The normal pericardial sac contains 10–50 ml of pericardial fluid as a plasma ultrafiltrate that acts as a lubricant between the pericardial layers.
Pericardial effusion may be classified according to its onset (acute, subacute, chronic when lasting >3 months), distribution (circumferential or loculated), haemodynamic impact (none, cardiac tamponade, effusive-constrictive), composition (exudate, transudate (hydropericardium), blood (hemopericardium), rarely air, or gas (pneumopericardium) and in by its size based on a simple semiquantitative echocardiographic assessment as mild (<10 mm), moderate (10–20 mm) or large (>20 mm).
Image 1 Pericardial effusion classification
Adapted from: Adler, Y., Charron, P., & Imazio, M. (2015, November 7). 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC). Academic.Oup.Com. https://academic.oup.com/eurheartj/article/36/42/2921/2293375#204378284
Clinical findings (Image 2)
Cardiac tamponade is a compressive status of the heart caused by accumulation of fluid, pus, blood, clots or gas as a result of inflammation, trauma, rupture of the heart or aortic dissection and resulting increased intrapericardial pressure that compresses the cardiac chambers and inhibits normal filling.
As fluid accumulates in the pericardial sac, pericardial pressure rises, and systemic and pulmonary venous pressures must increase to maintain cardiac filling.
As cardiac tamponade becomes more severe, these venocardiac gradients continue to diminish, resulting in a progressive decrease in cardiac output.
When compensatory mechanisms are exhausted, preload becomes insufficient to sustain cardiac filling and coronary and systemic perfusion.
Image 3 Causes of cardiac tamponade
The magnitude of clinical and haemodynamic abnormalities depends on the rate of accumulation and amount of pericardial contents, the distensibility of the pericardium and the filling pressures and compliance of the cardiac chambers.
Image 4 Clinical findings in Cardiac tamponade
Echocardiographic examination of pericardial effusion
Cardiac imaging should be performed whenever a PE is suspected, because a physical examination or chest x-ray cannot make a definitive diagnosis.
Echocardiography is the initial procedure of choice to detect the presence of a PE because it can be performed with minimal delay and has an accuracy of nearly 100%. It is also the best diagnostic tool for assessing the physiologic and hemodynamic effects of a PEff.
A separation of the two layers that is seen only in systole represents a normal or clinically insignificant amount of pericardial fluid (trivial PE), whereas a separation that is present in both systole and diastole is associated with effusions of >50 mL (small PE).
A left pleural effusion may mimic a PE. In these cases, a two-dimensional (2D) parasternal long-axis should be performed. View that shows fluid between the descending aorta and heart establishes the fluid as pericardial rather than pleural.
2D echocardiography followed by Doppler provides the easiest way to demonstrate and assess PE.
Two-dimensional echocardiography allows the qualitative assessment of the size and distribution of a PE as well as the detection of fluid that may be loculated or have density features consistent with an exudate or clot rather than a transudative fluid.
Epicardial fat is often brighter than the myocardium and tends to move in concert with the heart.
1) Small pericardial effusion
Video 1 Small pericardial effusion (maximum separation between visceral and parietal pericardium = 10mm), partially organised (echogenic) - PLAX view
Video 2 Small pericardial effusion, partially organized (echogenic) - PSAX view
Video 3 Small pericardial effusion (maximum separation between visceral and parietal pericardium =10mm), diastolic undulation of RA free wall (nonspecific finding) - A4C view
Video 4 IVC diameter shows more than 50% reduction during inspiration in patient with a small pericardial effusion - subxyphoideal view
Image 5 Normal IVC diameter (15 mm) in a patient with small pericardial effusion - subxyphoideal view
2. Moderate pericardial effusion
Video 5 Moderate pericardial effusion (separation between visceral and parietal pericardium 10-20mm), maximum located at inferolateral wall - PLAX view
Video 6 Moderate pericardial effusion (separation between visceral and parietal pericardium 10-20mm), maximum located at inferolateral wall - PSAX view
Image 6 Moderate pericardial effusion (separation between visceral and parietal pericardium of 15mm), maximum located by lateral wall - A4C
Image 7 Moderate pericardial effusion, maximum located at inferolateral wall - 15mm - subxyphoideal view
Image 8 Non significant changes in peak E-wave mitral flow velocity during respiration in patient with moderate pericardial effusion - max 1.42 m/s vs. min 1.18 m/s = 17%
Video 7 IVC diameter shows more than 50% reduction during inspiration in patient with moderate pericardial effusion - subxyphoideal view
Moderate to large chronic pericardial effusion
Video 8 Moderate to large chronic pericardial effusion without current hemodynamic signs of cardiac tamponade - PLAX view
Video 9 Moderate to large chronic pericardial effusion without current hemodynamic signs of cardiac tamponade - PSAX
Image 9. Non significant changes in peak E-wave mitral flow velocity during respiration in patient with moderate pericardial effusion - max. 1.16 m/s vs. min 0.95 m/s= 10%
Video 10 Moderate to large chronic pericardial effusion without current hemodynamic signs of cardiac tamponade; right atrium free wall undulation - A4C
Image 10 Moderate to large chronic pericardial effusion without current hemodynamic signs of cardiac tamponade, maximum 20mm localized around right atrium - A4C
Video 11 Moderate to large chronic pericardial effusion without current hemodynamic signs of cardiac tamponade - subxyphoideum
Image 11 DIlated IVC in patient with chronic pericardial effusion - subxyphoideum
The most important echocardiographic findings in heamodynamically compromising pericardial effusion are:
1) large pericardial effusion with swinging heart
2) a left ventricular reduced end-diastolic and end-systolic dimensions with evidence of reduced stroke volume and cardiac output
3) a dilated and non-compressible inferior vena cava (IVC)
4) right heart diastolic chamber collapse
5) an inspiratory bulge or ‘‘bounce’’ of the interventricular septum into the left ventricle
6) characteristic abnormal respiratory changes in Doppler flow velocity recordings - transmitral and transtricuspidal Pulse doppler velocities
7 changes in hepatic venous flow velocity
1) Large pericardial effusion with swinging heart
Swinging heart is characterized as counterclockwise rotational movement, which occurs in addition to the triangular movement of the heart, producing a dancelike motion.
Video 12 Swinging heart in a patient with cardiac tamponade
2) Left ventricle end-diastolic and end-systolic dimensions reduction
The parasternal short-axis view shows the effects of the cardiac compression and reduced filling.
LV cavity dimensions in systole and diastole are reduced, while the myocardium, which retains the same mass, appears ‘‘hypertrophied.’’
RV diastolic diameter increases during inspiration, while LV diastolic diameter decreases, with the opposite changes seen during expiration.
3) Dilated inferior vena cava (IVC)
An important 2D sign of tamponade is vena cava inferior (IVC) plethora.
A dilated IVC (>2.1 cm) with <50% reduction in diameter during inspiration reflects the elevation in systemic venous pressure that occurs as pericardial pressure increases the intracardiac pressures.
Video 13 IVC plethora during respiration
4) Right heart diastolic chamber collapse
Collapse in systole for the atria and during diastole for the ventricle.
Diastolic RA and RV chamber indentation or ‘‘collapse’’ on 2D echocardiography is usually seen in cardiac tamponade and is particularly important in the diagnosis of low-pressure tamponade, when IVC dilation is minimal or absent.
It is important to evaluate duration of the RA collapse. Duration of RA collapse that exceeds one third of the cardiac cycle is nearly 100% sensitive and specific for clinical cardiac tamponade.
The RV free wall stays indented until chamber pressure with diastolic filling exceeds pericardial pressure.
Right heart diastolic collapse may occur at higher levels of pericardial pressure in conditions in which right heart chamber pressures were elevated before the effusion accumulated, for example with RV hypertrophy, severe pulmonary hypertension, or coexisting severe LV dysfunction.
Conversely, collapse of the right heart chamber may occur earlier than normal when intracardiac pressures are low because of hypovolemia.
Posterior loculated effusions after cardiac surgery and severe pulmonary arterial hypertension may produce LA and LV diastolic collapse.
Video 14 Right heart diastolic chamber collapse
5) Inspiratory bulge or ‘‘bounce’’ of the interventricular septum
An inspiratory bulge of the interventricular septum into the left ventricle during inspiration is commonly seen in cardiac tamponade.
During inspiration, we observe an increase in RV dimension and a decrease in LV dimension due to septal movement toward the LV free wall.
Septal bulge or ‘‘bounce’’ is not specific for cardiac tamponade, while it is typically seen in constrictive pericarditis.
Video 15 Septal bounce example in a patient with contristive pericarditis
6) Changes in transvalvular velocities
The changes are tricuspid and pulmonary flow velocities increase in inspiration and flow velocities decrese in the mitral and aortic valves.
Under normal circumstances, the change in peak E-wave mitral flow velocity is about 5%.
In cardiac tamponade, changes in mitral and tricuspid flow velocity are much larger:
- Peak mitral E inflow- the maximal drop occurs with the first beat of inspiration and the first beat of expiration and exceeds >25% respiratory variation.
- Peak tricuspid E inflow- the maximal drop is on the first beat in expiration and exceeds >40% respiratory variation.
Formula: (expiration - inspiration)/expiration
Image 12 Severe variation of transmitral flow velocities - max. 1.01 m/s vs. min 0.55 m/s = 46%
7) Hepatic venous flow velocity with PW Doppler in assessing the hemodynamic effects of a Pericardial effusion
Normal hepatic venous flow is biphasic, the systolic velocity greater than diastolic velocity.
With inspiration, both peak systolic and diastolic flow velocities increase.
When a pericardial effusion inhibits cardiac filling, forward flow velocities decrease from the normal 50 cm/sec to 20–40 cm/sec and systolic venous flow predominates.
Diastolic flow velocity (DFV) can be absent but still exhibits some inspiratory augmentation or DFV can disappear completely.
With no hepatic forward flow is observed except during inspiration, systemic venous and intracardiac pressures are equalized, and cardiac arrest is imminent.
Video 16 Cardiac tamponade - PLAX view
Video 17 Cardiac tamponade - PSAX view
Video 18 Cardiac tamponade - A3C view
Video 19 Cardiac tamponade - subxyphoideal view
Image 13 Transmitral variation of flow during inspiration in a patient with cardiac tamponade - max. 1,08 m/s vs 0,74 m/s = 31%
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