Early Clinical Oxygen Supplementation
Oxygen supplementation grew gradually in medicine. First Mayow then Boyle demonstrated absence of air made mammalian life impossible by 1666. Priestly in 1774 and Lavoisier in 1777 isolated and demonstrated oxygen as air’s vital component. Beddoes medicalized oxygen as a panacea in 1789 through his Pneumatic Institute in Bristol, which closed in 1800. Thereafter oxygen use fell out of favor. (Warnock E, Tovell RM. Oxygen therapy and resuscitation. Anesthesiology. 1940; 1:187-204)
The roots of oxygen supplementation in anesthesia are also instructive. Availability, purity, equipment, logistics, and indications for use factored into acceptance. Most early anesthetics using ether, chloroform, and nitrous oxide were delivered in room air (FiO2 0.21) with the patient breathing spontaneously. The first inhaled ether anesthetic was reported in 1846. (Bigelow HJ. Insensibility during surgical operations produced by inhalation. Boston Med Surg J. 1846; 35:309-17) Hooper reported using oxygen after ether anesthesia to aid recovery in April 1847. (Hooper W. Inhalation of oxygen for resuscitating etherized patients. The Pharmaceutical Journal. 1847; 6:508-9)
Supplemental oxygen was first used to treat nitrous oxide poisoning in the 1860s. (Andrews E. The Oxygen Mixture, a new anaesthetic combination. Chicago Medical Examiner. 1868; 9:656-61) A common anesthetic technique then relied on 100% nitrous oxide inhalation until signs of adequate anesthesia appeared—stretor, jacitation, and lividity. With the patient obtunded near asphyxiation the procedure was performed. Blood loss was minimal as death was near. At surgery’s end oxygen was given for rescue treatment. (Smith WDA, The introduction of nitrous oxide and oxygen anaesthesia. Brit J Anaesth. 1966; 38: 950-62)
Volatile agent-oxygen combinations surfaced in the late 19th C. Who to credit is a matter of dispute. Kreutzmann cited Neudorfer in Vienna in his 1887 report. (Kreutzmann H. Anaesthesia by choloroform and oxygen combined: preliminary report. Pacif Med Surg J. 1887; 30:462-3) Suarez published his “Spanish method” in 1898. (Diz JC, Franco A. A Spanish pioneer in the use of oxygen in anaesthesia. International Congress Series. 2002; 1242:121-5) Routine oxygen supplementation during and after inhalation anesthesia grew in the mid-20th C. Increased muscle relaxant use likely hastened oxygen’s acceptance as part of anesthesia.
Awareness about how too little and too much oxygen affects life also grew gradually. Claude Bernard’s early lectures on anesthetics and asphyxia were published in 1875. (Bernard C. Lectures on anesthetics and on asphyxia. Translated by BR Fink. Park Ridge, IL:Wood Library-Museum of Anesthesiology. 1989) Paul Bert, a Bernard protégé, reported central nervous system oxygen toxicity effects in animals and other toxic effects on plants and animals in 1878. William Osler’s first textbook edition published in 1892 made no reference to supplemental oxygen. Lorrain Smith induced fatal pneumonia in rabbits with two to four days of 80% oxygen exposure in 1899. (Barach AL. Widening scope of oxygen therapy in the treatment of disease. Anesth Analg. 1932; :71-7)
Oxygen supplementation got a boost with efficacious poison gas-induced pulmonary injury treatment with 40% to 50 % oxygen during WW I. Barcroft and Haldane demonstrated hypoxemia’s relationship to harmful effects between 1914 and 1922. Enthusiasm built afterward to where Cohen, quoted by Buettner, said in 1931: “Oxygen to be efficacious must be used freely, frequently, fearlessly, and almost constantly, nor must its use be postponed until the patient is moribund for it will not revive the dead.” (Buettner JJ. Oxygen therapy. Anesth Analg. 193; 10:39-44) A new “oxygen culture” was thus born out of war-time experience.
By 1932 Barach endorsed specific indications for oxygen supplementation: lobar and bronchopneumonia; postoperative atelectasis; atelectasis of the new-born; acute and chronic cardiac failure; chronic pulmonary fibrosis; and (in combination with carbon dioxide) carbon monoxide poisoning and morphine poisoning. For these conditions he advocated an oxygen therapy range of between 30% and 60%. (Barach AL. Widening scope of oxygen therapy in the treatment of disease. Anesth Analg. 1932; :71-7) By 1940-41 the indications and physiological considerations applicable to oxygen supplementation were defined for cardiac disease, resuscitation, and “asphyxia neonatorum.” (Warnock E, Tovell RM. Oxygen therapy and resuscitation. Anesthesiology. 1940; 1:187-204) (Behkne AR. Certain physiological principles underlying resuscitation and oxygen therapy. Anesthesiology. 1941; 2:245-60)
