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Archives Classics
April 2010

Shock: Blalock and Cannon

Author Affiliations

Author Affiliation: Emory Center for Critical Care, Emory University Hospital, Atlanta, Georgia.

Arch Surg. 2010;145(4):393-394. doi:10.1001/archsurg.2010.34

Archives of Surgery

Shock: Further Studies With Particular Reference to the Effects of Hemorrhage

Alfred Blalock, MD

This paper reports on a continuation of experiments in dogs to determine the effects of hemorrhage on physiologic measurements of pulse rate and blood pressure along with the weight of vital organs by comparing normal controls to animals exposed to either sodium barbital anesthesia or ether anesthesia. Hemorrhage was caused by removal of blood in small increments (large blood vessel hemorrhage) or trauma (small vessel hemorrhage due to capillary congestion and loss of red blood cells and plasma into locally traumatized area). Changes found in the tissues were related to the length of time that the blood pressure remained low. In these experiments, shock, which is associated with an increased concentration of red blood cells, capillary congestion, and hemorrhage into the tissues, can be produced by hemorrhage alone. Treatment of shock due to loss of blood due to a large vessel injury that has been repaired with the transfusion blood results in the blood staying in the bloodstream and alleviates the shock. Whereas that is not true when the blood loss is due to trauma and the blood and fluid loss is from many small vessels that allow sequestration to occur in the tissues. If low blood pressure remains for several hours in either type of injury, fluid will not be retained intravascularly as then the capillaries become damaged.

November 2009 marked the 75th anniversary of Alfred Blalock's definitive article on shock.1 To appreciate the significance of the report, it is worth revisiting the scientific and social context of the day.

World War I brought the problem of traumatic shock to worldwide attention. In America, a young Harvard physiologist, Walter B. Cannon, toured the battlefields and brought the problem back to the laboratory. Cannon developed the standard shock model of the day: smashing a cat's hind limb with a heavy object to cause severe injury to the flexor muscles of the thigh. Cannon also performed vascular isolation of the limb to show that postinjury reperfusion resulted in shock, prompting Cannon to attribute the shock to an endogenous toxin.2 Pertinent to the unfolding of the tale is a detail of Cannon's analytic method: Cannon took great care to show that loss of fluid into the injured tissue did not account for the shock by amputating the injured and uninjured limbs at the upper thigh and comparing their weights.3,4

Cannon was an icon of the times. In addition to professional lectures and writing (eg, a 1923 monograph on traumatic shock4), Cannon's clarity of expression made him a popular speaker. He would later (1932) write a bestseller, The Wisdom of the Body,5 in which he described the principle of homeostasis (a word that he coined) for lay readers. With repetition, the toxin theory of shock became common belief.

A Johns Hopkins urology intern in 1923 when Traumatic Shock4 was published, Alfred Blalock failed to secure a permanent position in the surgical residency there and left for Nashville, Tennessee, to join the Vanderbilt University training program. There, Blalock set about organizing laboratory studies with his good friend Tinsley Harrison (whose textbook of medicine remains popular today).6 They became interested in derangements of cardiac output. Using the Fick principle and the Van Slyke device that determines the oxygen content of blood, they reported on changes in cardiac output in anemia, hemorrhage, anoxia, anesthesia, and thyroid disease. By 1927, Blalock had developed great facility in measurement of oxygen content and thus blood flow. In his initial report on shock's effect on cardiac output, Blalock cited Cannon, noting that the latter “did not mention diminished minute cardiac output”7(p792) despite observations of his contemporaries.

For the next 3 years, Blalock ruminated on the inconsistency between his results and those reported by Cannon. Blalock had a fair bit of time to think: he developed tuberculosis that forced him to spend a year away from the bench in a sanatorium, while Harrison and others kept the Blalock laboratory active in Nashville. By 1930, the laboratory had accumulated 15 different types of experiments that debunked the toxic theory that Cannon had advanced. The key to the experiments lay in a simple but telling observation: when the animal's hind limb was smashed, swelling advanced above the groin crease. In the Blalock laboratory, postexperiment amputation for weighing of the injured and control limbs was performed, not at the groin crease (as Cannon had done), but at the aortic bifurcation. Blalock, Vivien Thomas, and the others in the laboratory “found” the missing fluid, a volume sufficient to account for the decline in cardiac output and consequent shock. Blalock directly confronted Cannon in print: the concluding paragraph of the 1930 article begins, “the experiments which are presented offer no evidence that trauma to the extremities produces a toxin. . . . ”8(p996)

Blalock knew that Cannon would be nonplussed. He wrote to Cannon, declaring the latter to be “an authority,” asking him “to criticize to me very frankly my interpretation of the results” and saying that Cannon's book on traumatic shock was his “bible” and he was “seldom without it.”9 Cannon did not respond.

The inconsistency between the 2 lines of experiment emerging from the laboratories did not escape the notice of surgical leaders. The president of the American Surgical Association, Elliott Cutler, invited the 2 men to address that organization on “Old and New Views of Traumatic Shock” at the June 1934 meeting. Six weeks prior to the conference, Cannon finally wrote to Blalock, complimenting him on his work and asking for reprints. Blalock responded promptly, whereupon Cannon wrote once more in May saying that he intended to discuss “commonly acknowledged facts,” avoiding “theories,” but recognizing the “stress laid on toxic shock.”10 The gauntlet was thrown.

Cannon is said to have taken a balanced approach in his talk. Blalock did not. He discussed his published work and more recent studies, systematically dispatching toxins, vasoconstrictors, and other popular concepts. The cause of shock, argued Blalock, was simple fluid loss. Blalock's arguments were persuasive: during the discussion period, surgeons of the day (including Owen Wangensteen, whose remarks were transcribed) were vehement in their support of Blalock's position.11

Cannon and Blalock apparently did not communicate with one another for the next 6 years. The toxic theory of shock faded. The 2 men eventually enjoyed a warm relationship reflected in their personal correspondence.10,12

The article by Blalock,1 published 5 months after the Cannon-Blalock debate, surely contains data that Blalock discussed in Toronto. In the text, Blalock pays homage to Cannon's leadership. He begins his comments quoting directly from Cannon's 1923 monograph4 regarding the importance of shock. He returns to Cannon:

As Cannon has stated, the central problem in the study of traumatic shock has to do with the reason for the lowered blood pressure or the determination of the initiating factor.1(p851)

After paying those respects to Cannon, however, Blalock is forthright:

It seems conclusive that the cause of low blood pressure in experiments of the duration reported here in which large masses of muscle of dogs are traumatized is due to the loss of red blood cells and of plasma into the local injured area.1(p851)

No mysterious toxic factor, just volume loss.

Blalock grasped the lasting significance of the findings. Years later, amid professional and public adulation for the “Blue Baby” operation, he remained proudest of the work on shock. Blalock was again correct. The Blalock-Taussig shunt is long obsolete. In contrast, the quiet voice contemporary surgeons hear advising them to give additional fluid in the presence of injured tissue is that of Alfred Blalock, echoing over 75 years from these pages.

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Article Information

Correspondence: Dr Buchman, Emory University Hospital, Emory Center for Critical Care, 1364 Clifton Rd NE, Ste F524, Atlanta, GA 30322 (tbuchma@emory.edu).

Financial Disclosure: None reported.

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