MULTI-TRAUMA CARDIAC-ARREST 3
diminished reflow can lead to obstinate ischemia and trivial infarction in some parts of the
brain (Zima, 2015, p. 167). The main source of the diminished reflow is cerebral micro-
vascular obstruction ascribed to intravascular thrombosis in the course of a cardiac arrest.
Away from the first reperfusion stage, various aspects can possibly inhibit delivery of
oxygen to the cerebral and cause secondary injuries in a span of hours to weeks after the
cardiac arrest event. The inhibitors comprise hypoxemia, hypotension elevated intracranial
pressure and brain oedema (Zima, 2015, p. 168). Transitory oedema in brain is observed after
resuscitation while delayed hyperaemia is responsible for delayed brain oedema.
The clinical indicators of multi-trauma cardiac arrest causing injury to brain include
seizures, coma, brain demise, neuro-cognitive dysfunction (Trzeciak, 2013, p. 130). Coma is
a state of unconsciousness of the brain areas accountable for awareness and arousal. Early
recovery of the brain could however constitute to a vegetative state, where only arousal and
sleep-wake phases preserved. Loss in coordination and movement may rise from damaged
motor associated centres in the cerebellum and cortex.
Myocardial dysfunction
Immediately after a prolonged resumption of spontaneous circulation, normal or
increased blood pressure and pulse rate can be as a result of a short-lived increment in
concentrations of circulating and local catecholamine (Morley, 2016, p. 67). Detection of
myocardial dysfunction occurrence can be detected within a few minutes of resumption of
circulation. However, prolonged depression of the ejection fraction can be reported over
weeks. The clinical evidence points to reversibility of the condition.
Systematic Ischemia
A multi-trauma cardiac arrest denotes the severest state of shock, as oxygen delivery
and metabolic material transport is instantly terminated and metabolites are also not ejected

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A cardiac arrest is the cessation of cardiac

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