The Treatment of Shock with Beta Adrenergic Blockade

  • James L. Berk
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 9)


Hemodynamic inconsistencies in the Vasoconstrictor Theory of Shock and the unsatisfactory results of the treatment of shock founded on this concept, led to experimental studies designed to re-evaluate and clarify the role of adrenergic stimulation in shock. (1, 2) Based on these findings we suggested that in shock of various causations beta adrenergic stimulation with the opening of multiple arteriovenous shunts in the pulmonary and splanchnic areas was of major importance in the pathogenesis of late refractory shock and that excessive alpha adrenergic stimulation with arteriolar vasoconstriction was only of secondary importance. (3) It was suggested that the beta adrenergic stimulation causes a rapid arterial runoff with a fall in peripheral resistance and a lowering of the arterial pressure. The arterialized blood enters the thin walled venules causing dilatation and pooling. The resultant increase in capillary hydrostatic pressure and stagnant anoxia causes a loss of plasma and blood and a further decrease in the effective blood volume. In addition, in the lungs the bypassing of the alveolar capillary bed due to anatomical shunting leads to arterial unsaturation. The transudation of plasma can wash away pulmonary surfactant causing alveolar collapse. The hypoperfusion of the type II alveolar cells leads to a decrease in the biosynthesis of pulmonary surfactant resulting in more alveolar collapse. The pulmonary edema, hemorrhages, and atelectasis cause physiological shunting and a further increase in arterial unsaturation. The other effects of adrenergic stimulation are compensatory at this stage, beta stimulation resulting in an increased heart rate and increased myocardial contractility and the alpha stimulation resulting in compensatory arteriolar vasoconstriction in the renal and cutaneous areas. As shock progresses the pooling continues but due to the increasing metabolic acidosis of cellular hypoperfusion the catecholamines become less effective and there is a progressive loss of the compensation and the development of irreversible shock and death.


Arteriovenous Shunt Pulmonary Surfactant Adrenergic Stimulation Beta Blockade Beta Adrenergic Blockade 
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  1. 1.
    Berk, J. L., Pecic, I., Shields, E. and Natwick, R. (1964): The Role of Multiple Arteriovenous Anastomoses in the Pathogenesis of the Dumping Syndrome. Surgery, Gynecology & Obstetrics, 119, 817.Google Scholar
  2. 2.
    Berk, J. L., Hagen, J. F., Beyer, W. H. and Niazmand, R. (1967): The Effect of Epinephrine on Arteriovenous Shunts in the Pathogenesis of Shock. Surgery, Gynecology & Obstetrics, 124, 347.Google Scholar
  3. 3.
    Berk, J. L., Hagen, J. F., Beyer, W. H., Dochat, G. R. and LaPointe, R. (1967): The Treatment of Hemorrhagic Shock by Beta Adrenergic Receptor Blockade. Surgery, Gynecology & Obstetrics, 125, 311.Google Scholar
  4. 4.
    Berk, J. L., Hagen, J. F., Beyer, W. H., Gerber, M.J. and Dochat, G. R. (1969): The Treatment of Endotoxin Shock by Beta Adrenergic Blockade. Annals of Surgery, 169, 74.PubMedCrossRefGoogle Scholar
  5. 5.
    Berk, J. L., Hagen, J. F., Dunn, J. M. (1969): The Treatment of Septic Shock with Beta Adrenergic Blockade. Circulation (Supplement), 40, 44.Google Scholar
  6. 6.
    Berk, J. L., Hagen, J. F., Dunn, J. M. (1970): The Treatment of Septic Shock. Surgery, Gynecology & Obstetrics. To be published.Google Scholar

Copyright information

© Plenum Press, New York 1970

Authors and Affiliations

  • James L. Berk
    • 1
  1. 1.School of MedicineCase Western Reserve UniversityUSA

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