The cardiovascular response to burn injury

Severe burn injury has a profound and widespread effect on an individuals cardiovascular system. Early features include myocardial contractile dysfunction and increased vascular permeability. This progresses to a hyperdynamic/hypermetabolic state with oxygen consumption increasing by up to 200%. Animal studies have suggested that pro-inflammatory mediators may in part be responsible, with TNF alpha, nuclear factor-kappa B, p38 activated protein kinase, macrophage inhibitory factor and high mobility group box 1 all playing a role. Traditional markers of myocardial injury are often unreliable in the presence of severe burn injury, either being too non-specific or having uncertain clinical significance.The restoration of adequate organ perfusion without the development of significant peripheral oedema is one of the primary goals of cardiovascular resuscitation in the burn patient. Despite the use of resuscitation formulae and various methods of assessing cardiac output and perfusion to aid resuscitation, the burn patient is often over or under resuscitated. Over resuscitation has led to severe tissue oedema resulting in impaired tissue perfusion and complications including compartment syndromes in unburned limbs and abdominal compartment syndrome.Vasopressors have a role in supporting the circulation, particularly during septic episodes, although caution must be taken as progression of burn wound depth may occur. B-Blockers are being increasingly used to attenuate the hypermetabolic state in burn patients with some promising results, particularly in the paediatric population.This review will focus on the cardiovascular responses to burn injury and discuss early fluid resuscitation and pharmacological support.