ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Sidney Levitsky
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Levitsky, S.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Levitsky, S.
Related Collections
Right arrow Myocardial protection

Ann Thorac Surg 2001;72:S2243-S2244
© 2001 The Society of Thoracic Surgeons


Supplement: Monitoring and improving patient safety during and following cardiac surgery

Discussion

Sidney Levitsky, MDa

a Division of Cardiothoracic Surgery, Beth Israel-Deaconess Medical Center, 110 Francis Street, Suite 2A, Boston, MA 02215, USA

e-mail: slevitsk@caregroup.harvard.edu

I really want to compliment Dr Khuri, who has worked so hard over the years, beginning first with the mass spectrometer and now finally providing a functional probe with which one can really investigate myocardial acidosis. The probe allows us to look at a surrogate of anaerobic metabolism. Normally, myocardial metabolism is aerobic and myocardial pH remains within a normal range except, perhaps, in areas that are severely ischemic in association with coronary artery disease. We know from early physiologic studies conducted in the 1960s that, when we clamp the aorta, myocardial metabolism reverts from the aerobic to anaerobic state within 6 seconds, as high-energy phosphate moieties and glycogen stores are depleted and intracellular acidosis ensues. The advent of cardioplegia has provided buffering agents to prevent or partially ameliorate intracellular acidosis, hypothermia presumably to extend safely the time of surgically induced ischemia, and potassium to effect very rapid diastolic arrest. It is important to achieve an arrest within the first 1 or 2 minutes of aortic clamping to slow down the depletion of metabolic substrates and to delay the onset of acidosis.

Let me first answer the questions I’ve been asked. First, is hypothermia useful or injurious to the myocardium? Even though I still use hypothermia in the clinical setting, there is a real question as to whether putting cold water or ice slush on the surface of the heart is injurious to the myocardium. Is myocardial temperature measurement useful? I have not found it to be so, and have stopped using it. Is there any role for topographic thermography? I have not used this technology, but if temperature . . . [Full Text of this Article]







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 © 2001 by The Society of Thoracic Surgeons.