FOR MANY YEARS the heart has been implicated as an important factor in the production of irreversible shock. In 1942 Wiggers and Werle1 noticed that during the terminal stages of hemorrhagic shock effective atrial pressure rose while arterial pressure fell. This was interpreted as signifying myocardial insufficiency. Kondo and Katz in 1945 produced shock by venous occlusion of the hind limbs and found a consistent decline in heart size which was explained as the result of diminution in venous return.2 In 1944, Kohlstaedt and Page noticed that after an initial diminution in the size of the heart, progressive bleeding led to an increase in both the systolic and diastolic size of the heart.3 Apparently, the stroke volume was diminished, while the residual volume of the heart increased. Wiggers in extensive studies on hemorrhagic shock concluded that deterioration of myocardial expulsive power contributed to the progressive circulatory failure
Bing RJ, Ramos H. The Role of the Heart in Shock. JAMA. 1962;181(10):871–873. doi:10.1001/jama.1962.03050360057011
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