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The Normal and Diseased Pericardium: Current Concepts of Pericardial Physiology, Diagnosis and Treatment

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The Normal and Diseased Pericardium: Current Concepts of Pericardial Physiology, Diagnosis and Treatment View metadata, citation and similar papers at core.ac.uk brought to you by CORE 240 J AM CaLL CARDIOL 1983;1:240--51 provided by Elsevier - Publisher Connector The Normal and Diseased Pericardium: Current Concepts of Pericardial Physiology, Diagnosis and Treatment DAVID H. SPOmCK, MD, DSc, FACC Worcesrer, Massachusetts The past quarter century has seen remarkable contri• tricular myocardial infarction has been demonstrated. butions to understanding the role of the pericardium in Constrictive pericarditis, and the currently more common health and disease and to diagnostic methods in the con• effusive-constrictive pericarditis, have been studied, in text of significant changes in the clinical spectrum of depth, clinically and hemodynamically. acute pericarditis, pericardial effusion and their seque• Cardiography in pericardial disease now includes M• lae. Anatomic studies have demonstrated pericardial ul• mode and two-dimensional echographic studies, ena• trastructure and its relation to function and delineated bling rapid diagnosis and further physiologic study in the pericardiallymphatics and their participation in in• cardiac tamponade and constriction . The four stages of flammation and tamponade. Physiologic investigations typical electrocardiographic evolution in acute pericar• have revealed the pericardium's mechanical, membra• ditis and atypical variants have been codified and char• nous and ligamentous functions and its role in ventrlc• acteristic PR segment deviations identified. The non• ular interaction, pericardiaI modification of cardiac re• etiologic role of acute pericarditis in arrhythmias has sponses during acute cardiocirculatory loading and effects been clarified in prospective clinical and postmortem on diastolic function (and, at high filling pressures, sys• investigations. Electric alternation has been elucidated tolic function), including reduction by pericardial fluid and its relation to cardiac " swinging" has been at least of true filling pressure-the myocardial transmural partly explained. Special roles now exist for contrast pressure. The diastolic mean pressure plateau and phasic roentgenography , computed tomography (especially for venoatrial pressure and flow during cardiac tamponade cysts) and radionuclide imaging. Clinical advances in per• have been further characterized and the mechanisms icardial disease include changes in the prevalence of es• producing pulsus paradoxus have been elucidated, in• tablished etiologies and identification of new etiologies, cluding the importance of inspiratory increase in right for example, immunopathic processes to explain recur• ventricular filling. A far reaching compensatory re• rent pericarditis and the post-injury (including postop• sponse to tamponade has been revealed, particularly ad• erative) pericardial syndromes. New forms of constric• renergic stimulation, and, over time, blood volume ex• tion-uremic, postoperative, radiation-have appeared pansion. Right heart tamponade and low pressure in increasing numbers. The pericardial rub has been tamponade have been identified and the importance of characterized and codified, confirming a typical three• the pericardium in the restrictive dynamics of right ven- component structure (with frequent exceptions). The pericardium has fascin ated physicians since antiquity Fowler <7-19). Guntheroth (20,21). Reddy (22), Friedm an (I), largely becau se pericardial syndromes produce a range (23-25) and a host of physiologists (26-38). Clinical and of often spectacular clinical and physiologic abnormalities laboratory investigations have clarified the hemodynamics and because the pericardium is susceptible to involvement and the noninvasive registration of pericardial diseases and by every kind of disease. The last quarter century has seen have delineated the function s of the normal pericardium in five major books on the pericardium and its disorders (2• facilitating cardiac action and chamber interaction s. Disease 6) and brilliant advances in elucidating pericardial dynam• may compromise pericardial function s and convert the per• ics, particularl y by cardiology groups led by Shabetai and icardium from the heart 's protector to its deadl y enem y. Because of space limitations I have necessarily con• From the Division of Cardiology. SI. Vincent Hospital and Universi ty densed this review of salient contributions of the past 25 of Massachu setts Medical School. Worcester , Massachu setts. years into a synthesis of state-of-the-science and state-of• Address for reprints: David H. Spodick . MD. DSc . Director of Car• diology. SI. Vincent Hospital. 25 Winthrop Street . Worcester. Massachu• the-art concepts and have largely excluded discussion of sett s 0 1604. experimental and clinical method ology. Recent work sup- 1;)1983 by the AmericanCollege of Cardiology 0735-1097/8310 I0240-12$03.00 NORMAL AND DISEASED PERICARDIUM J AM cou, CARDIOl 1983;1:240-5I 241 ports some and refutes other earlier studies; important ref• Table 1. Physiology of the Normal Pericardium erences more than 25 years old are found in reference 6. Mechanical Function: Promotion of Cardiac Efficiency. Especially Dur• ing Hemodynamic Overloads I. Relatively inelastic cardiac envelope Pericardial Anatomy A. Limitation of excessive acute dilation B. Protection against excessive ventriculoatrial regurgitation Ultrastructure C. Maintenance of normal ventricular compliance (volume-elas• Gross pericardial anatomy, including mesothelial. fibrous, ticity relation) elastic, vascular and lymphatic elements, is well understood; D. Defense of the integrity of the Starling curve: Starling mech• even "subgross" analysis, the dynamic orientation of fibers anism operates uniformly at all intraventricular pressures be• cause presence of pericardium: in the parietal pericardium, has been characterized (6). Fer• I. Maintains ventricular function curves rans et al. (39) and Roberts and Spray (40) recently reported ~ Limits effect of increased left ventricular end-diastolic ultrastructural details, including serosal cell microvilli, that pressure presumably bear friction and facilitate fluid and ion ex• 3. Supports output responses to change. Although oblique during diastole, these become a) venous inflow loads and atrioventricular valve regurgi• more perpendicular during systole. Despite a basal lamina, tation (especially acute) b) rate fluctuations pericardial mesothelial cells detach easily. Yet, during sys• 4. Hydrostatic system (pericardium plus pericardial fluid) tole, the visceral pericardial serosa becomes corrugated and distributes hydrostatic forces over epicardial surfaces the cells bulge and thicken. Indeed, the mesothelial cell a) Favors equality of transmural end-diastolic pressure monolayer has considerable overlap and marked interdigi• throughout ventricle. therefore uniform stretch of mus• tations between adjacent cells, a design that would permit cle fibers (preload) b) Constantly compensates for changes in gravitational changes in the surface configuration but maintain mechan• and inertial forces. distributing them evenly around the ical stability. Among the many cell constituents are actin heart filaments, involved in active change in cell shape, and cvto• E. Ventricular interaction; relative pericardial stiffness skeletal filaments, providing structural support. I. Reduces ventricular compliance with increased pressure in the opposite ventricle (e.g .. limits right ventricular stroke Significance ofPericardial Lymphatics work during increased impedance to left ventricular outflow) Miller et al. (41) extensi vely studied the cardiopericardial 2. Provides mutually restrictive chamber favoring balanced lymphatics. Myocardial lymph drains to the subepicardium output from right and left ventricles integrated over sev• and ultimately to the mediastinum and right heart cavities. eral cardiac cycles In heart failure, hydropericardium results from interference 3. Permits either ventricle to generate greater isovolumic by elevated central venous pressure with myocardial venous pressure from any volume and lymph drainage. Inflammations damage the visceral F. Maintenance of functionally optimal cardiac shape pericardium, also interfering with epicardial venous and II. Provision of closed chamber with slightly subatmospheric pres• sure in which: lymph flow, with loss of interstitial fluid from the myocar• A. The level of transmural cardiac pressures will be low. rela• dium to the pericardial space. Because most pericarditis with tive to even large increases in "filling pressures" referred to effusion probably is myopericarditis, all inflammatory ef• atmospheric pressures fusions may exude through the epicardial surface. B. Pressure changes aid atrial filling via more negative pericar• dial pressure during ventricular ejection III. "Feedback" cardiocirculatory regulation via pericardial servo• mechanisms Pericardial Physiology: A. Neuroreceptors (via vagus): lower heart rate and blood A Synthesis of Laboratory pressure and Clinical Observations B. Mechanoreceptors: lower blood pressure and contract spleen Table I presents a concept derived from experimental and IV. ?? Limitation of hypertrophy associated with chronic exercise Membranous Function: Shielding the Heart clinical observations (2-38,42)-a synopsis of the compli• I. Reduction of external friction due to heart movements cated roles of the pericardium and its components. These roles are divided into mechanical. membranous and liga• II. Barrier to inflammation from contiguous structures mentous functions
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