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Changes in cardiac physiology after severe burn injury.

Authors
  • Williams, Felicia N
  • Herndon, David N
  • Suman, Oscar E
  • Lee, Jong O
  • Norbury, William B
  • Branski, Ludwik K
  • Mlcak, Ronald P
  • Jeschke, Marc G
Type
Published Article
Journal
Journal of burn care & research : official publication of the American Burn Association
Publication Date
Jan 01, 2011
Volume
32
Issue
2
Pages
269–274
Identifiers
DOI: 10.1097/BCR.0b013e31820aafcf
PMID: 21228708
Source
Medline
License
Unknown

Abstract

Cardiac stress, mediated by increased catecholamines, is the hallmark of severe burn injury typified by marked tachycardia, increased myocardial oxygen consumption, and increased cardiac output (CO). It remains one of the main determinants of survival in large burns. Currently, it is unknown for how long cardiac stress persists after a severe injury. Therefore, the aim of this study was to determine the extent and duration of cardiac stress after a severe burn. To determine persistence of cardiac alteration, the authors determined cardiac parameters of all surviving patients with burns ≥ 40% TBSA from 1998 to 2008. One hundred ninety-four patients were included in this study. Heart rate, mean arterial pressure, CO, stroke volume, cardiac index, and ejection fractions were measured at regular intervals from admission up to 2 years after injury. Rate pressure product was calculated as a correlate of myocardial oxygen consumption. All values were compared with normal nonburned children to validate the findings. Statistical analysis was performed using log transformed analysis of variance with Bonferroni correction and Student's t-test, where applicable. Heart rate, CO, cardiac index, and rate pressure product remained significantly increased in burned children for up to 2 years when compared with normal ranges (P < .05), indicating vastly increased cardiac stress. Ejection fraction was within normal limits for 2 years. Cardiac stress persists for at least 2 years postburn, and the authors suggest that attenuation of these detrimental responses may improve long-term morbidity.

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