Pericardial effusion: haemodynamic spectrum.

H aemodynamic 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 curve 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. 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, the pressure rise is appreciably less. This is the tamponade usually encountered in medical clinics and wards, whereas acute tamponade is found in interventional cardiac laboratories, as a consequence of puncture of a cardiac chamber or a vessel, in trauma units to which victims of mediastinal injury are admitted, and in intensive care units where acute tamponade is a sequel to rupture of a myocardial infarction or aortic aneurysm. Because the pressure–volume relation is curved, compliance decreases with increasing volume. Even in ‘‘medical tamponade’’ pericardial pressure may rise to 30 mm Hg as fluid continues to accumulate faster than it can be absorbed. However, this elevation occurs at much greater volume of pericardial fluid compared with acute tamponade. The volume of effusion at which this development occurs depends on how quickly the effusion grows and may be anywhere between a few hundred millilitres to several litres. The therapeutic consequence of the different haemodynamics of acute versus chronic tamponade is that, in the former, removal of 100 ml of fluid can drop pericardial pressure dramatically and be life saving, whereas in the latter, considerably more fluid must be removed to attain comparable relief of tamponade. Between these extremes is a broad spectrum of pericardial volume and pressure. CLASSIC TAMPONADE Pericardial pressure, by definition, is elevated. The circulation adapts by increasing central systemic and pulmonary venous pressures to equal the pericardial pressure, thereby preventing total collapse of the cardiac chambers. Left and right ventricular diastolic, right atrial, and pulmonary wedge pressures all rise to equal the pressure in the pericardium, making atrial and ventricular diastolic transmural pressures essentially zero. This equalisation of pressures is the hallmark of tamponade. Stroke volume is reduced, but cardiac output is partially preserved by tachycardia, driven by increased adrenergic tone. The increased ventricular diastolic pressure mandates commensurate pulmonary hypertension to maintain pulmonary circulation. Pulmonary arterial systolic pressure seldom significantly exceeds 40 mm Hg. When the pericardium is tightly stretched, it becomes virtually inextensible. As a result, total pericardial volume is constant throughout the respiratory cycle. Any change in the volume of one side of the heart then causes the opposite change in volume of the other side, a phenomenon referred to as ventricular interaction or interdependence. The manifestations of this greatly enhanced ventricular interaction are pulsus paradoxus 5 and increased respiratory variation in the velocity of atrioventricular filling. Inspiration increases systemic venous return by the same mechanism as in normal physiology. The resulting increase in right heart volume can only occur by bulging the atrial and ventricular septa into the left atrium and ventricle. This redistribution of blood volume within the heart accompanying each respiratory cycle is the cause of decreased left ventricular stroke input and output and systemic arterial systolic pressure (pulsus paradoxus). Pulsus paradoxus can be palpated in the peripheral pulses, or measured by sphygmomanometry, or by cannulating a systemic artery. Respiratory changes in the pulmonary circulation are nearly 180 ̊out of phase with those in the systemic circulation as a consequence of ventricular interaction.