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18
CHAPTER
Heart Failure and
Circulatory Shock
A
dequate perfusion of body tissues depends on the pump-
Heart Failure
Physiology of Heart Failure
Cardiac Output
Compensatory Mechanisms
Congestive Heart Failure
Types of Heart Failure
Manifestations of Heart Failure
Diagnosis and Treatment
Acute Pulmonary Edema
Manifestations
Treatment
Cardiogenic Shock
Manifestations
Treatment
Mechanical Support of the Failing Heart and
Heart Transplantation
Circulatory Failure (Shock)
Types of Shock
Hypovolemic Shock
Obstructive Shock
Distributive Shock
Sepsis and Septic Shock
Complications of Shock
Acute Respiratory Distress Syndrome
Acute Renal Failure
Gastrointestinal Complications
Disseminated Intravascular Coagulation
Multiple Organ Dysfunction Syndrome
Heart Failure in Children and the Elderly
Heart Failure in Infants and Children
Manifestations
Diagnosis and Treatment
Heart Failure in the Elderly
Manifestations
Diagnosis and Treatment
ing ability of the heart, a vascular system that transports
blood to the cells and back to the heart, sufficient blood
to fill the circulatory system, and tissues that are able to extract
and use the oxygen and nutrients from the blood. Heart failure
and circulatory shock are separate conditions that reflect failure
of the circulatory system. Both conditions exhibit common
compensatory mechanisms even though they differ in terms of
pathogenesis and causes.
HEART FAILURE
Heart failure affects an estimated 4.8 million Americans.
1
Although morbidity and mortality rates from other cardiovas-
cular diseases have decreased during the past several decades,
the incidence of heart failure is increasing at an alarming rate.
This change undoubtedly reflects treatment improvements
and survival from other forms of heart disease. Despite ad-
vances in treatment, the 5-year survival rate for heart failure is
only about 50%.
Physiology of Heart Failure
The term
heart failure
denotes the failure of the heart as a pump.
The heart has the amazing capacity to adjust its pumping abil-
ity to meet the varying needs of the body. During sleep, its out-
put declines, and during exercise, it increases markedly. The
ability to increase cardiac output during increased activity is
called the
cardiac reserve
. For example, competitive swimmers
and long-distance runners have large cardiac reserves. During
exercise, the cardiac output of these athletes rapidly increases
to as much as five to six times their resting level. In sharp con-
trast with healthy athletes, persons with heart failure often use
their cardiac reserve at rest. For them, just climbing a flight of
stairs may cause shortness of breath because they have ex-
ceeded their cardiac reserve.
The pathophysiology of heart failure involves an interaction
between two factors: (1) a decrease in cardiac output with a
consequent decrease in blood flow to the kidneys and other
body organs and tissues; (2) the recruitment of compensatory
mechanisms designed to maintain tissue perfusion.
320
321
Chapter 18: Heart Failure and Circulatory Shock
contraction (
i.e.
, positive inotropic action), and hypoxia and
ischemia decrease contractility (
i.e.
, negative inotropic effect).
The inotropic drug digitalis, which is used in the treatment of
heart failure, increases cardiac contractility such that the heart
is able to eject more blood at any level of preload filling.
KEY CONCEPTS
HEART FAILURE
The function of the heart is to move deoxygenated
blood from the venous system through the right
heart into the pulmonary circulation and to move
the oxygenated blood from the pulmonary circula-
tion through the left heart into the arterial system.
■
Compensatory Mechanisms
Heart failure is characterized by a decrease in cardiac output
with a consequent decline in blood flow to the kidneys as well
as other body organs and tissues. With a decrease in cardiac
performance, tissue and organ perfusion is largely maintained
through compensatory mechanisms such as the Frank-Starling
mechanism, activation of the sympathetic nervous system and
the renin-angiotensin-aldosterone mechanism, and myocardial
hypertrophy (Fig. 18-1). In the failing heart, early decreases in
cardiac function often go unnoticed because these compen-
satory mechanisms are used to maintain the cardiac output.
This state is called
compensated heart failure
. Unfortunately,
these mechanisms were not intended for long-term use. In
severe and prolonged heart failure, the compensatory mecha-
nisms are no longer effective and may themselves worsen the
failure, causing what is termed
decompensated failure
.
To function effectively, the right and left hearts must
maintain an equal output.
■
Right heart failure represents failure of the right
heart to pump blood forward into the pulmonary
circulation; blood backs up in the systemic circula-
tion, causing peripheral edema and congestion of
the abdominal organs.
■
Left heart failure represents failure of the left heart to
move blood from the pulmonary circulation into the
systemic circulation; blood backs up in the pul-
monary circulation.
■
Frank-Starling Mechanism.
The Frank-Starling mechanism re-
lies on an increase in venous return and a resultant increase in
diastolic filling of the ventricles. Known as the
end-diastolic vol-
ume
, this volume causes the tension in the wall of the ventricles
and the pressure in the ventricles to rise. With increased ven-
tricular end-diastolic volume, there is increased stretching of
the myocardial fibers, more optimal approximation of the actin
and myosin filaments, and a resultant increase in the stroke
volume in accord with the Frank-Starling mechanism (see
Chapter 14, Fig. 14-20).
In heart failure a decrease in cardiac output and renal blood
flow leads to increased salt and water retention, a resultant in-
crease in vascular volume and venous return to the heart, and
an increase in ventricular end-diastolic volume. Within limits,
as preload and ventricular end-diastolic volume increase, there
is a resultant increase in cardiac output. Thus, cardiac output
may be normal at rest in persons with heart failure. However,
as myocardial function deteriorates, the heart becomes over-
filled, the muscle fibers become overstretched, and the ventric-
ular function curve flattens (Fig. 18-2). The maximal increase
in cardiac output that can be achieved may severely limit activ-
ity, while producing an elevation in left ventricular and pul-
monary capillary pressure and development of dyspnea and
pulmonary congestion.
An important determinant of myocardial energy consump-
tion is ventricular wall tension. Overfilling of the ventricle
produces a decrease in wall thickness and an increase in wall
tension. Because increased wall tension increases myocardial
oxygen requirements, it can produce ischemia and further im-
pairment of cardiac function. The use of diuretics in the treat-
ment of heart failure helps to reduce vascular volume and
ventricular filling, thereby unloading the heart and reducing
ventricular wall tension.
Cardiac Output
The cardiac output is the amount of blood that the heart
pumps each minute. It reflects how often the heart beats each
minute (heart rate) and how much blood the heart pumps
with each beat (stroke volume) and can be expressed as the
product of the heart rate and stroke volume (cardiac output
=
heart rate
stroke volume). Heart rate is a function of sympa-
thetic nervous system reflexes, which accelerate heart rate and
parasympathetic nervous system reflexes, which slows it down.
Stroke volume is a function of preload, afterload, and cardiac
contractility.
×
Preload and Afterload.
The work that the heart performs con-
sists mainly of ejecting blood into the pulmonary or systemic
circulations. It is determined largely by the loading conditions
or what is called the
preload
and
afterload
.
Preload
reflects the loading condition of the heart at the end
of diastole just before the onset of systole. It is the volume of
blood stretching the resting heart muscle and is determined
mainly by the venous return to the heart.
Afterload
represents
the force that the contracting heart must generate to eject blood
from the filled heart. The main components of afterload are
ventricular wall tension and the peripheral vascular resistance.
The greater the peripheral vascular resistance, the greater the
ventricular wall tension and intraventricular pressure required
to open the aortic valve and pump blood into the peripheral
circulation.
Cardiac Contractility.
Cardiac contractility refers to the me-
chanical performance of the heart: the ability of the contractile
elements (actin and myosin filaments) of the heart muscle to
interact and shorten against a load. Contractility increases car-
diac output independent of preload filling and muscle stretch.
An
inotropic influence
is one that increases cardiac contractil-
ity. Sympathetic stimulation increases the strength of cardiac
Increased Sympathetic Nervous System Activity.
Stimulation
of the sympathetic nervous system plays an important role in
the compensatory response to decreased cardiac output and the
pathogenesis of heart failure.
2,3
Both cardiac sympathetic tone
322
Unit Four: Alterations in the Cardiovascular System
Vascular resistance
(afterload)
Frank-Starling
mechanism
Venous return
(preload)
Cardiac contractility
Heart rate
Cardiac
output
Sympathetic
reflexes
Myocardial
hypertrophy
Renal blood flow
Vascular
tone
Renin-
angiotensin-
aldosterone
mechanism
Angiotensin II
Aldosterone
■
FIGURE 18-1
■
Compensatory mecha-
nisms in heart failure. The Frank-Starling
mechanism, sympathetic reflexes, renin-
angiotensin-aldosterone mechanism, and
myocardial hypertrophy function in main-
taining the cardiac output for the failing
heart.
Vascular volume
Salt and water
retention
and circulating catecholamine (epinephrine and norepineph-
rine) levels are elevated during the late stages of most forms of
heart failure. By direct stimulation of heart rate and cardiac
contractility and by regulation of vascular tone, the sympa-
thetic nervous system helps to maintain perfusion of the vari-
ous organs, particularly the heart and brain.
The negative aspects of increased sympathetic activity in-
clude an increase in peripheral vascular resistance and the after-
load against which the heart must pump. Excessive sympathetic
stimulation also may result in decreased blood flow to skin,
muscle, kidney, and abdominal organs. The catecholamines
also may contribute to the high rate of sudden death by pro-
moting dysrhythmias.
4
Renin-Angiotensin Mechanism.
One of the most important ef-
fects of a lowered cardiac output in heart failure is a reduction
in renal blood flow and glomerular filtration rate, which leads
to salt and water retention. Normally, the kidneys receive ap-
proximately 25% of the cardiac output, but this may be de-
creased to as low as 8% to 10% in persons with heart failure.
With decreased renal blood flow, there is a progressive increase
in renin secretion by the kidneys along with parallel increases
in circulating levels of angiotensin II. The increased concen-
tration of angiotensin II contributes to a generalized vaso-
constriction and serves as a stimulus for aldosterone produc-
tion by the adrenal cortex (see Chapter 16). Aldosterone, in
turn, increases tubular reabsorption of sodium, with an accom-
panying increase in water retention. Because aldosterone is
metabolized in the liver, its levels are further increased when
heart failure causes liver congestion.
Recent evidence suggests that angiotensin is also a growth
factor for cardiac muscle cells and fibroblasts and, as such, may
play a central role in modifying the structure and function of
the myocardium in persons with heart failure.
2
Angiotensin-
converting enzyme (ACE) inhibitor drugs, which block the
conversion of angiotensin I to angiotensin II, are often used in
the treatment of heart failure.
2–4
323
Chapter 18: Heart Failure and Circulatory Shock
Myocardial Hypertrophy.
Myocardial hypertrophy is a long-
term compensatory mechanism. Cardiac muscle, like skeletal
muscle, responds to an increase in work demands by under-
going hypertrophy. Hypertrophy increases the number of con-
tractile elements in myocardial cells as a means of increasing
their contractile performance.
Myocardial hypertrophy occurs early in the course of heart
failure and is an important risk factor for subsequent morbid-
ity and mortality. Although hypertrophy increases the systolic
function of the heart, it also eventually can lead to diastolic dys-
function and myocardial ischemia. Some forms of hypertrophy
may lead to abnormal remodeling of the ventricular wall with
a reduction in chamber size, reduced diastolic filling, and in-
creased ventricular wall tension. For example, untreated hyper-
tension causes hypertrophy that may preserve systolic function
for a time, but eventually the work performed by the ventricle
exceeds the augmented muscle mass and the heart dilates.
2
The
increased muscle mass of the hypertrophied heart increases
the need for oxygen delivery. When the oxygen requirements
of the increased muscle mass exceed the ability of the coronary
vessels to bring blood to the area, myocardial hypertrophy is
no longer beneficial and may result in ischemia with decreased
contractility. In addition, hypertrophy of cardiac muscle cells
may be accompanied by the growth of nonmyocardial tissue
(
e.g.
, fibrous tissue) that produces stiffness of the ventricle and
further impairment of ventricular function.
Causes of Heart Failure
TABLE 18-1
Impaired Cardiac
Excess Work
Function
Demands
Myocardial Disease
Increased Pressure Work
Cardiomyopathies
Systemic hypertension
Myocarditis
Pulmonary hypertension
Coronary insufficiency
Coarctation of the aorta
Myocardial infarction
Valvular Heart Disease
Increased Volume Work
Stenotic valvular disease
Arteriovenous shunt
Regurgitant valvular disease
Excessive administration of
intravenous fluids
Congenital Heart Defects
Increased Perfusion Work
Thyrotoxicosis
Anemia
Constrictive Pericarditis
pair the pumping ability of the heart, such as ischemic heart
disease and cardiomyopathy.
Systolic Versus Diastolic Failure.
A recent classification separates
the pathophysiology of CHF into two categories—systolic dys-
function and diastolic dysfunction. Systolic dysfunction is
characterized by impaired ejection of blood from the heart dur-
ing systole and diastolic dysfunction by impaired filling of the
ventricles during diastole (Fig. 18-3). Many persons with heart
failure fall into an intermediate category, with combined ele-
ments of both systolic and diastolic failure.
Systolic dysfunction
involves a decrease in cardiac contractil-
ity and ejection fraction. It commonly results from conditions
that impair the contractile performance of the heart (
e.g.
, isch-
emic heart disease and cardiomyopathy), produce a volume
Congestive Heart Failure
Heart failure occurs when the pumping ability of the heart be-
comes impaired. The term
congestive heart failure
(CHF) refers to
heart failure that is accompanied by congestion of body tissues.
Heart failure may be caused by a variety of conditions, in-
cluding acute myocardial infarction, hypertension, valvular
heart disease, or degenerative conditions of the heart muscle
known collectively as
cardiomyopathies
(see Chapter 17). Heart
failure also may occur because of excessive work demands,
such as occurs with hypermetabolic states, or with volume
overload, such as occurs with renal failure. Either of these states
may exceed the work capacity of even a healthy heart. In per-
sons with asymptomatic heart disease, heart failure may be pre-
cipitated by an unrelated illness or stress. Table 18-1 lists major
causes of heart failure.
Diastolic
dysfunction
Systolic
dysfunction
Normal
Types of Heart Failure
Heart failure may be described as high-output or low-output
failure, systolic or diastolic failure, and right-sided or left-sided
failure.
End
systole
High- and Low-Output Failure.
High- and low-output failure
are described in terms of cardiac output.
High-output failure
is
an uncommon type of heart failure that is caused by an exces-
sive need for cardiac output. With high-output failure, the func-
tion of the heart may be supernormal but inadequate because
of excessive metabolic needs. Causes of high-output failure in-
clude severe anemia, thyrotoxicosis, and conditions that cause
arteriovenous shunting. High-output failure tends to be specif-
ically treatable.
Low-output failure
is caused by disorders that im-
End
diastole
■
FIGURE 18-3
■
Congestive heart failure due to systolic and di-
astolic dysfunction. The ejection fraction represents the difference
between the end-diastolic and end-systolic volumes. Normal sys-
tolic and diastolic function with normal ejection fraction (
mid-
dle
); diastolic dysfunction with decreased ejection fraction due to
decreased diastolic filling (
left
); systolic dysfunction with de-
creased ejection fraction due to impaired systolic function (
right
).
324
Unit Four: Alterations in the Cardiovascular System
overload (
e.g.
, valvular insufficiency and anemia), or generate
a pressure overload (
e.g.
, hypertension and valvular stenosis)
on the heart.
A normal heart ejects approximately 65% of the blood that
is present in the ventricle at the end of diastole when it con-
tracts. This is called the
ejection fraction
. In systolic heart failure,
the ejection fraction declines progressively with increasing de-
grees of myocardial dysfunction. In very severe forms of heart
failure, the ejection fraction may drop to a single-digit percent-
age. With a decrease in ejection fraction, there is a resultant in-
crease in diastolic volume, ventricular dilation, ventricular wall
tension, and ventricular end-diastolic pressure. The symptoms
of persons with systolic dysfunction result mainly from reduc-
tions in ejection fraction and cardiac output.
Diastolic dysfunction
, which reportedly accounts for approx-
imately 40% of all cases of CHF, is characterized by a smaller
ventricular chamber size, ventricular hypertrophy, and poor
ventricular compliance (
i.e.
, ability to stretch during filling).
5
Because of impaired filling, congestive symptoms tend to pre-
dominate in diastolic dysfunction. Among the conditions that
cause diastolic dysfunction are those that restrict diastolic fill-
ing (
e.g.
, mitral stenosis), those that increase ventricular wall
thickness and reduce chamber size (
e.g.
, myocardial hypertro-
phy caused by lung disease and hypertrophic cardiomyopa-
thy), and those that delay diastolic relaxation (
e.g.
, aging, isch-
emic heart disease). Aging often is accompanied by a delay in
relaxation of the heart during diastole; diastolic filling begins
while the ventricle is still stiff and resistant to stretching to ac-
cept an increase in volume.
6
A similar delay occurs with myo-
cardial ischemia, resulting from a lack of energy to break the
rigor bonds that form between the actin and myosin filaments
of the contracting cardiac muscle.
7
Because tachycardia pro-
duces a decrease in diastolic filling time, persons with diastolic
dysfunction often become symptomatic during activities and
situations that increase heart rate.
Right-Sided Versus Left-Sided Heart Failure.
Heart failure also
can be classified according to the side of the heart (right or left)
that is affected. An important feature of the circulatory system
is that the right and left ventricles act as two pumps that are
connected in series. To function effectively, the right and left
ventricles must maintain an equal output. Although the initial
event that leads to heart failure may be primarily right sided or
left sided in origin, long-term heart failure usually involves
both sides.
Right-Sided Heart Failure.
Right-sided heart failure impairs the
ability to move deoxygenated blood from the systemic venous
circulation into the pulmonary circulation. Consequently,
when the right heart fails, there is an accumulation of blood in
the systemic venous system (Fig. 18-4). This causes an increase
in the right atrial, right ventricular end-diastolic, and systemic
venous pressures.
A major effect of right-sided heart failure is the development
of peripheral edema. Because of the effects of gravity, the edema
is most pronounced in the dependent parts of the body—in the
lower extremities when the person is in the upright position
and in the area over the sacrum when the person is supine. The
Right heart failure
Left heart failure
Congestion of peripheral tissues
Decreased cardiac output
Pulmonary congestion
Dependent
edema
and ascites
Liver congestion
Activity
intolerance
and signs of
decreased
tissue
perfusion
Pulmonary
edema
Impaired gas
exchange
Signs related
to impaired liver
function
GI tract
congestion
Cough with
frothy sputum
Cyanosis
and signs of
hypoxia
Orthopnea
Anorexia, GI distress,
weight loss
Paroxysmal
nocturnal dyspnea
■
FIGURE 18-4
■
Manifestations of left- and right-sided heart failure.
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