 |
|
Experimental Cardiogenic ShockEffect of Low Molecular Weight Dextran
JACK H. BLOCH, MD;
CHARLES H. PIERCE, MSc;
WILLIAM G. MANAX, MD;
GARY W. LYONS, MD;
RICHARD C. LILLEHEI, MD, PhD
AMA Arch Surg. 1965;91(1):77-85.
|
|
| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
|
|
|
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
. . . [Full Text PDF of this Article]
Author Affiliations
MINNEAPOLIS
From the Department of Surgery, University of Minnesota Medical School. National Institutes of Health Postdoctoral Fellow, National Heart Institute (Dr. Bloch); Markle Scholar in Academic Medicine and Associate Professor of Surgery (Dr. Lillehei).
Footnotes
Read before the 22nd Annual Meeting of the Central Surgical Association, Milwaukee, March 4-5, 1965.
Reprint requests to Minneapolis 55455 (Dr. Bloch).
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter
What's this?
|
