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Anesth Analg 2002;94:479
© 2002 International Anesthesia Research Society

LETTERS TO THE EDITOR

Vasopressin Effect on Pulmonary Arterial Pressure

C. Chamorro, J. A. Silva, M. A. Romera, J. Márquez, and C. Pardo

Intensive Care Unit, Clínica Puerta de Hierro, Madrid, Spain

To the Editor:

We read the interesting article by Dünser et al. (1) regarding the effects of continuous arginine vasopressin infusion on systemic hemodynamics in patients with refractory shock to the catecholamine employment. The use of vasopressin caused a significant increase in systemic vascular resistance (SVR) and mean arterial pressure (MAP), along with a significant reduction in heart rate, cardiac index (CI) (maintaining the stroke volume index), and mean pulmonary arterial pressure (MPAP) in these patients. In the later discussion of their work, the authors emphasize the finding of the reduction in MPAP, and they even suggest a probable pulmonary vasodilator effect caused by the vasopressin employment.

Nevertheless, the authors do not express the pulmonary vascular resistance (PVR), which is the real marker of the pulmonary vasoconstrictor or vasodilator effect of a drug. If we calculate the PVR according to the data shown in Table 2 of their article, we observe that PVR increases, and therefore the contrary hemodynamic effect to which Dünser et al. (1) suggest occurs. The reduction in MPAP that they find in their study is the consequence of the reduction in CI that the vasopressin produced, not the consequence of a pulmonary vasodilator effect.

References

  1. Dünser MW, Mayr AJ, Ulmer H, et al. The effects of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock: a retrospective analysis. Anesth Analg 2001; 93: 7–13.[Abstract/Free Full Text]
 

Response

W. R. Hasibeder, MD, M. W. Dünser, MD, and A. J. Mayr, MD

Department of Anesthesia and Critical Care Medicine, The Leopold Franzens University of Innsbruck, Innsbruck, Austria

In Response:

We would like to thank Chamorro et al. for their important contribution. The pulmonary vascular resistance (PVR), not expressed in our work, is now presented in Table 1. We observed no significant change in PVR. In addition, there is not a significant difference between survivors and nonsurvivors nor is there one between patients in septic and patients in postcardiotomy shock.


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  		Table 1. Pulmonary Vascular Resistance (dyne · s · cm5) in Patients with Catecholamine-Resistant Vasodilatory Shock
 
From a physiological standpoint, the observed decrease in cardiac index (CI) of approximately 1 L · min-1 · m2 should not significantly contribute to the observed reduction in mean pulmonary arterial pressure (MPAP). In humans the pulmonary arterial system is very compliant and blood flow through the lungs may vary substantially before MPAP changes. Even in critically ill patients, small changes in cardiac output similar to that observed during this study usually do not affect MPAP. Nevertheless, a significant reduction in mean pulmonary arterial pressure should be accompanied by a decrease in right ventricular afterload.

The true mechanism of the observed decrease in MPAP in our patients remains to be resolved. However, we speculate that the significant reduction in norepinephrine requirements during vasopressin administration plays a major role.





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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press