This section is from the book "Materia Medica: Pharmacology: Therapeutics Prescription Writing For Students and Practitioners", by Walter A. Bastedo. Also available from Amazon: Materia Medica: Pharmacology: Therapeutics: Prescription Writing for Students and Practitioners.
Following severe trauma or a surgical operation, there develops at times a condition of pronounced muscular relaxation, with rapid, weak heart, low blood-pressure, and depressed respiration. There is a similar state into which a patient may pass as the result of severe disease or loss of blood. But whether the effects when produced by a severe infection acting steadily for days are the same as those from trauma, or are produced in the same manner, are questions not yet decided. And, further, there is not by any means an agreement as to just what does happen in a patient to bring him into the state described, which is known as shock or collapse. There is a tendency on the part of many writers to use the term "collapse" when the prostration results from toxic causes, as diseases or drugs, or from loss of blood, and to confine the term "shock" to the condition developed after trauma, either accidental or operative. But the fine of differentiation between the two cannot be satisfactorily drawn at the present time. It would seem to be established, however, that the central nervous system is involved, and it may be that shock is due to an overwhelming inflow of powerful afferent impulses, as from the cut nerves of a severed leg.
In abdominal operations Crile makes a block between the operative field and the brain by an infiltration of the skin and subcutaneous tissues with 1/4 per cent. novocaine, and of the peritoneum with 1/2 per cent. quinine and urea hydrochloride. He also lessens the perceptive faculties by a preliminary injection one hour before of morphine and scopolamine. He terms the whole process anoci-association.
J. M. Wainwright's experiments (1906) as to the value of spinal analgesia in shock from traumatism to the lower extremities lend support to this theory. After artificial traumatism, designed to imitate that of a railway accident, he used cocaine and stovaine to block the afferent impulses. Two series of his experiments are of interest, viz.:
1. Dogs completely anesthetized with ether had their hind limbs kept immersed in boiling water. Some were given spinal anesthesia, some not. Those without the preliminary spinal anesthesia showed a short rise in arterial pressure for rive to ten minutes, then a rapid fall in pressure, and death in twenty-five minutes (average). In the dogs with spinal anesthesia there was no change in the arterial pressure for one hour, then a gradual fall until death, presumably as the cocaine effect was wearing off.
2. Dogs were completely anesthetized with ether, and then had their hind legs crushed to a pulp by repeated blows of the blunt side of an ax. After twenty minutes, given for shock to develop, both hind legs were amputated at the knee. A preliminary ligation of the femoral arteries was done to exclude the effects of hemorrhage. In all the dogs without spinal analgesia there was marked shock, and 2 out of 7 dogs died during or immediately after the amputation. The dogs which had a spinal injection before the amputation were all in good condition after the amputation, and remained so until the cocaine effect had worn off.
Porter states that the vasoconstrictor center is not exhausted in shock, as it responds in the usual way to stimuli through sensory nerves. But in well-developed shock the center is evidently not easily influenced, or else the usual pressor influences are changed to depressor. (See Strychnine.) And it has been suggested that in shock the constrictor synapses are easily paralyzed, so that the usual vasoconstrictor stimuli become vasodilator. No matter what the underlying factors involved, Hill figures that the condition of shock or collapse is associated with cessation of the reflexes which maintain the body in a state of vascular tone and muscular activity.
Respiratory paralysis must be considered with collapse. It may be due to direct or reflex depression of the center, or to the failure of the circulation to bring the center sufficient Co2 for its stimulation. The symptoms are those of asphyxia, resulting in death unless artificial respiration is maintained. If the heart action remains good, artificial respiration may often be continued until the center regains its activity.
Whatever the cause or the condition, therapeutically there are about three distinct degrees:
1. Mild and transitory collapse is the result of a momentary suspension of the cerebral circulation, as a reflex effect from sudden emotional or psychic influences, or from a drug like amyl nitrite or nitroglycerin, or from momentary ventricular stoppage, as in heart-block. It is probably due to anemia of the brain, caused by the dilatation of the splanchnic arterioles, and this dilatation is in turn the result of a failure of the normal sensory impulses to have their usual effect upon the vasoconstrictor center. The symptoms are dizziness and faintness, or fainting. Treatment is directed toward favoring the blood-supply of the medulla. If the patient feels faint, he may sit with head down between the legs or may lie down; if he has fainted, he should be laid with head lower than feet. Ammonia smelling-salts, or any rapidly acting strong carminative, such as aromatic spirit of ammonia or (hot) whisky, will hasten the recovery.
2. A moderate degree of collapse from poisoning manifests itself by the gradual onset of nausea, and perhaps vomiting, diarrhea, and abdominal weakness, with profuse sweating, clammy skin, and general muscular weakness and prostration (a condition experienced by many embryo smokers after their first cigar).
3. Severe collapse may be gradual in its onset or sudden. It may or may not be accompanied by unconsciousness. The face is anxious, or if the patient is unconscious, may be expressionless - mask-like. The skin is cold and clammy and bathed in perspiration. It is usually cyanotic, but is pale if the collapse is due to hemorrhage or chloroform. The breathing is labored and inefficient, and may become slow and shallow, or of the Cheyne-Stokes type. The pulse is rapid and feeble, perhaps almost imperceptible. The temperature falls, and may reach as much as three or four degrees below normal. The mind becomes dulled or there is unconsciousness. There is great muscular weakness with prostration, and there may be vomiting and convulsions.
Crile's anoci-association would seem to be a successful prophylactic. Actual - all would seem to agree with Pike and Coombs that in surgical shock some means of raising the systemic arterial pressure is necessary. But the more we know of shock and collapse, the less we pin our faith to drugs. If we employ them, we must not let the stress of the emergency lead us into giving them in too large doses. In such an emergency we have seen drugs administered in amounts that might have proved fatal to a healthy person; and it seemed as if the patient might have died from the drugs rather than from the collapse.
There are two drugs that stand preeminent as of possible value in raising the arterial pressure, viz., epinephrine and pituitary. Their action is peripheral, therefore takes place whether the vasoconstrictor center is paralyzed or not. They may be added to a saline infusion and administered very slowly indeed; in this way the action may be obtained for an hour or two. But the shock may supervene at the end of this period.
Besides this there should be:
1. A position to favor cerebral blood-supply, i. e., with the body tilted so that the feet are higher than the head. The legs may even be raised in the air at a right angle to the body.
2. Mechanical measures to raise blood-pressure - the limbs may be bandaged from ringers to shoulders, or Crile's pneumatic jacket applied, or weights and tight binders placed over the abdomen. Meltzer says this last method may send up the blood-pressure and hold it.
3. Absolute repose.
4. Maintenance of body warmth by hot blankets, hot towels, hot-water bottles, hot drinks, hot enemata, etc.
5. Plenty of air, and, if necessary, artificial respiration and the inhalation of oxygen. In edema of lungs, dry-cupping and artificial respiration (Emerson), especially by Meltzer's intratracheal insufflation.
The treatment as outlined may need to be modified according to the cause of the collapse. For example, if the cause is hemorrhage, the chief end of the medication is to restore the volume of the blood; if the cause is heart failure, it may be desirable to avoid vasoconstriction, i. e., peripheral resistance and physical work; and if the heart failure is the result of malnutrition from failure of the digestive organs, as in some post-operative cases, transfusion of blood may be indicated. For nutrition, an intravenous of glucose may be employed (see Glucose).
When the heart has ceased to beat it may sometimes be resuscitated by an injection of epinephrine or tincture of digitalis into the ventricle or pericardial sac, especially if this is combined with massage of the heart through a thoracic or abdominal opening, or by simple compression of the thorax or abdomen. Gunn and Martin recommend that the compression be gradual and the relaxation abrupt.
Further treatment may be:
The administration, by stomach or rectum, of strong hot coffee. The hypodermatic administration of stimulants to the central nervous system, the respiration, and the circulation, such as atropine, caffeine, strychnine, or strophan-thin, according to the several indications.
2. The administration of carbon dioxide by inhalation. As this gas does not interfere with the oxygen-carrying power of the blood, it may be administered with oxygen. It stimulates the respiratory center and tends to overcome Cheyne-Stokes or shallow breathing. Henderson says that it should not be given in a concentration above 6 per cent.