Abstract
A variety of different patterns of deranged cardiovascular function can produce hypotension (1, 2, 5, 8, 9, 15, 16, 20). Consequently, quantitative determinations of the specific set of physiologic abnormalities responsible must influence the physician’s choice of a therapeutic program to support the failing circulation. In hypovolemic shock, produced either by hemorrhage or by a decrease in extra-cellular fluid secondary to a third space loss, appropriate replacement of the loss in circulatory volume is usually sufficient therapy and will generally result in an increase in both cardiac output and oxygen consumption reflecting an adequate peripheral perfusion (1, 6, 8, 9). However, in many patients the presence of occult myocardial failure compounded by the hypoxemia brought about by the low flow state, may make the use of a cardiac inotropic agent mandatory if cardiovascular competence is to be restored. An example of this is seen in the case demonstrated of an 83 year old male who presented with an acute gastrointestinal hemorrhage and a long history of chronic duodenal ulcer (Fig.1). The patient when first seen had profound hypotension, and a pulse rate of 120 beats per minute despite attempts at massive transfusion. Even though his cardiac index was only 0.82 liters/min/m2, the central venous pressure was noted to be elevated to 14 mm Hg.
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Siegel, J.H. (1970). The Recognition and Therapy of Patho-Physiologic Patterns in Human Shock. In: Bertelli, A., Back, N. (eds) Shock: Biochemical, Pharmacological, and Clinical Aspects. Advances in Experimental Medicine and Biology, vol 9. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3201-5_20
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DOI: https://doi.org/10.1007/978-1-4684-3201-5_20
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