Cardiac Failure pdf - The Circulation

sympathetics become strongly stimulated within a few seconds, and the

ing the sympathetic nervous system. But whatever the reflexes might be, the

reflexes that originate in the damaged heart

central nervous system ischemic response

, the

chemoreceptor reflex

, which is activated by diminished arterial pressure. It is probable

in Chapter 18 are immediately activated. The best known of these is the

cardiac output falls precariously low, many of the circulatory reflexes discussed

When the

Compensation for Acute Cardiac Failure by Sympathetic Nervous Reflexes.

heart, as follows.

reflexes occur immediately and compensate, to a great extent, for the damaged

perhaps a few hours, but it is likely to be associated with fainting. Fortunately,

the right atrium. This low cardiac output is still sufficient to sustain life for

4 mm Hg

two-fifths normal, whereas the right atrial pressure has risen to

than point A, illustrating that the cardiac output has fallen to 2 L/min, about

Within a few seconds, a new circulatory state is established at point B rather

becomes greatly lowered, falling to the lowest curve at the bottom of the graph.

Immediately after the heart becomes damaged, the cardiac output curve

resting conditions of 5 L/min and a right atrial pressure of 0 mm Hg.

curve is the normal operating point, showing a normal cardiac output under

top curve of this figure shows a normal cardiac output curve. Point A on this

after an acute myocardial infarction are shown graphically in Figure 22–1. The

The progressive changes in heart pumping effectiveness at different times

veins, resulting in increased venous pressure.

main effects occur: (1) reduced cardiac output and (2) damming of blood in the

tion, the pumping ability of the heart is immediately depressed. As a result, two

If a heart suddenly becomes severely damaged, such as by myocardial infarc-

Acute Effects of Moderate Cardiac Failure

Dynamics of the Circulation in Cardiac Failure

the heart to pump enough blood to satisfy the needs of the body.

The term “cardiac failure” means simply failure of

congenital heart disease.

blockage of the coronary blood vessels. In Chapter 23, we discuss valvular and

mality that makes the heart a hypoeffective pump. In this chapter, we discuss

heart, vitamin B deficiency, primary cardiac muscle disease, or any other abnor-

damaged heart valves, external pressure around the

blood flow. However, failure can also be caused by

The cause usually is decreased contractility of the

failure”). This can result from any heart condition

Cardiac Failure

258

One of the most important ailments that must be
treated by the physician is cardiac failure (“heart

that reduces the ability of the heart to pump blood.

myocardium resulting from diminished coronary

mainly cardiac failure caused by ischemic heart disease resulting from partial

Definition of Cardiac Failure.

because venous blood returning to the heart from the body is dammed up in

this acute stage usually lasts for only a few seconds because sympathetic nerve

barore-

ceptor reflex
that the

and even

also contribute to activat-

water to equal salt and water intake. Therefore, fluid

still more, blood flow to the kidneys finally becomes

When the heart’s pumping capability is reduced

in a quiet resting state.

reduced to as low as 40 to 50 per cent of normal, the

fact that even when the heart’s pumping ability is

for the heart’s diminished pumping ability—enough in

If the heart is not too greatly damaged, this

it distends the veins, which

. Second,

causing venous flow of blood toward the heart

pressure, which

in two ways: First, it increases the mean systemic filling

The increased blood volume increases venous return

always to have a detrimental effect in cardiac failure.

sure remain significantly less than normal, and urine

general, the urine output remains reduced below

output falls to one-half to two-thirds normal. In

function, sometimes causing anuria when the cardiac

Volume Occur for Hours to Days

Renal Retention of Fluid and Increase in Blood

trated by the light green curve in Figure 22–1; this was

heart itself over a period of weeks to months, as illus-

kidneys and (2) varying degrees of recovery of the

mainly by two events: (1) retention of fluid by the

prolonged semi-chronic state begins, characterized

After the first few minutes of an acute heart attack, a

Retention Helps to Compensate

Chronic Stage of Failure—Fluid

or she remains quiet, although the pain might persist.

thetic reflex compensations, the cardiac output may

fainting. Shortly thereafter, with the aid of the sympa-

a sudden, moderate heart attack might experience

oped in about 30 seconds. Therefore, a person who has

The sympathetic reflexes become maximally devel-

4.2 L/min and a right atrial pressure of 5 mm Hg.

is depicted by point C, showing a cardiac output of

blood. Thus, in Figure 22–1, the new circulatory state

usual, and the right atrial pressure rises still further,

the veins back into the heart. Therefore, the damaged

greatly increases the tendency for blood to flow from

cussed in Chapter 20, this increased filling pressure

mm Hg, almost 100 per cent above normal. As dis-

blood vessels of the circulation, especially the veins,

cardiac output curve.

strated in Figure 22–1, showing after sympathetic com-

. This effect is also demon-

one way or another

functional muscle. Thus,

tion, in this way partially compensating for the non-

functional and part of it is still normal, the normal

this damaged musculature. If part of the muscle is non-

still functional, sympathetic stimulation strengthens

and second on the peripheral vasculature. If all the

effects on the circulation: first on the heart itself,

reciprocally inhibited at the same time.

Cardiac Failure

Chapter 22

259

parasympathetic nervous signals to the heart become

Strong sympathetic stimulation has two major

ventricular musculature is diffusely damaged but is

muscle is strongly stimulated by sympathetic stimula-

the heart,

becomes a stronger pump

pensation about twofold elevation of the very low

Sympathetic stimulation also increases venous

return because it increases the tone of most of the

raising the mean systemic filling pressure to 12 to 14

heart becomes primed with more inflowing blood than

which helps the heart to pump still larger quantities of

nothing more than cardiac pain and a few seconds of

return to a level adequate to sustain the person if he

Cardiac Output

also discussed in Chapter 21.

A low cardiac output has a profound effect on renal

normal as long as the cardiac output and arterial pres-

output usually does not return all the way to normal
after an acute heart attack until the cardiac output and
arterial pressure rise either all the way back to normal
or almost to normal.

Moderate Fluid Retention in Cardiac Failure Can Be Beneficial.

Many cardiologists formerly considered fluid retention

But it is now known that a moderate increase in body
fluid and blood volume is an important factor in
helping to compensate for the diminished pumping
ability of the heart by increasing the venous return.

increases the pressure gradient for

reduces the venous resist-

ance and allows even more ease of flow of blood to the
heart.

increased venous return can often fully compensate

increased venous return can often cause an entirely
normal cardiac output as long as the person remains

too low for the kidneys to excrete enough salt and

+8 +10 +12 +14

Cardiac output (L

/min)

–4

–

Right atrial pressure (mm Hg)

Normal heart

Partially recovered heart

Damaged heart + sympathetic stimulation

Acutely damaged heart

sure change progressively from point A to point D (illustrated by

myocardial infarction. Both the cardiac output and right atrial pres-

Progressive changes in the cardiac output curve after acute

Figure 22–1

the black line) over a period of seconds, minutes, days, and
weeks.

compensation, either by sympathetic nervous reflexes

If the heart becomes severely damaged, no amount of

reserve is discussed more fully later in the chapter.

compensated heart failure. This concept of cardiac

cardiac reserve

fore, it is said that the

capacity to the levels required for the exercise. There-

When a person is in compensated heart failure, any

progressive stages of damage.

the damage often has occurred a little at a time, and

degrees of “compensated heart failure.” These persons

Thus many people, especially older people, have

normal. This demonstrates that an increase in right

light green curve, is still depressed to less than one-half

recovered heart, as depicted by the plateau level of the

Note especially in Figure

ery and fluid retention (point D). This final state is

by sympathetic stimulation (point C), and final return

B), the rise in cardiac output toward normal caused

(point A), the state a few seconds after the heart attack

by the black curve in Figure 22–1. The progression of

tion of fluid. All these changes are shown graphically

seconds to 1 minute; and (3) chronic compensations

nervous system, which occurs mainly within the first 30

cardiac damage; (2) compensation by the sympathetic

after an acute, moderate heart attack, we can divide

To summarize the events discussed in the past few sec-

After Acute Cardiac Failure

the acute stage of cardiac failure gradually disappear.

recovers even slightly, the fast pulse rate, cold skin,

sympathetic stimulation can. Therefore, as the heart

the following reasons: The partial recovery of the

adequate fluid volume has been retained, the sympa-

this figure, the person now has essentially normal car-

. Therefore, except for the

further fluid retention occurs, except that

renal output of fluid also returns to normal, and no

atrial pressure increased to 6 mm Hg.

culation is now changed from point C to point D, which

has risen even more. As a result, the state of the cir-

markedly as well; therefore, the right atrial pressure

the tendency for venous return has increased

or so after acute myocardial infarction. By this time,

Figure 22–1

The Cardiac Output Curve After Partial Recovery.

months.

final state of recovery within 5 to 7 weeks, although

infarction, the heart ordinarily recovers rapidly during

almost complete recovery. After acute myocardial

cardiac damage, and it varies from no recovery to

The degree of recovery depends on the type of

way offsetting much of the cardiac damage.

portion of the heart musculature hypertrophies, in this

to become functional again. Also, the undamaged

eral portions of the infarcted area of the heart, often

restore normal cardiac function. For instance, a new

of myocardial infarction, the natural reparative

Myocardial Infarction

Recovery of the Myocardium After

are discussed in later sections of this chapter.

of the body.These detrimental effects of excessive fluid

filtration of fluid into the lungs, causing pulmonary

the heart, thus weakening the heart still more; (2)

cal consequences. They include (1) overstretching of

ate fluid retention in cardiac failure, in severe failure

severe edema develops throughout the body, which

on the circulation. Instead,

, this excess fluid no

Furthermore, because the heart is already pumping at

major therapeutic procedures are used to prevent this.

retention begins and continues indefinitely, unless

260

Unit IV

The Circulation

its maximum pumping capacity
longer has a beneficial effect

can be very detrimental in itself and can lead to death.

Detrimental Effects of Excess Fluid Retention in Severe Cardiac
Failure.

In contrast to the beneficial effects of moder-

extreme excesses of fluid can have serious physiologi-

edema and consequent deoxygenation of the blood;
and (3) development of extensive edema in most parts

After a heart becomes suddenly damaged as a result

processes of the body begin immediately to help

collateral blood supply begins to penetrate the periph-

causing much of the heart muscle in the fringe areas

the first few days and weeks and achieves most of its

mild degrees of additional recovery can continue for

shows function of the partially recovered heart a week

considerable fluid has been retained in the body and

shows a normal cardiac output of 5 L/min but right

Because the cardiac output has returned to normal,

the retention

of fluid that has already occurred continues to maintain
moderate excesses of fluid
high right atrial pressure represented by point D in

diovascular dynamics as long as he or she remains at
rest.

If the heart recovers to a significant extent and if

thetic stimulation gradually abates toward normal for

heart can elevate the cardiac output curve the same as

and pallor resulting from sympathetic stimulation in

Summary of the Changes That Occur

—

“Compensated Heart Failure”

tions describing the dynamics of circulatory changes

the stages into (1) the instantaneous effect of the

resulting from partial heart recovery and renal reten-

this curve shows the normal state of the circulation

but before sympathetic reflexes have occurred (point

of the cardiac output almost exactly to normal after
several days to several weeks of partial cardiac recov-

called compensated heart failure.

Compensated Heart Failure.

22–1 that the maximum pumping ability of the partly

atrial pressure can maintain the cardiac output at a
normal level despite continued weakness of the heart.

normal resting cardiac outputs but mildly to moder-
ately elevated right atrial pressures because of various

may not know that they have cardiac damage because

the compensation has occurred concurrently with the

attempt to perform heavy exercise usually causes
immediate return of the symptoms of acute failure
because the heart is not able to increase its pumping

is reduced in

Dynamics of Severe Cardiac Failure—
Decompensated Heart Failure

reducing water and salt intake, which brings about a

tion normally again, or (2)

, so that

istration of a cardiotonic drug, such as

in any one of several ways, especially by admin-

The decompensation

Treatment of Decompensation.

hunger). All clinicians know that lack of appropriate

edema, especially edema of the lungs, which leads

completely. Clinically, one detects this serious condi-

even moderate quantities of blood and, therefore, fails

systemic filling pressure, and (3) progressive elevation

Thus, one can see from this analysis that failure of

the patient dies. This state of heart failure in which the

approached or reached incompatibility with life, and

the right atrial pressure 16 mm Hg. This state has

of the circulation has reached point F on the curve,

occurs). Consequently, within a few days, the state

normal renal function, so that fluid retention not

detrimental than beneficial to the circulation. Yet the

diminish the heart’s pumping performance. It is

edema of the heart muscle, and other factors that

level. This decline is caused by overstretch of the heart,

atrial pressure has risen still further, but by now,

After another few days of fluid retention, the right

balance.

becomes that depicted by point D. Still, the cardiac

pressure rises to 9 mm Hg, and the circulatory state

to be retained. After another day or so, the right atrial

normal renal output of fluid; therefore, fluid continues

and the cardiac output to 4.2 L/min. Note again that

the circulation changes in Figure 22–2 from point B to

the right atrial pressure. After 1 day or so, the state of

peripheral veins into the right atrium, thus increasing

increasing quantities of blood from the person’s

circulation continues to rise; this forces progressively

volume, the mean systemic filling pressure of the

and the body fluid volume increases progressively.

output below this level, all the fluid-retaining mecha-

to be as great as the intake of these. At any cardiac

fluid balance—that is, for the output of salt and water

output level of 5 L/min. This is approximately the crit-

Note the straight line in Figure 22–2, at a cardiac

tatively in the following way.

cause of death. These events can be explained quanti-

to cause adequate kidney excretion of fluid; therefore,

good condition, but this state will not remain stable

to 5 mm Hg. The person appears to be in reasonably

tion has begun. At this time, the cardiac output has

compensation has occurred, and point B, the state a

severely weakened. Point A on this curve represents

ent times (points A to F) after the heart has become

Figure

Thus, the main cause of decom-

pensated heart failure.

events eventually leads to death. This is called

develops more and more edema, and this state of

Therefore, fluid continues to be retained, the person

sequence, the cardiac output cannot rise high enough

ened heart pump a normal cardiac output. As a con-

or by fluid retention, can make the excessively weak-

Cardiac Failure

Chapter 22

261

to make the kidneys excrete normal quantities of fluid.

decom-

pensated heart failure is failure of the heart to pump
sufficient blood to make the kidneys excrete daily the
necessary amounts of fluid.

Graphical Analysis of Decompensated Heart Failure.

22–2 shows greatly depressed cardiac output at differ-

the approximate state of the circulation before any

few minutes later after sympathetic stimulation has
compensated as much as it can but before fluid reten-

risen to 4 L/min and the right atrial pressure has risen

because the cardiac output has not risen high enough

fluid retention continues and can eventually be the

ical cardiac output level that is required in the normal
adult person to make the kidneys re-establish normal

nisms discussed in the earlier section remain in play

And because of this progressive increase in fluid

point C—the right atrial pressure rising to 7 mm Hg

the cardiac output is still not high enough to cause

output is not enough to establish normal fluid

cardiac function is beginning to decline toward a lower

now clear that further retention of fluid will be more

cardiac output still is not high enough to bring about

only continues but accelerates because of the falling
cardiac output (and falling arterial pressure that also

with the cardiac output now less than 2.5 L/min and

failure continues to worsen is called decompensated
heart failure.

the cardiac output (and arterial pressure) to rise to the
critical level required for normal renal function results
in (1) progressive retention of more and more fluid,
which causes (2) progressive elevation of the mean

of the right atrial pressure until finally the heart is so
overstretched or so edematous that it cannot pump

tion of decompensation principally by the progressing

to bubbling rales in the lungs and to dyspnea (air

therapy when this state of events occurs leads to rapid
death.

process can often be stopped by (1) strengthening the
heart

digitalis

the heart becomes strong enough to pump adequate
quantities of blood required to make the kidneys func-

administering diuretic drugs

to increase kidney excretion while at the same time

balance between fluid intake and output despite low
cardiac output.

+12

+16

/min)

2.5

5.0

Cardiac output

–

Right atrial pressure (mm Hg)

Critical cardiac output level

for normal fluid balance

from point A to point F, until death occurs.

pressure over a period of days, and the cardiac output progresses

. Progressive fluid retention raises the right atrial

heart disease

Greatly depressed cardiac output that indicates

Figure 22–2

decompensated

can be elevated high enough, the coronary blood flow

to sustain the arterial pressure. If the arterial pressure

blood, plasma, or a blood pressure–raising drug is used

shows signs of deterioration. Also, infusion of whole

problems in the management of acute heart attacks.

pressure) to a life-sustaining level. Therefore, treat-

Physiology of Treatment.

this reason, in treating myocardial infarction, it is

set off a vicious circle of cardiac deterioration. For

even a small decrease in arterial pressure can now

pressure falls below 80 to 90 mm Hg. In other words,

vessel, deterioration sets in when the coronary arterial

before cardiac deterioration sets in. However, in a

For instance, in a healthy heart, the arterial pres-

pounded by already existing coronary vessel blockage.

by myocardial infarction, this problem is greatly com-

of cardiac deterioration. In cardiogenic shock caused

worse, the process eventually becoming a vicious circle

pressure fall still more, which makes the shock still

makes the heart still weaker, which makes the arterial

reduces the coronary blood supply even more. This

is, the low arterial pressure that occurs during shock

supply is reduced during the course of the shock. That

emphasizes the tendency for the heart to become pro-

The discussion of circulatory shock in Chapter 24

ops cardiogenic shock, the survival rate is often less

. Once a person devel-

cardiac shock

shock

cardiogenic

tening death. This circulatory shock syndrome caused

with the remainder of the body), deteriorates, thus has-

system suffers from lack of nutrition, and it, too (along

explained in Chapter 24. Even the cardiovascular

The picture then is one of circulatory shock, as

often leading to death within a few hours to a few days.

body tissues begin to suffer and even to deteriorate,

required to keep the body alive. Consequently, all the

cardiac deterioration, the heart becomes incapable of

Cardiogenic Shock

Low-Output Cardiac Failure—

which we discuss more fully later in the chapter.

it can cause death by suffocation in 20 to 30 minutes,

. In severe, acute left heart failure,

Thus, among the most important problems of left

stitial spaces and alveoli, resulting in pulmonary

osmotic pressure of the plasma, about 28 mm Hg, fluid

pulmonary capillary pressure increases, and if this rises

As the volume of blood in the lungs increases, the

a result, the

by the left heart into the systemic circulation. As

be pumped into the lungs with usual right heart vigor,

comitant failure of the right side, blood continues to

When the left side of the heart fails without con-

unilateral heart failure.

without significant failure of the left side. Therefore,

sided failure, and in rare instances, the right side fails

failure, left-sided failure predominates over right-

number of patients, especially those with early acute

sidered failure of the heart as a whole. Yet, in a large

In the discussions thus far in this chapter, we have con-

Unilateral Left Heart Failure

slightly.

mechanism a moderate amount using digitalis, allow-

increase the muscle contractile force. Therefore, it is

case of a failing heart, extra calcium is needed to

pumps calcium ions out of the muscle. However, in the

brane of the cardiac muscle fibers. This pump normally

cause full contraction of the muscle. One effect of dig-

therefore, cannot release enough calcium ions into

failing heart muscle, the sarcoplasmic reticulum fails

the quantity of calcium ions in muscle fibers. In the

heart failure.

myocardium as much as 50 to 100 per cent. Therefore,

person with a chronically failing heart, the same drugs

the cardiac muscle. However, when administered to a

administered to a person with a healthy heart, have

Cardiotonic drugs, such as digitalis, when

Mechanism of Action of the Cardiotonic Drugs Such as

re-establishing normal fluid balance, so that at least as

262

Unit IV

The Circulation

Both methods stop the decompensation process by

much fluid leaves the body as enters it.

Digitalis.

little effect on increasing the contractile strength of

can sometimes increase the strength of the failing

they are one of the mainstays of therapy in chronic

Digitalis and other cardiotonic glycosides are

believed to strengthen heart contraction by increasing

to accumulate normal quantities of calcium and,

the free-fluid compartment of the muscle fibers to

italis is to depress the calcium pump of the cell mem-

usually beneficial to depress the calcium pumping

ing the muscle fiber intracellular calcium level to rise

we need especially to discuss the special features of

whereas it is not pumped adequately out of the lungs

mean pulmonary filling pressure rises

because of shift of large volumes of blood from the sys-
temic circulation into the pulmonary circulation.

above a value approximately equal to the colloid

begins to filter out of the capillaries into the lung inter-

edema.

heart failure are pulmonary vascular congestion and
pulmonary edema
pulmonary edema occasionally occurs so rapidly that

In many instances after acute heart attacks and
often after prolonged periods of slow progressive

pumping even the minimal amount of blood flow

by inadequate cardiac pumping is called

or simply

than 15 per cent.

Vicious Circle of Cardiac Deterioration in Cardiogenic Shock.

gressively more damaged when its coronary blood

sure usually must be reduced below about 45 mm Hg

heart that already has a blocked major coronary

extremely important to prevent even short periods of
hypotension.

Often a patient dies of cardio-

genic shock before the various compensatory
processes can return the cardiac output (and arterial

ment of this condition is one of the most important

Immediate administration of digitalis is often used

for strengthening the heart if the ventricular muscle

cortex. But some of the increase in aldosterone

This results mainly from the effect of angiotensin

stage of heart failure, large quantities of

3. Increased aldosterone secretion.

body.

into the urine decreases greatly, and large

from the tubules. Therefore, loss of water and salt

surrounding the renal tubules, promoting greatly

the blood flow through the kidneys, which

19. The angiotensin in turn has a direct effect on

, as described in Chapter

by the kidneys, and this in turn causes the

The reduced blood flow to the

renal tubules.

increased reabsorption of water and salt by the

2. Activation of the renin-angiotensin system and

about one-half normal, this can result in almost

When the cardiac output falls to

filtration rate becomes less than normal. It is

mildest degrees of heart failure, the glomerular

. As a consequence, except in the

cardiac output has a tendency to reduce the

1. Decreased glomerular filtration.

equally important but in different ways.

output of urine during cardiac failure, all of which are

There are three known causes of the reduced renal

, thus causing loss of fluid into the tissues and

the capillary pressure now also rises

Therefore,

dency for blood to return to the heart. This elevates

systemic filling pressure, resulting in increased ten-

. The retention of fluid increases the mean

because of fluid retention by

right-ventricular heart failure, peripheral edema does

Heart Failure

Long-Term Fluid Retention by the Kidneys—

pheral edema.

rience in humans, show that acute cardiac failure

. Therefore, animal experiments, as well as expe-

severe acute cardiac failure often

of 13 mm Hg. Thus,

13 mm Hg. Capillary pressure also falls from its normal

cardiac output approaches zero, these two pressures

pressure falls and the right atrial pressure rises. As the

ously healthy heart acutely fails as a pump, the aortic

explained by referring to Figure 22–3. When a previ-

. This can best be

However, either left or right heart failure is very

hours.

congestion of the lungs, with development of

Cardiac Failure

if any, benefit after 3 hours.

within the first hour of cardiogenic shock but of little,

dissolution of the clot. The results occasionally are

coronary bypass graft, or (2) catheterizing the blocked

clot in the coronary artery, often in combination with

the following procedures: (1) surgically removing the

of deterioration. And this allows enough time for

Cardiac Failure

Chapter 22

263

often will increase enough to prevent the vicious circle

appropriate compensatory mechanisms in circulatory
system to correct the shock.

Some success has also been achieved in saving the

lives of patients in cardiogenic shock by using one of

coronary artery and infusing either streptokinase or
tissue-type plasminogen activator enzymes that cause

astounding when one of these procedures is instituted

Edema in Patients with

Inability of Acute Cardiac Failure to Cause Peripheral Edema.

Acute left heart failure can cause terrific and rapid

pul-

monary edema and even death within minutes to

slow to cause peripheral edema

approach each other at an equilibrium value of about

value of 17 mm Hg to the new equilibrium pressure

causes a fall in peripheral capillary pressure rather than
a rise

almost never causes immediate development of peri-

The Cause of Peripheral Edema in Persisting

After the first day or so of overall heart failure or of

begin to occur principally
the kidneys

the right atrial pressure to a still higher value and
returns the arterial pressure back toward normal.

markedly
development of severe edema.

A decrease in

glomerular pressure in the kidneys because
of (1) reduced arterial pressure and (2) intense
sympathetic constriction of the afferent arterioles
of the kidney

clear from the discussion of kidney function in
Chapters 26 through 29 that even a slight decrease
in glomerular filtration often markedly decreases
urine output.

complete anuria.

kidneys causes marked increase in renin secretion

formation of angiotensin

the arterioles of the kidneys to decrease further

especially reduces the pressure in the capillaries

increased reabsorption of both water and salt

quantities of salt and water accumulate in the
blood and interstitial fluids everywhere in the

In the chronic

aldosterone are secreted by the adrenal cortex.

to stimulate aldosterone secretion by the adrenal

secretion often results from increased plasma

Normal

1/2 Normal

Zero

100

Pressure (mm Hg)

Cardiac output

Mean aortic pressure

Capillary pressure

Right atrial pressure

13 mm Hg

falls from normal to zero.

capillary pressure, and right atrial pressure as the cardiac output

Progressive changes in mean aortic pressure, peripheral tissue

Figure 22–3

uses up the small amount of reserve that is available,

cardiac output. The increased load on the heart rapidly

down steps, either of which requires greatly increased

disease. However, a diagnosis of low cardiac reserve

rest, they usually will not know that they have heart

Diagnosis of Low Cardiac Reserve—Exercise Test.

which are shown in Figure 22–4.

valvular heart disease, and many other factors, some of

cardiac muscle, physical damage to the myocardium,

myocardial disease, vitamin deficiency that affects

This can result from ischemic heart disease, primary

blood satisfactorily will decrease the cardiac reserve.

a cardiac reserve of 400 per cent

cent—that is,

normal; this is an increase above normal of 400 per

reserve, during severe exercise the cardiac output of a

there is no cardiac reserve. As an example of normal

is occasionally 500 to 600 per cent. But in heart failure,

300 to 400 per cent. In athletically trained persons, it

Thus, in the healthy young adult, the cardiac reserve is

cardiac reserve

The maximum percentage that the cardiac output can

Cardiac Reserve

cessful must be instituted immediately.

to 1 hour. Therefore, any procedure that is to be suc-

This vicious circle of acute pulmonary edema can

drug, such as digitalis, to strengthen the heart

5. Giving the patient a rapidly acting cardiotonic

deterioration, and the peripheral vasodilation

reverse the blood oxygen desaturation, the heart

4. Giving the patient pure oxygen to breathe to

furosemide, to cause rapid loss of fluid from the

3. Giving a rapidly acting diuretic, such as

2. Bleeding the patient

therefore, decrease the workload on the left side

1. Putting tourniquets on both arms and legs to

ures that can reverse the process and save the patient’s

within minutes. The types of heroic therapeutic meas-

certain critical point, it will continue until death of the

Thus, a vicious circle has been established.

desaturation, more venous return, and so forth.

more transudation of fluid, more arterial oxygen

damming of the blood in the lungs, leading to still

6. The increased venous return further increases the

still more.

5. The peripheral vasodilation increases venous

everywhere in the body, thus causing peripheral

4. The decreased oxygen in the blood further

3. The increased fluid in the lungs diminishes the

pulmonary capillary pressure, and a small amount

2. The increased blood in the lungs elevates the

begins to dam up in the lungs.

limited pumping capacity of the left heart, blood

left ventricle initiates the vicious circle. Because of

1. A temporarily increased load on the already weak

The acute pulmonary edema is believed to result from

cise, some emotional experience, or even a severe cold.

heart, such as might result from a bout of heavy exer-

occurs in a person without new cardiac damage, it

had chronic heart failure for a long time. When this

Failure—Another Lethal Vicious Circle

Acute Pulmonary Edema in Late-Stage Heart

toms during cardiac failure. The renal effects of ANF

excretion of salt and water. Therefore, ANF plays a

to tenfold in severe heart failure. The ANF in turn has

culating levels of ANF in the blood increase fivefold

left atrial pressures that stretch the atrial walls, the cir-

they become stretched. Because heart failure almost

tubular reabsorption of water.

(discussed in Chapter 29). The antidiuretic

fluid everywhere in the body. This elicits

with the sodium, mainly chloride ions, increase

Second, the absorbed sodium and anions that go

pressure in the renal interstitial fluids; these

sodium is reabsorbed, it reduces the osmotic

in water reabsorption for two reasons: First, as the

tubules. This in turn leads to a secondary increase

The elevated aldosterone level further increases

to reduced renal function in cardiac failure.

potassium. Excess potassium is one of the most

264

Unit IV

The Circulation

powerful stimuli known for aldosterone secretion,
and the potassium concentration rises in response

the reabsorption of sodium from the renal

pressure in the tubules but increases the osmotic

changes promote osmosis of water into the blood.

the osmotic concentration of the extracellular

antidiuretic hormone secretion by the
hypothalamic–posterior pituitary gland system

hormone in turn promotes still greater increase in

Role of Atrial Natriuretic Factor to Delay Onset of Cardiac
Decompensation.

Atrial natriuretic factor (ANF) is a

hormone released by the atrial walls of the heart when

always causes excessive increase in both the right and

a direct effect on the kidneys to increase greatly their

natural role to help prevent extreme congestive symp-

are discussed in Chapter 29.

A frequent cause of death in heart failure is acute pul-
monary edema occurring in patients who have already

usually is set off by some temporary overload of the

the following vicious circle:

of fluid begins to transude into the lung tissues
and alveoli.

degree of oxygenation of the blood.

weakens the heart and also weakens the arterioles

vasodilation.

return of blood from the peripheral circulation

Once this vicious circle has proceeded beyond a

patient unless heroic therapeutic measures are used

life include the following:

sequester much of the blood in the veins and,

of the heart

body

proceed so rapidly that death can occur in 20 minutes

increase above normal is called the

healthy young adult can rise to about five times

Any factor that prevents the heart from pumping

As long as

persons with low cardiac reserve remain in a state of

usually can be easily made by requiring the person to
exercise either on a treadmill or by walking up and

is, at a right atrial pressure of

venous return curves now equilibrate at point C, that

the right and upward. The new cardiac output and

Hg up to 10 mm Hg. This increase in mean systemic

mercury—in this figure, from a normal value of 7 mm

output curve as much as 30 to 100 per cent. It can also

return curves, raising both of them

They affect both the cardiac output and the venous

seconds, the sympathetic reflexes become very active.

Within the next 30

ately to 4 mm Hg, whereas the cardiac output falls to

curve. Thus, the right atrial pressure rises immedi-

circulation is depicted by point B, where the new

still operating normally. Therefore, the new state of the

few seconds, the venous return curve still has not

. During these

lowermost curve

after a moderately severe heart attack, the cardiac

0 mm Hg.

is where the two curves cross at point A. Therefore, the

at which the circulatory system can operate. This point

20, there is only one point on each of these two curves

. As pointed out in Chapter

normal cardiac output curve

circulation. The two curves passing through Point A

cardiac output

Figure 22–5 shows

Chronic Compensation

Graphical Analysis of Acute Heart Failure and

using this graphical technique.

chapter, we analyze several aspects of cardiac failure,

duced in Chapter 20. In the remaining sections of this

tive approaches. One such approach is the graphical

logic, as we have done thus far in this chapter, one can

Quantitative Graphical Method for

in most clinical settings.

cardiologist. These tests take the place of cardiac

3. Excessive increase in heart rate because the

ischemia, thus limiting the person’s ability to

2. Extreme muscle fatigue resulting from muscle

heart to pump sufficient blood to the tissues,

1. Immediate and sometimes extreme shortness of

to sustain the body’s new level of activity. The acute

Cardiac Failure

Chapter 22

265

and the cardiac output soon fails to rise high enough

effects are as follows:

breath (dyspnea) resulting from failure of the

thereby causing tissue ischemia and creating a
sensation of air hunger

continue with the exercise

nervous reflexes to the heart overreact in an
attempt to overcome the inadequate cardiac
output

Exercise tests are part of the armamentarium of the

output measurements that cannot be made with ease

Analysis of Cardiac Failure

Although it is possible to understand most general
principles of cardiac failure using mainly qualitative

grasp the importance of the different factors in cardiac
failure with far greater depth by using more quantita-

method for analysis of cardiac output regulation intro-

and venous return

curves for different states of the heart and peripheral

are (1) the

and (2) the

normal venous return curve

normal state of the circulation is a cardiac output and
venous return of 5 L/min and a right atrial pressure of

Effect of Acute Heart Attack.

During the first few seconds

output curve falls to the

changed because the peripheral circulatory system is

cardiac output curve crosses the normal venous return

2 L/min.

Effect of Sympathetic Reflexes.

. Sympathetic stim-

ulation can increase the plateau level of the cardiac

increase the mean systemic filling pressure (depicted
by the point where the venous return curve crosses the
zero venous return axis) by several millimeters of

filling pressure shifts the entire venous return curve to

+5 mm Hg and a cardiac

output of 4 L/min.

100

200

300

400

500

600

Cardiac reserve (%)

Moderate

coronary

disease

Diphtheria

Severe

coronary

thrombosis

Mild

valvular
disease

Severe

valvular
disease

Athlete

Normal

operation

reserve for two of the conditions.

Cardiac reserve in different conditions, showing less than zero

Figure 22–4

venous return (L

/min)

–4

–

Cardiac output and

Right atrial pressure (mm Hg)

Normal

during different stages of cardiac failure.

Progressive changes in cardiac output and right atrial pressure

Figure 22–5

and a right atrial pressure of 4.6 mm Hg. This cardiac

digitalized heart at point H, at an output of 5 L/min

becomes the curve labeled “Several days later.” This

down to 11.5 mm Hg, and the new venous return curve

The progressive loss of fluid over a period of several

effect of digitalis.

, a well-known therapeutic

normally, causing

Therefore, the kidneys eliminate much more fluid than

make the kidneys excrete normal amounts of urine.

point G. The cardiac output is now 5.7 L/min, a value

the venous return curve. Therefore, the new cardiac

Figure 22–7, but there is not an immediate change in

time, digitalis is given to strengthen the heart. This

proceed to the same point E in Figure 22–7. At this

already reached point E in Figure 22–6, and let us

Treatment of Decompensated Heart Disease with Digitalis.

Thus, “decompensation” results from the fact that

erates downhill until death occurs.

mental effect on cardiac output. The condition accel-

cardiac output curve, so that further retention of fluid

to point D, to point E, and, finally, to point F. The equi-

venous return curve continues to shift to the right, and

mean systemic filling pressure continues to rise, the

renal function. Fluid continues to be retained, the

During the succeeding days, the cardiac output

atrial pressure to 7 mm Hg.

C. The cardiac output rises to 4.2 L/min and the right

venous return curve becomes that labeled “2nd day”

pressure rises from 10.5 to almost 13 mm Hg. Now the

tinues to be retained, and the mean systemic filling

the kidneys to function normally. Therefore, fluid con-

The cardiac output of 4 L/min is still too low to cause

pressure to 5 mm Hg.

equates with the cardiac output curve at point B. The

compensation.” Thus, the new venous return curve

the right to produce the curve labeled “autonomic

Hg. This shifts the venous return curve upward and to

this low cardiac output, increases the mean systemic

ulation of the sympathetic nervous system, caused by

give a cardiac output of about 3 L/min. However, stim-

curve to this low level. At point A, the curve at time

great as this heart can achieve. In this figure, we have

curve that has already reached a degree of recovery as

same as the curve shown in Figure 22–2, a very low

The black cardiac output curve in Figure 22–6 is the

Cardiac Failure

manner.

Figure 22–5, they are presented in a more quantitative

the same as those presented in Figure 22–1, but in

Note that the events described in Figure 22–5 are

degrees of heart failure.

culation in mild to moderate heart failure. And one

Using this technique for analysis, one can see espe-

curve.

pressure, until some additional extrinsic factor changes

continue to function at point D and remain stable, with

balance has been achieved. The circulatory system will

normal, so that a new state of equilibrated fluid

the cardiac output is now normal, renal output is also

6 mm Hg. Because

however, has risen still further to

now returned to normal. The right atrial pressure,

equilibrate at point D. Thus, the cardiac output has

12 mm Hg. The two new curves now

heart and (2) renal retention of salt and water, which

ensuing week, the cardiac output and venous return

266

Unit IV

The Circulation

Compensation During the Next Few Days.

During the

curves rise further because of (1) some recovery of the

raises the mean systemic filling pressure still further—
this time up to

a normal cardiac output and an elevated right atrial

either the cardiac output curve or the venous return

cially the importance of moderate fluid retention and
how it eventually leads to a new stable state of the cir-

can also see the interrelation between mean systemic
filling pressure and cardiac pumping at various

Graphical Analysis of “Decompensated”

added venous return curves that occur during succes-
sive days after the acute fall of the cardiac output

zero equates with the normal venous return curve to

filling pressure within 30 seconds from 7 to 10.5 mm

cardiac output has been improved to a level of 4 L/min
but at the expense of an additional rise in right atrial

and equilibrates with the cardiac output curve at point

never rises quite high enough to re-establish normal

the equilibrium point between the venous return curve
and the cardiac output curve also shifts progressively

libration process is now on the down slope of the

causes only more severe cardiac edema and a detri-

the cardiac output curve never rises to the critical level
of 5 L/min needed to re-establish normal kidney excre-
tion of fluid that would be required to cause balance
between fluid input and output.

Let

us assume that the stage of decompensation has

raises the cardiac output curve to the level shown in

output curve equates with the venous return curve at

greater than the critical level of 5 liters required to

diuresis

days reduces the mean systemic filling pressure back

curve equates with the cardiac output curve of the

Cardiac output and venous return (L

/min)

–4

–

Right atrial pressure (mm Hg)

8th day

6th day

4th day

2nd day

Critical cardiac

output level

for normal

fluid balance

onomic

com

pens

ation

Normal ven

ous

return

of continued fluid retention.

progressive shift of the venous return curve to the right as a result

Graphical analysis of decompensated heart disease showing

Figure 22–6

level of the cardiac output curve.

weak heart, as demonstrated by the depressed plateau

normal; this high cardiac output occurs despite the

beriberi, with a right atrial pressure in this instance of

point C, which describes the circulatory condition in

The two blue curves (cardiac output curve and

explained in Chapter 17.

minosis has dilated the peripheral blood vessels, as

the right. Finally, the venous return curve has rotated

11 mm Hg. This has shifted the venous return curve to

fluid, which in turn has increased the mean systemic

decreased the blood flow to the kidneys. Therefore, the

the beriberi syndrome. The weakening of the heart has

. The decreased level of the cardiac output

Figure 22–8 shows the approximate changes

and is called “high-output failure,” but in reality, the

fistula. This condition resembles a failure condition

eral congestion. If the person attempts to exercise, he

is slightly elevated, and there are mild signs of periph-

has become greatly elevated, the right atrial pressure

atrial pressure of 3 mm Hg. Thus, the cardiac output

point B, with a cardiac output of 12.5 L/min and a right

the curve labeled “AV fistula.” This venous return

vein). The venous return curve rotates upward to give

min and a normal right atrial pressure of 0 mm Hg.

venous return curves. These equate with each other at

The “normal” curves of Figure

cular resistance, but at the same time, the pumping

, in which the venous return is

capability of the heart is not depressed. The other is

of excessive venous return, even though the pumping

arteriovenous fistula

output cardiac failure. One of these is caused by an

Figure 22–8 gives an analysis of two types of high-

Cardiac Failure

for normal fluid balance. The compensatory mecha-

curve, the venous return curve, and the critical level

the crossing point of three curves: the cardiac output

pensated.” And to state this another way, the final

decompensation of the heart failure has been “com-

system has now stabilized, or in other words, the

none will be gained. Consequently, the circulatory

balance. Therefore, no additional fluid will be lost and

Cardiac Failure

Chapter 22

267

output is precisely that required for normal fluid

steady-state condition of the circulation is defined by

nisms automatically stabilize the circulation when all
three curves cross at the same point.

Graphical Analysis of High-Output

that overloads the heart because

caused by beriberi
greatly increased because of diminished systemic vas-

capability of the heart is depressed.

Arteriovenous Fistula.

22–8 depict the normal cardiac output and normal

point A, which depicts a normal cardiac output of 5 L/

Now let us assume that the systemic resistance (the

total peripheral resistance) becomes greatly decreased
because of opening a large arteriovenous fistula (a
direct opening between a large artery and a large

curve equates with the normal cardiac output curve at

or she will have little cardiac reserve because the heart
is already being used almost to maximum capacity to
pump the extra blood through the arteriovenous

heart is overloaded by excess venous return.

Beriberi.

in the cardiac output and venous return curves caused
by beriberi
curve is caused by weakening of the heart because of
the avitaminosis (mainly lack of thiamine) that causes

kidneys have retained a large amount of extra body

filling pressure (represented by the point where the
venous return curve now intersects the zero cardiac
output level) from the normal value of 7 mm Hg up to

upward from the normal curve because the avita-

venous return curve) intersect with each other at

9 mm Hg and a cardiac output about 65 per cent above

venous return (L

/min)

10 12 14 16

–4 –

Cardiac output and

Right atrial pressure (mm Hg)

Critical cardiac output

level for normal

fluid balance

veral d

ays

later

ver

ely

failing

hea

git

ali

d h

ear

First da

increased urine output and progressive shift of the venous return

digitalis in elevating the cardiac output curve, this in turn causing

Treatment of decompensated heart disease showing the effect of

Figure 22–7

curve to the left.

venous return (L

/min)

10 12 14 16

–4 –

Cardiac output and

Right atrial pressure (mm Hg)

AV fistula

Normal cardiac

output curve

Beriberi

heart

disease

Normal
venous

return

curve

beriberi heart disease.

output cardiac failure: (1) arteriovenous (AV) fistula and (2)

Figure 22–8

Graphical analysis of two types of conditions that can cause high-

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