Pericardial and cardiac pressure.

ASSESSMENT OF pericardial pressure is beset with a number of conceptual and technical obstacles. One of the most formidable of these is that the clinical or experimental conditions under which a specific investigation is carried out strongly influence pericardial volume and the compliance of pericardium, myocardium, and the cardiac chambers. Of perhaps equal importance, operational conditions alter juxtapericardial pressure through alterations in pulmonary volume and transpulmonary pressure. Finally, comparison of results of different studies of pericardial pressure or restraint depends on knowledge of at what point on the pressurevolume relationship data have been obtained, and whether myocardial, pericardial, or juxtapericardial compliance dominated. The publication of a series of articles15 dealing with the concept of pericardial surface contact pressure therefore has important implications for normal pericardial physiology and the pathophysiology of acute and chronic cardiac enlargement, cardiac tamponade, and constrictive pericarditis. The concept that conventional measurement of pressure in a film of liquid between two serous membranes may give a falsely low estimate of the contact force between them originated in discussions of pleural mechanics.6 However, in 1960 Holt et al.7 measured pericardial pressure in dogs with the use of open-ended catheters and cylindrical and flat balloons filled with liquid. They, like subsequent investigators, found that a cylindrical balloon seriously overestimated pericardial pressure, whereas a flat balloon yielded a pericardial pressure slightly higher than the pressure measured directly from the end of a catheter. These investigators assumed that the true pressure was that yielded by the catheter, and introduced a correction factor for use by investigators employing flat balloons. When Holt et al. sequentially subjected dogs to acute hemorrhage and plethora they measured substantial changes in intrapericardial pressure without change in intrapleural pressure, and concluded that cardiac transmural pressure cannot be estimated from intrapleural pressure. This result emphasized that under all except the mostabnormal circumstances, true ventriculartransmural pressure is the difference between ventricular end-diastolic and pericardial end-diastolic pressure and does not usually exceed 2 or 3 mm Hg. This last observation takes measurement of intrapericardial pressure in experimental studies to the limit of accuracy, and beyond it in most clinical studies. This limitation explains why investigators tend to emphasize the extremes of hypovolemia and hypervolemia, thereby making specific and important observations, but at the risk of obscuring normal physiology. The argument for surface contact pressure as opposed to liquid pressure is that in normal cardiac chambers there must exist a static equilibrium whereby the pericardial pressure is equal to ventricular pressure minus ventricular transmural pressure. Liquid pressure is exerted in all directions, obeying Pascal's law, but surface pressure is the sum of liquid pressure and the force exerted by the heart and pericardium on each other. It is argued that the pericardial space is a potential one, because the film of normal pericardial liquid is too thin to separate the layers from one another; thus, introducing a catheter tip into the pericardial space creates an isolated area of artificial separation of the pericardial layers such that the catheter lumen is not in continuity with the pericardial liquid and yields an intrapericardial pressure too low to be meaningful. Unfortunately we lack an imaging technique that has