Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2.
Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4+/-10.9 mm Hg. The baseline MABP and CPP were 90+/-20 and 84+/-19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9+/-7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5+/-7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7+/-11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2.
Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.
"The impact of nimodipine administration on Pbto 2 was studied in 11 patients with SAH. The investigators found that the Pbto 2 decreased significantly in 7 of 11 patients, and it persisted for up to 2 hours . Vasospasm has the potential to impact oxygen delivery to the brain. "
[Show abstract][Hide abstract] ABSTRACT: This article describes the potential application of brain tissue oxygen monitoring technology in the care of patients who have sustained traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH). To accomplish this objective, a review of the intracranial dynamics that are created by primary and secondary brain injury, and the challenges of optimizing oxygen delivery to the injured brain are presented. Furthermore, interventions that facilitate cerebral oxygen supply and reduce oxygen consumption are identified. Finally, application of this technology is highlighted by using case vignettes of patients who have TBI or SAH.
Critical Care Nursing Clinics of North America 07/2006; 18(2):243-56, xi. DOI:10.1016/j.ccell.2006.01.003 · 0.49 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Use of technology in the management of the severely brain-injured patient has increased over the past decade and can be confusing and overwhelming to the critical care nurse clinicians who are new to the field of neurology. This article will describe normal physiology and cerebral dynamics and potential abnormal physiology encountered after brain injury. The technology reviewed will include intracranial pressure monitoring, cerebral blood flow monitoring and autoregulation, cerebral oxygen consumption and tissue oxygen monitoring, metabolism, sedation, and temperature monitoring. Integration of appropriate technology into patient management will be discussed using a case study to explore the utility of information at the bedside. Recognizing the difficult task of trying to control secondary injury in our patients is the first step to better outcomes. Implementing the use of technology to mitigate the situation must be done with careful consideration and a team approach to achieve the greatest benefit for the patient.
AACN Clinical Issues Advanced Practice in Acute and Critical Care 10/2005; 16(4):501-14.
[Show abstract][Hide abstract] ABSTRACT: The cerebrovascular effects of nimodipine are stillpoorly understood even in the healthy condition; in par-ticular, its effects on tissue oxygenation have neverbeen investigated. The aim of the present study was to investigatechanges in cerebral oxygenation and blood volume up-on oral administration of nimodipine (90 mg) in thehealthy condition. In eight subjects, changes in cerebral tissue oxygena-tion and blood volume were determined simultaneous-ly with changes in blood velocity of the middle cerebralartery (VMCA) by using, respectively, near infrared spec-troscopy (NIRS) and transcranial Doppler ultrasonogra-phy (TCD). The subjects also underwent non-invasiveassessment of arterial blood pressure (ABP) and end-tidal CO2. TCD and NIRS CO2reactivity indices were al-so extracted. Nimodipine signiﬁcantly reduced ABP (11±13%) and in-creased heart rate, as well as NIRS oxygenation(6.0±4.8%) and blood volume indices (9.4±10.1%), whileVMCAwas not signiﬁcantly decreased (2.0±3.5%). Ni-modipine slightly but signiﬁcantly reduced the VMCAre-sponse to changes in pCO2whereas the CO2reactivityof NIRS parameters was improved. The observed changes in cerebral tissue oxygenationand blood volume indicate nimodipine-induced cere-brovascular dilation and increased perfusion, while theeffect on VMCApossibly results from dilation of the in-sonated artery. The present results cast doubt on theputative nimodipine-induced impairment of CO2reac-tivity.
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