Volume 13 Supplement 1

29th International Symposium on Intensive Care and Emergency Medicine

Open Access

Alteration of cardiopulmonary function after subarachnoid hemorrhage

  • E Isotani1,
  • Y Otomo1 and
  • K Ohno1
Critical Care200913(Suppl 1):P99

https://doi.org/10.1186/cc7263

Published: 13 March 2009

Introduction

Volume management is crucial in intensive care; however, in some patients it is very hard to achieve optimal water balance. The subarachnoid hemorrhage (SAH) patient is a representative example [13]. Cardiopulmonary complications are common after SAH: neurogenic pulmonary edema, cardiac failure, and so on. In this study we will present the time course of catecholamines and natriuretic polypeptides and fluid redistribution on pulse contour analysis calibrated by transpulmonary thermodilution PiCCO-plus monitoring after SAH.

Methods

Plasma catecholamines and natriuretic polypeptides of 54 consecutive patients were measured every other day during 2 weeks after SAH. The cardiopulmonary functions of 37 consecutive patients were monitored by PiCCO-plus daily during 2 weeks after SAH.

Results

Noradrenalin, dopamine and brain natriuretic polypeptide concentrations were significantly high during the entire study period. Intrathoracic blood volume was maintained in spite of systemic hypovolemia, and this fluid redistribution caused hydrostatic fluid retention in lung tissues on PiCCO-plus monitoring after SAH. See Figures 1 and 2.
Figure 1

Plasma catecholamine and natriuretic peptide concentrations after SAH. NOR, noradrenalin; DOA, dopamine.

Figure 2

PiCCO-plus monitoring after SAH. ELWI, extravascular lung water index; PVPI, pulmonary vascular permeability index; EVLW, extravascular lung water; PBV, pulmonary blood volume.

Conclusion

Persistent catecholamine release and the different sensitivity of blood vessels to catecholamine cause the blood volume redistribution: systemic hypovolemia and hydrostatic pulmonary edema. The excess cardiac preload due to catecholamine release leads to BNP release resulting in natriuresis.

Authors’ Affiliations

(1)
Tokyo Medical and Dental University

References

  1. Isotani E, et al.: Alterations in plasma concentrations of natriuretic peptides and antidiuretic hormone after sub-arachnoid hemorrhage. Stroke 1994, 25: 2198-2203.View ArticleGoogle Scholar
  2. Isotani E, et al.: Impaired endothelium-dependent relaxation in rabbit pulmonary artery after subarachnoid hemorrhage. J Cardiovasc Pharmacol 1996, 28: 639-644. 10.1097/00005344-199611000-00005View ArticleGoogle Scholar
  3. Kubota Y, et al.: Alterations of intracellular calcium concentration and nitric oxide generation in pulmonary artery endothelium after subarachnoid hemorrhage of the rabbit. Vasc Pharmacol 2007, 47: 90-98. 10.1016/j.vph.2007.04.004View ArticleGoogle Scholar

Copyright

© Isotani et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.

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