Normal Pericardial Physiology

Nick Tehrani, MD

Normal Pericardial Physiology

Mechanical function (Theoretical):
Limits ventricular filling affects
chamber compliance
More significant vis--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 Mmode

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)

<

cavity collapse occurs when local transmural

local transmural
gradient becomes negative

gradient becomes negative

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