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Does Inhalational Nitrous Oxide Affect Induction Dose of Propofol and Haemodynamic

Received: 26 October 2014     Accepted: 10 November 2014     Published: 17 November 2014
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Abstract

Background: Propofol is a commonly used induction agent. Propofol does not possess any strong analgesic effect, when used alone for induction of anaesthesia. In dose of more than 2 mg/kg bolus known to cause hypotension even requiring vasopressors. Nitrous oxide (N2O) has been in use for more than 150 years. Although N2O reduces the requirement of propofol for induction and maintenance, the effects of both the drugs on overall haemodynamic remain controversial. The aim of this study was to evaluate the efficacy and safety of induction dose of propofol when N2O was concurrently administered and haemodynamic alteration with addition of N2O to therapeutic dose of propofol. Materials and Methods: This was a prospective, randomized and double blinded comparison study that was conducted after obtaining institutional ethical approval. The study population consisted of eighty patients aged between 18 to 60 years from either sex and classified as American Society of Anaesthesiologists (ASA) physical status I or II which were scheduled for various elective surgical procedures under general anaesthesias. Participants were randomly allocated into two groups comprising 40 subjects each. Group PN received breathed 67% N2O (4 L/min) + 33% O2 (2L/min) and propofol. Group PO: breathed 100 % O2 (6L/min) and propofol. Changes in heart rate (HR), systolic blood pressure (SBP), mean arterial pressure (MAP) and Oxygen saturation (SpO2) were measured Preoperatively (baseline T0), After 3minutes of premedication (T1), After 1minute of inhalation of 100% O2 before induction of anesthesia (T2), After induction (T3), At 2, 5 and 10 minutes after induction (T4), (T5), and (T6). Results: Induction time and dose of propofol in PN group were significantly less. As 42.5% of the patients were induced in less than 100 sec, 57.5% in less than 200 sec and none of the patients required more than 200 sec for induction as compare to group PO where 77.5% required more than 200 sec, 22.5% in less than 200 sec and none of the patients were induced in less than 100 sec. The mean ± SD of induction time in groups PN and PO were 113.38±35.93 and 258.00±59.43 seconds respectively with p < 0.001. In group PN, 57.5% required 0.5-1.0mg/kg, 40% required less than 0.5mg/kg unlike group PO where 77.5% required 1-2mg/kg. The mean ± SD induction dose required for induction of anesthesia were 0.58±0.19 mg/kg and 1.43±0.40 mg/kg with and without 67% N2O in O2. Increase in HR in groups PN and PO 16.38% and 6.42% respectively. Conclusions: Co-administration of N2O during induction of anaesthesia achieves significant reduction in induction dose as well as induction time of propofol. It provides significant stability in SBP, and MAP, without affecting arterial oxygen saturation. N2O causes significant increase in HR.

Published in Journal of Anesthesiology (Volume 2, Issue 5)
DOI 10.11648/j.ja.20140205.11
Page(s) 32-39
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2014. Published by Science Publishing Group

Keywords

Blood Pressure, Heart Rate, Nitrous Oxide, Propofol (Source: Mesh, NLM)

References
[1] Perouansky M, Hemmings HC Jr. Intravenous anesthetic agents. In: HC Hemmings Jr, PM Hopkins, eds. Foundations of Anesthesia: Basic Science and Clinical Practice. 2nd ed. London: Mosby Elsevier; 2006:295-310.
[2] Krzych LJ ,Szurlej D, Bochenek A. Rationale for propofol use in cardiac surgery. Journal of Cardiothoracic and Vascular Anesthesia. 2009;23:878-85.
[3] Rasooli S, Parish M, Mahmoodpoor A, Moslemi F, Sanaie S, Faghfuri S. The effect of intramuscular ephedrine in prevention of hypotension due to propofol. Pak J Med Sci. 2007;23:893-897.
[4] Hashiba E, Hirota K, Suzuki K, Matsuki A. Effects of propofol on bronchoconstriction and bradycardia induced by vagal nerve stimulation. Acta Anaesthesiologica Scandinavica. 2003; 47:1059-63.
[5] Vasconcellos KD, Sneyd JR. Nitrous oxide: are we still in equipoise? A qualitative review of current controversies. BJA. 2013;111:877-85.
[6] Davidson JAH, Macleod AD, Howie JC, White M, Kenny GNC. Effective concentration 50 for propofol with and without 67% nitrous oxide. Acta Anesthesiol Scand 1993; 37: 458-64.
[7] Stuart PC, Stott SM, Millar A, Kenny GNC, Russell D. CP50 of propofol with and without nitrous oxide 67%. Br J Anaesth 2000; 84: 638-9.
[8] Shiga T, Wajima Z , Inoue T, Ogawa R. Nitrous oxide produces minimal hemodynamic changes in patients receiving a propofol-based anesthetic: an esophageal Doppler ultrasound study. Can J Anaesth. 2003; 50 :649-52.
[9] Annamalai A, Singh S, Singh A, Mahrous DE. Can Intravenous Dexmedetomidine Prolong Bupivacaine Intrathecal Spinal Anesthesia? J Anesth Clin Res. 2013; 12: 1-5.
[10] Ehrenfeld JM, Funk LM, Schalkwyk JV, Merry AF, Sandberg WS, Gawande A. The incidence of hypoxemia during surgery: evidence from two institutions. Can J Anaesth. 2010; 57:888-897.
[11] Tanaka M, Nishikawa T. Propofol requirement for insertion of cuffed oropharyngeal airway versus laryngeal mask airway with and without fentanyl: a dose finding study. Br J Anaesth 2003; 90: 14-20.
[12] Ju-Mei Ng and Nian-Chih Hwang. Inhaling nitrous oxide reduces the induction dose requirements of propofol. Anesth Analg 2000; 90: 1213-6.
[13] Uzun S, Ozkaya BA, Yilbaş SO, Ayhan B, Sahin A, Aypar U. Effects of different propofol injection speeds on blood pressure, dose, and time of induction. Turk J Med Sci 2011; 41: 397-401.
[14] Kumar AA, Sanikop CS, Kotur PF. Clinical investigation effect of priming principle on the induction dose requirements of propofol - a randomized clinical trial. Indian J. Anaesth. 2006; 50:283- 87.
[15] Peacock JE, Lewis RP, Reilly CS, Nimmo WS. Effect of different rates of propofol for induction of anaesthesia in elderly patients. Br J Anaesth. 1990; 65: 346-52.
[16] McKinney MS, Fee JPH. Cardiovascular effects of 50% nitrous oxide in older adult patients anaesthetized with isoflurane or halothane.BJA. 1998; 80: 169–173.
[17] Robert K. Stoelting. Inhaled Anesthetics. In: Pharmacology and Physiology in Anesthetic Practice. Stoelting RK, Hiller SC, 4th Edition. Philadelphia: Lippincott Williams and Wilkins; 2006: p .42-86.
[18] Edmond I. Eger II. Inhaled Anesthetics: Uptake and Distribution. In: Miller’s Anaesthesia. Miller RD. 7th Edition. Philadelphia: Churchill Livingstone; 2010: p.539-60.
[19] Singh S, Laing EF, Owiredu WKBA, Singh A. Comparison of esmolol and lidocaine for attenuation of cardiovascular stress response to laryngoscopy and endotracheal intubation in a Ghanaian population. Anesthesia: Essays and Researches. 2013; 7: 83-88.
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  • APA Style

    Sanjeev Singh. (2014). Does Inhalational Nitrous Oxide Affect Induction Dose of Propofol and Haemodynamic. International Journal of Anesthesia and Clinical Medicine, 2(5), 32-39. https://doi.org/10.11648/j.ja.20140205.11

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    ACS Style

    Sanjeev Singh. Does Inhalational Nitrous Oxide Affect Induction Dose of Propofol and Haemodynamic. Int. J. Anesth. Clin. Med. 2014, 2(5), 32-39. doi: 10.11648/j.ja.20140205.11

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    AMA Style

    Sanjeev Singh. Does Inhalational Nitrous Oxide Affect Induction Dose of Propofol and Haemodynamic. Int J Anesth Clin Med. 2014;2(5):32-39. doi: 10.11648/j.ja.20140205.11

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  • @article{10.11648/j.ja.20140205.11,
      author = {Sanjeev Singh},
      title = {Does Inhalational Nitrous Oxide Affect Induction Dose of Propofol and Haemodynamic},
      journal = {International Journal of Anesthesia and Clinical Medicine},
      volume = {2},
      number = {5},
      pages = {32-39},
      doi = {10.11648/j.ja.20140205.11},
      url = {https://doi.org/10.11648/j.ja.20140205.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ja.20140205.11},
      abstract = {Background: Propofol is a commonly used induction agent. Propofol does not possess any strong analgesic effect, when used alone for induction of anaesthesia. In dose of more than 2 mg/kg bolus known to cause hypotension even requiring vasopressors. Nitrous oxide (N2O) has been in use for more than 150 years. Although N2O reduces the requirement of propofol for induction and maintenance, the effects of both the drugs on overall haemodynamic remain controversial. The aim of this study was to evaluate the efficacy and safety of induction dose of propofol when N2O was concurrently administered and haemodynamic alteration with addition of N2O to therapeutic dose of propofol. Materials and Methods: This was a prospective, randomized and double blinded comparison study that was conducted after obtaining institutional ethical approval. The study population consisted of eighty patients aged between 18 to 60 years from either sex and classified as American Society of Anaesthesiologists (ASA) physical status I or II which were scheduled for various elective surgical procedures under general anaesthesias. Participants were randomly allocated into two groups comprising 40 subjects each. Group PN received breathed 67% N2O (4 L/min) + 33% O2 (2L/min) and propofol. Group PO: breathed 100 % O2 (6L/min) and propofol. Changes in heart rate (HR), systolic blood pressure (SBP), mean arterial pressure (MAP) and Oxygen saturation (SpO2) were measured Preoperatively (baseline T0), After 3minutes of premedication (T1), After 1minute of inhalation of 100% O2 before induction of anesthesia (T2), After induction (T3), At 2, 5 and 10 minutes after induction (T4), (T5), and (T6). Results: Induction time and dose of propofol in PN group were significantly less. As 42.5% of the patients were induced in less than 100 sec, 57.5% in less than 200 sec and none of the patients required more than 200 sec for induction as compare to group PO where 77.5% required more than 200 sec, 22.5% in less than 200 sec and none of the patients were induced in less than 100 sec. The mean ± SD of induction time in groups PN and PO were 113.38±35.93 and 258.00±59.43 seconds respectively with p < 0.001. In group PN, 57.5% required 0.5-1.0mg/kg, 40% required less than 0.5mg/kg unlike group PO where 77.5% required 1-2mg/kg. The mean ± SD induction dose required for induction of anesthesia were 0.58±0.19 mg/kg and 1.43±0.40 mg/kg with and without 67% N2O in O2. Increase in HR in groups PN and PO 16.38% and 6.42% respectively. Conclusions: Co-administration of N2O during induction of anaesthesia achieves significant reduction in induction dose as well as induction time of propofol. It provides significant stability in SBP, and MAP, without affecting arterial oxygen saturation. N2O causes significant increase in HR.},
     year = {2014}
    }
    

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  • TY  - JOUR
    T1  - Does Inhalational Nitrous Oxide Affect Induction Dose of Propofol and Haemodynamic
    AU  - Sanjeev Singh
    Y1  - 2014/11/17
    PY  - 2014
    N1  - https://doi.org/10.11648/j.ja.20140205.11
    DO  - 10.11648/j.ja.20140205.11
    T2  - International Journal of Anesthesia and Clinical Medicine
    JF  - International Journal of Anesthesia and Clinical Medicine
    JO  - International Journal of Anesthesia and Clinical Medicine
    SP  - 32
    EP  - 39
    PB  - Science Publishing Group
    SN  - 2997-2698
    UR  - https://doi.org/10.11648/j.ja.20140205.11
    AB  - Background: Propofol is a commonly used induction agent. Propofol does not possess any strong analgesic effect, when used alone for induction of anaesthesia. In dose of more than 2 mg/kg bolus known to cause hypotension even requiring vasopressors. Nitrous oxide (N2O) has been in use for more than 150 years. Although N2O reduces the requirement of propofol for induction and maintenance, the effects of both the drugs on overall haemodynamic remain controversial. The aim of this study was to evaluate the efficacy and safety of induction dose of propofol when N2O was concurrently administered and haemodynamic alteration with addition of N2O to therapeutic dose of propofol. Materials and Methods: This was a prospective, randomized and double blinded comparison study that was conducted after obtaining institutional ethical approval. The study population consisted of eighty patients aged between 18 to 60 years from either sex and classified as American Society of Anaesthesiologists (ASA) physical status I or II which were scheduled for various elective surgical procedures under general anaesthesias. Participants were randomly allocated into two groups comprising 40 subjects each. Group PN received breathed 67% N2O (4 L/min) + 33% O2 (2L/min) and propofol. Group PO: breathed 100 % O2 (6L/min) and propofol. Changes in heart rate (HR), systolic blood pressure (SBP), mean arterial pressure (MAP) and Oxygen saturation (SpO2) were measured Preoperatively (baseline T0), After 3minutes of premedication (T1), After 1minute of inhalation of 100% O2 before induction of anesthesia (T2), After induction (T3), At 2, 5 and 10 minutes after induction (T4), (T5), and (T6). Results: Induction time and dose of propofol in PN group were significantly less. As 42.5% of the patients were induced in less than 100 sec, 57.5% in less than 200 sec and none of the patients required more than 200 sec for induction as compare to group PO where 77.5% required more than 200 sec, 22.5% in less than 200 sec and none of the patients were induced in less than 100 sec. The mean ± SD of induction time in groups PN and PO were 113.38±35.93 and 258.00±59.43 seconds respectively with p < 0.001. In group PN, 57.5% required 0.5-1.0mg/kg, 40% required less than 0.5mg/kg unlike group PO where 77.5% required 1-2mg/kg. The mean ± SD induction dose required for induction of anesthesia were 0.58±0.19 mg/kg and 1.43±0.40 mg/kg with and without 67% N2O in O2. Increase in HR in groups PN and PO 16.38% and 6.42% respectively. Conclusions: Co-administration of N2O during induction of anaesthesia achieves significant reduction in induction dose as well as induction time of propofol. It provides significant stability in SBP, and MAP, without affecting arterial oxygen saturation. N2O causes significant increase in HR.
    VL  - 2
    IS  - 5
    ER  - 

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Author Information
  • Department of Anaesthesia and Intensive care, School of Medical Sciences, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana, West Africa

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