diastolic heart failure: restrictive cardiomyopathy ... · although uncommon, restrictive...

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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 non- specific symptoms or may present with acute hemodynamic compromise. Echocardiogra- phy 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, Restric- tive 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 left- sided congestion, the syndrome of diastolic heart failure (1). Although diastolic dysfunction contrib- utes to heart failure in patients with abnormal sys- tolic 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 di- verse, ranging from nonspecific, insidious symp- toms such as exertional dyspnea to pulmonary edema or sudden hemodynamic collapse. The prevalence of diastolic heart failure is vari- ably reported depending on the age, diagnostic cri- teria, and referral patterns of the populations stud- ied (2). Hypertension, coronary artery disease, valvular heart disease, and hypertrophic cardiomy- opathy are the predominant myocardial disorders that result in diastolic dysfunction with relatively preserved systolic function (3). Restrictive cardio- myopathies are less common causes of diastolic dysfunction because of myocardial storage or infil- tration. All of these myocardial conditions cause diastolic dysfunction largely by their effect on ven- tricular relaxation and compliance (4). Constrictive pericarditis and cardiac tamponade are pericardial disorders that impede ventricular filling by extrinsic constraint or limitation of chamber loading. Pericar- dial disorders may result in a spectrum of acute and chronic hemodynamic disturbance. Distinguishing disorders that cause diastolic dys- function is important so that management can be tailored to the specific disease. This review dis- cusses the general principles of normal diastolic function and contrasts the abnormalities of diastolic dysfunction present with restrictive cardiomyopa- thy, constrictive pericarditis, and cardiac tampon- ade. The integral role of echocardiography in differ- entiating these diseases is highlighted. Department of Cardiovascular Medicine, Section of Cardiovascular Imaging, Cleveland Clinic Foundation, Cleveland, Ohio Address reprint requests to: Allan L. Klein, MD, Cleveland Clinic Founda- tion, Department of Cardiovascular Medicine, 9500 Euclid Avenue, Desk F15, Cleveland, OH 44195-0001. Cardiology in Review Volume 10, Number 4, pp. 218 –229 Copyright © 2002 Lippincott Williams & Wilkins 218 CARDIOLOGY IN REVIEW

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Diastolic Heart Failure: RestrictiveCardiomyopathy, Constrictive Pericarditis,and Cardiac Tamponade: Clinical andEchocardiographic EvaluationCRAIG R. ASHER, MD, and ALLAN L. KLEIN, MD

An understanding of the basic principles of diastolic function is important in order torecognize diseases that may result in diastolic dysfunction and diastolic heart failure.Although uncommon, restrictive cardiomyopathy, constrictive pericarditis, and cardiactamponade are among the disorders that may affect primarily diastolic function withpreservation of systolic function. Diastolic heart failure may manifest with chronic non-specific symptoms or may present with acute hemodynamic compromise. Echocardiogra-phy plays a vital role in the diagnosis of diastolic dysfunction and differentiation of thesedisease processes. It also provides a basis for clinical decisions regarding managementand surgical referral. This review summarizes the clinical features, pathophysiology, andhemodynamic and echocardiographic signs of restrictive cardiomyopathy, constrictivepericarditis, and cardiac tamponade.

Key Words: Cardiac tamponade, Constrictive pericarditis, Diastolic dysfunction, Restric-tive cardiomyopathy

Diastolic dysfunction is defined as the requirementfor elevated filling pressures to maintain cardiacoutput. Augmented filling pressures may result inexcessive cardiac volume and right-sided or left-sided congestion, the syndrome of diastolic heartfailure (1). Although diastolic dysfunction contrib-utes to heart failure in patients with abnormal sys-tolic function, it may occur in patients with normalfunction (2). Numerous disease processes affectingthe myocardium and pericardium are associatedwith diastolic dysfunction and heart failure. Theclinical manifestations of these conditions are di-verse, ranging from nonspecific, insidious symp-toms such as exertional dyspnea to pulmonaryedema or sudden hemodynamic collapse.

The prevalence of diastolic heart failure is vari-ably reported depending on the age, diagnostic cri-teria, and referral patterns of the populations stud-

ied (2). Hypertension, coronary artery disease,valvular heart disease, and hypertrophic cardiomy-opathy are the predominant myocardial disordersthat result in diastolic dysfunction with relativelypreserved systolic function (3). Restrictive cardio-myopathies are less common causes of diastolicdysfunction because of myocardial storage or infil-tration. All of these myocardial conditions causediastolic dysfunction largely by their effect on ven-tricular relaxation and compliance (4). Constrictivepericarditis and cardiac tamponade are pericardialdisorders that impede ventricular filling by extrinsicconstraint or limitation of chamber loading. Pericar-dial disorders may result in a spectrum of acute andchronic hemodynamic disturbance.

Distinguishing disorders that cause diastolic dys-function is important so that management can betailored to the specific disease. This review dis-cusses the general principles of normal diastolicfunction and contrasts the abnormalities of diastolicdysfunction present with restrictive cardiomyopa-thy, constrictive pericarditis, and cardiac tampon-ade. The integral role of echocardiography in differ-entiating these diseases is highlighted.

Department of Cardiovascular Medicine, Section of CardiovascularImaging, Cleveland Clinic Foundation, Cleveland, Ohio

Address reprint requests to: Allan L. Klein, MD, Cleveland Clinic Founda-tion, Department of Cardiovascular Medicine, 9500 Euclid Avenue, DeskF15, Cleveland, OH 44195-0001.

Cardiology in ReviewVolume 10, Number 4, pp. 218–229Copyright © 2002 Lippincott Williams & Wilkins

218 CARDIOLOGY IN REVIEW

DIASTOLIC FUNCTION: PHYSIOLOGY

Diastolic filling of the left ventricle (LV) encom-passes the period of the cardiac cycle between aorticvalve closure and mitral valve closure. Four distinctphases are distinguished: (1) isovolumic relaxation(between aortic valve closure and mitral valve open-ing), (2) rapid filling, (3) diastasis (slow filling), and(4) atrial contraction (5). There are multiple physi-ologic determinants of diastolic function. The majormyocardial factors that affect diastolic function in-clude LV myocardial relaxation, compliance, andleft atrial function (5). Other parameters includeheart rate, preload, afterload, atrioventricular con-duction, right ventricular (RV) function, intrathoracicpressure, viscoelastic properties, coronary engorge-ment, neurohormonal activation, and pericardialconstraint (6). RV diastolic function is concordantwith LV diastolic function in healthy people, al-though discordant filling and differing external in-teractions may occur in some disease states.

After LV contraction, diastole begins with theenergy-dependent cellular process of ventricularrelaxation, which extends into diastasis. LV relax-ation is best characterized by the time constant ofrelaxation (�), which describes the rate of LV pres-sure decay in an exponential equation. Until re-cently, only invasive methods were available toestimate (�)(7). Other, more dependent surrogateechocardiographic markers of relaxation includethe isovolumic relaxation time (IVRT) and infor-mation obtained by color M-mode and Dopplertissue imaging. The IVRT characterizes the timewhen LV pressure declines and LV volume re-mains constant. When LV pressure drops belowleft atrial pressure, the mitral valve opens and theearly rapid filling period begins.

During the early filling period (mitral E wave),there is a rapid increase in the LV chamber vol-ume, which contributes largely to the ventricularstroke volume (8). The amount of volume enteringthe LV cavity is influenced by many factors, in-cluding the pressure gradient between the pulmo-nary veins and LV, continued myocardial relax-ation, elastic recoil (ventricular suction), andstiffness properties of the myocardium (5). LVstiffness (or its reciprocal, compliance) character-izes the change in pressure within the chamberwith an increase in volume and is dependent onthe many inherent properties of myocardial con-tent, chamber dimension, and external constraintsof the pericardium and thorax (5).

The left atrial and LV pressures are equalizedduring diastasis, resulting in slow or minimal fill-

ing. Diastasis is followed by atrial contraction (mi-tral A wave), which contributes variably to LV end-diastolic volume. Aside from the left atrium’spassive role as a conduit receptacle, it functions as apump to regulate filling volume. When left atrialpressure is high at the end of diastole because ofsystolic heart disease, Frank-Starling mechanismsare activated (increased stretch, increased force ofcontraction), and atrial systole may contribute sig-nificantly to diastolic filling volume (9).

DIASTOLIC FUNCTION: ECHOCARDIOGRAPHY

The assessment of diastolic function has be-come an integral part of any echocardiographicstudy. Many causes of diastolic heart failure canbe identified, including restrictive, hypertrophic,and ischemic cardiomyopathies and pericardial,valvular, and congenital heart disease. Diastolicfilling patterns can be evaluated and stages ofdiastolic dysfunction determined that correlatewith left-sided and right-sided filling pressuresand disease-related prognosis (10–13). Othertechniques such as radionuclide angiography,magnetic resonance imaging, and cardiac cathe-terization are more time consuming, invasive, andtedious, and are generally used only as adjuncts toechocardiography.

Traditionally, the diastolic function exam fo-cuses on pulsed Doppler recordings of left-sidedmitral inflow E and A waves and pulmonary veinsystolic (S), diastolic (D), and atrial reversal (AR)waves and the corresponding right-sided tricus-pid inflow and hepatic vein flow waves (14).Measurements of deceleration and IVRT timesand responses to physiologic maneuvers such asValsalva provide more information. Using theseparameters, 4 stages of diastolic dysfunction canbe determined: (1) impaired relaxation, (2)pseudonormal stage, (3) restrictive, reversiblestage, and (4) restrictive, irreversible function (15)(Fig. 1).

Newer technologies have provided supplemen-tal data to differentiate normal from pseudonor-mal patterns and to estimate left atrial and LVfilling pressures more accurately (16) A color M-mode display shows a more precise spatial andtemporal distribution of flow velocities propagat-ing across the mitral valve into the LV. The flowpropagation velocity (vp) provides a relativelypreload-independent determination of relaxationin various disease states and can be used in aregression equation with the mitral inflow E wave

CARDIOLOGY IN REVIEW 219Volume 10, Number 4, 2002

to estimate pulmonary capillary wedge pressure(17). Doppler tissue imaging obtains the low ve-locity and high amplitude signals of the myocar-dium rather than the high velocity and low am-plitude blood signals (16). With this technique,spectral Doppler or color Doppler encoded veloc-ities can be recorded. Spectral Doppler myocar-dial velocities of the mitral annulus provide sys-tolic and diastolic velocities (Em, early filling; Eaor Am, atrial contraction) similar to the mitralinflow profiles. Studies have demonstrated thatEm is relatively preload-independent in manydisease states. As with vp, Em can be used todifferentiate disease states such as restrictive car-diomyopathy and constrictive pericarditis and toassess LV filling pressures more accurately (18).Additionally, recent reports have emphasized theimportance of assessing regional myocardial func-tion by Doppler echocardiographic strain rate im-aging (19).

RESTRICTIVE CARDIOMYOPATHY

As defined by the revised World Health Orga-nization Task Force, restrictive cardiomyopathy isa disease characterized by “restrictive filling andreduced diastolic volume of either or both ventri-cles with normal or near-normal systolic func-

tion.” (20) Despite this rigid definition requiringthat restrictive hemodynamics are present, severalstudies have demonstrated early forms of thesedisorders with earlier stages of diastolic impair-ment. These diseases may be idiopathic or asso-ciated with specific systemic conditions and maybe further characterized as myocardial (noninfil-trative, infiltrative, and storage) or endomyocar-dial types (21). The prognosis of restrictive car-diomyopathies is generally poor, except for thosewith reversible causes such as hemochromatosis.Cardiac amyloidosis is the most prevalent restric-tive cardiomyopathy, and the current literatureaddresses predominantly this specific disease(Fig. 2).

Because of the resistance to biventricular fill-ing, patients commonly develop a clinical profilerelated to congestive failure with fatigue, exerciseintolerance, right-sided or left-sided heart failure,and atrial fibrillation (22,23). The clinical exami-nation correlates with these symptoms. An ele-vated jugular venous pressure with an x andprominent y descent (early-stage, M wave), y de-scent only (late-stage), and Kussmaul’s sign maybe present, although pulsus paradoxus is alwaysabsent. Depending on the stage of disease, an S4(early) or S3 (late) may be present (21). The elec-trocardiogram of amyloidosis typically shows a

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 diastolicdysfunction can be determined. A, mitral A-wave velocity; Am, tissue Doppler atrial contraction wave; CMM-vp, colorM-mode flow propagation velocity; D, pulmonary venous diastolic wave; E, mitral E-wave velocity; Em, tissue Dopplerearly filling wave; PV, pulmonary vein; S, pulmonary venous systolic wave; Sm, tissue Doppler systolic wave; TDE, tissueDoppler 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 Cardiol1998;32:865–875.

220 CARDIOLOGY IN REVIEW Diastolic Heart Failure

large discordance between echocardiographicwall thickness and voltage (low voltage and in-creased wall thickness) (24).

PathophysiologyAs a result of myocardial or endocardial in-

volvement such as amyloid infiltration, the ven-tricle is noncompliant or stiff and resists ventric-ular filling. Therefore, as the volume of the heartis increased, there is a steep rise in the pressure.Diastolic right-sided or left-sided heart failuremay ensue (22).

Hemodynamic SignsIn the cardiac catheterization laboratory, inva-

sive determination of operating stiffness may bedemonstrated by pressure-volume curves, LV andRV hemodynamic tracings showing a dip andplateau or square root pattern (21). Other, lessspecific findings include a RV systolic pressure ofgreater than 50 mmHg with a RV end-diastolicpressure usually less than one third of the RVsystolic pressure. Typically, the LV end-diastolicpressure is greater that the RV end-diastolic pres-sure (25).

Echocardiographic signsEchocardiography is uniquely suited as a diag-

nostic modality to detect the anatomic and func-tional abnormalities associated with restrictivecardiomyopathies. A combination of 2-dimen-sional imaging, M-mode, and Doppler informa-tion is important to identifying specific features ofrestrictive cardiomyopathy. Amyloidosis is pri-marily discussed here because it is the prototypeof this class of diseases, and although endomyo-cardial disorders have very distinct features, theyare less commonly encountered in this country.

Two-dimensional Imaging and M-modeIncreased wall thickness of the LV and often the

RV is a hallmark of amyloidosis and almost all themyocardial disorders (26). Both ventricular cavi-ties are typically small with a decreased volumeand large atria. The atrial septum and cardiacvalves may also be thickened. A characteristic“granular sparkling” myocardial texture was de-scribed before harmonic and high frequency im-aging, but this may be a less sensitive and specificfinding with current imaging modalities. A peri-cardial effusion may be present. The inferior venacava is usually dilated and does not collapse withinspiration (plethoric), reflecting increased rightatrial pressure.

Doppler EchocardiographyDiastolic dysfunction is a requirement for a

restrictive cardiomyopathy, although not all pa-tients will have a restrictive diastolic filling pat-tern. In earlier stages of disease an impaired relax-ation pattern may be present before the onset ofabnormal compliance. Determination of the sever-ity of diastolic impairment is important not onlyfor diagnostic reasons; it has been demonstratedthat the prognosis of patients with restrictive fill-ing patterns have a nearly fivefold higher mortal-ity than the nonrestrictive patterns (27).

The classic Doppler pattern of advanced cardiacamyloidosis is as follows: (28)

(1) Mitral inflow: large E wave and small A wave;E/A ratio greater than 2; short decelerationtime (DT) less than 150 ms; short IVRT lessthan 60 ms; no significant change in mitral Ewave, deceleration time, or IVRT with phasesof respiration

(2) Pulmonary veins: small S wave; large D wave;

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 ClinicalEchocardiography. Philadelphia, WB Saunders, 1997; 473–493.

CARDIOLOGY IN REVIEW 221Volume 10, Number 4, 2002

S/D ratio less than 0.5; prominent AR (exceptwith atrial systolic failure) width greater thanmitral A wave and high amplitude; no signifi-cant respiratory variation of D wave

(3) Tricuspid inflow: similar to mitral inflowwith an increased E/A ratio and short DT;with inspiration, there is further shortening ofthe DT and minimal change in E/A ratio

(4) Hepatic veins: similar to pulmonary vein flowwith S/D ratio less than 0.5 and prominentatrial and ventricular reversals; with inspira-tion and expiration, there is increased promi-nence of the reversal waves

Superior vena cava flows are similar to hepaticvein flows, and right and left heart patterns areconcordant in most patients. Other findings in-clude the lack of respiratory variation of the tri-cuspid regurgitant jet with respiration and thepresence of at least mild mitral and tricuspidregurgitation.

Doppler tissue imaging and color M-mode flowpropagation have provided invaluable informa-tion for the differentiation of restrictive cardiomy-opathy and constrictive pericarditis. Patients withrestrictive cardiomyopathy have an abnormalityof both relaxation and compliance, whereas thosewith constrictive pericarditis generally have nor-mal relaxation and impaired compliance becauseof pericardial impedance to filling. For this rea-son, patients with constrictive pericarditis gener-ally have a normal or fast color M-mode vp and anormal or increased Em, differing from patientswith restrictive cardiomyopathy (16,18,29). A re-cent case report demonstrated that an exception tothe rule of higher Em velocities with constrictivepericarditis may occur when pericardial calcifica-tion and tethering involve the annulus (30). Inthese cases, Doppler imaging of the apex andstrain rate imaging may help confirm constriction.

Differential DiagnosisDifferentiation of restrictive cardiomyopathy

and constrictive pericarditis is essential becauseof the potential to relieve constrictive pericarditiseffectively with surgical pericardial stripping (Ta-ble 1). It should be appreciated that certain con-ditions such as radiation of the heart may cause amixed disease of constrictive pericarditis and re-strictive physiology.

Restrictive cardiomyopathy must also be distin-guished from other pathologic conditions thatcause an increase in wall thickness because ofhypertrophy. These diseases are caused by eitherprimary hypertrophy (hypertrophic cardiomyop-

athy) or secondary hypertrophy (ie, aortic valvedisease, hypertension).

CONSTRICTIVE PERICARDITIS

The majority of contemporary cases of nonidio-pathic constrictive pericarditis are caused by pre-vious cardiac surgery, radiation exposure, andchronic pericarditis with a myriad of etiologies(31). With the increasing rates of patients under-going cardiac surgery, the prevalence of constric-tive pericarditis may be increasing. Constrictivepericarditis can be surgically cured with pericar-dial stripping, with acceptable surgical mortalityrates and symptomatic benefits in most patients(31). Therefore, clinicians must consider the diag-nosis among patients seeking treatment withsymptoms that may be consistent with the condi-tion.

The clinical presentation of patients with con-strictive pericarditis may be nonspecific and in-dolent in the early stages. Symptoms may includefatigue or decreased exercise tolerance. In moreadvanced stages, patients may develop both leftand right heart failure, with the latter often pre-dominating. Physical findings in advanced dis-ease reflect the signs of cardiac congestion (32).The hallmarks of physical diagnosis include anelevated jugular venous pressure with a promi-nent y descent (Friedreich’s sign) reflecting thepredominance of filling in early diastole. Kuss-maul’s sign, an inspiratory increase in the jugularvenous pressure, may be present but is not spe-cific for constrictive pericarditis (32). Findingsspecific to constrictive pericarditis include a peri-cardial knock (occurs after an opening snap andbefore an S3 in timing) because of cessation indiastolic filling and retraction of the apical im-pulse in systole. In very advanced cases, patientsdevelop severe right heart failure.

In advanced cases, noninvasive diagnostic test-ing may be supportive of the diagnosis. The elec-trocardiogram may be low in voltage because ofthe pericardial encasement. The chest radiographmay show calcification of the pericardium andpleural effusions.

PathophysiologyMost conditions that lead to constrictive pericar-

ditis result in inflammation, fibrosis, adhesion,thickening, and calcification of the pericardium.Isolated constrictive pericarditis is characterized byan abnormality in compliance. Ventricular compli-

222 CARDIOLOGY IN REVIEW Diastolic Heart Failure

ance is impaired because of external interference todiastolic filling from a rigid pericardium. The myo-cardium is unaffected in isolated constrictive peri-carditis; therefore, systolic function and early dia-stolic filling are normal. Once ventricular diastolicfilling reaches the limitations of the pericardial re-straint, the pressure and volume in the cavity rise,

filling ceases, and congestion occurs (33). Becauseof the isolated encasement of the pericardium andnot the systemic veins or lungs, there is a dissocia-tion between intrathoracic and intracardiac pres-sures with marked interventricular dependence, re-spiratory variation, and discordance in right and leftheart filling (34).

Table 1. Differentiation between restrictive cardiomyopathy and constrictive pericarditis.

Evaluation Type Restrictive Cardiomyopathy Constrictive Pericarditis

Physical Examination Kussmaul’s sign may be present Kussmaul’s sign usually presentApical impulse may be prominent Apical impulse usually not palpableS3 (advanced disease), S4 (early disease) Pericardial knock may be presentRegurgitant murmurs common Regurgitant murmurs uncommonParodoxical pulse absent Parodoxical pulse rare

Electrocardiography Low voltage (especially in amyloidosis),pseudoinfarction, left-axis deviation, atrialfibrillation, conduction disturbancescommon

Low voltage (�50 percent)

Chest x-ray Absent calcification Calcification sometimesEchocardiography Small LV cavity with large atria

1 wall thickness sometimes present(especially thickened interatrial septum inamyloidosis)

Normal wall thickness

Thickened cardiac valves (amyloidosis) Pericardial thickening seenGranular sparking texture (amyloidosis) Prominent early diastolic filling with

abrupt displacement of interventricularseptum

Mitral inflow No resp variation of mitral inflow Inspiration � 2 mitral inflowE wave, IVRT, E wave, prolonged IVRTE/A ratio �2 Expiration � opposite changesShort DT Short DTDiastolic regurgitation Diastolic regurgitation

Pulmonary vein Blunted S/D ratio (0.5), prominent &prolonged AR

S/D ratio � 1

No resp variation D wave Inspiration � 2 PV, S and D waves,Expiration � opposite changes

Tricuspid inflow Mild resp variation of tricuspid inflow E wave Inspiration � 1 tricuspid inflow E wave,1 TR peak velocity

E/A ratio �2 Expiration � opposite changesTR peak velocity no significant resp change Short DTShort DT with inspiration Diastolic regurgitationDiastolic regurgitation

Hepatic vein Blunted S/D ratio, inspiratory 1 reversals Inspiration � Minimally 1 HV, S and DExpiration � 2 diastolic flow & 1

reversalsInferior vena cava Plethoric PlethoricColor M-mode Slow flow propagation Rapid flow propagation (�100 cm/s)Mitral annular motion Low velocity early filling (�8 cm/s) High velocity early filling (�8 cm/s)Cardiac catheterization “Dip and plateau” ‘‘Dip and plateau’’

LVEDP often �5 mmHg greater than RVEDP,but may be identical

RVEDP and LVEDP usually equal

RV systolic pressure � 50 mmHg Inspiration � 1 in RV systolic pressure 2in LV systolic pressure

RVEDP � one-third of RV systolic pressure Expiration � opposite changesEndomyocardial

biopsyMay reveal specific cause of restrictive

cardiomyopathyMay be normal or show nonspecific

myocyte hypertrophy or myocardialfibrosis

CT/MRT Pericardium usually normal 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.

CARDIOLOGY IN REVIEW 223Volume 10, Number 4, 2002

Hemodynamic SignsCardiac catheterization is usually reserved for

unclear cases of constrictive pericarditis inwhich the diagnosis is uncertain. The classicfeature of constrictive pericarditis is near equal-ization of chamber pressures between the leftatrium, right atrium, LV and RV in end-diastole(33). Other hemodynamic findings include anelevated right atrial pressure, a pulmonary ar-tery pressure of less than 50 mmHg, and a RVdiastolic pressure exceeding one third of the RVsystolic pressure (25). Characteristic pressuretracings include the atrial waveform showingthe W wave configuration with preserved x andprominent y descent and the simultaneous ven-tricular pressure waveform showing the dip andplateau configuration (33). Reciprocal changeswith respiration can be observed, with the RVsystolic pressure increasing with inspirationand the LV pressure decreasing.

Echocardiographic SignsAn integrated and dedicated echocardiographic

examination including 2-dimensional imaging,M-mode, and Doppler are capable of diagnosingthe anatomic and pathophysiologic features ofconstrictive pericarditis in most patients with sus-pected disease.

Two-dimensional Imaging and M-modeThe 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 ventricularcavities (Fig. 3). A pericardial effusion may bepresent. The inferior vena cava is usually dilated(plethoric). The septal bounce is a classic feature ofabnormal diastolic septal motion caused by abrupttermination of ventricular filling (35). LV and RVfunction are usually preserved in isolated cases.M-mode signs such as flattening of the LV free wallafter early diastole are less well appreciated (36).

Doppler EchocardiographyElucidation of the pathophysiologic features of

constrictive pericarditis requires a comprehensivededicated Doppler examination. The hallmark ofthe examination is reciprocal respiratory variationof right and left heart flows caused by interven-tricular dependence (37). Because the heart isencased in a rigid shell, when the right heart fillsduring inspiration, the left heart filling is re-stricted by the shift of the septum to the left. Theopposite changes occur with expiration.

The classic Doppler pattern of constrictive peri-carditis is as follows (37–39) (Fig. 4):

(1) Mitral inflow

Figure 3. Example of the utility of transesophageal echocardiography and magnetic resonance imaging for demonstratingthe location and extent of pericardial thickening and calcification with constrictive pericarditis. Reprinted withpermission from Klein AL, et al: Am Heart J 1999;138:880–889.

224 CARDIOLOGY IN REVIEW Diastolic Heart Failure

Inspiration: smaller E wave greater than Awave, longer IVRT and, usually shorter DT

Expiration: larger E wave greater than A wave,shorter IVRT and usually longer DT; E waveis typically increased more than 25% withexpiration, and the IVRT increased morethan 50% with inspiration

(2) Pulmonary veinsInspiration: S and D waves near equal in sizeExpiration: larger S and D waves

(3) Tricuspid inflow: same pattern, with recipro-cal changes compared with mitral inflow; tri-cuspid E wave increase is typically more than40% with inspiration

(4) Hepatic veinInspiration: S greater than D wave, with small

AR and ventricular reversalsExpiration: S greater than D wave, with smaller

or absent D wave and larger AR and ventric-ular reversals

Also described in constrictive pericarditis is aninspiratory increase in the tricuspid regurgitantjet velocity and duration of the signal (40). Supe-rior vena cava flow has been useful to distinguishrespiratory changes caused by chronic obstructivelung disease from constrictive pericarditis, withthe latter having less significant changes in sys-tolic forward flow during inspiration (41).

The Doppler findings of constrictive pericarditiswith the hallmark of reciprocal respiratory variationcontrast with the typical findings of restrictive car-diomyopathy. Doppler tissue imaging and colorM-mode techniques provide more information fordistinguishing these disorders. In addition, trans-esophageal echocardiography may be required for amore optimal Doppler examination and assessmentof anatomic features of constriction.

Differential DiagnosisThere are limitations to the Doppler echocardi-

ography differentiation of constrictive pericarditisand restrictive cardiomyopathy, and special clin-ical situations should be appreciated.

Particular attention must be paid to the loadingconditions and respiratory effort when perform-ing a study. A respirometer is used to assess thetiming of inspiration and expiration. The first beatafter inspiration is measured because it is leastlikely to be affected by factors affecting the respi-ratory effort such as chronic obstructive lung dis-ease (34). The optimal examination is performedduring a period of euvolemia, possibly requiringsaline loading for hypovolemic patients and ma-neuvers or diuresis for hypervolemic patients(42).

Figure 4. Diagram of left (A) and right (B) ventricular inflow velocities and pulmonary (C) and hepatic (D) venous flowsduring different phases of respiration differentiating constrictive pericarditis and restrictive cardiomyopathy as assessedby echocardiography. Reprinted with permission from Klein AL, Cohen GI: Doppler echocardiographic assessment ofconstrictive pericarditis, cardiac amyloidosis, and cardiac tamponade. Cleve Clin J Med 1992;59:278–290.

CARDIOLOGY IN REVIEW 225Volume 10, Number 4, 2002

The many special situations make interpretationparticularly challenging (43). Patients with irregularheart rhythms like atrial fibrillation may requireventricular pacing to equalize the R-R intervals.Conditions such as mixed restriction and constric-tion and effusive and constrictive states have fea-tures of both diseases. Other diseases that exaggeratethe rate or force of breathing such as pulmonaryembolism, obesity, and chronic obstructive lung dis-ease may cause reciprocal changes in right and leftheart flows that must be differentiated from con-strictive pericarditis.

CARDIAC TAMPONADE

Cardiac tamponade is a medical emergencycaused by the inability of the heart to fill ade-quately to maintain cardiac output. Although thecauses of pericardial effusions are numerous, indaily practice, most cases occur after cardiac sur-gery or with malignancy and any cause of acute orchronic pericarditis. Clinicians must be able torecognize and treat cardiac tamponade rapidly.Echocardiography is an essential modality toguide the choice of management. Patients mayseek treatment with symptoms of low cardiac out-put or unheralded hemodynamic collapse. Themedical or surgical history of the patient shouldprovide ample clues to the potential for this event,because many events occur in patients after pro-cedures or with known effusions.

The bedside diagnosis of cardiac tamponadeshould be considered in a patient with elevatedjugular veins, quiet heart sounds, tachycardia,and hypotension. The hallmark of the jugular ve-nous waveform is the loss of the y descent with amaintained x descent (33). A pulsus paradoxusmay be present but is not specific for cardiactamponade and may be absent in many disordersin which the LV or RV diastolic pressure is high orthere is decompression of respiratory changes inpressures, as with an atrial septal defect (44).Other supportive noninvasive tests include anelectrocardiogram with low voltage and electricalalternans, and a chest radiograph with cardiomeg-aly.

PathophysiologyA small volume of fluid is present in a normal

pericardial sac. When fluid accumulates becauseof injury inflammation or hemorrhage, the intra-pericardial volume and pressure rise proportion-ally with the compliance of the pericardial lining

and the intracardiac pressures. When intraperi-cardial pressure exceeds intracardiac pressure,there is interference of diastolic filling and subse-quent decreased cardiac output (44). With inspi-ration, intrathoracic pressure and pulmonary cap-illary wedge pressure decrease, whereasintracardiac pressure is unchanged because of thepericardial effusion. A decrease in gradient be-tween the pulmonary veins and LV results in adecreased mitral inflow E wave with inspirationand an increase in tricuspid E-wave flow (45).Reciprocal changes occur during expiration. Be-cause the cardiac chambers are in a finite spacewithin the pericardium, there is equalization ofpressures in all cardiac chambers.

Hemodynamic SignsRight heart catheterization is an important tool

to diagnose cardiac tamponade, particularly inpatients in the intensive care unit setting, wherephysical diagnosis and echocardiography mayhave limitations. The typical hemodynamic signsinclude elevation of the central venous pressurewith a prominent x descent and loss of the ydescent and near equalization of right atrial, RVend-diastolic, pulmonary capillary wedge, and LVdiastolic pressures (33). Tachycardia, a decreasedstroke volume, cardiac output, and hypotensionwith a pulsus paradoxus may be present.

Echocardiographic SignsIn most patients with adequate image quality,

echocardiography can rapidly and accuratelymake the diagnosis of cardiac tamponade. Causesof hemodynamic compromise other than cardiactamponade may be excluded. The decision canalso be made to evacuate the fluid via pericardio-centesis or surgery.

An integrated echocardiographic study incor-porating 2-dimensional imaging and Dopplermust be performed to assess the presence of apericardial effusion and the pathophysiologicconsequences. In the intensive care unit setting, atransesophageal echocardiogram may be requiredif transthoracic imaging is suboptimal.

Two-dimensional Imaging and M-modeA pericardial effusion is present in almost all

cases of cardiac tamponade. Most pericardial ef-fusions appear as an echocardiography-free spacethat is localized or circumferential, free-flowingor organized. Scanning in and out of the planemay be required to separate the visceral and pari-etal pericardium in order to distinguish a pericar-

226 CARDIOLOGY IN REVIEW Diastolic Heart Failure

dial effusion from a pleural effusion. Another clueis the presence of fluid anterior to the descendingaorta in the parasternal view. Even small effusionscan cause tamponade, depending on their loca-tion and rate of accumulation.

Cardiac chamber collapse is a critical feature ofcardiac tamponade. The chambers with the lowestintracardiac pressure are most likely to be com-pressed. Right atrial collapse is the earliest sign oftamponade, occurring toward the end of ventric-ular end-diastole and extending into ventricularsystole. Because the right atrium may often inverteven in normal hearts with low right atrial pres-sure, the specificity of right atrial collapse may below (46). Extension of collapse greater than 1/3 ofthe cardiac cycle increases the sensitivity of thisfinding to more than 90% (46). Although RV dia-stolic collapse is generally a more specific indica-tor of tamponade, the sensitivity can be reducedbecause of conditions that increase RV pressure(47). Left atrial and LV collapse are unusual andare observed generally with massive effusions or,in the case of left atrial collapse, loculated effu-sions.

A plethoric inferior vena cava (dilated withfailure to collapse by more than 50%) is a highlysensitive sign of cardiac tamponade. This findingconfirms high right atrial pressure, invariablewith few exceptions in cardiac tamponade (48).

Doppler EchocardiographyThe Doppler examination confirms the patho-

physiologic hemodynamic aberrations that occurduring cardiac tamponade.

The classic Doppler pattern of cardiac tampon-ade is as follows: (37,45)

(1) Mitral inflow: for inspiration, E wave de-creases and IVRT increases by more than 30%compared with expiration

(2) Tricuspid inflow: for inspiration, E wave in-creases more than 70% compared with expi-ration

(3) Pulmonary vein: for inspiration, D wave de-creases compared with expiration

(4) Hepatic vein: for inspiration, S is greater thanD; for expiration, an absent or very dimin-ished D wave with prominent reversals

Differential DiagnosisAside from the differentiation of pericardial

from pleural effusions, other echocardiography-free spaces around the pericardium must be rec-ognized. These include pericardial fat pads (moreoften anterior and echocardiography-dense), vas-

cular structures (descending aorta, pseudoaneu-rysm, coronary sinus), other pericardial structures(cysts found in right cardiophrenic angle, hema-toma, or tumor), and noncardiac structures (hiatalhernia) (49).

In many situations, an incorrect diagnosis ofcardiac tamponade is made based on the presenceof confounding factors that affect respiratory vari-ation or chamber collapse (50). Clinical historyand other echocardiographic findings are impor-tant in differentiating these conditions.

ConclusionThe clinical presentation of restrictive cardio-

myopathy, constrictive pericarditis, and cardiactamponade may vary vastly from chronic nonspe-cific symptoms to acute hemodynamic deteriora-tion. As diseases of diastolic dysfunction, thereare common hemodynamic and echocardio-graphic features of these diseases. A comprehen-sive echocardiographic evaluation includes two-dimensional imaging and pulsed Doppler with arespirometer. Color M-mode and Doppler tissueimaging should be performed. Volume loadingmaneuvers or transesophageal echocardiographymay also be required. Together, these techniqueshelp to distinguish anatomic and pathophysio-logic findings specific to each process and pro-vide the basis for clinical decisions regardingmanagement.

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