Arterial blood gas changes in progressively deeper breath-hold dives

Studies involving breath-hold dives as deep as 60m have identified a spike in arterial PO 2 (PaO 2 ) and PCO 2 (PaCO 2 ) apparently associated with lung compression by water pressure as depth increases. Competitive breath-hold dives may exceed 100m, raising the possibility that a spike in PaCO 2 might contribute to narcosis-like symptoms sometimes experienced. To predict the magnitude of this spike, three elite breath-hold divers were instrumented with radial artery catheters and had arterial blood specimens taken at the bottom on separate dives to 20, 40, 60, and 80m with another specimen either after beginning apnea but before leaving surface (one participant) or on arrival back at the surface while still apneic (two participants). Contrary to prior expectations, the greatest spike in PaO 2 was at 40m (mean 29.3 kPa, 220 mmHg) and the trajectory of rise in PaCO 2 also plateaued at 40m (mean 5.61 kPa, 42.1 mmHg [from a mean baseline of 2.53 kPa after pre-dive hyperventilation] and 5.54 kPa, 41.6 mmHg at 60m) before rising again after 60m (80m mean 6.9 kPa, 51.5 mmHg). This suggests that a spike in arterial gases associated with lung compression was detectable until the greatest proportional changes in lung volume with increasing pressure had occurred. Thereafter, PaO 2 decreased through metabolism and PaCO 2 increased through simple metabolic accumulation. That the compression effect seemed maximal at 40m (five atmospheres absolute pressure) may relate to the simple Boyle’s Law predication that the lung may be compressed to close to residual volume (20-30% of total lung capacity) at this pressure.