Experiments in dogs have shown that for brown snake (Pseudonaja) envenoming, there can be a brief period of true coagulation, with thrombus formation, as the venom first reaches the circulation and before fibrinolysis is activated (Tibballs et al., 1991 and Tibballs et al., 1992). The resultant thrombi can occlude critical vessels, notably coronary vessels, resulting in cardiac arrythmias and arrest. These thrombi are quickly destroyed once fibrinolysis activates, but even a few minutes of such thrombotic complications can be devastating for the victim. It is likely that this brief thrombotic window is the cause of the well documented cases of early cardiac collapse following brown snake bite, unhappily a cause of fatalities which no amount of antivenom can prevent, because this is generally a pre-hospital phenomenon (White, 2000). Potentially, of course, if injected intravenously, most procoagulant venoms could cause a cardiac catastrophe, as was shown many years ago for tiger snake (Notechis) venom, with massive coagulation of blood in the heart causing immediate and irremediable cardiac standstill in animals as large as sheep