Normal Pericardial Physiology

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Normal Pericardial Physiology

• Nick Tehrani, MD

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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

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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

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• DDx of Pericardial Effusion

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Pregnancy and pericardial effusion

• PE can be seen in late pregnancy
• Women with increased fluid retention more
  commonly affected
• Typically resolve spontaneously post-partum

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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

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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

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Pleural v.s. Pericardial Effusion

• Fig 35-16

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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

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Ab-Normal M-Mode

• Persistance of this separation beyond the rapid
  filling phase of the LV is suggestive of abnormal
  increase in pericardial fluid

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Post-CABG pericardial effusion

• Seen in approximately 85 of patients
• In 93 has peaked by the 10th post operative day

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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

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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

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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

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Loculated Hematomas

• Localized pericardial hematoma may occur after
• CABG,
• Cardiac laceration, or
• Rupture

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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

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Loculated Hematomas

• The appearance of the hematoma depends on the
  extent of thrombus formation

Echo free space
Highly reflective intrapericardial mass
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Loculated Hematomas

• Thrombus

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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

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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

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Overview

• Pericardial effusion
• Tamponade

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Definition

• TAMPONADE Physiology
• Impairment of diastolic filling of the LV during
  inspiration, caused by abnormally elevated
  intrapericardial pressure.

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Definition

• TAMPONADE
• Clinical syndrome, defined by a host of bedside
  findings, and
• Echocardiographic signs may precede the clinical
  manifestations.

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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.

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M-Mode TAMPONADE Physiology
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Spectrum of Tamponade Physiology
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Normal Pericardial Physiology

• Normal pericardial pressure is subatmospheric,
  i.e., negative throughout the cardiac cycle
• Normally Transmural pressure gt 0 at all times

• Transmural pressure across any cardiac chamber
• (Intracavitary pressure) - (Intrapericardial
  pressure)

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Tamponade Physiology

• With increasing intrapericardial pressure, i.e.,
• negative ? positive
• (Intracavitary pressure) - (Intrapericardial
  pressure)
• cavity collapse occurs when local transmural
  gradient becomes negative

lt
local transmural
gradient becomes negative
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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

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Tamponade Physiology

• Lower Pressure chambers (ATRIA)
• Affected Before
• Higher pressure chambers (VENTRICLES)

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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

?
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RA Compression

• Weyman (Pg.1122)
• RA Inversion
• Begins in late diastole
• Continues into ventricular systole for variable
  period before normalizing

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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.

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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 gt 1/3 of the cycle has a
  specificity of 100 and Sensitivity of 94 for
  clinical tampnade

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2-D Features of Tamponade

• The longer the duration of RA inversion the
  higher the probability of tampodane
• Inversion gt 1/3 of systole
• 94 Sensitive
• 100 Specific
• RA free wall is a thin flexible structure ? brief
  inversion can occur without Tamponade.

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RV Compression

• No controversy as to the exact timing of RV free
  wall inversion
• Early diastole
• May be transient
• OR
• May persist throughout diastole.

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RV diastolic collapse

• Occurs when
• Intrapericardial pressure gt RV pressure

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RV Diastolic Collapse (RVDC)

• Also affected by
• Intravascular volume
• Low pressure tamponade
• RV Pressure
• RVH and PHTN gt RVDC at higher pressures
• Chamber compliance
• RV Ischemia, Trauma, Post CABG adhesions
• LV Ditto
• LV less compliant gt shape alteration is minimal
  compared to Atria or RV despite pressure
  equalization

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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

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Rate of PE Accumulation also affects Tamponade
Physiology

• Volume of the fluid
• Rate of accumulation
• Slowly accumulating gt1Li
• Rapid accumulation of 50-100 cc

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Doppler Findings
Percent change in Doppler Flow Velocity with
Inspiration