| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
From the Perioperative Cardiac Research Group (PECARG), Departments of Anesthesiology and *Cardiac Surgery, Centre Hospitalier de l’Université de Montréal (CHUM), Hôtel-Dieu, Université de Montréal, Montréal, Québec, Canada
Address correspondence and reprint requests to Thomas M. Hemmerling, MD, DEAA, Centre Hospitalier de l’Université de Montréal (CHUM), Hôtel-Dieu, Université de Montréal, 3840, rue Saint-Urbain, Montréal, Québec, Canada. Address e-mail to thomashemmerling{at}hotmail.com.
 |
Abstract |
|---|
 Top Abstract IntroductionCase ReportDiscussionReferences |
|---|
|
Introduction |
|---|
|
TopAbstractIntroductionCase ReportDiscussionReferences |
|---|
Whereas monitoring of the cardiac ischemic complications during OPCAB is readily achieved using transesophageal echocardiography (TEE) and 5-lead electrocardiography (ECG), monitoring cerebral ischemia is neither easy nor routine. Measurement of cerebral perfusion (pressure) would be the most direct method of assessing for potential cerebral ischemia. However, this is invasive and not applicable during routine cardiac surgery. Monitoring based on 16-channel electroencephalography (EEG) has been advocated to identify focal ischemic changes (5). However, for routine use in cardiac theaters, this is not practical. We present a case of severe depression of the cortical EEG as noted on bispectral index (BIS) monitoring during the period of myocardial compromise during OPCAB.
|
Case Report |
|---|
|
TopAbstractIntroductionCase ReportDiscussionReferences |
|---|
At arrival in the operating room, a high thoracic epidural (TEA) catheter was inserted at the T3 dermatome for intraoperative and postoperative analgesia. Monitoring included invasive femoral artery blood pressure, 5-lead ECG, pulse oximetry, end-tidal carbon dioxide, TEE, and BIS using the A-2000 monitoring system (software version 2.10, update rate: 1 s to BIS/10 s to trend/DSA, bispectral smoothing = 15 s; BIS classic sensor, Aspect Medical, Newton, MA). The BIS sensor was applied to the forehead and left temporal area; the initial impedance test showed a very good impedance of less than 2 k
at all three sites. After anesthetic induction with fentanyl 3 µg/kg and propofol 1.5 mg/kg, endotracheal intubation was facilitated using rocuronium 0.6 mg/kg. Anesthesia was maintained with sevoflurane delivered in 50% oxygen. Analgesia was provided by TEA with bupivacaine 0.125% at 10 mL/h and one bolus of 8 mL of bupivacaine 0.25% 10–15 min before midline sternotomy and 10–15 min before the end of surgery. Sevoflurane was titrated to maintain BIS between 40 and 50. Maintenance of body temperature was achieved by means of a heated operating room (more than 22°C) and a warming blanket for the lower body. The initial bladder temperature was 36.5°C; it stayed above 35.8°C throughout surgery. Surgery commenced with hemodynamic stability throughout sternotomy and during preparation of the left internal mammary artery for grafting of the left anterior descending coronary artery. The heart was stabilized using the Cor-Vasc System (CoroNéo Inc., Montreal, Quebec, Canada). During the first myocardial ischemic period and grafting using the left internal mammary artery, his systolic blood pressure was 85 mm Hg and diastolic pressure was 45 mm Hg; grafting was performed in 5 min 28 sec and BIS remained at approximately 45.
After a period of 5 min during which TEE showed normal ventricular function and ECG monitoring no change in ST segments, the heart was positioned for grafting of the left circumflex coronary artery. His arterial blood pressure decreased to 70/35 mm Hg with TEE and ECG monitoring being impaired because of the position of the heart. BIS remained at 45–50. A phenylephrine bolus was given and the arterial blood pressure remained stable during the initial 3 min of grafting. Suddenly the BIS decreased from 45 to 0. At this point, the end-tidal sevoflurane concentration was 1.5 vol%; there was no change of this concentration throughout the period of distal and proximal bypass grafting. No other anesthetic was given. Physical examination revealed weak but palpable pulsation of both carotid arteries. With an expected completion of the distal anastomosis within 3 min, another phenylephrine bolus was given with no apparent increase in arterial blood pressure or BIS while grafting continued. The distal anastomosis was finished within 3 min and myocardial ischemia resolved at 5 min 48 s its onset, and the heart immediately positioned in the normal position. ECG and TEE monitoring did not show any abnormality and BIS returned to values of 50 within 1 min; arterial blood pressure returned to 105/55 mm Hg (Fig. 1). Manual palpation showed normal strong carotid pulsations. After 5 min of rest, the third distal anastomosis to the right coronary artery was performed without any hemodynamic or cerebral complication. Surgery finished within 45 min after the decrease in BIS values and the patient was tracheally extubated 5 min after the end of surgery on the operating table.
|
Immediate and postoperative recovery was uneventful. Immediate postoperative neurological status was assessed as normal; the patient had an uneventful recovery and was dismissed home at 5 days after surgery. Although no preoperative carotid artery Doppler study was performed in this patient, postoperative examination was normal.
|
Discussion |
|---|
|
TopAbstractIntroductionCase ReportDiscussionReferences |
|---|
The decrease in BIS occurred 2 min after the heart was positioned for circumflex artery grafting and the arterial blood pressure had diminished. Initial artifact check consisted of verification of good contact between BIS sensor and skin, impedance check (showing a value below 3 k), verification of electromyelogram (EMG) influences (EMG column remained clear), evaluation of signal quality index (which was optimal), and observation of the raw EEG that resembled a flat line with minimal activity. There was no anesthetic given during this time, and the end-tidal concentration of sevoflurane remained stable at 1.5 vol%.
Therefore, the anesthesiologist interpreted a BIS of 0 not as an artifact but as an indication of cerebral hypoperfusion after the distal anastomosis had already commenced. At this "point of no return," a bolus of phenylephrine was given although it had no apparent effect on arterial blood pressure, as would be expected in this position with angulated heart and very limited cardiac output. The only means to effectively increase the arterial blood pressure would have been to change the position of the heart. Because of the expected extremely short anticipated time of anastomosis, it was decided to finish grafting as quickly as possible. As anticipated, shortly afterwards with the release of the heart to the normal position, systemic blood pressure and cerebral perfusion increased. Immediate tracheal extubation facilitated neurological assessment and helped to evaluate possible neurological sequelae of cerebral hypoperfusion during OPCAB. Because the threshold systemic pressure for cerebral hypoperfusion is not individually known, it is speculative whether a higher systemic pressure might have avoided cerebral hypoperfusion. We usually allow arterial blood pressure to decrease up to 30% of baseline systemic blood pressure during grafting. Since BIS monitoring was introduced in our setting as monitoring in OPCAB, only this case of possible cerebral hypoperfusion has occurred in approximately 600 cases. However, had cerebral hypoperfusion been detected before distal grafting (after positioning the heart), the anesthesiologist would have asked the surgeon to change the position of the heart to increase systemic blood pressure.
Assessment of neurological damage in the form of global or focal cerebral hypoperfusion is even more difficult and cumbersome. Jugular bulb venous oxygen saturation has been used as a sensitive marker for cerebral oxygenation in cardiac surgery (6) but is invasive and not used in clinical routine; transcranial Doppler monitoring detecting high intensity transient signals does detect microemboli but does not reflect cerebral hypoperfusion or clinical neurocognitive outcomes (7). Near-infrared spectrometry might be an alternative and has been shown to be useful in carotid artery surgery but has not been systematically evaluated in cardiac surgery (8–9). However, one study (10) has already doubted its interchangeable use with jugular bulb venous oxygen saturation in cardiac surgery. BIS monitoring has been described for a variety of indications other than routine monitoring of anesthetic depth or sedation. The use of BIS during carotid artery surgery to monitor the effects of clamping on cerebral perfusion (3), during resuscitation to monitor the successfulness of resuscitation in terms of cerebral outcome (11,12), and during hypotensive periods as a monitor of cerebral hypoperfusion (3) have been documented. A recent study has presented a small series of 10 consecutive cases of children undergoing cardiac surgery in which a reduction of cerebral oxygen saturation was accompanied by simultaneous BIS decreases in five children (13). This might indicate that BIS monitoring could be an easily applicable monitor of cerebral hypoperfusion and might be an interesting method for a multimodal approach of neurologic monitoring in cardiac surgery (14).
Cerebral hypoperfusion is a risk during OPCAB. Bradycardia and systemic hypotension are common during distal grafting and because of positioning the heart using stabilizers. Although TEE and ECG monitoring are useful to detect cardiac ischemia (though both are limited by the extreme cardiac positioning), detection of cerebral hypoperfusion remains a challenge. BIS monitoring in OPCAB could help to titrate depth of anesthesia and, in addition, might be a useful indicator for cerebral hypoperfusion during distal coronary artery grafting.
|
Footnotes |
|---|
|
References |
|---|
|
TopAbstractIntroductionCase ReportDiscussionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  H. Yoshida, T. Kushikata, S. Kabara, H. Takase, H. Ishihara, and K. Hirota Flat Electroencephalogram Caused by Carbon Dioxide Pneumoperitoneum Anesth. Analg., December 1, 2007; 105(6): 1749 - 1752. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Lauwick, M. English, and T. M. Hemmerling An unusual case of cerebral hypoperfusion detected by bispectral index monitoring Can J Anesth, August 1, 2007; 54(8): 680 - 681. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
