👜Pericardial Disease

Assessment of pericardial space most frequently manifests as assessment for pericardial tamponade in the presence of a pericardial effusion.

Other pathology that must be interpreted includes constrictive pericarditis and differentiating this from restrictive cardiomyopathy.

In health – space between fibrous and serous pericardium contains around 50ml of lubricating fluid.

Pressure is roughly equal to interpleural pressure – drops slightly below zero with inspiration and rises with expiration.

FIbrous pericardium may become thickened:

  • Thick smooth appearance – acute inflammatory processes
  • Irregular thickening – chronic inflammatory process/post-surgical reaction. Rarely this results in calcification from chronic infiltrative or haemorrhagic process.

A small amount of fluid may be seen in diastole and is trivial, <5mm in depth. This should not be seen in systole.

Tamponade physiology:

Ventricular interdependence is a physiological consequence of the anatomy of the pericardium as it contains all four chambers.

A rise in volume of one chamber will have an impact on the chambers around it.

Effect most clearly seen in filling relationship between the two ventricles but also occurs between atria and ventricles.

Atrioventricular interdependence – adds to efficiency of heart. Ventricular systole pulls atrioventricular annulus longitudinally towards the apex creating space within the pericardium for atria to passively fill – hence encouraging atrial filling..

When pericardial pressure (PP) is elevated atrial filling is even more dependent on this process.

With accumulation of pericardial fluid the ventricles become compromised and are unable to pull the AV annulus around the blood column.

This manifests in early tamponade as the rise in RV pressure during filling causes exaggerated collapse of the RA as it empties.

Signs in tamponade reflect this AV interdependence:

  • RA collapse in diastole – exaggerated atrial emptying due to impaired ventricular relaxation.
  • RV collapse in systole – PP exceeds RV free wall pressure during diastole – geometric change in ventricular wall leading to worsening of diastolic and systolic function.
  • Symptoms usually occur when PP exceeds 10mmHg and all dyspnoeic & tachycardic at 15mmHg.

Ventricular independence – about 1/3 of the work done by the RV depends on the LV in health, and lesser extent LV also relies on RV function.

Inspiration reduces intrathoracic pressure and sucks blood into thoracic cavity filling the RV.

This process is exaggerated in tamponade:

  • Inspiration fills RV but RV free wall cannot expand due to high PP.
  • The septum bows significantly into the LV distorting the muscle and reducing the ventricular function.
  • Overall – exaggerates normal SVV with respiration & causes drop in SV with inspiration. This is pulsus paradoxus. LV Vmax/VTI can be used to demonstrate this on echo.
  • This can be seen with very negative intrathoracic pressure & high work of breathing.

The same physiological process occurs with massive pleural effusions or tension pneumothorax.

As decompensation progresses (20-25mmHg) gradient from mean systemic filling pressure to RA becomes negligible and atria cannot passively fill.

Further rise equalises pressure with LV filling pressure – SV will precipitously fall and obstructive shock occurs.

Established tamponade – equalisation of diastolic pressure in all chambers and blood cannot flow through the heart.

Rate of accumulation dictates how quickly this process advances.

Phase of compensation is shorter in patients with hypovolaemia or with a railing RV/impaired LV.


Pericardial thickness on echo very poorly correlates to operative or post-mortem findings so care should be taken.

Awareness of fat pads anterior to heart of deep to sternum.

Retrosternal haematomas may appear anterior to the heart but rarely compresses RVOT.

Remember that pleural effusions and pericardial effusions may be differentiated by the location of the descending aorta. A pleural effusion will never separate the aorta from the LA.

Effusion size:

Circumferential of localised.

Measured at the deepest region in end-diastole.

Localised effusions occur in cardiac surgical patients – early with haematoma & later with infection.

High pulmonary venous pressures can cause effusion contained within oblique fissure which may compress LA.

Anterior-posterior distance on PLAX of over 12cm (measured from outer all by probe to posterior pericardial wall behind LVPW) correlates well with onset of symptoms in chronic effusions.

Can use this to estimate volume:

volume = (0.8 x APD – 0.6)^3

2D & M-mode

  1. RA diastolic collapse (lowest diastolic pressure – occurs in ventricular, not atrial, diastole) affected first with free wall collapse for >1/3 of diastole. M-mode can be used in subcostal view. Can see spontaneous echo contrast (‘smoke’) within RA once this occurs. Agitated saline may be seen to flow slowly/stall within RA during spontaneous expiration..
  2. RV diastolic collapse affected next – diastolic collapse almost always signifying cardiac compromise. RVOT affected first, then entire RV.
  3. IVS shift towards LV.
  4. LA and LV last chambers to show diastolic collapse in non-localised effusions.
  5. Swinging heart is visual representation of pulsus alternans.

Also – RA pressure is high so IVC will be dilated with minimal respiratory variation.

Doppler studies:

Intracardiac flow:

MV and TV inflow variability.

MV – normally will have <20% variation. Abnormal if >25%.

TV – normally will have <30% variation. Abnormal if >40%

These values can also be used for LVOT/RVOT flow variability.

Restrictive filling pattern in LV – will show pattern of moderate to severe diastolic impairment.

In rare case of effusive constrictive pericarditis (where patient with constrictive pericarditis develops effusion) both diastology and flow variation are devalued.

Intrahepatic flow:

  • Pronounced S wave during inspiration that reduces in amplitude during expiration.
  • Diminished D wave during inspiration which may disappear.
  • Large positive a waves during expiration.

Positive pressure ventilation:

The impact of positive pressure ventilation may increase RV diastolic pressure and free wall collapse may be seen at a later stage.

Flow variation across MV/TV/RVOT/LVOT cannot be as accurately relied on. There is a degree of uncoupling of ventricular interdependence making flow variation more dependent on filling and afterload seen in each ventricle.

Sensible to err on the side of caution.

Constrictive Pericarditis:

Thickening and fibrosis of serous pericardium constricts the heart in fibrous envelope which impairs filling of ventricles and leads to equalisation of diastolic pressures.

Filling during early diastole becomes rapid but then abruptly stops (plateaus).

Ventricles becomes interdependent.

Can occur as a result of pericardial inflammation – often after a long period of time, e.g. after cardiac surgery, radiotherapy and pericardial tuberculosis.



Assess for pericardial thickening. As mentioned above this can be v challenging and inaccurate on TTE. TOE has 90% accuracy.

In 20% of cases the pericardium is not thickened and presence of thickened pericardium does not necessarily imply constriction.

LV dimensions and function are often normal.

Ventricular septum:

  • Abrupt posterior motion in diastole caused by rapid RV diastolic filling.
  • Little motion in mid diastole.
  • Abrupt anterior motion at the end of diastole (after atrial contraction) as there is further RV filling.
  • May be ‘septal bounce’ during inspiration due to ventricular interdependence.

Raised RA and LA size due to chronically raised diastolic pressure.

IVC will be dilated with absent/minimal respiratory collapse.

PW doppler:

Mitral inflow pattern:

  • Exaggeration of normal E/A ratio with very large E and very small A.
  • Rapid E deceleration time.
  • Exaggerated respiratory variation.

Difference between pericardial constriction and restrictive cardiomyopathy can be challenging and is a popular BSE exam question.