A chill is considered to be the result of surface cooling from constriction of the cutaneous arterioles, the skin being the site of the nerve-endings through which temperature changes are perceived. In a chill, shivering is the heat-producing response of the regulators to the cold at the surface rather than to general body temperature. The subsequent fever results from this excessive heat production at a time when the skin vessels are still constricted and sweating absent, i. e., when heat loss is at a minimum.

In those of the infectious fevers which have been studied in this regard there is a great increase in the nitrogen elimination during the fever, but no material increase in the amount of fats and carbohydrates oxidized, as shown by the elimination of Co2; therefore heat production is not greatly increased. Just the opposite condition is found in active exercise, in which there is great increase in the elimination of Co2 and only a moderate increase in the nitrogen of the urine.

Liebermeister has likened the heat-regulating centers to the heat-regulator of a room. The heat regulator is set at a certain temperature; if the room gets warmer, the mercury rises or a metallic band expands, and by making an electric connection operates on one or more dampers in the furnace so that the fire burns less briskly, or shuts down the registers so that the room receives less heat. If the temperature of the room falls below that at which the regulator is set, the dampers or registers are opened and more heat comes into the room. Now, to carry out the analogy, the heat-regulating centers in the human body may be thought of as being normally set for a temperature between 98° and 990 F. If the temperature goes up a degree or two, the centers send out impulses which result either in a lessening of heat production, i. e., by diminution in muscular and circulatory activity, or an increase in heat loss, i. e., by dilatation of the cutaneous vessels and sweating. On the contrary, if the temperature falls a degree or two, the heat production may be increased by muscular activity, shivering, etc., or the heat loss diminished by contraction of the cutaneous vessels and the stoppage of sweating.

The temperature-regulating centers have little discriminating power, and a surface chill may induce the centers to constrict the vessels and lessen heat loss, and at the same time to increase the production of heat, so that fever may result. To what extent the body reaction which results in fever is beneficial or harmful, we are not yet able to state. Recently certain infections seem to have been cured by the repeated artificial production of a chill with high fever, as by the intravenous administration of foreign protein, usually typhoid vaccine.

In some fevers the regulating centers may lose their control at certain times of the day only. In tuberculosis there is a tendency to afternoon fever, accompanied by headache, discomfort, and weakness from failure of heat loss, while at night there may be an overaction of the mechanism for cooling, with diminished metabolism and the production of profuse sweat, the result being chilling of the surface (cold night-sweats) and a fall of temperature to subnormal. Frequently, in tuberculosis fever cases, the morning temperature is normal and the patient feels at his best at that time. But in tuberculosis the centers are incompetent, so that a slight exertion tends to produce fever at any time.

In malaria there is a severe chill with contraction of the skin vessels and the generation of much heat (by shivering). After a time this results in great fever and discomfort, the contraction of the skin vessels and the absence of sweating preventing heat loss. But presently the centers gain control, and great activity of the cooling mechanism follows. The result is dilatation of the skin vessels and profuse sweating, with a fall in temperature to normal or even subnormal, and the restoration of the patient's comfort till the next chill comes on a day or two later.

In a continuous fever like typhoid, apparently the heat-regulating centers are set at a high point, 102o F., 1030 F., 1040 F. The centers are just as sensitive to changes as ordinarily, for shivering follows a drop of 2 or 3 degrees in the temperature, and sweating results from a rise of 1 or 2 degrees. But the temperature at which the centers tend to keep the body is not 98.6° F., but 102° F., 103° F., or 1040 F., as the case may be.

But even in typhoid fever there is a tendency to a morning remission of temperature, with rise to the highest point in the afternoon or evening. And it would seem as if, preceding the rise in temperature in these cases, the heat regulators are affected by the poisons of the disease, so that they allow the temperature to rise above normal; but that, at a certain point, the centers gather themselves together and are able to assert themselves and regain their control, and the temperature is brought backtoward normal. This makes a daily rhythm.

Action Of Drugs

A drug may tend to lessen the temperature in fever by decreasing metabolism, as quinine, by lessening the activity of the circulation, as veratrum, by dilating the cutaneous vessels, as whisky, or by inducing perspiration, as solution of ammonium acetate. But antipyrine, acetanilid, acet-phenetidin, and their allies act centrally, and they result in a lowering of the temperature in fever either by increasing the resistance of the regulating centers to the disease poisons, or by lowering the degree at which the heat-regulating centers are set (if we may use such an analogy). Meyer regards them as mild narcotics to irritated thermogenic centers. The effect of these drugs is not to any extent to reduce heat production, for they do not diminish metabolism, and acetanilid even increases metabolism. They act by enabling the center to improve its control over the mechanisms of heat dissipation, which are the ones at fault in the infectious fevers.