Diver Risk & Physiology

Problems Beneath the Surface

What Kills Divers

The DAN/UHMS 2014 Medical Examination of Diving Fatalities Symposium challenged a long-standing assumption: that most diving deaths are drowning. The symposium's central finding is that medical examiners routinely classify in-water deaths as drowning by default, when the true cause is often cardiac, neurological, or barotrauma-related. Cardiac arrest in water produces a victim found submerged — which looks like drowning. The autopsy findings are frequently indistinguishable without a proper protocol.

When diving deaths are investigated properly, cardiac events account for approximately 25% or more of diving fatalities. Immersion triggers the mammalian dive response — bradycardia and peripheral vasoconstriction — which increases myocardial wall stress. This can precipitate arrhythmias in divers with pre-existing cardiac disease, often undiagnosed. Gas management failure is the leading root cause of the sequence ending in death. Running out of gas, or making decisions under the pressure of a low gas situation, precipitates the majority of fatal incidents through panic ascent (causing AGE), drowning, or cardiac arrest from extreme exertion.

Arterial gas embolism from pulmonary barotrauma is identifiable at autopsy by intravascular gas in the cardiac cavities, but this finding is only present in a minority of AGE cases — most are missed without proper investigative protocol. Decompression sickness is rarely the direct cause of death in recreational divers, but contributes to fatalities through incapacitation: neurological DCS producing paralysis or loss of consciousness underwater.

The implication for fitness-to-dive assessment is that cardiovascular screening is the highest-yield medical intervention.

What Is Decompression Sickness?

Decompression sickness (DCS), also called "the bends," occurs when inert gas — nitrogen on air or nitrox, nitrogen and helium on trimix — that dissolved into body tissues under pressure forms bubbles as ambient pressure decreases too rapidly during ascent.

Henry's Law governs the mechanism: the amount of gas dissolved in a liquid is proportional to the partial pressure of that gas above it. At depth, elevated partial pressure of nitrogen drives more nitrogen into solution in blood and tissues. The longer and deeper the dive, the more nitrogen is absorbed. During ascent, as pressure drops, that nitrogen must be eliminated through respiration. If ascent is too rapid, nitrogen comes out of solution before it can be exhaled, forming bubbles within tissues and blood.

The body is modelled as a set of tissue compartments with different gas exchange rates — fast compartments (brain, blood, heart) load and off-gas quickly; slow compartments (fat, tendon, bone) exchange gas over hours. This is the basis of all decompression algorithms, from Haldane's original 1908 tables through to modern Bühlmann ZHL-16 implementations in dive computers.

What Bubbles Do

Bubbles cause injury through several mechanisms simultaneously. Mechanical compression and distortion of tissues at the site of formation (joints, spinal cord, inner ear). Vascular obstruction — bubbles large enough to lodge in small vessels cause ischaemia distal to the blockage. Endothelial damage — bubbles in contact with vessel walls trigger inflammation and complement cascade activation. Coagulation activation — the damaged endothelium and bubble surfaces activate platelets and clotting factors, worsening perfusion. The result depends on where bubbles form and how large the load is.

DCS Type I and Type II

Type I DCS (musculoskeletal and lymphatic) produces joint and limb pain — most commonly shoulders, elbows, and knees — skin marbling or mottling, and lymphatic swelling. Painful and debilitating, but not immediately life-threatening.

Type II DCS (neurological and cardiopulmonary) involves the spinal cord, brain, or inner ear, producing paresthesias, weakness, paralysis, bladder or bowel dysfunction, vertigo, or the "chokes" — pulmonary DCS with chest pain, dyspnoea, and respiratory distress from bubbles in pulmonary vasculature. These are emergencies.

When Symptoms Appear

Published onset data from compiled clinical series: approximately 42% of cases are symptomatic within 30 minutes of surfacing; 60% within 1 hour; 83% within 3 hours; 95% within 6 hours; 99% within 24 hours. Symptoms appearing more than 6 hours after surfacing warrant consideration of alternative diagnoses. In-water symptom onset does occur but is less common in recreational diving and more typical of technical or saturation exposures.

The Medical Dimension

Given that cardiac events account for a substantial proportion of diving fatalities, cardiovascular screening is the most clinically significant component of fitness-to-dive assessment.

The mammalian dive response generates a significant increase in myocardial wall stress in divers with coronary artery disease, hypertension, or structural heart disease. Standard fitness-to-dive evaluation includes resting ECG, and in older divers or those with risk factors, exercise testing to screen for exercise-induced arrhythmia or ischaemia. Pollock et al (2024) identified untreated hypertension as a contributing factor in a review of arterial dissection cases in divers.

PFO — present in approximately 25–30% of the population — is relevant to fitness-to-dive because it allows venous gas emboli to bypass the pulmonary filter and enter arterial circulation. Most divers with PFO dive without incident for years; the shunt only becomes problematic when venous bubble loads are high enough to produce paradoxical embolism. The DAN/UHMS 2015 PFO workshop concluded that divers with known PFO should use more conservative decompression profiles and that those with recurrent unexplained neurological DCI should be evaluated with bubble contrast echocardiography.

Several medication classes interact with diving physiology in ways not always discussed at pre-dive medical screening. Beta-blockers blunt the heart rate response and may mask exertion warning signs. First-generation antihistamines cause sedation that interacts with nitrogen narcosis. Diuretics cause dehydration, an established DCS risk modifier. Anticoagulants complicate the management of DCS as well as the risk of intracranial haemorrhage if AGE occurs. None are absolute contraindications, but all require specific consideration in context.

The majority of fatal incidents involve a recognisable human factors chain rather than simple physiological failure. Gas management errors, task loading, inadequate situational awareness, and decision-making under stress are consistent findings in incident investigation.

Risk Factors

DCS risk increases with deeper, longer dives; rapid ascent or missed decompression stops; repetitive dives with short surface intervals; dehydration; cold water or thermal stress; and pre-existing conditions including PFO, cardiovascular disease, obesity, and significant age-related decline. These are explored in detail in Predisposing Factors for DCS.

Prevention

Ascend no faster than 9–10 m/min throughout the dive. Complete all scheduled decompression and safety stops — the 5 m/3 min safety stop is a minimum, not a ceiling. Use a dive computer, but understand what it is and is not accounting for. Stay hydrated before, during surface intervals, and after diving. Avoid strenuous post-dive exercise for at least an hour. Wait 12–24 hours before flying depending on dive type (see the predisposing factors article for DAN-specific intervals). Declare medical conditions accurately at screening — the fitness-to-dive system only works with accurate information.

First Aid

1. Lay the diver horizontal — not seated, not upright; horizontal
2. Administer 100% oxygen via tight-fitting non-rebreather mask at 15 L/min
3. Hydrate if the diver is conscious and can swallow without risk of aspiration
4. Call DAN emergency line: +1-919-684-9111 (Americas); +65-6492-9299 (SE Asia); +39-06-4211-8685 (Europe)
5. Evacuate to the nearest hyperbaric facility — do not wait to see if symptoms improve

References

• Denoble PJ (ed) (2015). Medical Examination of Diving Fatalities Symposium Proceedings. DAN/UHMS.
• Denoble PJ, Holm JR (eds) (2015). Patent Foramen Ovale and Fitness to Dive: Consensus Workshop Proceedings. DAN/UHMS.
• Denoble PJ, Marroni A (eds) (2019). Differential Diagnosis of Decompression Illness Workshop Proceedings. DAN/UHMS.
• Pollock NW, Lippmann J, Pearn J, Hayman J (2024). Arterial dissection in scuba divers. Diving and Hyperbaric Medicine 54(3):188–195.
• Workman RD (1965). Calculation of decompression schedules for nitrogen-oxygen and helium-oxygen dives. US Navy Experimental Diving Unit Report NEDU-RR-6-65.
• Bühlmann AA (1983). Dekompression — Dekompressionskrankheit. Springer.

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