Assessment and treatment of central nervous system abnormalities in the emergency patient (original) (raw)
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Circulatory effects of moderately and severely increased intracranial pressure in the dog
Journal of Neurosurgery, 1972
✓ Anesthetized dogs were subjected to elevated intracranial pressure (ICP) of 60 and 100 mm Hg. At 60 mm Hg, decreases in heart rate and arterial blood pressure were observed associated with an increase in femoral blood flow that suggested vasodilation in the somatic areas. Cardiac output showed little change. Subsequent elevation of ICP to 100 mm Hg was followed by an increase in arterial blood pressure; cardiac output increased, and femoral flow increased still further. Since resistance to flow did not change, the hypertension was thought to be due to an increase in flow rather than peripheral resistance. An increase in heart rate was associated with the elevation in cardiac output; the fact that femoral blood flow increased proportionately more than cardiac output suggested a redistribution of blood flow. The changes in peripheral blood flow and in cardiac output were associated with a decrease in the arteriovenous oxygen (A–VO2) difference. No signs of tissue hypoxia were observ...
Cerebral hemodynamics: concepts of clinical importance
Arquivos de Neuro-Psiquiatria, 2012
Cerebral hemodynamics and metabolism are frequently impaired in a wide range of neurological diseases, including traumatic brain injury and stroke, with several pathophysiological mechanisms of injury. The resultant uncoupling of cerebral blood flow and metabolism can trigger secondary brain lesions, particularly in early phases, consequently worsening the patient's outcome. Cerebral blood flow regulation is influenced by blood gas content, blood viscosity, body temperature, cardiac output, altitude, cerebrovascular autoregulation, and neurovascular coupling, mediated by chemical agents such as nitric oxide (NO), carbon monoxide (CO), eicosanoid products, oxygen-derived free radicals, endothelins, K+, H+, and adenosine. A better understanding of these factors is valuable for the management of neurocritical care patients. The assessment of both cerebral hemodynamics and metabolism in the acute phase of neurocritical care conditions may contribute to a more effective planning of t...
Background: Severe head injury is an important cause of disability and death. Despite the implementation of international consensus guidelines, the treatment of Traumatic Brain Injury (TBI) is sustained on global measures, bypassing the relevance of individualised therapies. In an era where "Big Data" consortiums emphasise the relevance of utilising multi-monitoring with the view of adjusting to individual patient's needs, still fundamental aspects of brain physiology such as cerebral perfusion and oxygen delivery, remain controversial. In the acute phase of TBI, multiple concomitant pathophysiological processes such as axonal tearing, cytogenic or vasogenic edema, impaired cerebral autoregulation and subsequent perfusion mismatch, xiv This project was initially registered on 28 March 2013 as a part-time PhD. Over the past four years, an intense series of surgical procedures took place at the Medical Engineering Research Facility within The Prince Charles Hospital campus to the completion of six experimental studies and the use of 45 animal models. The rhythm of work became so strategically important that it made me realise and value the assistance provided by many people around me. Among others, I would like to acknowledge and sincerely thank Sia Athanasas (research manager, Burns Trauma and Critical Care Research Centre; Faculty of Medicine, UQ). Sia has been a friend and a colleague. She has always contributed on my language editing, my grant applications, and financial statements and accounts. For me, Sia has been the human side of the UQ Research Centre. Her sincerity and warmth have made tough moments into pleasant and unforgettable ones. I also want to acknowledge the initial advisory support from Professor John Finnie (senior veterinary pathologist, University of Adelaide) regarding the ovine model management: specifically, the various brain fixation methods strategies and their downsides. During the two years following the completion of the last experimental study, the animal specimens were stored at the RBWH research laboratory, within the intensive care department. Our critical care research nurses and coordinators have been crucial in the maintenance and preservation of these specimens. We acknowledge their contribution to this project and thank them for the sparing space that our specimens took in our small laboratory. Capstone Editing provided copyediting and proofreading services, according to the guidelines laid out in the university-endorsed national 'Guidelines for Editing Research Theses'.
Cerebral hemodynamics, autoregulation, and blood pressure management
Journal of Stroke and Cerebrovascular Diseases, 1999
Despite a wealth of clinical research in acute stroke, physicians today do not know how to optimally manage blood pressure in these patients. 1 The major focus of clinical research in acute stroke is not, at present, on supportive care issues such as blood pressure, but rather on developing thrombolytic and neuroprotective treatments. Blood pressure (BP) changes in acute stroke are clinically important, 2 because autoregulation is impaired under these circumstances, and cerebral blood flow (CBF) is dependent on systemic BP. Initially, elevated BP in a stroke victim may be beneficial because it will increase blood flow to an ischemic penumbra, but if sustained, such hypertension may increase the likelihood of cerebral edema and hemorrhagic transformation. We review the state of our knowledge, experimental and clinical regarding cerebral hemodynamics, autoregulation, and blood pressure management in acute cerebral infarction and intracerebral hemorrhage. Cerebral Blood Flow Regulation of cerebral blood flow in a normal brain is determined by a variety of intrinsic control mechanisms. Despite wide variations in blood flow throughout the body, the brain extracts the amount of blood required for its tissue nutrition and for ensuring homeostasis. This process of autoregulation can be defined as the controlled pairing of CBF with metabolic demand. Autoregulation is accomplished through the complex interplay of a variety of mechanisms. These mechanisms include myogenic/ stretch, chemical metabolic, and neurogenic control.
Cerebrospinal Fluid Physiology and the Management of Increased Intracranial Pressure
Mayo Clinic Proceedings, 1990
Increased intracranial pressure can result in irreversible ii^jury to the central nervous system. Among the many functions of the cerebrospinal fluid, it provides protection against acute changes in venous and arterial blood pressure or impact pressure. Nevertheless, trauma, tiunors, infections, neurosurgical procedures, and other factors can cause increased intracranial pressure. Both siurgical and nonsur gical therapeutic modalities can be used in the management of increased intracranial pressure attributable to traumatic and nontraumatic causes. In patients with cerebral injury and increased intracranial pressure, monitoring of the intracranial pressure can provide an objective measure of the response to therapy and the pressure dynamics. Intraventricular, intraparenchymal, subarachnoid, and epidural sites can be used for monitoring, and the advantages and disadvantages of the varioiis devices available are discussed. With the proper understanding of the physiologic features of the cerebrospinal fluid, the physician can apply the management prin ciples reviewed herein to minimize damage from intracranial hsφerten8ion. An increase in intracranial pressure (ICP), also tension may also shift brain structures and cause termed intracranial hypertension, can result in herniation of brain tissue, irreversible injury to the central nervous sys-Because the skull is a rigid structure, an tem. ICP is considered normal when it is less increase in ICP will cause compression of inthan 10 mm Hg. When ICP increases above 20 tracranial contents. The intracranial contents mm Hg, neuronal injury may develop. The ma-can be categorized into three compartments: jor pathophysiologic problems associated with brain parenchyma, vascular tissue, and the cereincreased ICP are ischemia and herniation. As hrospinal fluid (CSF) of the ventricular and ICP approaches the level of the systolic blood subarachnoid spaces. An increase in any one pressure, cerebral perfusion pressure decreases, constituent as a result of trauma, ischemia, and the resultant failure of cerebrovascular space-occupying lesions, or metabolic causes will autoregulation (described in the subsequent result in an increase in ICP. paragraph) may lead to irreversible ischemic An increase in cerebral blood volume occurs injury. Cerebral perfusion pressure is defined as with either vasodilatation or obstruction of the difference between mean systemic arterial venous outflow. Cerebral blood vessels dilate in blood pressure and the ICP. Intracranial hyper-order to maintain normal cerebral blood flow during periods of decline in cerebral perfusion pressure. Conversely, cerebral vessels con-Address reprint requests to Dr. F. B. Meyer, Department of strict when systemic arterial blood pressure Neurologic Surgery, Mayo Clinic, Rochester, MN 55905. (arid thus cerebral perfusion pressure) increases; Mayo Clin Proc 65:684-707, 1990 684 Mayo Clin Proc, May 1990, Vol 65 INCREASED INTRACRANIAL PRESSURE 685
On completion of this article, the reader should be able to: 1. Define " triple-H " therapy. 2. Explain the usefulness of triple-H therapy. 3. Use this information in a clinical setting. All authors have disclosed that they have no financial relationships with or interests in any commercial companies pertaining to this educational activity. Lippincott CME Institute, Inc., has identified and resolved all faculty conflicts of interest regarding this educational activity. Visit the Critical Care Medicine Web site (www.ccmjournal.org) for information on obtaining continuing medical education credit. Objective: Hypertensive, hypervolemic, hemodilution therapy (triple-H therapy) is a generally accepted treatment for cerebral vasospasm after subarachnoid hemorrhage. However, the particular role of the three components of triple-H therapy remains controversial. The aim of the study was to investigate the influence of the three arms of triple-H therapy on regional cerebral blood flow and brain tissue oxygenation. Design: Animal research and clinical intervention study. Setting: Surgical intensive care unit of a university hospital. Subjects and Patients: Experiments were carried out in five healthy pigs, followed by a clinical investigation of ten patients with subarachnoid hemorrhage. Interventions: First, we investigated the effect of the three components of triple-H therapy under physiologic conditions in an experimental pig model. In the next step we applied the same study protocol to patients following aneurysmal subarachnoid hemorrhage. Mean arterial pressure, intracranial pressure, cere-bral perfusion pressure, cardiac output, regional cerebral blood flow, and brain tissue oxygenation were continuously recorded. Intrathoracic blood volume and central venous pressure were measured intermittently. Vasopressors and/or colloids and crys-talloids were administered to stepwise establish the three components of triple-H therapy. Measurements and Main Results: In the animals, neither induced hypertension nor hypervolemia had an effect on intracra-nial pressure, brain tissue oxygenation, or regional cerebral blood flow. In the patient population, induction of hypertension (mean arterial pressure 143 10 mm Hg) resulted in a significant (p < .05) increase of regional cerebral blood flow and brain tissue oxygenation at all observation time points. In contrast, hypervol-emia/hemodilution (intrathoracic blood volume index 1123 152 mL/m 2) induced only a slight increase of regional cerebral blood flow while brain tissue oxygenation did not improve. Finally, triple-H therapy failed to improve regional cerebral blood flow more than hypertension alone and was characterized by the drawback that the hypervolemia/hemodilution component reversed the effect of induced hypertension on brain tissue oxygen-ation. Conclusions: Vasopressor-induced elevation of mean arterial pressure caused a significant increase of regional cerebral blood flow and brain tissue oxygenation in all patients with subarach-noid hemorrhage. Volume expansion resulted in a slight effect on regional cerebral blood flow only but reversed the effect on brain tissue oxygenation. In view of the questionable benefit of hyper-volemia on regional cerebral blood flow and the negative consequences on brain tissue oxygenation together with the increased risk of complications, hypervolemic therapy as a part of triple-H therapy should be applied with utmost caution. (Crit Care Med 2007; 35:1844–1851)
Critical Care Medicine, 2002
Background: Impaired cerebral autoregulation is frequent after severe traumatic head injury. This could result in intracranial pressure fluctuating passively with the mean arterial pressure. Objective: This study examines the influence of autoregulation on the amplitude and direction of changes in intracranial pressure in patients with severe head injuries during the management of cerebral perfusion pressure. Design: Prospective study. Setting: Neurosurgical intensive care unit Patients: A total of 42 patients with severe head injuries. Interventions: Continuous recording of cerebral blood flow velocity, intracranial pressure, and mean arterial pressure during the start or change of continuous norepinephrine infusion. Measurements and Main Results: Cerebrovascular resistance was calculated from the cerebral perfusion pressure and middle cerebral artery blood flow velocity. The strength of autoregulation index was calculated as the ratio of the percentage of change in cerebrovascular resistance by the percentage of change in cerebral perfusion pressure before and after 121 changes in mean arterial pressure at constant ventilation between day 1 and day 18 after trauma. The strength of autoregulation index varied widely, indicating either preserved or severely perturbed autoregulation during hypotensive or hypertensive challenge in patients with or without intracranial hypertension at the basal state (strength of autoregulation index, 0.51 ؎ 0.32 to 0.71 ؎ 0.25). The change in intracranial pressure varied linearly with the strength of autoregulation index. There was a clinically significant change in intracranial pressure (>5 mm Hg) in the same direction as the change in mean arterial pressure in five tracings of three patients. This was caused by the mean arterial pressure dropping below the identified lower limit of autoregulation in three tracings for two patients. It seemed to be caused by a loss of cerebral autoregulation in the remaining two tracings for one patient. Conclusion: Cerebral perfusion pressure-oriented therapy can be a safe way to reduce intracranial pressure, whatever the status of autoregulation, in almost all patients with severe head injuries.