In contrast to this our experiments give a relatively simple explanation of cold-death under these conditions. With the exception of a single case, a total irregularity of the heart chamber could be definitely demonstrated in all cases of cooling under 30° C. [86° F.], (50 experiments), when the rectal temperature reached 29° C. [84° F.] and usually already at a cooling of 31° C. [88° F.]. The exception was an experiment on an intoxicated subject, which is to be gone into more fully below (see sec. VII).
Furthermore heart-death was established clinically in all cases of death observed by us. In two cases breathing ceased simultaneously with the heart activity. These were cases in which it was specially noted that the neck and the back of the head lay deep in the water. In all remaining cases breathing outlasted the clinical chamber cessation by as much as 20 minutes. In part this was “normal, much decelerated breathing,” in part an angonal form of gasping. As already referred to, an auricular flutter could be demonstrated cardiographically during the irregularity.
In cases in which a special cooling of neck and back of head had existed before death, the autopsy showed a marked brain oedema, a tight filling of the general brain cavity [Hirngefaesse] blood in the spinal fluid as well as blood in the Michaelisrhomboid.
The heart findings warrant our taking a certain attitude toward the question of rescue collapse. Death occurred relatively quickly after removal from the water, which may be compared with rescue. The longest interval involved was 14 minutes. It is to be noted, however, in the first place, that almost certainly a much larger number of deaths would have been observed if an active heat therapy had not almost regularly been coupled directly with the completion of the experiment; in the second place, that in such cases there would have been very much longer intervals. We have already called attention repeatedly to the after-cooling following the experiment. In every case where this had proceeded to a certain point, countermeasures were taken, since the experiments were never planned to end in death. One may well imagine, however, that in mass catastrophes, in which almost exclusively rescue collapse has heretofore been described, the therapeutic measures were confined to an undressing and drying off of the rescued together with a subsequent wrapping in covers. Under these conditions after-drops of great magnitude and long duration were to be expected. In the course of this delayed fall in temperature, a heart-death might occur as in our experiments.
We should like to emphasize that the irregularity per se is not to be regarded in our experiments as a symptom of danger to life any more than in the clinic, but rather as a sign of direct heart damage, which increases continuously with further falling off of temperature, until finally the heart fails. If the temperature drop is arrested, the slow form of irregularity passes over into a rapid form. This transition is a favorable sign for survival; for this irregularity virtually always passes over of itself after a time averaging 90 minutes into normal heart activity. It continues therefore for a long time after the body temperature has already risen markedly. A danger to the circulatory system could not be demonstrated at this stage. In three cases the return of the heart action to normal occurred in spite of simultaneous energetic physical work.
With the demonstration that cold-death of man is primarily a heart-death, the essential points for therapy are also cleared up. The cause of the severe heart damage is another question. Since our studies were primarily aimed at the development of practical methods of treatment, we will not go very far into the theoretical concepts which may be developed in this connection. Still, several hints may be drawn from the blood studies:
1. The great increase of the viscosity causes an increased loading upon the heart.
2. The choking of peripheral vessel areas by the severe vessel contraction leads to an over-filling of the central areas. This appears not only from our autopsies. In all available records of autopsies which pertain to cases of death from cold in the water after sea disaster, we find uniformly a severe over-filling of the right heart.
3. It is to be calculated that, under the effect of the low blood temperature, the heart itself becomes severely hypodynamic. It has been proved long ago in animal experimentation that a Vorhof flutter can be developed by the overloading and cooling of the isolated heart.
Besides a physical damaging of the heart musculature by the cold, we must also keep in mind the damaging by pathological products of metabolism. Next, the sharp increase in blood sugar may be connected with the increased outpouring of adrenalin. The constancy of this increase of blood sugar during the temperature drop is, however, remarkable. One may well assume that this flow of adrenalin exhausts itself with the continuance of the temperature drop. With this there would have to be a rapid decrease in the blood sugar if the oxidation processes were to continue undisturbed. The decrease in the alkali reserve or the development of an acidosis argues strongly for an injury.