George C. Kramer writes:
“Hemodynamic consequences of acute burns
The cause of reduced cardiac output during the resuscitative phase of burn injury has been the subject of considerable debate. There is an immediate depression of cardiac output before any detectable reduction in plasma volume. The rapidity of the response may result from impaired electrical activity of cardiac nerves and muscle and increased afterload due to vasoconstriction. Soon after injury developing hypovolemia and reduced venous return undeniably contribute to the reduced cardiac output. The subsequent persistence of reduced CO after apparently adequate fluid therapy, as evidenced by restoration of arterial blood pressure and urinary output, has been attributed to circulating myocardial depressant factor(s), which possibly originates from the burn wound. It was concluded that the depression of CO resulted not only from decreased blood volume and venous return, but also from and increased SVR and from the presence of a circulating myocardial depressant substance. After the resuscitation phase of burn shock, patients can have supranormal CO. This is associated with a hypermetabolic state and systemic inflammatory response syndrome (SIRS).”
Herndon, David N. "Pathophysiology of burn shock and burn edema" Total Burn Care. Fourth ed. Edinburgh: Saunders Elsevier, 2012. 110. Print.
