JTCS Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gravlee, G. P.
Right arrow Articles by Toole, J. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gravlee, G. P.
Right arrow Articles by Toole, J. F.

The Journal of Thoracic and Cardiovascular Surgery, Vol 88, 742-747, Copyright © 1984 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association


ARTICLES

Bilateral brachial paralysis from watershed infarction after coronary artery bypass. A report of two cases and review of the predisposing anatomic and physiological mechanisms

GP Gravlee, AS Hudspeth and JF Toole

Bilateral brachial paralysis and bilateral visual field defects developed after coronary artery bypass in two patients. These deficits, caused by cerebral watershed infarctions, probably resulted from global cerebral hypoperfusion during cardiopulmonary bypass, although bypass had been maintained with high perfusion flows (2.0 to 3.0 L/min/m2) and perfusion pressures from 50 to 90 mm Hg. No systemic hypoperfusion or hypotension occurred before or after cardiopulmonary bypass. Cerebral watershed infarctions occur predominantly in the boundary zones between the anterior, middle, and posterior cerebral arteries. In previous reports, watershed infarctions most often occurred as preterminal events in patients after sustained episodes of obvious hypoperfusion. The occurrence of such major neurological deficits in two patients without systemic hypoperfusion suggests that traditionally accepted flows and perfusion pressures do not assure adequate cerebral blood flow during cardiopulmonary bypass.


This article has been cited by other articles:


Home page
StrokeHome page
M. A. Sloan, T. R. Price, M. L. Terrin, S. Forman, J. M. Gore, B. R. Chaitman, M. Hodges, H. Mueller, W. J. Rogers, G. L. Knatterud, et al.
Ischemic Cerebral Infarction After rt-PA and Heparin Therapy for Acute Myocardial Infarction : The TIMI-II Pilot and Randomized Clinical Trial Combined Experience
Stroke, June 1, 1997; 28(6): 1107 - 1114.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 1984 by The American Association for Thoracic Surgery.