Resuscitation techniques for lifeguards
Mike Tipton, Adam Wooler in The Science of Beach Lifeguarding, 2018
In drowning, the physiological process is different: in general during at least the first one to two minutes underwater, the heart continues to beat and the circulation continues to transport available oxygen reservoirs to the cells. The oxygen reserve in the lungs and blood decreases as a result of the oxygen consumed by the cells and gradually all cells have to deal with hypoxia (lowered oxygen). To the brain, hypoxia initially means a decrease in consciousness. To the heart, it initially means a slower and reduced pumping function, which is reflected in a slower and weaker pulse. At a certain point, the oxygen supply to the cells of the heart muscles becomes so low that the heart stops beating. At that point, the cells in the brain might already have started to suffer hypoxic damage, but this may temporarily be delayed when there has been a rapid decline in brain temperature [16,17]. However, in most cases the preceding and prolonged hypoxia will have caused gradual and severe neurological damage [18,19].
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.
Pathophysiology
Burkhard Madea in Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
At rest, adrenaline and noradrenaline are released from the adrenal medulla in an amount of about 70 ng/min/kg body weight. In normal circumstances, the adrenaline serum level is less than 100 ng/L. Exceptional physical and psychological exertion, trauma of all kinds, even asphyxiation, lead to a considerable sympathetic effect. The same applies to fighting and escape situations. As a result, the serum level of both hormones, especially adrenaline, increases many times over. The adrenaline causes a complex adaptation of the body to emergency situations. A rapid increase in metabolism is triggered, whereby a higher performance can be achieved. For example, increases in the frequency and contractility of the heart and improvements in the ability of the muscles to work can be observed. The increase in the organism's performance is accompanied by a considerable increase in the O2 requirement of various body tissues. It should be noted that high concentrations of adrenaline can cause arrhythmias. Apparently, the excessive increase of catecholamines can also lead to changes in the ST range and T wave in the ECG, as well as to an increase in QT time, as has been observed in a case of near-hanging [2]. Cerebral hypoxia can be promoted or even induced as a result of the adrenaline effect. The effects are to be considered to varying degrees for the individual types of asphyxiation. In cases of strong defence by the victims, which can be observed during neck holds or blocking the respiratory passages, positional asphyxia syndrome is of importance. It should be noted that hypoglycaemia, certain drugs and alcohol can additionally increase the adrenaline level [29, 50].
Narirutin-rich fraction from grape fruit peel protects against transient cerebral ischemia reperfusion injury in rats
Published in Nutritional Neuroscience, 2022
Paresh Patel, Kalyani Barve, Lokesh Kumar Bhatt
During brain hypoxia/ ischemia, pathological and cellular mechanisms involved in cerebral function are unclear. Studies have proved that cerebral hypoperfusion results in cognitive and memory dysfunction [23]. A four-year follow-up assessment of stroke survivors in hospitals showed that approximately one-third of the patients met the criteria of dementia [22]. The study carried out by Yan et al. revealed that bilateral common carotid artery occlusion model of global cerebral ischemia caused a marked cognitive and memory dysfunction in rats [24]. Furthermore, global cerebral ischemia has been reported to cause marked decrease in muscle strength of the limbs, which has been demonstrated in rotarod experiments [25,26]. Consistent with the studies mentioned above, a marked decrease in muscle strength was observed in the present study after 30 min of bilateral common carotid artery occlusion followed by 24 h of reperfusion. These effects were significantly attenuated by NRF pretreatment, which suggests that NRF has therapeutic potential against I/R injury. The hippocampus is an area of the brain that is important for the regulation of memory [27]. Global cerebral ischemia causes memory dysfunction because of its influence on hippocampal neurons [20,26]. Results of the present experiment are in line with the above findings, which showed a marked reduction in memory retention in the I/R control rats in elevated plus maze paradigm. NRF pretreatment significantly prevented this decline in memory performance. This suggested potential of NRF against stroke-induced cognitive dysfunction.
LncRNA SNHG1 protects SH-SY5Y cells from hypoxic injury through miR-140-5p/Bcl-XL axis
Published in International Journal of Neuroscience, 2021
Da-Wei Wang, Xiao-Qian Lou, Zuo-Long Liu, Nan Zhang, Li Pang
Hypoxic brain injury can lead to many central nervous system diseases. The brain hypoxia-ischemia insult to cerebellum and brainstem has been shown to cause neurological injury [1]. Hypoxic-ischemic brain injury results in neuronal death and probably leads to multiple human neurological dysfunctions, such as movement and learning disabilities, epilepsy, cerebral palsy, and even death, during which multiple apoptosis-associated signal pathways were involved [2,3]. It has been demonstrated that oxygen and hypothermia therapies are used for the treatment of hypoxic brain damage [4,5]. However, even though the hypothermia therapy has been recognized for years, there are still some controversies and problems needs to be solved, such as the increased risk of interference with blood clotting or infection. Therefore, to reveal the mechanism of the development of hypoxic brain injury and to find new treatment methods and targets are the urgent problems to be solved in the treatment of hypoxic brain injury in the future.
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).