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Accident
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
In this context the observation that some children who lost their balance and fell into shallow water got into a state of shock, immediately lying face down in the water without struggling, is of interest. (Krauland [10] reported that a 6-year-old boy who observed his sister drowning in the bathtub thought that she had lain down to sleep. Diagnosis of drowning was confirmed and internal disease excluded by autopsy.) This behaviour may support the development of a rapid and efficient diving reflex [29] but may gain fatal relevance if the children are not rescued before they start to aspirate water or hypoxic damage occurs to the brain.
Physiology Related to Special Environments
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Several cardiovascular changes are associated with diving. On first immersion and exposure to water, especially when it is colder than 15°C, there is a dramatic decrease in heart rate, apnoea and selective vasoconstriction (especially cutaneous), and this is called the ‘diving reflex’. The vasoconstriction occurs in those organs that can utilize anaerobic metabolism such as the skin, muscle, kidneys and gastrointestinal tract. The brain requires a constant supply of oxygen as it relies on oxidative metabolism. During the diving reflex, the oxygen supply to the brain is maintained by the redistribution of the cardiac output to the cerebral circulation. The initial stimulus for the diving reflex appears to be the immersion of skin of the face to cold water. The afferent fibres responsible for this reflex are in the trigeminal nerve. Immediately following face immersion, the heart rate decreases by about 50%, and this is mediated by increased vagal activity. This is usually associated with an increase in arterial pressure that occurs because of profound peripheral vasoconstriction due to increased sympathetic activity. The apnoea is induced partly by voluntary control and partly by reflex inhibition of respiration mediated by stimulation of the trigeminal receptors. Prolonged breath holding leads to severe hypoxaemia and hypercapnia, which stimulate the carotid body chemoreceptors and initially cause bradycardia and peripheral vasoconstriction. Under these conditions, the chemoreceptor stimulus is strongly inhibited by the activation of the trigeminal receptors. Eventually, the hypercapnia is so severe that the trigeminal inhibition is overcome and the desire to breathe is compelling. This is called the break point, which is largely determined by arterial Pco2.
Special environments
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2015
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Several cardiovascular changes are associated with diving. On first immersion and exposure to water, especially when it is colder than 15°C, there is a dramatic decrease in heart rate, apnoea and selective vasoconstriction (especially cutaneous) and this is called the ‘diving reflex’. The vasoconstriction occurs in those organs that can utilize anaerobic metabolism such as the skin, muscle, kidneys and gastrointestinal tract. The brain requires a constant supply of oxygen as it relies on oxidative metabolism. During the diving reflex, the oxygen supply to the brain is maintained by the redistribution of the cardiac output to the cerebral circulation. The initial stimulus for the diving reflex appears to be the immersion of skin of the face to cold water. The afferent fibres responsible for this reflex are in the trigeminal nerve. Immediately following face immersion, the heart rate decreases by about 50% and this is mediated by increased vagal activity. This is usually associated with an increase in arterial pressure that occurs because of profound peripheral vasoconstriction due to increased sympathetic activity. The apnoea is induced partly by voluntary control and partly by reflex inhibition of respiration mediated by stimulation of the trigeminal receptors. Prolonged breath holding leads to severe hypoxaemia and hypercapnia, which stimulate the carotid body chemoreceptors and initially cause bradycardia and peripheral vasoconstriction. Under these conditions, the chemoreceptor stimulus is strongly inhibited by the activation of the trigeminal receptors. Eventually, the hypercapnia is so severe that the trigeminal inhibition is overcome and the desire to breathe is compelling. This is called the break point, which is largely determined by arterial Pco2.
Correlations of Enzyme Levels at Birth in Stressed Neonates with Short-Term Outcomes
Published in Fetal and Pediatric Pathology, 2018
Junya Nakajima, Norito Tsutsumi, Shonosuke Nara, Hiroki Ishii, Yusuke Suganami, Daisuke Sunohara, Hisashi Kawashima
Intracellular enzymes, such as AST, ALT, LDH, and CK, leak from damaged cells (3, 6). Levels of these enzymes are widely used to evaluate neonatal status. However, using these data to evaluate short- and long-term severity of stressed neonates remains controversial (10). We reevaluated these classical indices of multi-organ injury and their applicability for the intensive care of stressed neonates. These enzymes appeared to correlate with some short-term outcomes that are thought to result from perinatal stress. A 1-min Apgar score of < 7 suggests some sort of perinatal hypoxic and/or ischemic stress, including perinatal asphyxia (1). Acute hypoxia during delivery induces the diving reflex in the newborn, reducing circulation to peripheral areas such as skin and the gastrointestinal tract, to divert perfusion to more vital organs such as the brain and heart (13, 14). This reflex results in ischemic injury to organs and damage to cells, resulting to leakage of intracellular enzymes (3, 6). In a hypoxic–ischemic insult, the patient needs to be treated with multiple organ support, including mechanical ventilation.
Cardiovascular diseases, cold exposure and exercise
Published in Temperature, 2018
Heart rate (HR) responses depend on the type of cold exposure, but are not generally altered much with whole-body cold exposure [39]. Only with the cold pressor test [27,34,40,41] or cold air inhalation [34] is an increase in HR observed which is related to strong activation of the sympathetic nervous system. However, with whole body cooling of skin in cold air or water, and depending on whether the face is exposed or not, a parallel activation of both the sympathetic and parasympathetic nerve branches may occur. Hence, whole-body skin cooling including facial exposure results in either decreased [25,27,28,38,42,43] or unaltered [24,26,44,45] HR. Also skin surface cooling without facial cold exposure demonstrated either reduced [46,47] or no effect on HR [32,33]. Application of cold to the face (ice-packs), on the other hand, stimulates the trigeminal nerve and evokes a non-baroreflex mediated vagal response resembling the diving reflex [29]. Hence, many experimental studies applying facial cooling report reduced HR [25,27,29–31,48,49].
Dysautonomia in the pathogenesis of migraine
Published in Expert Review of Neurotherapeutics, 2018
Parisa Gazerani, Brian Edwin Cairns
It may even be that the generating mechanism of migraine headache is a malfunctioning central neurogenic reflex. The trigeminal cardiac reflex causes rapid increase in parasympathetic tone (leading to cerebral vasodilation and gastric hypermotility) and decrease of sympathetic tone (leading to hypotension), in response to stimulation of any of the branches of the trigeminal nerve. This pathway may function to increase blood flow to the brain or within it, and may serve a similar purpose as the diving reflex. Relatively little is known about the normal role of this reflex, or whether it is altered in migraine sufferers; however, the effects produced by its activation mirror the autonomic tone changes associated with initiation of a migraine attack. Future research may identify how this reflex is modified in migraine and whether treatment aimed at modulating it can contribute to migraine treatment or prophylaxis. Ultimately, by understanding the role of autonomic changes in pathogenesis of migraine, it may be possible to develop even more effective treatments through targeting both trigeminal sensory input and autonomic efferent output simultaneously.