Echocardiographic Evaluation of Pericardial Disease - Casecag.com

Avery EG/Pericardial Disease Page 2 of 10respiratory cycle demonstrating pressures of approximately –6 mm Hg at end inspiration and –3 mm Hg at end expiration(NB – as measured by a fluid filled, non-balloon tipped catheter). It is the lowering of intrathoracic and pericardial pressureduring inspiration that permits increased filling of the right-sided chambers in that venous return is augmented. The truefilling pressure of the heart is determined by transmural pressure which is calculated by subtracting the pericardial pressurefrom the intracardiac pressure. For example, in a spontaneously breathing patient with a right atrial (RA) pressure of 6mmHg and a pericardial pressure of – 6 mmHg the actual filling pressure is 6 – (-6) = 12 mmHg, during inspiration. Thesame inspiratory negative intrapleural pressures create a pooling of the increased right ventricular (RV) output in thepulmonary circulation which reduces left atrial (LA) pulmonary venous return. The decrease in LA return results in adecrease in left ventricular (LV) stroke volume and output. Additionally, the decrease in intrathoracic pressure duringspontaneous inspiration relative to higher extrathoracic systemic arterial pressures may contribute to a decrease in left heartoutput 4,6 . Measurable Doppler changes in the transatrioventricular valvular velocities accompany these intrapericardialpressure dynamics. During the inspiratory phase of spontaneous respiration normal transtricuspid velocities increase byapproximately 20% inspiration (Figure 2a). Transmitral velocities normally decrease by approximately 10% duringspontaneous inspiration (Figure 2b) 1 . Intermittent positive pressure ventilation (IPPV) will produce opposite changes invelocities (Figures 2c-d) 7 . The increase in intrathoracic pressures relative to extrathoracic systemic pressures during IPPVinspiration favors an increase in left heart output. Additionally, the increased intrathoracic pressures during IPPV inspirationexpels blood from the pulmonary veins into the LA and thus augments left heart filling and output 4 . The changes oftransatrioventricular valvular velocities have been termed respirophasic variation.Figure 2a – Spontaneous Respiration: Transtricuspid Figure 2b – Spontaneous Respiration: TransmitralFigure 2c – IPPV: TranstricuspidFigure 2d – IPPV: TransmitralThe absolute values of these velocities are affected by several physiologic variables that include age, heart rate, rhythm,preload, volume flow rate, ventricular systolic function, diastolic function and atrial contractile function. The transmissionof intrathoracic pressures to the intrapericardial structures appears blunted in patients with certain pericardial pathologies(e.g., pericarditis or pericardial effusions severe enough to elicit tamponade physiology 7 ).Figure 2e – IPPV: Transmitral, volume depletedNote that under conditions of intravascular volume depletion that an alternative profile of transmitral velocity has beendescribed in an animal model. In one report using a canine model 45% of the observed transmitral profiles revealed a slightdecrease in maximal amplitude during IPPV inspiration that even further decreased during expiration and eventually reacheda nadir during expiration (Figure 2e). The author’s attributed the observation of this pattern to intravascular volumedepletion which was manifest as a direct result of reduced pulmonary venous vascular reserve 7 .III. PERICARDIAL PATHOLOGYEchocardiographic evaluation of pericardial disease is performed to rule out specific pathologies that can affect myocardialfunction. There are five basic categories of pericardial pathology that one must consider (Table 1).