The Origin and Nature of Emotions [68]
difference in potential may be restored and the life processes will be renewed. Bearing especially on this point is the fact that if adrenalin in sufficient quantities be administered simultaneously with an acid, it will not only prevent the fall in blood-pressure usually caused by the acid, but will also prevent the histologic changes in the brain, adrenals, and liver which are usually caused by the intravenous injection of acids.
This hypothesis regarding the cause of anesthesia and unconsciousness explains and harmonizes many facts. It explains how asphyxia, overwhelming emotion, and excessive muscular exertion, by causing acidity, may produce unconsciousness. It explains the acidosis which results from starvation, from uremia, from diabetes, from Bright's disease, and supplies a reason for the use of intravenous infusions of sodium bicarbonate to overcome the coma of diabetes and uremia (Fig. 76). It may explain the quick death from chloroform and nitrous oxid; and may perhaps show why unconsciousness is so commonly the immediate precursor of death.
One of the most noticeable immediate effects of the administration of an inhalation anesthetic is a marked increase in the rapidity and force of the respiration. The respiratory center has evidently been evolved to act with an increase of vigor which is proportional-- within certain limits--to the increase in the H-ion concentration, whereas the centers governing the voluntary muscles are inhibited. In this antithetic reaction of the higher cortical centers and the lower centers in the medulla to acidity we find a remarkable adaptation which prevents the animal from killing itself by the further increase in acidity which would be produced by muscular activity. That is, as the acidity produced by muscular action increases and threatens life, the respiratory action, by which carbon dioxid is eliminated and oxygen supplied, is increased, while the driving power of the brain, which produces acidity, is diminished or even inhibited entirely; that is, the state of unconsciousness or anesthesia is reached. We conclude first that, without this life-saving regulation, animals under stress would inevitably commit suicide; and, second, that it is probable that the remarkable phenomenon of anesthesia-- the coincident existence of unconsciousness and life--is due to this antithetic action of the cortex and the medulla.
In the human, as in the animal, the degree of acidity parallels the depth of inhalation anesthesia.
Within a few seconds after beginning nitrous oxid anesthesia the acidity of the blood is increased. This rapid acidulation is synchronous with almost instantaneous unconsciousness and increased respiration. If the oxygen in the inhaled mixture be increased, a decrease in acidity is again synchronous with lighter anesthesia and a decrease in the respiratory rate.
If these premises be sound, we are justified in asserting that the state of anesthesia is due to an induced acidity of the blood. If the acidity is slight, then the anesthesia is slight and the force of the nerve impulses is lessened, but the patient is still conscious of them. As the acidity increases associative memory is lost, and the patient is said to be unconscious: the centers governing the voluntary muscles are not inhibited, however, and cutting the skin causes movements. If the acidity is further increased, there is loss of muscular tone and even the strong contact ceptor stimuli of a surgical operation do not cause any muscular response, and, finally, the acidity may be increased to the point at which the respiratory and circulatory centers can no longer respond by increased effort, and anesthetic death-- that is, ACID death--follows.
Certain clinical phenomena are clarified by this theory and serve to substantiate it. For example, it is well known that inhalation anesthesia precipitates the impending acidosis which results from starvation, from extreme Graves' disease, from great exhaustion, from surgical shock, and from hemorrhage, and which is present when death from any cause
This hypothesis regarding the cause of anesthesia and unconsciousness explains and harmonizes many facts. It explains how asphyxia, overwhelming emotion, and excessive muscular exertion, by causing acidity, may produce unconsciousness. It explains the acidosis which results from starvation, from uremia, from diabetes, from Bright's disease, and supplies a reason for the use of intravenous infusions of sodium bicarbonate to overcome the coma of diabetes and uremia (Fig. 76). It may explain the quick death from chloroform and nitrous oxid; and may perhaps show why unconsciousness is so commonly the immediate precursor of death.
One of the most noticeable immediate effects of the administration of an inhalation anesthetic is a marked increase in the rapidity and force of the respiration. The respiratory center has evidently been evolved to act with an increase of vigor which is proportional-- within certain limits--to the increase in the H-ion concentration, whereas the centers governing the voluntary muscles are inhibited. In this antithetic reaction of the higher cortical centers and the lower centers in the medulla to acidity we find a remarkable adaptation which prevents the animal from killing itself by the further increase in acidity which would be produced by muscular activity. That is, as the acidity produced by muscular action increases and threatens life, the respiratory action, by which carbon dioxid is eliminated and oxygen supplied, is increased, while the driving power of the brain, which produces acidity, is diminished or even inhibited entirely; that is, the state of unconsciousness or anesthesia is reached. We conclude first that, without this life-saving regulation, animals under stress would inevitably commit suicide; and, second, that it is probable that the remarkable phenomenon of anesthesia-- the coincident existence of unconsciousness and life--is due to this antithetic action of the cortex and the medulla.
In the human, as in the animal, the degree of acidity parallels the depth of inhalation anesthesia.
Within a few seconds after beginning nitrous oxid anesthesia the acidity of the blood is increased. This rapid acidulation is synchronous with almost instantaneous unconsciousness and increased respiration. If the oxygen in the inhaled mixture be increased, a decrease in acidity is again synchronous with lighter anesthesia and a decrease in the respiratory rate.
If these premises be sound, we are justified in asserting that the state of anesthesia is due to an induced acidity of the blood. If the acidity is slight, then the anesthesia is slight and the force of the nerve impulses is lessened, but the patient is still conscious of them. As the acidity increases associative memory is lost, and the patient is said to be unconscious: the centers governing the voluntary muscles are not inhibited, however, and cutting the skin causes movements. If the acidity is further increased, there is loss of muscular tone and even the strong contact ceptor stimuli of a surgical operation do not cause any muscular response, and, finally, the acidity may be increased to the point at which the respiratory and circulatory centers can no longer respond by increased effort, and anesthetic death-- that is, ACID death--follows.
Certain clinical phenomena are clarified by this theory and serve to substantiate it. For example, it is well known that inhalation anesthesia precipitates the impending acidosis which results from starvation, from extreme Graves' disease, from great exhaustion, from surgical shock, and from hemorrhage, and which is present when death from any cause