ABSTRACT
BACKGROUND: Clinical studies of deep hypothermic circulatory arrest (DHCA) have focused only on the immediate postoperative period. However, experimental findings suggest impairment of cerebral oxygenation at 2 to 8 hours after reperfusion. METHODS: In 10 children who had DHCA for heart operations, transcerebral differences of hemoglobin oxygen saturation and plasma hypoxanthine, xanthine, and lactoferrin concentrations were measured in concurrently obtained cerebral venous, arterial, and mixed venous samples up to 10 hours postoperatively. RESULTS: Compared with preoperative levels (57% +/- 7%), cerebral venous oxygen saturation was not significantly reduced until 2 hours (44% +/- 6%) and 6 hours (42% +/- 5%) after DHCA (p < 0.05). A statistically significant transcerebral (ie, cerebral vein versus artery) concentration difference of hypoxanthine was observed at 30 minutes (3.6 +/- 0.9 micromol/L), 1 hour (3.4 +/- 1.1 micromol/L), and 2 hours (3.1 +/- 0.8 micromol/L) after DHCA but not preoperatively (0.4 +/- 0.2 micromol/L). A transcerebral concentration difference of lactoferrin occurred 30 minutes after DHCA (196 +/- 70 microg/mL) but not preoperatively (16 +/- 20 microg/mL). CONCLUSIONS: Cerebral venous oxygen saturation of hemoglobin decreased as late as 2 to 6 hours after DHCA, in association with impaired cerebral energy status. Neutrophil activation in the cerebral circulation occurred 30 minutes after reperfusion.
Subject(s)
Brain/metabolism , Heart Arrest, Induced , Heart Defects, Congenital/surgery , Hypothermia, Induced , Oxygen/metabolism , Female , Hemoglobins/metabolism , Humans , Hypoxanthine/blood , Infant , Infant, Newborn , Lactoferrin/blood , Male , Neutrophil Activation , Postoperative Period , Time Factors , Xanthine/bloodABSTRACT
The study describes long term ventilatory effects of 50 or 100 micrograms.kg-1 of morphine or 1.5 or 3.0 micrograms.kg-1 of buprenorphine when given in repeated intravenous (i.v.) doses, in a double blind fashion, to achieve equal levels of analgesia after thoracotomy. The patients were 56 children, six months to six years of age. Ventilatory rate (VR) was measured over the 24 h study period, and arterial carbon dioxide tension (PaCO2) was measured on arrival in the Paediatric Intensive Care Unit (PICU) and at 1, 6, 12 and 18 h. In the buprenorphine groups VRs progressively decreased during the first 2 h and remained significantly lower (P < 0.05) than in the morphine groups for 7 h. For the rest of the study period there were no differences. The PaCO2 values did not differ significantly at any point. For safety, prolonged observation of children is needed after intravenous administration of buprenorphine to ensure the ventilatory rate has stabilized.
Subject(s)
Analgesics, Opioid/pharmacology , Buprenorphine/pharmacology , Morphine/pharmacology , Respiration/drug effects , Analgesia , Analgesics, Opioid/administration & dosage , Blood Pressure/drug effects , Buprenorphine/administration & dosage , Carbon Dioxide/blood , Child , Child, Preschool , Critical Care , Double-Blind Method , Heart Rate/drug effects , Humans , Infant , Injections, Intravenous , Morphine/administration & dosage , Pain, Postoperative/prevention & control , Safety , Thoracotomy/adverse effectsABSTRACT
Presently myocardial protection can be obtained in three main ways: 1) energy conservation through chemical induction of rapid and complete diastolic arrest, 2) slowing of the metabolic rate and degradative process through the use of hypothermia, and 3) prevention or reversal of unfavourable ischemic-induced changes with various protective agents. These methods of myocardial protection and their effectiveness, the calcium metabolism during myocardial ischemia, and the effects of calcium channel blockers are briefly reviewed and discussed. It is stressed that myocardial protection during ischemic arrest is a complex entity, and that new modes of myocardial protection are needed in the future.
