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From the Department of Anaesthesia, The Queen Elizabeth Hospital, Woodville South, Australia.
Address correspondence to: Dr. John Pfitzner, Department of Anaesthesia, The Queen Elizabeth Hospital, 28 Woodville Road, Woodville South, SA 5011, Australia. Phone: +61-8-8222-6000; Fax: +61-8-8222-7065; E-mail: pfitznerwines{at}ozemail.com.au
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Abstract |
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Source: Of the historical and recent references quoted, most are from aviation-medicine journals that are not often readily available to anesthesiologists.
Principal findings: Pressure breathing at moderate levels of airway pressure gave World War II fighter pilots a tactical altitude advantage. With today’s fast and highly maneuvrable jet fighters, very much higher airway pressures of the order of 8.0 kPa (
60 mmHg) are used. They are used in conjunction with a counterpressure thoracic vest and an anti-G suit for the abdomen and lower body. Pressurization is activated automatically in response to +Gz accelerations, and to a potentially catastrophic loss of cabin pressurization at altitude. During +Gz accelerations, pressure breathing has been shown to maintain cerebral perfusion by raising the systemic arterial pressure, so increasing the level of G-tolerance that is afforded by the use of anti-G suits and seat tilt-back angles alone. This leaves the pilot less reliant on rigorous, and potentially distracting, straining maneuvers. With loss of cabin pressurization at altitude, pressure breathing of 100% oxygen at high airway pressures enables the pilot’s alveolar PO2 to be maintained at a safe level during emergency descent.
Conclusion: Introduced in military aviation, pressure breathing for G-tolerance and pressure breathing for altitude presented as concepts that may be of general physiological interest to many anesthesiologists.
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Introduction |
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TOPAbstractIntroductionWorld War IIToday’s fighter aircraftElusive informationConclusionReferences |
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World War II |
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TOPAbstractIntroductionWorld War IIToday’s fighter aircraftElusive informationConclusionReferences |
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), gave pilots a tactical advantage by enabling them to fly at higher altitudes.4,5 The practical and theoretical aspects of this so-called pressure breathing are well documented in an informative article by Gagge et al. from Wright Field Aeromedical Laboratory.4 By the time this paper was published in February 1945, the authors were able to report that the practical ceiling for the breathing of pure oxygen was approximately 12.8 km (42,000 ft) for brief periods. However, by using pressure breathing at airway pressures of 2.0 to 3.3 kPa (equivalent to 15 to 25 mmHg at sea level), a few minutes at 15.2 km (50,000 ft) could be tolerated.
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Today’s fighter aircraft |
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TOPAbstractIntroductionWorld War IIToday’s fighter aircraftElusive informationConclusionReferences |
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12 mmHg) with each +1Gz increase, to a design maximum of 8.0 kPa ( 60 mmHg) at +9Gz.8,9 Also very important in elevating systemic arterial pressure during +Gz accelerations is the pilot’s performance of rigorous active straining.9 However, it is believed that the use of pressure breathing will lessen pilot reliance on these rigorous straining practices, and so reduce the physical and mental stresses that occur during high +Gz maneuvers.9
Second, pressure breathing has a vital role, as pressure breathing for altitude (PBA), in the event of a sudden and potentially catastrophic loss of cabin pressurization at altitude.10 Because an adequate alveolar PO2 (PAO2) requires an adequate inspired PO2 (PIO2), pilot oxygenation in the event of loss of cabin pressurization becomes increasingly precarious at the low ambient barometric pressures seen at high altitude. The influence of altitude on PAO2 is summarized in the Table, for subjects breathing either air or 100% oxygen. The PAO2 values (in mmHg) were calculated using the formula, PAO2 = PIO2 - (PACO2 * 1.25); where PIO2 = (barometric pressure - 47) * FIO2; and where different values for PACO2 were used.
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calculations is to demonstrate the very relevant effect that hyperventilation has on PAO2, especially at altitude. A good example is that of acclimatized mountaineers climbing Mount Everest. Without gross hyperventilation to a PACO2 of the order of 1.5 kPa ( 11 mmHg), it would be impossible to conquer Mount Everest breathing air11 (see Table). Even climbing Mount Kilimanjaro breathing air requires hyperventilation and a PACO2 of the order of 2.7 kPa ( 20 mmHg). In aircraft below 12.8 km (42,000 ft), as in commercial jets flying at about 12.2 km (40,000 ft), the ambient pressure is such that prompt use of oxygen via facemask allows consciousness to be maintained while the aircraft makes an emergency descent.12 However, to maintain full fighter pilot capability in the event of loss of cabin pressurization, pressure breathing is used at altitudes above 11.9 km (39,000 ft).
With pressure breathing it has been shown that at an airway pressure of 9.3 kPa ( 70 mmHg), physiologically safe PAO2 levels can be achieved following rapid decompression at simulated altitudes of 18.3 km (60,000 ft) and higher.13,14 Thus, the pilot can initiate a rapid emergency descent or if necessary safely eject. The use of pressure breathing at airway pressures of the order of 8.0 kPa ( 60 mmHg) has enabled the approved and published ceiling of operation of planes such as the ‘Eurofighter’ to be increased from 15.2 km (50,000 ft) to 18.3 km (60,000 ft).
The practical use of PBA systems in emergency ‘get me down’ exercises has recently been assessed by Lindeis et al.14 in six trained volunteers who underwent rapid pressure-chamber decompression from a simulated operational15 altitude of 6.9 km (22,500 ft) to a simulated postemergency altitude of either 18.3 km (60,000 ft) or 21.9 km (72,000 ft). The decompression was initiated in 0.6 sec and was maintained for 180 sec in all six subjects following decompression to 18.3 km, and for 60 sec in all six subjects following decompression to 21.9 km. Only four of the six subjects were able to complete the second 60 sec of the study at the 21.9 km simulated altitude. The inspired oxygen was 100%, and the airway pressure of the PBA system was activated to either 9.3 kPa ( 70 mmHg) or 10.6 kPa ( 80 mmHg) for the two different decompression altitudes. Using a sophisticated visual-serial-choice assessment, it was found that there was a greater impairment of reaction time following a rapid decompression to 21.9 km (72,000 ft) than to 18.3 km (60,000 ft). This greater impairment of reaction time was considered to be due not to hypoxia, but rather to an impairment of vision caused by the vaporization of tears and subsequent increased tear production.14 Vaporization, or boiling, of tears occurs at altitudes above about 19.2 km (63,000 ft), where the barometric pressure is 6.26 kPa ( 47 mmHg), the saturated vapour pressure of H2O at 37°C.
With sudden loss of cabin pressurization there is also the possibility of arterial gas embolism16 as with rapid ascent from an underwater dive,17,18 and also a considerable risk of decompression sickness from dissolved gas coming out of solution with time.19–21 This latter risk is very much reduced by preoxygenation to achieve denitrogenation,15,22 as employed with high flying surveillance aircraft.22
Today’s fighter pilots therefore operate in cabins pressurized according to a pressurization schedule,15 they breathe up to 100% oxygen,15 and they wear and use pressure breathing equipment. Pressure breathing, without appreciably restricting pilot mobility, improves G-tolerance and hence pilot performance, and also reduces the grave risks inherent in loss of cabin pressurization at altitude.
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Elusive information |
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Conclusion |
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TOPAbstractIntroductionWorld War IIToday’s fighter aircraftElusive informationConclusionReferences |
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Revision received December 13, 2002. Accepted for publication September 26, 2002.
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References |
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2 Gregory GA, Kitterman JA, Phibbs RH, Tooley WH, Hamilton WK. Treatment of the idiopathic respiratory-distress syndrome with continuous positive airway pressure. N Engl J Med 1971; 284: 1333–40.
3 Gregory GA, Edmunds LH Jr, Kitterman JA, Phibbs RH, Tooley WH. Continuous positive airway pressure and pulmonary and circulatory function after cardiac surgery in infants less than three months of age. Anesthesiology 1975; 43: 426–31.[Medline]
4 Gagge AP, Allen SC, Marbarger JP. Pressure breathing. J Aviat Med 1945; 16: 2–8.
5 Barach AL, Eckman M, Ginsburg E, et al. Studies on positive pressure respiration. I. General aspects and types of pressure breathing. II. Effects on respiration and circulation at sea level. J Aviat Med 1946; 17: 290–320, 356.
6 Balldin UI, Wranne B. Hemodynamic effects of extreme positive pressure breathing using a two-pressure flying suit. Aviat Space Environ Med 1980; 51: 851–5.[Medline]
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11 Sutton JR, Reeves JT, Wagner PD, et al. Operation Everest II: oxygen transport during exercise at extreme simulated altitude. J Appl Physiol 1988; 64: 1309–21.
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14 Lindeis AE, Fraser WD, Fowler B. Performance during positive pressure breathing after rapid decompression up to 72 000 feet. Human Factors 1997; 39: 102–10.[Medline]
15 Webb JT, Balldin UI, Pilmanis AA. Prevention of decompression sickness in current and future fighter aircraft. Aviat Space Environ Med 1993; 64: 1048–50.[Medline]
16 Rudge FW. Altitude-induced arterial gas embolism: a case report. Aviat Space Environ Med 1992; 63: 203–5.[Medline]
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19 Balldin UI, Borgström P. Intracardial bubbles during decompression to altitude in relation to decompression sickness in man. Aviat Space Environ Med 1976; 47: 113–6.[Medline]
20 Ryles MT, Pilmanis AA. The initial signs and symptoms of altitude decompression sickness. Aviat Space Environ Med 1996; 67: 983–9.[Medline]
21 Webb JT, Krause KM, Pilmanis AA, Fischer MD, Kannan N. The effect of exposure to 35,000 ft on incidence of altitude decompression sickness. Aviat Space Environ Med 2001; 72: 509–12.[Medline]
22 Webb JT, Fischer MD, Heaps CL, Pilmanis AA. Exercise-enhanced preoxygenation increases protection from decompression sickness. Aviat Space Environ Med 1996; 67: 618–24.[Medline]
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