Alteration of cardiopulmonary function after subarachnoid hemorrhage
© Isotani et al; licensee BioMed Central Ltd. 2009
Published: 13 March 2009
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 [1–3]. 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.
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.
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.
- 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
- 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
- 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
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