Echo in pericardial diseases: effusion, cardiac tamponade, constriction

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Basic Principles
In normal pericardium, there is approximately 30 to 50 mL of fluid between the visceral and parietal pericardium. This amount of fluid usually is not visible on ultrasound. The pericardium should appear echogenic. If there is an effusion, an anechoic space will be evident between the pericardium and the heart. With a large or rapidly developed pericardial effusion, this anechoic space surrounding the heart may be associated with diastolic collapse of the right atrium or the right ventricle.

A subcostal view is helpful in identifying a pericardial effusion because there is no pleural reflection between the heart and the liver. Therefore, a large effusion seen in a subcostal view is either between the pericardial or in the free abdominal space. The main way to differentiate between these two locations of fluid is to understand that the pericardial fluid follows the shape of the heart. A parasternal short axis (PSAX) is also helpful because it allows the operator to view possible effusions in the dependent areas of the pericardium.

Emergency medicine physicians can reliably perform bedside echocardiography to detect pericardial effusions. Ultrasound use in the emergency department is fast, noninvasive, and easy. Depending on the image interpretation, cardiac ultrasound can direct the management of penetrating chest trauma and improve outcomes for patients with this type of injury.

It is especially useful in diagnosing impending cardiac tamponade when classic clinical signs are not present. Beck’s triad of jugular venous distension, muffled heart sounds, and hypotension are present in less than 40% of patients with tamponade. When these signs are present, it is not until late in the clinical scenario.

Even though emergency medicine physicians are fully capable of performing quality cardiac ultrasound scans, the study is operator-dependent and can be susceptible to misinterpretations. Specifically, pericardial fat can be mistaken for pericardial effusions. Epicardial fat (i.e., fat over the apical portion of the heart) is commonly seen in obese patients and is routinely seen in the subcostal view. Confusing epicardial fat for pericardial effusion could result in unnecessary surgical procedures.

To prevent misinterpretations, the cardiac ultrasound be performed in more than one view. In addition, a modified subcostal view can be used to evaluate the pericardium. The probe should be angled longitudinally so that the inferior vena cava can be seen entering the right atrium. The operator will be able to view the right side of the heart adjacent to the diaphragm and any associated amount of pericardial fluid.

In addition to detecting pericardial effusion, ultrasound can be used to perform pericardiocentesis. In the emergency department, pericardiocentesis usually is a blind procedure. Risks of the procedure include pneumothorax, laceration of cardiac chambers, pneumopericardium, and liver lacerations.

Ultrasound guidance may decrease the incidence of these complications. Once the pericardial effusion is visualized, the optimal needle entry site is where the fluid collection is closest to the body surface.

For a Discussion of the Pathophysiology of Pericardial Disease click here

Pericardial anatomy
(Outside) Fibrous (parietal) pericardium->serous pericardium->pericardial cavity >epidcardium->myocardium->endoderm (visceral)->heart chamber (inside)

Pathophysiology

 * 1)  Composition of pericardial fluid: Ultrafiltrate of plasma, normally the volume is less than 50 cc.
 * 2)  Function of pericardial fluid: Although there is controversy about the true function of pericardial fluid, it is generally thought to serve a lubricating function, allowing for normal movement of the heart.
 * Etiology of Pericardial effusion
 * 1) Inflammatory [Dressler’s syndrome, uremia, collagen vascular disease (i.e Lupus, rheumatoid arthritis), s/p cardiac surgery]
 * 2) Infectious (bacterial, post-viral, fungal)
 * 3) Malignant (metastatic disease, primary cardiac malignancy, direct extension)
 * 4) Iatrogenic (chest trauma, post- catheterization, LV rupture, radiation).
 * 5) Idiopathic


 * tamponade physiology: Compression of the heart and impairment of diastolic filling. In other words, when the intrapericardial pressure exceeds the chamber pressures, it impairs the ability for the heart to fill. This can occur with a low volume of pericardial fluid (50-100cc) in an acute, quickly accumulating, effusion or, at higher volumes (greater than 1000 ml) in a slowly accumulating chronic effusion.


 * For a detailed explaination of the Hemodynamic physiology of cardiac tamponade see below under title of the same


 * Remember that tamponade is primarily a clinical and hemodynamic diagnosis. Practically, cardiac output and MAP initially fall when the pericardial pressure is greater than the right atrial pressure.

Echocardiographic findings in pericardial effusions/ tamponade

 * A pericardial effusion is seen in 2D echo as an echolucency adjacent to the heart


 * Right atrial systolic collapse (RA inversion): Best visualized in the apical four chamber view.
 * 1) RA inversion occurs during the period of end-diastole to early systole when the RA pressure is minimal.
 * 2) The sensitivity and specificity of this finding increases with the length of time of RA collapse. This can be quantified by the RA inversion time index (RAITI): duration of inversion/cardiac cycle length. At a RAITI of >0.34 (roughly >1/3 of systole)
 * 3) sensitivity: 94% specificity: 100%.

 RA collapse

 RV diastolic collapse
 * Right ventricular diastolic collapse (RVDC): Best visualized in the subcostal view or potentially the parasternal RA/RV view.
 * 1) RVDC occurs during during early diastole, when the intrapericardial pressure is greater than the right ventricular diastolic pressure.
 * 2) Sensitivity: 60-90%, Specificity: 85-100%
 * 3) When RVDC is seen, it can be assumed that the cardiac output is at least 20% reduced from normal
 * 4) Caveat: This finding is dependant on a normal RV. If there is RVH or infiltrative disease of the RV or other issues which effect RV compliance, then one may not see collapse of the RV with increased intrapericardial pressure.


 * Reciprocal ventricular volume variation with respiration (aka: Interventricular Dependence): Best visualized in the apical four-chambered view and in the Subcostal long axis view with M-mode.

Hemodynamic Physiology of Cardiac Tamponade
--Hemodynamic 08:20, 9 December 2010 (UTC)
 * 1) During Normal Inspiration intrathoracic pressures decrease and this decrease in pressure is transmitted to both ventricles.  This decrease in pressure around the right ventricle (RV) and right atrium (RA) effectively makes the RA and RV like a syringe "sucking" the blood in from the inferior vena cava (IVC) and superior vena cava (SVC) increasing preload.  This is because the drop in intrathoracic is greater in the RA/RV than on the SVC and IVC creating an increased pressure gradient (Remember the greater the pressure gradient the faster the flow and larger the volume). The result is increased right ventricular filling which can be quantified by Doppler at the right ventricular inflow (RVIF); however, on the left atria (LA), left ventricle (LV) and pulmonary vein (PV) side, the drop in intrathoracic pressure is equal on and in all three anatomic structures so blood flow pressures remain constant (NO change in preload).  That is why there is no change in left ventricular inflow with respiration in the normal heart.  Again, easily quantified with Doppler.
 * 2) In tamponade, however, the pericardial effusion "compresses" the cardiac chambers transmitting a constant pressure on the heart effectively shielding it from experiencing the normal decrease in intrathoracic pressure with inspiration. Importantly, remember that the increased pressure from the pericardial effusion is only "felt" by the structures encased within the pericardium.  The pulmonary veins (and some of the Left Atrium), however, are not encased in the pericardial membrane and, therefore, do not experience the increased pressures exerted by the pericardial fluid.  This is an important point.  So when inspiration occurs during cardiac tamponade the drop in intrathoracic pressure that was once transmitted to all cardiac structures is now ONLY transmitted to the Pulmonary Veins (PV).  Therefore, the PV pressure decreases but the pressures in the LA, LV (and RA/RV) remain constant!  This leads to a significantly decreased pressure gradient (preload) from the pulmonary veins to the LA/LV thus decreasing inflow.  This is easily measured and quantified with Doppler Echocardiography at the left ventricular inflow (LVIF) in the Apical four chamber view.  This is also the physiology responsible for Pulsus Paradoxus.
 * 3) So in tamponade there is an increase in RV filling because of the decrease in LA/LV inflow volume not because of the normal drop in intrathoracic pressure. This decrease in LV volume allows expanse of the RV (it now has the greater pressure pushing the septum into the LV) causing the ventricular septum to "bow" toward the LV.
 * 4) Reciprocally, during expiration, intrathoracic pressure rises causing a concomitant increase in pulmonary vein pressure which increases the filling gradient from PV to LA to LV and LV inflow/volume increases.  Now the pressure/volume is greater in the LV which subsequently forces the interventricular septum to bow into the RV.  This is known as Interventricular Dependence--the interventricular septum "seesawing" back and forth between the RV and LV with respiration.
 * 5) This Hemodynamic physiology of Cardiac Tamponade is responsible for the physical finding of pulsus paradoxus--the decrease in systolic blood pressure with inspiration with reciprocal increase in systolic blood pressure with expiration.
 * 6) A pulsus paradoxus of > 10mmHg is considered Hemodynamically significant for pericardial effusions causing tamponade. (Circulation. 1985 Apr;71(4):829-33.)

 IVC plethora
 * Respiratory variations in flow velocities across valves in tamponade: This occurs most significantly in left ventricular inflow at the Mitral valve (It usually has NO respiratory variation) and is interrogated using pulsed wave Doppler. As severity of pericardial effusion/tamponade increases significant flow variations with respiration can be seen in the Aortic and Pulmonic valve outflows as well.  Right ventricular inflow at the Tricuspid valve always has respiratory variation which is normal and therefore is not as reliable for measuring respiratory hemodynamic variation for diagnosing cardiac tamponade.--Hemodynamic 08:20, 9 December 2010 (UTC)
 * Inferior vena cava plethora: Best visualized and only measured in the sub-costal view.
 * 1) Due to increased RA pressure in tamponade, the IVC is dilated (increased IVC diameter usually > 23mm) and with inspiration there is less than a 50% reduction in diameter measured at least 1cm proximal to the IVC-RA junction.
 * 2) Sensitivity: 97% Specificity: 40%.


 * Effusion size on Echocardiography
 * 1) Small effusion: <0.5cm (roughly corresponds to <100cc)
 * 2) Moderate effusion: 0.5cm-2cm (roughly corresponds to 100-500cc)
 * 3) Large effusion: >2.0 cm (roughly corresponds to >500cc)

Pathophysiology

 * Constrictive pericarditis has numerous etiologies with an end result of formation of a fibrotic and calcified "rigid" pericardium which inhibits diastolic filling of the ventricles.


 * Etiology
 * 1) infectious (bacterial, viral, fungal)
 * 2) radiation
 * 3) cardiac surgery
 * 4) drugs
 * 5) trauma
 * 6) connective tissue disease
 * 7) neoplasm
 * 8) sarcoidosis
 * 9) renal failure
 * 10) idiopathic

2D Echocardiogram findings in Constriction

 * Pericardial thickening: This can be visualized by transesophageal echo (often requiring multiple views), however, this is best seen using other imaging modalities such as CT or MRI.
 * Reciprocal ventricular volume variation with respiration: This is the same phenomenon as described above in echo findings of cardiac tamponade- During inspiration there is an increase in right ventricular filling accompanied by decreased left ventricular filling. During expiration there is a increase in left ventricular filling with a concommitant decrease in right ventricular filling.
 * diastolic septal bounce: This is due to the rapid filling during early diastole leading to asymmetrical filling of the right and left ventrical which creates a fluctuating pressure gradient that manifests as an abrupt shift of the septum.
 * atrial dilatation (mild): Secondary to elevated atrial pressures. Of note, more severe atrial dilatation is a marker of a restrictive cardiomyopathy.
 * IVC plethora and dilation of the hepatic veins: Secondary to elevated right atrial pressures. Hepatic vein doppler reveals pressure tracings significant for a prominant "a" wave and prominent "y" descent.