4/10/2018

Respiratory: An Integrated Approach to Disease >

Chapter 1: Respiratory System Nomenclature and

Ambient Conditions
Andrew J. Lechner

INTRODUCTION AND CONCEPTUAL OVERVIEW OF OXYGEN TRANSPORT

Learning Objectives

The student will be able to describe the general process of oxygen transport and identify steps in this
cascade that depend upon the lung to be achieved.

The student will be able to translate key words and phrases of pulmonary medicine into their
internationally recognized abbreviations and acronyms.

The student will be able to calculate the partial pressures of constituent gases in normal dry air using
Dalton's law and explain the e ects of altitude upon them.

The student will be able to use Boyle's law and Charles's law to convert gas volumes between standard
conditions [Standard Temperature and Pressure, Dry (STPD)] and ambient conditions [Body Temperature
and Pressure, Saturated (BTPS)].

The student will be able to compute the content of gases equilibrated with aqueous media using Henry's
law and their established solubility coe icients.

There is little argument that the urge to breathe is the most compelling drive that humans face, one they
must satisfy every minute of life. Our dependence on aerobic metabolism to perform life's complex
functions requires coordinated interaction among multiple organ systems to deliver su icient O2 for those
demands (Fig. 1.1). Although only the upper elements of this O2 transport cascade are the formal purview
of this book, physicians need to appreciate each aspect since failure at any step can become an O2
transport bottleneck with catastrophic consequences for their patients.

FIGURE 1.1
The oxygen transport cascade. See text for details.

1/9
4/10/2018

From this perspective, respiration really consists of two sequential processes within the lung, ventilation
and di usion. Each will require several chapters to describe their constituent parts and boundary
conditions. As an obvious example, ventilation is the algebraic product of respiratory frequency, f,
multiplied by the amount of air moved per breath, termed the tidal volume (VT). Less obvious is the fact
that only a portion of each VT enters the alveolar volume (VA) where di usion can occur, while the
remaining portion of VT is confined to anatomical regions unsuitable for di usion, collectively called the
dead space volume (VD). Thus, one goal of this text is to provide the intellectual tools both to determine the
fraction of VA in each VT, and to identify possible treatments for patients whose VA/VT is not optimal. As will
be seen, the work of breathing and the calories required are substantial to inhale the 8,000-12,000 L of air
per day just to support basal oxygen consumption. Clinicians must be able to distinguish if a patient's work
of breathing is excessive, and if so, whether due to altered recoil properties of the lungs and chest wall, or
to reduced airway diameters which increase dynamic resistance. Such functional distinctions, and the
structural changes that underlie them, form the central framework for sorting lung disorders into the so-
called restrictive lung diseases and obstructive airway diseases. Later subsections of this book are devoted
to providing a detailed introduction to both disease categories.

Even when the physical forces that regulate ventilation are ideal, the inhaled O2 must still di use through
the delicate membrane sandwich that separates alveolar airspace from blood within the underlying
pulmonary capillaries (Fig. 1.2). The resistance that the septal barrier poses to di usion is related to its
thickness and total surface area, which are modified in diseases like interstitial fibrosis and emphysema,
respectively. Alveolar di usion may be enhanced by interventions like increasing the fraction of inspired O2
in the ambient air, thereby increasing the pressure gradient for oxygen between the airspace and blood
that is the driving force for di usion. Much importance will be placed in the following chapters on training

2/9
4/10/2018

the clinician to determine when such supplemental O2 will probably improve tissue oxygenation versus
when that tactic alone will fail.

FIGURE 1.2
Representative electron micrograph of the air-tissue barrier to be traversed by di usion if oxygenation is to
succeed. In addition to the three tissue layers of alveolar septa, a thin fluid layer sits above the epithelium
but was removed during intratracheal fixation.

RESPIRATORY SYSTEM NOMENCLATURE

Numerous terms and phrases pertaining to respiratory biology and pulmonary medicine will be introduced
in this book. Among the most fundamental are abbreviations and acronyms that succinctly describe the
origin and contents of a gas or fluid sample. With such shorthand, the phrase carbon dioxide partial
pressure of alveolar gas usefully compresses to just PAco2, with its most common units of mm Hg implied.
Likewise, the phrase fractional concentration of oxygen in the inspired gas mixture reduces to FIo2. The
proper labeling of respiratory gases begins with the notation of F (fractional concentration, as a decimal
from 0.0-1.0), or P (for pressure in mm Hg, torr, kilopascals, etc). The second letter (o en subscripted) states
the source or location of the gas, if known, including: A = alveolar; AW = airway; a = arterial; B = ambient
barometric; c = capillary; ć = end-capillary; E = expired or expiratory; Ē = mean expiratory; É = end-
expiratory (sometimes called end-tidal); I = inspired; IP = intrapleural; IT = intratracheal; v = venous; and v̄ =
mixed or mean venous. Note that conventional usage may specify upper versus lower case lettering to
distinguish locations. The final designation is to the gas species: O2, N2, CO2, H2O, etc. Thus, the phrases
FĒco2 = 0.08 and Pćo2 = 105 mm Hg indicate respectively that the average fractional CO2 concentration in a
sample of expired air is 8%, and that the partial pressure of O2 in blood exiting an alveolar capillary to enter
a pulmonary venule is 105 mm Hg.

3/9
4/10/2018

Comparable examples of widely used abbreviations and acronyms for gas volumes in the lung, like VT for
tidal volume, will be introduced as needed. These and other terms for more complex functions are
accompanied by units of measure that serve as helpful reminders to students of their derivation. For
example, pulmonary vascular resistance (PVR) is a key measure of vascular tone across the lungs, usually
expressed in mm Hg/L/min. This PVR is derived from the physiological restatement of Ohm's law (I = ΔV/R
and thus R = ΔV/I). Thus, PVR is equal to the di erence between pulmonary arterial and pulmonary venous
pressures, divided by the cardiac output (Q̇, in L/min). Note: a dot placed over a symbol like Q̇ is shorthand
for a rate function, in this case the liters of blood pumped per minute by the right ventricle.

REVIEW OF BASIC GAS LAWS

Dalton's Law

The total pressure of a gas mixture is equal to the sum of the partial pressures of individual gases in that
mixture. The partial pressure of each gas is proportional to its fractional composition within such a mixture,
and thus is the pressure each gas would exert if it alone occupied the total volume available. In ambient air,
several gases comprise the total barometric pressure (PB) [reported in mm Hg, torr, kilopascals, or
atmospheres (atm) depending on local convention]:

PB = Po2 + Pco2 + Pn2 + Ph2o

Boyle's Law

The pressure of a gas varies inversely with its volume. This relationship becomes critical when attempting
to optimize mechanical ventilation to oxygenate patients whose thoracic and abdominal tissues naturally
resist lung expansion.

Charles's Law

The volume of a gas varies directly with its temperature, due to changes in molecular energy as a closed
gas system is heated or cooled. This principle has many ramifications in medicine, particularly when water
vapor is present that displaces other gases (by Dalton's law) in a temperature-dependent manner. It also
underlies whole-body plethysmography, an advanced form of pulmonary function testing (PFT) that will be
described in Chap. 16. The technique utilizes gas expansion caused by the small di erential between
ambient temperature (TA) and body temperature (TB) to estimate inhaled volumes and intrapleural
pressures (Chap. 6).

Historically, certain gas volumes in medicine, like oxygen consumption, are reported under STPD
conditions of 0°C, 760 mm Hg (1 atm) of pressure, and Ph2o = 0 mm Hg at 0% relative humidity (RH). Many
other gas volumes are consistently expressed as BTPS conditions of actual TB (o en assumed as 37°C) and
ambient PB, and fully saturated with water vapor (100% RH) so that Ph2o = 47 mm Hg, as exists throughout
the normal respiratory system. This discordance between STPD data and those in BTPS occasionally
requires clinicians and students to be able to convert from one set of units to the other. Recall the General
Gas law which states that:

4/9
4/10/2018

P·V=n·R·T
When the same molar amount (= n) of gas in a closed system under condition #1 (STPD or ambient) is
heated, cooled, compressed, or decompressed to a new condition #2, it follows that:

(P1 · V1)/T1 = (P2 · V2)/T2

Thus, to convert a starting volume in STPD units into a final volume in BTPS units:

1. Assign STPD data the subscript 1, and assign BTPS data the subscript 2.

2. Rearrange terms: V2 = (P1 · V1 · T2)/(P2 · T1).

3. Substitute known terms: VBTPS = (760 · VSTPD · TB)/[(PB – 47) · 273].

4. Solve for the desired volume. Note: failing to make this correction will result in an average error of
22%-28%, arguably a consequential oversight.

Henry's Law

The content or concentration of a gas dissolved in a liquid is proportional to its partial pressure that is in
equilibrium above the liquid. In practice, this becomes:

[CXy] (in g or mL/L) = KXy · PXy (in mm Hg)

where KXy = temperature-dependent solubility coe icient of gas Xy (in g or mL/L/mm Hg), and PXy = its
equilibrium partial pressure by Dalton's law.

By this relationship, it is clear that twice as much O2 would be dissolved in water that is equilibrated with
two atmospheres of pure oxygen than water equilibrated with one atmosphere of 100% O2. Importantly,
the solubility coe icient in aqueous media for CO2 is 20-30 times higher than that for O2. Indeed, the metal-
containing pigments like hemoglobin (Hb) and myoglobin (Mb) likely evolved specifically to increase the O2
carried in solution by orders of magnitude over the dissolved amount alone. The greater solubility of CO2,
due to its ready combination with water to form carbonic acid, H2CO3, obviates the need for an analogous
pigment system simply to excrete this waste gas. Henry's law finds several practical applications in
pulmonary medicine, notably during calculation of the total oxygen content of arterial blood (Cao2) (Chap.
3) and the use of that number to estimate physiological shunt (Qs) (Chap. 9).

AMBIENT ATMOSPHERIC CONDITIONS

The earth's atmosphere is detectable to a height of at least 80 km above sea level, and for at least 50 km
closest to the earth it is of constant composition: 79.02% N2; 20.93% O2; 0.03% CO2; plus trace quantities of
inert and rare gases (helium, argon, ozone, etc) that collectively comprise <0.02%. When the total mass of
this 80 km-deep atmosphere is multiplied by the acceleration of gravity, its barometric pressure, PB (force
or weight per unit area) is su icient to displace a column of mercury (Hg) to a height of 760 mm (Fig. 1.3). In
the English (nonmetric) units of measure common in America, the earth's atmosphere weighs about 14.2
lb/in2 at sea level.
5/9
4/10/2018
FIGURE 1.3
Barometric pressure PB is reduced by half for every 5,500 m (18,000 ) above sea level. From West et al:
High Altitude Medicine and Physiology. 4th ed. London, UK:Hodder-Arnold; 2007.

Although atmospheric composition is invariant, gravity compresses the air downward, making its density
highest closest to earth. Data show that atmospheric density decreases by half every ~5,500 m (18,000 ) of
elevation gained above sea level. This means that hikers standing on the summit of Alaska's Mt. Denali
(elev. 6,194 m) have more than half the atmosphere's molecules below them in the 5.5 km closest to the
surface, and less than half of all atmospheric gas between their hats and deep space, a distance of at least
50 km. At 5,500 m elevation, PB is ~380 mm Hg, or in English units ~7.1 lb/in2. Similarly, at 11,000 m
elevation (~36,000 ) where commercial jets cruise, ambient PB outside the plane's windows is ~190 mm
Hg, only one-fourth the PB at Los Angeles International Airport (Fig. 1.4). Thus, hikers breathing ambient air
on Denali's summit and animals in a non-pressurized baggage compartment on the jet, all experience
"shortness of breath." They do so not because their FIo2 is less than at sea level, but because their PIo2 is
less. We will see in Chap. 9 that it is this PIo2 and ultimately the alveolar partial pressure for oxygen, PAo2
that drive the process of di usive O2 uptake in the alveoli.

FIGURE 1.4
Decreasing PB with altitude eventually lowers Pao2 to levels incompatible with human life (see Chap. 8).
Native populations in the Andes of South America and the Himalayas of Tibet living at 5,500 m show
physiological adaptations to altitude, both genetic and developmental. Mountaineering above this
elevation by sea level natives is usually possible only for short durations and carries considerable risk.

6/9
4/10/2018

CLINICAL CORRELATION 1.1

This situation can be visualized as a thought experiment in which 100 people are stacked upon each other
in the prone position. Everyone in the pile has essentially the same body composition as the person on top,
but who is most likely to be squashed? In a relative sense, how will bodily distortion of the 75th person
from the top compare to that of the 25th person from the top? Like a fluid-filled body, the atmosphere has
real mass. Unlike those fluids, however, the atmosphere is compressible and conforms to the terrain
around it, whether hill or hole.

Atmospheric water content varies over both time and space, o en being very low and never approaching
100% RH globally. In addition, the atmosphere is generally much cooler than the human body at TB of 37°C.
Thus, atmospheric Ph2o rarely exceeds the PAh2o of 47 mm Hg found within the warmer and fully
humidified alveoli. Indeed, ventilation invariably represents a net loss of water to the body as a whole
(Chap. 13). Putting all this information together with Dalton's law, we can calculate the partial pressures of
ambient atmospheric gases in dry air at sea level to be: Po2 = 159 mm Hg, Pn2 = 600 mm Hg, Pco2 = 0.23 mm
Hg, and Ph2o = 0 mm Hg. As will be derived in Chap. 8, dilution of this ambient air during inspiration with

7/9
4/10/2018

the body's water vapor and Co2 results in an alveolar PAO2 that cannot exceed about 110 mm Hg at sea
level, with PAn2 equal to ~560 mm Hg and PAco2 of ~40 mm Hg. All atmospheric values are reduced
proportionally by altitude, so that the ambient Po2 is ~80 mm Hg at 5,500 m, and PAo2 cannot exceed about
55 mm Hg at that elevation (Fig. 1.5). The consequences of such ambient hypoxic hypoxia (reduced PAo2)
will be evident when the Po2 required to fully oxygenate hemoglobin is formally considered (Chap. 3).

FIGURE 1.5
The unavoidable reductions in ambient Po2 at altitude inevitably result in lower PAo2, Pao2, and reduced
oxygen content in systemic capillaries. At 5,500 m elevation, Pao2 is about 45 mm Hg, at which normal
human hemoglobin is still >80% oxygenated. Compensatory increases in red cell mass and other elements
of the O2 transport cascade (Fig. 1.1) result in a mixed venous Pv̄o2 that is only 7-10 mm Hg below that at
sea level.

CLINICAL CORRELATION 1.2

As implied in Fig. 1.5, the Pv̄o2 of mixed venous blood rarely falls below 35-40 mm Hg in normal subjects at
sea level. The Po2 required to oxygenate 50% of hemoglobin's binding sites is only 26-27 mm Hg (Chap. 3).
These observations indicate that systemic venous blood normally returns to the lungs for reoxygenation
despite being still at ~75% of its binding capacity. Among other causes, both anemia and exercise will lower
Pv̄ o2 slightly (Chap. 13) in otherwise healthy subjects. However, there appear to be other physiological
constraints that prevent Pv̄o2 from falling proportionally to the reductions in PAo2 and Pao2 that are
unavoidable when breathing air at an altitude. These constraints may include tissue Po2 levels in key
organs like the heart and brain that cannot be lowered without causing irreversible injury by such blood-
borne hypoxemic hypoxia.

SUGGESTED READINGS

8/9
4/10/2018

1. West  JB, Schoene  RB, Milledge  JS. High Altitude Medicine and Physiology . 4th ed. London, UK: Hodder-
Arnold; 2007. Each new edition of this highly rated text integrates the best of classic literature with the
most recent findings in the field, with an excellent introduction to atmospheric conditions.

2. Weinberger  SE. Principles of Pulmonary Medicine . 2nd ed. Philadelphia, PA: WB Saunders; 1992. One of
the first attempts to combine within one text the fundamentals of respiratory physiology and the
particulars of the many subcategories of pulmonary medicine.

McGraw Hill
Copyright © McGraw-Hill Global Education Holdings, LLC.
All rights reserved.
Your IP address is 14.102.151.192

Access Provided by: International Medical University

Silverchair

9/9