  Blood clotting is an important physiological process to suppress bleeding
upon injury, but when it occurs inadvertently, it can cause thrombosis, which
can lead to life threatening conditions. Hence, understanding the microscopic
mechanistic factors for inadvertent, spontaneous blood clotting, in absence of
a vessel breach, can help in predicting and adverting such conditions. Here, we
present a minimal model -- reminiscent of the SIR model -- for the initiating
stage of spontaneous blood clotting, the collective activation of blood
platelets. This model predicts that in the presence of very small initial
activation signals, macroscopic activation of the platelet population requires
a sufficient degree of heterogeneity of platelet sensitivity. To propagate the
activation signal and achieve collective activation of the bulk platelet
population, it requires the presence of, possibly only few, hyper-sensitive
platelets, but also a sufficient proportion of platelets with intermediate, yet
higher-than-average sensitivity. A comparison with experimental results
demonstrates a qualitative agreement for high platelet signalling activity.
