To elucidate the mechanism responsible for the occurrence of negative transmural atrial pressures in pericardial tamponade, saline or air was progressively injected into the pericardial sac. In 14 anesthetized, open-chest dogs, left atrial (LA), left ventricular (LV), and pericardial pressures (PP) were measured with catheter tip manometers. In beating and fibrillated hearts, measurements were carried out at normovolemia, hypovolemia and hypervolemia. Transmural atrial pressure (TAP = LA - PP) became negative when the PP reached 130 mm H 2 O whether the heart was beating or not. In normovolemia the relation between TAP and PP was: TAP (mm H 2 O) = 38.1--0.237PP--0.00042PP 2 . In anesthetized, closed-chest dogs, air inflation of pleural space produced pressures around the heart similar to those obtained in pericardial tamponade. With such pneumothorax, no negative TAP occurred either with beating or quiescent hearts. It is hypothesized that pericardial filling stiffens the pliable structures surrounding the heart and thereby diminishes the collapsibility of the atrial walls which form the inner part of the pericardial sac. Veins entering the atria through the filled pericardial sac are held open like the hole in an inflated inner tube. Through these mechanisms some cardiac filling is assured even with marked pericardial tamponade.