Two hypotheses on how tree mortality progresses are proposed in the literature: Manionís gradual decline and Bosselís sudden death hypotheses. Bossel already formulated a mechanism in his model, BAUMTOD, as the cause of sudden death phenomena. His model, however, cannot be used to generate a causal understanding to Manionís hypothesis. Therefore, a causal mechanism for the gradual decline pattern is suggested and incorporated in BAUMTOD; the modified model is called BAUMTOD-M. The suggested mechanism concerns the internal imbalance of respiration demand and available photosynthate supply. The eigenvalue elasticity analysis (EEA) is employed to study the likely structural causes behind tree mortality according to the two hypotheses. The analyses of both models suggest that, in stress-free conditions, a tree functions as an integrated organism. The analyses further suggest that the inability to supply respiration demand plays a crucial role at the onset of mortality. Differences in assumed mechanisms regarding the impact of this inability cause different paths to mortality in each model. This may mean either 1) Bosselís hypothesis is a special case of Manionís hypothesis or 2) there are truly different mechanisms at work in various observed mortality cases. More data and research is needed to clarify these points.