IN BROAD terms, shock may be defined as a state in which cardiac output is insufficient to meet the normal nutritional needs of tissues. The shock syndrome may have a variety of initiating causes, but shock becomes progressive, not necessarily because the initial cause is becoming more severe, but because intrinsic changes in the animal deprived of adequate tissue blood supply tend to perpetuate circulatory deterioration. One of these intrinsic changes is associated with alterations in the rheologic properties of the blood.
Cardiogenic shock, a syndrome of progressive circulatory deterioration initiated by myocardial damage, is the most common clinical etiological factor associated with shock, and has a mortality approaching 80%.1 In common with other forms of shock, reduced venous return, low cardiac output, high peripheral resistance, and microcirculatory insufficiency are self-propagating. It is commonly held that there is something "different" about cardiogenic shock that removes it from other forms
BLOCH JH, PIERCE CH, MANAX WG, LYONS GW, LILLEHEI RC. Experimental Cardiogenic Shock: Effect of Low Molecular Weight Dextran. Arch Surg. 1965;91(1):77–85. doi:10.1001/archsurg.1965.01320130079011
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