Sm. Millar et al., Cerebral hypoperfusion in immediate postoperative period following coronary artery bypass grafting, heart valve, and abdominal aortic surgery, BR J ANAEST, 87(2), 2001, pp. 229-236
Citations number
21
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Perioperative levels of jugular bulb oxyhaemoglobin saturation (Sj(O2)) and
lactate concentration (Lj), and postoperative duration of Sj(O2) <50% were
compared between patients undergoing coronary artery bypass grafting (CABG
) (n=86), heart valve (n=14) and abdominal aortic (n=16) surgery. Radial ar
tery and jugular bulb blood samples were aspirated after induction of anaes
thesia, during re-warming on cardiopulmonary bypass (CPB) (36<degrees>C), o
n arrival in the intensive care unit (ICU) and, subsequently, at 1, 2 and 6
h after ICU admission. Most patients having heart surgery were hypocapnic
at 36 degreesC on CPB. Following CABG and heart valve surgery, many patient
s were hypocapnic whereas after abdominal aortic surgery, most were hyperca
pnic. During CPB and postoperatively, Sj(O2) and Lj were significantly corr
elated to Pa-CO2 and the arterial concentration of lactate (La) respectivel
y (P<0.05). After correction for arterial carbon dioxide tension (Pa-CO2) a
nd La, there were no significant changes in Sj(O2) or Lj on CPB. Postoperat
ively, having corrected for Pa-CO2, there were significant effects on Sj(O2
) over all groups as a result of time from surgery (P<0.001) and its intera
ction with operation type (P<0.001). Following correction for La, there wer
e no postoperative effects on Li. No significant differences (P=0.2) in dur
ation of Sj(O2) <50% existed between patients undergoing CABG (1054 (82) mi
n), abdominal aortic (893 (113) min) and heart valve (1073 (91) min) surger
y. The lack of significant reciprocal effects on Lj combined with the frequ
ency of hypocapnia and strong influence of Pa-CO2 on Sj(O2), suggest that S
j(O2) <50% during CPB and after cardiac surgery represents hypoperfusion as
a consequence of hypocapnia rather than cerebral ischaemia.