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Cardiology in Review
Volume 10, Number 4, pp. 218 –229
Copyright © 2002 Lippincott Williams & Wilkins
Diastolic Heart Failure: Restrictive
Cardiomyopathy, Constrictive Pericarditis,
and Cardiac Tamponade: Clinical and
Echocardiographic Evaluation
CRAIG R. ASHER, MD, and ALLAN L. KLEIN, MD
An understanding of the basic principles of diastolic function is important in order to
recognize diseases that may result in diastolic dysfunction and diastolic heart failure.
Although uncommon, restrictive cardiomyopathy, constrictive pericarditis, and cardiac
tamponade are among the disorders that may affect primarily diastolic function with
preservation of systolic function. Diastolic heart failure may manifest with chronic nonspecific symptoms or may present with acute hemodynamic compromise. Echocardiography plays a vital role in the diagnosis of diastolic dysfunction and differentiation of these
disease processes. It also provides a basis for clinical decisions regarding management
and surgical referral. This review summarizes the clinical features, pathophysiology, and
hemodynamic and echocardiographic signs of restrictive cardiomyopathy, constrictive
pericarditis, and cardiac tamponade.
Key Words: Cardiac tamponade, Constrictive pericarditis, Diastolic dysfunction, Restrictive cardiomyopathy
Diastolic dysfunction is defined as the requirement
for elevated filling pressures to maintain cardiac
output. Augmented filling pressures may result in
excessive cardiac volume and right-sided or leftsided congestion, the syndrome of diastolic heart
failure (1). Although diastolic dysfunction contributes to heart failure in patients with abnormal systolic function, it may occur in patients with normal
function (2). Numerous disease processes affecting
the myocardium and pericardium are associated
with diastolic dysfunction and heart failure. The
clinical manifestations of these conditions are diverse, ranging from nonspecific, insidious symptoms such as exertional dyspnea to pulmonary
edema or sudden hemodynamic collapse.
The prevalence of diastolic heart failure is variably reported depending on the age, diagnostic criteria, and referral patterns of the populations studDepartment of Cardiovascular Medicine, Section of Cardiovascular
Imaging, Cleveland Clinic Foundation, Cleveland, Ohio
Address reprint requests to: Allan L. Klein, MD, Cleveland Clinic Foundation, Department of Cardiovascular Medicine, 9500 Euclid Avenue, Desk
F15, Cleveland, OH 44195-0001.
218
CARDIOLOGY IN REVIEW
ied (2). Hypertension, coronary artery disease,
valvular heart disease, and hypertrophic cardiomyopathy are the predominant myocardial disorders
that result in diastolic dysfunction with relatively
preserved systolic function (3). Restrictive cardiomyopathies are less common causes of diastolic
dysfunction because of myocardial storage or infiltration. All of these myocardial conditions cause
diastolic dysfunction largely by their effect on ventricular relaxation and compliance (4). Constrictive
pericarditis and cardiac tamponade are pericardial
disorders that impede ventricular filling by extrinsic
constraint or limitation of chamber loading. Pericardial disorders may result in a spectrum of acute and
chronic hemodynamic disturbance.
Distinguishing disorders that cause diastolic dysfunction is important so that management can be
tailored to the specific disease. This review discusses the general principles of normal diastolic
function and contrasts the abnormalities of diastolic
dysfunction present with restrictive cardiomyopathy, constrictive pericarditis, and cardiac tamponade. The integral role of echocardiography in differentiating these diseases is highlighted.
DIASTOLIC FUNCTION: PHYSIOLOGY
Diastolic filling of the left ventricle (LV) encompasses the period of the cardiac cycle between aortic
valve closure and mitral valve closure. Four distinct
phases are distinguished: (1) isovolumic relaxation
(between aortic valve closure and mitral valve opening), (2) rapid filling, (3) diastasis (slow filling), and
(4) atrial contraction (5). There are multiple physiologic determinants of diastolic function. The major
myocardial factors that affect diastolic function include LV myocardial relaxation, compliance, and
left atrial function (5). Other parameters include
heart rate, preload, afterload, atrioventricular conduction, right ventricular (RV) function, intrathoracic
pressure, viscoelastic properties, coronary engorgement, neurohormonal activation, and pericardial
constraint (6). RV diastolic function is concordant
with LV diastolic function in healthy people, although discordant filling and differing external interactions may occur in some disease states.
After LV contraction, diastole begins with the
energy-dependent cellular process of ventricular
relaxation, which extends into diastasis. LV relaxation is best characterized by the time constant of
relaxation (␶), which describes the rate of LV pressure decay in an exponential equation. Until recently, only invasive methods were available to
estimate (␶)(7). Other, more dependent surrogate
echocardiographic markers of relaxation include
the isovolumic relaxation time (IVRT) and information obtained by color M-mode and Doppler
tissue imaging. The IVRT characterizes the time
when LV pressure declines and LV volume remains constant. When LV pressure drops below
left atrial pressure, the mitral valve opens and the
early rapid filling period begins.
During the early filling period (mitral E wave),
there is a rapid increase in the LV chamber volume, which contributes largely to the ventricular
stroke volume (8). The amount of volume entering
the LV cavity is influenced by many factors, including the pressure gradient between the pulmonary veins and LV, continued myocardial relaxation, elastic recoil (ventricular suction), and
stiffness properties of the myocardium (5). LV
stiffness (or its reciprocal, compliance) characterizes the change in pressure within the chamber
with an increase in volume and is dependent on
the many inherent properties of myocardial content, chamber dimension, and external constraints
of the pericardium and thorax (5).
The left atrial and LV pressures are equalized
during diastasis, resulting in slow or minimal fillVolume 10, Number 4, 2002
ing. Diastasis is followed by atrial contraction (mitral A wave), which contributes variably to LV enddiastolic volume. Aside from the left atrium’s
passive role as a conduit receptacle, it functions as a
pump to regulate filling volume. When left atrial
pressure is high at the end of diastole because of
systolic heart disease, Frank-Starling mechanisms
are activated (increased stretch, increased force of
contraction), and atrial systole may contribute significantly to diastolic filling volume (9).
DIASTOLIC FUNCTION: ECHOCARDIOGRAPHY
The assessment of diastolic function has become an integral part of any echocardiographic
study. Many causes of diastolic heart failure can
be identified, including restrictive, hypertrophic,
and ischemic cardiomyopathies and pericardial,
valvular, and congenital heart disease. Diastolic
filling patterns can be evaluated and stages of
diastolic dysfunction determined that correlate
with left-sided and right-sided filling pressures
and disease-related prognosis (10 –13). Other
techniques such as radionuclide angiography,
magnetic resonance imaging, and cardiac catheterization are more time consuming, invasive, and
tedious, and are generally used only as adjuncts to
echocardiography.
Traditionally, the diastolic function exam focuses on pulsed Doppler recordings of left-sided
mitral inflow E and A waves and pulmonary vein
systolic (S), diastolic (D), and atrial reversal (AR)
waves and the corresponding right-sided tricuspid inflow and hepatic vein flow waves (14).
Measurements of deceleration and IVRT times
and responses to physiologic maneuvers such as
Valsalva provide more information. Using these
parameters, 4 stages of diastolic dysfunction can
be determined: (1) impaired relaxation, (2)
pseudonormal stage, (3) restrictive, reversible
stage, and (4) restrictive, irreversible function (15)
(Fig. 1).
Newer technologies have provided supplemental data to differentiate normal from pseudonormal patterns and to estimate left atrial and LV
filling pressures more accurately (16) A color Mmode display shows a more precise spatial and
temporal distribution of flow velocities propagating across the mitral valve into the LV. The flow
propagation velocity (vp) provides a relatively
preload-independent determination of relaxation
in various disease states and can be used in a
regression equation with the mitral inflow E wave
CARDIOLOGY IN REVIEW
219
Figure 1. Stages of diastolic function as assessed by Doppler echocardiography mitral inflow, pulmonary venous flow,
tissue Doppler, and color M-mode. Using an integrated approach with these 4 modalities, the stages of diastolic
dysfunction can be determined. A, mitral A-wave velocity; Am, tissue Doppler atrial contraction wave; CMM-vp, color
M-mode flow propagation velocity; D, pulmonary venous diastolic wave; E, mitral E-wave velocity; Em, tissue Doppler
early filling wave; PV, pulmonary vein; S, pulmonary venous systolic wave; Sm, tissue Doppler systolic wave; TDE, tissue
Doppler echocardiography; vp, color M-mode flow propagation velocity. Reprinted with permission from Garcia MJ,
Thomas JD, Klein AL: New Doppler echocardiographic applications for the study of diastolic function. J Am Coll Cardiol
1998;32:865– 875.
to estimate pulmonary capillary wedge pressure
(17). Doppler tissue imaging obtains the low velocity and high amplitude signals of the myocardium rather than the high velocity and low amplitude blood signals (16). With this technique,
spectral Doppler or color Doppler encoded velocities can be recorded. Spectral Doppler myocardial velocities of the mitral annulus provide systolic and diastolic velocities (Em, early filling; Ea
or Am, atrial contraction) similar to the mitral
inflow profiles. Studies have demonstrated that
Em is relatively preload-independent in many
disease states. As with vp, Em can be used to
differentiate disease states such as restrictive cardiomyopathy and constrictive pericarditis and to
assess LV filling pressures more accurately (18).
Additionally, recent reports have emphasized the
importance of assessing regional myocardial function by Doppler echocardiographic strain rate imaging (19).
RESTRICTIVE CARDIOMYOPATHY
As defined by the revised World Health Organization Task Force, restrictive cardiomyopathy is
a disease characterized by “restrictive filling and
reduced diastolic volume of either or both ventricles with normal or near-normal systolic func220
CARDIOLOGY IN REVIEW
tion.” (20) Despite this rigid definition requiring
that restrictive hemodynamics are present, several
studies have demonstrated early forms of these
disorders with earlier stages of diastolic impairment. These diseases may be idiopathic or associated with specific systemic conditions and may
be further characterized as myocardial (noninfiltrative, infiltrative, and storage) or endomyocardial types (21). The prognosis of restrictive cardiomyopathies is generally poor, except for those
with reversible causes such as hemochromatosis.
Cardiac amyloidosis is the most prevalent restrictive cardiomyopathy, and the current literature
addresses predominantly this specific disease
(Fig. 2).
Because of the resistance to biventricular filling, patients commonly develop a clinical profile
related to congestive failure with fatigue, exercise
intolerance, right-sided or left-sided heart failure,
and atrial fibrillation (22,23). The clinical examination correlates with these symptoms. An elevated jugular venous pressure with an x and
prominent y descent (early-stage, M wave), y descent only (late-stage), and Kussmaul’s sign may
be present, although pulsus paradoxus is always
absent. Depending on the stage of disease, an S4
(early) or S3 (late) may be present (21). The electrocardiogram of amyloidosis typically shows a
Diastolic Heart Failure
Figure 2. Working classification of restrictive cardiomyopathy. Reprinted with permission from Leung D, Klein AL:
Restrictive cardiomyopathy: diagnosis and prognostic implications. In Otto CM, ed: Practice of Clinical
Echocardiography. Philadelphia, WB Saunders, 1997; 473– 493.
large discordance between echocardiographic
wall thickness and voltage (low voltage and increased wall thickness) (24).
Pathophysiology
As a result of myocardial or endocardial involvement such as amyloid infiltration, the ventricle is noncompliant or stiff and resists ventricular filling. Therefore, as the volume of the heart
is increased, there is a steep rise in the pressure.
Diastolic right-sided or left-sided heart failure
may ensue (22).
Hemodynamic Signs
In the cardiac catheterization laboratory, invasive determination of operating stiffness may be
demonstrated by pressure-volume curves, LV and
RV hemodynamic tracings showing a dip and
plateau or square root pattern (21). Other, less
specific findings include a RV systolic pressure of
greater than 50 mmHg with a RV end-diastolic
pressure usually less than one third of the RV
systolic pressure. Typically, the LV end-diastolic
pressure is greater that the RV end-diastolic pressure (25).
Echocardiographic signs
Echocardiography is uniquely suited as a diagnostic modality to detect the anatomic and functional abnormalities associated with restrictive
cardiomyopathies. A combination of 2-dimensional imaging, M-mode, and Doppler information is important to identifying specific features of
restrictive cardiomyopathy. Amyloidosis is primarily discussed here because it is the prototype
of this class of diseases, and although endomyocardial disorders have very distinct features, they
are less commonly encountered in this country.
Volume 10, Number 4, 2002
Two-dimensional Imaging and M-mode
Increased wall thickness of the LV and often the
RV is a hallmark of amyloidosis and almost all the
myocardial disorders (26). Both ventricular cavities are typically small with a decreased volume
and large atria. The atrial septum and cardiac
valves may also be thickened. A characteristic
“granular sparkling” myocardial texture was described before harmonic and high frequency imaging, but this may be a less sensitive and specific
finding with current imaging modalities. A pericardial effusion may be present. The inferior vena
cava is usually dilated and does not collapse with
inspiration (plethoric), reflecting increased right
atrial pressure.
Doppler Echocardiography
Diastolic dysfunction is a requirement for a
restrictive cardiomyopathy, although not all patients will have a restrictive diastolic filling pattern. In earlier stages of disease an impaired relaxation pattern may be present before the onset of
abnormal compliance. Determination of the severity of diastolic impairment is important not only
for diagnostic reasons; it has been demonstrated
that the prognosis of patients with restrictive filling patterns have a nearly fivefold higher mortality than the nonrestrictive patterns (27).
The classic Doppler pattern of advanced cardiac
amyloidosis is as follows: (28)
(1) Mitral inflow: large E wave and small A wave;
E/A ratio greater than 2; short deceleration
time (DT) less than 150 ms; short IVRT less
than 60 ms; no significant change in mitral E
wave, deceleration time, or IVRT with phases
of respiration
(2) Pulmonary veins: small S wave; large D wave;
CARDIOLOGY IN REVIEW
221
S/D ratio less than 0.5; prominent AR (except
with atrial systolic failure) width greater than
mitral A wave and high amplitude; no significant respiratory variation of D wave
(3) Tricuspid inflow: similar to mitral inflow
with an increased E/A ratio and short DT;
with inspiration, there is further shortening of
the DT and minimal change in E/A ratio
(4) Hepatic veins: similar to pulmonary vein flow
with S/D ratio less than 0.5 and prominent
atrial and ventricular reversals; with inspiration and expiration, there is increased prominence of the reversal waves
Superior vena cava flows are similar to hepatic
vein flows, and right and left heart patterns are
concordant in most patients. Other findings include the lack of respiratory variation of the tricuspid regurgitant jet with respiration and the
presence of at least mild mitral and tricuspid
regurgitation.
Doppler tissue imaging and color M-mode flow
propagation have provided invaluable information for the differentiation of restrictive cardiomyopathy and constrictive pericarditis. Patients with
restrictive cardiomyopathy have an abnormality
of both relaxation and compliance, whereas those
with constrictive pericarditis generally have normal relaxation and impaired compliance because
of pericardial impedance to filling. For this reason, patients with constrictive pericarditis generally have a normal or fast color M-mode vp and a
normal or increased Em, differing from patients
with restrictive cardiomyopathy (16,18,29). A recent case report demonstrated that an exception to
the rule of higher Em velocities with constrictive
pericarditis may occur when pericardial calcification and tethering involve the annulus (30). In
these cases, Doppler imaging of the apex and
strain rate imaging may help confirm constriction.
Differential Diagnosis
Differentiation of restrictive cardiomyopathy
and constrictive pericarditis is essential because
of the potential to relieve constrictive pericarditis
effectively with surgical pericardial stripping (Table 1). It should be appreciated that certain conditions such as radiation of the heart may cause a
mixed disease of constrictive pericarditis and restrictive physiology.
Restrictive cardiomyopathy must also be distinguished from other pathologic conditions that
cause an increase in wall thickness because of
hypertrophy. These diseases are caused by either
primary hypertrophy (hypertrophic cardiomyop222
CARDIOLOGY IN REVIEW
athy) or secondary hypertrophy (ie, aortic valve
disease, hypertension).
CONSTRICTIVE PERICARDITIS
The majority of contemporary cases of nonidiopathic constrictive pericarditis are caused by previous cardiac surgery, radiation exposure, and
chronic pericarditis with a myriad of etiologies
(31). With the increasing rates of patients undergoing cardiac surgery, the prevalence of constrictive pericarditis may be increasing. Constrictive
pericarditis can be surgically cured with pericardial stripping, with acceptable surgical mortality
rates and symptomatic benefits in most patients
(31). Therefore, clinicians must consider the diagnosis among patients seeking treatment with
symptoms that may be consistent with the condition.
The clinical presentation of patients with constrictive pericarditis may be nonspecific and indolent in the early stages. Symptoms may include
fatigue or decreased exercise tolerance. In more
advanced stages, patients may develop both left
and right heart failure, with the latter often predominating. Physical findings in advanced disease reflect the signs of cardiac congestion (32).
The hallmarks of physical diagnosis include an
elevated jugular venous pressure with a prominent y descent (Friedreich’s sign) reflecting the
predominance of filling in early diastole. Kussmaul’s sign, an inspiratory increase in the jugular
venous pressure, may be present but is not specific for constrictive pericarditis (32). Findings
specific to constrictive pericarditis include a pericardial knock (occurs after an opening snap and
before an S3 in timing) because of cessation in
diastolic filling and retraction of the apical impulse in systole. In very advanced cases, patients
develop severe right heart failure.
In advanced cases, noninvasive diagnostic testing may be supportive of the diagnosis. The electrocardiogram may be low in voltage because of
the pericardial encasement. The chest radiograph
may show calcification of the pericardium and
pleural effusions.
Pathophysiology
Most conditions that lead to constrictive pericarditis result in inflammation, fibrosis, adhesion,
thickening, and calcification of the pericardium.
Isolated constrictive pericarditis is characterized by
an abnormality in compliance. Ventricular compliDiastolic Heart Failure
Table 1. Differentiation between restrictive cardiomyopathy and constrictive pericarditis.
Evaluation Type
Restrictive Cardiomyopathy
Constrictive Pericarditis
Physical Examination
Kussmaul’s sign may be present
Apical impulse may be prominent
S3 (advanced disease), S4 (early disease)
Regurgitant murmurs common
Parodoxical pulse absent
Low voltage (especially in amyloidosis),
pseudoinfarction, left-axis deviation, atrial
fibrillation, conduction disturbances
common
Absent calcification
Small LV cavity with large atria
1 wall thickness sometimes present
(especially thickened interatrial septum in
amyloidosis)
Thickened cardiac valves (amyloidosis)
Granular sparking texture (amyloidosis)
Kussmaul’s sign usually present
Apical impulse usually not palpable
Pericardial knock may be present
Regurgitant murmurs uncommon
Parodoxical pulse rare
Low voltage (⬍50 percent)
Electrocardiography
Chest x-ray
Echocardiography
Mitral inflow
Pulmonary vein
No resp variation of mitral inflow
E wave, IVRT,
E/A ratio ⬎2
Short DT
Diastolic regurgitation
Blunted S/D ratio (0.5), prominent &
prolonged AR
No resp variation D wave
Tricuspid inflow
Mild resp variation of tricuspid inflow E wave
Hepatic vein
E/A ratio ⬎2
TR peak velocity no significant resp change
Short DT with inspiration
Diastolic regurgitation
Blunted S/D ratio, inspiratory 1 reversals
Inferior vena cava
Color M-mode
Mitral annular motion
Cardiac catheterization
Plethoric
Slow flow propagation
Low velocity early filling (⬍8 cm/s)
“Dip and plateau”
LVEDP often ⬎5 mmHg greater than RVEDP,
but may be identical
RV systolic pressure ⬎ 50 mmHg
Endomyocardial
biopsy
RVEDP ⬍ one-third of RV systolic pressure
May reveal specific cause of restrictive
cardiomyopathy
CT/MRT
Pericardium usually normal
Calcification sometimes
Normal wall thickness
Pericardial thickening seen
Prominent early diastolic filling with
abrupt displacement of interventricular
septum
Inspiration ⫽ 2 mitral inflow
E wave, prolonged IVRT
Expiration ⫽ opposite changes
Short DT
Diastolic regurgitation
S/D ratio ⫽ 1
Inspiration ⫽ 2 PV, S and D waves,
Expiration ⫽ opposite changes
Inspiration ⫽ 1 tricuspid inflow E wave,
1 TR peak velocity
Expiration ⫽ opposite changes
Short DT
Diastolic regurgitation
Inspiration ⫽ Minimally 1 HV, S and D
Expiration ⫽ 2 diastolic flow & 1
reversals
Plethoric
Rapid flow propagation (ⱖ100 cm/s)
High velocity early filling (ⱖ8 cm/s)
‘‘Dip and plateau’’
RVEDP and LVEDP usually equal
Inspiration ⫽ 1 in RV systolic pressure 2
in LV systolic pressure
Expiration ⫽ opposite changes
May be normal or show nonspecific
myocyte hypertrophy or myocardial
fibrosis
Pericardium may be thickened
Modified from Kushwaha SS, Fallon JT, Fuster V. N Engl J Med 1997; 336: 267–76, with permission in reference 43.
ance is impaired because of external interference to
diastolic filling from a rigid pericardium. The myocardium is unaffected in isolated constrictive pericarditis; therefore, systolic function and early diastolic filling are normal. Once ventricular diastolic
filling reaches the limitations of the pericardial restraint, the pressure and volume in the cavity rise,
Volume 10, Number 4, 2002
filling ceases, and congestion occurs (33). Because
of the isolated encasement of the pericardium and
not the systemic veins or lungs, there is a dissociation between intrathoracic and intracardiac pressures with marked interventricular dependence, respiratory variation, and discordance in right and left
heart filling (34).
CARDIOLOGY IN REVIEW
223
Figure 3. Example of the utility of transesophageal echocardiography and magnetic resonance imaging for demonstrating
the location and extent of pericardial thickening and calcification with constrictive pericarditis. Reprinted with
permission from Klein AL, et al: Am Heart J 1999;138:880 – 889.
Hemodynamic Signs
Cardiac catheterization is usually reserved for
unclear cases of constrictive pericarditis in
which the diagnosis is uncertain. The classic
feature of constrictive pericarditis is near equalization of chamber pressures between the left
atrium, right atrium, LV and RV in end-diastole
(33). Other hemodynamic findings include an
elevated right atrial pressure, a pulmonary artery pressure of less than 50 mmHg, and a RV
diastolic pressure exceeding one third of the RV
systolic pressure (25). Characteristic pressure
tracings include the atrial waveform showing
the W wave configuration with preserved x and
prominent y descent and the simultaneous ventricular pressure waveform showing the dip and
plateau configuration (33). Reciprocal changes
with respiration can be observed, with the RV
systolic pressure increasing with inspiration
and the LV pressure decreasing.
Echocardiographic Signs
An integrated and dedicated echocardiographic
examination including 2-dimensional imaging,
M-mode, and Doppler are capable of diagnosing
the anatomic and pathophysiologic features of
constrictive pericarditis in most patients with suspected disease.
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Two-dimensional Imaging and M-mode
The anatomic features of constrictive pericarditis
may be recognized by 2-dimensional imaging (35).
These include pericardial thickening, calcification,
and localized tethering of the atrial or ventricular
cavities (Fig. 3). A pericardial effusion may be
present. The inferior vena cava is usually dilated
(plethoric). The septal bounce is a classic feature of
abnormal diastolic septal motion caused by abrupt
termination of ventricular filling (35). LV and RV
function are usually preserved in isolated cases.
M-mode signs such as flattening of the LV free wall
after early diastole are less well appreciated (36).
Doppler Echocardiography
Elucidation of the pathophysiologic features of
constrictive pericarditis requires a comprehensive
dedicated Doppler examination. The hallmark of
the examination is reciprocal respiratory variation
of right and left heart flows caused by interventricular dependence (37). Because the heart is
encased in a rigid shell, when the right heart fills
during inspiration, the left heart filling is restricted by the shift of the septum to the left. The
opposite changes occur with expiration.
The classic Doppler pattern of constrictive pericarditis is as follows (37–39) (Fig. 4):
(1) Mitral inflow
Diastolic Heart Failure
Figure 4. Diagram of left (A) and right (B) ventricular inflow velocities and pulmonary (C) and hepatic (D) venous flows
during different phases of respiration differentiating constrictive pericarditis and restrictive cardiomyopathy as assessed
by echocardiography. Reprinted with permission from Klein AL, Cohen GI: Doppler echocardiographic assessment of
constrictive pericarditis, cardiac amyloidosis, and cardiac tamponade. Cleve Clin J Med 1992;59:278 –290.
Inspiration: smaller E wave greater than A
wave, longer IVRT and, usually shorter DT
Expiration: larger E wave greater than A wave,
shorter IVRT and usually longer DT; E wave
is typically increased more than 25% with
expiration, and the IVRT increased more
than 50% with inspiration
(2) Pulmonary veins
Inspiration: S and D waves near equal in size
Expiration: larger S and D waves
(3) Tricuspid inflow: same pattern, with reciprocal changes compared with mitral inflow; tricuspid E wave increase is typically more than
40% with inspiration
(4) Hepatic vein
Inspiration: S greater than D wave, with small
AR and ventricular reversals
Expiration: S greater than D wave, with smaller
or absent D wave and larger AR and ventricular reversals
Also described in constrictive pericarditis is an
inspiratory increase in the tricuspid regurgitant
jet velocity and duration of the signal (40). Superior vena cava flow has been useful to distinguish
respiratory changes caused by chronic obstructive
lung disease from constrictive pericarditis, with
the latter having less significant changes in systolic forward flow during inspiration (41).
Volume 10, Number 4, 2002
The Doppler findings of constrictive pericarditis
with the hallmark of reciprocal respiratory variation
contrast with the typical findings of restrictive cardiomyopathy. Doppler tissue imaging and color
M-mode techniques provide more information for
distinguishing these disorders. In addition, transesophageal echocardiography may be required for a
more optimal Doppler examination and assessment
of anatomic features of constriction.
Differential Diagnosis
There are limitations to the Doppler echocardiography differentiation of constrictive pericarditis
and restrictive cardiomyopathy, and special clinical situations should be appreciated.
Particular attention must be paid to the loading
conditions and respiratory effort when performing a study. A respirometer is used to assess the
timing of inspiration and expiration. The first beat
after inspiration is measured because it is least
likely to be affected by factors affecting the respiratory effort such as chronic obstructive lung disease (34). The optimal examination is performed
during a period of euvolemia, possibly requiring
saline loading for hypovolemic patients and maneuvers or diuresis for hypervolemic patients
(42).
CARDIOLOGY IN REVIEW
225
The many special situations make interpretation
particularly challenging (43). Patients with irregular
heart rhythms like atrial fibrillation may require
ventricular pacing to equalize the R-R intervals.
Conditions such as mixed restriction and constriction and effusive and constrictive states have features of both diseases. Other diseases that exaggerate
the rate or force of breathing such as pulmonary
embolism, obesity, and chronic obstructive lung disease may cause reciprocal changes in right and left
heart flows that must be differentiated from constrictive pericarditis.
CARDIAC TAMPONADE
Cardiac tamponade is a medical emergency
caused by the inability of the heart to fill adequately to maintain cardiac output. Although the
causes of pericardial effusions are numerous, in
daily practice, most cases occur after cardiac surgery or with malignancy and any cause of acute or
chronic pericarditis. Clinicians must be able to
recognize and treat cardiac tamponade rapidly.
Echocardiography is an essential modality to
guide the choice of management. Patients may
seek treatment with symptoms of low cardiac output or unheralded hemodynamic collapse. The
medical or surgical history of the patient should
provide ample clues to the potential for this event,
because many events occur in patients after procedures or with known effusions.
The bedside diagnosis of cardiac tamponade
should be considered in a patient with elevated
jugular veins, quiet heart sounds, tachycardia,
and hypotension. The hallmark of the jugular venous waveform is the loss of the y descent with a
maintained x descent (33). A pulsus paradoxus
may be present but is not specific for cardiac
tamponade and may be absent in many disorders
in which the LV or RV diastolic pressure is high or
there is decompression of respiratory changes in
pressures, as with an atrial septal defect (44).
Other supportive noninvasive tests include an
electrocardiogram with low voltage and electrical
alternans, and a chest radiograph with cardiomegaly.
Pathophysiology
A small volume of fluid is present in a normal
pericardial sac. When fluid accumulates because
of injury inflammation or hemorrhage, the intrapericardial volume and pressure rise proportionally with the compliance of the pericardial lining
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and the intracardiac pressures. When intrapericardial pressure exceeds intracardiac pressure,
there is interference of diastolic filling and subsequent decreased cardiac output (44). With inspiration, intrathoracic pressure and pulmonary capillary wedge pressure decrease, whereas
intracardiac pressure is unchanged because of the
pericardial effusion. A decrease in gradient between the pulmonary veins and LV results in a
decreased mitral inflow E wave with inspiration
and an increase in tricuspid E-wave flow (45).
Reciprocal changes occur during expiration. Because the cardiac chambers are in a finite space
within the pericardium, there is equalization of
pressures in all cardiac chambers.
Hemodynamic Signs
Right heart catheterization is an important tool
to diagnose cardiac tamponade, particularly in
patients in the intensive care unit setting, where
physical diagnosis and echocardiography may
have limitations. The typical hemodynamic signs
include elevation of the central venous pressure
with a prominent x descent and loss of the y
descent and near equalization of right atrial, RV
end-diastolic, pulmonary capillary wedge, and LV
diastolic pressures (33). Tachycardia, a decreased
stroke volume, cardiac output, and hypotension
with a pulsus paradoxus may be present.
Echocardiographic Signs
In most patients with adequate image quality,
echocardiography can rapidly and accurately
make the diagnosis of cardiac tamponade. Causes
of hemodynamic compromise other than cardiac
tamponade may be excluded. The decision can
also be made to evacuate the fluid via pericardiocentesis or surgery.
An integrated echocardiographic study incorporating 2-dimensional imaging and Doppler
must be performed to assess the presence of a
pericardial effusion and the pathophysiologic
consequences. In the intensive care unit setting, a
transesophageal echocardiogram may be required
if transthoracic imaging is suboptimal.
Two-dimensional Imaging and M-mode
A pericardial effusion is present in almost all
cases of cardiac tamponade. Most pericardial effusions appear as an echocardiography-free space
that is localized or circumferential, free-flowing
or organized. Scanning in and out of the plane
may be required to separate the visceral and parietal pericardium in order to distinguish a pericarDiastolic Heart Failure
dial effusion from a pleural effusion. Another clue
is the presence of fluid anterior to the descending
aorta in the parasternal view. Even small effusions
can cause tamponade, depending on their location and rate of accumulation.
Cardiac chamber collapse is a critical feature of
cardiac tamponade. The chambers with the lowest
intracardiac pressure are most likely to be compressed. Right atrial collapse is the earliest sign of
tamponade, occurring toward the end of ventricular end-diastole and extending into ventricular
systole. Because the right atrium may often invert
even in normal hearts with low right atrial pressure, the specificity of right atrial collapse may be
low (46). Extension of collapse greater than 1/3 of
the cardiac cycle increases the sensitivity of this
finding to more than 90% (46). Although RV diastolic collapse is generally a more specific indicator of tamponade, the sensitivity can be reduced
because of conditions that increase RV pressure
(47). Left atrial and LV collapse are unusual and
are observed generally with massive effusions or,
in the case of left atrial collapse, loculated effusions.
A plethoric inferior vena cava (dilated with
failure to collapse by more than 50%) is a highly
sensitive sign of cardiac tamponade. This finding
confirms high right atrial pressure, invariable
with few exceptions in cardiac tamponade (48).
Doppler Echocardiography
The Doppler examination confirms the pathophysiologic hemodynamic aberrations that occur
during cardiac tamponade.
The classic Doppler pattern of cardiac tamponade is as follows: (37,45)
(1) Mitral inflow: for inspiration, E wave decreases and IVRT increases by more than 30%
compared with expiration
(2) Tricuspid inflow: for inspiration, E wave increases more than 70% compared with expiration
(3) Pulmonary vein: for inspiration, D wave decreases compared with expiration
(4) Hepatic vein: for inspiration, S is greater than
D; for expiration, an absent or very diminished D wave with prominent reversals
Differential Diagnosis
Aside from the differentiation of pericardial
from pleural effusions, other echocardiographyfree spaces around the pericardium must be recognized. These include pericardial fat pads (more
often anterior and echocardiography-dense), vasVolume 10, Number 4, 2002
cular structures (descending aorta, pseudoaneurysm, coronary sinus), other pericardial structures
(cysts found in right cardiophrenic angle, hematoma, or tumor), and noncardiac structures (hiatal
hernia) (49).
In many situations, an incorrect diagnosis of
cardiac tamponade is made based on the presence
of confounding factors that affect respiratory variation or chamber collapse (50). Clinical history
and other echocardiographic findings are important in differentiating these conditions.
Conclusion
The clinical presentation of restrictive cardiomyopathy, constrictive pericarditis, and cardiac
tamponade may vary vastly from chronic nonspecific symptoms to acute hemodynamic deterioration. As diseases of diastolic dysfunction, there
are common hemodynamic and echocardiographic features of these diseases. A comprehensive echocardiographic evaluation includes twodimensional imaging and pulsed Doppler with a
respirometer. Color M-mode and Doppler tissue
imaging should be performed. Volume loading
maneuvers or transesophageal echocardiography
may also be required. Together, these techniques
help to distinguish anatomic and pathophysiologic findings specific to each process and provide the basis for clinical decisions regarding
management.
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