Annals of Cardiac Anaesthesia Annals of Cardiac Anaesthesia Annals of Cardiac Anaesthesia
Home | About us | Editorial Board | Search | Ahead of print | Current Issue | Archives | Submission | Subscribe | Advertise | Contact | Login 
Users online: 4732 Small font size Default font size Increase font size Print this article Email this article Bookmark this page


    Advanced search

    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  


 Article Access Statistics
    PDF Downloaded138    
    Comments [Add]    

Recommend this journal


Table of Contents
Year : 2014  |  Volume : 17  |  Issue : 1  |  Page : 7-9
Time to manage gas based on research

Senior Lecturer, Department of Surgery and Consultant Cardiothoracic Anaesthetist, Department of Anaesthesia and Pain Management, Royal Melbourne Hospital, and Monash Medical Centre, Melbourne, Australia

Click here for correspondence address and email

Date of Web Publication2-Jan-2014

How to cite this article:
Canty D. Time to manage gas based on research . Ann Card Anaesth 2014;17:7-9

How to cite this URL:
Canty D. Time to manage gas based on research . Ann Card Anaesth [serial online] 2014 [cited 2022 Nov 29];17:7-9. Available from:

Although the mechanism of volatile anesthesia is still not fully understood, it has attracted much attention in the past 10 years with mounting evidence of its organ-protective effects during cardiac surgery [1] and development of an objective measure of anesthetic depth with spectral electroencephalography. The decision on whether or not to use inhalational agents for cardiac surgery is now fairly clear, but the questions now may be: 1) how much inhalational agent should be administered, 2) should we titrate the dose with the EEG, and 3) does this differ in patients with severely impaired cardiac function? Most research on the pharmacology of volatile anesthesia was done before the period of EEG monitoring of anesthetic depth and in patients with normal cardiac function. Although reduced cardiac output is known to reduce the uptake of volatile anesthetic into the blood thus increasing the speed of onset of the effects on the brain, little is known about the maintenance requirements in patients with a reduced cardiac output.

The report by Bautin et al., [2] from Saint Petersburg in this edition of Annals of Cardiac Anesthesia is truly a study relevant to cardiac anesthesia. Although they have not answered these three important questions in their study, they have provided some interesting proof-of-concept data that suggests that in patients with a reduced cardiac output there is a reduction in requirement of sevoflurane during the maintenance phase of anesthesia. In their prospective observational study, sevoflurane general anesthesia was titrated to an entropy index of < 40 in 36 patients undergoing on pump coronary artery bypass graft (CABG) surgery, and the end-tidal concentrations and cardiac index were measured with standard methods at three time points to determine any correlation between end-tidal concentration of sevoflurane and cardiac index. Although no correlation was found, a significantly lower concentration of sevoflurane was measured in seven patients with a cardiac index < 2.2 L/min/m 2 . This seems to be irrespective of the other recorded factors that are known to influence anesthetic depth requirement, such as age and total dose of intravenous fentanyl administration, which appeared equal in both groups, although administration of other anesthetic drugs such as premedication and intraoperative benzodiazepines were not recorded. The degree of surgical stimulus was accounted for by measurements at defined steps of surgery. Thus, it appears that less volatile anesthetic was required for a "standardized" depth of anesthesia in patients with reduced cardiac output during the maintenance phase of anesthesia. In fact, the end-tidal sevoflurane concentrations required to achieve entropy index < 40 were quite low (1.15-1.37%). However, due to the observational nature of the study in only a small number of patients and the lack of reporting of the mean entropy index in both groups, the findings provide only evidence of association and proof-of-concept, which may be used to direct further studies in this interesting area.

An interesting observation has been made that when an acute reduction in cardiac output occurs, the end expired concentration of volatile anesthetic increases, which may not only provide a clue to the reduced cardiac output but may also worsen its negative inotropic effects, producing a potentially dangerous positive feedback loop. [3] The data from Bautin's group suggest that there is less requirement for volatile anesthesia in patients with a reduced cardiac output. The implications are that volatile anesthesia should not be titrated to a target end-tidal concentration as this may lead to an unnecessary overdose with potential further cardiac depression, but instead spectral EEG monitoring such as that of entropy index should be used. Careful titration of volatile anesthetic delivery may be important in these patients during anesthesia maintenance as well as during induction. Volatile anesthetic use is common during cardiopulmonary bypass (CPB), which could cause cardiac depression from excessive volatile anesthesia during separation from CPB, a time when the cardiac output is commonly low and patients with poor baseline cardiac function are most vulnerable. The risk of intraoperative awareness is also greater at this time due to increased cerebral metabolic activity during rewarming and potential reduction of anesthetic depth during periods of hemodynamic instability. Furthermore, measurement of end-tidal volatile concentration may be unreliable due to variable pulmonary blood flow and alveolar ventilation.

In large randomized trials, bispectral index EEG guided anesthesia has been demonstrated to reduce the amount of anesthetic delivered, which has been associated with faster recovery from non-cardiac surgery, [4] and there is some retrospective evidence that morbidity and mortality may also be reduced. [5],[6] On the other hand, sevoflurane and desflurane, in particular, have been demonstrated to exert significant myocardial protection in patients undergoing CABG surgery with and without the use of CPB. [7] Multicenter randomized clinical trials have shown less release of cardiac troponin I, less need for inotropic support, and reduced hospital stay following CABG surgery in patients receiving volatile anesthesia compared with patients receiving propofol. [1] Thus, it is unclear where to strike the balance between reduction of volatile anesthetic delivery and the associated benefits in recovery without losing the benefits of myocardial protection. Clearly, this area deserves further research.

   References Top

1.Yu CH, Beattie WS. The effects of volatile anesthetics on cardiac ischemic complications and mortality in CABG: a meta-analysis. Can J Anaesth 2006;53:906-18.  Back to cited text no. 1
2.Bautin AE, Siganevich AV, Malaya EY, Khomenko EA, Gordeev ML, Solntsev VN. Correlation of cardiac output and sevoflurane required to maintain anesthetic depth targeted with entropy index. Ann Card Anaesth 2014;17:4-7.  Back to cited text no. 2
  Medknow Journal  
3.Kennedy RR, Baker AB. The effect of cardiac output changes on end-tidal volatile anaesthetic concentrations. Anaesth Intensive Care 2001;29:535-8.  Back to cited text no. 3
4.Liu SS. Effects of Bispectral Index monitoring on ambulatory anesthesia: a meta-analysis of randomized controlled trials and a cost analysis. Anesthesiology 2004;101:311-5.  Back to cited text no. 4
5.Leslie K, Myles PS, Forbes A, Chan MT. The effect of bispectral index monitoring on long-term survival in the B-aware trial. Anesth Analg 2010;110:816-22.  Back to cited text no. 5
6.Monk TG, Saini V, Weldon BC, Sigl JC. Anesthetic management and one-year mortality after noncardiac surgery. Anesth Analg 2005;100:4-10.  Back to cited text no. 6
7.Lin E, Symons JA. Volatile anaesthetic myocardial protection: a review of the current literature. HSR Proc Intensive Care Cardiovasc Anesth 2010;2:105-9.  Back to cited text no. 7

Correspondence Address:
David Canty
Consultant Cardiothoracic Anaesthetist, Royal Melbourne Hospital and Monash Medical Centre, Melbourne
Login to access the Email id

Source of Support: None, Conflict of Interest: None

Rights and PermissionsRights and Permissions