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Normal Pericardial Physiology
Nick Tehrani, MD
Normal Pericardial Physiology
Mechanical function (Theoretical):
Limits ventricular filling  affects chamber
compliance
More significant vis-à-vis RV than LV
Limits the extent of acute dilitation of the
ventricle
Even distribution of pressure over the
ventricles  Balancing RV/LV outputs
Normal Pericardial Physiology
Other functions of the Pericardium
Decreasing friction
Mechanical barrier to contiguous spread of
infection
Normal pericardium contains 20-30 cc of
lymphoid fluid
DDx of
Pericardial
Effusion
Pregnancy and pericardial effusion
PE can be seen in late pregnancy
Women with increased fluid retention more
commonly affected
Typically resolve spontaneously postpartum
Localization of Effusion
Increased pericardial fluid tends to collect
initially behind the posterior wall of the left
ventricle just distal to the A-V groove.
Readily visualized in the parasternal long
view in this position
2-D Diagnosis
Echolucent space
adjacent to the cardiac
structures
Effusions usually are
clear, diffuse and
symmetric in the
absence of prior
pericardial disease or
surgery
Pleural v.s. Pericardial Effusion
Fig 35-16
Normal M-Mode
Normal pericardium and
epicardium are in close
apposition and move in
unison
In systole this motion is
inward
In diastole this motion is
outward
Normal variant, slight
systolic separation of the
visceral and parietal layers
recorded on M-mode
Ab-Normal M-Mode
Persistance of
this separation
beyond the rapid
filling phase of
the LV is
suggestive of
abnormal
increase in
pericardial fluid
Post-CABG pericardial effusion
Seen in approximately 85% of patients
In 93% has peaked by the 10th post
operative day
Loculated effusion
Seen post CABG
Recurrent pericardial disease
Percutaneous drainage may not be possible
A small loculation in the right place can be
hemodynamically significant
Loculated effusion
Loculated effusion can be difficult to
assess in certain locations
Atrial region, where the effusion itself
may be mistaken for normal cardiac
chamber
Effect of positional change on
Pericardial Fluid Distribution
Moderate and large effusions are
redistributed toward the cardiac apex after
two minutes in the sitting position
This does not occur with smaller effusions, or
with loculated effusions
Documentation of apical shift may be
useful in demonstrating absence of
loculation
Loculated Hematomas
Localized pericardial hematoma may occur
after
CABG,
Cardiac laceration, or
Rupture
Post-op Loculated Hematomas
Post-op collection of blood is often localized
anterior and lateral to the RA free wall, but
may be found anywhere around the heart
Chamber compression is particularly common
when the hematomas abut the atria
Loculated Hematomas
The appearance of the
hematoma depends on the
extent of thrombus formation:
Echo free space
Highly reflective
intrapericardial mass
Loculated Hematomas
Thrombus
Other Findings simulating Peircardial
Effusion
Epicardial Fat
Mot pronounced in Older, ovese, diabetic
patinets, usually women.
Also commonly associated with steroids
Anterior Mediastimal Tumor
Most tend to be echodense
Peritoneal Fluid
Echo free space anterior to the heart
Midline appearance of the falciform
ligament bisects the echo-free space
Fibrinous stranding
Fibrinous stranding within the
fluid and on the epicardial
surface of the heart may
be seen with
Longstanding or
recurrent pericardial
disease, and
Malignancy
Nodularity, and
Extension into the
myocardium
Overview
Pericardial effusion
Tamponade
Definition
TAMPONADE Physiology
Impairment of diastolic filling of the LV
during inspiration, caused by
abnormally elevated intrapericardial
pressure.
Definition
TAMPONADE
Clinical syndrome, defined by a host of
bedside findings, and
Echocardiographic signs may precede the
clinical manifestations.
Breakdown: TAMPONADE Physiology
Decreased expansion of the cardiac chambers
due to elevated pericardial pressure.
Increased venous return to the right side with
inspiration.
This increased return necessarily compromises
diastolic filling of the LV during inspiration.
M-Mode: TAMPONADE Physiology
Spectrum of Tamponade Physiology
Normal Pericardial Physiology
Normal pericardial pressure is subatmospheric, i.e.,
negative throughout the cardiac cycle
Transmural pressure across any cardiac chamber:
(Intracavitary pressure) - (Intrapericardial pressure)
Normally Transmural pressure > 0 at all times
Tamponade Physiology
With increasing intrapericardial pressure, i.e.,
negative  positive
(Intracavitary pressure)<
- (Intrapericardial pressure)
local transmural
transmural
cavity collapse occurs when local
gradient becomes
becomes negative
negative
gradient
Tamponade Physiology
Filling pressure elevation is a compensatory
mechanism to maintain cardiac output
In fully developed tamponade
Diastolic pressure in all four chambers is
elevated, and
Equalized
Tamponade Physiology
Lower Pressure chambers (ATRIA)
Affected Before
Higher pressure chambers (VENTRICLES)
Tamponade Physiology
The compressive effects of the pericardial
pressure is most prominent during the phase
of the cardiac cycle when the pressure of the
chamber in question is the lowest.
Ventricles  Early Diastole
Atria  Systole
?
RA Compression
Weyman
(Pg.1122)
RA Inversion
Begins in late
diastole
Continues
into
ventricular
systole for
variable
period before
normalizing
RA Compression
Feigenbaum
pg.561
“The most common finding [of tamponade] is
diastolic invagination of the Rt. Ventricular and/or
Rt. Atrial wall during diastole.”
RA Compression
RA inversion
Extremely sensitive sign of clinical
tamponade
Specificity only 50%
Correlation with likelihood of tamponade:
Extent of inversion
NO
Duration of inversion
YES
RA inversion lasting > 1/3 of the cycle has a
specificity of 100% and Sensitivity of 94% for
clinical tampnade
2-D Features of Tamponade
The longer the duration of RA
inversion the higher the
probability of tampodane
Inversion > 1/3 of systole
94% Sensitive
100% Specific
RA free wall is a thin flexible
structure  brief inversion can
occur without Tamponade.
RV Compression
No controversy as to
the exact timing of RV
free wall inversion
Early diastole
May be transient
OR
May persist throughout
diastole.
RV diastolic collapse
Occurs when:
Intrapericardial pressure
> RV pressure
RV Diastolic Collapse (RVDC)
Also affected by:
Intravascular volume
Low pressure tamponade
RV Pressure
RVH and PHTN => RVDC at higher pressures
Chamber compliance
RV: Ischemia, Trauma, Post CABG adhesions
LV : Ditto

LV less compliant => shape alteration is minimal
compared to Atria or RV despite pressure equalization
RV Inversion
RV inversion preceeds the onset of clinical
tamponade
Significant Drop in MAP
Onset of Pulsus
Continued increase in intrapericardial
pressure 
Increasing prominence of RV inversion
In severe tamponade RV inversion persists
throughout diastole
Rate of PE Accumulation also affects
Tamponade Physiology
Volume of the fluid
Rate of accumulation
Slowly accumulating
>1Li
Rapid accumulation
of 50-100 cc
Doppler Findings
Percent change in Doppler Flow Velocity with Inspiration