O2 has yet to oxygenate the RBCs. Therefore,
the lung’s overall di using capacity for O2 consists of two linked components: its membrane di using capacity for O2, DMo2
representing the distance from alveolar airspace through the surfactant liquid, tissue, and plasma layers; and its erythrocytic
di using capacity. As will be described in Chap. 16, this latter component depends on the blood transfer conductance
coe icient for oxygen (Θo2) between Hb and O2, and on total pulmonary capillary blood volume, Vc. Perhaps surprisingly, the
di usive resistance of the membrane barrier (1/DMo2) accounts for only about half of overall resistance to O2 uptake in the
lung, with the balance of that resistance being due to the erythrocytes themselves.

ESTIMATING OXYGEN DELIVERY AND PHYSIOLOGICAL SHUNT

To this point, the Po2 gradient in the body has encountered only one unavoidable reduction from the inspired PIo2, that
occurring in conducting airways by Dalton’s law, as O2 is displaced by CO2 and H2O vapor. Thus PAo2 always is less than PIo2.
The preceding discussion also implies that if O2 is a perfusion-limited gas under most conditions, then the PĆo2 of blood
draining alveoli should equal PAo2. However, as was seen in Chap. 8, a subject’s actual Pao2 as reported from blood gas
analyses is always at least slightly less than PAo2. Indeed, this (A − a) Po2 di erence can be quite large in some patients,
implying that the higher PĆo2 of blood draining their alveolar capillaries is diluted downstream with blood with a Po2 nearer
to that of mixed venous blood. This venous admixture, or contamination of well-oxygenated blood draining the alveoli by less
oxygenated blood, comprises the essence of physiological shunt.

By analogy to comments regarding anatomical and physiological dead space (Chap. 8), there can exist anatomical and
physiological shunts in the pulmonary or systemic circulations. As for dead space, physiological shunt always includes
anatomical shunt, that is, blood flow through pulmonary arteries that never enters the respiratory parenchyma to permit
alveolar gas exchange. Examples of anatomical shunts include a patent ductus arteriosus (PDA) and patent foramen ovale
(PFO) that allow systemic venous blood to bypass the lungs entirely (Chap. 7). Importantly, physiological shunt includes that
blood flow plus any mixed venous blood that passes through the septal capillaries in the respiratory parenchyma without
gaining access to ventilated alveoli. Such physiological shunt was noted earlier in the low V̇A/Q̇ ratios of patients with type B
emphysema, as documented with the multiple inert gas technique (Chap. 8). In simplified form, the development of
physiological shunt is shown in Fig. 9.4.

FIGURE 9.4
Measurement of physiological shunt Q̇S assumes that the Cao2 of systemic arterial blood reflects the high CĆo2 of alveolar
capillary blood diluted by shunted blood with its lower CV̄o2. From West, Respiratory Physiology; 2005.

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A working version of the shunt equation can be derived from Fig. 9.4, where Q̇T equals total cardiac output, and Q̇S is that
portion of Q̇T being shunted around alveolar capillaries, either anatomically or due to low V̇A/Q̇ ratios. The blood O2
concentrations needed to solve the shunt equation for Q̇S include that of blood in alveolar capillaries (CĆO2) with very high
O2 content, as well as blood in the systemic arteries (Cao2) and in the pulmonary artery (CV̄o2). One can report a patient’s
physiological shunt (Q̇S) either in absolute terms (L/min) or as a percent of Q̇T. Deriving the shunt equation begins with the
principle of mass balance for O2 as expressed in the following equation:

Q̇T · (Cao2) = [ Q̇S · (CV̄o2)] + [(Q̇T − Q̇S) · (CĆo2)]

Rearranging terms and making a sign change so that Q̇S/Q̇T is a positive value, yields the working version of the shunt
equation that is solvable using a patient’s data:

Q̇S/Q̇T = (CĆo2 − Cao2)/(CĆo2) − (CV̄o2)

In practice, shunt studies are done while subjects are breathing pure oxygen (FIo2 = 1.00). This minor intervention permits
some simplifying assumptions about the amounts of HbO2 versus dissolved O2 needed in the calculation of total O2 contents
for each blood compartment. Shunt studies can be done on alert or sedated patients, provided that arterial and venous blood
samples are available for determinations of Pao2 and PV̄o2, blood [Hb], and mixed venous % oxygenation or saturation, SV̄o2
(%). The calculated Q̇S/Q̇T is generally <10% in most healthy adults, but it may exceed 20% in disease conditions that are
characterized by low V̇A/Q̇ ratios as described in Chap. 8. Several examples of shunt calculation problems are included at the
end of this chapter.

CLINICAL CORRELATION 9.1

Shunt fractions approaching 50% are life-threatening and require aggressive management to restore at least some ventilation
to lung regions where V̇A/Q̇ ratios are extremely low. To do so o en requires judicious application of mechanical ventilation
with positive end-expiratory pressure, PEEP that attempts to provide an "air stent" to recruit alveoli that are consolidated
into a nearly solid state by edema or are atelectatic due to excessive surface tension recoil (Chaps. 28 and 30).

ROLE OF ALVEOLI IN CO2 EXCRETION AND ACID-BASE BALANCE

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As detailed in Chap. 3, CO2 is transported in blood as: dissolved CO2 gas by Henry’s law; as HCO–3 from dissociated H2CO3
a er CO2 combines with H2O (facilitated by carbonic anhydrase, CA); and as HbCO2 from its reversible binding to Hb (Fig. 9.5).

Recall that deoxy-Hb is a weaker acid than oxy-Hb and so binds H+ more readily (the Haldane e ect), particularly in active
tissues where H2CO3 formation predominates.

FIGURE 9.5
(a) Processes that absorb CO2 in active tissues are reversed in pulmonary capillaries during excretion of CO2 from mixed
venous blood, even as oxygenation is occurring. Here, the roles of carbonic anhydrase (CA) within RBCs and on endothelial
cells are emphasized. (b) About 91% of CO2 in mixed venous blood exists as HCO3−, with 5% as HbCO2 and 4% as dissolved
CO2 gas. Only ~7% of CO2 in venous blood is excreted during one passage through the alveolar capillaries. Of that amount,

~80% is from HCO3− and ~9%-10% each from HbCO2 and dissolved CO2 pools. (a): From Fox, Human Physiology, 10th ed.
2008.

If the relationship is plotted between Pco2 and total [CO2] in a blood sample at equilibrium, a CO2 dissociation curve is
obtained (Fig. 9.6) that is analogous to such graphs for the O2 content of whole blood (Chap. 3). Because such plots of Pco2
versus [CO2] include all three forms of CO2, the resulting curves are not linear, owing to the saturable HbCO2 component and

also to the exhaustible supply of donor H+ from hemoglobin. Due to the Haldane e ect, the [CO2] for deoxygenated blood is
higher than for oxygenated blood at all physiological values for Pco2.

FIGURE 9.6
CO2 dissociation curves for whole blood at di erent O2 saturations. Oxygenated blood carries less CO2 than deoxygenated
blood at the same Pco2, but both transport far more CO2 than occurs as dissolved gas. The inset depicts di erences between

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arterial and mixed venous blood. Modified from West, Respiratory Physiology; 2005.

As shown in the inset to Fig. 9.6, the physiological range for CO2 exchange is normally between Paco2 = 40 mm Hg and PV̄co2 =
45 mm Hg, which yields a net loss of about 5 mL CO2/dL blood during each passage of blood through the lungs. Note that an
essentially equivalent di erence of 5 mL O2/dL blood exists between arterial and venous bloods, although the required
di erence in Pao2 and PV̄o2 is closer to 50-60 mm Hg to achieve this same amount of gas exchange, and that is normally
occurring on the upper shoulder of the O2 dissociation curve. The transport and release of CO2 by the respiratory system have
profound e ects on the body’s pH regulation and acid-base status. The following equation has been presented in the context
of CO2 transport, both for CO2 uptake in metabolically active tissues, and for CO2 excretion in the lungs:

CO2 + H2O ⇒ H2CO3 ⇔ H+ + HCO3−

The equation as written represents events in the tissues, while the right-to-le direction would describe the reaction in the
lungs. Importantly, mass action considerations apply in both directions: increasing the concentration of either substrates or
products will shi the equilibrium points accordingly in response to those changed conditions. The equilibrium between the
weak acid H2CO3 and its dissociated ions, H+ and HCO–3, is described by the dissociation constant Ka:

Ka = [H+] · [HCO–3]/[H2CO3]
Taking logarithms of both sides and then substituting for H2CO3 based on Henry’s law, yields the Henderson-Hasselbalch
equation (see Chap. 17 for more detailed steps):

pHa = pKa + log [HCO–3] − log [H2CO3]

pHa = pKa + log [HCO–3] − log [(0.03) · (Paco2)]
where 0.03 represents the solubility coe icient to convert Paco2 (in mm Hg) at 37°C into H2CO3 (in mM). In physiological
systems, the value of pKa for this first dissociation is 6.10 at 37°C, and an arterial pH of 7.40 is normally carefully regulated.
Thus:

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Given a typical Paco2 = 40 mm Hg, a normal resting [HCO3−] is calculated to be:

Thus, to achieve a stable pHa = 7.40 using the CO2 bu er system requires maintaining an anion/acid ratio of approximately

20:1. Obviously, this 20:1 ratio can be satisfied by an infinite range of molarities for [HCO–3] and [H2CO3] (ie, Paco2). Several
decades ago it was presumed that all mammals operate at Paco2 = 40 mm Hg. However smaller animals o en function with a

Paco2 of 25-30 mm Hg, and have [HCO–3] values that are appropriately lower, in the range of 18-20 mM. Nevertheless, at 37°C
all mammals appear to protect a pHa of ~7.40. Indeed, subsequent investigations confirmed that maintaining pHa near 7.40 is
far more important than is a particular value for total blood CO2 content. Among healthy adults, total CO2 is about 25.2 mM (=

24 mM HCO–3 + 1.2 mM H2CO3). However this total can vary widely, such that the measured [HCO–3] and total CO2 content for
individuals reflect either acute perturbations to their acid-base balance, or the chronic compensatory responses to such a
perturbation (Chap. 17).

With the Henderson–Hasselbalch equation, knowing any two parameters among pHa, Paco2, and HCO–3 fixes the third. Some
years ago Davenport wrote The ABC of Acid-Base Chemistry that popularized the eponymous diagram in Fig. 9.7. It features
an abscissa in pH units and an ordinate of [HCO–3]. Since knowing any pair of pH and [HCO–3] values determines Paco2, one
can draw a family of Pco2 isobars (lines of equal pressure) whose center point A shows that at 37°C, pHa = 7.40 if Paco2 = 40

mm Hg and [HCO–3] = 24 mM. The line CAB here is the CO2 Blood Bu er Line and describes the e ects on pH and [HCO–3] of
blood titrated with acid in the form of H2CO3 and thus Paco2. A similar CO2 Plasma Bu er Line would have a shallower slope
since plasma contains fewer proteins and is thus a weaker bu er than whole blood.

FIGURE 9.7

A Davenport diagram showing the basic relationships among blood HCO3−, pHa, and Paco2. Point A represents the normal
values for healthy subjects at rest and with Paco2 = 40 mm Hg; the center line BAC illustrates the normal bu ering capacity for
whole blood. Modified from West, Respiratory Physiology; 2005.

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There are four principal ways to perturb acid-base homeostasis within the CO2-based bu er system, namely raising or

lowering either Paco2 or [HCO–3]. Compensation usually involves altering the previously stable of the two (Fig. 9.8). Point A

here and in Fig. 9.7 represents the normal, ideal balance among pHa, Paco2, and [HCO–3]. If Paco2 abruptly increases toward a
higher CO2 isobar, this acute change in acid-base status to point B is termed respiratory acidosis. In the uncompensated

phase of this response, Paco2 is too high, pHa is too low, and blood [HCO–3] has not increased enough to reestablish a 20:1

ratio between [HCO–3] and [H2CO3]. Remembering that homeostatic mechanisms will first and foremost attempt to restore a
normal pHa, one can easily predict the appropriate response. Since respiratory impairment already exists (Paco2 is elevated),

the appropriate compensation is to move along this new Paco2 isobar toward point D by retaining [HCO–3] in the kidneys and

thereby regain a 20:1 ratio. Note that the uncompensated acidosis at point B does cause a slight increase in [HCO–3] by simple
mass action. However, this e ect is not su icient to correct the acidosis unless Paco2 is allowed to increase very slowly from
40 to 60 mm Hg.

FIGURE 9.8

An expanded view of the physiological ranges encountered clinically for plasma HCO–3, pHa, and Paco2. Point A illustrates
typical normal values at rest. The several paths to respiratory and metabolic disturbances are shown, and the typical
compensatory responses to reestablish pHa. Modified from West, Respiratory Physiology; 2005.

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Acute respiratory acidosis may begin with food aspiration, heart attack, drug overdose, pneumothorax, head injury a ecting
ventilatory drive, etc. Chronic acidosis with some compensation via renal HCO–3 retention is common with V̇A/Q̇
abnormalities due to obstructive disease. As the term implies, respiratory acidosis is mainly a lung disorder, whether it is
acute and uncompensated, or chronic and partially or fully compensated.

In the opposite direction, an individual may abruptly increase V̇A, causing Paco2 to fall below 40 mm Hg. Such respiratory
alkalosis is most o en due to hyperventilation during pain or anxiety (or accidentally during mechanical ventilation), or as a
direct result of exposure to environmental hypoxia, as occurs at high altitude. In Fig. 9.8, respiratory alkalosis is seen acutely
as moving from point A to point C toward a lower Paco2 isobar. Again in attempting to reestablish pHa = 7.40, compensation

will occur toward point F by promoting renal excretion of HCO–3. Again, such a respiratory disturbance could maintain the

20:1 ratio of [HCO–3]/[H2CO3] if it occurred slowly, since HCO–3 is eventually converted to H2CO3 by mass action. For example,
ascent to altitude can be staged slowly enough to minimize such alkalotic increases in pHa.

Numerous nonrespiratory diseases can a ect pHa, and their onset may be either acute or more chronic than respiratory
acidosis and alkalosis. Excessive ingestion of antiacids or prolonged vomiting can induce metabolic alkalosis, shown in Fig.
9.8 as moving from point A to point E along a constant Paco2 isobar. Respiratory compensation occurs toward point D in the
form of hypoventilation, again to restore the 20:1 ratio between anion and acid. This compensation increases total blood CO2

content above that caused by the excessive [HCO–3] in the acute, uncompensated phase. Assuming patients survive any
immediate crisis caused by this elevated pHa, their hypoventilation can be reversed later to excrete the additional CO2
content that compensation induced.

Metabolic acidosis is a serious perturbation caused primarily by the excessive production of organic acids that overwhelm the
body’s supply of [HCO–3]. Diabetic ketoacidosis, septic shock, aspirin overdose, renal failure, and diarrhea are common
causes. By observing movement from point A to point G in Fig. 9.8, the life-threatening nature of metabolic acidosis is
apparent. Respiratory compensation from point G to point F requires lowering blood CO2 content via hyperventilation, which

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consumes additional [HCO–3]. Thus, the 20:1 ratio for [HCO–3]/[H2CO3] is restored in such a manner that if the underlying

cause of acid generation is not corrected, blood [HCO–3] stores are depleted, and irreversible acidosis and death ensue.

The numerous clinical variations of these acid-base disorders will be more extensively reviewed in Chap. 17, in the form of
patient scenarios and their solutions.

CLINICAL CORRELATION 9.2

Why is arriving at point F in Fig. 9.8 via point G more dangerous than getting to point F via point C, as occurs in respiratory
alkalosis? The answer relates to the causes that lead to lost pH equilibrium. The hyperventilation of uncompensated
respiratory alkalosis is more easily corrected (by descending from altitude or reducing anxiety with sedation) than is the
ketoacidosis of diabetes or the ischemia and lactate acidemia of septic shock.

SUGGESTED READINGS

1. Davenport  HW. The ABC of Acid-Base Chemistry , 6th ed. Chicago, IL: University of Chicago Press; 1974. Many have tried
and most have failed to teach as much about the fundamentals of acid-base balance in the lung as this author, whose
contribution to the field continue in the diagrams bearing his name.

2. Scheid  P, Piiper  J. Di usion. In: Crystal  RG, West  JB, eds. The Lung: Scientific Foundations . New York, NY: Raven Press;
1991. Working predominantly at the Max Planck Institute in Gottingen, Germany, Drs. Piiper and Scheid pushed the
experimental and mathematical boundaries of gas exchange to unprecedented heights, while influencing innumerable
physiologists and clinicians with their insights and personalities .

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