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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