Controlled transient hypercapnia: a novel approach for the treatment of delayed cerebral ischemia after subarachnoid hemorrhage?

Clinical article

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  • 1 Departments of Neurosurgery and
  • 2 Anaesthesia and Critical Care, University Hospital Wuerzburg, Wuerzburg, Germany
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Object

The authors undertook this study to investigate whether the physiological mechanism of cerebral blood flow (CBF) regulation by alteration of the arterial partial pressure of carbon dioxide (PaCO2) can be used to increase CBF after aneurysmal subarachnoid hemorrhage (aSAH).

Methods

In 6 mechanically ventilated patients with poor-grade aSAH, the PaCO2 was first decreased to 30 mm Hg by modification of the respiratory rate, then gradually increased to 40, 50 and 60 mm Hg for 15 minutes each setting. Thereafter, the respirator settings were returned to baseline parameters. Intracerebral CBF measurement and brain tissue oxygen saturation (StiO2), measured by near-infrared spectroscopy (NIRS), were the primary and secondary end points. Intracranial pressure (ICP) was controlled by external ventricular drainage.

Results

A total of 60 interventions were performed in 6 patients. CBF decreased to 77% of baseline at a PaCO2 of 30 mm Hg and increased to 98%, 124%, and 143% at PaCO2 values of 40, 50, and 60 mm Hg, respectively. Simultaneously, StiO2 decreased to 94%, then increased to 99%, 105%, and 111% of baseline. A slightly elevated delivery rate of cerebrospinal fluid was noticed under continuous drainage. ICP remained constant. After returning to baseline respirator settings, both CBF and StiO2 remained elevated and only gradually returned to pre-hypercapnia values without a rebound effect. None of the patients developed secondary cerebral infarction.

Conclusions

Gradual hypercapnia was well tolerated by poor-grade SAH patients. Both CBF and StiO2 reacted with a sustained elevation upon hypercapnia; this elevation outlasted the period of hypercapnia and only slowly returned to normal without a rebound effect. Elevations of ICP were well compensated by continuous CSF drainage. Hypercapnia may yield a therapeutic potential in this state of critical brain perfusion. Clinical trial registration no.: NCT01799525 (ClinicalTrials.gov).

Abbreviations used in this paper:aSAH = aneurysmal SAH; CBF = cerebral blood flow; DCI = delayed cerebral ischemia; ICP = intracranial pressure; NIRS = near-infrared spectroscopy; PaCO2 = arterial partial pressure of carbon dioxide; PaO2 = arterial partial pressure of oxygen; SAH = subarachnoid hemorrhage; StiO2 = brain tissue oxygen saturation; TCD = transcranial Doppler sonography.

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Contributor Notes

Address correspondence to: Thomas Westermaier, M.D., Department of Neurosurgery, University Hospital Wuerzburg, Josef-Schneider-Str. 11, 97080 Wuerzburg, Germany. email: westermaier.t@nch.uni-wuerzburg.de.

Please include this information when citing this paper: published online August 22, 2014; DOI: 10.3171/2014.7.JNS132611.

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