PAUTA DE EVALUACIÓN EL M
EN RELACION A LA PROMOCION DEL VINCULO MADRE HIJO/A
Anaesthesia (anesthesiology) as an academic discipline.
Ralph M Waters (1883 – 1979), was the first professor of anaesthesia in the world. He was professor in Madison, Wisconsin from 1927 until 1949. He said his mission was ‗to work toward bringing back anesthesia into the medical profession where it originally was and where it undoubtedly belongs. The only way I could see of really basically helping this movement was through the educational institutions.‘81
80
Mushin WW, Rendell-Baker L. The principles of thoracic anaesthesia past and present. London: Blackwell Scientific Publications; 1953. page 66.
81
Waters RM. Letter to Frederick W. Clement, M.D., February 3, 1933. The collected papers of Ralph M. Waters, M.D., Steenbock Library, University of Wisconsin Archives, Madison,
At a time when anesthesiology was just being defined as a medical specialty, Waters worked to ensure that it was set on an equal footing within the university with surgery, internal medicine and paediatrics as well as the traditional hospital-based specialties of radiology and pathology.
In addition to his seminal influence on raising the status of anaesthesia and anaesthetists in the US and abroad Waters made several advances in anaesthetic practice which were later used by anaesthetists such as Ibsen to treat patients with respiratory paralysis. The first was the introduction of carbon dioxide absorption in a closed breathing system (the Waters closed circuit) in 1924.82 A mixture of oxygen and the anaesthetic gas nitrous oxide (N2O) is supplied to a large rebreathing bag.
(figure 4).
Figure 4. Diagramatic [sic] sketch of carbon dioxid [sic] filtration system.70 A. Mask with well fitting rubber face cushion
B. Cylinder of granular soda lime 3 ½ inches in diameter and 4 inches long. C. Wire gauze dams to hold soda lime in place.
D. Cone shaped ends of filter, the distal one bearing a stopcock through which to obtain gas for carbon dioxide test.
E. Rebreathing bag.
Wisconsin. Cited in Bacon DR. Why Celebrate Ralph Milton Waters? ASA Newsletter 2010; 65 (9).
82
Waters RM. Clinical scope and utility of carbon dioxid filtration in inhalation anesthesia. Anesth. Analg. 1924; Feb. (Volumes were not at that time numbered): 20–22 and 26. Note: The unusual spelling of dioxide (dioxid) and diagramatic (diagrammatic) is reproduced from the article. It is not a typographical error; all Waters‘ papers use these spellings.
The patient breathes this mixture through a cylinder containing soda lime. During expiration the carbon dioxide in the expired air is absorbed by the soda lime. The expired gas can therefore be re-breathed indefinitely, only oxygen which is absorbed by the patient (about 200 ml per minute) needs to be replaced. This system could be used for anaesthesia using nitrous oxide, ethylene, ether or ethyl chloride. Its advantages were simplicity and economy of agents, particularly of nitrous oxide which was expensive. It was not described as having been used to ventilate the lungs, the patients continued to breathe through the circuit spontaneously.
Waters‘ next step towards positive pressure ventilation of the lungs in anaesthesia was his introduction of cyclopropane into clinical practice in 1934. Cyclopropane is a gaseous anaesthetic which was more pleasant for the patient than the previously used ether or chloroform (induction of anaesthesia by intravenous agents had yet to be invented), produced better relaxation of the abdominal muscles and allowed easier access to the abdomen for the surgeon. In their preliminary report on its use in 10 dogs and 447 patients Waters and his colleagues make little mention of respiratory depression but emphasise that it was fully as easy to introduce an endotracheal catheter with this agent as with ether. ‗In fact the laryngeal reflex is eliminated more quickly than with ether and [vocal] cord relaxation is quite as complete.‘83
A further paper in the same year (1934) stated that ‗Respiratory excursion was definitely less in patients receiving cyclopropane‘, but added ‗often adding considerably to the convenience of the surgeon‘.84
So respiratory depression was seen as an advantage and no mention was made of assisted or controlled respiration.
In the following year, 1935, Schmidt and Waters stated briefly what they believed the surgeon could reasonably expect from his anaesthetist in the light of (then) modern anaesthetic knowledge. In quite a long list of expected capabilities and also in a separate paragraph they wrote ‗under operating conditions which demand a specialized technique the surgeon should be able to expect of the anaesthetist;
83
Styles JA, Neff WB, Rovenstine EA, Waters RM. Cyclopropane as an anaesthetic agent: A preliminary clinical report. Anesth Analg. 1934; March-April:56–60.
84
abilities to provide positive pressure respiration during thoracotomies, passive respiration for difficult abdominal closures, closed endotracheal airways to preclude the possibility of aspiration in oral or stomach surgery.‘ 85
This list is in stark contrast to Meyer‘s 1909 dictum about what should be demanded of a thoracic surgeon (Page 21) ‗He should not be obliged to put a cannula into the trachea, either through the mouth or directly through a tracheal incision to produce anesthesia.‘86
By 1935 the anaesthetist should be appropriately skilled and not be simply anyone who was ‗at hand‘ to assist the surgeon with the minor task of ‗etherizing‘ the patient while the surgeon performed his operation.
It was left to Arthur Guedel, writing in 1940, to grasp the nettle and realise that if a patient‘s respiration is depressed by cyclopropane then the anaesthetist must ventilate the lungs.87 The first full page of his paper ‗Cyclopropane anaesthesia‘ was devoted to ‗Controlled Respiration‘. He described the normal mechanism in which the carbon dioxide level in the blood stimulates respiration. If the subject‘s breathing is less than required, the carbon dioxide level in the blood rises, the respiratory centre in the brain is stimulated and emits impulses which increase the activity of the respiratory muscles. The increased rate and depth of breathing cause more carbon dioxide to be exhaled so that its level in the blood is reduced to normal and the emissions from the respiratory centre returned to produce normal breathing. The threshold level of carbon dioxide to which the respiratory centre will respond by hyperventilation can be elevated by anaesthetic agents. So a person anaesthetised by cyclopropane will not hyperventilate when the carbon dioxide level rises in the blood. His breathing will actually be depressed. If deep anaesthesia is require to produce relaxation of the abdominal muscles to allow surgical access to the abdomen, the respiratory centre will not respond at all to the rising CO2; breathing
will stop. The anaesthetist must be prepared to take over the patient‘s breathing completely by rhythmically and continuously squeezing the rebreathing bag. She or he must do this for as long as the operation requires muscular relaxation. Guedel called this ‗passive‘ respiration – the patient plays no part in ventilating his lungs –
85
Schmidt ER, Waters RM. Cyclopropane anesthesia: Post operative morbidity in 2200 cases. Anesth Analg. 1935;14:1-3
86
Meyer W. Pneumonectomy with the aid of differential air pressure. JAMA 1909;LIII:1978-87.
87
he is passive. It is now called controlled ventilation. When relaxation is no longer required the cyclopropane is turned off or reduced and the patient will start to breath spontaneously again. ‗Controlled ventilation had become an essential part of the anaesthetist‘s armamentarium.‘80
A second insight provided by Guedel was that raised concentration of carbon dioxide in the blood was more dangerous than a lowered concentration. This was important because at that time and for decades thereafter there was no way of monitoring the arterial carbon dioxide pressure (pCO2) in clinical practice. The
anaesthetist could not know whether in controlled ventilation the lungs were being ventilated more or less than was required to maintain a normal pCO2.
As has been shown in the previous section, in normal breathing the volume of air inhaled and exhaled (the minute volume of ventilation) will be regulated by the brain to be sufficient to remove from the blood the amount of carbon dioxide produced by the body each minute so the level of carbon dioxide in the blood will stay within normal limits (36 – 44 mm Hg.) If an anaesthetist applied controlled ventilation she or he will not know whether the lungs are being ventilated too much or too little. Guedel stated that the anaesthetist should not be deterred from controlling respiration by the fear that he might ventilate the lungs ‗too much‘. He showed that little if any damage had resulted from over-ventilating the lungs (hyperventilation) and thereby reducing the amount of carbon dioxide in the blood. More damage would be produced by a raised carbon dioxide level if the anaesthetist accepted the depression of respiration during cyclopropane anaesthesia and did nothing about it.
It had been known that excessive positive pressure within the chest can cause deleterious effects on the circulation. This can be seen if one tries to further inflate an already distended balloon. As one blows hard against the unyielding resistance of the fully inflated balloon one creates a very high pressure in the thorax. Blood can not return to the heart against this pressure so the blood pressure falls, and the organs become starved of blood. Because the circulation to the brain is reduced one becomes dizzy and, if stupid enough to persist (and the balloon does not burst), one may faint.
When early anaesthetists started to maintain positive pressure in the lungs to prevent them deflating during thoracic surgery, they were aware of the potentially
negative effects on the circulation of raised intrathoracic pressure. As they progressed to assisted respiration by squeezing the rebreathing bag, they tried to limit the extent and duration of positive intrathoracic pressure and were deterred from adopting continuous controlled respiration. Instead they gently squeezed the bag from time to time (and usually ineffectively) when the patient‘s respiration was seen to be obviously and severely depressed, as in deep cyclopropane anaesthesia.
In 1948 André Cournand and his colleagues at Columbia University, New York published the results of their research into the effects of intermittent positive pressure breathing on cardiac output.88 They found that the effect on cardiac output depended upon the type of respirator and the way it inflated the lungs. Crucially they found that if the expiration part of the respiratory cycle (when the machine stops inflating the lung) is twice as long as the inflation time, and if the pressure is allowed to fall to atmospheric during expiration, there was little if any effect on cardiac output. There may be a slight fall during the inflation phase but it is compensated during the deflation phase. Cournand‘s group were studying different types of lung ventilators, but their findings applied equally to manual ventilation of the lungs (bag squeezing).