Vascular disease A series of events lasting for hrs to several days after an initial ischemic event that results in extensive necrosis and tissue damage beyond the tissue zone first affected by the initial lack of blood flow
Management of acute Stroke: Techniques that are used to minimize the injury to the brain in the event of an ischemic insult can be thought of as having three broad purposes: to increase the supply of oxygen to the injured tissue, to reduce the metabolic demands, or to affect specific pathways in the ischemic cascade to reduce the production of unwanted metabolites.
Known as an ischemic cascade, this drop-off of oxygen results in a sudden crush of metabolic waste that damages cell membranes as well as the mitochondria, a part of the cell that generates chemical energy and is involved in cell growth and death.
Intensive basic scientific research during the last two decades has given healthcare professionals an increased understanding of the ischemic cascade in the format of the precise environmental alterations involved in the pathophysiology of ischemic injury at the cellular level.
The impact of systemic blood pressure and subsidiary maintenance of cerebral perfusion pressure are basic elements of stroke pathophysiology, yet colossal research efforts have been diverted toward the more elusive goal of identifying critical molecular targets in the ischemic cascade.
Decreased blood flow to the brain deprives the brain of oxygen, triggering the ischemic cascade that includes calcium influx, overstimulation of excitatory amino acids, and overproduction of free radicals.