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Alteration of cardiopulmonary function after subarachnoid hemorrhage

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
figure1

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

Figure 2
figure2

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.

References

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    Isotani E, et al.: Alterations in plasma concentrations of natriuretic peptides and antidiuretic hormone after sub-arachnoid hemorrhage. Stroke 1994, 25: 2198-2203.

  2. 2.

    Isotani E, et al.: Impaired endothelium-dependent relaxation in rabbit pulmonary artery after subarachnoid hemorrhage. J Cardiovasc Pharmacol 1996, 28: 639-644. 10.1097/00005344-199611000-00005

  3. 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.2007.04.004

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Isotani, E., Otomo, Y. & Ohno, K. Alteration of cardiopulmonary function after subarachnoid hemorrhage. Crit Care 13, P99 (2009). https://doi.org/10.1186/cc7263

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Keywords

  • Catecholamine
  • Pulmonary Edema
  • Subarachnoid Hemorrhage
  • Catecholamine Release
  • Pulse Contour