Hyponatremia in Congestive Heart Failure

  • C. T. G. Flear
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 102)

Abstract

Dyspnoea on effort, venous congestion of the lungs and the liver, distension of neck veins and oedema are features of congestive heart failure (CHF) which result from a progressive accumulation of sodium, chloride, bicarbonate and water. The interstitial fluid (ISF) increases in all tissues and and body weight rises despite obvious wasting that may develop in some patients. Resting energy expenditure increases in progressive failure, as Na+ influx into skeletal muscle cells increases. With oedema accumulation, there is a fall in the concentrations of proteoglycans that structure tissue ISF. This increases the mobility of ISF and enables the clinical sign of pitting oedema to be demonstrated.

Keywords

Filtration Mercury Urea Shrinkage Arginine 

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References

  1. 1.
    Flear CTG. Disturbance of volume and composition of body fluids in congestive heart failure. In: Bajusz E. (ed) Electrolytes and Cardiovascular Diseases. Karger, Basel/New York, 1966. Vol 2, pp.357–85.Google Scholar
  2. 2.
    Flear CTG, Rorence I, Williams JA. Water and electrolytes in muscle. Lancet 1968a; 1:45–6.PubMedCrossRefGoogle Scholar
  3. 3.
    Flear CTG, Rorence I, Williams JA. Water, sodium, potassium and chloride content of skeletal muscle in fit and ill subjects. J Clin Path 1968b;21:555–563.PubMedCrossRefGoogle Scholar
  4. 4.
    Flear CTG. Water and electrolyte metabolism in congestive heart failure. Postgrad Med J 1960a;36:104–119.PubMedCrossRefGoogle Scholar
  5. 5.
    Flear CTG. Studies in congestive heart failure: Therapeutic and theoretical problems. MD Thesis, Birmingham Univ, 1960b.Google Scholar
  6. 6.
    Lee WH, Packer M. Prognostic importance of serum sodium concentration and its modification by converting enzyme inhibition in patients with severe chronic heart failure. Circulation 1986;73:257–267.PubMedCrossRefGoogle Scholar
  7. 7.
    Flear CTG, Cawley RH. Potassium supplements and congestive heart failure: some biochemical and clinical observations. Brit Heart J 1962;24:337–348.PubMedCrossRefGoogle Scholar
  8. 8a.
    Landell WSS, Waterlow JC, Hudson MF. Desert climate: Physiological and clinical observations. Lancet 1944;2:491–7.Google Scholar
  9. 8b.
  10. 9.
    Adolph EF, et al. Physiology of Man in the Desert. Hafner, New York/London, 1947.Google Scholar
  11. 10.
    Edelman, I. The pathogenesis of hyponatremia: Physiologic and therapeutic implications. Metabolism 1956;5:500–507.PubMedGoogle Scholar
  12. 11.
    Gill GV, Rear CTG. Hyponatraemia. In: Price CP, Alberti KGMM (eds) Recent Advances in Clinical Biochemistry. Churchill Livingstone, Edinburgh, 1985. Vol 3, pp. 149–176.Google Scholar
  13. 12.
    Clowdus BF, Summerskill DM, Casey TH, Higgins JA, Orvis AL. Isotope studies of the development of water and electrolyte disorders and azotemia during the treatment of ascites. Gastroenterology 1961;41:360–70.PubMedGoogle Scholar
  14. 13.
    Flear CTG. Significance of potassium and sodium masses in cardiac disease. In: Bergner P-EE, Lushbough CC, Anderson EB. (eds) Compartments, Pools and Spaces in Medical Physiology. US Atomic Commission Divn of Tech Inf. 1967. pp.53–93.Google Scholar
  15. 14.
    Rear CTG, Singh CM. Hyponatraemia and sick cells. Brit J Anaesth 1973;45:976–94.CrossRefGoogle Scholar
  16. 15.
    Schrier RW, Bichet DG. Osmotic and non-osmotic control of vasopressin release and the pathogenesis of impaired water excretion in adrenal, thyroid and oedematous disorders. Journal 1978;98:1–15.Google Scholar
  17. 16.
    Szatalowicz VL, Arnold PE, Chaimoritz C, Bichet D, Berl T, Schrier RW. Radioimmunoassay of plasm arginine vasopressin in hyponatraemic patients with congestive heart failure. New Engl J Med 1981;263–6.Google Scholar
  18. 17.
    Flear CTG. Hyponatraemia. Lancet 1974;2:164–166.PubMedCrossRefGoogle Scholar
  19. 18.
    Flear CTG, Singh CM. The sick cell concept and hyponatraemia in congestive heart failure and liver disease. Lancet 1982;2:101–2.PubMedCrossRefGoogle Scholar
  20. 19.
    Flear CTG, Singh CM. The sick cell concept and hypoinatraemia. In: Taylor K, Bain WH (eds) Handbook of Intensive Care. John Wright, Bristol, 1983. pp.165–195.Google Scholar
  21. 20.
    Bichet D, Schrier RW. Evidence against concept of hyponatraemia and “sick cells”. Lancet 1982;1:742.PubMedCrossRefGoogle Scholar
  22. 21.
    Flear CTG, Cawley RH, Quinton A, Cooke WT. The simultaneous determination of total exchangeable sodium and potassium and its significance with particular reference to congestive cardiac failure and the steatorrhoea syndrome. Clin Sci 1958;17:81–104.PubMedGoogle Scholar
  23. 22.
    Flear CTG. Potassium chloride and intestinal ulceration. Lancet 1965;2:293–4.CrossRefGoogle Scholar
  24. 23.
    Flear CTG. Alterations in water and electrolyte distribution on congestive heart failure and their significance. In: Bajusz E. (ed) Experimental “Metabolic” cardipathies and their relationship to human heart diseases. Annals New York Acad Sci 1969;156(1):421–44.Google Scholar
  25. 24.
    Flear CTG, Hughes P. Electrolyte content of extracellular fluid in health and in congestive heart failure. Brit Heart J 1963;25:166–172.PubMedCrossRefGoogle Scholar
  26. 25.
    Davidson C, Burkinshaw L, McLachlan MSF, Morgan DB. Effects of long-term diuretic treatment on body-potassium in heart disease. Lancet 1976;2:1044–1047.PubMedCrossRefGoogle Scholar
  27. 26.
    Morgan DB, Burkinshaw L, Davidson C. Potassium depletion in heart failure and its relation to long-term treatment with diuretics: a review of the literature. Postgraduate Med J 1978;54:72–79.CrossRefGoogle Scholar
  28. 27.
    Singh CM, Flear CTG, Nandra A, Ross DN. Electrolyte change in the human myocardium seen after anoxic arrest. Cardiology 1971;56:128–135.PubMedCrossRefGoogle Scholar

Copyright information

© Kluwer Academic Publishers 1989

Authors and Affiliations

  • C. T. G. Flear
    • 1
  1. 1.University Department of Clinical Biochemistry and Metabolic MedicineUniversity of Newcastle upon TyneUK

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