Analysis of Shock

V. H. Moon
1944 BMJ (Clinical Research Edition)  
During a period of 40 years shock has been the subject of extensive and intensive study, both clinical and experimental. This has resulted in a mass of well-attested factual evidence, but agreement on the pathophysiological mechanisms has not been reached. Writers differ widely in their views, and readers are bewildered by the evidence set forth in support of the conflicting opinions. It appears that a logical correlation of the known facts is needed now rather than a search for new facts. A
more » ... for new facts. A realistic examination of the causes for disagreement may be illuminating. What is Shock? The broad and indefinite use of this term is not the least among several causes for disagreement. Shock has been applied to a number of unrelated conditions. Many regard it as a state of acute circulatory failure characterized clinically by prostration, apathy or stupor, tachycardia, feeble regular pulse, and diminished blood pressure. The peripheral temperature frequently is subnormal. When used in this sense shock includes several forms of circulatory disturbance having no other features in common; their pathogenesis and disorders of function are various. The effects of syncope, fright, exhaustion, anaesthesia, haemorrhage, primary shock, cardiac failure, or of secondary shock may produce the clinical signs mentioned. Each of these conditions may cause low blood pressure; hence it cannot be used as the criterion for differentiating them. The attention of surgeons is focused chiefly upon shock seen in battle casualties and in those injured in accidents or air raids, and upon shock following extensive surgery. If, under these or other circumstances, a patient manifests the signs mentioned above, shock is regarded as present. Some writers recognize that at least three unrelated mechanisms may combine to cause weakness, pallor, feeble rapid pulse, and low blood pressure -interpreted clinically as shock-after traumatic injuries. Attention is invited to a brief consideration of each of these mechanisms. Primary or Neurogenic Shock.-This is a neurovascular reaction like that of syncope or fainting. It may be excited by pain, fear, and the emotional effects of the injury, or by non-sensory nerve impulses arising in the damaged tissues. Primary shock comes on promptly, and is usually transient unless accompanied by extensive trauma or haemorrhage. In cases of -severe abdominal injury, visceral perforations, pancreatitis, bums, or extensive damage to other parts, primary shock may merge gradually into secondary shock without an interval of partial recovery. This feature was emphasized by Cope (1928 Cope ( , 1935 , Blalock (1940), and others. Recent experiments (Phemister and associates, 1944) show that prolonged low arterial pressure can be produced in animals by continuous mild stimulation of afferent depressor nerves. Arterial pressures between 40 and 60 mm. Hg were maintained In some instances for several hours. The blood of such animals showed dilution regularly. This feature is opposite to that seen in secondary shock. It indicates that the mechanism of fluid balance is functioning normally and that the capillary walls are not abnormally permeable. Fluid balance and haemoconcentration will be discussed later. A decrease in total blood volume has not been shown in uncomplicated primary shock. Haemorrhage.-The effects of haemorrhage are an obvious cause for low blood pressure and other signs of disturbed circulation after injuries. These signs may develop promptly from voluminous haemorrhage or gradually after slow or repeated small haemorrhages. The clinical signs of haemorrhage are like those of secondary shock, but they differ in other important particulars, as will appear presently. Haemorrhage directly lowers the total blood volume and is followed by a rapid dilution of the blood. This is accomplished by absorption of fluid from the tissues into the blood, tending to restore the blood volume. It is evident that the mechanism of fluid balance is operating physiologically. Low blood pressure developing shortly after trauma is due chiefly to neurogenic and haemorrhagic effects. Secondary Shock.-This is the third mechanism by which circulatory deficiency may develop after extensive injuries. It is due to atony and abnormal permeability of capillary walls, and has been discussed (Moon, 1938a (Moon, , 1942a (Moon, , 1942b as circulatory failure of capillary origin. Products of tissue autolysis or of infection, absorbed from damaged tissues, produce permeability of endothelium like the effects of histamine, peptone, venoms, and other capillarv poisons. When this effect is produced in extensive areas it involves the mechanism of fluid balance.-Osmosis requires the presence of a semi-permeable membrane-the endothelium. If the latter becomes so permeable that plasma colloids escape through it, osmotic attraction ceases to act and the mechanism of fluid balance is vitally deranged. Leakage of fluid from the blood into the tissues lowers the blood volume and causes haemoconcentration, which is evidence in itself that the mechanism of fluid balance is not functioning adequately. Under normal conditions fluid lost from the blood is restdred by absorption; haemoconcentration is thereby prevented. Decreased blood volume, combined with increased volume capacity of the capillary bed, tends to cause circulatory deficiency, which is manifested by clinical signs like those of primary shock or the effects of haemorrhage. But the mechanism of capillary damage requires time for development; it is never seen immediately after injury, hence it is called delayed or secondary shock. Confusion in Shock Analysis Numerous reports, both from British and from American authors, indicate confusion in attempting to analyse the causes of shock resulting from injuries. Space does not permit detailed examination of each of these. Since the reports are similar in nature and in the conclusion drawn, one will be cited as an example. Evans and his associates (1944) made haematocrit and bloodvolume determinations in 143 cases of knife wounds, bullet wounds, and accidental injuries. Many of these developed shock, as indicated by low blood pressure and other clinical signs. Haemodilution was present in the majority; a few showed haemoconcentration. The authors concluded that low arterial pressure is the most useful criterion for shock and that haemorrhage is its most important cause. It was stated that the injured were seen soon after the wounds were received. Hence probably the time factor was not sufficient for the development of secondary shock. In many instances there was haemodilution, and evidence of extensive haemorrhage which averaged 38% of the estimated blood volume. It is probable that primary shock and haemorrhage were chiefly responsible for the low blood pressure, 4353
doi:10.1136/bmj.1.4353.773 fatcat:e6unv7zdsra6bieedlcjos5tbe