Brain Monitoring

EEG monitoring during myocardial revascularization without cardiopulmonary bypass

Aida Sehic MD, Aarti Prabhune MD, Samuel B. Pollock Jr MD*, Harvey L. Edmonds Jr PhD
Departments of Anesthesiology and Surgery (Division of Cardiothoracic Surgery)*,
University of Louisville School of Medicine
Louisville, KY USA

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Introduction

Myocardial revascularization without cardiopulmonary bypass, also known as off-pump coronary artery bypass (OPCAB), is enjoying an explosive rise in popularity. The interest in this new surgical approach is due both to clinical and economic factors. A number of recent comparisons with conventional coronary bypass using the heart-lung machine have demonstrated improved outcome (1,2). The reduced complications and faster recovery are thought due, at least in part, to marked reduction in the bypass circuit-mediated systemic inflammatory response (3).

Despite improved outcomes, OPCAB still places the brain at significant risk of hemodynamic injury. Both intentional blood pressure reduction and manipulation of the inverted beating heart can result in compromised cerebral perfusion. This case illustrates such a hemodynamic insult, identified by EEG monitoring.

Case Description

A 75 year-old female patient underwent revascularization of three coronary arteries without cardiopulmonary bypass. Her history was remarkable for chronic severe hypertension and transient confusion, but no evidence of neurologic abnormality. Pre-operative blood pressure was 160/95.

In addition to routine physiologic monitors, multimodality neuromonitoring was used. This included transcranial Doppler ultrasound (Neuroguard, Nicolet Vascular, Golden, Colorado, USA) that measured left middle cerebral artery blood flow velocity and quantified the presence of microemboli. Doppler recording began prior to incision and continued until sternal closure. In addition, a four-channel EEG recording was made using the Datex-Ohmeda CS/3 monitor equipped with an EEG and auditory evoked potential module. EEG signals were obtained with gold cup electrodes affixed to the scalp with conductive paste. Electrodes were located over the anterior and posterior watershed regions using the International 10-20 Electrode Placement System at Fp1-T7, Fp2-T8, C3-O1 and C4-O2 with a ground at FPz. All electrode impedances were maintained below 5 kOhms. The digitized, but otherwise unprocessed, EEG waveforms were permanently stored on magnetic media using a notebook computer equipped with the Datex-Ohmeda WinColl3 program. The recording was initiated prior to anesthesia induction and continued until sternal closure.

Anesthesia was induced with thiopental and maintained with balanced anesthesia comprised of hypnosis (desflurane), analgesia (sufentanil), amnesia (midazolam) and neuromuscular blockade (pancuronium). Following anesthetic induction and patient positioning, the EEG was characterized by diffuse high amplitude low frequency activity. A modest asymmetry was evident in the left posterior region characterized by lower amplitude slow waves and a relative paucity of faster frequency activity (Fig. 1)

Fig. 1 illustrates the asymmetric EEG at the beginning of the case. Note the slightly lower amplitude and reduced high frequency components in the left posterior derivation (Channel 3: C3-O1) when compared with that from the right hemisphere (Channel 4: C4-O2).

Hemodynamic instability with episodes of severe hypertension (systolic >200 mm Hg) during sternotomy and surgical exposure required increased hypnosis, including supplemental thiopental. Aggressive attempts at hypertension correction were successful, with systolic pressures ranging between 140 and 90 mm Hg. During this period of hemodynamic instability, the middle cerebral artery blood flow velocity never fell more than 20% below the pre-incision baseline. However, the increased hypnotic use obliterated EEG activity for 45 minutes and upon its return, the EEG asymmetry had become prominent (Fig. 2). The remainder of the procedure was uneventful except that the asymmetry persisted. The Doppler recording identified no evidence of cerebral microembolization in the left middle cerebral artery.

Fig. 2 shows the growing asymmetry with the reappearance of EEG activity following pharmacological suppression with high dose anesthetic. Peak-to-peak amplitude in left hemispheric Channel 3 is clearly much smaller than in right hemispheric Channel 4. Also note the near absence of high frequency activity in Channel 3.

Upon recovery from anesthesia, the patient remained confused with episodic aphasia and an initially sluggish right pupillary response. Subsequent CT revealed multiple infarcts in periventricular regions and the cortical watersheds bilaterally (Fig. 3).

Fig. 3 illustrates ischemic changes in both hemispheres, signified by the pen marks on the CT images.

Discussion

This case illustrates several important points about the etiology of brain injury during cardiac surgery and the role of neuromonitoring in preventing it. First, the patient’s history of hypertension and confusion suggested an increased risk for ischemic brain damage. The asymmetric pre-induction EEG provided objective support for this concern and documented a pre-existing focal neurologic abnormality prior to surgery that would have been otherwise unappreciated.

Second, transcranial Doppler demonstrated that at no time during the surgery did the absolute blood flow velocity in the critical left middle cerebral artery ever fall to abnormally low levels (i.e., <20% of pre-incision baseline). Doppler recording also verified the absence of microemboli in this off-pump procedure. This is consistent with several recent reports that have noted a marked reduction in cerebral emboli through avoidance of the heart-lung machine (4,5).

Third, in order for the EEG to detect and prevent ischemic injury, interpretable waveforms must be present. In this case, sole reliance on high doses of hypnotic agents for blood pressure control effectively obliterated the EEG for a substantial portion of the surgery. Thus, eventual return of the EEG activity could

serve only to document disaster, not prevent it. The use of additional means for pressure control would have retained continuous EEG activity and enabled immediate detection of the ischemic insult.

Fourth, this case illustrates the phenomenon of relative ischemia, inadequate perfusion in the presence of "normal" blood pressure and the role of the EEG in preventing it. Chronic hypertension shifts the autoregulatory curve to the right or eliminates it completely. In either case, following a modest lowering of chronically elevated pressure, cerebral perfusion in the susceptible cortical watersheds may become inadequate even though arterial pressure remains at or above the normal range. During general anesthesia, this phenomenon can be detected only through monitoring of cerebral electrical activity or oxygen saturation (6). In the present case, this was manifested by the marked decrease in EEG amplitude and loss of high frequency activity.

In summary, this case illustrates ischemic brain injury during an OPCAB procedure. EEG monitoring, when not suppressed by high dose hypnotics, offers a continuous sensitive measure of cerebral cortical function that can be used effectively to prevent damage.

References

1. Koutlas TC, Elbeery Jr, Williams JM et al. Myocardial revascularization in the elderly using beating heart coronary artery bypass surgery. Ann Thorac Surg 69(4):1042-7, 2000.
2. Ricci M, Karamanoukian HL, Abraham R et al. Stroke in octogenarians undergoing coronary artery surgery with and without cardiopulmonary bypass. Ann Thorac Surg 69(5):1471-5, 2000.
3. Ascione R, Lloyd CT, Underwood MJ et al. Inflammatory response after coronary revascularization with and without cardiopulmonary bypass. Ann Thorac Surg 69(4):1198-1204, 2000.
4. Diegeler A, Hirsch R, Schneider F et al. Neuromonitoring and neurocognitive outcome in off-pump versus conventional coronary bypass operation. Ann Thorac Surg 69(4):1162-6, 2000.
5. Watters MP, Cohen AM, Monk CR et al. Reduced cerebral embolic signals in beating heart coronary surgery detected by transcranial Doppler ultrasound. Br J Anaesth 84(5):629-31, 2000.
6. Edmonds HL Jr Rodriguez RA, Audenaert SM et al. The role of neuromonitoring in cardiovascular surgery. J Cardiothorac Vasc Anesth 10(2):15-23

Last updated: 1 June 2001Created
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