Abstract

Research Article

Assessing the Neurocognitive function effects of ketamine in Cardiac Surgical patients

Demet Dogan Erol*

Published: 23 October, 2018 | Volume 2 - Issue 1 | Pages: 018-022

Background: Despite remarkable progress in surgical, cardiopulmonary bypass (CPB) and anesthetic tecniques, neurocognitive damage still remains an important cause of postoperative morbidity in cardiac surgery. The aetiology of neurocognitive damage is likely to be multifocal; including macro and microemboli, cerebral hypoperfusion, inflammation and nonpulsatile flow. N-methyl-D-asparticAcid (NMDA) receptors play an important role during neurocognitive damage. Ketamine is a non-competitive antagonist to the phencyclidine site of NMDA receptor for glutamate and directly suppresses proinflammatory cytokine production. The aim of the present study was to evaluate whether ketamine has neuroprotective effects during open-heart surgery through the use of neurocognitive tests.

Methods: We considered all patients aged between 58-76 years who were referred to a single cardiothoracic surgical team for elective, primary coronary revascularization. Patients were excluded from the study for the following reasons: a history of neurological, psychiatric, gastrointestinal, hepatic, renal, hematologic and clotting systems disorder and repeat procedures. Undergoing CPB were randomized 2 groups: Group1 (ketamine)(n=25) or Group2 (propofol)(n= Patients 25) In the propofol group, anesthesia was induced with 3mg/kg propofol, 1µg/kg remifentanyl, 0.1mg/kg vecuronium. Remifentanyl 0.5-1μg/kg/min was infused intravenously throughout the whole procedure. In the ketamine group, anesthesia was induced with 1-2mg/kg propofol, 1-2mg ketamin, 0.1mg/kg vecuronium. Ketamin 1mg/kg/hour was infused intravenously. Pressors, inotropic agents and antiarrhythmics were used as needed. The Mini-Mental State Examination(MMSE) was administered the day before surgery and three days later. The change in scores for MMSE was calculated for each patient and all the group. The results were compared statistically with paired simple t-test.

Results: The mean age, CBP duration, lowest temperature was not statistically significant (Table1). Peroperative and postoperative blood pressures and pulse rates showed differences between groups. There were no preoperative differences between the groups on any of the mean MMSE score (Table2). The ECG monitoring revealed that most patients remained in sinus rhythm, with no difference between groups.

Conclusions: We could not demonstrate that intraoperatively administered ketamine resulted in greater neuroprotective effects compared with propofol. Ketamine in combination with propofol during cardiac surgery is associated with a stable hemodynamic profile. Propofol may reduce the delivery of microemboli to the cerebral circulation by decreasing the cerebral blood flow. Propofol has a direct neuroprotective effect in vitro, although Roach et al. could not demonstrate a protective effect of propofol during open-heart surgery. Propofol enhances the antiinflammatory response to surgery by several mechanisms. This might have masked a neuroprotective effect of ketamine because propofol was administered in both groups in our study.

Read Full Article HTML DOI: 10.29328/journal.ijcar.1001007 Cite this Article Read Full Article PDF

Keywords:

Cardiac surgical procedures; Cardiopulmonary bypass; General anesthesia; Ketamine; Propofol; Neuroprotective agents

References

  1. Lombard FW, Mathew JP. Neurocognitive dysfunction following cardiac surgery. Sem Cardiothorac Vasc Anesth. 2010; 14: 102-110. Ref.: https://goo.gl/4R41sv
  2. Arrowsmith J, Grocott H, Reves J, Newman MF. Central nervous system complications of cardiac surgery. Br J Anaesth. 2000; 84: 378–393. Ref.: https://goo.gl/4WJr1t
  3. Pugsley W, Klinger L, Paschalis C, Treasure T, Harrison M, et al. The impact of microemboli in cardiopulmonary bypass on neuropsychological functioning. Stroke. 1994; 25: 1393–1399. Ref.: https://goo.gl/Ya8K6Z
  4. Smith QR. Transport of glutamate and other amino acids at the blood-brain barrier. J Nutr. 2000; 130: 1016-1022. Ref.: https://goo.gl/eCC29Q
  5. Kawasaki T, Ogata M, Kawasaki C, Ogata J, Inoue Y, et al. Ketamine suppresses proinflammatory cytokine production in human whole blood in vitro. Anesth Analg. 1999; 89: 665–669. Ref.: https://goo.gl/3tmdxB
  6. Nagels W, Demeyere R, Hemelrijck JV, Vandenbussche E, Gijbels K, et al. Evaluation of the Neuroprotective Effects of S(+)-Ketamine During Open-Heart Surgery. Anesth Analg. 2004; 98: 1595-1603. Ref.: https://goo.gl/cqVBqe
  7. Hindman BJ, Todd MM. Improving Neurologic Outcome after Cardiac Surgery. Anesthesiology. 1999; 90: 1243-1247. Ref.: https://goo.gl/zVU3wU
  8. Laffey JG, Boylan JF, Cheng DC. The systemic inflammatory response to cardiac surgery. Anesthesiology. 2002; 97: 215–252. Ref.: https://goo.gl/qcTDq2
  9. Smith P, Treasure T, Newman SP, Joseph P, Ell PJ, et al. Cerebral consequences of cardiopulmonary bypass. Lancet. 1986; 1: 823–825. Ref.: https://goo.gl/RZwu4J
  10. Gladstone DJ, Black SE, Hakim AM; Heart and Stroke Foundation of Ontario Centre of Excellence in Stroke Recovery. Toward Wisdom from Failure: Lessons from Neuroprotective Stroke Trials and New Therapeutic Directions. Stroke. 2002; 33: 2123 - 2136. Ref.: https://goo.gl/GRZ34D
  11. Newman MF, Murkin JM, Roach G, Croughwell ND, White WD, et al. Cerebral physiologic effects of burst suppression doses of propofol during nonpulsatile cardiopulmonary bypass: CNS Subgroup of McSPI. Anesth Analg. 1995; 81: 452–457. Ref.: https://goo.gl/yLm8bV
  12. Hollrigel G, Toth K, Soltesz I. Neuroprotection by propofol in acute mechanical injury: role of GABAergic inhibition. J Neurophysiol. 1996; 76: 2412–2422. Ref.: https://goo.gl/h8oUmn
  13. Bhudia SK, Cosgrove DM, Naugle RI, Rajeswaran J, Buu-Khanh Lam, et al. Magnesium as a neuroprotectant in cardiac surgery: A randomized clinical trial. J Thorac Cardiovasc Surg. 2006; 131: 853-861. Ref.: https://goo.gl/g737xX
  14. Butterworth J, Hammon JW. Lidocaine for Neuroprotection: More Evidence of Efficacy. Anesth Analg. 2002; 95: 1131-1133. Ref.: https://goo.gl/Y2Nw8F
  15. Arrowsmith JE, Harrison MJG, Newman SP, Stygall J, Timberlake N, et al. Neuroprotection of the Brain During Cardiopulmonary Bypass A Randomized Trial of Remacemide During Coronary Artery Bypass in 171 Patients. Stroke. 1998; 29: 2357–2362. Ref.: https://goo.gl/4Dy7D4
  16. Ozyurt E, Graham DI, Woodruff GN, Culloch J. Protective effect of the glutamate antagonist MK801 in focal cerebral ischaemia in the cat. J Cereb Blood Flow Metab. 1988; 8: 138–143. Ref.: https://goo.gl/TSzGxt
  17. Bruno V, Copani A, Knöpfel T, Kuhn R, Casabona G, et al. Activation of metabotropic glutamate receptors coupled to inositol phospholipid hydrolysis amplifies NMDA-induced neuronal degeneration in cultured cortical cells. Neuropharmacology. 1995; 34: 1089-1098. Ref.: https://goo.gl/ZFdjQ5
  18. Burker EJ, Blumenthal JA,Feldman M, Thyrum E, Mahanna E, et al. The Mini Mental State Exam as a predictor of neuropsychological functioning after cardiac surgery. Int J Psychiatry Med 1995; 25: 263-276. Ref.: https://goo.gl/Ciet9a
  19. Lewis MS, Maruff PT, Silbert BS. Examination of the Use of Cognitive Domains in Postoperative Cognitive Dysfunction after Coronary Artery Bypass Graft. Surgery. Ann Thorac Surg 2005; 80: 910 - 916. Ref.: https://goo.gl/kUPVNq
  20. Weissrock S, Levy F, Balabaud V, Thiranos JC, Dupeyron JP, et al. Interest of the Mini Mental State Examination to detect cognitive defects after cardiac surgery. Ann Fr Anesth Reanim. 2005; 24: 1255-1261. Ref.: https://goo.gl/BmesV8

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