Abstract
After a brief historical survey, the exptl. conditions under which shock is best studied and its criteria are discussed. The evidence for reduced venous return and decreased cardiac output is reviewed. Mechanisms which may initiate the reduction in venous return are carefully analyzed, and it is concluded that "the operation of none of the suggested mechanisms[long dash]arteriolar dilatation or constriction, capillary dilatation and changes in permeability, failure of a venopressor force[long dash]has been proved by existing experimental evidence. On the other hand, obvious loss of blood (hemorrhage) or plasma (e.g., in traumatic shock) remains a clearly demonstrated initiating factor in many types of shock." The author suggests that after a circulatory imbalance has been inaugurated by initiating factors, it still requires a precipitating mechanism (or agent) to convert it into a stage of irreversible circulatory failure. Possible precipitatory factors are discussed under the following headings: the time factor. ischemia, irretrievable capillary damage; cortico-adrenal influences; translocation of K; reduction of blood vol. to a critical minimum; default of compensatory or emergency mechanisms; vasomotor failure; myocardial depression; the problem of aortic adaptation. Finally the author''s conception of the sequence of dynamic events during hemorrhage and shock is given. There is a bibliography of 269 references. The review is unusually critical, and no particular hypothesis is favored. Discrepancies and gaps of information are emphasized. In a few instances the author has reassigned priority of ideas in accordance with exptl. evidence therefor.

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