![]() ![]() Each supports 1000 g (stress) and undergoes similar elongation from its resting baseline (strain). Let us assume that a load of 10 kg is sustained by 10 parallel and interconnected elastic cords that suspend it. Apart from opening and closing, these too are relevant forms of ‘atelectrauma’.Īnother important but often neglected physical amplifier of stress and strain (‘drop-out’) is rather intuitive. One consequence of microatelectasis is the generation of these stress risers, which encourage shearing stresses and also amplify the consequences of applied power to the ‘baby lung’. For injured lungs, the stress multiplier (which varies with PL) may exceed 2.0. Treatment consists of reducing oxygen exposure and dive depth and, if necessary, managing seizures.Stress and strain amplify at interfaces between regions with different elasticity these junctions act as “stress risers”. 4 The cause of oxygen toxicity to the nervous system mainly involves oxygen-free radical formation, as well as reduction of the inhibitory neurotransmitter, gamma-aminobutyric acid. Although uncommon, generalized seizures at depth are often fatal, because divers may drown or arterial gas embolism may be precipitated during rescue to the surface. 18 Generalized seizures or syncope can also occur in 5 to 10 percent of patients. Symptoms develop at depth without warning and consist of focal seizures (e.g., facial or lip twitching occurs in 50 to 60 percent of patients), vertigo, nausea and emesis, paresthesias, visual constriction and respiratory changes. In general, the higher the oxygen content in the Nitrox mixture, the shallower the dive to minimize the potential for oxygen toxicity. When diving with Nitrox, the diver is at risk of oxygen toxicity if the maximum oxygen depth limit and/or the oxygen time limit is exceeded. Nitrox is a breathing mixture that contains more than 21 percent oxygen (usually 32 to 36 percent), and allows extended bottom time. In the recreational diver, the most likely cause of oxygen toxicity is diving with oxygen enriched air (i.e., Nitrox). Reduce depth and oxygen exposure, supportive care, seizure management see arterial gas embolism treatment Usually precipitated during pre-dive activities or at depthĪvoid precipitating stimuli, dive conservatively, consider prophylactic therapyįocal seizures, visual constriction, nausea, emesis, vertigo, paresthesias, rare generalized seizures Pounding, throbbing pain nausea, emesis, photophobia Usually develops within minutes of ascent, may persist without recompression treatment Severe generalized headache associated with alteration of consciousness and other signs Paresthesias/sensory loss in trunk and/or extremities, leg weakness, loss of bowel/bladder function Within 30 to 60 minutes of surfacing (> 50 percent), 90 percent by six hours significant time-depth exposure requiredĬonfusion, focal weakness, fatigue, visual loss, diplopia, speech dysfunction, gait abnormality, headache Within five minutes of surfacing (> 80 percent) or during ascent significant time-depth exposure not requiredġ00 percent oxygen, United States Navy Table 6 algorithm recompression, supportive careĪcute vertigo, nausea, emesis, nystagmus, tinnitus, sensorineural hearing loss Stupor, confusion, coma, seizures, focal weakness, visual loss Ipsilateral facial paralysis, resolves within hoursĪcute vertigo, nausea, emesis, tinnitus, sensorineural hearing loss often associated with middle ear barotraumaĮNT evaluation, bed rest, head elevation, stool softeners consider surgical exploration if symptoms persist Improved equalization techniques, oral and nasal decongestants with otorrhea use antibiotics Acute pain, vertigo, hearing loss, rupture or hemorrhage of tympanic membraneĭuring descent usually, possible during ascent ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |