![]() ![]() The early (ebb) phase of burn injury is characterized by decreased cardiac output and decreased blood flow to all organs. Pathophysiologic changes in the early phase (24–48 h) of burn injury. ![]() 3, 4 Elderly patients may not exhibit signs of the hyperdynamic state, but protein catabolism is ubiquitous. The onset of sepsis further increases the cardiac output and decreases systemic vascular resistance. 3, 4 Pari Passu with the hypermetabolism is the hyperdynamic phase evidenced by supranormal cardiac output (often more than two to three times normal), tachycardia, and decreased systemic vascular resistance ( fig. 2 The hypermetabolic and hyperdynamic phase that develops over 48 to 72 h after injury is characterized by increased oxygen consumption, carbon dioxide production, and protein wasting. The depressed cardiac output continues for 24 to 36 h. Depression of cardiac output occurs even before any detectable reduction in plasma volume. Burn shock occurs not only because of depletion of intravascular volume but also because of increased systemic vascular resistance (due to release of catecholamines, antidiuretic hormone, and hemoconcentration) and depressed cardiac output ( fig. Thus, the initial therapeutic goal is the repletion of intravascular volume with clear fluids to preserve tissue perfusion and minimize the ischemia and inflammatory responses. In contrast to nonburn trauma, burn-induced fluid loss occurs in the absence of marked red cell volume loss resulting in hemoconcentration rather than anemia. Loss of intravascular fluid into burned areas and edema formation (in nonburned sites) can quickly result in burn shock with impaired tissue and organ perfusion. After major burn injury, continued loss of plasma into burned tissue can occur up to the first 48 h or even longer. Generalized edema even in noninjured tissues occurs when the injury exceeds 25 to 30% total body surface area (TBSA). Operating room concerns for the burn-injured patient include airway abnormalities, impaired lung function, vascular access, deceptively large and rapid blood loss, hypothermia, and altered pharmacology. Burn injury is associated basal and procedural pain requiring higher than normal opioid and sedative doses. Formulae for fluid resuscitation should serve only as guideline fluids should be titrated to physiologic endpoints. Electrical burns result in morbidity much higher than expected based on burn size alone. Approximately 2 to 5 days after major burn injury, a hyperdynamic and hypermetabolic state develops. Hemodynamics in the early phase of severe burn injury is characterized by a reduction in cardiac output and increased systemic and pulmonary vascular resistance. Massive airway and/or lung edema can occur rapidly and unpredictably after burn and/or inhalation injury. It does not store any personal data.Care of burn-injured patients requires knowledge of the pathophysiologic changes affecting virtually all organs from the onset of injury until wounds are healed. The cookie is set by the GDPR Cookie Consent plugin and is used to store whether or not user has consented to the use of cookies. The cookie is used to store the user consent for the cookies in the category "Performance". This cookie is set by GDPR Cookie Consent plugin. The cookie is used to store the user consent for the cookies in the category "Other. The cookies is used to store the user consent for the cookies in the category "Necessary". The cookie is set by GDPR cookie consent to record the user consent for the cookies in the category "Functional". The cookie is used to store the user consent for the cookies in the category "Analytics". These cookies ensure basic functionalities and security features of the website, anonymously. ![]() Necessary cookies are absolutely essential for the website to function properly. ![]()
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