Can we prevent significant brain desaturation during defibrillator testing by increasing the brain saturation reserve?
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In patients undergoing electrophysiology procedures, programmed threshold testing for internal cardioverter and defibrillator (ICD) insertion involves testing of the apparatus and repeated inductions of ventricular fibrillation (VF), which can result in global cerebral hypoperfusion similar to cardiac arrest.1 Hypercapnia is known to increase cerebral blood flow (CBF) and cerebral vasodilation. The adjustment of ventilation to raise cerebral regional saturation (rSO2) is a common intervention in correcting brain desaturation and part of a previously reported and validated algorithm.2
Preliminary evidence has shown that hypoventilation (with resulting hypercarbia) may prevent cerebral desaturations during ICD insertion and cardiac arrest.3 It is possible that deeper sedation with increased hypoventilation and hypercapnia may increase CBF to compensate for decreases in cardiac output associated with VF and reduce the risk of cerebral desaturation. The use of near-infrared spectroscopy (NIRS) to monitor and prevent brain desaturation by pre-emptively increasing CBF has not been reported. The purpose of this study is to test the effectiveness of permissive sedation-induced hypercapnia in decreasing the severity of cerebral desaturation episodes during ICD insertion.
This randomized-controlled study was approved (03-2009 #03-076) by the Montreal Heart Institute ethics review board. After informed consent, all patients undergoing ICD insertion were sedated with remifentanil and propofol and randomized in two groups: a “light sedation” (LS) and a “deep sedation” (DS) group. Monitoring using NIRS and blood gases was performed in both groups. The VF test was induced via pre-programmed electrical stimulations. The primary endpoint was a reduction in episodes of significant cerebral desaturation in the group with permissive hypercapnia. Unfortunately, the trial was stopped before completion because, unexpectedly, recommendations were made to avoiding testing the defibrillators.4 A total of 13 (out of 20) patients were recruited for the study with six LS and six DS patients and one exclusion. On average, patients were older in the LS than DS group (69 yr vs 58 yr) and more frequently males (LS: six males; DS: two males/four females). The DS group had lower mean (standard deviation [SD]) pH [7.35 (0.01), DS vs 7.43 (0.04), L; P = 0.006] and higher mean (SD) partial pressure of carbon dioxide (PaCO2) [50 (5), DS vs 34 (3) mmHg, LS; P < 0.001] prior to VF and higher remifentanil infusion rates compared with controls (P = 0.03). There were no significant differences between groups in terms of propofol infusion rates, total duration of VF, number of VFs, and number of shocks. Ventricular fibrillation was associated with a reduction in cerebral rSO2 values in all patients. Brief desaturations after VF below baseline occurred in three DS patients (50%) and in five LS patients (83%). The area over the baseline cerebral rSO2 values was higher in the DS compared with LS group [left: 1241 (463), DS vs 303 (124) %.min, LS; P = 0.004; and right: 1282 (490), DS vs 259 (108) %.min, LS; P = 0.003], even when corrected for procedural time (P < 0.001). The Figure illustrates four patients. Patients with lower ejection fractions (EF) had reduced baseline rSO2values compared with those with normal EF. Ventricular fibrillation was associated with brief episodes of desaturation in both groups but it remained above baseline in the DS group because of the increased saturation reserve.
These observations are pertinent for the increased role of NIRS in cardiac arrest5 suggesting that patients with good resuscitation outcomes have significantly higher NIRS values. Deeper sedation and consequently a higher PaCO2 value increase rSO2 and may attenuate the reduction in rSO2 and consequently cerebral blood flow during VF.
Dr. Denault is on the Speakers Bureau for CAE-Healthcare, Edwards, Masimo, and Medtronic.
Conflicts of interest
This submission was handled by Dr. Philip M. Jones, Associate Editor, Canadian Journal of Anesthesia.
Supported by the Montreal Heart Institute Foundation.