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Canadian Anaesthetists’ Society Journal

, Volume 25, Issue 3, pp 191–197 | Cite as

ETUDE CRITIQUE DE ĽEXPLORATION HEMODYNAMIQUE PER-ANESTHESIQUE

  • P. Stieglitz
  • P. Girardet
Article
  • 118 Downloads

Résumé

Le praticien qui doit choisir des méthodes ďanesthésie et de surveillance hémodynamique adaptées à ľétat de ses patients, cherche dans la littérature réponses à ses questions. Il n’y trouve pas toujours des notions utilisables dans son exercice courant.

En effet, la réaction circulatoire à un agent phaimaco-dynamique est diffuse et non spécifique, comme le rappelent divers exemples théoriques et pratiques. En particulier, il n’est pas sûr que diminuer la perfusion coronaire soit “mauvais“ si la Vo2 myocardique diminue en proportion.

D’autre part, les indices hémodynamiques (PA, PV, dP/dt) sont composés à partir de données élémentaires interdépendantes; il en résulte qu’ils sont eux aussi interdépendants.

Un dernier fait est troublant: les agents anesthésiques dépresseurs peuvent déclencher des crises hémodynamiques sévères mal supportées par les viscères en général mais, semble-t-il mieux par le myocarde qui ne souffre pas irrémédiablement si Panoxie ischémique infligée ac compagne une diminution brutale du travail cardique externe. Ceci explique la bonne tolérance cardiaque à un surdosage anesthésique passager.

Il est difficile de déterminer quelles sont les premières modifications hémodynamiques duês à ľanesthésie que ľon doit traiter. La biochimie du sang veineux coronaire elle-même n’apporte pas aujourďhui la solution.

Summary

Physicians must choose the anaesthetics for their patients and select the methods to check their haemodynamic status. Experimental works do not always bring sufficient information to help them in their daily practice.

Circulatory reaction to a pharmacodynamic agent is diffuse and non-specific. Some examples drawn from theoretical considerations and practical situations support this view. The difficulty of assessing the actual damage caused by one apparent variation still remains. On the other hand, haemodynamic indices such as PA, CVP, dP/dt are composed of elementary data that are interdependent; so indices are interdependent, too.

A puzzling fact is that depressing anaesthetics can initiate severe haemodynamic crisis, generally badly tolerated by tissues, but better tolerated by myocardium which is not definitely altered if the anoxia inflicted is accompanied by a real decrease in cardiac work. This explains the often slight effect of short anesthetic overdosage.

Previous haemodynamic variations to be countered relative to anaesthesia are not really known. Biochemistry of the venous coronary blood does not yet bring striking features in this field.

Bibliographie

  1. 1.
    Patschke, D., Bruckner, J.B., Eberlein, H.J., Hess, W., Tarnow, J., &Weymar, A. Effects of althesin, etomidate and fentanyl on haemodynamics and myocardial oxygen consumption in man. Can. Anaesth. Soc. J.24: 57–69 (1976).Google Scholar
  2. 2.
    Merin, R.G., Kumazawa, T., &Luka, N.L. Enflurane depresses myocardial function, perfusion and metabolism in the dog. Anesthesiology,45: 501–507 (1976).PubMedCrossRefGoogle Scholar
  3. 3.
    Dauchot, P.J., Rasmussen, J.P., Nicholson, D.H., Divers, R.T., Katona, P.G., Zollinger, R.M., Knoke, J.D., Kyo, E.W., &Gravenstein, J.S. On-line systolic time intervals during anesthesia in patients with and without heart disease. Anesthesiology44: 472–480 (1976).PubMedGoogle Scholar
  4. 4.
    Byrick, R.J.,Teasdale, S.J., &Young, A. Systolic time interval changes after aorto-coronary bypass. Canad. Anaesth. Soc. J.24: 175-185.Google Scholar
  5. 5.
    Filner, B.E. &Karliner, J.S. Alterations of normal left ventricular performance by general anesthesia. Anesthesiology,45: 610–621 (1976).PubMedCrossRefGoogle Scholar
  6. 6.
    Brutsaert, D.L. &Sonnenblick, E.H. Cardiac muscle mechanics in the evaluation of myocardial contractility and pump function: problems, concepts and directions. Progress Cardiovasc. Dis.16: 337–361 (1973).CrossRefGoogle Scholar
  7. 7.
    Guyton, A.C., Jones, C.E., &Coleman, T.G. Circulatory physiology: cardiac output and its regulation. W.B. Saunders Cy. Ed. Philadelphia, 556 PP. (1973).Google Scholar
  8. 8.
    Roberts, J.G., Foex, P., Clarke, T.N.S., Bennett, M.J., &Saner, C.A. Haemodynamic interactions of high-dose propranolol pretreatment and anaesthesia in the dog. 3. The effects of haemorrhage during halothane and trichloroethylene anaesthesia. Brit. J. Anaesth.48: 411–418 (1976).PubMedCrossRefGoogle Scholar
  9. 9.
    Swan, H.J.C., Forrester, J.S., Diamond, G., Chatterjee, K., &Parmley, W.W. Haemodynamic spectrum of myocardial infarction and cardiogenic shock. Circulation45: 1097–1110 (1972).PubMedGoogle Scholar
  10. 10.
    Giuntini, C. Communication personnelle.Google Scholar
  11. 11.
    Braunwald, E. On the difference between the heart’s output and its contractile state. Circulation43: 171–174 (1971).PubMedGoogle Scholar
  12. 12.
    Braunwald, E. Control of myocardial oxygen consumption. Physiologic and clinical considerations. Amer. J. Cardiol.,27: 416–432 (1971).PubMedCrossRefGoogle Scholar
  13. 13.
    Braunwald, E. Current concepts in cardiology. Determinants and assessment of cardiac function. New Engl. J. Med.296: 86–89 (1977).PubMedGoogle Scholar
  14. 14.
    Cross, CE., Rieben, P.A., Barron, C.I., &Salisbury, P.F. Effects of arterial hypoxia on the heart and circulation: an integrative study. Amer. J. Physiol.,205: 963–970 (1963).PubMedGoogle Scholar
  15. 15.
    Diaz, F.A., Bianco, J.A., Bello, A., Beer, N., Velarde, H., Izquierdo, J. P., &Jaén, R. Effects of ketamine on canine cardiovascular function. Brit. J. Anaesth.45: 941–945 (1976).CrossRefGoogle Scholar
  16. 16.
    Foex, P. &Prys-Roberts, C. Interactions of beta-receptor blockage and Pco2 levels in the anaesthetized dog. Brit. J. Anaesth.,46: 397–405 (1974).PubMedCrossRefGoogle Scholar
  17. 17.
    Gersh, B.J., Prys-Roberts, C., Reuben, S.R., &Schultz, D.L. The effects of halothane on the interactions between myocardial contractility, aortic impedance and left ventricular performance. 2. Aortic imput impedance and the distribution of energy during ventricular ejection. Brit. J. Anaesth.,44: 767–774 (1972).PubMedCrossRefGoogle Scholar
  18. 18.
    Giudicelli, J.F. Pharmacologie cardiaque. Asclepios Ed., Paris, 279 pp. (1976).Google Scholar
  19. 19.
    Gorlin, R. Current concepts in cardiology. Practical cardiac hemodynamics. New Engl. J. Med.296: 203–205 (1977).PubMedGoogle Scholar
  20. 20.
    Graham, T.P., Covell, J.W., Sonnenblick, E.H., Ross, J., &Braunwald, E. Control of myocardial oxygen consumption: relative influence of contractile state and tension development. J.Clin. Invest.47: 375–385 (1968).PubMedGoogle Scholar
  21. 21.
    Guyton, A.C. Regulation of cardiac output. New Engl. J. Med.277: 805–812 (1967).PubMedGoogle Scholar
  22. 22.
    Harlan, W.R., Oberman, A., Grimm, R., &Rosati, R.A. Chronic congestive heart failure in coronary artery disease: clinical criteria. Ann. Internal. Med.86: 133–138 (1977).Google Scholar
  23. 23.
    Hill, D.W. &Merrifield, A.J. Left ventricular ejection and the Heather index measured by noninvasive methods during postural changes in man. Acta Anaesth. Scand.20: 313–320 (1976).PubMedGoogle Scholar
  24. 24.
    Kanter, S.F. &Samuels, S.I. Anesthesia for major operations on patients who have transplanted hearts. A review of 29 cases. Anesthesiology46: 65–68 (1977).PubMedCrossRefGoogle Scholar
  25. 25.
    Lappas, D.G., Buckley, M.J., Laver, M.B., Daggett, W.M., &Lowenstein, E. Left ventricular performance and pulmonary circulation following addition of nitrous oxide to morphine during coronary artery surgery. Anesthesiology,43: 61–69 (1975).PubMedCrossRefGoogle Scholar
  26. 26.
    Levy, M.N. The cardiovascular physiology of the critically ill patient. Surg. Clin. North Amer.,55: 483–499 (1975).Google Scholar
  27. 27.
    Marino, R.J., Romagnoli, A., &Keats, A.S. Selective venoconstriction by Dopamine in comparison with Isoproterenol and Phenylephrine. Anesthesiology,41: 570–572 (1975).Google Scholar
  28. 28.
    Marshall, M. Williams, W.G., Creighton, R.E., Volgyesi, G.A., &Steward, D.J. A technique for measuring regional myocardial blood flow and its application in determining the effects of hyperventilation and halothane. Canad. Anaesth. Soc. J.23: 244–251 (1976).Google Scholar
  29. 29.
    Mason, D.T., Spann, J.F., &Zelis, R. Quantification of the contractile state of the intact human heart. Amer. J. Cardiol.26: 248–257 (1970).PubMedCrossRefGoogle Scholar
  30. 30.
    Mjchalot, G. Oxygénation extra-corporelle ďas sistance dans rhypoxémie réfractaire. Etude expérimentale de la voie de réinjection aortique rétrograde. Données gazométriques et hémodynamiques. Thèse de Médecine, Grenoble (1977).Google Scholar
  31. 31.
    Nandan, R.M. Action du Nitroprussiate en neurochirurgie. Thèse de Médecine, Grenoble. Sous presse.Google Scholar
  32. 32.
    Parisi, A.F., Tow, D.E., Felix, W.R., &Sasahara, A.A. Noninvasive cardiac diagnosis. New Engl. J. Med.296: 427–432 (1977).PubMedCrossRefGoogle Scholar
  33. 33.
    Payne, R.M., Horwitz, L.D., &Mullins, C.B. Comparison of isometric exercise and angiotensin infusion as stress test for evaluation of left ventricular function. Amer. J. Cardiol.31: 428–433 (1973).PubMedCrossRefGoogle Scholar
  34. 34.
    Philips, P.A., Marty, A.T., Miyamoto, A.M. A clinical method for detecting subendocardial ischemia after cardio-pulmonary bypass. J. Thor. Cardiovasc. Surg.69: 30–39 (1975).Google Scholar
  35. 35.
    Prys-Roberts, C., Greene, L.T., Meloche, R., &Foex, P. Studies of anaesthesia in relation to hypertension. Hemodynamic consequences of induction and endotracheal intubation. Brit. J. Anaesth.43: 531–547 (1971).PubMedCrossRefGoogle Scholar
  36. 36.
    Roberts, J.G., Foex, P., Clarke, T.N.S., &Bennett, M.J. Haemodynamic interactions of high-dose propranolol pretreatment and anaesthesia in the dog. I. Halothane dose-response studies. Brit. J. Anaesth.48: 315–324 (1976).Google Scholar
  37. 37.
    Roberts, J.G., Foex, P., Clarke, T.S.N., Prys-Roberts, C., &Bennett, M.J. Haemodynamic interactions of high-dose propranol pretreatment and anaesthesia in the dog. 2. The effects of acute arterial hypoxaemia at increasing depths of halothane anaesthesia. Brit. J. Anaesth.48: 403–409 (1976).PubMedCrossRefGoogle Scholar
  38. 38.
    Roizen, M.F., Moss, J., Henry, D.P., &Kopin, I.J. Effects of halothane on plasma catecholamines. Anesthesiology41: 432–439 (1974).PubMedCrossRefGoogle Scholar
  39. 39.
    Sarnoff, S.J., Baunwald, E., Welch, G.H., Case, R.B., Stainsby, W.H., &Macrez, R. Hemodynamic determinants of oxygen consumption of the heart with special reference to tension time index. Amer. J. Physiol.,192: 148–155 (1958).PubMedGoogle Scholar
  40. 40.
    Sanghvi, V.R., Khaja, F., Mark, A.L., Parker, J.P. Effects of blood volume expansion on left ventricular haemodynamics in man. Circulation46:708–787 (1972).Google Scholar
  41. 41.
    Smith, G. The coronary circulation and anaesthesia. Brit. J. Anaesth.48: 933–934 (1976).PubMedCrossRefGoogle Scholar
  42. 42.
    Starling, E.H. The linacre lecture on “the Law of the heart“. London and New York: Longman, Green and Co. (1918).Google Scholar
  43. 43.
    Swan, H.J.C. &Ganz,W. Use of balloon flotation catheters in criticialiy ill patients. Surg. Clinics North Amer.55: 501–520 (1975).Google Scholar
  44. 44.
    Tomlin, P.J. &Duck, F.A. Transoesophageal aortic velography in man. Canad. Anaesth. Soc. J.22: 561–571 (1975).CrossRefGoogle Scholar
  45. 45.
    Wexler, L.F. &Pohost, G.M. Hemodynamic monitoring: noninvasive techniques. Anesthesiology45: 156–183 (1976).PubMedCrossRefGoogle Scholar
  46. 46.
    Yang, S.S. From cardiac catheterisation data to hemodynamics parameters. Davis Ed., Philadelphia, 307 pp. (1972).Google Scholar

Copyright information

© Canadian Anesthesiologists 1978

Authors and Affiliations

  • P. Stieglitz
  • P. Girardet
    • 1
  1. 1.Département ďAnesthésie-RéanimationCentre Hospitalier, Universitaire de GrenobleLa TroncheFrance

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