Abstract:During exposure to 280 kPa oxygen at rest a constant delay of approximately 20 min precedes the onset of central nervous oxygen toxicity. An increase in CBFV may indicate the impending seizure.
“…Interestingly, in contrast to the cerebral vasoconstriction normally observed during pure O 2 breathing, symptoms are preceded by a paradoxical increase in cerebral blood flow velocity [ 88 ] (Fig. 2 ), which is referred to peroxynitrite (ONOO − ) formation resulting from the reaction of NO with the superoxide radical (O 2 − ) [ 89 ], and thereby causing a dysregulation of the endogenous NO availability [ 46 , 90 ]. Fig.…”
Section: (Patho)physiology Of Hyperoxia: Pulmonary Vascular Metabolmentioning
This review summarizes the (patho)-physiological effects of ventilation with high FiO2 (0.8–1.0), with a special focus on the most recent clinical evidence on its use for the management of circulatory shock and during medical emergencies. Hyperoxia is a cornerstone of the acute management of circulatory shock, a concept which is based on compelling experimental evidence that compensating the imbalance between O2 supply and requirements (i.e., the oxygen dept) is crucial for survival, at least after trauma. On the other hand, “oxygen toxicity” due to the increased formation of reactive oxygen species limits its use, because it may cause serious deleterious side effects, especially in conditions of ischemia/reperfusion. While these effects are particularly pronounced during long-term administration, i.e., beyond 12–24 h, several retrospective studies suggest that even hyperoxemia of shorter duration is also associated with increased mortality and morbidity. In fact, albeit the clinical evidence from prospective studies is surprisingly scarce, a recent meta-analysis suggests that hyperoxia is associated with increased mortality at least in patients after cardiac arrest, stroke, and traumatic brain injury. Most of these data, however, originate from heterogenous, observational studies with inconsistent results, and therefore, there is a need for the results from the large scale, randomized, controlled clinical trials on the use of hyperoxia, which can be anticipated within the next 2–3 years. Consequently, until then, “conservative” O2 therapy, i.e., targeting an arterial hemoglobin O2 saturation of 88–95 % as suggested by the guidelines of the ARDS Network and the Surviving Sepsis Campaign, represents the treatment of choice to avoid exposure to both hypoxemia and excess hyperoxemia.
“…Interestingly, in contrast to the cerebral vasoconstriction normally observed during pure O 2 breathing, symptoms are preceded by a paradoxical increase in cerebral blood flow velocity [ 88 ] (Fig. 2 ), which is referred to peroxynitrite (ONOO − ) formation resulting from the reaction of NO with the superoxide radical (O 2 − ) [ 89 ], and thereby causing a dysregulation of the endogenous NO availability [ 46 , 90 ]. Fig.…”
Section: (Patho)physiology Of Hyperoxia: Pulmonary Vascular Metabolmentioning
This review summarizes the (patho)-physiological effects of ventilation with high FiO2 (0.8–1.0), with a special focus on the most recent clinical evidence on its use for the management of circulatory shock and during medical emergencies. Hyperoxia is a cornerstone of the acute management of circulatory shock, a concept which is based on compelling experimental evidence that compensating the imbalance between O2 supply and requirements (i.e., the oxygen dept) is crucial for survival, at least after trauma. On the other hand, “oxygen toxicity” due to the increased formation of reactive oxygen species limits its use, because it may cause serious deleterious side effects, especially in conditions of ischemia/reperfusion. While these effects are particularly pronounced during long-term administration, i.e., beyond 12–24 h, several retrospective studies suggest that even hyperoxemia of shorter duration is also associated with increased mortality and morbidity. In fact, albeit the clinical evidence from prospective studies is surprisingly scarce, a recent meta-analysis suggests that hyperoxia is associated with increased mortality at least in patients after cardiac arrest, stroke, and traumatic brain injury. Most of these data, however, originate from heterogenous, observational studies with inconsistent results, and therefore, there is a need for the results from the large scale, randomized, controlled clinical trials on the use of hyperoxia, which can be anticipated within the next 2–3 years. Consequently, until then, “conservative” O2 therapy, i.e., targeting an arterial hemoglobin O2 saturation of 88–95 % as suggested by the guidelines of the ARDS Network and the Surviving Sepsis Campaign, represents the treatment of choice to avoid exposure to both hypoxemia and excess hyperoxemia.
“…Simultaneous to this increase in CBF, the cortical electroencephalography (EEG) activity increases (Bean and Coulson, 1971; Visser et al, 1996b). This increase in CBF and cortical EEG activity precedes convulsions (Bean and Coulson, 1971; Visser et al, 1996a,b; Demchenko et al, 2001; Koch et al, 2008). The exact mechanism though which ROS cause convulsions is not entirely clear.…”
Section: Central Nervous System Toxicitymentioning
confidence: 99%
“…Although the exact mechanism is not fully understood, currently, the most plausible explanation is related to an overflow of reactive oxygen species (ROS) in the brain after an increase of cerebral blood flow (CBF) (Visser et al, 1996a; Koch et al, 2008). Due to the increased PO 2 in plasma there is an auto oxidation of nitric oxide ( · NO) to several ROS, of which peroxynitrite (ONOO − ) is the most important (Goldstein and Czapski, 1995; de Groot et al, 2004).…”
Section: Central Nervous System Toxicitymentioning
In Special Operations Forces (SOF) closed-circuit rebreathers with 100% oxygen are commonly utilized for covert diving operations. Exposure to high partial pressures of oxygen (PO2) could cause damage to the central nervous system (CNS) and pulmonary system. Longer exposure time and higher PO2 leads to faster development of more serious pathology. Exposure to a PO2 above 1.4 ATA can cause CNS toxicity, leading to a wide range of neurologic complaints including convulsions. Pulmonary oxygen toxicity develops over time when exposed to a PO2 above 0.5 ATA and can lead to inflammation and fibrosis of lung tissue. Oxygen can also be toxic for the ocular system and may have systemic effects on the inflammatory system. Moreover, some of the effects of oxygen toxicity are irreversible. This paper describes the pathophysiology, epidemiology, signs and symptoms, risk factors and prediction models of oxygen toxicity, and their limitations on SOF diving.
“…Data for hyperoxic exposures at rest in immersion or in dry conditions -exposure time, partial pressure of oxygen (PO 2 ), and appearance or absence of CNS-OT, were extracted from a number of studies compiled by Harabin (1993), and from Koch et al (2008). Evidently there are ample data on hyperoxic exposures at rest which were not reported in a proper way for our analysis (exact condition for each single exposure).…”
Section: Data Derivationmentioning
confidence: 99%
“…However, because these were gathered from naval oriented studies, we believe that the subjects were healthy males. Koch et al (2008) state that their data were from healthy, elite Navy combat divers. As in our previous study (Arieli et al, 2002), we selected the symptoms suggested by Harabin et al (1995) as indicating a positive finding of CNS-OT: nausea, numbness, dizziness, twitching, hearing and visual disturbances, convulsions and unconsciousness.…”
Patients undergoing hyperbaric oxygen therapy and divers engaged in underwater activity are at risk of central nervous system oxygen toxicity. An algorithm for predicting CNS oxygen toxicity in active underwater diving has been published previously, but not for humans at rest. Using a procedure similar to that employed for the derivation of our active diving algorithm, we collected data for exposures at rest, in which subjects breathed hyperbaric oxygen while immersed in thermoneutral water at 33 • C (n = 219) or in dry conditions (n = 507). The maximal likelihood method was employed to solve for the parameters of the power equation. For immersion, the CNS oxygen toxicity index is K I = t 2 × PO 2 10.93 , where the calculated risk from the Standard Normal distribution is Z I = [ln(K I 0.5)-8.99)]/0.81. For dry exposures this is K D = t 2 × PO 2 12.99 , with risk Z D = [ln(K D 0.5)-11.34)]/0.65. We propose a method for interpolating the parameters at metabolic rates between 1 and 4.4 MET. The risk of CNS oxygen toxicity at rest was found to be greater during immersion than in dry conditions. We discuss the prediction properties of the new algorithm in the clinical hyperbaric environment, and suggest it may be adopted for use in planning procedures for hyperbaric oxygen therapy and for rest periods during saturation diving.
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