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J Thorac Cardiovasc Surg 1994;107:942-943
© 1994 Mosby, Inc.


LETTERS TO THE EDITOR

Vasoplegic syndrome: A new dilemma

Walter J. Gomes, MD, Antonio C. Carvalho, MD, J. Honório Palma, MD, Iran Gonçalves, Jr., MD, Enio Buffolo, MD

Division of Cardiovascular Surgery and Cardiology
Escola Paulista de Medicina
Rua Botucatú, 740
04023-900—São Paulo, Brazil

To the Editor:

The postperfusion syndrome is a well-known entity and its consequences are fully documented. Among them are variable degrees of lung and kidney dysfunction, hemorrhagic diathesis, increased tendency to infection, swelling, leukocytosis, fever, vasoconstriction, and hemolysis.Go 1

Recently, a new form of postperfusion syndrome has been worrying us. We have observed a vasoplegic syndromeGo 2 in the early postoperative period with severe hypotension and normal or elevated cardiac output, decreased filling pressures, and low systemic vascular resistance. Physical examination reveals normal capillary filling at the extremities, normal oxygen saturation, but oliguria and hypotension.

Our comments are based on six cases in which thermodilution monitoring was done in the immediate postoperative period. The hemodynamic data showed low wedge and right atrial pressures (wedge pressure from 4 to 11 mm Hg), mean arterial pressure in the range of 40 to 65 mm Hg, cardiac index from 2.97 to 3.82 L· min-1· m-2, and systemic vascular resistance index (SVRI) from 700 to 1200 dyne· sec· cm-5· mGo 2 with heart rates in the range 120 to 130 beats/min. Restoration of volume was not sufficient to restore normal hemodynamic parameters. These patients needed a high dosage of vasoconstrictor drugs (norepinephrine) for hours or even days until symptoms were completely reversed. A chart relating sequential values of norepinephrine and SVRI in one of our patients demonstrates an initial response of SVRI to norepinephrine and then the need for further increases of norepinephrine until SVRI stabilizes and increases (Fig. 1). In this patient norepinephrine was withdrawn after a little more than 24 hours; in some other patients norepinephrine was continued for more than 72 hours. Interestingly, even high dosages of norepinephrine in these patients did not produce the classic situation of cool extremities and faint peripheral pulses. The morbidity and mortality in this patient group is high, however.



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Fig. 1. Relation of norepinephrine (NOR) administration and systemic vascular resistance index (SVRI) in a patient with a vasoplegic syndrome in the immediate postoperative (PO) period.

 
No isolated or predictive risks could be incriminated in the development of this syndrome. Several aspects may be related to the emergence of this complication. Plasticizers—contaminants of tubes and oxygenators—affect cardiovascular dynamics,Go 3 and leukocyte activation with cytokines andrelease of tumor necrosis factor,Go 4 as occur in endotoxic shock, could produce similar clinical features.

Curiously, this syndrome was observed in our service after blood hypothermic cardioplegia had been introduced as a method of myocardial protection.

Despite its infrequent appearance (the prevalence in our series is 1/120 cases), the deleterious effects of the vasoplegic syndrome, as well as its mortality, have been worrisome. Efforts should be directed to determine the cause of this syndrome and to prevent its onset. Once it has developed, treatment with intravenous vasoconstrictors is usually necessary.

References

  1. Kirklin JK. The postperfusion syndrome: inflammation and the damaging effects of cardiopulmonarybypass. In: Tinker JH, ed. Cardiopulmonary bypass: current concepts and controversies. Philadelphia: WB Saunders, 1989:131-46.
  2. Gonçalves I Jr, Carvalho AC, Castello HJ, et al. Vasodilatação periféricano pós-operatório de cirurgia cardíaca: síndromevasoplégica. Arq Bras Cardiol 1992;59(suppl II):84.
  3. Aronson CE, Serlick R, Preti G. Effects of di-2-ethylhexyl phthalate on the isolated perfused rat heart. Toxicol Appl Pharmacol 1978;44:155-69.[Medline]
  4. Michie HR, Spriggs DR, Manogue KR, et al. Tumor necrosis factor and endotoxin induce similar metabolic responses in human beings. Surgery 1988;104:280-7.[Medline]



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