Echocardiography:

Pericardial Effusions &

CardiacTamponade
David M. Whitaker, MD
Pericadial Anatomy
2 layers  visceral and parietal

Most diseases involve both, even though the parietal

layer is most commonly called the pericardium

Normally 5-10 mL buffering fluid in space

Extends up to great vessels and reflects around the

pulmonary veins

In disease free states – rarely visualized

Pericardial Purpose
Restrains 4 chambers in a relatively confined volume.
Thus the total volume of all 4 chambers is limited
Changes in volume of one chamber must be reflected in
a change in volume in the opposite direction in another
chamber
This “linking” of volumes forms the basis for the
physiology of pulsus paradox and findings seen in
tamponade
Fluid Accumulation Rates
Space is limited, so a significant accumulation of fluid
reduces total volume the 4 chambers can contain at any
one time  may result in hemodynamic compromise
Hemodynamic compromise related to intrapericardial
pressure, which in turn is related to volume of
pericardial fluid and compliance/distensibility of
pericardium
Fluid Accumulation Rates
An effusion which accumulates slowly may become large
with little to no hemodynamic compromise

Smaller effusions which accumulate rapidly may cause

deterioration
Detecting & Quantifying Fluid
Can use all traditional techniques

M-mode  echo free space anterior and posterior

No accurate way to quantitate volume in M-mode

Isolated echo free space in anterior side may not be

fluid – could be mediastinal fat, fibrosis, thymus or
other tissue
Detecting & Quantifying Fluid
2D echo most commonly used

Commonly visually quantified as:

 Minimal, small, moderate or large

Further characterized as free or loculated

Should always report on presence or absence of

hemodynamic compromise
Effusions in General
Tend to be more prominent in dependent area

Frequently appears maximal in the posterior AV groove

Effusions in General
Short axis and apical views can help you determine the
circumferential nature
Definitions
Small effusions – as much as 1cm fo posterior echo-free
space with or without fluid accumulation elsewhere
 Definitions
Moderate – 1-2 cm of echo free space

Large – greater than 2cm of max separation

Different labs may have slightly different cut points for

definition
Effusions in General
May be localized or loculated rather than
circumferential

Not uncommon after cardiac surgery or trauma where

inflammation results in an unequal distribution of fluid
in the pericardial space
 Pericardial vs. Pleural Fluid
Left pleural effusions result in echo free space posterior
to the heart when pt is supine or left lateral
Can be confused with pericardial effusions
Recall pericardial reflections surround the pulmonary
veins – this tends to limit the potential space behind the
LA
Fluid appearing exclusively behind the LA more likely to
be pleural
Pericardial vs. Pleural Fluid
A more reliable distinguishing factor is location of fluid
filled space in relation to descending aorta

The pericardial reflection typicall anterior, so fluid

appearing posterior to the aorta likely to be pleural.
Fluid anterior likely pericardial

This, of course, is in the PLAX view

Cardiac Tamponade - Physiology
Normal intrapericardial pressure ranges from -5 to +5
cm H2O and fluctuates with respiration
Recall the constraining effect the pericardium has on
the combined volume of all 4 chambers
Respiratory variation in intrapericardial pressure results
in a “linked” variation in filling of the right & left
ventricles
Cardiac Tamponade - Inspiration
During inspiration, intrathoracic & intrapericardial
pressure decrease

Increased flow into right heart and decreased flow out

of pulmonary veins

Result is augmented RV filling and stroke volume with a

compensatory decrease in LV stroke volume in early
inspiration
Cardiac Tamponade - Expiration
Intrathoracic & intrapericardial pressure increase
Mild decrease in RV diastolic filling with
subsequent increase in LV filling
This cyclic variation of left & right ventricular
filling is sufficient to create mild changes in
stroke volume and BP with the respiratory cycle
Normal respiratory variation in stroke volume
results in no more than 10 mmHg decrease in
systemic arterial pressure with inspiration
Cardiac Tamponade - Physiology
Increased fluid  further increased intrapericardial
pressure affecting right heart filling

Overall effect is to limit total blood volume allowable

within the 4 chambers

This exaggerates the respiratoyr dependent ventricular

volume interaction
Cardiac Tamponade - Physiology
Intrapericardial pressure can equal or exceed
normal filling pressures of the heart – thus
becomes the determining factor for the passive
intracardiac pressures
 RA, LA, RV diastolic, PADP, PCWP

With elevation of intrapericardial pressure

above normal filling pressure, the diastolic
pressure in all 4 chambers equalizes and is
determined by the intrapericardial pressure 
the hallmark of tamponade
Echo Features of Tamponade
Always remember that tamponade is a clinical diagnosis

Echo findings may suggest a hemodynamic abnormality

that may be the substrate for tamponade, but echo
abnormalities alone do not establish the diagnosis
Echo Features of Tamponade
One of earliest features is swinging heart

Swinging is just a marker of large effusion

A large effusion is more likely than a small effusion to

be associated with intrapericardial pressure elevation –
so the swinging heart and pressure elevation is indirect
rather than direct evidence of elevated pressure
Echo Features of Tamponade
More specific signs of elevated intrapericardial pressure
and hemodynamic compromise:
 Diastolic RV outflow collapse
 Exaggerated RA collapse in atrial systole

Remember these are indirect evidence that peric

pressure is high and the substrate for tamponade is
likely present
Doppler Findings in Tamponade
Exaggerated phasic variation in flow can be documented
with doppler

Normally, peak velocity of mitral inflow varies by 15% or

more with respiration

Tricuspid inflow by 25% or more

Variation in peak velocity and VTI of aortic and

pulmonary flow profiles are typically less than 10%
Doppler Findings in Tamponade
With a hemodynamically significant effusion, respiratory
variation in filling is exaggerated above these thresholds

So, respiratory variation in outflow tract velocities and

VTI is likewise exaggerated

These doppler findings are the corollary to pulsus

paradoxus
Doppler Findings in Tamponade
Normally vena caval flow occurs in both systole
& diastole – nearly continuous
With elevated intrapericardial pressure, the
diastolic vena caval flow is truncated and most
of the flow occurs during ventricular systole
Hepatic vein flow may also reflect the
exaggerated respiratory phase dependency of
RV filling
These are confirmatory findings, not diagnostic
Doppler Findings in Tamponade
Some order to these findings
 Typically, the earliest feature to be noticed is exaggerated
respiratory variation of tricuspid inflow
 Exaggeration of mitral inflow is usually next
 Abnormal RA collapse typically occurs at lower levels of
intrapericardial pressure elevation than does RV outflow
tract collapse
 RV free wall collapse is seen only later in the development
of elevated pericardial pressures