37. Pulmonary Ventilation 38. Pulmonary Circulation, Pulmonary Edema, Pleural Fluid

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37. Pulmonary Ventilation

38. Pulmonary Circulation, Pulmonary Edema,

Pleural Fluid

39. Physical Principles of Gas Exchange; Diffusion

of Oxygen and Carbon Dioxide Through the

Respiratory Membrane

40. Transport of Oxygen and Carbon Dioxide in

Blood and Tissue Fluids

41. Regulation of Respiration

42. Respiratory Insufficiency—Pathophysiology,

Diagnosis, Oxygen Therapy
C H A P T E R 3 7


Pulmonary Ventilation

The goals of respiration are to provide oxygen to

the tissues and to remove carbon dioxide. To

achieve these goals, respiration can be divided into

four major functions: (1) pulmonary ventilation,

which means the inflow and outflow of air between

the atmosphere and the lung alveoli; (2) diffusion

of oxygen and carbon dioxide between the alveoli

and the blood; (3) transport of oxygen and carbon

dioxide in the blood and body fluids to and from the body’s tissue cells; and

(4) regulation of ventilation and other facets of respiration. This chapter is a

discussion of pulmonary ventilation, and the subsequent five chapters

cover other respiratory functions plus the physiology of special respiratory


Mechanics of Pulmonary Ventilation

Muscles That Cause Lung Expansion and Contraction

The lungs can be expanded and contracted in two ways: (1) by downward and

upward movement of the diaphragm to lengthen or shorten the chest cavity,

and (2) by elevation and depression of the ribs to increase and decrease the

anteroposterior diameter of the chest cavity. Figure 37–1 shows these two


Normal quiet breathing is accomplished almost entirely by the first method,

that is, by movement of the diaphragm. During inspiration, contraction of the

diaphragm pulls the lower surfaces of the lungs downward. Then, during expiration,

the diaphragm simply relaxes, and the elastic recoil of the lungs, chest

wall, and abdominal structures compresses the lungs and expels the air. During

heavy breathing, however, the elastic forces are not powerful enough to cause

the necessary rapid expiration, so that extra force is achieved mainly by contraction

of the abdominal muscles, which pushes the abdominal contents

upward against the bottom of the diaphragm, thereby compressing the lungs.

The second method for expanding the lungs is to raise the rib cage. This

expands the lungs because, in the natural resting position, the ribs slant downward,

as shown on the left side of Figure 37–1, thus allowing the sternum to fall

backward toward the vertebral column. But when the rib cage is elevated, the

ribs project almost directly forward, so that the sternum also moves forward,

away from the spine, making the anteroposterior thickness of the chest about

20 per cent greater during maximum inspiration than during expiration.Therefore,

all the muscles that elevate the chest cage are classified as muscles of inspiration,

and those muscles that depress the chest cage are classified as muscles

of expiration. The most important muscles that raise the rib cage are the external

intercostals, but others that help are the (1) sternocleidomastoid muscles,

which lift upward on the sternum; (2) anterior serrati, which lift many of the

ribs; and (3) scaleni, which lift the first two ribs.

The muscles that pull the rib cage downward during expiration are mainly

the (1) abdominal recti, which have the powerful effect of pulling downward on

the lower ribs at the same time that they and other abdominal muscles also compress

the abdominal contents upward against the diaphragm, and (2) internal


472 Unit VII Respiration

Figure 37–1 also shows the mechanism by which the

external and internal intercostals act to cause inspiration

and expiration. To the left, the ribs during

expiration are angled downward, and the external

intercostals are elongated forward and downward. As

they contract, they pull the upper ribs forward in relation

to the lower ribs, and this causes leverage on the

ribs to raise them upward, thereby causing inspiration.

The internal intercostals function exactly in the opposite

manner, functioning as expiratory muscles because

they angle between the ribs in the opposite direction

and cause opposite leverage.

Movement of Air In and Out of the

Lungs and the Pressures

That Cause the Movement

The lung is an elastic structure that collapses like a

balloon and expels all its air through the trachea whenever

there is no force to keep it inflated. Also, there

are no attachments between the lung and the walls of

the chest cage, except where it is suspended at its hilum

from the mediastinum. Instead, the lung “floats” in the

thoracic cavity, surrounded by a thin layer of pleural

fluid that lubricates movement of the lungs within the

cavity. Further, continual suction of excess fluid into

lymphatic channels maintains a slight suction between

the visceral surface of the lung pleura and the parietal

pleural surface of the thoracic cavity. Therefore, the

lungs are held to the thoracic wall as if glued there,

except that they are well lubricated and can slide

freely as the chest expands and contracts.

Pleural Pressure and Its Changes

During Respiration

Pleural pressure is the pressure of the fluid in the thin

space between the lung pleura and the chest wall

pleura. As noted earlier, this is normally a slight

suction, which means a slightly negative pressure. The

normal pleural pressure at the beginning of inspiration

is about –5 centimeters of water, which is the amount

of suction required to hold the lungs open to their

resting level. Then, during normal inspiration, expansion

of the chest cage pulls outward on the lungs with

greater force and creates more negative pressure, to an

average of about –7.5 centimeters of water.

These relationships between pleural pressure and

changing lung volume are demonstrated in Figure

37–2, showing in the lower panel the increasing negativity

of the pleural pressure from –5 to –7.5 during

inspiration and in the upper panel an increase in lung

volume of 0.5 liter.Then, during expiration, the events

are essentially reversed.

Alveolar Pressure

Alveolar pressure is the pressure of the air inside the

lung alveoli. When the glottis is open and no air is

flowing into or out of the lungs, the pressures in all

parts of the respiratory tree, all the way to the alveoli,

are equal to atmospheric pressure, which is considered

to be zero reference pressure in the airways—that is,

0 centimeters water pressure. To cause inward flow of

air into the alveoli during inspiration, the pressure in

the alveoli must fall to a value slightly below atmospheric

pressure (below 0). The second curve (labeled

“alveolar pressure”) of Figure 37–2 demonstrates that

during normal inspiration, alveolar pressure decreases

to about –1 centimeter of water. This slight negative




rib cage





vertical diameter


A–P diameter







Figure 37–1

Contraction and expansion of the thoracic cage during expiration

and inspiration, demonstrating diaphragmatic contraction, function

of the intercostal muscles, and elevation and depression of

the rib cage.

Pressure (cm H2O) Volume change (liters)










Inspiration Expiration

Transpulmonary pressure

Lung volume

Alveolar pressure

Pleural pressure

Figure 37–2

Changes in lung volume, alveolar pressure, pleural pressure, and

transpulmonary pressure during normal breathing.

Chapter 37 Pulmonary Ventilation 473

pressure is enough to pull 0.5 liter of air into the lungs

in the 2 seconds required for normal quiet inspiration.

During expiration, opposite pressures occur: The

alveolar pressure rises to about +1 centimeter of water,

and this forces the 0.5 liter of inspired air out of the

lungs during the 2 to 3 seconds of expiration.

Transpulmonary Pressure. Finally, note in Figure 37–2 the

difference between the alveolar pressure and the

pleural pressure. This is called the transpulmonary

pressure. It is the pressure difference between that in

the alveoli and that on the outer surfaces of the lungs,

and it is a measure of the elastic forces in the lungs

that tend to collapse the lungs at each instant of respiration,

called the recoil pressure.

Compliance of the Lungs

The extent to which the lungs will expand for each unit

increase in transpulmonary pressure (if enough time is

allowed to reach equilibrium) is called the lung compliance.

The total compliance of both lungs together in

the normal adult human being averages about 200 milliliters

of air per centimeter of water transpulmonary

pressure. That is, every time the transpulmonary pressure

increases 1 centimeter of water, the lung volume,

after 10 to 20 seconds, will expand 200 milliliters.

Compliance Diagram of the Lungs. Figure 37–3 is a diagram

relating lung volume changes to changes in transpulmonary

pressure. Note that the relation is different for

inspiration and expiration. Each curve is recorded by

changing the transpulmonary pressure in small steps

and allowing the lung volume to come to a steady level

between successive steps. The two curves are called,

respectively, the inspiratory compliance curve and the

expiratory compliance curve, and the entire diagram is

called the compliance diagram of the lungs.

The characteristics of the compliance diagram are

determined by the elastic forces of the lungs.These can

be divided into two parts: (1) elastic forces of the lung

tissue itself and (2) elastic forces caused by surface

tension of the fluid that lines the inside walls of the

alveoli and other lung air spaces.

The elastic forces of the lung tissue are determined

mainly by elastin and collagen fibers interwoven

among the lung parenchyma. In deflated lungs, these

fibers are in an elastically contracted and kinked state;

then, when the lungs expand, the fibers become

stretched and unkinked, thereby elongating and exerting

even more elastic force.

The elastic forces caused by surface tension are

much more complex. The significance of surface

tension is shown in Figure 37–4, which compares the

compliance diagram of the lungs when filled with

saline solution and when filled with air.When the lungs

are filled with air, there is an interface between the

alveolar fluid and the air in the alveoli. In the case of

the saline solution–filled lungs, there is no air-fluid

interface; therefore, the surface tension effect is not

present—only tissue elastic forces are operative in the

saline solution–filled lung.

Note that transpleural pressures required to expand

air-filled lungs are about three times as great as those

required to expand saline solution–filled lungs. Thus,

one can conclude that the tissue elastic forces tending

to cause collapse of the air-filled lung represent only

about one third of the total lung elasticity, whereas the

Lung volume change (liters)






–4 –5 –6

Pleural pressure (cm H2O)

Figure 37–3

Compliance diagram in a healthy person. This diagram shows

compliance of the lungs alone.

Lung volume change (liters)




0 –2 –4 –6 –8

Pleural pressure (cm H2O)

Saline-filled Air-filled



Figure 37–4

Comparison of the compliance diagrams of saline-filled and airfilled

lungs when the alveolar pressure is maintained at atmospheric

pressure (0 cm H2O) and pleural pressure is changed.

474 Unit VII Respiration

fluid-air surface tension forces in the alveoli represent

about two thirds.

The fluid-air surface tension elastic forces of the

lungs also increase tremendously when the substance

called surfactant is not present in the alveolar fluid. Let

us now discuss surfactant and its relation to the surface

tension forces.

Surfactant, Surface Tension, and Collapse

of the Alveoli

Principle of Surface Tension. When water forms a surface

with air, the water molecules on the surface of the

water have an especially strong attraction for one

another. As a result, the water surface is always

attempting to contract. This is what holds raindrops

together: that is, there is a tight contractile membrane

of water molecules around the entire surface of the

raindrop. Now let us reverse these principles and see

what happens on the inner surfaces of the alveoli.

Here, the water surface is also attempting to contract.

This results in an attempt to force the air out of the

alveoli through the bronchi and, in doing so, causes the

alveoli to try to collapse. The net effect is to cause an

elastic contractile force of the entire lungs, which is

called the surface tension elastic force.

Surfactant and Its Effect on Surface Tension. Surfactant is a

surface active agent in water, which means that it

greatly reduces the surface tension of water. It is

secreted by special surfactant-secreting epithelial cells

called type II alveolar epithelial cells, which constitute

about 10 per cent of the surface area of the alveoli.

These cells are granular, containing lipid inclusions

that are secreted in the surfactant into the alveoli.

Surfactant is a complex mixture of several

phospholipids, proteins, and ions. The most important

components are the phospholipid dipalmitoylphosphatidylcholine,

surfactant apoproteins, and calcium

ions. The dipalmitoylphosphatidylcholine, along with

several less important phospholipids, is responsible

for reducing the surface tension. It does this by not

dissolving uniformly in the fluid lining the alveolar

surface. Instead, part of the molecule dissolves,

while the remainder spreads over the surface of the

water in the alveoli. This surface has from one

twelfth to one half the surface tension of a pure water


In quantitative terms, the surface tension of different

water fluids is approximately the following: pure

water, 72 dynes/cm; normal fluids lining the alveoli but

without surfactant, 50 dynes/cm; normal fluids lining

the alveoli and with normal amounts of surfactant

included, between 5 and 30 dynes/cm.

Pressure in Occluded Alveoli Caused by Surface Tension. If the

air passages leading from the alveoli of the lungs are

blocked, the surface tension in the alveoli tends to collapse

the alveoli. This creates positive pressure in the

alveoli, attempting to push the air out. The amount of

pressure generated in this way in an alveolus can be calculated

from the following formula:

For the average-sized alveolus with a radius of about

100 micrometers and lined with normal surfactant, this

calculates to be about 4 centimeters of water pressure

(3 mm Hg). If the alveoli were lined with pure water

without any surfactant, the pressure would calculate to

be about 18 centimeters of water pressure, 4.5 times as

great. Thus, one sees how important surfactant is in

reducing alveolar surface tension and therefore also

reducing the effort required by the respiratory muscles

to expand the lungs.

Effect of Alveolar Radius on the Pressure Caused by Surface

Tension. Note from the preceding formula that the pressure

generated as a result of surface tension in the

alveoli is inversely affected by the radius of the alveolus,

which means that the smaller the alveolus, the

greater the alveolar pressure caused by the surface

tension. Thus, when the alveoli have half the normal

radius (50 instead of 100 micrometers), the pressures

noted earlier are doubled. This is especially significant

in small premature babies, many of whom have alveoli

with radii less than one quarter that of an adult person.

Further, surfactant does not normally begin to be

secreted into the alveoli until between the sixth and

seventh months of gestation, and in some cases, even

later than that.Therefore, many premature babies have

little or no surfactant in the alveoli when they are born,

and their lungs have an extreme tendency to collapse,

sometimes as great as six to eight times that in a normal

adult person. This causes the condition called respiratory

distress syndrome of the newborn. It is fatal if

not treated with strong measures, especially properly

applied continuous positive pressure breathing.

Effect of the Thoracic Cage

on Lung Expansibility

Thus far, we have discussed the expansibility of the

lungs alone, without considering the thoracic cage.The

thoracic cage has its own elastic and viscous characteristics,

similar to those of the lungs; even if the lungs

were not present in the thorax, muscular effort would

still be required to expand the thoracic cage.

Compliance of the Thorax and the

Lungs Together

The compliance of the entire pulmonary system (the

lungs and thoracic cage together) is measured while

expanding the lungs of a totally relaxed or paralyzed

person.To do this, air is forced into the lungs a little at

a time while recording lung pressures and volumes.To

inflate this total pulmonary system, almost twice as

much pressure is needed as to inflate the same lungs

after removal from the chest cage.Therefore, the compliance

of the combined lung-thorax system is almost

exactly one half that of the lungs alone—110 milliliters

of volume per centimeter of water pressure for

the combined system, compared with 200 ml/cm for

the lungs alone. Furthermore, when the lungs are

expanded to high volumes or compressed to low

volumes, the limitations of the chest become extreme;


Surface tension

Radius of alveolus


2 ¥

Chapter 37 Pulmonary Ventilation 475

when near these limits, the compliance of the combined

lung-thorax system can be less than one fifth

that of the lungs alone.

Work” of Breathing

We have already pointed out that during normal quiet

breathing, all respiratory muscle contraction occurs

during inspiration; expiration is almost entirely a

passive process caused by elastic recoil of the lungs and

chest cage. Thus, under resting conditions, the respiratory

muscles normally perform “work” to cause inspiration

but not to cause expiration.

The work of inspiration can be divided into three

fractions: (1) that required to expand the lungs against

the lung and chest elastic forces, called compliance work

or elastic work; (2) that required to overcome the viscosity

of the lung and chest wall structures, called tissue

resistance work; and (3) that required to overcome

airway resistance to movement of air into the lungs,

called airway resistance work.

Energy Required for Respiration. During normal quiet respiration,

only 3 to 5 per cent of the total energy expended

by the body is required for pulmonary ventilation. But

during heavy exercise, the amount of energy required

can increase as much as 50-fold, especially if the person

has any degree of increased airway resistance or decreased

pulmonary compliance. Therefore, one of the

major limitations on the intensity of exercise that can

be performed is the person’s ability to provide enough

muscle energy for the respiratory process alone.

Pulmonary Volumes

and Capacities

Recording Changes in Pulmonary


A simple method for studying pulmonary ventilation

is to record the volume movement of air into and out

of the lungs, a process called spirometry. A typical

basic spirometer is shown in Figure 37–5. It consists of

a drum inverted over a chamber of water, with the

drum counterbalanced by a weight. In the drum is a

breathing gas, usually air or oxygen; a tube connects

the mouth with the gas chamber.When one breathes

into and out of the chamber, the drum rises and falls,

and an appropriate recording is made on a moving

sheet of paper.

Figure 37–6 shows a spirogram indicating changes in

lung volume under different conditions of breathing.

For ease in describing the events of pulmonary ventilation,

the air in the lungs has been subdivided in this

diagram into four volumes and four capacities, which

are the average for a young adult man.

Pulmonary Volumes

To the left in Figure 37–6 are listed four pulmonary

lung volumes that, when added together, equal the

maximum volume to which the lungs can be expanded.

The significance of each of these volumes is the


1. The tidal volume is the volume of air inspired or

expired with each normal breath; it amounts to

about 500 milliliters in the adult male.

2. The inspiratory reserve volume is the extra volume

of air that can be inspired over and above the

normal tidal volume when the person inspires

with full force; it is usually equal to about

3000 milliliters.

3. The expiratory reserve volume is the maximum

extra volume of air that can be expired by

forceful expiration after the end of a normal

tidal expiration; this normally amounts to about

1100 milliliters.

4. The residual volume is the volume of air

remaining in the lungs after the most forceful

expiration; this volume averages about

1200 milliliters.

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