The acute phase lasts about 48 h and is followed by a
hypermetabolic phase characterized by increased blood
flow to the tissues and organs and increased internal core
temperature. During the hypermetabolic phase rapid
edema formation occurs and this has been attributed to
hypoproteinemia, which favors the outward movement of
water from the capillary to the interstitium. Secondly, an
increase in the water permeability of the interstitial space
is evident, which further increases edema formation (29).
Patients with acute burn injuries develop a
hypermetabolic state with associated catecholamine
production and release. Increased adrenergic stimulation
is one of the triggers of myocardial infarction and cardiac
arrhythmias. In burn patients, end-diastolic volume
indices increase while right ventricular ejection fractions
decrease, which strongly indicate myocardial dysfunction
(30). Cardiac instability in burned patients is associated
with hypovolemia, increased afterload and direct
myocardial depression. Additionally, the
hyperaggregability, hypercoagulability, and impaired
fibrinolysis resulting from any acute injury may
predispose to myocardial infarction
The acute phase lasts about 48 h and is followed by ahypermetabolic phase characterized by increased bloodflow to the tissues and organs and increased internal coretemperature. During the hypermetabolic phase rapidedema formation occurs and this has been attributed tohypoproteinemia, which favors the outward movement ofwater from the capillary to the interstitium. Secondly, anincrease in the water permeability of the interstitial spaceis evident, which further increases edema formation (29).Patients with acute burn injuries develop ahypermetabolic state with associated catecholamineproduction and release. Increased adrenergic stimulationis one of the triggers of myocardial infarction and cardiacarrhythmias. In burn patients, end-diastolic volumeindices increase while right ventricular ejection fractionsdecrease, which strongly indicate myocardial dysfunction(30). Cardiac instability in burned patients is associatedwith hypovolemia, increased afterload and directmyocardial depression. Additionally, thehyperaggregability, hypercoagulability, and impairedfibrinolysis resulting from any acute injury maypredispose to myocardial infarction
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