Update in the Treatment of Acute Circulatory Failure

  • E. C. Rackow
Conference paper
Part of the Anaesthesiologie und Intensivmedizin / Anaesthesiology and Intensive Care Medicine book series (A+I, volume 167)

Abstract

The pathophysiological defect which characterizes shock is that of perfusion failure in which blood flow to maintain the function of vital organ systems is critically reduced. As a clinical syndrome, it is characterized by protracted prostration, pallor, coldness and moistness of the skin, collapse of the superficial veins, alterations in pressure is typically less than 90 mmHg or has declined more than 50 mm from the basal level, and the urine flow is less than 20 ml/h.

Keywords

Ischemia Dopamine Lactate Glycoside Quinone 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Braunwald E (1974) Regulation of the circulation. N Engl J Med:290, 1124, 1420PubMedCrossRefGoogle Scholar
  2. 2.
    Eichna LS (1960) Circulatory congestion and heart failure. Circ 22:864Google Scholar
  3. 3.
    Forrester JS, Diamond GA, Swan HJC (1977) Correlative classification of clinical and hemodynamic function after acute myocardial infarction. Am J Card 39:173CrossRefGoogle Scholar
  4. 4.
    Forrester JS, Diamond G, Kanu Chatterjee MD, Swan HJC (1977) Medical therapy of acute myocardial infarction by application of hemodynamic subsets. N Engl J Med 295:1356CrossRefGoogle Scholar
  5. 5.
    Gaasch WH, Levine JH, Quinones MA, Alexander JK (1976) Left ventricular compliance: Mechanisms and clinical implications. Am J Card 38:645PubMedCrossRefGoogle Scholar
  6. 6.
    Henning RJ, Weil MH (1978) Effect of afterload reduction of plasma volume during acute heart failure. Am J Card 42:823PubMedCrossRefGoogle Scholar
  7. 7.
    Mason DT (ed) (1978) Symposium on vasodilator and inotropic therapy of heart failure. Am J Med 15:101Google Scholar
  8. 8.
    Mikulic E, Cohn JM, Franciosa JA (1977) Comparative hemodynamic effects of inotropic and vasodilator drugs in severe heart failure. Circ 56:528Google Scholar
  9. 9.
    Mueller HS, Evans R, Ayers SM (1978) Effect of dopamine on hemodynamics and myocardial metabolism in shock following acute myocardial infarction. Circ 45:361Google Scholar
  10. 10.
    Rahimtoola HS, Sinno MZ, Chuqiumea R, Loeb HS, Rosen KM, Gunnar RM (1972) Effects of ouabain on impaired left ventricular function in myocardial infarction. N Engl J Med 287:527PubMedCrossRefGoogle Scholar
  11. 11.
    Ross J Jr (1976) Afterload mismatch and preload reserve: A conceptual framework for the analysis of ventricular function. Prog Cardiovas Dis 18:255CrossRefGoogle Scholar
  12. 12.
    Ruiz CE, Weil MH, Carlson RC (1979) Treatment of circulatory shock with dopamine: studies on survival. JAMA 242:165PubMedCrossRefGoogle Scholar
  13. 13.
    Scheuer J, Bhan AK (1979) Cardiac contractile proteins: adenosine triphosphate activity and physiologic function. Circ Res 45:1PubMedGoogle Scholar
  14. 14.
    Sonnenblick EH (1962) Force-velocity relations in mammalian heart muscle. Am J Physiol 202:931PubMedGoogle Scholar
  15. 15.
    Sonnenblick EH et al (1979) Dobutamine: A new synthetic cardioactive sympathetic amine. N Engl J Med 300:17PubMedCrossRefGoogle Scholar
  16. 16.
    Stemple DR, Kleiman JH, Harrison DC (1979) Combined nitroprusside dopamine therapy in severe chronic congestive heart failure. Dose related hemodynamic advantages over single drug infunctions. Am J Cardiol 42:267Google Scholar
  17. 17.
    Swan HJC (1975) The role of hemodynamic monitoring in the management of the critically ill. Crit Care Med 3:83PubMedCrossRefGoogle Scholar
  18. 18.
    Weil MH, Shubin H, Carlson (1975) Treatment of circulatory shock: use of sympathomimetic and related vasoactive agents. JAMA 23a:1280CrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1984

Authors and Affiliations

  • E. C. Rackow

There are no affiliations available

Personalised recommendations