The pericardial sac typically has 15-30 ml fluid. Cardiac tamponade is caused by an increased amount of fluid in the pericardial sac, which compresses the heart. To a point, the body can adapt by increased adrenergic tone which in turn increases systemic venous pressure and heart rate. This increase in pressure prevents the heart chambers from collapsing. And the increased heart rate preserves cardiac output despite decreased stroke volume.
At some point in the accumulation of fluid (around 250-300 ml), the pericardium reaches maximal distension and results in a phenomenon called pulsus paradoxus. Basically, the two ventricles are competing for space within the pericardial sac, so any increase in right ventricular volume (increased venous return during inspiration) results in the interatrial/ventricular septae to bulge leftwards. The opposite happens during expiration. This can be observed on the blood pressure waveform (defined by a drop in systolic blood pressure exceeding 10 mm Hg during inspiration), and on echocardiography.
Cardiac tamponade is the classic cause of pulsus paradoxus, but it can also be seen from a PE or hypovolemic shock. Many cardiac tamponade patients exhibit the classic “Beck Triad”: low blood pressure, increased JVP, and distant heart sounds.
Anesthestic management for suspected cardiac tamponade could include arterial monitoring and CVP. Keep the heart “fast, full, and strong”. Minimize positive pressure ventilation, especially high-volumes. And avoid drugs that cause myocardial depression or bradycardia.