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Dive Medicine Aide-Memoire Lt(N) K Brett Reviewed by Lcol a Grodecki Diving Physics Physics

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Dive Medicine Aide-Memoire Lt(N) K Brett Reviewed by Lcol a Grodecki Diving Physics Physics Dive Medicine Aide-Memoire Lt(N) K Brett Reviewed by LCol A Grodecki Diving Physics Physics • Air ~78% N2, ~21% O2, ~0.03% CO2 Atmospheric pressure Atmospheric Pressure Absolute Pressure Hydrostatic/ gauge Pressure Hydrostatic/ Gauge Pressure Conversions • Hydrostatic/ gauge pressure (P) = • 1 bar = 101 KPa = 0.987 atm = ~1 atm for every 10 msw/33fsw ~14.5 psi • Modification needed if diving at • 10 msw = 1 bar = 0.987 atm altitude • 33.07 fsw = 1 atm = 1.013 bar • Atmospheric P (1 atm at 0msw) • Absolute P (ata)= gauge P +1 atm • Absolute P = gauge P + • °F = (9/5 x °C) +32 atmospheric P • °C= 5/9 (°F – 32) • Water virtually incompressible – density remains ~same regardless • °R (rankine) = °F + 460 **absolute depth/pressure • K (Kelvin) = °C + 273 **absolute • Density salt water 1027 kg/m3 • Density fresh water 1000kg/m3 • Calculate depth from gauge pressure you divide press by 0.1027 (salt water) or 0.10000 (fresh water) Laws & Principles • All calculations require absolute units • Henry’s Law: (K, °R, ATA) • The amount of gas that will dissolve in a liquid is almost directly proportional to • Charles’ Law V1/T1 = V2/T2 the partial press of that gas, & inversely proportional to absolute temp • Guy-Lussac’s Law P1/T1 = P2/T2 • Partial Pressure (pp) – pressure • Boyle’s Law P1V1= P2V2 contributed by a single gas in a mix • General Gas Law (P1V1)/ T1 = (P2V2)/ T2 • To determine the partial pressure of a gas at any depth, we multiply the press (ata) • Archimedes' Principle x %of that gas Henry’s Law • Any object immersed in liquid is buoyed up by a force equal to weight of the fluid • Gas molecules enter liquid – add to gas displaced by the object tension (=partial press gas in liquid) • Pressure gradient = Δ between gas • Daltons’ Law P(total) = P1+P2+…+Pn tension in the liquid and gas partial • The total pressure exerted by a mixture of gases is the sum of the pressures that press outside liquid would be exerted by each gas if it alone • High gradient (low tension high PP) = high were present and occupied the total rate absorption of gas into liquid volume Physiologic Implications Underwater Breathing Apparatus Physiologic Implications Underwater Breathing • Increased CO2 levels • Immersion Effects • CO2 retention if breathing inadequate • P Δ feet to chest ~120cm H2O, to eliminate CO2 produced. negative static lung load dev when • Common in all diving due to ↑WOB lungs deeper than reg/counterlung • Immersion effects • Fluid shift to central circulation • Gas density • ↑cardiac afterload, ↑blood to lungs = • Equipment effects ↓lung compliance, ↓ VC, ↑ airway resistance, diuresis • Exacerbated by exercise/work, panic, hyperventilation, dynamic airway • Equipment Effects compression • All underwater breathing equipment • Gas Density increases breathing resistance • i.e. Demand valve, dead space in • increased depth = increased density helmet/face masks/hoses (Gas law) = decreased flow • Movement of CO2 from blood to (Poiseuille’s law) = increased WOB lungs based on gradient/press Δ • Rebreathers – if inhaling Co2 = smaller Δ = less CO2 ventilated Dynamic Airway Compression (DAC) • Normal Expiration – gas flows out along airway because P1 >P2 • P1 -> P2 declines more quickly with Palv P1 P2 dense gas • At some point along the tube, airway P = intrapleural P (Ppl ) = equal pressure point (EPP) Equal • Beyond this point, P along airway is Pressure less than Ppl = airway compression Point • Catch 22 P Pl • Harder you try to exhale, • higher the PPl = shift EPP to the left • ↑ WOB which ↑ CO Palv P1 P2 2 • Distal movement of EPP • Increased a/w resistance (asthma, gas density), reduced lung elastic recoil, negative static lung load 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 Oxygen Toxicity Ocular OxTox • Toxic effects due to PPO2 (not %) • Decreased peripheral vision • CNS main concern but pulm may ~2.5-3.0 hrs at 3.0 ATA become an issue with extended • Central vision unaffected, usually dive ops (serial bounce, sat) resolved within 30-45mins after treatment stops • PPO2 limits CF diving • Progressive myopia • 1.6 ATA routine • Generally 2-4 weeks of treatment • 1.8 ATA exceptional (requires CO and usually completely reversed sign-off) after ~3-4 weeks (sometimes up to 1 year) • DM, elderly more susceptible • Unclear whether hood/monoplace increase risk vs. facemask CNS Ox Tox • 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 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) 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 Nitrogen Narcosis “Rapture of the deep” • Reversible depression of neuronal • S/Sx excitability due to inert gas • ↓performance mental/manual work • Potency Xe > Kr > Ar > N > H > Ne > (higher fx affected most) He • Dizzy, euphoria, uncontrolled laughter • Interfere with transmission of EP • Overconfidence, overly talkative across synaptic gap • Memory loss/post-dive amnesia • Immediate onset at depth, stable after • Perceptual narrowing (fixation) few mins at depth, rapid resolution • Impaired sensory functioning upon ascent • LOC >100msw • Potentiated by ↑CO2 levels • Prevention • No true acclimatization, divers may • Depth <30msw, plan dive ahead & dev short term tolerance practice tasks • RFs • If affected – decrease depth • Depth, gas mix, anxiety, task loading, • Heliox cold, fatigue, exercise, EtOH, sedatives, ↑CO2 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
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