Anaesthesia in the Sixties, Bristol Fashion

reprinted from the GAT meeting programme April 1992

Iin 1964 the establishment for Senior Registrars in Anaesthetics in the South West Region of England was increased from one to three; two of the registrars at the Bristol Royal Infirmary (BRI) were promoted to SR and a young man at the end of his National Service landed one of the vacant registrar posts. He remembers three things about his first day in Bristol:

1. the advice given by a worldly wise SR (PJFB) to a colleague on his way to the cardiac theatre: "If the surgeon asks you anything, just say '100'; it will do for the pulse, the blood pressure or the temperature."

2. the answer given by an elderly consultant anaesthetist when asked why he was not going to take the patient's blood pressure during a thyroidectomy: "We have not taken it during the last twenty five years, so I don't think we will start this afternoon." (The anaesthetic was Pentothal 600mg, Scoline 100mg, gas-oxygen- Trilene.)

3. a comment in an anaesthetic nurse's notebook about the Senior Lecturer (who was later to become Bristol's first professor of anaesthesia): "Does not like being interfered with!"

It was a fascinating mixture of the old and the new in Bristol. At the BRI the old timers let the patients breathe on their own and did not intubate children who were being anaesthetized for post-tonsillectomy haemorrhage[1]. In contrast the University department taught that it was often better to relax and ventilate (though not to hyperventilate in the Liverpool style).

At Southmead they did nephrectomies under paravertebral block and gastrectomies under epidural anaesthesia[11] (Xylocaine 1.2% 48cc, Evipan 10%m, Scoline, Xylocaine spray, ET tube, N20, spontaneous respiration; uneventful!).

At Frenchay they gave the patients pentolinium so that only one swab was needed for a thoracotomy ("I never did master the differential diagnosis between induced hypotension and imminent death"[2]), and a classic book on neonatal anaesthesia was published[3].

Back in the BRI the academic department's standard anaesthetic for straightforward surgery was as follows: premedication, one and a half hours preoperatively, with intramuscular pethidine 50mg, phenergan 25mg and atropine 0.6mg; induction with Pentothal 50mg (sic), a 'mask acceptance dose', 75% N20-25% 02, d-tubocurarine 15mg as a test dose followed by a further 30mg; ET tube; IPPR, most commonly by a BOC Cyclator. Large muscular men were sometimes given 75mg of thiopentone whilst seriously ill patients who were being anaesthetised for cardiac surgery might receive only 12.5mg (or on one occasion only 6.25mg) if their saccharin arm-tongue time approached 90 seconds.

Intraoperative opiates and volatile agents were rarely added; the risk of awareness under anaesthesia was not thought to be important as long as (a) the anaesthetist talked to the patient throughout the operation ("Everything is going very nicely, Mrs. Jones. Are you comfortable?"), and (b) the cylinder of nitrous oxide did not run out!

The preoperative antihistamine was used not only for its sedative effect but also to counter the histamine released by the curare; the dose of thiopentone was kept small because larger doses were thought to be anti-analgesic[4] ("antanalgesic") and so might antagonise the effect of postoperative opiates , or even antagonize the effect of the nitrous oxide during the surgery.

This style of anaesthesia was so light that there were often wide swings of pulse rate and blood pressure; these were accepted without concern, since they were the very reflexes which had allowed Man to evolve successfully. If tears formed it indicated only that the patient had not been taken unnecessarily deep.

Complaints of "awareness" were rare; when they did occur, they were always put down to an error in technique, such as failing to talk to the patients at the moment they regained consciousness, especially if they were still intubated and people were still putting the dressings on the wound. In an case the few patients who said they remembered the spoken voice never said that they had felt pain during the operation. Postoperatively it was different: ten minutes after the nitrous oxide had been discontinued patients were in urgent need of analgesia. Since oxygen was not given routinely at the end of the anaesthetic diffusion hypoxia may have played a part in keeping them analgesic for the first few minutes.

Much of the open heart surgery was carried out under profound hypothermia, which was fondly known as the Deep Freeze. Two pumps were used, one to replace each side of the heart, while the patient's own lungs continued as the oxygenator; after cooling, sometimes to as low as 8oC, total respiratory and circulatory arrest was possible for periods up to 2 hours. During this time the patient looked and felt as though he or she had been in the mortuary fridge for a week. In the words of one visitor from Houston "sure is pretty damn cold, professor."

The infra-red C02 analyzer used in the cardiac theatre was the size of a bus and needed two hours to warm up and two cylinders for calibration. It was fascinating to see the effect of the cold temperature on the solubility of carbon dioxide in the blood and to watch a patient being ventilated with 10% C02, this being necessary in order to maintain an end tidal C02 of 5%.

It was the experience he gained in the care of these patients that led Burton to write his three classic papers[5,6,7]; the one on carbon dioxide monitoring is as fresh today as when it was written, and it should be compulsory reading for every young modern anaesthetist.

Before the sixties the real expertise in what we now call Intensive Care was found, in the South West, only in the fever hospital at Ham Green[10]. By 1965 the ITU at the BRI had been opened, so that now patients who needed IPPR in the city centre were no longer to be found scattered throughout the hospital attached precariously to intinerant Cyclators. The Professor of Medicine, who had fought hard against the establishment of the ITU and who had sworn that "no patient of mine will ever be nursed there", was no doubt surprised to find that the first patient admitted to the ITU was in fact one of his.

Near the beginning of September 1966 a batch of nitrous oxide cylinders filled by the British Oxygen Co. was contaminated with 1.5% nitric oxide. Two patients at the Bristol General Hospital were exposed to this mixture; one of them died. As a precaution until the matter had been fully investigated all operating lists were cancelled and only emergency cased were operated upon. It is interesting to read[8] : "the junior staff were comparatively inexperienced in techniques not involving the use of nitrous oxide, so it was decided that any necessary anaesthetics should be administered only by Senior Registrars and Consultants". No doubt today our juniors would be able to cope well enough, even at the teaching hospital!

Incidentally, this was not the first time that impure nitrous oxide had been inhaled in Bristol, for Humphry Davy himself wrote[9] in 1800: "A considerable time elapsed before I was able to produce the gas in a state of purity, and my first experiments were made on the mixtures of nitrous oxide, nitrogene and Nitrous gas (Nitric oxide)." It was lucky that he did not do himself an injury!


1. Gorham A P. The role of the anaesthetist in the management of post-tonsillectomy haemorrhage in children. Anaesthesia 1964; 19: 565-569.

2. Powell, Isabel. Recollections of a recovery ward nurse. Anaesthesia Points West 1973; 6:14.

3. Wilton T N P, Wilson F. Neonatal Anaesthesia and Allied Problems. Blackwell Scientific Publications Ltd, Oxon 1965.

4. Clutton-Brock J. Pain and the barbiturates. Anaesthesia 1961; 16: 80-88.

5. Burton G W. Metabolic acidosis during profound hypothermia. Anaesthesia 1964; 19: 365-375.

6. Burton G W, Holderness M C. On the management of massive blood transfusion. Anaesthesia 1964; 19: 408-420.

7. Burton G W The value of carbon dioxide monitoring during anaesthesia. Anaesthesia 1966; 21: 173-183.

8. Clutton-Brock. Two cases of poisoning by contamination of nitrous oxide with higher oxides of nitrogen during anaesthesia. Brit. J. Anaesth. 1967; 39: 388-392. See also GASMAN Chap 1. AD 1966

9. Davy H. Researches, chemical and philosophical; chiefly concerning nitrous oxide. London: Johnson J., 1800.

10. for more on this see The Clevedon Ventilator

11. for further details see Two weeks in August, Southmead 1958