• DOI:10.1161/01.RES.61.5.659
• Corpus ID: 27991910

Group B Streptococcal Sepsis in the Piglet: Effects of Fluid Therapy on Venous Return, Organ Edema, and Organ Blood Flow

@article{Bressack1987GroupBS,
  title={Group B Streptococcal Sepsis in the Piglet: Effects of Fluid Therapy on Venous Return, Organ Edema, and Organ Blood Flow},
  author={Michael Bressack and Neil S Morton and John Hortop},
  journal={Circulation Research},
  year={1987},
  volume={61},
  pages={659–669}
}

• M. Bressack, N. Morton, J. Hortop
• Published 1 November 1987
• Medicine
• Circulation Research

We investigated the physiologic effects of normal saline versus 5% albuminated saline fluid resuscitation on 10-12-day-old piglets infected with group B streptococci for four hours. After intravenously receiving 1 ± 1010 bacteria/kg over 45 minutes, one group was untreated while the two fluid-treated groups received enough intravenous fluid to maintain the baseline cardiac output. An increase in the resistance to venous blood return was the major limitation to cardiac output. The resistance nearly quadrupled in the untreated piglets as shown by a 50% decrease in cardiac output with a nearly doubling of the driving pressure for venous return (mean circulatory pressure was normal and atrial pressures decreased by 70%). In both fluid-treated groups, resistance doubled as shown by an unchanged cardiac output with a doubling of the driving pressure (mean circulatory pressure increased by 50%) and atrial pressures remained at baseline). Blood volume was 9% below control in the untreated group and 13% above control in both fluid-treated groups. Much more crystalloid (155 ml/kg) than colloid (58 ml/kg) was necessary to maintain baseline cardiac output; this resulted in a 36% decrease in the plasma protein oncotic pressure of the former group and a 15% increase in the oncotic pressure of the latter group. Organ edema formation (ileum, pancreas, kidney, adrenal gland, lung) occurred only in the saline-treated animals. We conclude that increased resistance to venous return was the primary cause of shock in our model and that this can be effectively treated by giving enough intravenous fluid to elevate the mean circulatory pressure. However, if the plasma protein oncotic pressure is also lowered (saline group), organ edema results. (Circulation Research 1987;61:659-669)