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LETTER TO EDITOR  
Year : 2011  |  Volume : 14  |  Issue : 1  |  Page : 68
Anesthetic induction in coronary artery disease patients with left ventricular dysfunction


Department of Anaesthesiology, Command Hospital (CC), Lucknow - 226002, UP, India

Click here for correspondence address and email

Date of Web Publication31-Dec-2010
 

How to cite this article:
Kapoor MC. Anesthetic induction in coronary artery disease patients with left ventricular dysfunction. Ann Card Anaesth 2011;14:68

How to cite this URL:
Kapoor MC. Anesthetic induction in coronary artery disease patients with left ventricular dysfunction. Ann Card Anaesth [serial online] 2011 [cited 2020 Aug 13];14:68. Available from: http://www.annals.in/text.asp?2011/14/1/68/74412


The Editor,

I read with interest the article by Singh et al. titled "A randomized trial of anesthetic induction agents in patients with coronary artery disease and left ventricular dysfunction." [1] The study has presented findings contrary to contemporary literature on established induction agents - etomidate, propofol, midazolam and thiopentone.

The hemodynamic data presented show that the systemic vascular resistance index (SVRI) increased 3 min after induction with etomidate (20%), propofol (18.5%), midazolam (23.7%) as well as with thiopentone (22.5%). All the above drugs are known to vasodilate the arterial tree by their sympatholytic effects. The authors have used lower than standard doses for the first three drugs, possibly in view of the left ventricular dysfunction, but still a rise in SVRI has been elicited. Interestingly, the stroke volume index (SVI) was found to fall 2-3 min after induction with use of etomidate (38%), propofol (33.4%), midazolam (35.5%) and thiopentone (33.5%). There was a corresponding reduction in cardiac index (CI) too.

Most intravenous induction agents are known to reduce the SVRI. In individuals with normal cardiac function, this fall in SVRI and the consequent rise in heart rate may in fact raise the CI marginally. In left ventricular dysfunction, patients rely on the sympathetic drive to maintain adequate cardiac output. Induction of anesthesia is associated with depression of sympathetic activity, on which many patients with diminished cardiac reserve rely to maintain their hemodynamics. [2]

Hemodynamic stability has been a hallmark of the induction of anesthesia with etomidate since this drug was introduced into clinical practice in the late 1970s. [3] Etomidate produces minimal cardiovascular effects in healthy patients, as it maintains autonomic nervous system reflexes and preserves myocardial contractility. [4],[5],[6],[7] The clinical efficacy of etomidate has also been demonstrated in patients with coronary artery or valvular heart disease. [8],[9] The arterial pressure is maintained during etomidate anesthesia as a consequence of increases in left ventricular (LV) afterload which diminishes LV systolic and diastolic performance in the presence of impaired LV function [3] The fall in CI with the use of etomidate, in the study by Singh et al., may be explained by this. However, the fall in mean arterial pressures by a mean value of 25%, with the use of etomidate counters this argument.

The fall in CI in all the groups with a rise in SVRI is unexplainable. The rise in SVRI with the use of thiopentone, midazolam and propofol almost parallels that with etomidate. The authors' view that the fall in CI was due to withdrawal of sympathetic drive is untenable as the effects of such a withdrawal would not be restricted to the heart alone. The loss of sympathetic drive would have resulted in a fall in SVRI too.

Singh et al. also report that most of their patients had a fall in blood pressure and CI of 30-40%, which is unacceptable in the patient population they studied. The study should have been terminated or the protocol modified, when they reviewed their preliminary data.

 
   References Top

1.Singh R, Choudhury M, Kapoor PM, Kiran U. A randomized trial of anesthetic induction agents in patients with coronary artery disease and left ventricular dysfunction. Ann Card Anaesth 2010;13:217-23.   Back to cited text no. 1
[PUBMED]  Medknow Journal  
2.Bovill JG. Intravenous anesthesia for the patient with left ventricular dysfunction. Semin Cardiothorac Vasc Anesth 2006;10:43-8.   Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Pagel PS, Hettrick DA, Kersten JR, Tessmer JP, Lowe D, Warltier DC. Etomidate adversely alters determinants of left ventricular afterload in dogs with dilated cardiomyopathy. Anesth Analg 1998;86:932-8.  Back to cited text no. 3
[PUBMED]  [FULLTEXT]  
4.Criado A, Maseda J, Navarro E, Escarpa A, Avello F. Induction of anaesthesia with etomidate: haemodynamic study of 36 patients. Br J Anaesth 1980;52:803-6.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Ebert TJ, Muzi M, Berens R, Goff D, Kampine JP. Sympathetic responses to induction of anesthesia in humans with propofol or etomidate. Anesthesiology 1992;76:725-33.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Stowe DF, Bosnjak ZJ, Kampine JP. Comparison of etomidate, ketamine, midazolam, propofol, and thiopental on function and metabolism of isolated hearts. Anesth Analg 1992;74:547-58.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.Riou B, Lecarpentier Y, Viars P. Effects of etomidate on the cardiac papillary muscle of normal hamsters and those with cardiomyopathy. Anesthesiology 1993;78:83-90.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Gooding JM, Weng JT, Smith RA, Berninger GT, Kirby RR. Cardiovascular and pulmonary responses following etomidate induction of anesthesia in patients with demonstrated cardiac disease. Anesth Analg 1979;58:40-1.  Back to cited text no. 8
[PUBMED]  [FULLTEXT]  
9.Colvin MP, Savege TM, Newland PE, Weaver EJ, Waters AF, Brookes JM, et al. Cardiorespiratory changes following induction of anaesthesia with etomidate in patients with cardiac disease. Br J Anaesth 1979;51:551-6.  Back to cited text no. 9
[PUBMED]  [FULLTEXT]  

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Correspondence Address:
Mukul C Kapoor
16 Church Road, Delhi Cantt - 110 010
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.74412

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