When practising scuba diving, we use a gas mixture that allows us to breathe underwater. Oxygen is vital for humans, but it can become toxic beyond a certain partial pressure, along with other factors such as exposure time.
Oxygen Toxicity
The partial pressure (Pp) of a gas within a mixture is the result of multiplying its concentration (%) by the absolute pressure to which it's subjected. The tolerable partial pressure values of oxygen (Pp O2) over a given period without immediate or delayed alterations fall between the limits of 0.17 to 1.7 ATA.
- If Pp O2 < 0.17 Atm, hypoxic syncope (loss of consciousness) may occur.
- If Pp O2 is between 0.4 and 1.7 Atm, pulmonary hyperoxic accidents may occur
- If Pp O2 > 1.7 Atm, convulsive neurological accidents may arise.
Causes of oxygen toxicity during diving occur from breathing pure O2 under pressure (closed-circuit rebreather below 7 metres), or compressed air beyond 72 metres depth.
Clinical Presentation
Neurotoxicity
An initial phase typically appears with general malaise, nausea, facial muscle tics, muscle cramps, tachycardia, followed by an epileptiform convulsive episode resembling "Grand mal" (epileptic seizure). The episode is dramatic and dangerous, potentially causing trauma if in a hyperbaric chamber, or pulmonary overpressure and drowning if occurring during the dive.
If removed from the hyperoxic environment, the subject recovers without sequelae, but persistence in said environment increases the frequency of episodes, potentially leading to death.
- Prevention: avoid descending with compressed air beyond 80 metres depth. When using nitrox, calculate according to the mixture percentage, the O2 Pp to determine the maximum achievable depth with that mixture.
- Treatment: remove the affected subject from the hyperoxic environment (ascend during dive or reduce pressure within hyperbaric chamber).
Medical staff will treat the patient as a "Grand mal" episode (epileptic seizure).
Pneumotoxicity (pulmonary irritation)
This is a slow, progressive effect dependent on the Pp O2 value established according to exposure time, manifesting as: cough, expectoration, respiratory difficulty, chest pain behind the sternum, reduced vital capacity, potentially developing pulmonary alveolar oedema (lung flooding).
Very rare in recreational divers, as at least ten hours at six metres depth breathing pure O2 are required for initial signs to appear.
Carbon Monoxide Poisoning
A relatively common clinical presentation in daily life caused by inhaling gases from incomplete carbon combustion (braziers, exhaust fumes, fire smoke, etc.).
In underwater activities, the problem arises when divers breathe CO-contaminated air, which at surface pressure isn't toxic (25 parts per million CO), but that same air breathed at 30 metres depth would contain 100 ppm CO, becoming toxic. It's an odourless, colourless and tasteless gas, very difficult to detect when breathing from our tank.
Pathophysiology
CO has 240 times greater affinity for haemoglobin (protein transporting oxygen vital for cellular metabolism) than O2, and 40 times greater affinity for myoglobin (muscle transport protein), causing disruption at the cellular respiration level.
Symptoms
Acute Form
Presents primarily neurological symptoms: headache, nausea, vomiting, visual and auditory hallucinations, respiratory difficulty and confusion. Pyramidal and extrapyramidal signs (tremors, uncontrolled movements) may appear, with frequent erythematous plaques (red patches) and facial flushing. In severe cases, loss of consciousness.
Cardiac abnormalities with arrhythmias and ECG changes (ST segment alterations and T wave flattening/inversion), plus pulmonary issues like acute pulmonary oedema, form part of CO poisoning. After the initial phase, a delayed and irreversible demyelinating neurological syndrome (nerve conduction deterioration) may occur.
Chronic Form
Characterised by headaches, appetite loss, insomnia, irritability, facial paresthesia (tingling), vertigo, and anaemia. Diagnosis primarily based on clinical history supplemented by plasma carboxyhaemoglobin level determination.
Prevention and Treatment
Use appropriate lubricants and filters in the filling compressor, and avoid CO sources in compressor air intake (e.g., car exhaust fumes). Pre-hospital treatment: highest possible oxygen concentration. Hospital treatment involves hyperbaric oxygen therapy to:
- Increase dissolved O2, immediately correcting tissue anoxia (O2 lack in tissues).
- Promote separation of haemoglobin from carbon monoxide (carboxyhaemoglobin) transforming it into oxygenated haemoglobin (oxyhaemoglobin).
- Prevent delayed neurological sequelae.
Recommended protocol: 46 minutes at 3 ATA followed by 30-60 minute decompression. Most cases show dramatic improvement within first 30 minutes.
For severe poisoning, repeat sessions one hour later to displace CO fixed at tissue level, then conduct 2-5 sessions of 45 minutes at 3 ATA within first 48 hours to prevent delayed demyelinating neurological syndrome.
Not a common clinical presentation, but could explain many fatal accidents of unclear cause in deep-diving divers.
Carbon Dioxide Poisoning
Carbon dioxide is a colourless gas, slightly denser than air, present in the environment from animal respiration and plant fermentation. Normal atmospheric CO2 proportion is below 2%; above 9% becomes toxic. CO2 normal at surface would be toxic when breathed at depth.
Causes of hypercapnia (increased blood CO2 concentration) include: high CO2 concentration in inhaled mixture, or gas accumulation in (closed) breathing circuit, but most common cause is poor compressor air intake. Another endogenous source (from diver) is hypercapnia from intense muscle activity and/or increased inspiratory resistance from poorly adjusted regulator or breathing very dense gas mixtures.
CO2 elimination becomes inefficient with agitated breathing, causing accumulation. Poor diver breathing technique may cause inadequate pulmonary ventilation with incomplete CO2 exhalation. Intense exercise, cold and stress increase CO2 production.
As CO2 Pp increases, these symptoms appear: mild hyperventilation, panting, headaches, loss of breathing rhythm making voluntary breath-holds impossible, throbbing temporal headache, initial carbonic narcosis, severely altered breathing rhythm with shallow respiration, severe headache with facial congestion, dizziness and vomiting potentially causing unconsciousness.
When arterial CO2 levels rise, bulbar respiratory centres become excited causing excessive respiratory rate acceleration making breathing inefficient; surfacing worsens symptoms with vomiting risks causing drowning or pulmonary overpressure in final ascent metres.
Prevention relies on better breathing control and awareness of physical condition, plus maintaining dive equipment properly. At slightest breathing rhythm disruption, cease activity, alert buddies and control respiration.
Optimal ventilation for divers involves short inhalations, brief respiratory pauses and long, deep exhalations. Deep breath-holds to conserve air are counterproductive as they hinder nitrogen elimination.
Regulating regulator airflow isn't particularly useful either, creating false air reserve sensation, as the problem is expiratory not inspiratory. Increased CO2 promotes oxygen toxicity, potentiates inert gas narcotic effects and favours decompression accidents.
Nitrogen Narcosis
When breathing air above atmospheric pressure due to increased nitrogen Pp, our body experiences gradual alterations:
- Initially affects reasoning and short-term memory.
- Secondly impacts motor coordination and reaction time, worsening with increasing depth.
- If N2 Pp isn't reduced, may lead to loss of consciousness and fatal drowning.
Individual susceptibility to narcosis is highly personal.
Tolerance thresholds vary enormously between individuals, with symptom ranges from 35 to 120 metres, disappearing as absolute pressure decreases.
Narcosis from inert gases (nitrogen and helium), also caused by increased partial pressure, will be covered in more detail in a future chapter.
