Cardiac problems associated with burns

Burns represent a major cause of accidental death in industrialized countries. Before the recognition of the key role of aggressive volume resuscitation in successful management, early mortality was common secondary to burn shock. Salvage of patients with major burns is optimized only if the pathophysiology of burn injury and the time course of hemodynamic derangements is understood. The effects of the neuroendocrine response to burning and the release of mediators from the burn wound on intravascular volume status, ventricular function, peripheral vascular tone, and metabolism must be addressed. In the early postburn period, crystalloid should be administered at a rate prescribed by any of several burn resuscitation formulas. The Parkland formula, providing 4 mL/kg/% burn over the first 24 hours, is the most widely used and has met with consistent success when used as a guideline for resuscitation over the early period of management. Colloid may be added to minimize resuscitation volumes and reduce edema once capillary endothelial competency has been restored. Ongoing resuscitation should be modified based on the clinical response of the patient, primarily the urine output, heart rate, and base deficit. In selected high-risk patients and in those failing resuscitation to clinical goals, invasive hemodynamic monitoring should be used to refine fluid management and identify those patients who may benefit from cardiotonic drugs. The potential contribution of carbon monoxide or cyanide intoxication to hemodynamic instability should be considered in all patients with a compatible history, including a history of inadequate response to treatment. With resolution of the phase of potential burn shock, the increased metabolic needs of the patient and the demands imposed by those needs on the cardiovascular system should be anticipated and supported.