 | Viet Tran When it comes to pressure, you can always have too much of a good thing. Nitrogen narcosis, oxygen toxicity - seemingly innocent enough at the surface, but under pressure, the body shows cracks... |
Summary
- N2 causes both DCS (biophysical) and "nitrogen narcosis" (biochemical effect) - onset around 35-50 m and relieved with ascent
- O2 toxicity occurs > ~ 1.6 ATA , relieved with reducing O2 (either by ascent or decreasing FiO2)
- Most profound manifestations of O2 toxicity include Pulmonary (Lorrain Smith effect) & CNS (Paul Bert effect)
- He can cause High Pressure Neurological Syndrome (HPNS) at depths > 150m on He mix
Nitrogen (N2)
- DCS from N2 is caused by both biophysical and biochemical effects (see post on DCI), whereas N2 Narcosis is a direct biophysical effect on CNS
- N2 solubility: Fat > Blood
- Effects higher cognitive function ie "stuck on stupid"
Causes
- Increased partial pressure of N2 has a direct effect on neurotransmitters
- Meyer-Overton theory of inhaled anaesthetics suggests that once a threshold for lipid solubility is reached, enough gas will have dissolved through the lipid soluble membrane to exert an anaesthetic effect (rather than any specific gas) - since N2 is highly lipid soluble, it is also a potent anaesthetic agent
Onset
- 4-6 ATA (30-50m): Insidious Onset
- 6-8 ATA (50-70m): More severe symptoms
- > 8 ATA: Incapacitating
| Early Effects
| Late Effects
Long Term
| Risk Factors
|
Prevention/Protection
Management
- Avoid threshold exposure by limiting air diving to 30-50m (dependent on task and experience)
- Acclimatisation
- Task training
- Motivation
- Stimulants (controversial)
Management
- Ascend (reduces partial pressure N2)
- Usually results in rapid resolution - suggesting that there is a direct toxic effect and that N2 solubility is high
Oxygen (O2)
- O2 toxicity occurs > ~ 1.6 ATA eg breathing air at 7.6 ATA (66m) = 7.6 x 0.21 = 1.6 ATA or breathing 100% O2 at 1.6 ATA (16m) = 1.6 ATA
- Don't forget that onset is related (in an unknown relationship) to the ATA eg 6ATA O2 has a much faster onset of toxicity than 2ATA O2 - this is important because a typical Table RN62 dives to 18m (2.8ATA) on FiO2 100% = 2.8ATA O2 (ie > 1.6 ATA threshold) with 5 min air breaks to "reset" risk (but probably not back to baseline)
- Used to prevent, treat and avoid DCS
Circulating O2
- FiO2 21% @ 1 ATA = 0.2 ATA = 100 mmHg (760 x 0.21 - water vapour) = 50 mmHg (in tissues) = 3ml/L blood/min
- FiO2 100% @ 2.8 ATA (ie RN62) = 2.8 ATA = 2000 mmHg (760 x 2.8 - water vapour) = 500 mmHg (in tissues) = 60ml/L blood/min
Benefits
- Angiogenesis (one reason for HBOT in wound healing)
- Immunomodulation (by impairing white cell diapedesis)
- Free radical formation
- Vasoconstriction (which is why it is no longer routine in acute AMI)
- Other: bradycardia, increased ventilation, small decrease in cardiac output
- Normobaric O2 paradox: less red cell mass
Toxicity
- Due to a high partial pressure of O2 > 1.6 ATA that can be achieved either by increasing FiO2 or ATA or both
- Precise mechanisms of toxicity unknown but a combination of effects most likely:
- Depression of cellular metabolism
- Enzymatic inactivation
- O2 free radical theory: reactive O2 species from aerobic metabolism (overwhelming normal antioxidant mechanisms) leading to direct cellular toxic effects
O2 on Lungs
- aka Lorrain Smith effects
- More relevant for chamber diving, saturation diving and submarine
- Occurs earlier on in dive (eg 1.6 ATA) vs CNS toxicity - to prevent suggest limiting dives: RCC 18m, Diving 7m (working) or 9m (resting)
- PTU = Pulmonary Toxic Dose: 1 PTU = 1 minute at 100% FiO2 @ 1 ATA - threshold for Lung toxicity > 600 PTU
- Causes
- Respiratory distress from damage by free radicals (FVC is most sensitive for monitoring this)
- Acute: Exudative phase -> Proliferative phase
- Chronic: Hypeplasia & Fibrosis
- Symptoms
- Mild tracheal irritation
- Chest tightness
- Retrosternal pain
- Cough
- Dyspnoea
- Signs
- Rales, Nasal mucousal hyperaemia
- Often a normal Cxr early
O2 on CNS
- aka Paul Bert effect
- More relevant for wet diving (lower threshold - 10x higher incidence)
- Exacerbating factors: wet diving, cold, severe exercise, increased CO2
- Symptoms
- Visual: tunnel, blurring
- Oto-vestibular (calssic): tinnitus, hearing loss, vertigo, dizziness
- Nausea (classic): persistant or intermittent
- Muscle twitching (pathogneumonic)
- Mental: confusion, anxiety, agitation, irritbailty, amnesia
- Motor: inco-ordination, unusual fatigue
- Seizures
- Death
- The O2 off effect
- Paradoxical seizures after removing O2
- Though ti be due to sudden reduction in PO2 -> responsive vasodilation -> seizures
O2 on other systems
- Lenticular (cataracts)
- Lens (reversible myopia)
- Immunomodulation
Treatment of O2 Toxicity
- Reduce the PO2 by ascending (if safe) and/or reducing FiO2 (eg 'air break' in chamber)
- Supportive
- +/- BZDP etc if recalcitrant seizures
Carbon Dioxide (CO2)
- CO2 endogenously produced therefore PCO2 @ 1ATA = 40 mmHg, PCO2 @ 2ATA = 40 mmHg
- Production 200ml/min (rest), 3L/min (work)
- CO2 is primary resp stimulus
Causes of CO2 toxicity
- Failure of absorbent/scrubber system
- Dirty gas
- Under breathing/skip breathing (to maximise tank time)
Dose-Response of CO2Symptoms
- Opposite of O2 - uncomfortable, headache, flushed, SOB
- Increases chance of N2 or O2 toxicity
Treatment
- Remove from toxic environment = rapid recovery of most symptoms
- Headache can persist for > 24hrs
Prevention
- Teach CO2 signature
- CO2 monitors (in chambers)
Carbon Monoxide (CO)
- 240x binding kinetics of O2
- SSG diving or dirty gas
Weaver's Criteria for HBOT in CO poisoning, any of:
- Loss of consciousness at any stage
- Age > 50 years
- COHb > 25%
- Metabolic Acidosis
- Failure of treatment after 6hrs FiO2 100%
- Pregnant (despite being a relative contraindication for HBOT in general)
- Delayed neurological sequelae (after initial recovery)
If Weaver's Criteria Met: Treatment Table
A local guideline
- Within the first 24hrs start with RN61/USN5 then 2 sessions of 14:90:20 (14m for 90min with air breaks and 20min ascent)
- Then continue 14:90:20 BD until normal + 1 or plateau + 1
- Delayed neurological Sequelae: 5-10 days of 14:90:20 table
If Weaver's Criteria not Met
- 72 hrs of 100% O2
Helium (he)
- Used to offset issues with N2 and He
- He toxicity occurs at 43 ATA
- Weak narcotic (at best)
- Better heat transfer -> hypothermia
High Pressure Neurological Syndrome (HPNS)
- Symptoms: tremor, eeg changes, somnolence, headache
- Occur at depths > 16ATA (150m)
Other
- Will become more common when He runs out
- Neon
- Hydrogen
- Argon
