Gas Issues in Diving Gas Issues • TOO MUCH • O2, CO2, inert gas narcosis, High Pressure Neurological Syndrome • TOO LITTLE • Hypoxia, hyperventilation • WRONG GAS • CO poisoning, contaminants CNS Ox Tox “VENTID-C” • Vision changes (↓acuity, dazzle, lat • Risk Factors movement, constricted fields) • Exercise • Ears (tinnitus, auditory hallucinations, • Hyper/hypothermia music, bells, knocking) • Hypoventilation, hypercapnia • Immersion • Nausea/vomiting • Metabolic activity, blood flow to brain • Twitch (lips, cheek, eyelid, tremors…) • Hypoglycemia (DM) • Irritability, behaviour, mood changes • Seizure D?O, +/- meds that lower sx (incl apprehension, apathy, euphoria) threshold • VitE deficiency • Dizzy • Pseudoephedrine, amphetamines, ASA, • Convulsions acetazolamide • Spherocytosis, hypercortisolism • Also pallor, sweaty, palpitations, brady, tachy, panting, grunting, unpleasant gustatory/ olfactory sensations, hiccups CNS OxTox • No consistent pre-convulsion • Tx warning sx • Remove O2 • • Stop travel Often not preceded by other sx • Protect from injuries if seizing • O2 convulsions not inherently • Check DDx (don’t forget hypoglycemia) harmful • Keep patient off O2 for 15 mins after all sx are gone • No pathologic changes in human • Ignore treatment time lost and resume brain, no evidence of clinical sequelae table where last interrupted • No apparent predisposition to future • Don’t forget to compensate for extra sz disorder time for chamber attendants • Harm based on context (seizure • Preventive Measures underwater = drowning) • Air breaks • Clinical HBOT setting (rarely used) • Very high intra & inter-individual • Glutathione variation in susceptibility • Lithium • ?increased risk with drugs that lower • GABA agonists sz threshold (not much evidence) CNS OxTox • No consistent pre-convulsion • Tx warning sx • Remove O2 Often not preceded by other sx • Protect from injuries if seizing • • Check DDx (don’t forget hypoglycemia) • O2 convulsions not inherently • Keep patient off O2 for 15 mins after all sx harmful are gone • Ignore treatment time lost and resume • No pathologic changes in human table where last interrupted brain, no evidence of clinical sequelae • Don’t forget to compensate for extra • No apparent predisposition to future time for chamber attendants sz disorder • Preventive Measures • Harm based on context (seizure • Air breaks underwater = drowning) • Clinical HBOT setting (rarely used) • Glutathione • Very high intra & inter-individual • Lithium variation in susceptibility • GABA agonists • ?increased risk with drugs that lower sz threshold (not much evidence) Pulmonary Oxygen Toxicity • Cumulative dose = fx of exposure time, ATA, and • Acute Exudative (reversible) FiO2 • Interstitial and alveolar edema, hemorrhage, • Acute Δ with FiO2 > 0.8 ATA destruction of pulm capillary endothelium, • Chronic Δ with FiO2 > 0.5 ATA loss of type I alveolar cells (surfactant), inflam. cell infiltrates • Typically insidious mild substernal irritation, chest tightness -> ↑cough -> constant burning • Acute Proliferative (non-reversible) exacerbated by inspiration -> dyspnea (exertion or • Type II alveolar cells replace damaged type I rest) (blood-air barrier thickens), fibroblast • ~12-16 hrs @ 1 ATA, ~3-6 hrs @ 2.0 ATA infiltration, increased alveolar-capillary • CXR usually N, +/- patchy infiltrates distance, ↓alveolar air vol, ↑collagen content • Mechanical fx impaired earlier than gas exchange • Chronic (CO diffusing capabilities) • Progressive pulmonary fibrosis, similar to • No change FEV1 ARDS • ↓FVC • Preventions: • 2%, asx, completely reversible over hrs • Air breaks • 10% = mild sx, reversible over several days • Unit Pulmonary Toxicity Dose (UPTD) • 20% = mod sx, probably reversible over • 1 UPT = pulm poisoning produced by 100% O2 weeks, acceptable for a TT x 1 min at 1 ATA • ↓Diffusion capacity, FEF 25-75, V/Q defect • HBOT Max 1440 UPTD/24hrs (TT6 = 750 UPTDs) Nitrogen Narcosis “Rapture of the deep” • Reversible depression of neuronal • S/Sx excitability due to inert gas • ++Inter/intra-variability (~60-120ft • Potency Xe >Kr > Ar > N > H > Ne > He onset) • • ?Interfere with transmission of EP ↓performance mental/manual work across synaptic gap (higher fx affected most) • • Meyer-Overton theory: ↑solubility = DiZZy, euphoria, uncontrolled laughter ↑narcotic effect • Overconfidence, overly talkative • • Immediate onset at depth, stable after Memory loss/post-dive amnesia few mins at depth, rapid resolution • Perceptual narrowing (fixation) upon ascent • Impaired sensory functioning • Potentiated by ↑CO2 levels • LOC >100msw • No true acclimatization, divers may • Prevention dev short term subjective tolerance, • Depth <30msw, plan dive ahead & NO objective tolerance practice tasks • RFs • If affected – decrease depth • Depth, gas mix, anxiety, task loading, • Heliox cold, fatigue, exercise, EtOH, sedatives, ↑CO2 CO2 Toxicity • Inadequate ventilation • S/Sx • Helmet diving, hyperbaric chamber • H/A, flushing, sweating • Alveolar hypoventilation • Dizzy • Dyspnea • Higher inspired CO2 = failure of CO2 scrubbers in rebreather systems • Decreased cognition, disorientation • LOC/convulsions • CO2 retention (increased WOB • Makes everything else worse (NN, underwater) OxTox) • Increased CO2 levels unpredictable, even in normal healthy divers • Tx • End dive • Inadequate pulmonary ventilation • Fresh air, +/-O • Increased density of gas 2 • Deliberate hypoventilation or ‘skip- breathing’ – NEVER skip breath, esp. at high PP High Pressure Neurological Syndrome (HPNS) • General excitation of brain • Prevention • Opposite to narcosis • Diver selection • Occurs in very deep diving >16 ATA • ↓compression rate, long • Usually Heliox mixtures at this depth stages/holds (allow adaptation) • Affected by rate of compression • Use of N2 (or other narcotic) in • Rapid rate = increased severity at trimix shallower depth • S/Sx • Marked tremor hands/arms/whole body, dizzy, anorexia, nausea, vomiting • Fatigue, somnolence • Can progress to myoclonic jerks -> clonic seizures Hypoxia • Same sx as on the surface • Shallow-Water Blackout • Important to know onset for • Breath-hold diving rebreathers • Remember – CO2 produces drive to breathe • Open circuit • Hypoxia at depth – almost never O • Hyperventilation reduces CO2 2 levels below normal levels issue, gen CO2 issue • Hypoxia at surface – almost always • O2 levels may fall to a level causing LOC before CO increases to O2 issue 2 breakpoint trigger for breathing • Closed circuit LOC underwater is never a good • Hypoxia – sensor failure • thing… • Prevention • Maintain gear & checks • Don’t run out of breathing gas CO Toxicity • Typically contaminated air from • S/Sx improperly directed compression • Headache, N/V, dizzy, weakness, vision engine exhaust changes, disorientation, ↓LOC, auditory dysfunction, cardiac arrhythmias, skeletal • Pathophys muscle necrosis -> ARF, pulm edema • CO relative affinity for Hb 250x greater than • Concomitant smoke inhalation sx O2 • Cherry red skin colour rare, very late • ↓O2 carrying capacity, ↑unbound Hb = left shift = ↓tissue/intracellular O2 • CO best assessed by blood • Disturbs mitochondrial e- transport, ↑NO carboxyhemoglobin (COHb) radicals, lipid peroxidation in brain • Mortality/morbidity not correlated with • Cerebral vessels dilate, ↑coronary blood COHb level flow with ↓central resp -> cerebral hypoxia • Pulse oximetry overestimate arterial O2 & cardiac arrhythmias • Acute mortality often due to ventricular • Tx arrhythmias due to hypoxic stress, • ABCs, preserve airway myocardial impairment • Ventilation, oxygenation • HBOT hastens CO dissociation beyond rate achievable by surface 100% O2.