Pathophysiology of Haemorrhagic Shock

Open Access
Publisher Website
Google Scholar
Abstract
The immediate effect of sudden blood loss is the activation of a variety of homeostatic responses. These include increased sympathetic activity and increased release or production of renin, angiotensin, anti-diuretic hormone, aldosterone, adrenocorticotrophic hormone, beta-endorphins, glucocorticoids, glucagon, erythropoeitin, 2-3 diphosphoglycerate, prostaglandins and complement. This may be followed by the release of many substances, some initially appropriate locally, and some the products of damaged cells, which may go on to cause both local and systemic damage. These include lysozomal enzymes, kinins, histamines, serotonin, lactic acid, free oxygen radicals, neutrophil proteases, fibrinogen degradation products, endotoxins, myocardial depressant polypeptides, and passive transferable lethal factor. The early and late effects on the cardiovascular and respiratory systems, and on the blood, brain, kidneys, gut, liver, pancreas, and on overall metabolism and cellular function, are considered in turn. Although an enormous research effort has increased our understanding of the pathophysiology of haemorrhagic shock, no special measures have yet been shown to influence morbidity or mortality in man. Management still hinges on the early recognition and treatment of bleeding, on general supportive measures, and on safeguarding each link in the oxygen delivery chain.