مواضيع المحاضرة:
background image

electrode is surrounded by a thin plastic membrane. In the space between the

in blood, a miniature glass

When the glass electrode is used to measure CO

explained in Chapter 30; that is,

solution until an equilibrium state is established. In this equilibrium state, the

bonate is exposed to carbon dioxide gas, the carbon dioxide dissolves in the

in the following way: When a weak solution of sodium bicar-

direct measure of pH, and this is generally read directly from a voltmeter scale,

purpose are miniaturized. The voltage generated by the glass electrode is a

the type used in all chemical laboratories. However, the electrodes used for this

minutes, using no more than a few drops of blood. They are the following.

respiratory distress or acute abnormalities of acid-base balance. Several simple

, and pH. It is often important to make these

, CO

Study of Blood Gases and Blood pH

clinical pulmonary physiologist. Some other interesting tools are described here.

space. This array of measurements is only part of the armamentarium of the

tional residual capacity, dead space, physiologic shunt, and physiologic dead

ing respiratory abnormalities, including measuring vital capacity, tidal air, func-

In the previous few chapters, we have discussed a number of methods for study-

Useful Methods for Studying Respiratory Abnormalities

a diagnosis of “respiratory insufficiency.”

entirely different for these diseases, so it is no longer satisfactory simply to make

between the lungs and tissues. Therapy is often

inadequate ventilation. Others result from abnor-

exchange. Some respiratory diseases result from

Oxygen Therapy

Pathophysiology, Diagnosis,

Respiratory Insufficiency—

C

H

A

P

T

E

R

 

4

2

524

Diagnosis and treatment of most respiratory disor-
ders depend heavily on understanding the basic
physiologic principles of respiration and gas

malities of diffusion through the pulmonary mem-
brane or abnormal blood transport of gases

Among the most fundamental of all tests of pulmonary performance are deter-
minations of the blood Po

2

2

measurements rapidly as an aid in determining appropriate therapy for acute

and rapid methods have been developed to make these measurements within

Determination of Blood pH.

Blood pH is measured using a glass pH electrode of

or it is recorded on a chart.

Determination of Blood CO

2

.

A glass electrode pH meter can also be used to deter-

mine blood CO

2

pH of the solution is a function of the carbon dioxide and bicarbonate ion con-
centrations in accordance with the Henderson-Hasselbalch equation that is

2

electrode and plastic membrane is a solution of sodium bicarbonate of known

pH

HCO

CO

3

2

=

-

lo

+

g

6.1


background image

capacity (TLC) and reduced residual volume (RV).

constricted lungs and partial airway obstruction. Note

ow-volume curve, along with two additional 

Figure 42

Abnormalities of the Maximum Expiratory Flow-Volume Curve.

pressure, thus progressively reducing the maximum

structures are relaxed, so that the bronchi and bron-

elements; however, as the lung becomes smaller, these

The main reason for this is that in the enlarged lung

ow rate also becomes less.

Note also that as the lung volume becomes smaller,

ow rate that he or she can achieve.

tional expiratory effort the person exerts, this is still

than 400 L/min. But regardless of how much addi-

maximum expiratory airflow

can expire at no greater rate. Note that the person

ow. The curve

Figure 42

Therefore, beyond a critical degree of expiratory force,

ow.

amount, thus preventing further increase in 

alveolar pressure, but it also increases the degree of

will oppose movement of air to the exterior. Once 

to collapse the bronchioles at the same time, which 

the alveoli toward the bronchioles, but it also tends 

fore, not only does this pressure force air from 

outsides of both the alveoli and the bronchioles.There-

ways caused by compressing the chest cage.The arrows

Figure 42

Figure 42

These principles can be understood by referring to

large volume of air than when they are almost empty.

ow. The maximum expiratory

with greatly increased additional force. This is the

follows: When a person expires with great force, the

, which can be de

maximum expiratory flow

culty in breathing. This has led to the concept called

during expiration, sometimes causing tremendous dif-

In many respiratory diseases, particularly in asthma,

almost moment by moment at the bedside.

so using a single, droplet-size sample of blood. Thus,

are built into the same apparatus, and all

, and Po

the electrode.

limeter is used, and this is separated from the blood 

as well). In practice, a negative platinum

deposit on the electrode. Furthermore, the rate of

different from the voltage of the solution, oxygen will

. Electric current is made to 

The concentration of oxygen

the pH is measured by the glass electrode, and the CO

solution. Only a drop or so of blood is required. Next,

surface of the plastic membrane, allowing carbon

concentration. Blood is then superfused onto the outer

Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy

Chapter 42

525

dioxide to diffuse from the blood into the bicarbonate

2

is calculated by use of the above formula.

Determination of Blood PO

2

.

in a fluid can be measured by a technique called
polarography

flow

between a small negative electrode and the solution.
If the voltage of the electrode is more than 

-0.6 volt

current flow through the electrode will be directly pro-
portional to the concentration of oxygen (and there-
fore to PO

2

electrode with a surface area of about 1 square mil-

by a thin plastic membrane that allows diffusion of
oxygen but not diffusion of proteins or other sub-
stances that will “poison”

Often all three of the measuring devices for pH,

CO

2

2

these measurements can be made within a minute or

changes in the blood gases and pH can be followed

Measurement of Maximum 
Expiratory Flow

the resistance to airflow becomes especially great

fi

fined as

expiratory airflow reaches a maximum flow beyond
which the flow cannot be increased any more even

maximum expiratory fl
flow is much greater when the lungs are filled with a

–1.

–1shows the effect of increased pressure

applied to the outsides of the alveoli and air passage-

indicate that the same pressure compresses the 

the bronchioles have almost completely collapsed,
further expiratory force can still greatly increase the

bronchiolar collapse and airway resistance by an equal

fl

a maximum expiratory flow has been reached.

–1shows the effect of different degrees

of lung collapse (and therefore of bronchiolar collapse
as well) on the maximum expiratory fl
recorded in this section shows the maximum expira-
tory  flow at all levels of lung volume after a healthy
person  first inhales as much air as possible and then
expires with maximum expiratory effort until he or she

quickly reaches a 

of more

the maximum fl

the maximum expiratory fl

the bronchi and bronchioles are held open partially by
way of elastic pull on their outsides by lung structural

chioles are collapsed more easily by external chest

expiratory flow rate as well.

–2 shows the normal maximum expiratory

fl

flow-

volume curves recorded in two types of lung diseases:

that the constricted lungs have both reduced total lung

Total lung

6

0

1

2

3

A

B

Residual

volume

capacity

Maximum expiratory flow

4

5

Expiratory air flow (L/min)

Lung volume (liters)

0

500

400

300

200

100

becomes smaller.

decreasing maximum expiratory air flow as the lung volume

lung volume on the maximum expiratory air flow, showing

Effect of

ratory effort, an effect that limits expiratory flow rate. 

Collapse of the respiratory passageway during maximum expi-

Figure 42–1

A,

B,


background image

excess air in the lungs. However, this term is usually

The term 

Abnormalities

of Specific Pulmonary

obstruction, as often occurs in acute asthma, this can

decreased to only 47 per cent. In serious airway

that, with airway obstruction, this value

/FVC%) is 80 per cent. However, note in Figure

), the percentage of the FVC that is

(see Figure 42

) with the normal. In the normal person

rst second. Therefore, it is customary to compare

, especially during

these persons can expire each second

however, a 

in basic lung volumes in the two persons. There is,

greatly different, indicating only a moderate difference

tion. The total volume changes of the FVCs are not

Now, study the difference between the two records

gure.

FVC, as shown in the 

and as completely as possible. The total distance of the

to the total lung capacity, then exhales into the

the FVC maneuver, the person 

person with partial airway obstruction. In performing

person with normal lungs and in Figure 42

. Such a record is shown in Figure 42

and one that is also simple, is to make a record on a

Forced Expiratory Volume

Forced Expiratory Vital Capacity and

. Serious airway obstruction also

The classic disease that causes severe airway

normal airways, the maximum expiratory 

2. Also, because of the obstruction of the

in Figure 42

both the TLC and the RV, as shown by the green curve

Over a period of months or years, this effect increases

lung easily but then becomes trapped in the lungs.

expands the alveoli. Therefore, air tends to enter the

to cause expiration. By contrast, the extra negative

the closing tendency of the airways is greatly increased

, it is usually

airway obstruction

, and 

kyphosis

eases that constrict the chest cage, such as 

, and dis-

lung itself, such as 

cannot rise to equal that of the normal curve. Con-

sible expiratory effort, the maximal expiratory 

normal maximum volume, even with the greatest pos-

Furthermore, because the lung cannot expand to a

526

Unit VII

Respiration

flow

stricted lung diseases include fibrotic diseases of the

tuberculosis  and silicosis

,

scoliosis

fibrotic pleurisy.

In diseases with 

much more difficult to expire than to inspire because

by the extra positive pressure required in the chest 

pleural pressure that occurs during inspiration actually
“pulls” the airways open at the same time that it

airways and because they collapse more easily than

flow rate is

greatly reduced.

obstruction is asthma
occurs in some stages of emphysema.

Another exceedingly useful clinical pulmonary test,

spirometer of the forced expiratory vital capacity
(FVC)

–3for a

–3for a

first inspires maximally

spirometer with maximum expiratory effort as rapidly

downslope of the lung volume record represents the

fi

(1) for normal lungs and (2) for partial airway obstruc-

major difference in the amounts of air that

the fi
the recorded forced expiratory volume during the first
second (FEV

1

–3A

expired in the first second divided by the total FVC
(FEV

1

42–3B

decrease to less than 20 per cent.

Physiologic Peculiarities 

Chronic Pulmonary Emphysema

pulmonary emphysema literally means

6

5

4

3

2

1

0

7

TLC

RV

Expiratory air flow (L/min)

Lung volume (liters)

0

500

Normal
Airway obstruction
Constricted lungs

400

300

200

100

curve. TLC, total lung capacity; RV, residual volume.

airway obstruction—-on the maximum expiratory flow-volume

Effect of two respiratory abnormalities—constricted lungs and

Figure 42–2

0

1

2

3

4

5

6

7

0

1

2

3

4

5

6

7

Maximum

inspiration

FEV

1

FVC

FEV

1

/FVC%

= 80%

Lung volume change (liters)

AIRWAY OBSTRUCTION

Seconds

NORMAL

4

3

2

1

0

A

FEV

1

FVC

FEV

1

/FVC%

= 47%

4

3

2

1

0

B

(The “zero” on the volume scale is residual volume.)

in a person with partial airway obstruction.

Recordings during the forced vital capacity maneuver: 

Figure 42–3

A, in a

healthy person and B,


background image

This disease begins with infection in the alveoli; the

, caused most frequently by 

5. A common type of pneumonia is 

uid and blood cells, as shown in Figure

The term 

smoking.

all these effects is severe, prolonged, devastating 

alveoli plus loss of alveolar walls. The net result of 

many years. The person develops both hypoxia and

frequently causes right-sided heart failure.

. This in

markedly, causing 

through which blood can pass. As a result, the

4. Loss of large portions of the alveolar walls also

same lungs.

in wasted ventilation, both effects occurring in the

), resulting

in poor aeration of the blood, and very high V

), resulting

, with a very low 

ventilated. This often causes 

ventilated, while other portions are poorly

in some parts of the lungs than in other parts,

3. The obstructive process is frequently much worse

of the lung, which

2. The marked loss of alveolar walls greatly

alveoli but also compresses the bronchioles,

breathing. It is especially dif

increases airway

1. The bronchiolar obstruction 

struction versus lung parenchymal destruction.Among

extremely varied, depending on the severity of the

The physiologic effects of chronic emphysema are

emphysematous lung is that shown in Figures

. Therefore, the 

destruction of as much as 50 to 80 per cent of the

combined with the lung infection, causes 

and overstretching them. This,

cult to expire, thus causing 

3. The obstruction of the airways makes it especially

airways.

chronic obstruction

2. The infection, excess mucus, and in

alveolar macrophages occurs, so that they become

exacerbates the condition. Too, inhibition of the

of excess mucus secretion occurs, which further

easily out of the passageways. Also, stimulation 

nicotine. As a result, mucus cannot be moved

the respiratory epithelium, an effect caused by

airways, including partial paralysis of the cilia of

bronchioles. The chronic infection seriously

, caused by inhaling smoke or

process of the lungs caused by many years of smoking.

Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy

Chapter 42

527

used to describe complex obstructive and destructive

It results from the following major pathophysiologic
changes in the lungs:
1. Chronic infection

other substances that irritate the bronchi and

deranges the normal protective mechanisms of the

less effective in combating infection.

flammatory

edema of the bronchiolar epithelium together
cause 

of many of the smaller

diffi

entrapment of 

air in the alveoli

marked

alveolar walls

final picture of the

42–4 (top) and 42–5.

disease and the relative degrees of bronchiolar ob-

the different abnormalities are the following:

resistance and results in greatly increased work of

ficult for the person

to move air through the bronchioles during
expiration because the compressive force on the
outside of the lung not only compresses the

which further increases their resistance during
expiration.

decreases the diffusing capacity
reduces the ability of the lungs to oxygenate the
blood and remove carbon dioxide from the blood.

so that some portions of the lungs are well

extremely abnormal

ventilation-perfusion ratios
V

.

a/Q

.

in some parts (physiologic shunt

.

a/Q

.

in other parts (physiologic dead space

decreases the number of pulmonary capillaries

pulmonary vascular resistance often increases

pulmonary hypertension

turn overloads the right side of the heart and

Chronic emphysema usually progresses slowly over

hypercapnia because of hypoventilation of many

air

hunger that can last for years until the hypoxia and
hypercapnia cause death—a high penalty to pay for

Pneumonia

pneumonia includes any inflammatory con-

dition of the lung in which some or all of the alveoli
are filled with fl
42–

bacterial pneu-

monia

pneumococci.

pulmonary membrane becomes inflamed and highly
porous so that fluid and even red and white blood cells

and the Department of Anatomy, The Medical College of 

emphysema. (Reproduced with permission of Patricia Delaney

bottom figure

) with the normal

top figure

Figure 42–4

Contrast of the emphysematous lung (
lung (

), showing extensive alveolar destruction in

Wisconsin.)


background image

monary vessels of the collapsed lung. This resistance

resistance to blood flow

7. Collapse of the lung tissue not

shown in Figure 42

The effects on overall pulmonary function caused by

lung.

atelectatic, a condition called 

uid. This almost always is the

illaries into the alveoli, thus causing the alveoli to 

the alveoli, which pull 

brotic tissue and cannot collapse, absorption of air

the alveoli. However, if the lung is rigid because of

is pliable enough, this will lead simply to collapse of

owing in the pulmonary capillaries. If the lung tissue

object such as a tumor. The air entrapped beyond the

The airway obstruction type of

Airway Obstruction.

in localized areas of a lung or in an entire lung. Its most

Atelectasis means collapse of the alveoli. It can occur

about 78 per cent, which is far below normal.

cent saturated.Therefore, the average saturation of the

97 per cent saturated with oxygen, whereas that

ventilation-perfusion ratio in pneumonia, showing that

Figure 42

hypoxemia

perfusion ratio. Both these effects cause 

This results in two major pulmonary abnormalities: (1)

ow through the lung continues normally.

to only one lung, with alveolar ventilation reduced

stages, the pneumonia process might well be localized

lungs change in different stages of the disease. In early

In pneumonia, the gas exchange functions of the

uid and cellular debris.

lung, become 

of the lungs, sometimes whole lobes or even a whole

virus from alveolus to alveolus. Eventually, large areas

uid and cells,

leak out of the blood into the alveoli.Thus, the infected

528

Unit VII

Respiration

alveoli become progressively filled with fl
and the infection spreads by extension of bacteria or

“consolidated,” which means that they

are filled with fl

while blood fl

reduction in the total available surface area of the res-
piratory membrane and (2) decreased ventilation-

(low blood oxygen) and hypercapnia (high blood
carbon dioxide).

–6 shows the effect of the decreased 

the blood passing through the aerated lung becomes

passing through the unaerated lung is about 60 per

blood pumped by the left heart into the aorta is only

Atelectasis

common causes are (1) total obstruction of the airway
or (2) lack of surfactant in the fluids lining the alveoli.

atelectasis usually results from (1) blockage of many
small bronchi with mucus or (2) obstruction of a major
bronchus by either a large mucus plug or some solid

block is absorbed within minutes to hours by the blood
fl

fi
from the alveoli creates very negative pressures within

fluid out of the pulmonary cap-

fill

completely with edema fl
effect that occurs when an entire lung becomes

massive collapse of the

massive collapse (atelectasis) of an entire lung are

only occludes the alveoli but also almost always
increases the 

through the pul-

Normal

Pneumonia

Emphysema

Fluid and blood cells

Confluent alveoli

Edema

Figure 42–5

Lung alveolar changes in pneumonia and emphysema.

Mean      = 78%

          

Pneumonia

Pulmonary arterial blood

60% saturated with O

2

Left
pulmonary
vein 60%
saturated

Right

pulmonary

vein 97%

saturated

Aorta:
Blood 

1

/

2

 = 97%

1

/

2

 = 60%

pulmonary artery, the right and left pulmonary veins, and the aorta.

Effect of pneumonia on percentage saturation of oxygen in the

Figure 42–6


background image

years, the chest cage becomes permanently enlarged,

expiring air from the lungs. Also, over a period of

The 

this chapter.

air hunger,

dyspnea, or 

ratory volume. Also, all of this together results in

ing. Clinical measurements show (1) greatly reduced

expiration. That is, the asthmatic person often can

occluded, further occlusion resulting from the external

the outsides of the bronchioles. Because the bronchi-

than during inspiration in asthma, caused by bronchi-

As discussed earlier in this chapter, the bronchiolar

Therefore, the airway resistance increases greatly.

and (2) spasm of the bronchiolar smooth muscle.

secretion of thick mucus into the bronchiolar lumens,

edema in the walls of the small bronchioles, as well as

substance of anaphylaxis, are to produce (1) localized

effects of all these factors, especially the slow-reacting

. The combined

, and (d) 

chemotactic factor

(which is a mixture of leukotrienes), (c) 

slow-reacting substance of anaphylaxis

, (b)

several different substances. Among them are (a) 

IgE antibodies), the pollen reacts with the mast cell

sensitive (that is, to which the person has developed

with the bronchioles and small bronchi. When the asth-

antibodies are mainly attached to mast cells

rst place, as explained in Chapter 34. In asthma,

mally large amounts of IgE antibodies, and these anti-

typical allergic person has a tendency to form abnor-

of asthma is believed to occur in the following way: The

The allergic reaction that occurs in the allergic type

the air, such as irritants in smog.

pollens. In older people, the cause is almost always

allergic hypersensitivity, especially sensitivity to plant

younger than age 30 years, the asthma is caused by

stances in the air. In about 70 per cent of patients

The usual cause of asthma is contractile hypersensi-

at some time in life.

cult breathing. It occurs in 3 to 5 per cent of all people

smooth muscle in the bronchioles, which partially

atelectatic.

explained in Chapter 37, many of these infants die of

uid. As

This causes a serious tendency for the lungs of these

babies, the quantity of surfactant secreted by the

), which often occurs in newborn premature

However, in a number of conditions, such as in 

plays a major role in preventing alveolar collapse.

tension in the alveoli 2- to 10-fold, which normally

alveoli. The surfactant in turn decreases the surface

discussed in Chapter 37. It was pointed out that the

The secre-

an entire lung.

promised, so that the aortic blood has only mild

through the unaerated lung. As a result, the overall

situation shown in Figure 42

lated lung and therefore becomes well aerated. In the

nately, most of the blood is routed through the venti-

through the atelectatic lung becomes slight. Fortu-

Because of the vascular constriction, blood 

tion, as explained in Chapter 38.

volume of the lung decreases. In addition, hypoxia in

itself, which compresses and folds the vessels as the

Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy

Chapter 42

529

increase occurs partially because of the lung collapse

the collapsed alveoli causes additional vasoconstric-

flow

–7, five sixths of the blood

passes through the aerated lung and only one sixth

ventilation-perfusion ratio is only moderately com-

oxygen desaturation despite total loss of ventilation in

Lack of “Surfactant” as a Cause of Lung Collapse.

tion and function of surfactant  in the alveoli were 

surfactant is secreted by special alveolar epithelial
cells into the fluids that coat the inside surface of the

hyaline

membrane disease (also called respiratory distress syn-
drome

alveoli is so greatly depressed that the surface tension
of the alveolar fluid becomes several times normal.

babies to collapse or to become filled with fl

suffocation when large portions of the lungs become

Asthma

Asthma is characterized by spastic contraction of the

obstructs the bronchioles and causes extremely diffi-

tivity of the bronchioles in response to foreign sub-

hypersensitivity to nonallergenic types of irritants in

bodies cause allergic reactions when they react with the
specific antigens that have caused them to develop in
the  fi
these 

that

are present in the lung interstitium in close association

matic person breathes in pollen to which he or she is

attached antibodies and causes the mast cells to release

histamine

eosinophilic

bradykinin

diameter becomes more reduced during expiration

olar collapse during expiratory effort that compresses

oles of the asthmatic lungs are already partially

pressure creates especially severe obstruction during

inspire quite adequately but has great difficulty expir-

maximum expiratory rate and (2) reduced timed expi-

” which is discussed later in

functional residual capacity and residual volume

of the lung become especially increased during the
acute asthmatic attack because of the difficulty in

causing a “barrel chest,” and both the functional resid-
ual capacity and lung residual volume become perma-
nently increased.

               = 91%

          

Atelectasis

Pulmonary arterial blood

60% saturated with O

2

Left
pulmonary
vein 60%
saturated-
flow 

1

/

5

 normal

Right

pulmonary

vein 97%

saturated

Aorta:
Blood 

5

/

6

 = 97%

1

/

6

 = 60%

Mean saturation

Effect of atelectasis on aortic blood oxygen saturation.

Figure 42–7


background image

value of about 100 mm Hg to as high as 600 mm Hg.

hypoventilation hypoxia, because oxygen therapy can

, essentially the same result occurs as in

hypoxia caused by impaired alveolar membrane

cial. (However, this provides no

normal air. Therefore, here again oxygen therapy can

per cent oxygen can move 

, a person breathing 100

hypoventilation hypoxia

effective therapy.

inspired gases and, therefore, provide 100 per cent

, oxygen therapy can com-

atmospheric hypoxia

valuable.

when oxygen therapy will be of value and, if so, how

different types of hypoxia, one can readily decide

intranasal tube.

a mask, or (3) administering oxygen through an

with oxygen, (2) allowing the patient to breathe either

s head in a 

of Hypoxia

Oxygen Therapy in Different Types 

high-altitude physiology.

(2) reduced work capacity of the muscles. These effects

mental activity, sometimes culminating in coma, and

can cause death of cells throughout the body, but in

Hypoxia, if severe enough,

Effects of Hypoxia on the Body.

, in which several

system can lead to this type of hypoxia. A special

tissue cellular oxidative

cannot use oxygen even when plenty is available. Also,

cyanide

cytochrome oxidase

, in which the action of the enzyme

The classic

Inadequate Tissue Capability to Use Oxygen.

needs further elaboration: this is the hypoxia caused

self-evident from the discussions earlier in the chapter.

This classi

ciency, or

oxygen, because of toxicity, vitamin de

b. Diminished cellular metabolic capacity for using

a. Poisoning of cellular oxidation enzymes

5. Inadequate tissue capability of using oxygen

d. Tissue edema

cerebral, coronary vessels)

ciency (peripheral,

c. Localized circulatory de

ciency

b. General circulatory de

a. Anemia or abnormal hemoglobin

4. Inadequate oxygen transport to the tissues by the

3. Venous-to-arterial shunts (

c. Diminished respiratory membrane diffusion

b. Abnormal alveolar ventilation-perfusion ratio

a. Hypoventilation caused by increased airway

2. Pulmonary disease

b. Hypoventilation (neuromuscular disorders)

ciency of oxygen in the atmosphere

a. De

1. Inadequate oxygenation of the blood in the lungs

principles of oxygen therapy. The following is a

types of hypoxia; then we can discuss the physiologic

Therefore, it is important to understand the different

value; and, at still other times, it is of almost no value.

therapy is of great value; other times, it is of moderate

of bodywide cellular hypoxia. Sometimes, oxygen

sion of oxygen and carbon dioxide.

in the lungs, further reducing overall pulmonary diffu-

increased thickness of the respiratory membrane

These effects cause (1) increased 

as reduced total amount of functional lung tissue.

brosis throughout the lungs, as well

Thus, tuberculosis in its late stages is characterized

large abscess cavities.

bacilli spread throughout the lungs, often causing

untreated, the walling-off process fails and tubercle

cent of all people who develop tuberculosis, if

extension of the infection. However, in about 3 per

. This walling-off process helps to limit further

tissue reaction in the lungs, including (1) invasion of

In tuberculosis, the tubercle bacilli cause a peculiar

Tuberculosis

530

Unit VII

Respiration

the infected tissue by macrophages and (2) “walling
off” of the lesion by fibrous tissue to form the so-called
tubercle
transmission of the tubercle bacilli in the lungs and
therefore is part of the protective process against

extreme destruction of lung tissue with formation of

by many areas of fi

“work” on the part

of the respiratory muscles to cause pulmonary venti-
lation and reduced vital capacity and breathing capac-
ity; 
(2) reduced total respiratory membrane surface area
and 

,

causing progressively diminished pulmonary diffusing
capacity; 
and (3) abnormal ventilation-perfusion ratio

Hypoxia and Oxygen Therapy

Almost any of the conditions discussed in the past 
few sections of this chapter can cause serious degrees

descriptive classification of the causes of hypoxia:

because of extrinsic reasons

fi

resistance or decreased pulmonary compliance

(including either increased physiologic dead
space or increased physiologic shunt)

“right-to-left” cardiac

shunts)

blood

fi

fi

fi

other factors

fication of the types of hypoxia is mainly

Only one of the types of hypoxia in the classification

by inadequate capability of the body’s tissue cells to
use oxygen.

cause of inability of the tissues to use oxygen is cyanide
poisoning

is completely blocked by the

—to such an extent that the tissues simply

deficiencies of some of the 
enzymes or of other elements in the tissue oxidative

example occurs in the disease beriberi
important steps in tissue utilization of oxygen and
formation of carbon dioxide are compromised because
of vitamin B deficiency.

less severe degrees it causes principally (1) depressed

are specifically discussed in Chapter 43 in relation to

Oxygen can be administered by (1) placing the
patient’

“tent” that contains air fortified

pure oxygen or high concentrations of oxygen from 

Recalling the basic physiologic principles of the 

In 

pletely correct the depressed oxygen level in the

In 

five times as much oxygen

into the alveoli with each breath as when breathing

be extremely benefi
benefit for the excess blood carbon dioxide also caused
by the hypoventilation.)

In 

diffusion

increase the Po

2

in the lung alveoli from the normal


background image

circle: (1) more carbon dioxide, (2) further decrease in

piration rather than stimulate it, thus causing a vicious

to 120 to 150 mm Hg. At these higher levels of P

becomes lethargic and sometimes even semicomatose.

rises to 80 to 100 mm Hg, the person

severe.

, becomes

air hunger,

can, and 

75 mm Hg, an otherwise normal person by then is

When the alveolar P

oxygen, so that the resulting tissue hypercapnia is

hypoxia. However, the transport capacity of the blood

decreases carbon dioxide removal from the tissues,

ciency, diminished 

Hypercapnia then occurs along with the hypoxia. And

atmosphere is affected as much as is oxygen transfer.

Conversely, in hypoxia caused by hypoventilation,

rapidly as oxygen. If hypercapnia does begin to occur,

the pulmonary membrane or through the tissues,

or use of oxygen by the tissues. Therefore, it is readily

poisoning of the oxidative

, or 

too little oxygen in the air

The reasons for this are the following.

hypoventilation

is caused by 

hypercapnia. However, hypercapnia usually occurs 

rst thought, that any respi-

One might suspect, on 

uids.

Hypercapnia

conditions.

frequently to cyanosis, even under otherwise normal

, the great excess of avail-

Conversely, in a person with excess red blood cells, as

almost never becomes cyanotic

genated hemoglobin in each 100 milliliters of blood. A

nite cyanosis appears whenever the

In general, de

laries. This deoxygenated hemoglobin has an intense 

bin in the skin blood vessels, especially in the capil-

means blueness of the skin, and its

The term 

Therefore, oxygen therapy is of hardly any measura-

tissues. Instead, the tissue metabolic enzyme system is

, there is abnormality neither

quate tissue use of oxygen

hypoxia caused by inade-

altered. This small amount of extra oxygen may be the

extra oxygen, between 7 and 30 per cent, can be 

cient. Even so, a small amount of

alveoli. The problem instead is that one or more of the

, oxygen therapy is of much less value

transport of oxygen

hypoxia caused by anemia, abnormal hemoglobin

as would occur with no therapy.

8, which shows that the

demonstrated in Figure 42

an increase of more than 800 per cent. This highly ben-

normal value of 60 mm Hg to as high as 560 mm Hg,

This raises the oxygen pressure gradient for diffusion

Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy

Chapter 42

531

of oxygen from the alveoli to the blood from the

eficial effect of oxygen therapy in diffusion hypoxia is

pulmonary blood in this patient with pulmonary
edema picks up oxygen three to four times as rapidly

In 

circulatory deficiencyor physio-

logic shunt
because normal oxygen is already available in the

mechanisms for transporting oxygen from the lungs to
the tissues is defi

trans-

ported in the dissolved state in the blood when alveo-
lar oxygen is increased to maximum even though the
amount transported by the hemoglobin is hardly

difference between life and death.

In the different types of 

of oxygen pickup by the lungs nor of transport to the

simply incapable of using the oxygen that is delivered.

ble benefit.

Cyanosis

cyanosis

cause is excessive amounts of deoxygenated hemoglo-

dark blue-purple color that is transmitted through the
skin.

fi

arterial blood contains more than 5 grams of deoxy-

person with anemia
because there is not enough hemoglobin for 5 grams
to be deoxygenated in 100 milliliters of arterial blood.

occurs in polycythemia vera
able hemoglobin that can become deoxygenated leads

Hypercapnia means excess carbon dioxide in the body
fl

fi

ratory condition that causes hypoxia would also cause

in association with hypoxia only when the hypoxia 

or circulatory deficiency.

Hypoxia caused by 

too

little hemoglobin
enzymes 
has to do only with the availability of oxygen

understandable that hypercapnia is not a concomitant
of these types of hypoxia.

In hypoxia resulting from poor diffusion through

serious hypercapnia usually does not occur at the same
time because carbon dioxide diffuses 20 times as

this immediately stimulates pulmonary ventilation,
which corrects the hypercapnia but not necessarily the
hypoxia.

carbon dioxide transfer between the alveoli and the

in circulatory defi

flow of blood

resulting in tissue hypercapnia in addition to tissue

for carbon dioxide is more than three times that for

much less than the tissue hypoxia.

co

2

rises above about 60 to 

breathing about as rapidly and deeply as he or she 

” also called dyspnea

If the Pco

Anesthesia and death can result when the Pco

2

rises

co

2

,

the excess carbon dioxide now begins to depress res-

Arterial end

Venous end

P

O

2

 in alveoli and blood (mm Hg)

Blood in pulmonary capillary

0

100

Capillary blood

Alveolar P

O

2

 with tent therapy

Normal alveolar P

O

2

Pulmonary edema 

+

  O

therapy

Pulmonary edema with no

 

therapy

200

300

monary edema with and without oxygen tent therapy.

Absorption of oxygen into the pulmonary capillary blood in pul-

Figure 42–8


background image

30 mm Hg positive pressure in the lungs can cause

sometimes to lethal levels. For instance, continuous

peripheral veins becomes impeded. As a result, use 

greater than pressure everywhere else in the body.

respirator, the pressure inside the lungs becomes

tive pressure by a resuscitator, or when the pressure

When air is forced into the lungs under posi-

Effect of the Resuscitator and the Tank Respirator on Venous

5 cm H

negative pressures. Ordinarily these pressures are

outward, negative pressure causes inspiration. Check

body and causes expiration; as the diaphragm moves

moves inward, positive pressure develops around the

the pressure inside the tank. As the leather diaphragm

head a motor-driven leather diaphragm moves back

collar. At the end of the tank opposite the patient

Figure 42

Tank Respirator (the “Iron-Lung”).

that are commonly set at 12 to 15 cm H

usage was at one time greatly decried. However, resus-

lungs because of excessive positive pressure. Their

the lungs during the remainder of the cycle.

during the positive-pressure cycle of the resuscitator

cheal tube. This apparatus forces air through the mask

and, with some machines, negative pressure as well;

consists of a tank supply of oxygen or air; a

ciples of operation. The resuscitator shown in Figure

are available, and each has its own characteristic prin-

Resuscitator.

Artificial Respiration

small or crowded rooms.

cient quantity of air, such as on entering

dyspnea. This feeling is greatly enhanced in people

. For instance, almost

of an abnormal state of mind. This is called 

Finally, the person

breathe forcefully. In these instances, the forceful

normality of the respiratory gases, the person has to

uids are normal, but to attain this

times, however, the levels of both carbon dioxide and

uids. At

piratory muscles to provide adequate ventilation; and

hypercapnia and, to a much less extent, hypoxia; (2)

uids, especially

ment of the sensation of dyspnea. They are (1) abnor-

ity to ventilate enough to satisfy the demand for air. A

respiration, (3) then more carbon dioxide, and so

532

Unit VII

Respiration

forth—culminating rapidly in a respiratory death.

Dyspnea

Dyspnea means mental anguish associated with inabil-

common synonym is air hunger.

At least three factors often enter into the develop-

mality of respiratory gases in the body fl

the amount of work that must be performed by the res-

(3) state of mind.

A person becomes very dyspneic especially from

excess buildup of carbon dioxide in the body fl

oxygen in the body fl

activity of the respiratory muscles frequently gives the
person a sensation of dyspnea.

’s respiratory functions may be

normal and still dyspnea may be experienced because

neurogenic

dyspnea or  emotional dyspnea
anyone momentarily thinking about the act of breath-
ing may suddenly start taking breaths a little more
deeply than ordinarily because of a feeling of mild

who have a psychological fear of not being able to
receive a suffi

Many types of respiratory resuscitators

42–9A
mechanism for applying intermittent positive pressure

and a mask that fits over the face of the patient or a
connector for joining the equipment to an endotra-

or endotracheal tube into the lungs of the patient

and then usually allows the air to flow passively out of

Earlier resuscitators often caused damage to the

citators now have adjustable positive-pressure limits

2

O pressure for

normal lungs (but sometimes much higher for non-
compliant lungs).

–9shows the

tank respirator with a patient’s body inside the tank

and the head protruding through a flexible but airtight

’s

and forth with sufficient excursion to raise and lower

valves on the respirator control the positive and 

adjusted so that the negative pressure that causes
inspiration falls to 

-10 to -20 cm H

2

O and the positive

pressure rises to 0 to 

+

2

O.

Return.

around the patient’s body is reduced by the tank 

Flow of blood into the chest and heart from the

of excessive pressures with either the resuscitator or
the tank respirator can reduce the cardiac output—

exposure for more than a few minutes to greater than

death because of inadequate venous return to the
heart.

Positive

pressure

valve

Negative
pressure
valve

Mechanism

for applying

positive and

negative

pressure

A

B

Leather diaphragm

Tank respirator.

Resuscitator. 

Figure 42–9

A,

B,


background image

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References

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flammation

fi

infl

porary management of chronic obstructive pulmonary

fi

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.

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رفعت المحاضرة من قبل: Mostafa Altae
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