Echocardiographic Evaluation of Pericardial Disease - Casecag.com

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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).
Avery EG/Pericardial Disease Page 3 of 10Table 1. General Categories of Pericardial PathologyCongenital Pericardial DefectsPericarditisPericardial EffusionPericardial TamponadePericardial MassesCongenital pericardial defects are rare and consist of partial or total absence of the pericardium and Mulibrey nanism, anautosomal recessive disorder, primarily found in the Finnish population that can lead to congestive heart failure in early adultlife and is partially characterized by the development of constrictive pericarditis in some affected individuals. TEE findings ofconstrictive pericarditis will be discussed in a later section. The significance of pericardial absence varies although appearsminor in that most of these patients are clinically asymptomatic (Table 2). One small observational study (n=10) reviewingthis disorder found that paroxysmal stabbing chest pain that mimicked coronary ischemia was the most common clinicalpresentation 8 . Individuals with congenital absence of the pericardium are at increased risk for additional congenitalabnormalities in that 30% of these patients will have some additional congenital pathology 3,23,24 .Table 2. Pathologic Characteristics of Forms of Pericardial AbsenceFormIncidence Clinical SignificanceTotal Bilateral Absence Rare Mostly asymptomaticPartial Left Absence 70% Increased risk for aortic dissection if augmented heart mobility;possible herniation or strangulation of heart structures throughthe defect with chest pain, shortness of breath, syncopePartial Right Absence 17% Increased risk for aortic dissection if augmented mobilityof the heart exists as a result of the defectOverall 0.01%Incidence values represent a percentage of the overall incidence of 0.01%.Echocardiographically, one may observe paradoxic ventricular septal motion, an exaggerated posterior left ventricular wall andpossibly the appearance of a dilated right ventricle when assessed through the transthoracic parasternal window. A small seriesof patients (n=8) from a Japanese group reported more marked alterations in venous return in the right heart (measured in thesuperior vena cava) than in the left heart (measured in the pulmonary veins) 9 . CXR and cardiac MRI are the two imagingmodalities that appear to be most useful in making the definitive diagnosis of congenital absence of the pericardium 9 .Pericarditis is an inflammation of the pericardium and can occur as the result of multiple pathologies. Pericarditis maypresent as either a chronic or acute process and is often associated with the development of a pericardial effusion. Clinically,one examines the patient suspected of having pericarditis for the presence of the classic triad of chest pain, ECG evidence ofpericarditis (e.g., diffuse ST segment elevations), and a pericardial rub on auscultation. Etiologies of pericarditis include thefollowing:• Infections (e.g., postviral, bacterial-especially tuberculosis)• Neoplastic (e.g., primary-mesothelioma or fibrosarcoma; secondary metastatic disease-melanoma, lymphoma, leukemia or directextension of a pulmonic or breast tumor)• Immune/Inflammatory (e.g., rheumatoid arthritis, systemic lupus erythematosus, scleroderma, acute rheumatic fever, dermatomyositis,Wegener’s granulomatosis, mixed collagen vascular disease; post-myocardial infarction (Dressler’s syndrome); uremia; postcardiacsurgery• Intracardiac-pericardial communications (e.g., chest trauma, post-interventional catheter procedures, postmyocardial ventricularrupture) 2 .Echocardiographically, one inspects the pericardium for evidence of thickening that appears as an increase in the brightness, orechogenicity of the ultrasound signal. Normal pericardial thickness is approximately 2-3 mm. M-mode analysis of a patientwith pericarditis will reveal multiple parallel ultrasound reflections and can be helpful to discern the thickened pericardium(Figure 3). Multiple echo windows should be obtained to verify the diffuse or localized nature of the pericarditis.Echocardiography lacks sufficient fidelity to consistently quantify the degree of pericarditis and thus carries an unreliablesensitivity and specificity for detecting this disorder compared to other imaging techniques (e.g, cardiac MRI or high resolution(64 slice) computed tomography).
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