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18
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Acute Heart Failure and Pulmonary Edema
Theo E. Meyer, Jeffrey A. Shih, Colleen Harrington
OUTLINE
Introduction, 180
Pathophysiologic Considerations, 181
Chronic Progressive Fluid and Water Retention, 181
Pulmonary Edema, 181
Left Ventricular Pump Performance in Acute Heart
Failure, 182
Chamber Stiffness, 182
Compensatory Mechanisms in Acute Heart Failure, 183
Mechanistic Considerations in Acute Heart Failure
Syndromes, 183
Clinical Presentation of Acute Heart Failure, 185
Group 1: Acute-on-Chronic Decompensated Heart
Failure, 185
Group 2: Hypertensive Acute Heart Failure, 186
Group 3: Acute Heart Failure With Severe Pulmonary
Edema, 187
Group 4: Cardiogenic Shock and Low-Output
Syndrome, 187
Group 5: High-Output Heart Failure, 187
Group 6: Right-Sided Heart Failure, 188
Diagnosis of Acute Heart Failure, 188
Differentiating Cardiogenic From Noncardiogenic
Pulmonary Edema, 188
Evaluation and Triage of Patients With Acute Heart
Failure, 189
Step 1: Define Clinical Severity of Acute Heart
Failure, 189
Step 2: Establish Etiology of Acute Heart
Failure, 190
Step 3: Identify Precipitating Causes of Acute Heart
Failure, 190
Step 4: Decide on Disposition of Patient, 190
Ongoing Evaluation of the Patient, 190
Pulmonary Artery Catheter, 191
Treatment of Acute Heart Failure, 191
General Measures, 191
Oxygenation, 191
Deep Venous Thrombosis Prophylaxis, 191
Diabetes, 191
Medications, 191
Treatment of Triggers of Decompensation, 191
Acute Coronary Syndrome, 191
Rapid Arrhythmias and Severe Bradycardia, 191
Acute Mechanical Instability, 192
Hemodynamic Goals of Treatment, 192
Specific Interventions, 192
Vasodilators, 192
Nitroglycerin, 192
Nitroprusside, 193
Nesiritide, 194
Other Vasodilators, 194
Decongestive Therapy, 194
Diuretics, 194
Vasopressin Antagonists, 195
Ultrafiltration, 195
Circulatory Support, 196
Inotropic Agents, 196
Dopamine, 196
Dobutamine, 196
Milrinone, 196
Digitalis, 197
Vasopressors, 197
Mechanical Support, 197
Continued Therapy for Chronic Heart Failure, 197
Choice of Therapeutic Regimen, 197
Hypertensive Acute Heart Failure,
Acute Heart Failure With Preserved Ejection
Fraction, 197
197
INTRODUCTION
Acute heart failure (AHF) is a clinical syndrome of new or
worsening signs and symptoms of heart failure (decompensated),
often leading to hospitalization or a visit to the emergency
department. Patients with AHF represent a heterogeneous
population with high hospital readmission rates.
180
1–9
The most
common reason for hospitalization is significant volume overload
and, subsequently, congestive symptoms. Fewer patients present
with hypotension and symptoms of reduced organ perfusion,
and some present with AHF due to “flash pulmonary edema,”
usually from uncontrolled hypertension or atrial fibrillation with
a rapid ventricular response. In general, most patients have a
slow progression of disease, resulting from cardiac ischemia,
1,2
CHAPTER 18 Acute Heart Failure and Pulmonary Edema 180.e1
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Keywords
acute heart failure
pulmonary edema
noncardiogenic pulmonary edema
diagnosis of acute heart failure
treatment of acute heart failure
hemodynamic goals of treatment
decongestive therapy
choice of therapeutic regimen
CHAPTER 18 Acute Heart Failure and Pulmonary Edema 181
Qf Kf Pv Pint Kf pV pint=− −−()()
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medication noncompliance, dietary indiscretion, or exacerbation
of hypertension.1 The average patient has had symptoms for
about 5 to 7 days before seeking medical attention.
10,11
AHF is the most common cause of hospital admission in
patients older than 65 years, accounting for 1 million admissions
annually.12 AHF represents a period of high risk for patients,
with a 20% to 30% mortality rate within 6 months after
admission.
13–15
Early medical care of AHF and time to initiation
of treatment are linked to outcome. These patients are generally
cared for in telemetry units in the United States. Only 10% to
20% of these patients are admitted to intensive care units (ICUs).
8,9
PATHOPHYSIOLOGIC CONSIDERATIONS
Integral to the understanding of the pathogenesis and treatment of
AHF and pulmonary edema is a basic understanding of the forces
involved in fluid retention, capillary–interstitial fluid exchange
(Starling relationship), and myocardial pump performance.
Chronic Progressive Fluid and Water Retention
Renal sodium and water excretion normally parallels sodium
and water intake so that an increase in plasma and blood volume
is associated with increased renal sodium and water excretion.
In patients with heart failure, sodium and water are retained
despite an increase in intravascular fluid volume. Renal sodium
and water retention in these patients may be regulated not by
the total blood volume but rather by the degree of filling of the
arterial compartment—the so-called effective blood volume. The
dynamic equilibrium of the arterial circulation, as determined
by cardiac output and peripheral vascular resistance or compliance, is the predominant determinant of renal sodium and water
excretion.
Arterial underfilling is sensed by mechanoreceptors in the left
ventricle, carotid sinus, aortic arch, and renal afferent arterioles.16
Decreased activation of these receptors due to a decrease in
systemic arterial pressure, stroke volume, renal perfusion, or
peripheral vascular resistance leads to an increase in sympathetic outflow from the central nervous system, activation of
the renin-angiotensin-aldosterone system, and the nonosmotic
release of arginine vasopressin, as well as the stimulation of
16
These factors—together with increased release of vaso-
thirst.
constrictors, such as endothelin and vasopressin, and resistance
to endogenous natriuretic peptides—contribute to sodium and
water retention leading to decompensation of chronic heart
failure.
Pulmonary Edema
The flux of fluid out of any vascular bed results from the sum of
forces promoting extravasation of fluid from the capillary lumen
versus forces acting to retain intravascular fluid. This concept of
a dynamic equilibration between opposing forces in the lung is
given mathematical expression in the Starling equation17:
where Qf is net transvascular fluid flow across the pulmonary
capillary endothelium; Kf is the filtration coefficient of the
microvascular endothelium (hydraulic conductivity of the
capillary wall × surface area); Pv is hydrostatic pressure in
the pulmonary capillaries; Pint is hydrostatic pressure in the
pulmonary interstitium; pV is plasma protein oncotic pressure;
and pint is protein oncotic pressure within the interstitial space.
Under normal conditions, the sum of the forces is slightly
positive, producing a small vascular fluid flux into the precapillary
interstitium of the lung that is drained as lymph into the systemic
veins. The capillary coefficient (Kf) determines the effectiveness
of the endothelial barrier to protein permeability, establishing
the functionality of the oncotic gradient. Because the intravascular
pressure in the pulmonary capillaries is always higher than plasma
osmotic pressure, transcapillary fluid flux out of the pulmonary
capillary is continuous. When the interstitial fluid exceeds the
interstitial space capacity, fluid floods into the alveoli.18 The
interstitial space is drained by a rich bed of lymphatics. It is
estimated that pulmonary lymph flow may increase threefold
before fluid extravasates into the alveolar airspaces. The two
most common forms of pulmonary edema are either initiated
by an imbalance of Starling forces or caused by disruption of
one or more components of the alveolar-capillary membrane.
Box 18.1 lists the causes of pulmonary edema based on the initiat-
ing mechanism. Similar to the genesis of interstitial lung edema,
pleural effusion occurs when lung interstitial pressure exceeds
pleural pressure and fluid redistributes across the visceral pleura.
It has been shown experimentally that pulmonary edema
occurs if the pulmonary capillary pressure exceeds the plasma
colloid osmotic pressure, which is approximately 28 mm Hg in
humans. The normal pulmonary capillary wedge pressure is
approximately 8 mm Hg, which allows a margin of safety of
about 20 mm Hg in the development of pulmonary edema.19
Although pulmonary capillary pressure must be abnormally high
to increase the flow of the interstitial fluid, these pressures may
not correlate with the severity of pulmonary edema when edema
is clearly present.20 These pressures may have returned to normal
when there is still considerable pulmonary edema because time
is required for removal of interstitial and pulmonary edema.
The rate of increase in lung fluid at any given elevation of
pulmonary capillary pressure is related to the functional capacity
of the lymphatics, which may vary from patient to patient, and
to variations in osmotic and hydrostatic pressures. Chronic
elevations in left atrial pressures are associated with hypertrophy
in the lymphatics, which then clear greater quantities of capillary
filtrate during acute increases in pulmonary capillary pressure.
21
The removal of edema fluid from the alveolar and interstitial
compartments of the lung depends on active transport of sodium
and chloride across the alveolar epithelial barrier. Reabsorption
of these electrolytes is mediated by the epithelial ion channels
located on the apical membrane of alveolar epithelial type I and
type II cells and distal airway epithelia. Water follows passively,
probably through aquaporins that are found predominantly on
alveolar epithelial type I cells.
22
Clinical experience with patients who have chronically elevated
atrial pressures suggests that these patients show minimal or no
evidence of interstitial lung edema. The mechanisms by which
pulmonary capillary pressure increases when the pumping ability
of the ventricle is suddenly impaired are discussed later. When
the alveolar-capillary membrane is injured, proteins leak from
182 PART IV Noncoronary Diseases: Diagnosis and Management
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BOX 18.1 Classification of Acute Pulmonary Edema
Cardiogenic Pulmonary Edema
A. Acute increase in pulmonary capillary pressure
1. Increased LA pressure with normal LV diastolic pressure
a. Thrombosed prosthetic mitral valve
b. Obstructive left atrial myxoma
2. Increased LA pressure due to elevated LV diastolic pressure
a. Increased myocardial stiffness or impaired relaxation
i. Myocardial ischemia
ii. Acute myocardial infarction
iii. Hypertrophic heart disease complicated by tachycardia or
ischemia
iv. Stress-induced cardiomyopathy
b. Acute volume load
i. Acute mitral or aortic regurgitation
ii. Ischemic myocardial septal rupture
c. Acute increases in LV afterload
i. Hypertensive crisis
ii. Thrombosed prosthetic aortic valve
B. Exacerbation of chronically elevated pulmonary capillary pressures
1. Increase in elevated LA pressure with normal LV diastolic pressure
a. Mitral stenosis and atrial fibrillation with rapid heart rate
b. Left atrial myxoma
2. Increase in elevated LA pressure due to a further increase in LV diastolic
pressure
a. Further increases in myocardial stiffness or impaired relaxation
i. Cardiomyopathy complicated by myocardial ischemia or
infarction
ii. Hypertrophic heart disease complicated by tachycardia or
ischemia
b. Volume load imposed on preexisting LV diastolic dysfunction
i. Worsening mitral regurgitation
ii. Vigorous postoperative fluid administration
iii. Dietary indiscretion
c. Pressure load imposed on preexisting LV systolic dysfunction
i. Accelerated hypertension
Noncardiogenic Pulmonary Edema
A. Altered alveolar capillary membrane permeability (adult respiratory distress
syndrome)
1.
Infectious or aspiration pneumonia
2. Septicemia
3. Acute radiation or hypersensitivity pneumonitis
4. Disseminated intravascular coagulopathy
5. Shock lung
6. Hemorrhagic pancreatitis
7. Inhaled or circulating toxins
8. Massive trauma
B. Acute decrease in interstitial pressure of the lung
1. Rapid removal of unilateral pleural effusion
C. Unknown mechanisms
1. High-altitude pulmonary edema
2. Neurogenic pulmonary edema
3. Narcotic overdose
4. Pulmonary embolism
5. After cardioversion
6. After anesthesia or cardiopulmonary bypass
LA, Left atrial; LV, left ventricular.
the capillary into the interstitium, reducing the oncotic counterpressure tendency to oppose capillary filtration. Interstitial edema
and the consequent alveolar edema formation can occur in the
presence of low hydrostatic pressures.
Left Ventricular Pump Performance in Acute
Heart Failure
The factors involved in regulating cardiac output are discussed
in Chapter 5. The following discussion briefly reviews left
ventricular (LV) pump performance in terms of the LV pressurevolume relationship as it pertains to a patient with AHF.
To appreciate fully the factors that contribute to AHF, it is
appropriate to review briefly the pressure-volume relationships
of normal and diseased hearts. The relationship between pressure
and volume throughout the cardiac cycle can be presented as a
pressure-volume loop (Fig. 18.1). The pressure-volume loop
encapsulates the systolic and diastolic functions of the heart.
Because these loops also circumscribe end-systolic and enddiastolic volumes, the stroke volume and ejection fraction can
be derived. The bottom limb of the loop, also termed the diastolic
pressure-volume curve, describes LV diastolic compliance. The
pressure-volume loop can provide a simple, but comprehensive,
description of LV pump function.
Progressive increases in systolic pressure produce a nearly
linear increase in end-systolic volume. By matching the endsystolic pressure and volume coordinates from multiple, variably
loaded beats, a near-linear relationship is established. The slope
of this relationship (E
), determined by altering load, reflects
max
LV contractility (see Fig. 18.1).23 A positive inotropic intervention
is associated with an increased end-systolic pressure and stroke
volume and a decreased end-diastolic volume. This results in an
increased E
and a shift of the pressure-volume relationship
max
to the left (Fig. 18.2A). Conversely, a negative inotropic intervention decreases end-systolic pressure and stroke volume and
increases end-diastolic volume. This results in a decrease in E
max
and a shift of the pressure-volume relationship to the right (see
Fig. 18.2B).
In the intact human heart, an increase in systolic pressure is
associated with an increase in end-systolic volume, and if the
LV fails to dilate, stroke volume decreases (Fig. 18.3A). An increase
in preload is accompanied by an increase in stroke volume and
a modest increase in end-systolic pressure (see Fig. 18.3B). Acute
and chronic changes in the pressure-volume relationship in the
failing heart depend on the underlying myocardial structure and
function, the type and extent of injury (e.g., infarction or
myocarditis, regional or global myocardial depression), and the
severity and nature of the hemodynamic load (pressure vs.
volume).
Chamber Stiffness
Chamber stiffness is determined by analyzing the curvilinear
diastolic pressure-volume relationships (Fig. 18.4). The slope of
CHAPTER 18 Acute Heart Failure and Pulmonary Edema 183
Ventricular volume
cb
Ventricular pressure
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Fig. 18.1 Schematic representation of the left ventricular (LV)
pressure-volume loop. The aortic valve opens at b and closes
at c. The mitral valve opens at d and closes at a. The slope of
the broken line through c represents the end-systolic pressure-
volume relationship (E
represents the end-diastolic pressure-volume relationship. As
contractile force develops in the LV in systole, the pressure
rapidly increases in the ventricular chamber (a → b) without
changing its volume (i.e., isovolumic phase of systole). When
the pressure exceeds the diastolic aortic pressure, the aortic
valve opens and the ventricle ejects its contents into the arterial
circulation (b → c, the ejection phase of systole). At the end of
ejection (point c), LV pressure decreases and the aortic valve
closes. Pressure rapidly declines at a constant volume (c → d,
isovolumic relaxation) to levels below that of the left atrium. At
this point, the mitral valve opens (point d), and the relaxing LV
fills along the segment d → a. The trajectory a → b → c represents
the contractile or inotropic function of the LV at any given enddiastolic volume, whereas the trajectory c → d → a represents
the lusitropic function (relaxation and filling) of the heart at any
given end-systolic pressure. The area within the loop graphically
depicts the external work (i.e., stroke work) of the ventricle.
the tangent (dP/dV) to this curvilinear relationship defines the
chamber stiffness at a given filling pressure. An increase in dP/
dV due to an increase in volume, shown in Fig. 18.4 (A → B),
has been called a preload-dependent change in stiffness. When
the pressure-volume relationship shifts to the left (A → C), the
tangent is steeper at the same diastolic pressure. The latter may
be caused by an increase in myocardial mass or intrinsic myocardial stiffness or by changes in several extramyocardial factors.
Chamber stiffness of the left ventricle is determined by static
factors (e.g., chamber volume, wall mass, stiffness of the wall)
and dynamic factors (e.g., pericardium, right ventricle [RV],
myocardial relaxation, erectile effects of the coronary vasculature).
from a preload-dependent increase in chamber stiffness, a shift
to a different pressure-volume curve, or a combination of the
two. All can result in elevated left atrial pressures, pulmonary
venous hypertension, and the signs and symptoms of AHF.
Ejection
Contraction
Relaxation
d
), and the broken line through d and a
max
24,25
Most acute alterations in LV chamber stiffness result
Filling
a
Compensatory Mechanisms in Acute Heart Failure
Rapid activation of neurohormonal systems occurs in the setting
of decreased blood pressure and reduced cardiac output related
to acute depression of LV pump performance. This causes an
increase in heart rate and arterial resistance and a decrease in
capacity of the venous system.
26,27
This decreased systemic vascular
capacity after sympathetic activation is brought on predominantly
by changes in the splanchnic vascular bed that result in a leftward
shift of the venous pressure–volume relationship, causing a
redistribution of blood from the unstressed to the stressed circulating pool (i.e., central blood pool).
28,29
In normal adults, sympathoadrenal stimulation can increase systemic blood volume by
redistribution of up to 2 units of blood from the splanchnic
venous reservoir.
29
Mechanistic Considerations in Acute Heart
Failure Syndromes
During the early phase of myocardial infarction (MI) or with
acute ischemia, reduced ventricular ejection increases endsystolic volume (residual volume) and, together with reduced
LV compliance, leads to rapid increases in LV filling pressures. It
is thought that lusitropic dysfunction associated with ischemia is
the result of an increase in stiffness in the ischemic myocardial
segment (possibly caused by slowing and incompleteness of the
relaxation process)30 and dilation of the nonischemic segment,
causing a preload-dependent increase in chamber stiffness.31 The
increase in LV filling pressure that occurs with acute infarction or
ischemia is caused by the combination of a preload-dependent
increase in chamber stiffness and a leftward shift of the diastolic
pressure-volume curve. Increased diastolic pressures after an acute
ischemic insult may also result from the redistribution of blood
from the periphery to the central blood pool.29 The effects of
these changes on the pressure–volume relationship are shown in
Fig. 18.5A.
In acute volume overload, as seen in patients with sudden
and severe valvular regurgitation or after ischemic ventricular
septal rupture, the LV dilates, causing the ventricle to operate
on the steeper portion of the pressure-volume curve. Consequently, small increments in volume result in a marked increase
in filling pressures. The effects of these changes on the pressurevolume relationship are shown in Fig. 18.5B.
The lusitropic abnormalities of LV hypertrophy secondary to
aortic stenosis, severe hypertension, or hypertrophic cardiomyopathy are caused by abnormalities of the static and dynamic
determinants of chamber stiffness. Increased passive stiffness
of the hypertrophied heart results in part from the increased
myocardial mass and the low volume-to-mass ratio; abnormal
intrinsic myocardial stiffness also may contribute to increased
chamber stiffness. Abnormalities of myocardial relaxation further
impair filling in the hypertrophied heart. The effects of these
changes on the pressure-volume relationship are shown in
Fig. 18.5C.
Chronic heart failure is characterized by a compressed pressurevolume loop. This compressed loop, characterized by a decrease
in end-systolic pressure and an increase in end-diastolic pressure,
means that the work of the failing heart is reduced while
184 PART IV Noncoronary Diseases: Diagnosis and Management
A
Ventricular pressure
Ventricular pressure
B
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Inotropic
state
A
Fig. 18.2 Schematic diagrams illustrating the effects of inotropic interventions on the pressure-
volume loop. (A) With a positive inotropic intervention, the pressure-volume loop (broken line) is
shifted to the left and the slope of the end-systolic pressure-volume line is increased. (B) With
a negative inotropic intervention, the pressure-volume loop is shifted to the right and the slope
of the end-systolic pressure-volume line is decreased.
Ventricular volume
Baseline
Ventricular pressure
Ventricular volume
Baseline
Inotropic
state
maintaining a near-normal stroke volume. Comparable to the
changes with ischemia, the elevated filling pressures in chronic
heart failure is caused by a combination of a preload-dependent
increase in chamber stiffness (i.e., the LV operates at higher
end-diastolic volumes to optimize the Starling relationship) and
Ventricular pressure
Ventricular volume
Fig. 18.3 Schematic diagrams illustrating the effects of changing loading conditions on the
pressure-volume loop in the intact heart. (A) An increase in afterload shifts the pressure-volume
loop (broken line) to the right, increasing the end-systolic and end-diastolic volumes and the
end-systolic and end-diastolic pressures while decreasing the stroke volume. The slope of the
end-systolic pressure-volume line is usually not affected by a pure change in afterload. (B) An
increase in preload also shifts the pressure-volume loop (broken line) to the right, increasing the
end-diastolic volume and end-diastolic pressure. The increase in preload may be associated
further with a small increase in end-systolic volume and a modest increase in end-systolic pressure;
in contrast to the case with an increase in afterload, however, the stroke volume increases.
Similar to an increase in afterload, the slope of the end-systolic pressure-volume line is not
affected by a change in preload.
B
Ventricular volume
a preload-independent increase in chamber stiffness (see Fig.
18.5D). It should also be evident from the pressure-volume curve
that these hearts operate near the limit of their preload reserve;
therefore they are extremely vulnerable to any myocardial injury
or insult. Even a minor perturbation, such as an arrhythmia,
CHAPTER 18 Acute Heart Failure and Pulmonary Edema 185
Diastolic volume
Diastolic pressure
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A= Baseline stiffness (dP/dV)
B= Preload-dependent change
C= Increased intrinsic stiffness
B
infection, or a small area of infarction, is likely to precipitate
acute decompensation in these patients.
CLINICAL PRESENTATION OF ACUTE
HEART FAILURE
The onset and severity of symptoms of AHF vary and depend
to a great extent on the nature of the underlying cardiac disease
and the rate at which the syndrome develops. The largest proportion of patients (70%) with AHF are admitted due to worsening
chronic heart failure; up to 15% to 20% of patients present with
heart failure for the first time and approximately 5% are admitted
for advanced or end-stage heart failure. A few patients with AHF
present with low blood pressure (<8%) or shock (<3%).
patients are elderly, with an average age of approximately 70 to
75 years. Patients with new-onset heart failure are more likely
to present with pulmonary edema or cardiogenic shock. The
heterogeneity of this patient population is evident when one
considers that almost half of these patients have preserved LV
ejection fraction. A history of coronary disease is present in 60%
of patients, 45% of whom have had a prior MI, hypertension
in 70%, atrial fibrillation in 30%, diabetes mellitus in 40%, and
chronic obstructive pulmonary disease in 30%.
mitral regurgitation due to LV dilation is common.
For practical purposes, it is helpful to view the presentation
of AHF according to the predominant clinical characteristics on
admission. The European Society of Cardiology guidelines for
the diagnosis and treatment of AHF classifies patients into 1 of
6 groups on the basis of the clinical and hemodynamic profiles.5
These include (1) AHF, either new-onset or decompensated
chronic heart failure, (2) hypertensive AHF, (3) AHF with
pulmonary edema, (4) cardiogenic shock, (5) high output failure,
C
A
Fig. 18.4 Schematic diagram of the diastolic left ventricular pressure-volume curve. The slope
of the tangent (dP/dV) to this curvilinear relationship defines chamber stiffness at a given filling
pressure. An increase in dP/dV owing to an increase in volume, shown diagrammatically as
A → B, has been termed a preload-dependent change in stiffness. When the pressure-volume
relationship shifts to the left, A → C, the tangent is steeper (increased chamber stiffness) at the
same diastolic pressure.
and (6) right heart failure. These syndromes are discussed here
and are outlined in Table 18.1.
Group 1: Acute-on-Chronic Decompensated
Heart Failure
This syndrome is seen in patients with an established diagnosis
of heart failure who develop increasing signs or symptoms of
decompensation after a period of relative stability. This scenario
accounts for greater than 70% of all heart failure admissions.
New-onset HF is seen much less frequently (15% to 20%) but
may present with the same phenotype as chronic heart failure.
Progressive dyspnea is the most common complaint of patients
10,32
10,32
Secondary
Most
presenting with decompensated chronic heart failure. Patients
may report lower extremity edema and epigastric tenderness or
a sensation of abdominal fullness. Abdominal tenderness is often
due to hepatic congestion and distention of the hepatic capsule.
With severe hepatic congestion, the patient may also complain
of nausea and anorexia. Other symptoms include nocturia and
neurologic symptoms such as confusion, headaches, insomnia,
anxiety, disorientation, and impaired memory.
Physical signs vary according to the severity of the volume
overload. An elevated jugular venous pressure, positive hepatojugular reflux test, and a tender, enlarged liver are frequent findings
in these patients. Rales and wheezing are not common but may
be heard in patients with significant pulmonary congestion. The
absence of rales does not imply that the pulmonary venous
pressures are not elevated. Diminished air entry at the lung bases
is usually caused by a pleural effusion, which is often more
frequent in the right pleural cavity than in the left. Leg edema
is frequently evident in both legs, particularly in the pretibial
region and ankles in ambulatory patients. Sacral edema can be
detected in patients who are bedridden.
186 PART IV Noncoronary Diseases: Diagnosis and Management
AB
CD
Ventricular pressure
Ventricular pressure
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Ventricular pressure
Ventricular volume
Ventricular pressure
Ventricular volume
Fig. 18.5 Schematic diagrams of four different pathophysiologic states. In each diagram, the
control pressure-volume loop and the diastolic pressure-volume relationship (curve) are shown
in solid lines. The effects of different pathologic states on the pressure-volume relationship are
depicted by the broken lines (A). With acute ischemia or infarction, the pressure-volume curve
is shifted upward and to the right. (B) In a volume-overloaded heart (i.e., valvular regurgitation),
the pressure-volume relationship is shifted to the right along the same diastolic pressure-volume
curve. The increase in diastolic pressure is the result of the left ventricle operating on the steeper
portion of the diastolic pressure-volume relationship. (C) With excessive hypertrophy, the pressurevolume relationship is shifted to the left, so that the heart operates at smaller end-diastolic and
end-systolic volumes. The increase in chamber stiffness is reflected by the steep diastolic pressurevolume curve. (D) In chronic advanced heart failure, the pressure-volume loop is often compressed
and shifted to the right. This compressed loop, characterized by a lower end-systolic and increased
end-diastolic pressure, implies that the work of the heart is reduced, while maintaining a nearnormal stroke volume. Comparable to the situation in (A), the elevated diastolic pressure is caused
by preload-dependent and preload-independent increases in chamber stiffness.
Ventricular volume
Ventricular volume
The cardiac examination may be entirely normal in patients
with heart failure with preserved ejection fraction, whereas many
patients with advanced systolic dysfunction exhibit a third heart
sound and a laterally displaced point of maximal impulse. A
murmur of mitral regurgitation is often audible when the left
ventricle is markedly enlarged, or a tricuspid regurgitation
murmur is present when the RV is volume or pressure overloaded.
These patients often do not have radiographic signs of marked
interstitial lung edema.
Group 2: Hypertensive Acute Heart Failure
The syndrome of AHF is characterized by the rapid onset of
symptoms or signs of heart failure. This phenotype is more
common in females and the systolic blood pressure on admission
usually exceeds 180 mm Hg.33 There is usually predominant
pulmonary rather than systemic congestion, as is manifest by
minimal weight gain prior to admission. Virtually all patients
have a preserved LV ejection fraction. Blood pressure elevation
CHAPTER 18 Acute Heart Failure and Pulmonary Edema 187
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TABLE 18.1 Acute Heart Failure Syndromes
Phenotype Rate of Onset Signs and Symptoms Hemodynamic Profile Diagnostics
1a.
Acute-on-chronic HF Gradual Dyspnea and fluid overload Normal or low normal BP CR: normal or mild
interstitial edema
Adequate tissue perfusion Possible pleural effusion
1b.
New-onset AHF Gradual or rapid Dyspnea, variable fluid overload Normal or low BP CR: normal or mild
interstitial edema
Variable tissue perfusion Possible pleural effusion
2.
Hypertensive AHF Rapid Acute dyspnea SBP >180 mm Hg CR: interstitial lung edema
Minimal fluid overload Adequate tissue perfusion
3.
AHF and pulmonary edema Rapid or gradual Severe dyspnea, tachypnea Low normal BP Hypoxic on room air
Tachycardia Variable tissue perfusion
4a.
Cardiogenic shock (low
output syndrome)
4b.
Severe cardiogenic shock Rapid Weakness/fatigue
5. High output HF Rapid or gradual Dyspnea; tachycardia and warm
6.
Acute right HF Rapid or gradual; marked
Modified from Nieminen MS, Bohm M, Cowie MR, et al. for the ESC Committee for Practice Guideline: Executive summary of the guidelines on
the diagnosis and treatment of acute heart failure: The Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J
2005;26:384–416; and Joseph SM, Cedars AM, Ewald GA, et al. Acute decompensated heart failure: contemporary medical management. Tex
Heart Inst J. 2009;36(6):510–20.
BP, Blood pressure; CR, chest radiograph; HF, heart failure; SBP, systolic blood pressure.
Usually gradual Weakness/fatigue
Alterered mental status
Poor tissue perfusion
Oliguria/anuria
periphery
Variable tissue perfusion Severe dyspnea Low normal BP
fluid overload
Low normal BP Echo shows severe LV
dysfunction
Low BP (< 90 mm Hg)
Normal BP
could develop rapidly, which is associated with increased filling
pressures and enhanced sympathetic tone.
Group 3: Acute Heart Failure With Severe
Pulmonary Edema
Severe pulmonary edema is seen in less than 3% of all patients
admitted with AHF.32 Patients typically experience a sudden and
overwhelming sensation of suffocation and air hunger; this is
invariably accompanied by extreme anxiety, cough, expectoration
of a pink frothy liquid, and a sensation of drowning. The patient
sits bolt upright, is unable to speak in full sentences, and may
thrash about. The respiratory rate is increased, the alae nasi
are dilated, and there is inspiratory retraction of the intercostal
spaces and supraclavicular fossae. Respiration is often noisy,
and there may be audible inspiratory and expiratory gurgling
sounds. An ominous sign is obtundation, which may be a sign
of severe hypoxemia. Sweating is profuse, and the skin tends to
be cool, ashen, and cyanotic, reflecting increased sympathetic
outflow.
The pulse rate is most often elevated secondary to an increased
adrenergic drive. When the blood pressure is found to be markedly
elevated, it is more likely to be the cause of, or an important
contributing factor to, pulmonary edema rather than the consequence of the condition. The oxygen saturation is usually less
than 90% on room air before treatment. Auscultation of the
lung usually reveals coarse airway sounds bilaterally with rhonchi,
wheezes, and moist fine crepitant rales that are detected first at
the lung bases, but then extend upward to the apices as the lung
edema worsens. Cardiac auscultation may be difficult in the
acute situation, but third and fourth heart sounds may be present.
When valvular abnormalities or mechanical complications after
MI result in AHF, the murmurs of mitral and aortic regurgitation
and ischemic septal rupture are often audible, but detection
requires a careful and skillful auscultator.
Group 4: Cardiogenic Shock and
Low-Output Syndrome
Systolic blood pressure is less than 90 mm Hg in approximately
8% of patients with decompensated chronic heart failure.
Low-output heart failure is characterized by symptoms and signs
that are related to decreased end-organ perfusion. A typical patient
with this clinical syndrome has severely impaired LV function
and usually presents with symptoms of fatigue, altered mental
status, or signs of organ hypoperfusion, such as prerenal azotemia,
abnormal hepatic enzymes, or elevated lactic acid. The patient
may present with tachypnea at rest, tachycardia, and a cold and
cyanotic periphery. The degree of peripheral hypoperfusion may
be so advanced that the skin over the lower extremities is mottled
and cool. A diminished pulse pressure, consistent with a reduced
stroke volume, is often found in patients with AHF. Occasionally,
the clinician may detect pulsus alternans—when a strong or
normal pulse alternates with a weak pulse during normal sinus
rhythm. This physical finding is rare but, when present, is a sign
of severe LV dysfunction.
5,10
Group 5: High-Output Heart Failure
The phenotype is an uncommon cause of AHF and generally
presents with warm extremities, pulmonary congestion, tachycardia, and a wide pulse pressure. Underlying conditions include
anemia, thyrotoxicosis, advanced liver failure, and Paget disease.
188 PART IV Noncoronary Diseases: Diagnosis and Management
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by a constellation of symptoms owing to a heterogeneous group
Group 6: Right-Sided Heart Failure
This syndrome occurs commonly in patients with severe isolated
tricuspid regurgitation; right ventricular dysfunction; chronic
lung disease, such as those with chronic obstructive and/or
insterstitial lung disease; or long-standing pulmonary hyperten-
of cardiac and vascular disorders; the diagnosis cannot be based
on a single laboratory test. Results of BNP or NT-proBNP testing
must be interpreted in the context of the overall clinical evaluation;
such testing must support, rather than override, careful clinical
judgment.
sion. These patients are often oxygen dependent and present
with signs and symptoms of right-sided volume overload.
Differentiating Cardiogenic From Noncardiogenic
Pulmonary Edema
DIAGNOSIS OF ACUTE HEART FAILURE
The rapid diagnosis of AHF is a necessary first step to initiate
appropriate treatment. This is critical since early treatment is
linked to outcome. The diagnosis of decompensated chronic heart
failure is generally straightforward, especially when a patient
presents with the triad of fluid retention, exertional dyspnea, and
a history of heart failure. It is also essential to rule out alternate
causes of the patient’s signs and symptoms. Worsening exertional
dyspnea could also be due to a range of other conditions, including
pulmonary embolism, pneumonia, chronic obstructive pulmonary
disease, asthma, pulmonary fibrosis, pleural effusion, anemia,
hyperthyroidism, and musculoskeletal disorders.
For patients without a prior cardiac history, the diagnosis
of AHF should be based primarily on signs and symptoms and
supported by appropriate investigations, such as electrocardiogram (ECG), chest radiograph, biomarkers, and Doppler
echocardiography according to the American Heart Association/
American College of Cardiology and European Society of Cardiology Guidelines.
AHF (resulting in a high negative predictive value).35 The chest
radiograph can be helpful for the diagnosis of AHF. The most
specific findings in patients with AHF are pulmonary venous
congestion, pleural effusions, interstitial or alveolar edema, and
cardiomegaly. Up to 20% of patients with AHF may have normal
chest radiographs.36 Echocardiography is indicated early on only
in patients with hemodynamic instability.
When the diagnosis is uncertain, determination of plasma
B-type natriuretic peptide (BNP) or N-terminal pro-B-type
natriuretic peptide (NT-proBNP) concentration should be
considered in patients being evaluated for dyspnea who have
signs and symptoms compatible with AHF. The natriuretic
peptide concentration should not be interpreted in isolation
but rather in the context of all available clinical data bearing
on the diagnosis of AHF.
There is considerable overlap in BNP and NT-proBNP levels
in patients with and without heart failure, which makes the test
less robust in an individual patient with intermediate levels of
BNP (~200 to 400 pg/mL). Because many conditions increase
natriuretic pepide levels, low values of BNP (<100 pg/mL) or
NT-proBNP (<300 pg/mL) are most useful because the diagnosis
of decompensated heart failure is very unlikely as an explanation
for dyspnea.38 Decision analysis suggests that BNP or NT-proBNP
testing is generally most useful in patients who have an intermediate probability of heart failure.39 Unexpected low biomarkers
are occasionally found in some patients with end-stage HF, acute
pulmonary edema, constrictive pericarditis, and right-sided heart
failure.35 AHF remains a clinical syndrome that is characterized
34,35
The electrocardiogram is rarely normal in
It is crucial to establish whether respiratory failure (pulmonary
edema) is due to cardiogenic or noncardiogenic causes. This
distinction can invariably be made by assessment of the clinical context in which it occurs and through examination of the
clinical data available (Table 18.2). The clinical data include tests
that are routinely performed on all critically ill patients, such
as ECG, blood gas analysis, blood count, electrolytes, and chest
radiograph.
Noncardiogenic pulmonary edema (NCPE) is invariably
associated with an underlying disease, which may or may not
be readily apparent. The diagnosis of NCPE often depends on
pretest probabilities: acute respiratory distress in a patient with
documented sepsis (i.e., peritonitis) or pancreatitis should raise
the strong possibility that the respiratory failure is due to NCPE.
In contrast to cardiogenic pulmonary edema (CPE), NCPE is
uncommonly associated with a well-defined acute cardiac event
(i.e., MI). Subtle physical signs may also aid in differentiating
NCPE from CPE. NCPE is usually a component of a hyperdynamic
illness, clinically apparent as a warm, vasodilated periphery,
whereas CPE is frequently associated with a cold and sweaty
periphery. The findings of a third heart sound or murmurs of
TABLE 18.2 Differentiation of
Noncardiogenic From Cardiogenic
Pulmonary Edema Based on Clinical Data
Noncardiogenic Cardiogenic
History Underlying disease (e.g.,
pancreatitis, sepsis)
Physical
examination
ECG ECG usually normal ST segment and QRS
Chest radiograph Peripheral infiltrates Perihilar infiltrates
Laboratory test Normal enzymes BNP
Ventilatory
needs
Modified from Sibbald WJ, Cunningham DR, Chin DN. Non-cardiac or
cardiac pulmonary edema? A practical approach to clinical
differentiation in critically ill patients. Chest. 1983;84:452–61.
BNP, Brain natriuretic peptide; FIo2, inspired oxygen concentration;
JVP, jugular venous pressure; MI, myocardial infarction; PEEP,
positive end-expiratory pressure.
Warm periphery Cool, mottled periphery
Bounding pulses Small-volume pulse
Normal-sized heart Cardiomegaly
Normal JVP Elevated JVP
No S
3
No murmurs Systolic and diastolic
<
100 mg/mL
Higher F
IO
oxygenate
and PEEP to
2
Acute cardiac event
(e.g., MI)
S
3
murmurs
abnormalities
Elevated biomarkers
Lower FIO2 and PEEP to
oxygenate
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