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Pathophysiology
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Wolfgang Keil, Claire Delbridge
The venae vertebrales consist of an inner and an outer plexus. The inner system runs in the spinal canal and cannot be compressed by strangulation. The outer part of the venous plexus is located in the vertebral muscles and apparently has a larger cross-section than the venae jugulares. However, compression of the neck can significantly impede blood flow from the brain. If the impairment of the blood flow is greater than the reduction of the inflow, a considerable passive hyperaemia develops above the compression. In this case, considerably more O2 is withdrawn from the accumulated blood than normally, so that cyanosis develops in the head and neck region. If the obstruction persists, oxygenated blood cannot enter and cerebral hypoxia occurs. Due to the suppressed cleansing function of the blood, mainly acidic metabolites accumulate, resulting in particularly pronounced cell damage. In addition, tissue fluid can be expressed, which can lead to swelling of the face.
Regional blood flow
Published in Burt B. Hamrell, Cardiovascular Physiology, 2018
Cerebral hypoxia due to inadequate cerebral blood flow develops below a mean arterial blood pressure of 60 mm Hg. There is autoregulation of cerebral blood flow that operates above this arterial blood pressure level, as discussed above.
Dementia Associated with Medical Conditions
Published in Marc E. Agronin, Alzheimer's Disease and Other Dementias, 2014
Both acute and chronic oxygen deprivation to the brain can result in brain damage and a dementia syndrome that is characterized by confusion, impaired memory, apathy, irritability, and somnolence (Lin, 2013). Individuals who survive severe anoxia caused by sustained cardiac or respiratory arrest or other traumatic causes often suffer from profound, permanent neuropsychological impairment. Less severe cognitive impairment can sometimes result from a variety of acute and chronic conditions that produce cerebral hypoxia, including brief cardiopulmonary failure, inadequate surgical ventilation, open heart surgery, sleep apnea, bradycardia, chronic obstructive pulmonary disease, congestive heart failure, anemia, and hyperviscous or hypercoagulable states.
Optimizing Physiology During Prehospital Airway Management: An NAEMSP Position Statement and Resource Document
Published in Prehospital Emergency Care, 2022
Daniel P. Davis, Nichole Bosson, Francis X. Guyette, Allen Wolfe, Bentley J. Bobrow, David Olvera, Robert G. Walker, Michael Levy
Physiological derangement is common following advanced airway insertion, and efforts should be focused on maintaining optimal perfusion, oxygenation, and ventilation (57,58). Hypoxemia contributes to morbidity and mortality from multiple disease processes, particularly those involving cerebral injury, and should be prevented or reversed in all patients (8,59). Some data suggest that extreme hyperoxemia may contribute to free radical injury and hypoperfusion resulting in worsened neurological outcomes following brain injury (34). EMS clinicians should achieve systemic normoxemia for most patients, targeting SpO2 values of 94-98%. Traumatic brain injury patients may suffer cerebral hypoxia despite systemic normoxemia. For these patients, increasing FiO2 to 40-60% while maintaining SpO2 values of 99-100% may be reasonable (35). Potential strategies to reverse hypoxemia include increasing FiO2 and increasing available alveolar surface area for gas exchange, either through recruitment [tidal volume, inspiratory time] or through PEEP to prevent atelectasis and atelectrauma. Other strategies for improving oxygenation include ensuring good pulmonary toilet, treating underlying pulmonary disease, optimizing perfusion status, and positioning the patient to ensure efficient ventilation/perfusion matching.
Brugada syndrome and the story of Dave
Published in Neuropsychological Rehabilitation, 2018
Samira Kashinath Dhamapurkar, Barbara A Wilson, Anita Rose, Gerhard Florschutz
The cognitive deficits seen following cardiac arrest depend on the extent and severity of brain damage, with memory and executive disorders being the most typical (Caine & Watson, 2000; Wilson, 1996). There is a subgroup of people with cerebral hypoxia who have very severe intellectual impairment such that they cannot be assessed with traditional neuropsychological tests and have to be assessed with tests for people with special needs (Wilson, 1996). There is another subgroup who remain with a disorder of consciousness (DOC). They are either in a vegetative state (VS) or a minimally conscious state (MCS). Giacino and Whyte (2005) recognised that patients who are in VS or MCS following hypoxic damage do less well than those whose DOC follows a tramatic brain injury (TBI). Dhamapurkar, Wilson, Rose, and Florschutz (2015) found that 18% of 28 people who had a DOC for 12 or more months recovered consciousness and that survivors of a TBI were more likely to show delayed recovery than non-TBI patients, most of whom had sustained hypoxic brain damage. Rehabilitation for survivors of hypoxic brain damage mirrors that provided for survivors of any other type of brain injury (Wilson & Van Heugten, in press).
The effect of intravenous ginkgolide on clinical improvement of patients with acute ischemic stroke
Published in Neurological Research, 2020
Yi Dong, Huiqin Li, Qiang Dong
The pathogenesis of cerebral infarction [33] is complex and associated with platelet adhesion, vascular endothelial injury, platelet aggregation, lipid metabolism disorders, atherosclerosis and a hypercoagulable state, as well as vascular stenosis and occlusion. Acute cerebral infarction leads to cerebral hypoxia-induced anoxia, which results in disorders of cell metabolism, neurotoxicity, oxidative stress and a cascade of cellular changes. Studies have revealed that, following cerebral infarction, the neurons in the ischemic penumbra lose their function but retain an intact structure. The function of these neurons may be restored to varying degrees if the blood supply is recovered in time, thereby reducing delayed neuronal damage [34].