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Haemodynamic abnormalities, caused by pericardial effusion, range from undetectable or mild, to life threatening, depending on the determinants discussed below. These include the rate at which the effusion accumulates and whether or not the pericardium is scarred and thus adds an element of constrictive pericarditis. Pericardial adhesions or organisation of the fluid can result in localised, and thus atypical, tamponade. Pericardial effusion is the cause of a number of distinct clinical and haemodynamic syndromes.
Fundamental to understanding their pathophysiology are the biomechanical properties of the pericardium. The pressure–volume relation of normal pericardium, after an initial short shallow portion that allows the pericardium to stretch slightly in response to physiological events, such as changes in posture or volume status, shows a minimal increase in pericardial pressure. Thereafter, the pressure increase is extremely steep. This J shaped curve1 indicates that a sudden increase in the volume of pericardial fluid can slightly stretch the pericardium, and thus an increase of as little as 100 or 200 ml may elevate pericardial pressure from its normal ambient, or slightly sub-ambient value, to 30 mm Hg or more, defining severe cardiac tamponade.
At the other extreme, a pericardial effusion developing over several weeks or months may reach a volume measured in litres accompanied by a considerably more modest increase in pericardial pressure.2 The explanation for this difference is that the response of the pericardium to gradual stretch differs from its response to acute stretch. A slower accumulation of pericardial fluid causes pericardial compliance to increase; its pressure–volume curve is shifted to the right and the slope of the steep portion is greatly reduced, such that for a given increment in volume, …
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