Circulatory Shock and Physiology of Its Treatment pdf - The Circulation

lar waste products from the tissues.

to critical tissues and critical organs and also cause inadequate removal of cellu-

The specific causes of shock are discussed later in the chapter. For the present,

tissue perfusion patterns, so that most of the cardiac output is passing through

the body, so that even a normal cardiac output is inadequate,

person is in circulatory shock. This can result from (1)

Occasionally, the cardiac output is normal or even greater than normal, yet the

Circulatory Shock That Occurs Without Diminished

in the circulation, especially in the venous return pathway to the heart.

obstruction to blood flow

of the venous blood reservoirs, or

decreased vascular tone,

diminished blood volume,

the heart cannot pump blood that does not flow into it. The most common

Factors that decrease venous return

who develop cardiogenic shock do not survive.

Chapter 22, where it is pointed out that as many as 85 per cent of people

This is discussed in detail in

cardiogenic shock.

conditions. The circulatory shock that results from diminished cardiac

arrhythmias,

toxic states

myocardial infarction

These include especially

Cardiac abnormalities that decrease the ability of the heart to pump blood.

shock. Two types of factors can severely reduce cardiac output:

Shock usually results from inadequate cardiac output. Therefore, any condition

that the shock, once begun, is prone to become progressively worse.

other circulatory parts—begins to deteriorate, so

walls of the blood vessels, vasomotor system, and

diovascular system itself—the heart musculature,

nutrients delivered to the tissue cells. Even the car-

body tissues are damaged because of too little flow,

blood flow through the body, to the extent that the

Circulatory shock

Physiology of Its Treatment

278

Circulatory Shock and

means generalized inadequate

especially because of too little oxygen and other

Physiologic Causes of Shock

Circulatory Shock Caused by Decreased Cardiac Output

that reduces the cardiac output far below normal will likely lead to circulatory

but also

the heart, severe heart valve dysfunction, heart

and other

pumping ability is called

also decrease cardiac output because

cause of decreased venous return is

but venous

return can also be reduced as a result of

especially

at some point

Cardiac Output

excessive metabolism of

or (2) abnormal

blood vessels besides those that supply the local tissues with nutrition.

it is important to note that all of them lead to inadequate delivery of nutrients

venous reservoirs constrict, thereby helping to main-

the total peripheral resistance. (2) The veins and

parts of the systemic circulation, thereby increasing

important effects: (1) The arterioles constrict in most

tor system throughout the body, resulting in three

These reflexes stimulate the sympathetic vasoconstric-

vascular stretch receptors, as explained in Chapter 18).

The decrease in arte-

Value to Maintain Arterial Pressure.

Sympathetic Reflex Compensations in Shock—Their Special

arterial pressure, both of which fall to zero when about

rial pressure or cardiac output, but greater blood loss

minutes. About 10 per cent of the total blood volume

Figure 24–1 shows the approximate effects on both

Cardiac Output and Arterial Pressure

Relationship of Bleeding Volume to

normal, and shock may ensue.

return. As a result, the cardiac output falls below

and, as a consequence, decreases venous

shock. Hemorrhage

means diminished blood volume. Hem-

Hypovolemia

teristics of shock initiated by other causes.

basic principles. Then we can consider special charac-

caused by decreased blood volume, which illustrate the

Now, let us discuss the stages of circulatory shock

person is still alive.

person’s life, even though, for the moment, the

irreversible stage,

3. An

in which, without therapy,

progressive stage,

2. A

therapy.

), in which the normal

1. A

change with different degrees of severity, shock is

shock, and so forth until death. It is with this late stage

culatory shock, less adequate tissue perfusion, more

vicious circle ensues, with progressively increasing cir-

an even greater decrease in cardiac output, and a

ing the heart and circulatory system itself. This causes

causes the body tissues to begin deteriorating, includ-

That is, the inadequate blood flow

breeds more shock.

the shock itself

ity, regardless of its initiating cause,

Tissue Deterioration Is the End Result

at the same time as the cardiac output decreases,

severe blood loss, the arterial blood pressure decreases

In most types of shock, especially shock caused by

arterial pressure can fall to half of normal, but the

keep the pressure from falling. At other times, the

be seriously misleading. At times, a person may be in

tory function. However, the arterial pressure can often

level is the principal measure of adequacy of circula-

In the minds of many physicians, the arterial pressure

What Happens to the Arterial Pressure

Circulatory Shock and Physiology of Its Treatment

Chapter 24

279

in Circulatory Shock?

severe shock and still have an almost normal arterial
pressure because of powerful nervous reflexes that

person still has normal tissue perfusion and is not in
shock.

although usually not as much.

of Circulatory Shock, Whatever
the Cause

Once circulatory shock reaches a critical state of sever-

of circulatory shock that we are especially concerned,
because appropriate physiologic treatment can often
reverse the rapid slide to death.

Stages of Shock

Because the characteristics of circulatory shock

divided into the following three major stages:

nonprogressive stage (sometimes called

the compensated stage
circulatory compensatory mechanisms eventually
cause full recovery without help from outside

the shock becomes steadily worse until death.

in which the shock has

progressed to such an extent that all forms of
known therapy are inadequate to save the

Shock Caused by
Hypovolemia—Hemorrhagic
Shock

orrhage is the most common cause of hypovolemic

decreases the filling pressure of the

circulation

cardiac output and arterial pressure of removing blood
from the circulatory system over a period of about 30

can be removed with almost no effect on either arte-

usually diminishes the cardiac output first and later the

35 to 45 per cent of the total blood volume has been
removed.

rial pressure after hemorrhage—as well as decreases
in pressures in the pulmonary arteries and veins in the
thorax—causes powerful sympathetic reflexes (initi-
ated mainly by the arterial baroreceptors and other

tain adequate venous return despite diminished blood

Cardiac output and

arterial pressure

(percentage of normal)

100

Percentage of total blood removed

Arterial

pressure

Cardiac

output

Effect of hemorrhage on cardiac output and arterial pressure.

Figure 24–1

gression, the person eventually recovers. Therefore,

Nonprogressive Shock—Compensated Shock

the shock itself causes still more shock,

That is,

progressive.

life and death. Thus, hemorrhage beyond a certain crit-

This experiment demonstrates that the circulatory

V, and VI), all the dogs died, although many of them

the arterial pressure fell below 45 mm Hg (groups IV,

it fell almost to the 45 mm Hg level (group III). When

recovered; the recovery occurred rapidly if the pres-

than 45 mm Hg (groups I, II, and III) all eventually

their arterial pressures fell to different levels. Those

of arterial pressure. The dogs were bled rapidly until

Figure 24–2 shows an experiment that we performed

does not fall below about 70 mm Hg, despite the fact

cantly decreasing their blood flows. Therefore, blood

blood flow autoregulation is excellent, which prevents

vessels. In addition, in both these vascular beds, local

The sympathetic stimulation does not cause significant

through the coronary and cerebral circulatory systems.

Protection of Coronary and Cerebral Blood Flow by

low.

“last-ditch stand” of the sympathetic reflexes in their

discussed in Chapter 18. This effect of the central

oxygen or from excess buildup of carbon dioxide, as

central nervous system ischemic response, which

of Figure 24–1. This results from activation of the

to their role in maintaining arterial pressure.

, in addition

and cardiac output from falling too much

effect on cardiac output; however, the

total peripheral resistance, which has no beneficial

arterial pressure than for maintaining output. They

is the cardiac output. The reason for this is that the

Referring again to Figure 24–1, note

Maintaining Arterial Pressure than in Maintaining

twice that which is possible in their absence.

Therefore, the reflexes extend the amount of blood

period of 30 minutes before a person dies; this is in

absence of the sympathetic reflexes, only 15 to 20 per

Value of the Sympathetic Nervous Reflexes.

volume. (3) Heart activity increases markedly, some-

280

Unit IV

The Circulation

times increasing the heart rate from the normal value
of 72 beats/min to as high as 160 to 180 beats/min.

In the

cent of the blood volume can be removed over a

contrast to a 30 to 40 per cent loss of blood volume
that a person can sustain when the reflexes are intact.

loss that can occur without causing death to about

Greater Effect of the Sympathetic Nervous Reflexes in

Cardiac Output.

that the arterial pressure is maintained at or near
normal levels in the hemorrhaging person longer than

sympathetic reflexes are geared more for maintaining

increase the arterial pressure mainly by increasing the

sympathetic con-

striction of the veins is important to keep venous return

Especially interesting is the second plateau occur-

ring at about 50 mm Hg in the arterial pressure curve

causes extreme stimulation of the sympathetic nervous
system when the brain begins to suffer from lack of

nervous system ischemic response can be called the

attempt to keep the arterial pressure from falling too

the Reflexes.

A special value of the maintenance

of normal arterial pressure even in the presence of
decreasing cardiac output is protection of blood flow

constriction of either the cerebral or the cardiac

moderate decreases in arterial pressure from signifi-

flow through the heart and brain is maintained essen-
tially at normal levels as long as the arterial pressure

that blood flow in some other areas of the body might
be decreased to as little as one third to one quarter
normal by this time because of vasoconstriction.

Progressive and Nonprogressive
Hemorrhagic Shock

in dogs to demonstrate the effects of different degrees
of sudden acute hemorrhage on the subsequent course

dogs whose pressures fell immediately to no lower

sure fell only slightly (group I) but occurred slowly if

hovered between life and death for hours before the
circulatory system deteriorated to the stage of death.

system can recover as long as the degree of hemor-
rhage is no greater than a certain critical amount.
Crossing this critical threshold by even a few milliliters
of blood loss makes the eventual difference between

ical level causes shock to become

and the condi-

tion becomes a vicious circle that eventually leads to
deterioration of the circulation and to death.

If shock is not severe enough to cause its own pro-

shock of this lesser degree is called nonprogressive

120

180

240

300

360

Arterial pressure

(percentage of control value)

100

Time in minutes

III

represents average results from six dogs.

ferent degrees of acute hemorrhage. Each curve

Time course of arterial pressure in dogs after dif-

Figure 24–2

flow, large amounts of acid, both carbonic acid and

blockage is sluggish blood flow in the microvessels.

the shock to progress. The initiating cause of this

vessels in the circulatory system, and this also causes

In time,

Blockage of Very Small Vessels—“Sludged Blood.”

pressure remains above 30 mm Hg.

strated. Fortunately, the vasomotor center usually does

discharges, but by the end of 10 to 15 minutes, the vaso-

first 4 to 8 minutes, the most intense of all sympathetic

causes, during the

plete circulatory arrest to the brain

active and finally totally inactive. For instance,

center so much that it, too, becomes progressively less

flow to the brain’s vasomotor center depresses the

However, there comes a point when diminished blood

especially helps prevent decreased arterial pressure.

sympathetic nervous system. This, as discussed earlier,

In the early stages of shock, various

Vasomotor Failure.

nutrition. In the latest stages of shock, however, dete-

hour or so of shock, but mainly because the heart has

little role in the condition of the person, partly because

the heart. In the early stages of shock, this plays very

another way, is eventual progressive deterioration of

shock, whether it is hemorrhagic in origin or caused in

Thus, one of the important features of progressive

heart deteriorated completely.

(after 4 hours of low coronary blood pressure), the

then, rapidly, during the last hour of the experiment

hours, the heart had deteriorated about 40 per cent;

oration of the heart during the first 2 hours, but by 4

or retransfusion of blood as required. Note from the

bled until the arterial pressure fell to 30 mm Hg, and

at different times after the onset of shock. A dog was

lated to the human heart from experiments in dogs,

Figure 24–4 shows cardiac output curves extrapo-

and more severe.

cycle has developed, whereby the shock becomes more

the cardiac output more. Thus, a positive feedback

This weakens the heart muscle and thereby decreases

required for adequate nutrition of the myocardium.

coronary blood flow decreases below that

When the arterial pressure falls low

important feedbacks are the following.

the shock to become progressive. Some of the more

further depress cardiac output in shock, thus causing

Figure 24–3 shows some of the positive feedbacks that

Circle of Cardiovascular Deterioration

“Progressive Shock” Is Caused by a Vicious

progressive stage.

hours, but recovery eventually takes place, provided

quantities of water and salt, may require from 1 to 48

Finally, readjustment of blood volume by absorption

all require 10 minutes to 1 hour to respond completely,

contraction of the blood vessels and venous reservoirs,

The angiotensin and vasopressin mechanisms, as

after hemorrhage.

The sympathetic reflexes provide immediate help

foods if able.

conservation of water and salt by the kidneys, and

from the interstitial spaces of the body,

tract, absorption of fluid into the blood capillaries

volume back toward normal,

Compensatory mechanisms that return the blood

increases water retention by the kidneys.

by the posterior pituitary gland,

Formation of vasopressin (antidiuretic hormone)

kidneys, both of which help prevent progression

Formation of angiotensin by the kidneys,

the diminished blood volume, so that the blood

falls below 50 mm Hg.

Central nervous system ischemic response,

Baroreceptor reflexes,

back to normal levels. They include the following:

The factors that cause a person to recover from

compensated shock,

shock.

Circulatory Shock and Physiology of Its Treatment

Chapter 24

281

It is also called

meaning

that the sympathetic reflexes and other factors com-
pensate enough to prevent further deterioration of the
circulation.

moderate degrees of shock are all the negative feed-
back control mechanisms of the circulation that
attempt to return cardiac output and arterial pressure

which elicit powerful

sympathetic stimulation of the circulation.

which elicits even more powerful sympathetic
stimulation throughout the body but is not
activated significantly until the arterial pressure

3. Reverse stress-relaxation of the circulatory system,

which causes the blood vessels to contract around

volume that is available more adequately fills the
circulation.

which

constricts the peripheral arteries and also causes
decreased output of water and salt by the

of shock.

which constricts

the peripheral arteries and veins and greatly

including absorption

of large quantities of fluid from the intestinal

increased thirst and increased appetite for salt,
which make the person drink water and eat salty

toward bringing about recovery because they become
maximally activated within 30 seconds to a minute

well as the reverse stress-relaxation that causes

but they aid greatly in increasing the arterial pressure
or increasing the circulatory filling pressure and
thereby increasing the return of blood to the heart.

of fluid from the interstitial spaces and intestinal tract,
as well as oral ingestion and absorption of additional

the shock does not become severe enough to enter the

Cardiac Depression.

enough,

demonstrating progressive deterioration of the heart

the pressure was held at this level by further bleeding

second curve in the figure that there was little deteri-

deterioration of the heart is not severe during the first

tremendous reserve capability that normally allows
it to pump 300 to 400 per cent more blood than is
required by the body for adequate bodywide tissue

rioration of the heart is probably the most important
factor in the final lethal progression of the shock.

circulatory reflexes cause intense activity of the

helps delay depression of the cardiac output and

com-

motor center becomes so depressed that no further
evidence of sympathetic discharge can be demon-

not fail in the early stages of shock if the arterial

blockage occurs in many of the very small blood

Because tissue metabolism continues despite the low

the chapter.

of shock, especially “septic shock,” discussed later in

cardiac depres-

cific effect on the heart muscle, causing

despite inadequate nutrition of the cells; this has a spe-

absorption of this toxic substance. The circulating

bacteria in the intestines. Diminished blood flow to

Endotoxin

endotoxin,

latory system. Quantitative studies have proved the

enzymes, that cause further deterioration of the circu-

substances, such as histamine, serotonin, and tissue

history of research in the field of shock, it has been

Throughout the

Release of Toxins by Ischemic Tissue.

making the shock still more severe. Capillary hypoxia

tissues. This decreases the blood volume even more,

permeability of the capillaries gradually increases,

capillary hypoxia and lack of other nutrients, the

Increased Capillary Permeability.

ficult for blood to flow through the microvasculature,

not become plugged, an increased tendency for the

small plugs in the small vessels. Even if the vessels do

nation, resulting in minute blood clots, leading to very

from the ischemic tissues, causes local blood aggluti-

blood. This acid, plus other deterioration products

lactic acid, continue to empty into the local blood

282

Unit IV

The Circulation

vessels and greatly increase the local acidity of the

blood cells to stick to one another makes it more dif-

giving rise to the term sludged blood.

After many hours of

and large quantities of fluid begin to transude into the

with a resultant further decrease in cardiac output,

does not cause increased capillary permeability until
the late stages of prolonged shock.

suggested that shock causes tissues to release toxic

significance of at least one toxin,

in some

types of shock.

Cardiac Depression Caused by Endotoxin.

is released from the bodies of dead gram-negative

the intestines often causes enhanced formation and

toxin then causes increased cellular metabolism

sion. Endotoxin can play a major role in some types

Decreased systemic blood flow

Increased

capillary

permeability

Decreased nutrition of tissues

Decreased cardiac nutrition

Decreased nutrition of brain

Decreased venous return

Decreased

blood volume

Tissue ischemia

Decreased cardiac output

Decreased arterial pressure

Decreased vasomotor

activity

Cardiac depression

Vascular dilation

Venous pooling

of blood

Decreased nutrition

of vascular system

Release of

toxins

Intravascular clotting

Different types of “positive feedback” that can lead to progression of shock.

Figure 24–3

tive metabolism of the foodstuffs. When this occurs,

oxygen to the tissues, which greatly diminishes oxida-

through the body. This results from poor delivery of

shock lung syndrome.

later. Deterioration of the lungs also often leads to res-

the epithelium of the kidney tubules, leading to kidney

orative lesions also occur in the kidneys, especially in

leading to the final irreversible stage of shock. Deteri-

theless, the cardiac lesions play an important role in

occurs in the liver, cannot be demonstrated. Never-

although here a definite repetitive pattern, such as

Similar punctate lesions occur in heart muscle,

passes through the liver sinusoids.

necrosis in the center of a liver lobule, the portion of

parts of the body. For instance, Figure 24–5 shows

laries than elsewhere. This is precisely the effect that

nutritive deficiency around the venous ends of capil-

same capillaries. Therefore, one would expect more

blood supplies than others. For instance, the cells adja-

damaged by shock, because some tissues have better

Different Organs.

Patchy Areas of

Tissue Necrosis in Severe Shock

depressing its contractility.

oxygenate the blood; and (3) the

lungs,

detoxification functions; (2) the

liver,

of many organs of the body, including especially (1)

are depressed as well, including almost 100 per

stages of shock. The actions of some hormones

4. Cellular metabolism of nutrients, such as glucose,

begin to break open, with intracellular release of

3. Lysosomes in the cells in widespread tissue areas

severely depressed.

in many other tissues of the body, becomes

2. Mitochondrial activity in the liver cells, as well as

addition, the cells begin to swell.

the cells, and potassium is lost from the cells. In

As a result, sodium and chloride accumulate in

1. Active transport of sodium and potassium

cells, but also partly because of the extreme exposure

as illustrated in Figure 24–5. This

liver,

tion occur throughout the body. One organ especially

severe, many signs of generalized cellular deteriora-

Circulatory Shock and Physiology of Its Treatment

Chapter 24

283

Generalized Cellular Deterioration.

As shock becomes

affected is the
occurs mainly because of lack of enough nutrients to
support the normally high rate of metabolism in liver

of the liver cells to any vascular toxin or other abnor-
mal metabolic factor occurring in shock.

Among the damaging cellular effects that are

known to occur in most body tissues are the following:

through the cell membrane is greatly diminished.

hydrolases that cause further intracellular
deterioration.

eventually becomes greatly depressed in the last

cent depression of the action of insulin.

All these effects contribute to further deterioration

the

with depression of its many metabolic and

with eventual

development of pulmonary edema and poor ability to

heart, thereby further

—

Necrosis Occur Because of Patchy Blood Flows in

Not all cells of the body are equally

cent to the arterial ends of capillaries receive better
nutrition than cells adjacent to the venous ends of the

Crowell discovered in studying tissue areas in many

the lobule that is last to be exposed to the blood as it

failure and occasionally uremic death several days

piratory distress and death several days later—called
the

Acidosis in Shock.

Most metabolic derangements that

occur in shocked tissue can lead to blood acidosis all

the cells obtain most of their energy by the anaerobic

Cardiac output (L

/min)

–

Right atrial pressure (mm Hg)

0 time

2 hours

4 hours

hours

5 hours

heart from data obtained in dog experiments by Dr. J. W. Crowell.)

rhagic shock begins. (These curves are extrapolated to the human

Cardiac output curves of the heart at different times after hemor-

Figure 24–4

tory shock. (Courtesy Dr. J. W. Crowell.)

Necrosis of the central portion of a liver lobule in severe circula-

Figure 24–5

without loss of red blood cells, can sometimes be

Loss of plasma from the circulatory system, even

energy compounds.

irreversibility, is this cellular depletion of these high-

deterioration in shock, and the one that is perhaps

Thus, one of the most devastating end results of

depleted, they are difficult to replenish.

the normal cellular amount an hour, meaning that

the adenosine phosphate system. New adenosine can

circulating blood and is converted into uric acid, a

Then

adenosine.

and, eventually,

monophosphate,

adenosine diphosphate, adenosine

degraded, and almost all the

shock. Essentially all the

the heart, are greatly diminished in severe degrees of

in the tissues of the body, especially in the liver and

The high-energy phosphate reserves

Depletion of Cellular High-Energy Phosphate Reserves in

normal for short periods.

ration. Therefore, in severe shock, a stage is eventually

developed, and so many other destructive factors are

released into the body fluids, so much acidosis has

has occurred, so many destructive enzymes have been

death. Beyond a certain point, so much tissue damage

a long period, depress heart pumping enough to cause

ability to pump blood but, over

the heart’s

fusions have less and less effect. By this time, multiple

output soon begins to fall again, and subsequent trans-

pressure) to return to normal. However, the cardiac

Figure 24–6 demonstrates this effect, showing that

few hours.

riorate, and death ensues in another few minutes to

output to normal or near normal for short periods, but

this irreversible stage, therapy can, on rare occasions,

Ironically, even in

irreversible stage of shock.

of saving the person’s life. The person is then said to

After shock has progressed to a certain stage, transfu-

feedback and vicious circle discussed in Chapter 1, one

powerful, leading to such rapid deterioration of the

recovery. But in severe degrees of shock, the deterio-

the positive feedback influences and, therefore, cause

interstitial spaces, and others—can easily overcome

reservoirs, absorption of fluid into the blood from the

anisms of the circulation—sympathetic reflexes,

In mild degrees of shock, the negative feedback mech-

lead to a vicious circle. Whether a vicious circle devel-

However, positive feedback does not necessarily

That is, each increase in the degree of shock causes a

positive feedback.

Progressive Shock

in Shock and the Vicious Circle of

leading to further progression of the shock itself.

of shock is both generalized and local tissue acidosis,

lar acidic substances. Thus, another deteriorative effect

intracellular carbonic acid; this, in turn, reacts with

of carbon dioxide. The carbon dioxide reacts locally

in the blood. In addition, poor

process of glycolysis, which leads to tremendous quan-

284

Unit IV

The Circulation

tities of excess lactic acid
blood flow through tissues prevents normal removal

in the cells with water to form high concentrations of

various tissue chemicals to form still other intracellu-

Positive Feedback Deterioration of Tissues

All the factors just discussed that can lead to further
progression of shock are types of

further increase in the shock.

ops depends on the intensity of the positive feedback.

reverse stress-relaxation mechanism of the blood

rative feedback mechanisms become more and more

circulation that all the normal negative feedback
systems of circulatory control acting together cannot
return the cardiac output to normal.

Considering once again the principles of positive

can readily understand why there is a critical cardiac
output level above which a person in shock recovers
and below which a person enters a vicious circle of cir-
culatory deterioration that proceeds until death.

Irreversible Shock

sion or any other type of therapy becomes incapable

be in the

return the arterial pressure and even the cardiac

the circulatory system nevertheless continues to dete-

transfusion during the irreversible stage can some-
times cause the cardiac output (as well as the arterial

deteriorative changes have occurred in the muscle
cells of the heart that may not necessarily affect

immediate

now in progress that even a normal cardiac output for
a few minutes cannot reverse the continuing deterio-

reached at which the person will die even though vig-
orous therapy might still return the cardiac output to

Irreversible Shock.

creatine phosphate has been

adenosine triphosphate

has downgraded to

much of this adenosine diffuses out of the cells into the

substance that cannot re-enter the cells to reconstitute

be synthesized at a rate of only about 2 per cent of

once the high-energy phosphate stores of the cells are

most significant for development of the final state of

Hypovolemic Shock Caused
by Plasma Loss

severe enough to reduce the total blood volume

120

150

Cardiac output

(percentage of normal)

100

Minutes

Progressive

stage

Hemorrhage

Transfusion

Irreversible shock

Failure of transfusion to prevent death in irreversible shock.

Figure 24–6

capillary permeability, with rapid loss of fluid and

reduced arterial pressure; and (3) greatly increased

(2) dilation of the arterioles, resulting in greatly

tion, thus causing a marked decrease in venous return;

The histamine causes (1) an

histamine-like substance.

is sensitive enters the circulation. One of the principal

drastically. This is discussed in Chapter 34. It results

neurons in the brain stem, with consequent

stimulation, prolonged ischemia (lasting longer

Also, even though brain ischemia for a few

paralysis. Many patients who have had brain

the way up the spinal cord, blocks the sympathetic

paralysis, with resulting neurogenic shock.

venous return to the heart. Diminished venous return

the mean systemic filling pressure,

The role of vascular capacity in helping to regulate

neurogenic shock.

massive dilation of the veins. The resulting condition

throughout the body, resulting especially in

incapable of filling the circulatory system adequately.

volume. Instead, the

Vascular Capacity

Neurogenic Shock—Increased

shock caused by loss of vasomotor tone, as discussed

mainly from hypovolemia, although there might also

In summary, traumatic shock seems to result

failed to show significant toxic elements.

the causes of shock after trauma. However, cross-

Various attempts have been made to implicate toxic

tissues. This results in greatly reduced plasma volume,

occur even without hemorrhage, because extensive

from hemorrhage caused by the trauma, but it can also

is trauma to the body. Often the shock results simply

by Trauma

the adrenocortical hormone aldosterone.

chloride, and water, which occurs in the absence of

cortices, with loss of aldosterone secretion and conse-

fluid and electrolytes, or (5) destruction of the adrenal

fluid by nephrotic kidneys, (4) inadequate intake of

loss in severe diarrhea or vomiting, (3) excess loss of

this type of shock are (1) excessive sweating, (2) fluid

that resulting from hemorrhage. Some of the causes of

this, too, can reduce the

gishness of blood flow.

the remaining blood, and this exacerbates the slug-

plicating factor: the blood viscosity increases greatly as

caused by hemorrhage, except for one additional com-

The hypovolemic shock that results from plasma

other denuding conditions of the skin, so much

2. In almost all patients who have

well as reduced plasma volume.

increases intestinal capillary pressure. This in turn

venous blood flow in the intestinal walls, which

reduced plasma volume. Distention of the

almost all details to that caused by hemorrhage. Severe

markedly, causing typical hypovolemic shock similar in

Circulatory Shock and Physiology of Its Treatment

Chapter 24

285

plasma loss occurs in the following conditions:
1. Intestinal obstruction is often a cause of severely

intestine in intestinal obstruction partly blocks

causes fluid to leak from the capillaries into the
intestinal walls and also into the intestinal lumen.
Because the lost fluid has a high protein content,
the result is reduced total blood plasma protein as

severe burns or

plasma is lost through the denuded skin areas
that the plasma volume becomes markedly
reduced.

loss has almost the same characteristics as the shock

a result of increased red blood cell concentration in

Loss of fluid from all fluid compartments of the

body is called dehydration;
blood volume and cause hypovolemic shock similar to

quent failure of the kidneys to reabsorb sodium,

Hypovolemic Shock Caused

One of the most common causes of circulatory shock

contusion of the body can damage the capillaries
sufficiently to allow excessive loss of plasma into the

with resultant hypovolemic shock.

factors released by the traumatized tissues as one of

transfusion experiments into normal animals have

be a moderate degree of concomitant neurogenic

next.

Shock occasionally results without any loss of blood

vascular capacity increases so

much that even the normal amount of blood becomes

One of the major causes of this is sudden loss of vaso-
motor tone

is known as

circulatory function was discussed in Chapter 15,
where it was pointed out that either an increase in vas-
cular capacity or a decrease in blood volume reduces

which reduces

caused by vascular dilation is called venous pooling of
blood.

Causes of Neurogenic Shock.

Some neurogenic factors

that can cause loss of vasomotor tone include the
following:
1. Deep general anesthesia often depresses the

vasomotor center enough to cause vasomotor

2. Spinal anesthesia, especially when this extends all

nervous outflow from the nervous system and can
be a potent cause of neurogenic shock.

3. Brain damage is often a cause of vasomotor

concussion or contusion of the basal regions of
the brain develop profound neurogenic shock.

minutes almost always causes extreme vasomotor

than 5 to 10 minutes) can cause the opposite
effect—total inactivation of the vasomotor

development of severe neurogenic shock.

Anaphylactic Shock and
Histamine Shock

Anaphylaxis is an allergic condition in which the
cardiac output and arterial pressure often decrease

primarily from an antigen-antibody reaction that takes
place immediately after an antigen to which the person

effects is to cause the basophils in the blood and mast
cells in the pericapillary tissues to release histamine or
a
increase in vascular capacity because of venous dila-

molecular size to exert colloid osmotic pressure. One

To remain in the circulation, the plasma substitute

ment of the body’s extracellular fluid electrolytes on

In addition, the solution must be nontoxic and must

filter through the capillary pores into the tissue spaces.

that it remain in the circulatory system—that is, not

The principal

tions as plasma. One of these is dextran solution.

Sometimes plasma is unavailable. In these instances,

Therefore, in emergency conditions, it is reasonable to

sequences result, if cardiac output is adequate.

Plasma cannot restore a normal hematocrit, but the

blood volume and restores normal hemodynamics.

battlefield conditions. Plasma can usually substitute

Whole blood is not always available, such as under

tion of plasma; when dehydration is the cause, admin-

caused by plasma loss, the best therapy is administra-

usually transfusion of whole blood. If the shock is

caused by hemorrhage, the best possible therapy is

Blood and Plasma Transfusion.

Physiology of Treatment

the two conditions.

ent from the end stages of hemorrhagic shock, even

The end stages of septic shock are not greatly differ-

walls. There finally comes a point at which deteriora-

from the bacteria, with resultant loss of plasma into the

becomes more severe, the circulatory system usually

signs of the bacterial infection. As the infection

In early stages of septic shock, the patient usually

hemorrhaging occurs in many tissues, especially in

blood clotting factors to be used up, so that

Also, this causes the

areas of the body, a condition called

5. Development of micro–blood clots in widespread

agglutination in response to degenerating tissues.

4. Sludging of the blood, caused by red cell

high body temperature.

elsewhere in the body, resulting from bacterial

3. High cardiac output in perhaps half of patients,

especially in the infected tissues.

2. Often marked vasodilation throughout the body,

1. High fever.

condition. Some features often observed are:

types of septic shock, it is difficult to categorize this

kidney or urinary tract, often caused by colon

5. Infection spreading into the blood from the

liver.

of the blood to the internal organs, especially the

first through peripheral tissues and finally by way

specifically from gas gangrene bacilli, spreading

4. Generalized gangrenous infection resulting

3. Generalized bodily infection resulting from

intestinal disease and sometimes by wounds.

gastrointestinal system, sometimes caused by

2. Peritonitis resulting from rupture of the

unsterile conditions.

uterus and fallopian tubes, sometimes resulting

1. Peritonitis caused by spread of infection from the

the most frequent cause of shock-related death in the

because other than cardiogenic shock, septic shock is

Septic shock is extremely important to the clinician,

produces different effects.

tissue to another and causing extensive damage. There

widely disseminated to many areas of the body, with

by most clinicians. This refers to a bacterial infection

septic shock

name “blood poisoning” is now called

causes “histamine shock,” which has characteristics

serious shock that the person dies within minutes.

protein into the tissue spaces. The net effect is a great

286

Unit IV

The Circulation

reduction in venous return and sometimes such

Intravenous injection of large amounts of histamine

almost identical to those of anaphylactic shock.

Septic Shock

A condition that was formerly known by the popular

the infection being borne through the blood from one

are many varieties of septic shock because of the many
types of bacterial infections that can cause it and
because infection in different parts of the body

modern hospital.

Some of the typical causes of septic shock include

the following:

from instrumental abortion performed under

spread of a skin infection such as streptococcal
or staphylococcal infection.

bacilli.

Special Features of Septic Shock.

Because of the multiple

caused by arteriolar dilation in the infected tissues
and by high metabolic rate and vasodilation

toxin stimulation of cellular metabolism and from

disseminated

intravascular coagulation.

the gut wall of the intestinal tract.

does not have signs of circulatory collapse but only

becomes involved either because of direct extension
of the infection or secondarily as a result of toxins

infected tissues through deteriorating blood capillary

tion of the circulation becomes progressive in the same
way that progression occurs in all other types of shock.

though the initiating factors are markedly different in

in Shock

Replacement Therapy

If a person is in shock

istration of an appropriate electrolyte solution can
correct the shock.

adequately for whole blood because it increases the

human body can usually stand a decrease in hemat-
ocrit to about half of normal before serious con-

use plasma in place of whole blood for treatment of
hemorrhagic or most other types of hypovolemic
shock.

various plasma substitutes have been developed that
perform almost exactly the same hemodynamic func-

Dextran Solution as a Plasma Substitute.

requirement of a truly effective plasma substitute is

contain appropriate electrolytes to prevent derange-

administration.

must contain some substance that has a large enough

of the most satisfactory substances developed for this

no intravascular blood clotting could occur. In this

all the blood was removed from the animal’s blood

instance, in animal experiments performed by Crowell,

rioration of the brain during circulatory arrest. For

the brain, this will also prevent most of the early dete-

However, experiments have shown that if blood clots

For many years, it was taught that this detrimental

amounts of mental power.

nent brain damage in more than half of patients.

In general, more than 5 to 8 minutes of total circula-

Effect of Circulatory Arrest

patient’s lungs with adequate quantities of ventilatory

procedures, while at the same time supplying the

effect of the anesthesia itself. A normal cardiac rhythm

strong electroshock of the heart, the basic principles

Ventricular fibrillation can usually be stopped by

cardiac arrest

culatory arrest, in which all blood flow stops. This

Circulatory Arrest

glucose by the severely damaged cells.

cells, thus preventing deterioration from this source;

release of lysosomal enzymes into the cytoplasm of the

heart in the late stages of shock; (2) glucocorticoids

reasons: (1) experiments have shown empirically that

Treatment with Glucocorticoids (Adrenal Cortex Hormones That

is far less beneficial than one might expect, because the

of benefit in many instances. However, this frequently

the tissues, giving the patient oxygen to breathe can be

Oxygen Therapy.

thereby also increasing cardiac output. This head-

hemorrhagic and neurogenic shock, placing the patient

falls too low in most types of shock, especially in

When the pressure

Treatment by the Head-Down Position.

reflexes already; so much norepinephrine and epi-

this type of shock, the sympathetic nervous system is

valuable in hemorrhagic shock. The reason is that in

thomimetic drug is often lifesaving.

Therefore, either norepinephrine or another sympa-

that opposes the vasodilating effect of histamine.

which excess histamine plays a prominent role. The

anaphylactic shock,

The second type of shock in which sympatho-

system is severely depressed. Administering a sympa-

neurogenic shock,

proved to be especially beneficial. The first of these is

In two types of shock, sympathomimetic drugs have

norepinephrine.

, and a large number of long-acting

pathetic stimulation. These drugs include

Treatment of Shock with

most fluid replacement therapy.

therefore, solutions containing this substance have

Few toxic reactions have been observed when using

agents.

fore, can replace plasma proteins as colloid osmotic

size do not pass through the capillary pores and, there-

the desired value. Dextrans of appropriate molecular

By varying the growth conditions of the bacteria, the

be manufactured using a bacterial culture procedure.

product of their growth, and commercial dextran can

glucose. Certain bacteria secrete dextran as a by-

Circulatory Shock and Physiology of Its Treatment

Chapter 24

287

purpose is dextran, a large polysaccharide polymer of

molecular weight of the dextran can be controlled to

purified dextran to provide colloid osmotic pressure;

proved to be a satisfactory substitute for plasma in

Sympathomimetic Drugs—Sometimes
Useful, Sometimes Not

A sympathomimetic drug is a drug that mimics sym-

norepineph-

rine, epinephrine
drugs that have the same effect as epinephrine and

in which the sympathetic nervous

thomimetic drug takes the place of the diminished
sympathetic actions and can often restore full circula-
tory function.

mimetic drugs are valuable is

sympathomimetic drugs have a vasoconstrictor effect

Sympathomimetic drugs have not proved to be very

almost always maximally activated by the circulatory

nephrine are already circulating in the blood that sym-
pathomimetic drugs have essentially no additional
beneficial effect.

Other Therapy

with the head at least 12 inches lower than the feet
helps tremendously in promoting venous return,

down position is the first essential step in the treat-
ment of many types of shock.

Because the major deleterious effect of

most types of shock is too little delivery of oxygen to

problem in most types of shock is not inadequate oxy-
genation of the blood by the lungs but inadequate
transport of the blood after it is oxygenated.

Control Glucose Metabolism).

Glucocorticoids are fre-

quently given to patients in severe shock for several

glucocorticoids frequently increase the strength of the

stabilize lysosomes in tissue cells and thereby prevent

and (3) glucocorticoids might aid in the metabolism of

A condition closely allied to circulatory shock is cir-

occurs frequently on the surgical operating table as a
result of

or ventricular fibrillation.

of which are described in Chapter 13.

Cardiac arrest often results from too little oxygen in

the anesthetic gaseous mixture or from a depressant

can usually be restored by removing the anesthetic and
immediately applying cardiopulmonary resuscitation

oxygen.

on the Brain

A special problem in circulatory arrest is to prevent
detrimental effects in the brain as a result of the arrest.

tory arrest can cause at least some degree of perma-

Circulatory arrest for as long as 10 to 15 minutes
almost always permanently destroys significant

effect on the brain was caused by the acute cerebral
hypoxia that occurs during circulatory arrest.

are prevented from occurring in the blood vessels of

vessels at the beginning of circulatory arrest and
then replaced at the end of circulatory arrest so that

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Wilson M, Davis DP, Coimbra R: Diagnosis and monitoring

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myocardial infarction: an interpretative review. J Surg Res

Wernly JA: Ischemia, reperfusion, and the role of surgery in

old disease, new hope. BMJ 327:974, 2003.

Toh CH, Dennis M: Disseminated intravascular coagulation:

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Directed Therapy Collaborative Group. Early goal-

Rivers E, Nguyen B, Havstad S, et al: The Early Goal-

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Proctor KG: Blood substitutes and experimental models of

evidence? BMJ 327:1332, 2003.

Adrenaline in the treatment of anaphylaxis: what is the

McLean-Tooke AP, Bethune CA, Fay AC, Spickett GP:

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Martin GS, Mannino DM, Eaton S, Moss M: The epidemiol-

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Ledgerwood AM, Lucas CE: A review of studies on the

Saunders, 1973.

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Guyton AC, Jones CE, Coleman TG: Circulatory Physiology:

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Granger DN, Stokes KY, Shigematsu T, et al: Splanchnic

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on blood coagulation: a comparative review. Crit Care

de Jonge E, Levi M: Effects of different plasma substitutes

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Crowell JW, Smith EE: Oxygen deficit and irreversible

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of the neurons.

blockage of many small blood vessels by blood clots,

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288

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The Circulation

to 30 minutes of circulatory arrest without permanent

tokinase (to prevent blood coagulation) before cardiac
arrest was shown to increase the survivability of the
brain up to two to four times longer than usual.

It is likely that the severe brain damage that occurs

from circulatory arrest is caused mainly by permanent

thus leading to prolonged ischemia and eventual death

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