Download Heart Failure and Circulatory Shock

CHAPTER
28
Heart Failure
and Circulatory Shock
HEART FAILURE
Physiology of Heart Failure
Cardiac Output
Adaptive Mechanisms
Congestive Heart Failure
High-Output Versus Low-Output Failure
Systolic Versus Diastolic Failure
Right-Sided Versus Left-Sided Heart Failure
Manifestations of Congestive Heart Failure
Diagnostic Methods
Treatment Methods
Acute Pulmonary Edema
Manifestations
Treatment
Cardiogenic Shock
Manifestations
Treatment
Mechanical Support and Heart Transplantation
CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Physiology of Hypovolemic Shock
Clinical Course
Obstructive Shock
Distributive Shock
Neurogenic Shock
Anaphylactic Shock
Sepsis and Septic Shock
Complications of Shock
Acute Respiratory Distress Syndrome
Acute Renal Failure
Gastrointestinal Complications
Disseminated Intravascular Coagulation
Multiple Organ Dysfunction Syndrome
CIRCULATORY 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
A
dequate perfusion of body tissues depends on the
pumping 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 oxygen and nutrients from
the blood. Impaired pumping ability of the heart 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
After completing this section of the chapter, you should be able to
meet the following objectives:
✦ Explain the effect of the cardiac reserve on symptom
development in heart failure
✦ Define the terms preload, afterload, and cardiac contractility
✦ Explain how increased Frank-Starling mechanism, sym-
✦
✦
✦
✦
✦
✦
✦
pathetic activity, the renin-angiotensin-aldosterone
mechanism, the natriuretic peptides, the endothelins,
and myocardial hypertrophy and remodeling contribute
to the initial adaptation to heart failure and then to its
progression
Differentiate high-output versus low-output heart failure,
systolic versus diastolic heart failure, and right-sided
versus left-sided heart failure
Describe the physiologic mechanisms underlying the
manifestations of congestive heart failure
Describe the methods used in diagnosis and assessment
of cardiac function in persons with heart failure
Relate the actions of diuretics, digoxin, angiotensinconverting enzyme inhibitors, and β-adrenergic–
blocking drugs to the treatment of heart failure
Relate the effect of left ventricular failure to the
development of and manifestations of pulmonary
edema
Describe the pathophysiology of cardiogenic shock
Compare the indications for use of ventricular support
devices, heart transplantation, and cardiomyoplasty in
treatment of heart failure
603
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Heart failure affects an estimated 5 million Americans,
with approximately 550,000 new cases diagnosed each
year.1 Although morbidity and mortality rates from other
cardiovascular diseases have decreased over the past several decades, the incidence of heart failure is increasing at
an alarming rate. This change undoubtedly reflects improved treatment methods and increased survival from
other forms of heart disease. Despite advances in treatment, 80% of men and 79% of women younger than age
65 who have heart failure will die within 8 years.1
This section of the chapter is divided into four parts:
pathophysiology of heart failure, congestive heart failure,
acute pulmonary edema, and cardiogenic shock.
PHYSIOLOGY OF HEART FAILURE
The heart has the amazing capacity to adjust its pumping
ability to meet the varying needs of the body. During
sleep, its output 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 contrast 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 exceeded their
cardiac reserve.
The pathophysiology of heart failure involves an interaction between two factors: a decrease in pumping ability of the heart with a consequent decrease in the cardiac
reserve and the adaptive mechanisms that serve to maintain the cardiac output while also contributing to the progression of heart failure.
Cardiac Output
The cardiac output is the amount of blood that the heart
pumps each minute. It reflects how often the heart beats
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 circulation through the left heart into
the arterial system.
➤ 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 circulation, 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 system circulation; blood backs up in the pulmonary circulation.
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. The heart rate
is regulated by a balance between the activity of the sympathetic nervous system, which produces an increase in
heart rate, and the parasympathetic nervous system, which
slows it down, whereas the stroke volume is a function of
preload, afterload, and cardiac contractility.
Preload and Afterload. The work that the heart performs
consists mainly of ejecting blood that has returned to the
ventricles during diastole into the pulmonary or systemic
circulations. As with skeletal muscle, the work of cardiac
muscle is determined by what is called loading conditions—
the stretch imposed by the load (i.e., blood volume) and
the force that the muscle must generate to move the
load. The terms preload and afterload often are used to
describe the workload of the heart.
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. For
any given cardiac cycle, the maximum volume of blood
filling the ventricle is present at the end of diastole. Known
as the end-diastolic volume, this volume causes the tension
in the wall of the ventricles and the pressure in the ventricles to rise. End-diastolic pressure can be measured clinically, providing an estimate of preload status. Within
limits, as end-diastolic volume or preload increases, the
stroke volume increases in accord with the Frank-Starling
mechanism (see Chapter 23, Fig. 23-16). In heart failure,
the ventricles may become overstretched because of excessive filling. When this happens, intraventricular pressure rises, and stroke volume may decrease. Preload may
be excessively elevated in conditions such as myocardial
infarction, in which the ventricles become distended because of impaired pumping ability; in valvular heart disease, such as aortic regurgitation, in which a portion of the
ejected systolic volume moves back into the ventricle and
is added to the diastolic volume; and in renal failure, in
which an increase in blood volume produces an increase
in venous return.
Afterload represents the force that the contracting
heart must generate to eject blood from the filled heart.
The main components of afterload are the systemic (peripheral) vascular resistance and ventricular wall tension.
When the systemic vascular resistance is elevated, as with
arterial hypertension or aortic stenosis, an increased intraventricular pressure must be generated first to open the
aortic valve and then, during the ejection period, to move
blood out of the heart and into the systemic circulation.
This equates to an increase in ventricular wall stress or tension. As a result, excessive afterload may impair ventricular ejection and increase wall tension if the ventricles
cannot generate sufficient pressure.
Cardiac Contractility. Cardiac contractility refers to the mechanical performance of the heart—the ability of the contractile elements (actin and myosin filaments) of the heart
muscle to interact with and shorten against a load. The ejec-
CHAPTER 28
tion of blood from the heart during systole depends on
cardiac contractility. Contractility increases cardiac output
independent of preload filling and muscle stretch.
An inotropic influence is one that increases cardiac contractility. Sympathetic stimulation increases the strength
of cardiac contraction (i.e., positive inotropic action), and
hypoxia and ischemia decrease contractility (i.e., negative
inotropic effect). The drug digitalis, which is classified as
an inotropic agent, increases cardiac contractility such that
the heart is able to eject more blood at any level of preload
filling. A decrease in cardiac contractility can result from
loss of functional muscle tissue due to myocardial infarction or from conditions such as cardiomyopathy that diffusely affect the myocardium.
Adaptive Mechanisms
In heart failure, the cardiac reserve is largely maintained
through compensatory or adaptive mechanisms such as
the Frank-Starling mechanism; activation of neurohumoral
influences such as the sympathetic nervous system, the
renin-angiotensin-aldosterone mechanism, natriuretic peptides, and locally produced vasoactive substances; and myocardial hypertrophy and remodeling (Fig. 28-1). The first
two of these adaptations occur rapidly over minutes to
hours of myocardial dysfunction and may be adequate to
maintain the overall pumping performance of the heart at
relatively normal levels. Myocardial hypertrophy and remodeling occur slowly over weeks to months and play an
important role in the long-term adaptation to hemodynamic overload. These adaptive mechanisms contribute not
Heart Failure and Circulatory Shock
605
only to the adaptation of the failing heart but also to the
pathophysiology of heart failure.
Frank-Starling Mechanism. The Frank-Starling mechanism increases stroke volume by means of an increase in
ventricular end-diastolic volume (Fig. 28-2). With increased
diastolic filling, there is increased stretching of the myocardial fibers, more optimal approximation of the actin
and myosin filaments, and a resultant increase in the force
of the next contraction. In the normally functioning
heart, the Frank-Starling mechanism serves to match the
outputs of the two ventricles.
In heart failure, the Frank-Starling mechanism helps
to support the cardiac output. Cardiac output may be normal at rest in persons with heart failure because of increased ventricular end-diastolic volume and the FrankStarling mechanism. However, this mechanism becomes
ineffective when the heart becomes overfilled and the
muscle fibers are overstretched. With deterioration of myocardial function, the ventricular function curve depicted
in Figure 28-2 flattens, and when an increase in cardiac
output is needed, as occurs with increased physical activity, there is a lesser increase in cardiac output at any given
increase in left ventricular end-diastolic volume or pressure. In this situation, the maximal increase in cardiac output that can be achieved may severely limit activity, while
at the same time producing an elevation in left ventricular and pulmonary capillary pressure and development of
dyspnea and pulmonary congestion. At the point at which
the heart becomes overfilled to the extent that actin and
myosin filaments cannot produce an effective contraction,
Vascular resistance
(afterload)
Venous return
(preload)
Frank-Starling
mechanism
Cardiac
output
Cardiac contractility
Heart rate
Sympathetic
reflexes
Myocardial
hypertrophy
Renal blood flow
Vascular
tone
Reninangiotensinaldosterone
mechanism
Angiotensin II
Aldosterone
FIGURE 28-1 Compensatory mechanisms in
heart failure. The Frank-Starling mechanism,
sympathetic reflexes, renin-angiotensinaldosterone mechanism, and myocardial
hypertrophy function in maintaining the
cardiac output for the failing heart.
Vascular volume
Salt and water
retention
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Cardiovascular Function
catecholamines also may contribute to the high rate of sudden death by promoting arrhythmias.6
Renin-Angiotensin-Aldosterone Mechanism. One of the
FIGURE 28-2 Frank-Starling curves. R, resting; E, exercise; LVED, left
ventricular end-diastolic; CHF, congestive heart failure. (Iseri L.T.,
Benvenuti D.J. [1983]. Pathogenesis and management of congestive heart failure—revisited. American Heart Journal 105 [2], 346)
further increases in ventricular filling may produce a decrease in cardiac output.
An important determinant of myocardial energy consumption 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 impairment of cardiac function. The
use of diuretics in persons with heart failure helps to reduce vascular volume and ventricular filling, thereby unloading the heart and reducing ventricular wall tension.
Sympathetic Nervous System Activity. Stimulation of the
sympathetic nervous system plays an important role in
the compensatory response to decreased cardiac output
and to the pathogenesis of heart failure.2–5 Both cardiac
sympathetic tone and catecholamine (epinephrine and
norepinephrine) 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 sympathetic nervous system helps to
maintain perfusion of the various organs, particularly the
heart and brain. In persons with more severe heart failure,
blood is diverted to the more critical cerebral and coronary
circulations.
The negative aspects of increased sympathetic activity
include an increase in systemic vascular resistance and the
afterload against which the heart must pump. Excessive
sympathetic stimulation also may result in decreased blood
flow to skin, muscle, kidney, and abdominal organs. This
not only decreases tissue perfusion but also contributes to
an increase in systemic vascular resistance and afterload
stress of the heart.
There also is evidence that prolonged sympathetic
stimulation may exhaust myocardial stores of norepinephrine and may lead to down-regulation and a reduction in
β-adrenergic receptors.2 Moreover, these effects adversely
affect the balance between oxygen supply and demand in
persons in whom this ratio is precariously balanced. The
most important effects 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 approximately
25% of the cardiac output, but this may be decreased 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 concentration of angiotensin II contributes to a
generalized and excessive vasoconstriction and provides a
powerful stimulus for aldosterone production by the adrenal cortex (see Chapter 25). Aldosterone increases tubular
reabsorption of sodium, with an accompanying increase
in water retention. Because aldosterone is metabolized in
the liver, its levels are further increased when heart failure
causes liver congestion. Angiotensin II also increases the
level of antidiuretic hormone (ADH), which serves as a
vasoconstrictor and inhibitor of water excretion7 (see Chapter 33). In addition to their individual effects on salt and
water balance, angiotensin II and aldosterone are also involved in regulating the inflammatory and reparative
processes that follow tissue injury.8 In this capacity, they
stimulate cytokine production, inflammatory cell (e.g., neutrophils and macrophages) adhesion, and chemotaxis;
activate macrophages at sites of injury and repair; and
stimulate the growth of fibroblasts and the synthesis of
collagen fibers.
Aldosterone-synthesizing enzymes have recently been
demonstrated in endothelial and vascular smooth muscle
cells as well as in the adrenal gland, suggesting that these
cells are capable of both producing aldosterone and responding to it.8,9 Thus, the progression of heart failure may
be augmented by aldosterone-mediated vascular remodeling in the heart and other organs. In the recent international (Randomized Aldactone Evaluation Study [RALES]) trial
involving more than 1600 patients with moderately severe
to severe heart failure, there was a 30% decrease in mortality from any cause among patients treated with standard
therapy plus spironolactone (an aldosterone antagonist) as
compared with those who received a placebo plus standard therapy.10
Natriuretic Peptides. The natriuretic peptide family consists of three peptides: atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide.11,12 Atrial
natriuretic peptide (ANP), which is released from atrial
cells in response to increased atrial stretch and pressure,
produces rapid and transient natriuresis, diuresis, and
moderate loss of potassium in the urine. It also inhibits aldosterone and renin secretion, acts as an antagonist to
angiotensin II, and inhibits the release of norepinephrine
from presynaptic nerve terminals. Brain natriuretic peptide (BNP), so named because it was originally found in extracts of porcine brain, is stored mainly in the ventricular
cells and is responsive to increased ventricular filling pressures. BNP has cardiovascular effects similar to ANP. The
CHAPTER 28
role of C-type natriuretic peptide (CNP), which is found
primarily in vascular tissue, has not as yet been clarified.
Circulating levels of both ANP and BNP are reportedly
elevated in persons with congestive heart failure. The concentrations are correlated with the extent of ventricular
dysfunction, increasing up to 30-fold in persons with advanced heart disease.11 Reliable assays of BNP are now
available and are used clinically in the diagnosis of heart
failure. Human BNP, synthesized by recombinant DNA
technology, is now available for treatment of persons with
acutely decompensated heart failure (discussed later).
Endothelin. The endothelins, released from the endothelial cells throughout the circulation, are potent vasoconstrictors. Other actions of the endothelins include
induction of vascular smooth muscle cell proliferation
and myocyte hypertrophy. Thus far, four endothelin peptides (endothelin-1 [ET-1], ET-2, ET-3, and ET-4) have
been identified.13 There are at least two types of endothelin receptors—type A and type B.2,13,14 Plasma ET-1 levels
correlate directly with pulmonary vascular resistance, and
it is thought that the peptide may play a role in mediating
pulmonary hypertension in persons with heart failure.2 An
endothelin receptor antagonist is now available for use in
the treatment of persons with pulmonary arterial hypertension due to severe heart failure.
Myocardial Hypertrophy and Remodeling. The development of myocardial hypertrophy constitutes one of the
principle mechanisms by which the heart compensates for
an increase in workload.2–4 Although ventricular hypertrophy improves the work performance of the heart, it also is
an important risk factor for subsequent cardiac morbidity
and mortality. Inappropriate hypertrophy and remodeling
can result in changes in structure (muscle mass, chamber
dilation) and function (impaired systolic or diastolic function) that often lead to further pump dysfunction and
hemodynamic overload.
It is now recognized that myocardial hypertrophy and
remodeling involve a series of complex events at both the
molecular and cellular levels.15 The myocardium is composed of myocytes, or muscle cells, and nonmyocytes. The
A
B
Heart Failure and Circulatory Shock
607
myocytes are the functional units of cardiac muscle. Their
growth is limited by an increment in cell size, as opposed
to an increase in cell number. The nonmyocytes include
cardiac macrophages, fibroblasts, vascular smooth muscle
cells, and endothelial cells. These cells, which are present
in the interstitial space and remain capable of an increase
in cell number, provide support for the myocytes. They
also determine many of the inappropriate changes that
occur during myocardial hypertrophy. For example, uncontrolled cardiac fibroblast growth is associated with increased synthesis of collagen fibers, myocardial fibrosis,
and ventricular wall stiffness.
Recent interest has focused on the type of hypertrophy that develops in persons with heart failure. At the cellular level, cardiac muscle cells respond to stimuli from
stress placed on the ventricular wall by pressure and volume overload by initiating several different processes that
lead to hypertrophy.15 These include stimuli that produce
symmetric hypertrophy with a proportionate increase in
muscle length and width, as occurs in athletes; concentric
hypertrophy with an increase in wall thickness, as occurs in
hypertension; and eccentric hypertrophy with a disproportionate increase in muscle length, as occurs in dilated cardiomyopathy2 (Fig. 28-3). When the primary stimulus for
hypertrophy is pressure overload, the increase in wall stress
leads to parallel replication of myofibrils, thickening of the
individual myocytes, and concentric hypertrophy. Concentric hypertrophy may preserve systolic function for a
period of time, but eventually the work performed by the
ventricle exceeds the vascular reserve, predisposing to ischemia. When the primary stimulus is ventricular volume
overload, increased diastolic wall stress leads to replication
of myofibrils in series, elongation of the cardiac muscle
cells, and eccentric hypertrophy. Eccentric hypertrophy
leads to a decrease in ventricular wall thickness with an increase in diastolic volume and wall tension.
The stimuli for hypertrophy and remodeling are
thought to reflect not only the mechanical stress placed
on the myocytes but also growth signals provided by the
release of substances such as angiotensin II, ANP, and
ET-1. Further research into the signals that cause specific
C
FIGURE 28-3 Different types of myocardial hypertrophy: (A) Normal symmetric hypertrophy with proportionate increases in myocardial wall thickness and length; (B) concentric hypertrophy with a disproportionate increase in wall thickness; and (C) eccentric hypertrophy with a disproportionate decrease in
wall thickness and ventricular dilatation.
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Cardiovascular Function
features of inappropriate myocardial hypertrophy and remodeling will hopefully lead to the identification of targets whose actions can be interrupted or modified.
and cardiomyopathy. As a result, treatment options tend
to be more limited and focus primarily on symptom management, with attempts to slow the natural progress of the
etiologic disease state.
CONGESTIVE HEART FAILURE
Systolic Versus Diastolic Failure
Heart failure occurs when the pumping ability of the heart
becomes impaired. Congestive heart failure (CHF) is heart
failure that is accompanied by congestion of body tissues.
After an initial compensatory period, the clinical manifestations of heart failure become complicated by pulmonary
or systemic venous congestion.
Heart failure may be caused by a variety of conditions, including acute myocardial infarction, hypertension, or degenerative conditions of the heart muscle
known collectively as cardiomyopathies. 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 persons with asymptomatic heart disease, heart
failure may be precipitated by an unrelated illness or
stress. Table 28-1 lists major causes of heart failure. Heart
failure may be described as high-output or low-output
failure, systolic or diastolic failure, and right-sided or leftsided failure.
Until recently, CHF was viewed mainly in terms of backward and forward failure. Backward failure represented failure of one of the ventricles to empty the heart effectively,
such that blood backs up in the venous system, causing
congestion. Forward failure was characterized by impaired
forward movement of blood into the arterial system emerging from the heart.
A more recent classification separates the pathophysiology of congestive failure into two categories—systolic
dysfunction and diastolic dysfunction. With systolic dysfunction, there is impaired ejection of blood from the
heart during systole; with diastolic dysfunction, there is
impaired filling of the ventricles during diastole (Fig. 28-4).
Many persons with heart failure fall into an intermediate
category, with combined elements of both systolic and
diastolic failure.16
High-Output Versus Low-Output Failure
High- and low-output heart failure are described in terms
of cardiac output. High-output failure is an uncommon type
of heart failure that is caused by an excessive need for cardiac output. With high-output failure, the function of the
heart may be supranormal but inadequate owing to excessive metabolic needs. Causes of high-output failure include severe anemia, thyrotoxicosis, conditions that cause
arteriovenous shunting, and Paget’s disease. High-output
failure tends to be specifically treatable.
Low-output failure is caused by disorders that impair the
pumping ability of the heart, such as ischemic heart disease
TABLE 28-1
Systolic Dysfunction. Systolic dysfunction involves a decrease in cardiac contractility and ejection fraction. It
commonly results from conditions that impair the contractile performance of the heart (e.g., ischemic heart disease and cardiomyopathy), produce a volume 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 contracts. This is called the ejection fraction. In systolic
heart failure, the ejection fraction declines progressively
with increasing degrees of myocardial dysfunction. In very
severe forms of heart failure, the ejection fraction may drop
Diastolic
dysfunction
Normal
Systolic
dysfunction
Causes of Heart Failure
Impaired Cardiac Function
Excess Work Demands
Myocardial Disease
Cardiomyopathies
Myocarditis
Coronary insufficiency
Myocardial infarction
Increased Pressure Work
Systemic hypertension
Pulmonary hypertension
Coarctation of the aorta
Valvular Heart Disease
Stenotic valvular disease
Regurgitant valvular disease
Increased Volume Work
Arteriovenous shunt
Excessive administration
of intravenous fluids
Congenital Heart Defects
Constrictive Pericarditis
Increased Perfusion Work
Thyrotoxicosis
Anemia
End
systole
End
diastole
FIGURE 28-4 Congestive heart failure due to systolic and diastolic
dysfunction. The ejection fraction represents the difference between the end-diastolic and end-systolic volumes. Normal systolic
and diastolic function with normal ejection fraction (middle); diastolic dysfunction with decreased ejection fraction due to decreased
diastolic filling (left); systolic dysfunction with decreased ejection
fraction due to impaired systolic function (right).
CHAPTER 28
to a single-digit percentage. With a decrease in ejection
fraction, there is a resultant increase in diastolic volume,
ventricular dilation, and ventricular wall tension and a rise
in ventricular end-diastolic pressure. The symptoms of persons with systolic dysfunction result mainly from reductions in ejection fraction and cardiac output.
Diastolic Dysfunction. Diastolic dysfunction, which reportedly accounts for approximately 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).17,18 Because of
impaired filling, congestive symptoms tend to predominate in diastolic dysfunction. Among the conditions that
cause diastolic dysfunction are those that restrict diastolic
filling (e.g., mitral stenosis), those that increase ventricular wall thickness and reduce chamber size (e.g., myocardial hypertrophy due to lung disease and hypertrophic
cardiomyopathy), and those that delay diastolic relaxation
(e.g., aging, ischemic 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 accept an increase in volume.19 A similar delay occurs with myocardial 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. Because tachycardia produces
a decrease in diastolic filling time, persons with diastolic
dysfunction often become symptomatic during activities
and situations that increase heart rate.
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. To understand the physiologic mechanisms
associated with heart failure, right- and left-sided failure
are considered separately (Fig. 28-5).
Right-Sided Heart Failure. The right heart pumps deoxygenated blood from the systemic circulation into the pulmonary circulation. Consequently, when the right heart
fails, there is accumulation or damming back of blood in
the systemic venous system. This causes an increase in
right atrial, right ventricular end-diastolic, and systemic
venous pressures.
A major effect of right-sided heart failure is the development of peripheral edema (see Fig. 28-5). 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 accumulation
of edema fluid is evidenced by a gain in weight (i.e., 1 pint
of accumulated fluid results in a 1-lb weight gain). Daily
measurement of weight can be used as a means of assessing fluid accumulation in a patient with chronic CHF. As
Left heart failure
Congestion of peripheral tissues
Liver congestion
GI tract
congestion
Signs related
to impaired liver
function
609
Right-Sided Versus Left-Sided Heart Failure
Right heart failure
Dependent
edema
and ascites
Heart Failure and Circulatory Shock
Decreased cardiac output
Activity
intolerance
and signs of
decreased
tissue
perfusion
Anorexia, GI distress,
weight loss
FIGURE 28-5 Manifestations of left-and right-sided heart failure.
Pulmonary congestion
Impaired gas
exchange
Cyanosis
and signs of
hypoxia
Pulmonary
edema
Cough with
frothy sputum
Orthopnea
Paroxysmal
nocturnal dyspnea
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Cardiovascular Function
a rule, a weight gain of more than 2 lb in 24 hours or 5 lb
in 1 week is considered a sign of worsening failure.
Right-sided heart failure also produces congestion of
the viscera. As venous distention progresses, blood backs
up in the hepatic veins that drain into the inferior vena
cava, and the liver becomes engorged. This may cause hepatomegaly and right upper quadrant pain. In severe and
prolonged right-sided failure, liver function is impaired,
and hepatic cells may die. Congestion of the portal circulation also may lead to engorgement of the spleen and the
development of ascites. Congestion of the gastrointestinal
tract may interfere with digestion and absorption of nutrients, causing anorexia and abdominal discomfort. The
jugular veins, which are above the level of the heart, are
normally collapsed in the standing position or when sitting with the head at higher than a 30-degree angle. In severe right-sided failure, the external jugular veins become
distended and can be visualized when the person is sitting
up or standing.
The causes of right-sided heart failure include conditions that restrict blood flow into the lungs. Stenosis or
regurgitation of the tricuspid or pulmonic valves, right
ventricular infarction, cardiomyopathy, and persistent
left-sided failure are common causes. Acute or chronic
pulmonary disease, such as severe pneumonia, pulmonary
embolus, or pulmonary hypertension, can cause right heart
failure, referred to as cor pulmonale.
Left-Sided Heart Failure. The left side of the heart moves
blood from the low-pressure pulmonary circulation into
the high-pressure arterial side of the systemic circulation. With impairment of left heart function, there is a
decrease in cardiac output, an increase in left atrial and
left ventricular end-diastolic pressures, and congestion
in the pulmonary circulation (see Fig. 28-5). When the
pulmonary capillary filtration pressure (normally approximately 10 mm Hg) exceeds the capillary osmotic pressure
(normally approximately 25 mm Hg), there is a shift of
intravascular fluid into the interstitium of the lung and development of pulmonary edema (Fig. 28-6). An episode of
pulmonary edema often occurs at night, after the person
has been reclining for some time and the gravitational
forces have been removed from the circulatory system. It
is then that the edema fluid that had been sequestered in
the lower extremities during the day is returned to the vascular compartment and redistributed to the pulmonary
circulation.
The most common causes of left-sided heart failure
are acute myocardial infarction and cardiomyopathy. Leftsided heart failure and pulmonary congestion can develop
very rapidly in persons with acute myocardial infarction.
Even when the infarcted area is small, there may be a surrounding area of ischemic tissue. This may result in a large
area of nonpumping ventricle and rapid onset of pulmonary edema. Stenosis or regurgitation of the aortic or mitral valves also creates the level of left-sided backflow that
results in pulmonary congestion. Pulmonary edema also
may develop during rapid infusion of intravenous fluids or
blood transfusions in an elderly person or in a person with
limited cardiac reserve.
Normal
Capillary
colloidal
osmotic
pressure
Venous 25 mm Hg
Capillary
filtration
pressure
10 mm Hg Arterial
Pulmonary edema
Capillary
filtration
pressure
>25 mm Hg Arterial
Capillary
colloidal
osmotic
pressure
Venous 25 mm Hg
FIGURE 28-6 Mechanism of respiratory symptoms in left-sided heart
failure. Normal exchange of fluid in the pulmonary capillaries (top).
The capillary filtration pressure that moves fluid out of the capillary
into the lung is less than the capillary colloidal osmotic pressure
that pulls fluid back into the capillary. Development of pulmonary
edema (bottom) occurs when the capillary filtration pressure exceeds the capillary colloidal osmotic pressure that pulls fluid back
into the capillary.
Manifestations of Congestive Heart Failure
The manifestations of heart failure depend on the extent
and type of cardiac dysfunction that is present and the rapidity with which it develops. A person with previously stable compensated heart failure may develop signs of heart
failure for the first time when the condition has advanced
to a critical point, such as with a progressive increase in
pulmonary hypertension in a person with mitral valve regurgitation. Overt heart failure also may be precipitated by
conditions such as infection, emotional stress, uncontrolled hypertension, administration of fluid overload, or
inappropriate reduction in therapy.16 Many persons with
serious underlying heart disease, regardless of whether they
have previously experienced heart failure, may be relatively
asymptomatic as long as they carefully adhere to their
treatment regimen. A dietary excess of sodium is a frequent
cause of sudden cardiac decompensation.
CHAPTER 28
The manifestations of heart failure reflect the physiologic effects of the impaired pumping ability of the heart,
decreased renal blood flow, and activation of the sympathetic compensatory mechanisms. The severity and progression of symptoms depend on the extent and type of
dysfunction that is present (systolic vs. diastolic failure).
The signs and symptoms include fluid retention and
edema, shortness of breath and other respiratory manifestations, fatigue and limited exercise tolerance, cachexia
and malnutrition, and cyanosis. Distention of the jugular
veins may be present in right-sided failure. Persons with severe heart failure may exhibit diaphoresis and tachycardia.
Fluid Retention and Edema. Many of the manifestations
of CHF result from the increased capillary pressures that
develop in the peripheral circulation in right-sided heart
failure and in the pulmonary circulation in left-sided heart
failure. The increased capillary pressure reflects an overfilling of the vascular system because of increased salt and
water retention and venous congestion resulting from the
impaired pumping ability of the heart.
Nocturia is a nightly increase in urine output that occurs relatively early in the course of CHF. It results from
the return to the circulation of edema fluids from the dependent parts of the body when the person assumes the
supine position for the night. As a result, the cardiac output, renal blood flow, glomerular filtration, and urine output increase. Oliguria is a late sign related to a severely
reduced cardiac output and resultant renal failure.
Respiratory Manifestations. Shortness of breath due to
congestion of the pulmonary circulation is one of the major
manifestations of left-sided heart failure. Perceived shortness of breath (i.e., breathlessness) is called dyspnea. Dyspnea related to an increase in activity is called exertional
dyspnea. Orthopnea is shortness of breath that occurs when
a person is supine. The gravitational forces that cause fluid
to become sequestered in the lower legs and feet when the
person is standing or sitting are removed when a person
with CHF assumes the supine position; fluid from the legs
and dependent parts of the body is mobilized and redistributed to an already distended pulmonary circulation.
Paroxysmal nocturnal dyspnea is a sudden attack of dyspnea
that occurs during sleep. It disrupts sleep, and the person
awakens with a feeling of extreme suffocation that resolves
when he or she sits up. Initially, the experience may be
interpreted as awakening from a bad dream.
A subtle and often overlooked symptom of heart failure is a chronic dry, nonproductive cough, which becomes
worse when the person is lying down. Bronchospasm due
to congestion of the bronchial mucosa may cause wheezing and difficulty in breathing. This condition is sometimes referred to as cardiac asthma.
Cheyne-Stokes respiration, also known as periodic breathing, is characterized by a slow waxing and waning of respiration. The person breathes deeply for a period when the
arterial carbon dioxide pressure (PCO2) is high and then
slightly or not at all when the PCO2 falls. In persons with
left-sided heart failure, the condition is thought to be
caused by a prolongation of the heart-to-brain circulation,
particularly in persons with hypertension and associated
Heart Failure and Circulatory Shock
611
cerebral vascular disease. Cheyne-Stokes breathing may
contribute to daytime sleepiness, and occasionally the
person awakens at night with dyspnea precipitated by
Cheyne-Stokes breathing.16
Fatigue and Limited Exercise Tolerance. Fatigue and limb
weakness often accompany diminished output from the
left ventricle. Cardiac fatigue is different from general fatigue in that it usually is not present in the morning but appears and progresses as activity increases during the day. In
acute or severe left-sided failure, cardiac output may fall to
levels that are insufficient for providing the brain with adequate oxygen, and there are indications of mental confusion and disturbed behavior. Confusion, impairment of
memory, anxiety, restlessness, and insomnia are common
in elderly persons with advanced heart failure, particularly
in those with cerebral atherosclerosis. These very symptoms
may confuse the diagnosis of heart failure in the elderly
because of the myriad other causes associated with aging.
Cachexia and Malnutrition. Cardiac cachexia is a condition of malnutrition and tissue wasting that occurs in persons with end-stage heart failure. A number of factors
probably contribute to its development, including the fatigue and depression that interfere with food intake, the
congestion of the liver and gastrointestinal structures that
impairs digestion and absorption and produces feelings of
fullness, and the circulating toxins and mediators released
from poorly perfused tissues that impair appetite and contribute to tissue wasting.
Cyanosis. Cyanosis is the bluish discoloration of the skin
and mucous membranes caused by excess desaturated
hemoglobin in the blood; it often is a late sign of heart failure. Cyanosis may be central, caused by arterial desaturation resulting from impaired pulmonary gas exchange, or
peripheral, caused by venous desaturation resulting from
extensive extraction of oxygen at the capillary level. Central cyanosis is caused by conditions that impair oxygenation of the arterial blood, such as pulmonary edema, left
heart failure, or right-to-left shunting. Peripheral cyanosis
is caused by conditions such as low-output failure that
cause delivery of poorly oxygenated blood to the peripheral tissues, or by conditions such as peripheral vasoconstriction that cause excessive removal of oxygen from the
blood. Central cyanosis is best monitored in the lips and
mucous membranes because these areas are not subject to
conditions such as cold that cause peripheral cyanosis.
Persons with right-sided or left-sided heart failure may develop cyanosis especially around the lips and in the peripheral parts of the extremities.
Diagnostic Methods
Diagnostic methods in heart failure are directed toward establishing the cause of the disorder and determining the
extent of the dysfunction.20 Because heart failure represents
the failure of the heart as a pump and can occur in the
course of a number of heart diseases or other systemic disorders, the diagnosis of heart failure often is based on signs
and symptoms related to the failing heart itself, such as
shortness of breath and fatigue. The functional classifica-
612
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Cardiovascular Function
tion of the New York Heart Association (NYHA) is one
guide to classifying the extent of dysfunction (Table 28-2).
The diagnostic methods include history and physical
examination, laboratory studies, electrocardiography, chest
radiography, and echocardiography. The history should include information related to dyspnea, cough, nocturia, generalized fatigue, and other signs and symptoms of heart
failure. A complete physical examination includes assessment of heart rate, heart sounds, blood pressure, jugular
veins for venous congestion, lungs for signs of pulmonary
congestion, and lower extremities for edema. Laboratory
tests are used in the diagnosis of anemia and electrolyte imbalances and to detect signs of chronic liver congestion.
Measurements of BNP are increasingly being used to confirm the diagnosis of heart failure; to evaluate the severity
of left ventricular compromise and estimate the prognosis
and predict future cardiac events, such as sudden death;
and to evaluate the effectiveness of treatment.21,22
Echocardiography plays a key role in assessing the
anatomic and functional abnormalities in CHF, which include the size and function of cardiac valves, the motion of
both ventricles, and the ventricular ejection fraction.22,23
Electrocardiographic findings may indicate atrial or ventricular hypertrophy, underlying disorders of cardiac
rhythm, or conduction abnormalities such as right or left
bundle branch block. Radionuclide angiography and cardiac catheterization are other diagnostic tests used to detect the underlying causes of heart failure, such as heart
TABLE 28-2
New York Heart Association
Functional Classification of Patients
With Heart Disease
Classification
Characteristics
Class I
Patients with cardiac disease but without
the resulting limitations in physical
activity. Ordinary activity does not
cause undue fatigue, palpitation,
dyspnea, or anginal pain.
Patients with heart disease resulting in
slight limitations of physical activity.
They are comfortable at rest. Ordinary
physical activity results in fatigue,
palpitation, dyspnea, or anginal pain.
Patients with cardiac disease resulting in
marked limitation of physical activity.
They are comfortable at rest. Less than
ordinary physical activity causes fatigue,
palpitation, dyspnea, or anginal pain.
Patients with cardiac disease resulting in
inability to carry on any physical
activity without discomfort. The
symptoms of cardiac insufficiency or of
the anginal syndrome may be present
even at rest. If any physical activity is
undertaken, discomfort increases.
Class II
Class III
Class IV
(From Criteria Committee of the New York Heart Association. [1964].
Diseases of the heart and blood vessels: Nomenclature and criteria for
diagnosis [6th ed., pp. 112–113]. Boston: Little, Brown)
defects and cardiomyopathy. Chest radiographs provide
information about the size and shape of the heart and pulmonary vasculature. The cardiac silhouette can be used to
detect cardiac hypertrophy and dilatation. X-ray films can
indicate the relative severity of the failure by revealing
whether pulmonary edema is predominantly vascular, interstitial, or advanced to the alveolar and bronchial stages.
Invasive hemodynamic monitoring often is used in
the management of acute, life-threatening episodes of
heart failure. These monitoring methods include central
venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), thermodilution cardiac output measurements, and intra-arterial measurements of blood pressure.
CVP reflects the amount of blood returning to the
heart. Measurements of CVP are best obtained by means
of a catheter inserted into the right atrium through a peripheral vein, or by means of the right atrial port (opening)
in a pulmonary artery catheter. This pressure is decreased
in hypovolemia and increased in right heart failure. The
changes that occur in CVP over time usually are more significant than the absolute numeric values obtained during
a single reading.
PCWP is obtained by means of a flow-directed, balloon-tipped pulmonary artery (Swan-Ganz) catheter. This
catheter is introduced through a peripheral or central vein
and then advanced into the right atrium. The balloon
is then inflated with air, enabling the catheter to float
through the right ventricle into the pulmonary artery until
it becomes wedged in a small pulmonary vessel (Fig. 28-7).
After the catheter is in place, the balloon is deflated and
then inflated only when the PCWP is being measured.
Continuous inflation of the balloon with its accompanying occlusion of a small pulmonary artery would cause
necrosis of pulmonary tissue. With the balloon inflated,
Swan-Ganz catheter
balloon tip
FIGURE 28-7 Swan-Ganz balloon-tipped catheter positioned in a pulmonary capillary. The pulmonary capillary wedge pressure, which
reflects the left ventricular diastolic pressure, is measured with the
balloon inflated.
CHAPTER 28
the catheter monitors pulmonary capillary pressures in direct communication with pressures from the left heart,
thus providing a means of assessing the pumping ability
of the left heart.
One type of pulmonary artery catheter is equipped
with a thermistor probe to obtain thermodilution measurements of cardiac output. A known amount of solution of a
known temperature (iced or room temperature) is injected
into the right atrium through an opening in the catheter,
and the temperature of the blood is measured downstream
in the pulmonary artery by means of a thermistor probe
located at the end of that catheter. A microcomputer
calculates the cardiac output from the time-temperature
curve resulting from the rate of change of the temperature
of the blood that flows past the thermistor. Catheters with
oximeters built into their tips that permit continuous
monitoring of oxygen saturation (SvO2) also are available,
as are catheters that provide continuous output data.
Intra-arterial blood pressure monitoring provides a
means for continuous monitoring of blood pressure. It is
used in persons with acute heart failure when aggressive
intravenous drug therapy or a mechanical assist device is
required. Measurements are obtained through the use of a
small catheter inserted into a peripheral artery, usually the
radial artery. The catheter is connected to a pressure transducer, and beat-by-beat measurements of blood pressure
are recorded. The monitoring system displays the contour
of the pressure waveform and a digital reading of the systolic, diastolic, and mean arterial pressures along with
heart rate and rhythm. Continuous digital display of respiratory rate and core temperature from the thermistor located at the end of the pulmonary artery catheter also may
be warranted.
Treatment Methods
The goals of treatment for chronic heart failure are directed toward relieving the symptoms and improving the
quality of life, with a long-term goal of slowing, halting,
or reversing the cardiac dysfunction.3,22,24,25 Treatment
measures include correction of reversible causes such as
anemia or thyrotoxicosis, surgical repair of a ventricular
defect or an improperly functioning valve, pharmacologic
and nonpharmacologic control of afterload stresses such
as hypertension, modification of activities and lifestyle to
a level consistent with the functional limitations of a reduced cardiac reserve, and the use of medications to improve cardiac function and limit excessive compensatory
mechanisms. Restriction of salt intake and diuretic therapy facilitate the excretion of edema fluid. Counseling,
health teaching, and ongoing evaluation programs help
persons with heart failure to manage and cope with their
treatment regimen.
In severe heart failure, restriction of activity, including bed rest if necessary, often facilitates temporary recompensation of cardiac function. However, there is no
convincing evidence that continued bed rest is of benefit.
Carefully designed and managed exercise programs for patients with CHF are well tolerated and beneficial to patients with stable NYHA class I to III heart failure.26,27
Heart Failure and Circulatory Shock
613
Pharmacologic Treatment. Once heart failure is moderate
to severe, polypharmacy becomes a management standard and often includes diuretics, digoxin, angiotensinconverting enzyme (ACE) inhibitors, and β-adrenergic–
blocking agents.28–30 The choice of pharmacologic agents
is determined by problems caused by the disorder (i.e., systolic or diastolic dysfunction) and those brought about
by activation of compensatory mechanisms (e.g., excess
fluid retention, inappropriate activation of sympathetic
mechanisms).
Diuretics are among the most frequently prescribed
medications for heart failure. They promote the excretion
of edema fluid and help to sustain cardiac output and tissue perfusion by reducing preload and allowing the heart
to operate at a more optimal part of the Frank-Starling
curve. Thiazide and loop diuretics are used. In emergencies, such as acute pulmonary edema, loop diuretics such
as furosemide can be administered intravenously. When
given intravenously, these drugs act quickly to reduce venous return through vasodilatation so that right ventricular output and pulmonary vascular pressures are decreased.
This response to intravenous drug administration is extrarenal and precedes the onset of diuresis.
Digitalis has been a recognized treatment for CHF for
more than 200 years. The various forms of digitalis are
called cardiac glycosides. They improve cardiac function by
increasing the force and strength of ventricular contraction.
By decreasing sinoatrial node activity and decreasing conduction through the atrioventricular node, they also slow
the heart rate and increase diastolic filling time. Although
not a diuretic, digitalis promotes urine output by improving cardiac output and renal blood flow. The digitalis drugs
act by binding to sodium-potassium adenosine triphosphatase (ATPase) on the cell membrane and inhibiting the
sodium-potassium pump. When intracellular sodium is increased because of inhibition of the sodium-potassium
pump by digitalis, the exchange of intracellular calcium
for extracellular sodium is inhibited; as a result, more calcium is available to activate the myocardial actin–myosin
contractile apparatus. The role of digitalis in the treatment
of heart failure is controversial and has been studied in
clinical trials over the past several decades. Although the
results of these studies remain controversial, there seems
to be a growing consensus that although it does not necessarily reduce mortality rates, digitalis prevents clinical
deterioration and hospitalization and improves exercise
tolerance.31,32
The ACE inhibitors, which prevent the conversion of
angiotensin I to angiotensin II, have been effectively used
in the treatment of heart failure. In heart failure, renin activity frequently is elevated because of decreased renal
blood flow. The net result is an increase in angiotensin II,
which causes vasoconstriction and increased aldosterone
production with a subsequent increase in salt and water retention by the kidney. Both mechanisms increase the
workload of the heart. The newer angiotensin II receptor
blockers have the advantage of not causing a cough, which
is a troublesome side effect of the ACE inhibitors for many
persons. The results of the previously mentioned RALES
trial suggest that the aldosterone antagonist, spironolac-
614
UNIT VI
Cardiovascular Function
tone, may be beneficial for persons with moderately severe
to severe heart failure.10
Large clinical trials have shown that long-term therapy with β-adrenergic–blocking agents reduces morbidity
and mortality in persons with CHF.24,29,33 Left ventricular
dysfunction is associated with activation of the reninangiotensin-aldosterone and sympathetic nervous systems.
Chronic elevation of norepinephrine levels has been shown
to cause cardiac muscle cell death and progressive left ventricular dysfunction and is associated with poor prognosis
in heart failure. Until recently, β-blockers were thought to
be contraindicated in left ventricular systolic dysfunction
because of their negative inotropic effects. Large clinical
trials involving more than 10,000 patients, most of whom
had stable NYHA class II and III heart failure, have demonstrated significant reductions in the overall mortality rate
with treatment with various β blockers. Several β-blockers
(i.e., carvedilol, metoprolol, and bisoprolol) are used in the
treatment of heart failure. The ongoing Carvedilol and
Metoprolol European Trial (COMET) is designed to evaluate the relative benefits of these agents.29
The new agent, nesiritide, a recombinant form of
human B-type natriuretic peptide, has recently been approved for treatment of acute and decompensated heart
failure.34,35 The drug, which has the same structure as the
endogenous natriuretic peptide, is a potent vasodilator that
reduces ventricular filling pressures and improves cardiac
output. Because it must be given intravenously in a closely
supervised clinical setting, it is usually reserved for patients
with severe heart failure who do not respond to other forms
of therapy.
Cardiac Resynchronization. Some patients with heart failure due to systolic dysfunction have abnormal intraventricular conduction that results in dyssynchronous and
ineffective contractions.36 Cardiac resynchronization therapy involves the placement of pacing leads into the right
and left ventricles as a means of resynchronizing the contraction of the two ventricles. Results of studies with up to
6 months of follow-up data have reported an increase in
ejection fraction and improvement in symptoms and exercise tolerance. Definitive data on more long-term morbidity and mortality are not yet available.
ACUTE PULMONARY EDEMA
Acute pulmonary edema is the most dramatic symptom of
left heart failure. It is a life-threatening condition in which
capillary fluid moves into the alveoli. The accumulated
fluid in the alveoli and respiratory airways causes lung stiffness, makes lung expansion more difficult, and impairs the
gas exchange function of the lung. With the decreased ability of the lungs to oxygenate the blood, the hemoglobin
leaves the pulmonary circulation without being fully oxygenated, resulting in shortness of breath and cyanosis.
Manifestations
Acute pulmonary edema usually is a terrifying experience.
The person usually is seen sitting and gasping for air, in obvious apprehension. The pulse is rapid, the skin is moist and
cool, and the lips and nail beds are cyanotic. As the lung
edema worsens and oxygen supply to the brain drops, confusion and stupor appear. Dyspnea and air hunger are accompanied by a cough productive of frothy (resembling
beaten egg whites) and often blood-tinged sputum—the
effect of air mixing with serum albumin and red blood cells
that have moved into the alveoli. The movement of air
through the alveolar fluid produces fine crepitant sounds
called crackles, which can be heard through a stethoscope
placed on the chest. As fluid moves into the larger airways,
the breathing becomes louder. The crackles heard earlier become louder and coarser. In the terminal stage, the breathing pattern is called the death rattle. Persons with severe
pulmonary edema literally drown in their own secretions.
Treatment
Treatment of acute pulmonary edema is directed toward reducing the fluid volume in the pulmonary circulation. This
can be accomplished by reducing the amount of blood that
the right heart delivers to the lungs or by improving the
work performance of the left heart. Several measures can
decrease the blood volume in the pulmonary circulation;
the seriousness of the pulmonary edema determines which
are used. One of the simplest measures to relieve orthopnea is assumption of the seated position. For many persons, sitting up or standing is almost instinctive and may
be sufficient to relieve the symptoms associated with mild
accumulation of fluid.
Measures to improve left heart performance focus on
decreasing the preload by reducing the filling pressure of
the left ventricle and on reducing the afterload against
which the left heart must pump. This can be accomplished
through the use of diuretics, vasodilator drugs, treatment
of arrhythmias that impair cardiac function, and improvement of the contractile properties of the left ventricle with
digitalis. Rapid digitalization can be accomplished with
intravenous administration of the drug. Although its
mechanisms of action are unclear, morphine sulfate usually is the drug of choice in acute pulmonary edema. Morphine relieves anxiety and depresses the pulmonary
reflexes that cause spasm of the pulmonary vessels. It also
increases venous pooling by vasodilatation.
Oxygen therapy increases the oxygen content of the
blood and helps relieve anxiety. Positive-pressure breathing increases the intra-alveolar pressure, opposes the capillary filtration pressure in the pulmonary capillaries, and
sometimes is used as a temporary measure to decrease the
amount of fluid moving into the alveoli. Positive-pressure
breathing can be administered through a specially designed, continuous positive airway pressure mask. In the
most severe cases, however, endotracheal intubation and
mechanical ventilation may be necessary.
CARDIOGENIC SHOCK
Cardiogenic shock implies failure of the heart to pump
blood adequately. Cardiogenic shock can occur relatively
quickly because of the damage to the heart that occurs during myocardial infarction; ineffective pumping caused by
CHAPTER 28
cardiac arrhythmias; mechanical defects that may occur as
a complication of myocardial infarction, such as ventricular
septal defect; ventricular aneurysm; acute disruption of
valvular function; or problems associated with open-heart
surgery. Cardiogenic shock also may ensue as an end-stage
condition of coronary artery disease or cardiomyopathy.
The most common cause of cardiogenic shock is myocardial infarction. Most patients who die of cardiogenic
shock have lost at least 40% of the contracting muscle of
the left ventricle because of a recent infarct or a combination of recent and old infarcts.37,38 Cardiogenic shock can
follow other types of shock associated with inadequate
coronary blood flow, or it can develop because substances
released from ischemic tissues impair cardiac function. One
such substance, myocardial depressant factor, is thought
to be released into the circulation during severe shock.
Myocardial depressant factor produces reversible (although
often severe) myocardial depression, ventricular dilation,
and decreased left ventricular ejection fraction and diastolic pressure.39
In all cases of cardiogenic shock, there is failure to
eject blood from the heart, hypotension, and inadequate
cardiac output. Increased systemic vascular resistance often
contributes to the deterioration of cardiac function by increasing afterload or the resistance to ventricular systole.
The filling pressure, or preload of the heart, also is increased as blood returning to the heart is added to blood
that previously returned but was not pumped forward, resulting in an increase in end-systolic ventricular volume.
Increased resistance to ventricular systole (i.e., afterload),
combined with decreased myocardial contractility, causes
the increased end-systolic ventricular volume and increased
preload, which further complicate cardiac status.
Manifestations
The signs and symptoms of cardiogenic shock are consistent with those of extreme heart failure. The lips, nail beds,
and skin are cyanotic because of stagnation of blood flow
and increased extraction of oxygen from the hemoglobin
as it passes through the capillary bed. The CVP and PCWP
rise as a result of volume overload caused by the pumping
failure of the heart.
Heart Failure and Circulatory Shock
615
ered systemic vascular resistance; this allows blood to be
redistributed from the pulmonary vascular bed to the systemic circulation. Catecholamines increase cardiac contractility but must be used with caution because they also
produce vasoconstriction and increased work of the heart
by increasing afterload.
The intra-aortic balloon pump provides a means of increasing aortic diastolic pressure and enhances coronary
and peripheral blood flow without increasing systolic pressure and the afterload, against which the left ventricle must
pump.40 The device, which pumps in synchrony with the
heart, consists of a 10-inch long balloon that is inserted
through a catheter into the descending aorta (Fig. 28-8).
The balloon is positioned so that the distal tip lies approximately 1 inch from the aortic arch. The balloon is filled
with helium and is timed to inflate during ventricular diastole and deflate just before ventricular systole. Diastolic
inflation creates a pressure wave in the ascending aorta that
increases coronary artery flow and a less intense wave in
the lower aorta that enhances organ perfusion. The sudden
balloon deflation at the onset of systole lowers the resistance to ejection of blood from the left ventricle, thereby
increasing the heart’s pumping efficiency and decreasing
myocardial oxygen consumption.
When cardiogenic shock is caused by myocardial infarction, several aggressive interventions can be used successfully. The rapid and aggressive administration of a
thrombolytic agent to dissolve intracoronary thrombi has
been shown to improve aortic pressure and survival significantly.41 Another alternative includes emergent direct
percutaneous transluminal angioplasty (see Chapter 26).
Left subclavian
artery
Treatment
Treatment of cardiogenic shock requires a precarious balance between improving cardiac output, reducing the workload and oxygen needs of the myocardium, and preserving
coronary perfusion. Fluid volume must be regulated within
a level that maintains the filling pressure (i.e., venous return) of the heart and maximum use of the Frank-Starling
mechanism without causing pulmonary congestion.
Pharmacologic treatment includes the use of vasodilators such as nitroprusside and nitroglycerin. Nitroprusside causes arterial and venous dilatation, producing
a decrease in venous return to the heart, with a reduction
in arterial resistance against which the left heart must
pump. Nitroglycerin focuses its effects on the venous vascular beds until, at high doses, it begins to dilate the arterial beds as well. The arterial pressure is maintained by an
increased ventricular stroke volume ejected against a low-
Renal arteries
FIGURE 28-8 Aortic balloon pump. (Hudak C.M., Gallo B.M. [1994].
Critical care nursing [6th ed.]. Philadelphia: J.B. Lippincott)
616
UNIT VI
Cardiovascular Function
MECHANICAL SUPPORT
AND HEART TRANSPLANTATION
Refractory heart failure reflects deterioration in cardiac
function that is unresponsive to medical or surgical interventions. With improved methods of treatment, more people are reaching a point at which a cure is unachievable and
death is imminent without mechanical support or heart
transplantation.
Since the early 1960s, significant progress has been
made in improving the efficacy of ventricular assist devices
(VADs), which are mechanical pumps used to support ventricular function. VADs are used to decrease the workload
of the myocardium while maintaining cardiac output and
systemic arterial pressure. This decreases the workload on
the ventricle and allows it to rest and recover. Most VADs
require an invasive open chest procedure for implantation. They may be used in patients who fail or have difficulty being weaned from cardiopulmonary bypass after
cardiac surgery; those who develop cardiogenic shock after
myocardial infarction; those with end-stage cardiomyopathy; and those who are awaiting cardiac transplantation.
Earlier and more aggressive use of VADs as a bridge to
transplantation has been shown to increase survival.40,42
VADs that allow the patient to be mobile and managed at
home are beginning to be considered as long-term or permanent support for treatment of end-stage heart failure,
rather than simply as a bridge to transplantation. VADs
can be used to support the function of the left ventricle,
right ventricle, or both.
Heart transplantation remains the treatment of choice for
end-stage cardiac failure. The number of successful heart
transplantations has been steadily climbing, with more than
2800 procedures performed per year. Patients with heart
transplants who are treated with triple-immunosuppressant
therapy have 5-year survival rates of 75% in men and 62%
in women.43 Despite the overall success of heart transplantation, donor availability and complications from infection,
rejection, and immunosuppression drug therapy remain
problems.
The current technique for orthotopic heart transplantation (the most common) was described in 1960 by Lower
and Shumway.43 The procedure is performed by placing
the recipient on cardiopulmonary bypass and excising the
diseased heart. The method involves retaining a large portion of the posterior wall of the right and left atrium in the
recipient and attaching the donor heart with relatively
long sutures (Fig. 28-9). Pacing wires are loosely attached
to the right ventricle to assist with temporary pacing of
the heartbeat in the event of bradycardia in the immediate postoperative phase.
An alternative to heart transplantation is a procedure
called cardiomyoplasty.44 This procedure involves fashioning one of the patient’s latissimus dorsi back muscles into
a wrap that embraces the heart. The muscle is native tissue; thus, rejection is not a problem. Because the proximal
end of the muscle remains intact, perfusion is optimal
with enhanced potential for healing and performance. A
pacemaker, which is placed between the heart and the
back muscle, stimulates the muscle to contract. After several weeks of rest and healing, the skeletal muscle is grad-
FIGURE 28-9 Orthotopic heart transplantation and sites of donor
heart attachment.
ually stimulated by the pacemaker to condition it in a necessary transformation into a more fatigue-resistant type of
muscle tissue. Although more work is needed to identify
the optimal way to wrap the muscle and condition it for
maximum ventricular assist, cardiomyoplasty provides an
alternative to transplantation for some persons, particularly when a donor heart is not available.
In summary, heart failure occurs when the heart fails to pump
sufficient blood to meet the metabolic needs of body tissues.
The physiology of heart failure reflects an interplay between a
decrease in cardiac output that accompanies impaired function
of the failing heart and the compensatory mechanisms designed to preserve the cardiac reserve. Adaptive mechanisms
include the Frank-Starling mechanism, sympathetic nervous
system activation, the renin-angiotensin-aldosterone mechanism, natriuretic peptides, the endothelins, and myocardial
hypertrophy, and remodeling. In the failing heart, early decreases in cardiac function may go unnoticed because these
compensatory mechanisms maintain the cardiac output. This
is called compensated heart failure. Unfortunately, the mechanisms were not intended for long-term use, and in severe and
prolonged decompensated heart failure, the compensatory
mechanisms no longer are effective, and instead contribute to
the progression of cardiac 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. With high-output failure, the function of the heart may
be supranormal but inadequate because of excessive metabolic
needs, and low-output failure is caused by disorders that impair
the pumping ability of the heart. With systolic dysfunction, there
is impaired ejection of blood from the heart during systole; with
diastolic dysfunction, there is impaired filling of the heart during
diastole. Right-sided failure is characterized by congestion in the
peripheral circulation, and left-sided failure by congestion in the
pulmonary circulation.
CHAPTER 28
Heart Failure and Circulatory Shock
617
The manifestations of heart failure include edema, nocturia,
fatigue and impaired exercise tolerance, cyanosis, signs of increased sympathetic nervous system activity, and impaired
gastrointestinal function and malnutrition. In right-sided failure,
there is dependent edema of the lower parts of the body, engorgement of the liver, and ascites. In left-sided failure, shortness of breath and chronic, nonproductive cough are common.
The diagnostic methods in heart failure are directed toward
establishing the cause and extent of the disorder. Treatment is
directed toward correcting the cause whenever possible, improving cardiac function, maintaining the fluid volume within
a compensatory level, and developing an activity pattern consistent with individual limitations in cardiac reserve. Among
the medications used in the treatment of heart failure are
diuretics, digoxin, ACE inhibitors, and β-blockers.
Acute pulmonary edema is a life-threatening condition in
which the accumulation of fluid in the interstitium of the lung
and alveoli interferes with lung expansion and gas exchange.
It is characterized by extreme breathlessness, crackles, frothy
sputum, cyanosis, and signs of hypoxemia. In cardiogenic
shock, there is failure to eject blood from the heart, hypotension, inadequate cardiac output, and impaired perfusion of peripheral tissues. Mechanical support devices, including the
intra-aortic balloon pump (for acute failure) and the VAD, sustain life in persons with severe heart failure. Heart transplantation remains the treatment of choice for many persons with
end-stage heart failure.
Circulatory shock can be described as a failure of the vascular system to supply the peripheral tissues and organs
of the body with an adequate blood supply. It is not a specific disease but a syndrome that can occur in the course
of many life-threatening traumatic conditions or disease
states. It can be caused by a decrease in blood volume
(hypovolemic shock), obstruction of blood flow through
the circulatory system (obstructive shock), or vasodilation
with redistribution of blood flow (distributive shock). These
three main types of shock are summarized in Chart 28-1
and depicted in Figure 28-10. Cardiogenic shock, which results from failure of the heart as a pump, was discussed earlier in the chapter. As with heart failure, circulatory shock
produces compensatory physiologic responses that eventually decompensate into various shock states if the condition is not properly treated in a timely manner.
Circulatory Failure (Shock)
Physiology of Hypovolemic Shock
After completing this section of the chapter, you should be able to
meet the following objectives:
✦ State a clinical definition of shock
✦ Compare the chief characteristics of hypovolemic shock,
obstructive shock, and distributive shock
HYPOVOLEMIC SHOCK
Hypovolemic shock is characterized by diminished blood
volume such that there is inadequate filling of the vascular
compartment (see Fig. 28-10). It occurs when there is an
acute loss of 15% to 20% of the circulating blood volume.
The decrease may be caused by an external loss of whole
blood (e.g., hemorrhage), plasma (e.g., severe burns), or extracellular fluid (e.g., gastrointestinal fluids lost in vomiting
or diarrhea). Hypovolemic shock also can result from an internal hemorrhage or from third-space losses, when extracellular fluid is shifted from the vascular compartment to
the interstitial space or compartment.
Hypovolemic shock has been the most widely studied
type of shock and usually serves as a prototype in discussions of the manifestations of shock. Figure 28-11 shows
the effect of removing blood from the circulatory system
during approximately 30 minutes.45 Approximately 10%
can be removed without changing the cardiac output or
✦ Describe the compensatory mechanisms that occur and
✦
✦
✦
✦
✦
relate them to the stages and manifestations of hypovolemic shock
State the causes of obstructive shock
Compare the pathophysiology of neurogenic shock,
anaphylactic shock, and septic shock as they relate to
the pathophysiology of distributive shock
Describe the complications of shock as they relate to the
lung, kidney, gastrointestinal tract, and blood clotting
State the rationale for treatment measures to correct and
reverse shock
Define multiple organ dysfunction syndrome and cite its
significance in shock
The functions of the circulatory system are to perfuse
body tissues and supply them with oxygen. Adequate perfusion of body tissues depends on the pumping ability of
the heart, a vascular system that transports blood to the
cells and back to the heart, sufficient blood to fill the vascular system, and tissues that are able to use and extract
oxygen and nutrients from the blood.
CHART 28-1
Classification of Circulatory Shock
Hypovolemic
Loss of whole blood
Loss of plasma
Loss of extracellular fluid
Obstructive
Inability of the heart to fill properly (cardiac tamponade)
Obstruction to outflow from the heart ( pulmonary
embolus, cardiac myxoma, pneumothorax, or
dissecting aneurysm)
Distributive
Loss of sympathetic vasomotor tone
Presence of vasodilating substances in the blood
(anaphylactic shock)
Presence of inflammatory mediators (septic shock)
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Normal
Shock
Hypovolemic
Obstructive
Distributive
FIGURE 28-10 Types of shock.
CIRCULATORY SHOCK
➤ Circulatory shock represents the inability of the circulation
to adequately perfuse the tissues of the body.
➤ It can result from a loss of fluid from the vascular compartment (hypovolemic shock), obstruction of flow
through the vascular compartment (obstructive shock),
or an increase in the size of the vascular compartment
that interferes with the distribution of blood
(distributive shock).
➤ The manifestations of shock reflect both the impaired perfusion of body tissues and the body’s attempt to maintain
tissue perfusion through conservation of water by the kidney, translocation of fluid from extracellular to the intravascular compartment, and activation of sympathetic nervous
system mechanisms that increase heart rate and divert
blood from less to more essential body tissues.
FIGURE 28-11 Effect of hemorrhage on cardiac output and arterial
pressure. (Guyton A.C. [1986]. Textbook of medical physiology [7th ed.].
Philadelphia: W.B. Saunders)
CHAPTER 28
arterial pressure. The average blood donor loses a pint of
blood without experiencing adverse effects. As increasing
amounts of blood (10% to 25%) are removed, the cardiac
output falls, but the arterial pressure is maintained because of sympathetic-mediated increases in heart rate and
vasoconstriction. Blood pressure is the product of cardiac
output and systemic vascular resistance (also known as
the peripheral vascular resistance); thus, an increase in
systemic vascular resistance can maintain the blood pressure in the presence of decreased cardiac output for a short
period of time. Cardiac output and tissue perfusion decrease before signs of hypotension occur. Cardiac output
and arterial pressure fall to zero when approximately 35%
to 45% of the total blood volume has been removed.45
Compensatory Mechanisms. Without compensatory
mechanisms to maintain cardiac output and blood pressure, the loss of vascular volume would result in a rapid progression from the initial to the progressive and irreversible
stages of shock. The most immediate of the compensatory
mechanisms are the sympathetic-mediated responses designed to maintain cardiac output and blood pressure.
Within seconds after the onset of hemorrhage or the loss
of blood volume, tachycardia, increased cardiac contractility, vasoconstriction, and other signs of sympathetic
and adrenal medullary activity appear. The sympathetic
vasoconstrictor response affects the arterioles and the
veins. Arteriolar constriction helps to maintain blood pressure by increasing the systemic vascular resistance, and venous constriction mobilizes blood that has been stored in
the capacitance side of the circulation as a means of increasing venous return to the heart. There is considerable
capacity for blood storage in the large veins of the abdomen and liver. Approximately 350 mL of blood that can
be mobilized in shock is stored in the liver. Sympathetic
stimulation does not cause constriction of the cerebral and
coronary vessels, and blood flow through the heart and
brain is maintained at essentially normal levels as long as
the mean arterial pressure remains above 70 mm Hg.45
During the early stages of hypovolemic shock, vasoconstriction causes a reduction in the size of the vascular
compartment and an increase in systemic vascular resistance. This response usually is all that is needed when the
injury is slight, and blood loss is arrested at this point. As
hypovolemic shock progresses, there are further increases
in heart rate and cardiac contractility, and vasoconstriction becomes more intense. There is vasoconstriction of
the blood vessels that supply the skin, skeletal muscles,
kidneys, and abdominal organs, with a resultant decrease
in blood flow and conversion to anaerobic metabolism
with lactic acid formation.
Compensatory mechanisms designed to restore blood
volume include absorption of fluid from the interstitial
spaces, conservation of salt and water by the kidneys, and
thirst. Extracellular fluid is distributed between the interstitial spaces and the vascular compartment. When there is
a loss of vascular volume, capillary pressures decrease, and
water is drawn into the vascular compartment from the
interstitial spaces. The maintenance of vascular volume is
Heart Failure and Circulatory Shock
619
further enhanced by renal mechanisms that conserve fluid.
A decrease in renal blood flow and glomerular filtration rate
results in activation of the renin-angiotensin-aldosterone
mechanism, which produces an increase in sodium reabsorption by the kidney. The decrease in blood volume also
stimulates centers in the hypothalamus that regulate ADH
release and thirst. A decrease in blood volume of 5% to
10% is sufficient to stimulate ADH release and thirst.46
ADH, also known as vasopressin, constricts the peripheral
arteries and veins and greatly increases water retention by
the kidneys. While more sensitive to changes in serum osmolality, a decrease of 10% to 15% in blood volume serves
as a strong stimulus for thirst.46
The compensatory mechanisms that the body recruits
in hypovolemic and other forms of circulatory shock were
not intended for long-term use. When injury is severe or
its effects prolonged, the compensatory mechanisms begin
to exert their own detrimental effects. The intense vasoconstriction causes a decrease in tissue perfusion, impaired
cellular metabolism, release of vasoactive inflammatory
mediators such as histamine, liberation of lactic acid, and
cell death. After circulatory function has been reestablished,
whether the shock will be irreversible or the patient will
survive is determined largely at the cellular level.
Cellular Function. Shock ultimately exerts its effect at the
cellular level with failure of the circulation to supply the
cell with the oxygen and nutrients needed for production
of adenosine triphosphate (ATP). The cell uses ATP for a
number of purposes, including operation of the sodiumpotassium membrane pump that moves sodium out of the
cell and potassium back into the cell. The cell uses two
pathways to convert nutrients to energy (see Chapter 4).
The first is the anaerobic (nonoxygen) glycolytic pathway,
which is located in the cytoplasm. Glycolysis converts glucose to ATP and pyruvate. The second pathway is the aerobic (oxygen-dependent) pathway, called the citric acid cycle,
which is located in the mitochondria. When oxygen is
available, pyruvate from the glycolytic pathway moves into
the mitochondria and enters the citric acid cycle, where it
is transformed into ATP and the metabolic byproducts carbon dioxide and water. Fatty acids and proteins also can be
metabolized in the mitochondrial pathway. When oxygen
is lacking, pyruvate does not enter the citric acid cycle; instead, it is converted to lactic acid.
In severe shock, cellular metabolic processes are essentially anaerobic, which means that excess amounts of
lactic acid accumulate in the cellular and the extracellular
compartment. The anaerobic pathway, although allowing
energy production to continue in the absence of oxygen,
is relatively inefficient and produces significantly less ATP
than does the aerobic pathway. Without sufficient energy
production, normal cell function cannot be maintained,
and the activity of the sodium-potassium membrane pump
is impaired. As a result, sodium chloride accumulates in
cells, and potassium is lost from cells. The cells then swell,
and their membranes become more permeable. Mitochondrial activity becomes severely depressed, and lysosomal
membranes rupture, resulting in the release of enzymes that
cause further intracellular destruction. This is followed by
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cell death and the release of intracellular contents into the
extracellular spaces. The resultant changes in the microcirculation reduce the chance of recovery.
Clinical Course
Stages. The progression of hypovolemic shock can be divided into four stages. During the initial stage, the circulatory blood volume is decreased, but not enough to cause
serious effects. The second stage is the compensatory stage;
although the circulating blood volume is reduced, compensatory mechanisms are able to maintain blood pressure
and tissue perfusion at a level sufficient to prevent cell
damage. The third stage is the progressive stage or stage of
decompensated shock. At this point, unfavorable signs
begin to appear: the blood pressure begins to fall, blood
flow to the heart and brain is impaired, capillary permeability is increased, fluid begins to leave the capillaries,
blood flow becomes sluggish, and the cells and their enzyme systems are damaged. The fourth stage is the final,
irreversible stage. In irreversible shock, even though the
blood volume may be restored and vital signs stabilized,
death ensues eventually. Although the factors that determine recovery from severe shock have not been clearly
identified, it appears that they are related to blood flow at
the level of the microcirculation. The severity of and clinical findings associated with hypovolemic shock are summarized in Table 28-3.
Manifestations. The signs and symptoms of hypovolemic shock depend on shock stage and are closely related
TABLE 28-3
to low peripheral blood flow and excessive sympathetic
stimulation. They include thirst, an increase in heart rate,
cool and clammy skin, a decrease in arterial blood pressure, a decrease in urine output, and changes in mentation. Laboratory tests of hemoglobin and hematocrit
provide information regarding the severity of blood loss
or hemoconcentration due to dehydration. Serum lactate
and arterial pH provide information about the severity of
acidosis.
Thirst is an early symptom in hypovolemic shock.
Although the underlying cause is not fully understood, it
probably is related to decreased blood volume and increased serum osmolality (see Chapter 33). An increase in
heart rate often is another early sign of shock. As shock
progresses, the pulse becomes weak and thready, indicating vasoconstriction and a reduction in filling of the vascular compartment.
Arterial blood pressure is decreased in moderate to severe shock (see Fig. 28-11). However, blood pressure measurements may not prove useful in the early diagnosis of
shock. This is because compensatory mechanisms tend to
preserve blood pressure until shock is relatively far advanced. Furthermore, an adequate arterial pressure does
not ensure adequate perfusion and oxygenation of vital
organs at the cellular level. This does not imply that blood
pressure should not be closely monitored in patients at
risk for development of shock, but it does indicate the
need for other assessment measures. Blood pressure often
is measured intraarterially in persons with severe shock because auscultatory (cuff and stethoscope) or oscillometric
Correlation of Clinical Findings and the Magnitude of Volume Deficit
in Hemorrhagic Shock
Severity of Shock
Clinical Findings
None
Mild
None; normal blood donation
Minimal tachycardia
Slight decrease in blood pressure
Mild evidence of peripheral vasoconstriction
with cool hands and feet
Tachycardia, 100–120 beats per minute
Decrease in pulse pressure
Systolic pressure, 90–100 mm Hg
Restlessness
Increased sweating
Pallor
Oliguria
Tachycardia over 120 beats per minute
Blood pressure below 60 mm Hg systolic and
frequently unobtainable by cuff
Mental stupor
Extreme pallor, cold extremities
Anuria
Moderate
Severe
Percentage of Reduction
in Blood Volume (mL)
≤10 (500)*
15–25 (750–1250)
25–35 (1250–1750)
Up to 50 (2500)
*Based on blood volume of 7% in a 70-kg male of medium build.
(Adapted from Weil M., Shubin H. [1967]. Diagnosis and treatment of shock [p. 118]. Baltimore:
Williams & Wilkins)
CHAPTER 28
(automatic blood pressure machines) methods may not always provide an accurate measurement. The Doppler
method, in which blood pressure is measured noninvasively by ultrasound, may provide a more accurate estimate of Korotkoff sounds when they are no longer audible
through the stethoscope. In some instances, this method
may be used as an alternative to continuous intraarterial
monitoring.
As shock progresses, the respirations become rapid and
deep. Decreased intravascular volume results in decreased
venous return to the heart and a decrease in CVP. When
shock becomes severe, the peripheral veins collapse, making it difficult to insert peripheral venous lines. Sympathetic stimulation also leads to intense vasoconstriction of
the skin vessels and activation of the sweat glands. As a result, the skin is cool and moist. When shock is caused by
hemorrhage, the loss of red blood cells leaves the skin and
mucous membranes looking pale.
Urine output decreases very quickly in hypovolemic
and other forms of shock. Compensatory mechanisms decrease renal blood flow as a means of diverting blood flow
to the heart and brain. Oliguria of 20 mL/hour or less
indicates severe shock and inadequate renal perfusion.
Continuous measurement of urine output is essential for
assessing the circulatory status of the person in shock.
Restlessness and apprehension are common behaviors
in early shock. As the shock progresses and blood flow to
the brain decreases, restlessness is replaced by apathy and
stupor. If shock is unchecked, the apathy progresses to
coma. Coma caused by blood loss alone and not related to
head injury or other factors is an unfavorable sign.
Treatment. The treatment of hypovolemic shock is directed toward correcting or controlling the underlying
cause and improving tissue perfusion. Persons who have
sustained blood loss are commonly placed in supine position with the legs elevated to maximize cerebral blood
flow. Oxygen is administered to persons with signs of
hypoxemia. Because subcutaneous administration is unpredictable, pain medications usually are administered
intravenously. Frequent measurements of heart rate and
cardiac rhythm, blood pressure, and urine flow are used to
assess the severity of circulatory compromise and to monitor treatment.
In hypovolemic shock, the goal of treatment is to restore vascular volume. This can be accomplished through
intravenous administration of fluids and blood. The crystalloids (e.g., isotonic saline) are readily available for emergencies and mass casualties. They often are effective, at least
temporarily, when given in adequate doses. Plasma expanders, including dextrans and colloidal albumin solutions, have a high molecular weight, do not necessitate
blood typing, and remain in the circulation for longer periods than the crystalloids, such as glucose and saline. The
dextrans must be used with caution because they may induce serious or fatal reactions, including anaphylaxis. Blood
or blood products (packed or frozen red cells) are administered based on hematocrit and hemodynamic findings. Fluids and blood are best administered based on volume
indicators such as CVP and PCWP. This is particularly im-
Heart Failure and Circulatory Shock
621
portant in pediatric patients, whose fluid balance allows less
variation from normal before compromise to tissue perfusion results, and who may respond better to hypertonic
saline than to other crystalloid or colloid solutions.47
Vasoactive drugs (e.g., adrenergic agents) are agents capable of constricting or dilating blood vessels. Considerable
controversy exists about the advantages or disadvantages
related to the use of these drugs. There are two types of
adrenergic receptors for the sympathetic nervous system:
α and β. The β receptors are further subdivided into β1 and
β2 receptors. In the cardiorespiratory system, stimulation of
the α receptors causes vasoconstriction; stimulation of β1
receptors causes an increase in heart rate and the force of
myocardial contraction; and stimulation of β2 receptors
produces vasodilatation of the skeletal muscle beds and relaxation of the bronchioles.
As a general rule, the adrenergic drugs are not used as
a primary form of therapy in shock. An increase in blood
pressure produced by vasopressor drugs usually has little
effect on the underlying cause of shock and in many cases
may be detrimental. These agents are given only when
hypotension persists after volume deficits have been corrected. Dopamine, which induces a more favorable array
of α- and β-receptor actions than many of the other adrenergic drugs, may be used in the treatment of severe and
prolonged shock. Dopamine is thought to increase blood
flow to the kidneys, liver, and other abdominal organs
while maintaining vasoconstriction of less vital structures,
such as the skin and skeletal muscles, when given in low
doses. In severe shock, higher doses may be needed to
maintain blood pressure. After dopamine administration
exceeds this low-dose range, it has vasoconstrictive effects
on blood flow to the kidneys and abdominal organs that
are similar to those of epinephrine.
OBSTRUCTIVE SHOCK
The term obstructive shock is used to describe circulatory
shock that results from mechanical obstruction of the flow
of blood through the central circulation (great veins, heart,
or lungs; see Fig. 28-10). Obstructive shock may be caused
by a number of conditions, including dissecting aortic
aneurysm, cardiac tamponade, pneumothorax, atrial myxoma, or evisceration of abdominal contents into the thoracic cavity because of a ruptured hemidiaphragm. The
most frequent cause of obstructive shock is pulmonary
embolism.
The primary physiologic results of obstructive shock
are elevated right heart pressure and impaired venous return to the heart. The signs of right heart failure are seen,
including elevation of CVP and jugular venous distention.
Treatment modalities focus on correcting the cause of the
disorder, frequently with surgical interventions such as
pulmonary embolectomy, pericardiocentesis (i.e., removal
of fluid from the pericardial sac) for cardiac tamponade, or
the insertion of a chest tube for correction of a tension
pneumothorax or hemothorax. In select cases of pulmonary embolus, thrombolytic drugs may be used to dissolve
the clots causing the obstruction.
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Cardiovascular Function
DISTRIBUTIVE SHOCK
Distributive or vasodilatory shock is characterized by loss
of blood vessel tone, enlargement of the vascular compartment, and displacement of the vascular volume away
from the heart and central circulation.48 With distributive
shock, the capacity of the vascular compartment expands
to the extent that a normal volume of blood does not fill
the circulatory system (see Fig. 28-10). Venous return is decreased in distributive shock, which leads to a diminished
cardiac output but not a decrease in total blood volume;
this type of shock is also referred to as normovolemic shock.
Loss of vessel tone has two main causes: a decrease in the
sympathetic control of vasomotor tone and the presence
of vasodilator substances in the blood. It can also occur as
a complication of vessel damage resulting from prolonged
and severe hypotension due to hemorrhage, known as irreversible or late-phase hemorrhagic shock.48 Three shock
states share the basic circulatory pattern of distributive
shock: neurogenic shock, anaphylactic shock, and septic
shock.
Neurogenic Shock
Neurogenic shock describes shock caused by decreased
sympathetic control of blood vessel tone due to a defect in
the vasomotor center in the brain stem or the sympathetic
outflow to the blood vessels. Output from the vasomotor
center can be interrupted by brain injury, the depressant
action of drugs, general anesthesia, hypoxia, or lack of glucose (e.g., insulin reaction). Fainting due to emotional
causes is a transient form of neurogenic shock. Spinal anesthesia or spinal cord injury above the midthoracic region
can interrupt the transmission of outflow from the vasomotor center. The term spinal shock is used to describe the
neurogenic shock that occurs in persons with spinal cord
injury. Many general anesthetic agents can cause a neurogenic shock-like reaction, especially during induction, because of interference with sympathetic nervous system
function. In contrast to hypovolemic shock, the heart rate
in neurogenic shock often is slower than normal, and the
skin is dry and warm. This type of distributive shock is
rare and usually transitory.
Anaphylactic Shock
Anaphylaxis is a clinical syndrome that represents the
most severe systemic allergic reaction.49,50 It results from
an immunologically mediated reaction in which vasodilator substances such as histamine are released into the
blood (see Chapter 21). These substances cause vasodilatation of arterioles and venules along with a marked increase in capillary permeability. The vascular response in
anaphylaxis is often accompanied by life-threatening laryngeal edema and bronchospasm, circulatory collapse,
contraction of gastrointestinal and uterine smooth muscle,
and urticaria or angioedema.
Among the most frequent causes of anaphylactic
shock are reactions to drugs, such as penicillin; foods, such
as nuts and shellfish; and insect venoms. The most common cause is stings from insects of the order Hymenoptera
(i.e., bees, wasps, and fire ants). Latex allergy has also
caused life-threatening anaphylaxis in a growing segment
of the population. Health care workers and others who are
exposed to latex are developing latex sensitivities that
range from mild urticaria, contact dermatitis, and mild respiratory distress to anaphylactic shock.51 Children with
spina bifida are at extreme risk for this increasingly serious
allergy (see Chapter 21).
The onset of anaphylaxis depends on the sensitivity
of the person and the rate and quantity of antigen exposure. Anaphylactic shock often develops suddenly;
death can occur within a matter of minutes unless appropriate medical intervention is promptly instituted.
Signs and symptoms associated with impending anaphylactic shock include abdominal cramps; apprehension;
burning and warm sensation of the skin, itching, and urticaria (i.e., hives); and coughing, choking, wheezing, chest
tightness, and difficulty in breathing. After blood begins to
pool peripherally, there is a precipitous drop in blood pressure, and the pulse becomes so weak that it is difficult to
detect. Life-threatening airway obstruction may ensue as a
result of laryngeal edema or bronchial spasm.
Treatment includes immediate discontinuance of the
inciting agent or institution of measures to decrease its absorption (e.g., application of ice to a beesting); close monitoring of cardiovascular and respiratory function; and
maintenance of adequate respiratory gas exchange, cardiac output, and tissue perfusion. Epinephrine constricts
the blood vessels and relaxes the smooth muscle in the
bronchioles; it usually is the first drug to be given to a patient believed to be experiencing an anaphylactic reaction.
Other treatment measures include the administration of
oxygen, antihistaminic drugs, and corticosteroids. Resuscitation measures may be required.
The prevention of anaphylactic shock is preferable to
treatment. Once a person has been sensitized to an antigen, the risk for repeated anaphylactic reactions with subsequent exposure is high. All health care providers should
question patients regarding previous drug reactions and
inform patients as to the name of the medication they are
to receive before it is administered or prescribed. Persons
with known hypersensitivities should carry some form of
medical identification to alert medical personnel if they
become unconscious or unable to relate this information.
Persons who are at risk for anaphylaxis should be provided
with emergency medications (e.g., epinephrine autoinjector) and instructed in procedures to follow in case they are
inadvertently exposed to the offending antigen. In some
situations, it may be medically necessary to administer
agents known to cause anaphylaxis. Protocols that have
been developed to prevent or decrease the severity of the
reaction involve pharmacologic pretreatment to block or
blunt the reaction.
Sepsis and Septic Shock
Septic shock, which is the most common type of vasodilatory shock, is associated with severe infection and the
systemic response to infection.48 It is associated most frequently with gram-negative bacteremia, although it can
be caused by gram-positive bacilli and other microorganisms such as fungi, which carry an even greater risk for
CHAPTER 28
mortality.52 Unlike other types of shock, septic shock commonly is associated with pathologic complications, such
as pulmonary insufficiency, disseminated intravascular
coagulation, and multiple organ dysfunction syndrome.
Severe sepsis accompanied by acute organ dysfunction
is a frequently occurring condition in critically ill patients,
affecting approximately 750,000 Americans annually and
causing more than 200,000 deaths.53,54 The growing incidence has been attributed to an increased awareness of the
diagnosis, increased numbers of immunocompromised
patients, increased use of invasive procedures, increased
number of resistant organisms, and an increased number
of elderly patients.55 Despite advances in treatment methods, the mortality rate remains approximately 40%.56
Septic shock has been described in the context of
what has been termed the systemic inflammatory response
syndrome. Although usually associated with infection, the
systemic inflammatory response syndrome can be initiated by noninfectious disorders such as acute trauma and
pancreatitis.52 To enable recognition, description, and
classification of persons with sepsis, the American College
of Chest Physicians and the Society of Critical Care Medicine published consensus terminology to describe and
define the clinical manifestations and progression of sepsis57 (Chart 28-2).
Mechanisms. The mechanisms of sepsis and septic shock
are thought to be related to mediators of the inflammatory
response.52–56,58 Although the immune system and the inflammatory response are designed to overcome infection
and eliminate bacterial breakdown products, the unregulated release of inflammatory mediators or cytokines (see
Chapter 20) may elicit toxic reactions, resulting in the
potentially fatal sepsis syndrome. The most widely investigated cytokines have been tumor necrosis factor-α (TNF-α),
interleukin-1, and interleukin-8, which usually are proinflammatory, and interleukin-6 and interleukin-10, which
tend to be anti-inflammatory. A trigger such as a microbial
toxin stimulates the release of TNF-α and interleukin-1,
which in turn promotes endothelial cell–leukocyte adhesion, release of cell-damaging proteases and prostaglandins,
and activation of the clotting cascade. The prostaglandins,
thromboxane A2 (a vasoconstrictor), prostacyclin (a vasodilator), and prostaglandin E2, participate in the generation
of fever, tachycardia, ventilation-perfusion abnormalities,
and lactic acidosis. Interleukin-8, a neutrophil chemotaxin,
may have a particularly important role in perpetuating
tissue inflammation. Interleukin-6 and interleukin-10,
which have anti-inflammatory actions and perhaps are
counter-regulatory, augment the acute-phase response and
consequent generation of additional proinflammatory
mediators.59
In addition to inducing the release of inflammatory
mediators, the sepsis-producing endotoxins may induce
tissue damage by directly activating pathways such as the
coagulation cascade, the complement cascade, vessel injury, or release of vasodilating prostaglandins.59 Thus, the
processes that result in the sepsis syndrome are complex
consequences of microbial products that profoundly dysregulate the release of inflammatory mediators and the
Heart Failure and Circulatory Shock
623
CHART 28-2
Definitions of Sepsis and Septic Shock
Infection: Microbial phenomenon characterized by an
inflammatory response to the presence of microorganisms and the invasion of normally sterile
host tissue by these organisms.
Bacteremia: The presence of viable bacteria in the
blood.
Systemic inflammatory response syndrome: The
systemic inflammatory response to a variety of severe
clinical insults. The response is manifested by two or
more of the following conditions:
Temperature >38°C or <36°C
Heart rate >90 beats per minute
Respiratory rate >20 breaths per minute or PaCO2
<32 mm Hg (pH <4.3)
WBC >12,000 cells/mm3, <4000 cells/mm3, or 10%
immature (band) forms
Sepsis: The systemic response to infection. This systemic
response is manifested by two or more of the above
conditions (temperature, heart rate, respiratory rate,
and WBC) as a result of infection.
Severe sepsis: Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion
and perfusion abnormalities may include, but are not
limited to, lactic acidosis, oliguria, or an acute alteration in mental status.
Septic shock: Sepsis with hypotension, despite adequate fluid resuscitation, along with the presence of
perfusion abnormalities that may include, but are not
limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are on inotropic
or vasopressor agents may not be hypotensive at the
time that perfusion abnormalities are measured.
Hypotension: A systolic blood pressure of <90 mm Hg
or a reduction of >40 mm Hg from baseline in the
absence of other causes of hypotension.
Multiple organ dysfunction syndrome: Presence
of altered organ function in an acutely ill patient
such that homeostasis cannot be maintained without
intervention.
(From American College of Chest Physicians/Society of Critical
Care Medicine Consensus Conference. [1992]. Definitions for
sepsis and organ failure and guidelines for use of innovative
therapies in sepsis. Critical Care Medicine 20 [6], 866)
regulation of several important inflammatory and coagulation pathways.
Manifestations. Septic shock typically manifests with fever,
vasodilatation, and warm, flushed skin. Mild hyperventilation, respiratory alkalosis, and abrupt changes in personality and behavior due to reduction in cerebral blood flow
may be the earliest signs and symptoms of septic shock.
These manifestations, which are thought to be a primary response to the bacteremia, commonly precede the usual
signs and symptoms of sepsis by several hours or days. Unlike other forms of shock (i.e., cardiogenic, hypovolemic,
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Cardiovascular Function
and obstructive) that are characterized by a compensatory
increase in systemic vascular resistance, septic shock often
presents with hypovolemia because of arterial and venous
dilatation and leakage of plasma into the interstitial spaces.
Aggressive treatment of the hypovolemia in septic
shock usually leads to a decrease in systemic vascular resistance and an increase in cardiac output. In the past, this
hyperdynamic pattern of response was thought to be present early in shock and was called warm shock. A second
pattern of cold shock accompanied by a low cardiac output
and cold extremities was thought to indicate the late
stages of septic shock and a poor prognosis. With the development of refined resuscitation methods and better
hemodynamic monitoring systems, approximately 90% of
patients in septic shock demonstrate a hyperdynamic response with high cardiac output and low systemic vascular resistance.59 Despite the fact that the cardiac output is
normal or increased, cardiac function is depressed, the heart
becomes dilated, and the ejection fraction decreases.
Treatment. The treatment of sepsis and septic shock focuses on the control of the causative agent and support of
the circulation. Although control of the source of infection is important and the use of antibiotics specific to the
infectious agent essential, antibiotics do not treat the inflammatory response to the infection.60 The cardiovascular status of the patient must be supported to maintain
oxygen delivery to the cells. Swift and aggressive fluid administration is needed to compensate for third spacing,
and equally aggressive use of vasopressor agents is needed
to counteract the vasodilation caused by endotoxins. Monitoring of central venous pressure, mean arterial pressure,
urine output, and laboratory measurements of serum lactate, base deficit, and pH is used to evaluate for the progression of sepsis and adequacy of treatment.54,60
Among the more recent advances in the treatment of
sepsis are the use of intensive insulin therapy for hyperglycemia54 and the administration of recombinant human
activated protein C.54,60 It has been demonstrated that intensive insulin therapy that maintained blood glucose levels at 80 to 110 mg/dL resulted in lower mortality and
morbidity than did conventional therapy that maintained
blood glucose levels at 180 to 200 mg/dL.61 The protective
mechanism of insulin in sepsis is unknown. The phagocytic
function of neutrophils is impaired in hyperglycemia, suggesting that this may be one of the reasons. Insulin also prevents apoptotic cell death by numerous stimuli, suggesting
a second reason. Recombinant human activated protein C,
a naturally occurring anticoagulant that acts by inactivating coagulation factors Va and VIII (see Chapter 15), is the
first anti-inflammatory agent that has proved effective in
the treatment of sepsis.62,63 In addition to its anticoagulant
actions, activated protein C has direct anti-inflammatory
properties, including blocking the production of cytokines
by monocytes and blocking cell adhesion. Activated protein
C also has antiapoptotic actions that may contribute to its
effectiveness. The use of corticosteroids, once considered a
mainstay in the treatment of sepsis, remains controversial.
The use of high doses of corticosteroids, in particular, has
not been shown to improve survival and may worsen outcomes by increasing the risk for secondary infections.
COMPLICATIONS OF SHOCK
Wiggers, a noted circulatory physiologist, stated, “Shock
not only stops the machine, but it wrecks the machinery.”64 Many body systems are wrecked by severe shock.
Five major complications of severe shock are shock lung,
acute renal failure, gastrointestinal ulceration, disseminated intravascular coagulation, and multiple organ dysfunction syndrome. The complications of shock are serious
and often fatal.
Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) is a potentially lethal form of respiratory failure that can follow
severe shock (see Chapter 31). The mortality rate remains
at greater than 50% despite advances in mechanical
ventilation.65
The symptoms of ARDS usually do not develop until
24 to 48 hours after the initial trauma; in some instances,
they occur later. The respiratory rate and effort of breathing increase. Arterial blood gas analysis establishes the
presence of profound hypoxemia with hypercapnia, resulting from impaired matching of ventilation and perfusion and from the greatly reduced diffusion of blood gases
across the thickened alveolar membranes.
The exact cause of ARDS is unknown. Neutrophils are
thought to play a key role in the pathogenesis of ARDS. A
cytokine-mediated activation and accumulation of neutrophils in the pulmonary vasculature and subsequent
endothelial injury is thought to cause leaking of fluid
and plasma proteins into the interstitium and alveolar
spaces.65,66 The fluid leakage impairs gas exchange and
makes the lung stiffer and more difficult to inflate. Abnormalities in the production, composition, and function of
surfactant may contribute to alveolar collapse and gas exchange abnormalities.66
Interventions for ARDS focus on increasing the oxygen concentration in the inspired air and supporting ventilation mechanically to optimize gas exchange while
avoiding oxygen toxicity and preventing further lung
injury.65–67 Despite the delivery of high levels of oxygen
using high-pressure mechanical ventilatory support and
positive end-expiratory pressure, many persons with ARDS
remain hypoxic, often with a fatal outcome.
Inhaled nitrous oxide is under investigation in the
treatment of ARDS. Nitrous oxide appears to improve gas
exchange but has not been demonstrated to significantly
decrease mortality.65,66 New interventions have focused on
more aggressive treatment of the underlying cause, with
the first line of treatment remaining supportive care.
Acute Renal Failure
The renal tubules are particularly vulnerable to ischemia,
and acute renal failure is one important late cause of
death in severe shock. Sepsis and trauma account for most
cases of acute renal failure. The endotoxins implicated in
septic shock are powerful vasoconstrictors that are capable of activating the sympathetic nervous system and
causing intravascular clotting. They have been shown to
trigger all the separate physiologic mechanisms that con-
CHAPTER 28
tribute to the onset of acute renal failure. The degree of
renal damage is related to the severity and duration of
shock. The normal kidney is able to tolerate severe ischemia for 15 to 20 minutes. The renal lesion most frequently seen after severe shock is acute tubular necrosis.
Acute tubular necrosis usually is reversible, although return to normal renal function may require weeks or months
(see Chapter 36). Continuous monitoring of urine output
during shock provides a means of assessing renal blood
flow. Frequent monitoring of serum creatinine and blood
urea nitrogen levels also provides valuable information regarding renal status.
Heart Failure and Circulatory Shock
625
come or merely a marker of the seriousness of the underlying condition causing the DIC.
The management of sepsis-induced DIC focuses on
treatment of the underlying disorder and measures to interrupt the coagulation process. Anticoagulation therapy
and administration of platelets and plasma may be used.
The use of antithrombin III, a coagulation inhibitor, is
under investigation. Clinical trails have shown modest to
marked reductions in mortality based on the dose of antithrombin III that was used.69 Other therapeutic options,
aimed at interrupting the intrinsic coagulation pathway at
the point at which tissue factor complexes with factor VIIa,
also are being investigated.69
Gastrointestinal Complications
The gastrointestinal tract is particularly vulnerable to
ischemia because of the changes in distribution of blood
flow to its mucosal surface. In shock, there is widespread
constriction of blood vessels that supply the gastrointestinal tract, causing a redistribution of blood flow that severely diminishes mucosal perfusion. Superficial mucosal
lesions of the stomach and duodenum can develop within
hours of severe trauma, sepsis, or burn.
Bleeding is a common symptom of gastrointestinal
ulceration caused by shock. Hemorrhage has its onset usually within 2 to 10 days after the original insult and often
begins without warning. Poor perfusion in the gastrointestinal tract has been credited with allowing intestinal
bacteria to enter the bloodstream, thereby contributing to
the development of sepsis and shock.68
Histamine type 2 receptor antagonists, proton-pump
inhibitors, or sucralfate may be given prophylactically to
prevent gastrointestinal ulcerations caused by shock.68
Nasogastric tubes, when attached to intermittent suction,
also help to diminish the accumulation of hydrogen ions
in the stomach.
Disseminated Intravascular Coagulation
Disseminated intravascular coagulation (DIC) is characterized by widespread activation of the coagulation system
with resultant formation of fibrin clots and thrombotic occlusion of small and mid-sized vessels (see Chapter 15). The
systemic formation of fibrin results from increased generation of thrombin, the simultaneous suppression of physiologic anticoagulation mechanisms, and the delayed
removal of fibrin as a consequence of impaired fibrinolysis.
Clinically overt DIC is reported to occur in as many as 30%
to 50% of persons with sepsis and septic shock.69 As with
other systemic inflammatory responses, the derangement
of coagulation and fibrinolysis is thought to be mediated
by inflammatory mediators.
The contribution of DIC to morbidity and mortality
in sepsis depends on the underlying clinical condition and
the intensity of the coagulation disorder. Depletion of the
platelets and coagulation factors increases the risk for
bleeding. Deposition of fibrin in the vasculature of organs
contributes to ischemic damage and organ failure. In a large
number of clinical trials, the occurrence of DIC appeared
to be associated with an unfavorable outcome and was an
independent predictor of mortality.69 However, it remains
uncertain whether DIC was a predictor of unfavorable out-
Multiple Organ Dysfunction Syndrome
Multiple organ dysfunction syndrome (MODS) represents
the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention. As the name implies, MODS commonly
affects multiple organ systems, including the kidneys,
lungs, liver, brain, and heart. MODS is a particularly lifethreatening complication of shock, especially septic shock.
It has been reported as the most frequent cause of death in
the noncoronary intensive care unit. Mortality rates vary
from 30% to 100%, depending on the number of organs
involved.70 Mortality rates increase with an increased number of organs failing. A high mortality rate is associated
with failure of the brain, liver, kidney, and lung. The pathogenesis of MODS is not clearly understood, and current
management therefore is primarily supportive. Major risk
factors for the development of MODS are sepsis, shock,
prolonged periods of hypotension, hepatic dysfunction,
trauma, infarcted bowel, advanced age, and alcohol abuse.70
Interventions for multiple organ failure are focused on
support of the affected organs.
In summary, circulatory shock is an acute emergency in
which body tissues are deprived of oxygen and cellular nutrients or are unable to use these materials in their metabolic
processes. Circulatory shock may develop because there is
not enough blood in the circulatory system (i.e., hypovolemic
shock), blood flow or venous return is obstructed (i.e., obstructive shock), or the tissues are unable to use oxygen and nutrients (i.e., distributive shock). Three types of shock share the
basic circulatory pattern of distributive shock: neurogenic
shock, anaphylactic shock, and septic shock. Septic shock,
which is the most common of these three types, is associated
with a severe, overwhelming infection and has a mortality rate
of approximately 40%.
The manifestations of hypovolemic shock, which serves as
a prototype for circulatory shock, are related to low peripheral
blood flow and excessive sympathetic stimulation. The low
peripheral blood flow produces thirst, changes in skin temperature, a decrease in blood pressure, an increase in heart
rate, decreased venous pressure, decreased urine output, and
changes in the sensorium. The intense vasoconstriction that
serves to maintain blood flow to the heart and brain causes a
decrease in tissue perfusion, impaired cellular metabolism, liberation of lactic acid, and, eventually, cell death. Whether the
626
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Cardiovascular Function
shock will be irreversible or the patient will survive is determined largely by changes that occur at the cellular level.
The complications of shock result from the deprivation of
blood flow to vital organs or systems, such as the lungs, kidneys, gastrointestinal tract, and blood coagulation system.
ARDS produces lung changes that occur with shock. It is
characterized by changes in the permeability of the alveolarcapillary membrane with the development of interstitial
edema and severe hypoxia that does not respond to oxygen
therapy. The renal tubules are particularly vulnerable to
ischemia, and acute renal failure is an important complication of shock. Gastrointestinal ischemia may lead to gastrointestinal bleeding and increased permeability to the intestinal
bacteria, which cause further sepsis and shock. DIC is characterized by formation of small clots in the circulation. It is
thought to be caused by inappropriate activation of the coagulation cascade because of toxins or other products released as a result of the shock state. Multiple organ failure,
perhaps the most ominous complication of shock, rapidly depletes the body’s ability to compensate and recover from a
shock state.
Circulatory Failure
in Children and the Elderly
After completing this section of the chapter, you should be able to
meet the following objectives:
✦ Describe the manifestations of heart failure in infants
and children
✦ Cite how the aging process affects heart failure in the
elderly
✦ State how the signs and symptoms of heart failure may
differ between younger and older adults
HEART FAILURE
IN INFANTS AND CHILDREN
As in adults, heart failure in infants and children results
from the inability of the heart to maintain the cardiac
output required to sustain metabolic demands.71–73 Congenital heart defects are the most common cause of CHF
during childhood. Surgical correction of congenital heart
defects may cause CHF as a result of intraoperative manipulation of the heart and resection of heart tissue, with
subsequent alterations in pressure, flow, and resistance relations.57 Usually, the heart failure that results is acute and
resolves after the effects of the surgical procedure have
subsided. Chronic congestive failure occasionally is observed in children with severe chronic anemia, inflammatory heart disease, end-stage congenital heart disease, or
cardiomyopathy. Chart 28-3 lists some of the more common causes of heart failure in children. Inflammatory heart
disorders (e.g., myocarditis, rheumatic fever, bacterial endocarditis, Kawasaki’s disease), cardiomyopathy, and congenital heart disorders are discussed in Chapter 26.
CHART 28-3
Causes of Heart Failure in Children
Newborn Period
Congenital heart defects
Severe left ventricular outflow disorders
Hypoplastic left heart
Critical aortic stenosis or coarctation of the aorta
Large arteriovenous shunts
Ventricular septal defects
Patent ductus arteriosus
Transposition of the great vessels
Heart muscle dysfunction (secondary)
Asphyxia
Sepsis
Hypoglycemia
Hematologic disorders (e.g., anemia)
Infants 1 to 6 Months
Congenital heart disease
Large arteriovenous shunts (ventricular septal defect)
Heart muscle dysfunction
Myocarditis
Cardiomyopathy
Pulmonary abnormalities
Bronchopulmonary dysplasia
Persistent pulmonary hypertension
Toddlers, Children, and Adolescents
Acquired heart disease
Cardiomyopathy
Viral myocarditis
Rheumatic fever
Endocarditis
Systemic disease
Sepsis
Kawasaki’s disease
Renal disease
Sickle cell disease
Congenital heart defects
Nonsurgically treated disorders
Surgically treated disorders
Manifestations
Many of the signs and symptoms of heart failure in infants
and children are similar to those in adults. They include fatigue, effort intolerance, cough, anorexia, and abdominal
pain. A subtle sign of cardiorespiratory distress in infants
and children is a change in disposition or responsiveness,
including irritability or lethargy. Sympathetic stimulation
produces peripheral vasoconstriction and diaphoresis. Decreased renal blood flow often results in a urine output of
less than 0.5 to 1.0 mL/kg/hour, despite adequate fluid intake.74 When right ventricular function is impaired, systemic venous congestion develops. Hepatomegaly due to
liver congestion often is one of the first signs of systemic
venous congestion in infants and children. However, dependent edema or ascites rarely is seen unless the CVP is
extremely high. Because of their short, fat necks, jugular
CHAPTER 28
venous distention is difficult to detect in infants; it is not
a reliable sign until the child is of school age or older.
A third heart sound, or gallop rhythm, is a common
finding in infants and children with heart failure. It results
from rapid filling of a noncompliant ventricle. However,
it is difficult to distinguish at high heart rates.
Most commonly, children develop interstitial rather
than alveolar pulmonary edema. This reduces lung compliance and increases the work of breathing, causing
tachypnea and increased respiratory effort. Older children
display use of accessory muscles (i.e., scapular and sternocleidomastoid). Head bobbing and nasal flaring may be
observed in infants. Signs of respiratory distress often are
the first and most noticeable indication of CHF in infants
and young children. Pulmonary congestion may be mistaken for bronchiolitis or lower respiratory tract infection.
The infant or young child with respiratory distress often
grunts with expiration. This grunting effort (essentially,
exhaling against a closed glottis) is an instinctive effort to
increase end-expiratory pressures and prevent collapse of
small airways and the development of atelectasis. Respiratory crackles (i.e., rales) are uncommon in infants and usually suggest development of a respiratory tract infection.
Wheezes may be heard, particularly if there is a large leftto-right shunt.
Infants with heart failure often have increased respiratory problems during feeding.70,74 The history is one of prolonged feeding with excessive respiratory effort and fatigue.
Weight gain is slow owing to high energy requirements
and low calorie intake. Other frequent manifestations of
heart failure in infants are excessive sweating (due to increased sympathetic tone), particularly over the head and
neck, and repeated lower respiratory tract infections. Peripheral perfusion usually is poor, with cool extremities;
tachycardia is common (resting heart rate >150 beats per
minute); and respiratory rate is increased (resting rate >50
breaths per minute).74
Diagnosis and Treatment
Diagnosis of congestive failure in infants and children is
based on symptomatology, chest radiographic films, electrocardiographic findings, echocardiographic techniques to
assess cardiac structures and ventricular function (i.e., endsystolic and end-diastolic diameters), arterial blood gases to
determine intracardiac shunting and ventilation-perfusion
inequalities, and other laboratory studies to determine
anemia and electrolyte imbalances.
Treatment of congestive failure in infants and children
includes measures aimed at improving cardiac function and
eliminating excess intravascular fluid. Oxygen delivery must
be supported and oxygen demands controlled or minimized. Whenever possible, the cause of the disorder is corrected (e.g., medical treatment of sepsis and anemia, surgical
correction of congenital heart defects). With congenital
anomalies that are amenable to surgery, medical treatment
often is needed for a time before surgery and usually is continued in the immediate postoperative period. For many
children, only medical management can be provided.
Medical management of heart failure in infants and
children is similar to that in adults, although it is tailored to
Heart Failure and Circulatory Shock
627
the special developmental needs of the child. Inotropic
agents such as digitalis often are used to increase cardiac
contractility. Diuretics may be given to reduce preload, and
vasodilating drugs may be used to manipulate the afterload.
Drug doses must be carefully tailored to control for the
child’s weight and conditions such as reduced renal function. Daily weighing and accurate measurement of intake
and output are imperative during acute episodes of failure.
Most children feel better in the semiupright position.
An infant seat is useful for infants with chronic CHF. Activity restrictions usually are designed to allow children to
be as active as possible within the limitations of their heart
disease. Infants with congestive failure often have problems feeding. Small, frequent feedings usually are more
successful than larger, less frequent feedings. Severely ill
infants may lack sufficient strength to suck and may need
to be tube fed.
The treatment of heart failure in children should be
designed to allow optimal physical and psychosocial development. It requires the full involvement of the parents,
who often are the primary care providers; therefore, parent
education and support is essential.
HEART FAILURE IN THE ELDERLY
Congestive heart failure is one of the most common causes
of disability in the elderly and is the most frequent hospital discharge diagnosis for the elderly. More than 75% of
patients with CHF are older than 65 years of age. CHF also
is a major cause of chronic disability, and annual expenditures exceed $10 billion.75 Among the factors that have
contributed to the increased numbers of older people with
CHF are the improved therapies for ischemic and hypertensive heart disease.75 Thus, persons who would have died
from acute myocardial disease 20 years ago are now surviving, but with residual left ventricular dysfunction. Similarly, improved blood pressure control has led to a 60%
decline in stroke mortality rates, yet these same people remain at risk for CHF as a complication of hypertension.
Also, advances in treatment of other diseases have contributed indirectly to the rising prevalence of CHF in the
older population.
Coronary heart disease, hypertension, and valvular
heart disease (particularly aortic stenosis and mitral regurgitation) are common causes of CHF in older adults.75,76
Although the pathophysiology of CHF is similar in younger
and older persons, elderly persons tend to develop cardiac
failure when confronted with stresses that would not produce failure in younger persons. There are four principal
changes associated with cardiovascular aging that impair
the ability to respond to stress.75 First, reduced responsiveness to β-adrenergic stimulation limits the heart’s capacity
maximally to increase heart rate and contractility. A second major effect of aging is increased vascular stiffness,
which results in an increased resistance to left ventricular
ejection (afterload) and contributes to the development
of systolic hypertension in the elderly. Third, in addition
to increased vascular stiffness, the heart itself becomes
stiffer and less compliant with age. The changes in diastolic
628
UNIT VI
Cardiovascular Function
stiffness result in important alterations in diastolic filling
and atrial function. A reduction in ventricular filling not
only affects cardiac output but also produces an elevation
in diastolic pressure that is transmitted back to the left
atrium, where it stretches the muscle wall and predisposes
to atrial ectopic beats and atrial fibrillation. The fourth
major effect of cardiovascular aging is altered myocardial
metabolism at the level of the mitochondria. Although
older mitochondria may be able to generate sufficient ATP
to meet the normal energy needs of the heart, they may
not be able to respond under stress.
Manifestations
The manifestations of CHF in elderly persons often are
masked by other disease conditions.77 Nocturia is an early
symptom but may be caused by other conditions such as
prostatic hypertrophy. Dyspnea on exertion may result
from lung disease, lack of exercise, and deconditioning.
Lower extremity edema commonly is caused by venous
insufficiency.
Among the acute manifestations of CHF in the elderly
are increasing lethargy and confusion, probably the result
of impaired cerebral perfusion. Activity intolerance is
common. Instead of dyspnea, the prominent sign may be
restlessness. Impaired perfusion of the gastrointestinal
tract is a common cause of anorexia and profound loss of
lean body mass. Loss of lean body mass may be masked by
edema.
The elderly also maintain a precarious balance between the managed symptom state and acute symptom
exacerbation. During the managed symptom state, they
are relatively symptom free while adhering to their treatment regimen. Acute symptom exacerbation, often requiring emergency medical treatment, can be precipitated by
seemingly minor conditions such as poor compliance with
sodium restriction, infection, or stress. Failure to seek medical care promptly is a common cause of progressive acceleration of symptoms.
Diagnosis and Treatment
The diagnosis of heart failure in the elderly is based on the
history, physical examination, chest radiograph, and electrocardiographic findings.77 However, the presenting symptoms of CHF often are difficult to evaluate. Symptoms of
dyspnea on exertion are often attributed to a sign of “getting older” or deconditioning from other diseases. Ankle
edema is not unusual in the elderly because the skin turgor
decreases and the elderly tend to be more sedentary with
the legs in a dependent position.
Treatment of CHF in the elderly involves many of the
same methods as in younger persons. Activities are restricted to a level that is commensurate with the cardiac
reserve. Seldom is bed rest recommended or advised. Bed
rest causes rapid deconditioning of skeletal muscles and
increases the risk for complications such as orthostatic
hypotension and thromboemboli. Instead, carefully prescribed exercise programs can help to maintain activity
tolerance. Even walking around a room usually is preferable to continuous bed rest. Sodium restriction usually is
indicated.
Age- and disease-related changes increase the likelihood of adverse drug reactions and drug–drug interactions. Drug dosages and the number of drugs prescribed
should be kept to a minimum. Compliance with drug regimens often is difficult; the simpler the regimen, the more
likely it is that the older person will comply. In general,
the treatment plan for the elderly person with CHF must
be put in the context of his or her overall needs. An improvement in the quality of life may take precedence over
increasing the length of survival.
In summary, the mechanisms of heart failure in children and
the elderly are similar to those in adults. However, the causes
and manifestations may differ because of age. In children, CHF
is seen most commonly during infancy and immediately after
heart surgery. It can be caused by congenital and acquired
heart defects and is characterized by fatigue, effort intolerance,
cough, anorexia, abdominal pain, and impaired growth. Treatment of CHF in children includes correction of the underlying
cause whenever possible. For congenital anomalies that are
amenable to surgery, medical treatment often is needed for a
time before surgery and usually is continued in the immediate
postoperative period. For many children, only medical management can be provided.
In elderly people, age-related changes in cardiovascular
functioning contribute to CHF but are not in themselves sufficient to cause heart failure. The manifestations of congestive
failure often are different and superimposed on other disease
conditions; therefore, CHF often is more difficult to diagnose in
the elderly than in younger persons. Because the elderly are
more susceptible to adverse drug reactions and have more
problems with compliance, the number of drugs prescribed is
kept to a minimum, and the drug regimen is kept as simple as
possible.
REVIEW EXERCISES
A 75-year-old woman with long-standing hypertension
and angina due to coronary heart disease presents with
ankle edema, nocturia, increased shortness of breath with
activity, and a chronic nonproductive cough. Her blood
pressure is 170/80 mm Hg, and her heart rate is 92 beats
per minute. Electrocardiograph and chest x-ray reports
indicate the presence of left ventricular hypertrophy.
A. Relate the presence of uncontrolled hypertension
and coronary artery disease to the development of
heart failure in this woman.
B. Explain the significance of left ventricular hypertrophy in terms of both a compensatory mechanism
and a pathologic mechanism in the progression of
heart failure.
C. Use Figure 28-2 to explain this woman’s symptoms,
including shortness of breath and nonproductive
cough.
A 26-year-old man is admitted to the emergency room
with excessive blood loss following an automobile in-
CHAPTER 28
jury. He is alert and anxious, his skin is cool and moist,
his heart rate is 135 beats per minute, and his blood
pressure 100/85 mm Hg. He is receiving intravenous
fluids, which were started at the scene of the accident by
an emergency medical technician. He has been typed
and cross-matched for blood transfusions, and a urinary
catheter has been inserted to monitor his urine output.
His urine output has been less than 10 mL since admission, and his blood pressure has dropped to 85/70 mm
Hg. Efforts to control his bleeding have been unsuccessful, and he is being prepared for emergency surgery.
A. Use information regarding the compensatory mechanisms in circulatory shock to explain this man’s
presenting symptoms, including urine output.
B. Use Figure 26-12 to hypothesize on this man’s blood
loss and maintenance of blood pressure.
C. The treatment of hypovolemic shock is usually directed at maintaining the circulatory volume through
fluid resuscitation rather than maintaining the blood
pressure through the use of vasoactive medications.
Explain.
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