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

Abstract

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).

The Association Between Spontaneous Hyperventilation, Delayed Cerebral Ischemia, and Poor Neurological Outcome in Patients with Subarachnoid Hemorrhage

“…In fact, induced hypercapnia has recently been proposed as an acute [35]. Unfortunately, in spontaneously breathing patients, therapeutic options are limited.…”

Multimodal MRI characterization of experimental subarachnoid hemorrhage

“…The relative hypointense MRV signals could arise from damages of the venous volume or decreased venous oxygen saturation. 5,56 The relative hypointense MRV signals could arise from increased venous volume or decreased venous oxygen saturation. 5,56 Given the venous blood T2* is likely much shorter than 14ms echo time used 57 , signals from the veins are likely invisible and any small changes in venous oxygen saturation is unlikely to significantly affect MRV signals.…”

Chronic Obstructive Pulmonary Disease and Stroke

“…Several studies suggested that routine oxygen delivery is associated with a small improvement in neurological recovery and a decrease in the frequency of episodes of desaturation (24)(25)(26)(27). On the other hand, recent studies suggested that hypoxia and hypercapnia, or hypercapnia alone, might provide neuroprotective effects (28,29).…”

“…It also decreases the number of nocturnal desaturations which may be one of the risk factor for seizures in stroke patients (26,27). But there is also data suggesting that hypoxia and hypercapnia, or hypercapnia alone, provides neuroprotective effects (28,29).…”