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A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care

Official Journal of the Italian Society of Anesthesiology, Analgesia, Resuscitation and Intensive Care
Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 2,036

Frequency: Monthly

ISSN 0375-9393

Online ISSN 1827-1596


Minerva Anestesiologica 2000 April;66(4):217-23



Systemic and pulmonary vascular resistances in brain death

Gravame V., Cardillo M. *, Paganoni G., Bonomi A., Candiani A. **, Chiaranda M. ***, Scalamogna M. ****, Taioli E. *****

Servizio di Anestesia e Rianimazione Ospedali Riuniti - Bergamo
*Centro Trasfusionale e di Immunologia dei Trapianti IRCCS Ospedale Maggiore - Milano
**II Servizio di Anestesia e Rianimazione Spedali Civili - Brescia
***Servizio di Anestesia e Rianimazione Ospedale - Varese
****Servizio per il Prelievo e la Conservazione di Organi e Tessuti IRCCS Ospedale Maggiore - Milano
*****Laboratorio di Epidemiologia IRCCS Ospedale Maggiore - Milano

Background. Hemodynamic instability is known to affect brain dead subjects and it can be dangerous for the viability of transplantable organs. Aim of the present study was to assess the hemodynamic performance in brain dead subjects, the changes during the legal observation period and the results of therapeutic management.
Methods. The authors evaluated 28 consecutive adult brain dead subjects, all in intensive treatment, controlled ventilation, infusion therapy and/or dopamine administration and continuous direct monitoring of arterial pressure. Ten hemodynamic parameters have been registered by the thermodilution method and the Swann-Ganz catheter. The Legal Committee performed measurements at the beginning (T0) and the end (T6) of the observation period, which lasts 6 hours according to the current law on death certification (Law N. 578/93).
Results. Low systemic and pulmonary vascular resistances have been documented in the majority of subjects (75%), both treated only with fluids and with the additional dopamine administration (dosage lower than 10 ug/Kg/min). The above-mentioned reduction was similar at the two different monitored times (T0 and T6).
Conclusions. This situation can be ascribed to the destruction of the cerebral vasoactive centers and the consequent hypotension is due to autonomic nervous system dysfunction. Hemodynamic instability must be treated by fluids and inotropic drugs, but they may cause cardiac and respiratory problems, thus it is suggested to use also low doses of vasoconstrictive drugs, provided that cardiac condition allows this therapeutic strategy.

language: Italian


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