Pathophysiology
Burkhard Madea in Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
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 In this case, considerably more O2 is withdrawn from the accumulated blood than normally, so that cyanosis develops in the head and neck region.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.
Dementia Associated with Medical Conditions
Marc E. Agronin in 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.
Physiology Related to Special Environments
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
Healthy individuals do not demonstrate any adverse effects below an altitude of 2500 m. Rapid exposure to altitudes in the range of 3000–6000 m results in ‘acute mountain sickness’. The symptoms usually appear in the first 24 hours, and they include headache, somnolence, nausea, vomiting, insomnia and muscle fatigue. These symptoms usually decrease after 3–4 days. At altitudes above 4000 m, cerebral hypoxia occurs with psychomotor impairment (diminished sensory acuity, manual skills and judgment and response times). Consciousness is lost within minutes above 6000 m, or within seconds at higher altitudes. These symptoms are the result of hypoxia and hypocapnia or alkalosis or both.
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).
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.
Establishing prognostic significance of hypoxia predictors in patients with acute cerebral pathology
Published in Neurological Research, 2022
Zhanslu Sarkulova, Ainur Tokshilykova, Alima Khamidulla, Aigul Utepkaliyeva, Dinmukhamed Ayaganov, Marat Sarkulov, Tomas Tamosuitis
In addition, considering the fact that biochemical reactions occur with the participation of cellular enzymes, it is relevant to study the state of some enzymes involved in metabolic processes during the acute period of brain damage. The severity of cerebral hypoxia is also determined by a violation of the energy transport system, the main component of which is lactate dehydrogenase (LDH) [22]. In the brain, LDH is expressed in astrocytes and neurons [14,23], and elevated levels of LDH in the cerebrospinal fluid have been observed in patients with TBI and stroke [24]. LDH levels also reportedly increase due to central nervous system disorders, such as brain infarction and hypoxic-ischemic encephalopathy [25].