Pericardial Diseases

22 Pericardial Diseases


Knowledge of pericardial anatomy and physiology is critical when assessing for the presence of pericardial diseases and their consequences. The combination of real-time two-dimensional (2D) imaging and Doppler (including tissue Doppler), especially when used in conjunction with respirometry, renders echocardiography a superb test to assess pericardial disorders.



Pericardial Effusions


Echocardiography is the test of choice to detect pericardial effusions.



Goals of Echocardiography in Pericardial Effusions




image To identify that pericardial effusion is present


image To distinguish or identify intrapericardial clot and blood from fluid


image To establish the presence of pericardial tamponade, if present


image To identify the cause of the pericardial effusion if possible


Description of the size of the pericardial effusion is inherently inaccurate and misleading because (1) the actual volume of the effusion is impossible to measure by echocardiography—only a dimensional measurement can be made of a highly complex three-dimensional (3D) structure; and (2) the physiologic relevance of the pericardial effusion does not correlate with the size of the effusion alone; parietal pericardial compliance is the other factor. At most tertiary hospitals many tamponade cases occur in the context of small, acute, effusions; therefore, the inference that size correlates with risk is disproven by daily practice.


Although conventions exist regarding the description of size by linear measurement of posterior effusion thickness, they assume that the “size” (i.e., linear measurement) correlates with volume, and, again, with physiologic consequence/clinical risk.


The impression of the size of the effusion is influenced by its second dimension and also by the size of the heart cavities, which are reduced in compressive states such as tamponade, compounding the impression of size of the pericardial effusion.


The only truism as to the size of pericardial effusion concerns the safety of drainage: small effusions entail greater risk of complication from drainage; conversely, entail fewer risks and are therefore safer to drain.


Epicardial fat is the most common coarsely specular echolucent material overlying the myocardium. Echolucent material within the pericardial space may also be fluid, clot, purulence, or markedly edematous (aqueous) pericardium. The epicardial and pericardial fat planes, although somewhat echolucent, have a coarse specular pattern. Most of the fat over the heart is anterior to the right ventricle; little fat is posterior to the left ventricle. Because fluid seeks a dependent position, with the patient positioned recumbent or in the left lateral position, it would be abnormal, without loculation, to have fluid located anteriorly alone.


Pericardial effusion is evident by a fluid space, usually widely distributed but possibly localized (“loculated”), seen within the pericardial space. To establish that the fluid is pericardial, its location must be pinpointed as within the recess between the descending thoracic aorta and the left atrium. Pleural effusion lies posterior to the descending aorta, and pericardial effusion tracks anterior to the descending aorta. The only times when this relation is not applicable are when a pericardial effusion is loculated or when the aortic arch is right-sided.


The free wall of chambers collapses when there is loss of the transmural distending pressure (i.e., the intracavitary pressure no longer is greater than the intrapericardial pressure) and there is sufficient extrinsic pressure to deform the wall of the chamber (chamber walls have some intrinsic stiffness, more in the ventricles than in the atria).



Pericardial Tamponade



Required Parameters to Obtain from Scanning




image Presence of pericardial fluid


image Distribution and orientation of pericardial fluid


image Cardiac chamber compression signs


• RA compression is sensitive (although imperfectly so), but poorly specific

• RV compression is less sensitive, but more specific


image Right heart obstruction sign


• Caval dilation, and lack of respiratory variation (in the absence of intravascular depletion)

image Signs of interdependence (use respirometer)


• Cyclical intracavitary flow variation depending on respiration phase can be measured using spectral recordings of LV inflow, which will show exaggerated decrease on the early diastolic inflow (E-wave) of the first or second cardiac cycles of inspiration), RV inflow, and LVOT-outflow, which will show a decrease of the velocity and integral of the first or second cardiac cycles of inspiration

• Ventricular interdependence, in which the RV fills and the LV underfills on the first or second cardiac cycle of inspiration

image Seek to determine the cause of tamponade (e.g., aortic dissection, AMI, pacer)


image Scan the pleural spaces as well


image Optimal site and orientation of potential drainage


• Site of shortest distance into fluid

• Orientation of transducer/needle to achieve greatest depth of fluid (and safety)


Echocardiographic Signs of Tamponade



Pericardial Effusion


Pericardial effusion must be present for the diagnosis of tamponade: no effusion equals no tamponade.



Right Atrial Collapse


Right atrial (systolic) collapse (i.e., inversion, or inflexion inward) is the most sensitive sign of tamponade, but it is not sufficiently specific to use by itself, unless a long proportion of the cardiac cycle is used. It is held to be more specific than it actually is. The RA pressure is lowest in tamponade with the X descent; therefore, the RA free wall transmural distending pressure is lowest at this point in the cardiac cycle. Therefore, RA collapse is most likely to occur at this time of the cardiac cycle (i.e., right atrial systolic collapse), although in severe tamponade, the RA may stay collapsed for longer, even for the entire cardiac cycle. Essentially, RA collapse is a linear risk variable for which the threshold of 40% of the cardiac cycle has been observed to help dichotomize tamponade cases (>40% of the cardiac cycle) from nontamponade cases (<40% of he cardiac cycle). If the patient is in sinus rhythm, the RA normally will diminish in size in late diastole, while maintaining its usual curvature.



Right Ventricular Diastolic Collapse


Right ventricular diastolic collapse is the most specific sign of tamponade. It typically occurs at a higher intrapericardial pressure than does RA collapse, because loss of the transmural distending pressure for the RV occurs at a higher pressure than it does for the RA as the RV wall has more intrinsic stiffness. In some cases, RV collapse may go underrecognized—for example, when there is persistent compression of the RV distal to the moderator band all the way through the cardiac cycle, and the interpreter assumes that the RV, rather than being compressed (i.e., having collapsed through the cardiac cycle), is just “small.” The key is whether or not the moderator band can be seen. RV diastolic collapse is a very good sign, but it is not perfect. In the presence of chronic pulmonary hypertension, compensatory right ventricular hypertrophy will resist collapse, and make the left atrium or right atrium the more likely site of compression or obstruction.



Caval Distention


Obstruction of the right heart by tamponade will, in the absence of intravascular depletion, result in raised central venous pressures that are apparent on echocardiography as inferior vena cava (IVC) dilation and lack of variation.



Augmented Respiratory Variation of Mitral Inflow Velocities


As with the other principal compressive disorders (constriction and effusoconstriction), the normal inspiratory fall in left heart filling is exaggerated in tamponade (represented by echocardiography as the transmitral E wave). Any form of increased respiratory distress will exaggerate tricuspid inflow variation; therefore, exaggerated tricuspid inflow variation is less helpful as a sign of tamponade. In fact, respiratory distress (increased effort) will also increase the variation of left heart filling (E wave height). Therefore, the sign of increased (>25%) variation of transmitral E-wave height is only applicable in the context of normal respiration. Ensure that the observation is made of the E wave, not the A wave.



Notes




image Hemodynamic studies have established that RA collapse compounds the detrimental effects of RV collapse; therefore, the more echocardiographic signs that are present, the greater the probability of tamponade.


image The echocardiographic findings are best applied to the context of clinical probability of tamponade (e.g., history, physical examination), and optimally serve to establish the post-test (clinical) probability.


The presence of the “usual” echocardiographic signs of tamponade assumes the following:



image Spontaneous ventilation with normal effort


image A normal underlying heart


image An absence of volume depletion or severe overload


image Normal pericardium (i.e., not previously opened during cardiac surgery or fibrotic from prior pericarditis)


image A regular cardiac rhythm


image Degrees of chronicity


Conversely, a case of acute tamponade occurring in a mechanically ventilated patient, post–valve surgery, with pulmonary hypertension is unlikely to have the usual gamut of echocardiographic signs.


Early postoperative tamponades usually are produced by bleeding, have a larger proportion of clot, and often consist of cardiac compression from clot, rather than from tamponade. Typically, early postoperative clot or compressive syndromes compress a right-sided chamber, including the superior vena cava or pulmonary artery. Such cases may benefit from transesophageal echocardiographic (TEE) imaging. Clot cannot be extracted by a needle and requires surgical drainage. Later postoperative tamponades (i.e., once the patient is on the ward, or has returned to the ER) usually are fluid.


A pulsus paradoxus assumes normal inspiratory effort and, therefore, is a confounding sign in the presence of significant dyspnea. Causes of absence of a pulsus paradoxicus include pathologies that overfill or that normalize filling of the left ventricle, such as the following:



image Positive end-expiratory pressure


image Severe aortic insufficiency or mitral regurgitation


image Severe congestive heart failure


image Large intracardiac shunt


The more signs of tamponade that are present, the greater the likelihood of the diagnosis. Echocardiographic false-negatives and false-positives do occur, so the final diagnosis is clinical.


If echocardiography is used to guide a pericardiocentesis, its roles are (see Chapter 25)



image To determine the optimal access route to fluid


• Site of entry: shortest distance into the fluid

• Orientation: orientation so that the pericardial fluid will be entered at its deepest point

image To provide echocardiographic guidance


• Visualization of the needle or wire in the pericardial space before dilation of a tract

• Visualization of the bubbles from agitated saline to denote the location of the needle tip or catheter sideholes

Causes of tamponade that may be seen or suggested by echocardiography are as follows:



image Post-infarction


• Rupture: suggested by blood or clot appearance in the space

• False aneurysm: evident by narrow neck and wide body with signs of tissue disruption at the margins of the neck

image Pacer wire—this is generally not seen in the pericardial space


image Type A aortic dissection or IMH


image Tumor in the pericardial space


image Tumor on the pericardium



Intrapericardial Blood Clot


A significant proportion of cases of pericardial tamponade involve bleeding into the pericardium (e.g., traumatic, procedural iatrogenic, postoperative, acute aortic dissection) and may result in intrapericardial blood clot. Intrapericardial blood is suggested by the presence of fine specular echoes, similar to spontaneous echocardiographic contrast within the heart in “low-flow” states). “Jiggling” of the material is consistent with clot, as is lamination.


Clot is nearly impossible to aspirate out with a needle; therefore, if drainage is required, surgical drainage is preferred.



Pericardial Constriction


Pericardial constriction, the other classic pericardial compressive state, results from contraction around the heart of (usually, but not always) thickened pericardium. Whether or not it is thickened, in constriction it is invariably stiff. The usual presentation is of predominant right-sided heart failure.


The prior contribution of echocardiography in the evaluation of pericardial constriction was to exclude significant valve disease or systolic dysfunction and obvious cases of amyloidosis, and to establish indirectly, and inconclusively, that constriction may be present. Due to better application of 2D echocardiography and Doppler, and appreciation that the signs of constriction are revealed over both cardiac and respiratory cycles, echocardiography is now able to make a diagnosis of constriction in more cases.


Many echocardiographic findings have been published that have relevance in pericardial constriction; unfortunately, there have been no broadly comparative studies of all the echocardiographic signs. Many signs seem dated. Use of the findings of ventricular interdependence—which appears to be the best sign of constriction—has been “borrowed” from cardiac catheterization, but it lacks actual echocardiographic validation.


When scanning, remember the following:



image The respirometer must be used with all recordings: 2D, M-mode and Doppler. Ensure that the patient is breathing regularly and with sufficient, not excessive, inspiratory effort.


image Record entire respiratory cardiac cycles for 2D cycle loops, not single cardiac cycle loops.



Required Parameters to Obtain from Scanning




image Optimal use of the respirometer. Digital capture should include the following:


• 8 to15 cardiac cycles

• One or more complete respiratory cycles that loop together appropriately

• Regular, normal or normalized, respirations. Panting, hypopnea, and apnea will not reveal the respiratory findings, and, conversely, hyperpnea will nonspecifically generate them.

image Signs of ventricular interdependence


• 2D and M-mode signs of ventricular interdependence (due to a combination of increased filling of the right heart, decreased filling of the left heart, and their competition for filling within the limited space imparted by constrictive pericardium). The interventricular septum shifts abruptly to the left side, then back, in the first or second beats of inspiration. This is best appreciated on the parasternal short-axis view at the mid-ventricle or on the apical four-chamber view.

image Doppler signs of ventricular interdependence


• LV inflow variation: >25%

• Ensure that the observation is made of the E-wave height, not the A wave. Do not assume that the tallest wave is the E wave, because the A wave may be dominant (impaired relaxation).

• Marked RV inflow variation: >40%

image Tissue Doppler imaging to exclude myopathic disease (e.g., restrictive cardiomyopathy)


image Hepatic venous flow pattern


• Increased diastolic flow reversal in the hepatic veins, a Kussmaul-like phenomenon, is specific for constriction (100%), although with limited sensitivity (60%).

image Tricuspid regurgitation


• For right ventricular systolic pressure (RVSP). RVSP > 60 mm Hg is typical of restrictive cardiomyopathy and unusual for constrictive pericarditis.

• For RVSP variation with the respiratory cycle: RVSP increases with inspirations, a Kussmaul-like phenomenon, may be detected in constriction.

image Exclusion of significant primary valve dysfunction or ventricular systolic dysfunction


image M-mode of the septum


• For the “early diastolic dip”

• For the “late systolic dip”

• For ventricular interdependence

image M-mode of the posterior wall


• Flattened mid-diastole motion due to limited filling imparted by the constrictive pericardium

image Dilated IVC


image Stroke volume and cardiac output/index


Use of a phonocardiograph as well is commendable, and affords teaching opportunities. About 50% of cases of constriction have a discernable “knock.”


The older approach to evaluating pericardial constriction employed observations seen per cardiac cycle. The contemporary approach is to view observations over the respiratory cycle; hence the need for respirometry physiologic tracing. Unfortunately, digital echocardiographic recording is inclined to single R-R interval acquisition, and acquisition of multiple cycles to establish a respiratory cycle requires the intention to do so from the outset. To conclusively associate respiratory phenomena and cardiac phenomena, use of the respirometer is critical.



Echocardiographic Signs of Constriction


Although the traditional presentation of echocardiographic signs was to group them by modality, it is more useful to group them by relevant pathophysiology and similarity to catheterization findings, because such an approach encourages physiologic insight and a means to scrutinize catheterization findings in cases of suspected constriction.



Signs of Ventricular Interdependence



Inspiratory Septal Shift


The inspiratory septal shift is the volume corollary of the catheterization pressure sign of ventricular interdependence. In constriction, with inspiration, the RV diastolic and systolic pressures increase, and the LV diastolic and systolic pressures decrease. This is evident on 2D imaging by the transient movement of the septum according to the fluctuations of the pressure gradient between the ventricles. Ventricular interdependence is evident on 2D imaging when the RV and RA (over)fill and the interventricular and interatrial septa shift over to the left during the first cardiac cycles of inspiration. The posterior short-axis and apical four-chamber 2D views are the most helpful. M-mode from the posterior long or short axis is useful to display the RV overfilling/LV underfilling associated with inspiration.



Inspiratory Fall in Left Ventricular Early Diastolic Inflow Velocities


Increased phasic variation of mitral and tricuspid inflow occurs in constriction, but is not specific for it. In fact, respiratory diseases are a more common cause. The effect of constriction is greater on right heart loading; typically, flow variations of over 40% occur, but respiratory diseases (increased respiratory effort) also increase right heart filling variations. Nonetheless, increased flow variation, especially across the tricuspid valve, should be seen in conjunction with 2D signs of interdependence. The Doppler sign is, therefore, of variation (>25%) in mitral inflow velocity from is 88% predictive of constriction.1,2 If typical variation of transmitral flow is not apparent with the patient supine, have him or her sit up.2


Some have advocated interrogation of the superior vena cava flow as well. In constriction, there is little variation (i.e., difference between inspiration and expiration) in the systolic and diastolic velocities, whereas with chronic obstructive pulmonary disease (COPD) the systolic difference averages 45% and the diastolic difference averages 35%.3 Although statistically significant, they are not clinically significant differences in variation.



Early Diastolic Pressure Dips


In some cases of constriction, the early diastolic pressure dip of the LV exceeds that of the RV. Typically, the difference is augmented in inspiration. The higher RV and LV diastolic pressure can transiently deflect the interventricular septum to the left side in early diastole. Best seen from a parasternal (long- or short-axis) view, this amounts to a brief dip into the LV of the septum in early diastole. It is most conclusively seen on M-mode tracing.



Reduced Right Ventricular (Extrinsic) Compliance



Early Diastolic Pressure Plateau




image Flattened LV posterior wall in mid-diastole


image Limitation of LV filling by the constrictive pericardium after the early diastolic dip renders the LV cavity of fixed volume through the rest of diastole


• On M-mode tracing, this is apparent as a lack of mid-diastolic expansion of the LV cavity.


Kussmaul Phenomena




image Increased end-expiratory flow reversal–hepatic veins


• The IVC and its branches typically are very distended unless the patient is volume contracted by high-dose diuretics. This generally facilitates pulsed-wave Doppler recording from the superior hepatic vein.

• Expiratory diastolic flow reversal in the hepatic veins is 68% sensitive, 100% specific4 for constriction.

image Inspiratory increase in RVSP


• An elegant sign of constriction is the surrogate of the catheterization observation that with constriction in inspiration, the RV systolic pressures increase and the LV systolic pressures decrease.

• Although maintaining alignment throughout the respiratory cycle is a challenge, the inspiratory increase in RV systolic pressure (TR velocity) is recorded with the use of a respirometer.

• Phasic inspiratory increases in RVSP associated with inspiration are present and describe the right heart pressure aspect of interdependence—that RV pressure increases while LV pressure decreases.

• Inspiratory increase in RVSP with constriction (13 ± 6%) versus fall in RVSP with restriction (–8 ± 7%).5


Pericardial Thickening




image Transthoracic echocardiography is notoriously poor for the detection of pericardial thickening, although TEE is validated to evaluate pericardial thickness and has very good correlation (r = 0.97, P < 0.001).6


image TEE is able to evaluate pericardium only over the RV free-wall.7


• Detection of pericardial thickening on TEE requires experience, more than most echocardiographic signs, and has considerable interphysician variation.

image Studies validating CT are very dated (sensitivity 78%, specificity 100%),8 because they were generated in lower temporal resolution nongated scanners.


image Later studies using cine-CT appeared better, studying small series of normal versus restrictive cardiomyopathy versus constriction.9 The advent of 32-, 40- and 64-detector scanners with cardiac gating has revolutionized pericardial imaging.


image The pericardium is most apparent over the RV free wall, as there is more pericardial fat to delineate it.

image CT is the best imaging test to identify pericardial calcification. Most cases of pericardial constriction are no longer calcified, unless they are tuberculous in origin.


image Gated MRI was considered, for a time, the definitive modality for detection of pericardial thickening (88% sensitivity, 100% specificity),10 using an extraordinarily improbable cut-off value of >4 mm to identify pericardial thickening. In contradistinction to CT, MRI is essentially insensitive to the presence of pericardial calcification.


image Gated cardiac CT is not proven to be more accurate at depicting pericardial thickness than is MRI, but it is far better able to depict calcification.



Tissue Doppler




image Normal tissue Doppler velocities. Tissue Doppler imaging plays an important role in excluding restrictive cardiomyopathy, where E′ is lower than normal. In (pure) pericardial constriction, with the caveat that the underlying heart is normal, myocardial relaxation is normal. Unfortunately, a few confusing cases, notably postradiotherapy cases, will have concurrent restrictive cardiomyopathy and constrictive pericarditis. Many postoperative heart surgery cases, especially post–valve replacement cases, have neither a normal left heart nor a normal tissue Doppler finding.


image Peak tissue Doppler >8 cm/sec is 89% sensitive and 100% specific for constriction versus restriction,11 but does not distinguish between constriction and normal without either constriction or restriction.12


image Another useful tissue finding in support of constriction is that the medial/septal tissue Doppler velocities are higher than are those of the lateral mitral annulus.



Elevated Cardiovascular Central Venous Pressure


IVC dilation and lack of variation indicate elevated cardiovascular pressure.



Elevated Right Ventricular Diastolic Pressure




image Late diastolic septal dip


• In constriction, the late diastolic A-wave pressure increase in the RV may exceed that in the LV, transiently deflecting the interventricular septum toward the LV in late diastole.

• The sign is best appreciated on M-mode tracing. Given variable PR intervals, the sign may be difficult to differentiate from the common presence of an early diastolic septal dip, but it is an elegant corollary of the elevated RV diastolic pressure catheterization sign of constriction.

image The emphasis of Doppler in constrictive pericarditis should stay focused on the following:


• Tissue Doppler to exclude restrictive cardiomyopathy

• Hepatic venous flow

• Mitral flow variations


The great confounder of 2D and Doppler signs of ventricular interdependence is atrial fibrillation, where R-R cycle variation produces effects that contaminate and may dominate those of respiration. Other confounders include severe underlying structural heart disease (e.g., valve disease, systolic dysfunction), which would confer abnormal hemodynamics that would mask those of constriction, and concurrence of restrictive cardiomyopathy and constrictive pericarditis.



Valid Means to Make the Diagnosis of Constriction




image No alternate pathology evident


image Ventricular interdependence on 2D and Doppler


image A septal diastolic dip


image Normal myocardial tissue Doppler imaging at annulus

Related posts:

  1. The Aortic Valve
  2. Coronary Artery Disease: Ischemia, Infarction, and Complications
  3. Coronary Artery Disease: Stress Echocardiography
  4. Mitral Insufficiency

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Jun 12, 2016 | Posted by in CARDIOLOGY | Comments Off on Pericardial Diseases

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