Hemodynamic Defects Underlying Shock with Indications for Treatment: An Appraisal of Vasopressors and Vasodilators

  • Max Harry Weil


Until the sphygmomanometer came into wide use after 1910, the character and rate of the pulse served as the primary objective measure of severity of circulatory failure. Subsequently, blood pressure became an index for both the diagnosis and estimation of severity of the shock state. In the search for therapy by which hypotension could be reversed, the clinician was attracted to drugs restoring blood pressure to more normal levels. This led to the early use of epinephrine and the subsequent use of its adrenergic analogs. Beginning in the 1940s synthetic adrenergic drugs came into wide use for treatment of shock states. Unlike epinephrine, phenylephrine and methaxamine increased blood pressure but more often decreased the heart rate. Except for the relatively conservative use of fluids, blood, blood components, and blood substitutes, vasopressor drugs were until recently the mainstay of therapy for shock, regardless of cause.


Shock State Fluid Challenge Arteriovenous Shunting Arterial Resistance Vasopressor Agent 
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  1. 1.
    Ahlquist, R. P. (1948). A study of adrenotropic receptors. Am. J. Physiol. 755:586–600.Google Scholar
  2. 2.
    Carriere, S. (1969). Effect of norepinephrine, isoproterenol and adrenergic blockers upon the intrarenal distribution of blood flow. Can. J. Physiol. Pharmacol. 47:199–208.PubMedCrossRefGoogle Scholar
  3. 3.
    Conn, J. N., and Luria, M. H. (1965). Studies in clinical shock and hypotension: II. Hemodynamic effects of norepinephrine and angiotension. J. Clin. Invest. 44:1494–1504.CrossRefGoogle Scholar
  4. 4.
    Cournand, A., et al. (1943). Studies of the circulation in clinical shock. Surg. 73:964–995.Google Scholar
  5. 5.
    da Luz, P. L., et al. (1974). Plasma volume prior to and following volume loading during shock complicating acute myocardial infarction. Circulation 49:98–105.PubMedGoogle Scholar
  6. 6.
    Gunnar, R. M., et al. (1967). Ineffectiveness of isoproterenol in shock due to acute myocardial infarction. J. Am. Med. Assoc. 202:1124–1128.CrossRefGoogle Scholar
  7. 7.
    Hershey, S. G., et al. (1964). Influence of a synthetic analogue of vasopressin on survival after hemorrhagic shock in rats. Proc. Soc. Exp. Biol. Med. 775:325–328.Google Scholar
  8. 8.
    Lillehei, R. C., Longerbeam, J. K., and Bloch, J. H. (1964). The nature of experimental irreversible shock with its clinical implications. In: Hershey, S. G. (ed.), Shock. Boston: Little, Brown, pp. 139–205.Google Scholar
  9. 9.
    Loeb, H. S., Winslow, E. B. J., and Rahimtoola, S. H. (1971). Acute hemodynamic effects of dopamine in patients with shock. Circulation 44:163–173.PubMedGoogle Scholar
  10. 10.
    Mueller, H. S., et al. (1970). Hemodynamics, coronary blood flow and myocardial metabolism in coronary shock. J. Clin. Invest. 49:1885–1902.PubMedCrossRefGoogle Scholar
  11. 11.
    Nickerson, M. (1955). Factors of vasoconstriction and vasodilation in shock. J. Mich. Med. Soc. 54:45–49.PubMedGoogle Scholar
  12. 12.
    Shnider, S. M., Lorimier, A. A., and Hefferson, J. L. (1970). Vasopressors in obstetrics: III. Fetal effects of metaraminol infusion during obstetrical spinal hypotension. Am. J. Obstet. Gynec. 705:1017–1022.Google Scholar
  13. 13.
    Shubin, H., and Weil, M. H. (1971). Shock associated with barbiturate intoxication. J. Am. Med. Assoc. 275:263–268.CrossRefGoogle Scholar
  14. 14.
    Talley, R. C., et al. (1969). A hemodynamic comparison of dopamine and isoproterenol in patients in shock. Circulation 39:361–378.PubMedGoogle Scholar
  15. 15.
    Taylor, S. H., et al. (1965). The circulatory effects of intravenous phentolamine in man. Circulation 37:741–754.Google Scholar
  16. 16.
    Weil, M. H. (1955). Clinical studies on a vasopressor agent: Metaraminol (Aramine). II. Observations on its use in the management of shock. Am. J. Med. Sci. 230:357–369.PubMedCrossRefGoogle Scholar
  17. 17.
    Weil, M. H., and Shubin, H. (1967). Diagnosis and Treatment of Shock. Baltimore: Williams and Wilkins, p. 10.Google Scholar
  18. 18.
    Weil, M. H., and Shubin, H. (1972). Proposed reclassification of shock with special reference to distributive defects. In: Hinshaw, L. B., and Cox, B. G. (eds.), The Fundamental Mechanisms of Shock. New York/London: Plenum, pp. 13–23.Google Scholar
  19. 19.
    Weil, M. H., Shubin, H., and Biddle, M. (1964). Shock caused by gramnegative microorganisms: Analysis of 169 cases. Ann. Intern. Med. 60:384–400.PubMedGoogle Scholar
  20. 20.
    Weil, M. H., Shubin, H., and Carlson, R. (1975). Treatment of circulatory shock: Use of sympathomimetic and related vasoactive agents. J. Am. Med. Assoc. 237:1280–1286.CrossRefGoogle Scholar

Copyright information

© Springer-Verlag New York Inc. 1978

Authors and Affiliations

  • Max Harry Weil
    • 1
  1. 1.Center for the Critically Ill and the Shock Research UnitUniversity of Southern California School of MedicineLos AngelesUSA

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