| Article Access Statistics|
| Viewed||2858 |
| Printed||143 |
| Emailed||5 |
| PDF Downloaded||254 |
| Comments ||[Add] |
| Cited by others ||1 |
Click on image for details.
|Year : 2011
: 14 | Issue : 3 | Page
|Effect of thoracic epidural anesthesia on oxygen delivery and utilization in cardiac surgical patients scheduled to undergo off-pump coronary artery bypass surgery: A prospective study
Sharadaprasad Suryaprakash1, Murali Chakravarthy1, Mamatha Gautam1, Anurag Gandhi1, Vivek Jawali2, Thimmannagowda Patil1, Krishnamoorthy Jayaprakash1, Saurabh Pandey1, Geetha Muniraju1
1 Department of Anesthesiology, Fortis Hospitals, Bannerughatta Road, Bangalore, Karnataka, India
2 Department of Cardiothoracic and Vascular Surgery, Fortis Hospitals, Bannerughatta Road, Bangalore, Karnataka, India
Click here for correspondence address and
|Date of Web Publication||20-Aug-2011|
| Abstract|| |
To evaluate the effect of thoracic epidural anesthesia (TEA) on tissue oxygen delivery and utilization in patients undergoing cardiac surgery. This prospective observational study was conducted in a tertiary referral heart hospital. A total of 25 patients undergoing elective off-pump coronary artery bypass surgery were enrolled in this study. All patients received thoracic epidural catheter in the most prominent inter-vertebral space between C7 and T3 on the day before operation. On the day of surgery, an arterial catheter and Swan Ganz catheter (capable of measuring cardiac index) was inserted. After administering full dose of local anesthetic in the epidural space, serial hemodynamic and oxygen transport parameters were measured for 30 minute prior to administration of general anesthesia, with which the study was culminated. A significant decrease in oxygen delivery index with insignificant changes in oxygen extraction and consumption indices was observed. We conclude that TEA does not affect tissue oxygenation despite a decrease in arterial pressures and cardiac output.
Keywords: Cardiac surgery, off-pump coronary artery bypass surgery, oxygen delivery, oxygen extraction, oxygen utilization, oxygen, thoracic epidural anesthesia
|How to cite this article:|
Suryaprakash S, Chakravarthy M, Gautam M, Gandhi A, Jawali V, Patil T, Jayaprakash K, Pandey S, Muniraju G. Effect of thoracic epidural anesthesia on oxygen delivery and utilization in cardiac surgical patients scheduled to undergo off-pump coronary artery bypass surgery: A prospective study. Ann Card Anaesth 2011;14:192-6
|How to cite this URL:|
Suryaprakash S, Chakravarthy M, Gautam M, Gandhi A, Jawali V, Patil T, Jayaprakash K, Pandey S, Muniraju G. Effect of thoracic epidural anesthesia on oxygen delivery and utilization in cardiac surgical patients scheduled to undergo off-pump coronary artery bypass surgery: A prospective study. Ann Card Anaesth [serial online] 2011 [cited 2019 May 27];14:192-6. Available from: http://www.annals.in/text.asp?2011/14/3/192/83997
| Introduction|| |
Thoracic epidural anesthesia (TEA) can potentially benefit patients undergoing surgical procedures.  In cardiac surgery, its advantages include early recovery of consciousness and spontaneous ventilation,  hemodynamic stability,  superior analgesia,  reduced oxygen demand, optimal redistribution of coronary blood flow,  reduced risk of depression and post-traumatic stress,  improved pulmonary function,  and early extubation.  The disadvantages of TEA are concerns of permanent neurologic deficits due to epidural hematoma formation , and delay in recognition of subtle neurologic deficits because of sedation or hemodynamic instability. 
TEA may affect tissue oxygen delivery and utilization in two ways. On one hand, after administration of TEA, oxygen delivery may decrease due to reduced cardiac output, while on the other, it may improve organ perfusion due to vasodilatation.  Ultimately, tissue-oxygen balance may be affected by the sum effect of the two. Understanding this may help clinicians to decide the clinical utility of TEA with respect to oxygen delivery and utilization. This prospective observational study was conducted in 25 patients to determine the effect of TEA on tissue oxygenation.
| Materials and Methods|| |
A total of 25 patients who consented to administration of TEA and participation in the study were enrolled. Inclusion criteria were elective surgery, isolated coronary artery bypass surgery, and eligibility to receive TEA. Exclusion criteria were ventricular dysfunction (left ventricular ejection fraction <50%), left main coronary artery disease, systemic hypertension, congestive heart failure, restrictive or obstructive pulmonary disease, resting hypoxia (room air SpO 2 <90%) of any etiology, preoperative mechanical ventilation, history of smoking, hepatic dysfunction, and renal dysfunction (any biochemical or radiological abnormality in hepatic or renal function). Cohorts with 'failed epidural analgesia' (failure to elicit adequate level of regional block after 20 minutes of completion of injection of the local anesthetic solution in the epidural space) were also excluded from the study.
Normal coagulation profile was a prerequisite for administering TEA (activated partial thromboplastin time <45 second, international normalization ration of <1.5, platelet count of >100,000) and in whom anti-platelet medications were withdrawn at least a week earlier. Aspirin 100 mg or less was not considered as contraindication. The epidural catheter was inserted in all patients in the evening before surgery.
Contraindications to TEA
The contraindications to epidural catheterization were the following: patient refusal, continued use of clopidogrel; heparin or low molecular weight heparin; bleeding disorders; past surgery of the cervical and upper thoracic spine; and infection at the site of injection.
Technique of epidural catheterization
Epidural catheterization was performed in a high-dependency area on the evening before surgery by an experienced anesthesiologist. Routine monitoring included electrocardiogram, non-invasive blood pressure, and pulse oximetry. A 16-gauge epidural catheter (Epidural minipack, Portex Ltd CT21 6JL, UK) was inserted at the most prominent inter-vertebral space between C7 and T3 space. The patient was positioned sitting upright and a midline approach was used. If hemorrhagic tap was encountered, the epidural catheter was inserted at a lower level. These patients were retained in the high-dependency unit for further 2-3 hours and observed for any evidence of extradural compression. Patients were transferred to the presurgical ward for observation until surgery.
Induction of TEA and assessment of block
All patients were fasted for 8 hours. Midazolam 20 μg/kg was administered intravenously 30 minute prior to surgery. In the operating room, invasive monitoring lines (femoral arterial catheter and continuous cardiac output catheter) were inserted under local anesthesia. Electrocardiogram and pulse oximetry were monitored in addition. An epidural test dose of 3 ml of 2% lignocaine with 1:200,000 epinephrine was administered prior to administering the full loading dose of 8-10 ml of a mixture of 0.5% bupivacaine and 2% lignocaine with 1:200,000 adrenaline, with bupivacaine and lignocaine in the ratio of 2:1. The full dose of the epidural local anesthetic was administered as an infusion over 10 minute. The level of the block was tested after 30 minute by loss of pinprick and temperature discrimination to ice, aiming for a block from C7 to T9. The patients received oxygen via the facemask. Patients with evidence of hypoventilation as a result of either respiratory depression or intercostals paralysis or diaphragmatic palsy or chest wall rigidity were not included in the study, and the plan was to administer conventional general anesthesia in such cases. The volume of oxygen administered via the facemask exceeded the patient's minute volume, which was calculated as tidal volume [10 ml/kg] times the breaths (15 per minute).
After insertion of monitoring lines, baseline data were recorded. Collection of data commenced after administration of test dose of the epidural analgesic and infusion of full dose of epidural analgesic solution. Heart rate, Mean Arterial Pressure (MAP), and Pulmonary Capillary Wedge Pressure (PCWP), and cardiac index (Swan Ganz CCO/VIP, Edward Lifesciences, LLC, Irvine, CA, USA) were measured for 30 minute at 5-minute intervals from the time of administration of epidural test dose. Arterial and mixed venous blood were subjected simultaneously to blood gas analyses. Partial pressures of oxygen in the arterial (PaO 2 ) and venous (PVO 2 ) blood were noted. The derived parameters such as oxygen delivery index (DO 2 I), systemic oxygen-consumption index (VO 2 I), and oxygen extraction ratio (ERO 2 ) were calculated by feeding in the measured data (mentioned above) into the cardiac output computer (Edward Lifesciences, LLC, Irvine, CA USA). Hypotension and bradycardia were defined as decrease in blood pressure or heart rate respectively by more than 30% of basal values. Hypotension was treated with intravenous infusion of dopamine 5-10 μg/kg/min and bradycardia by intravenous injection of atropine 0.6-1.2 mg, respectively. Lactated ringer's solution was administered deemed necessary determined by MAP, CVP, or PCWP. The study was terminated at the end of 30 minute from the completion of the full dose infusion. Induction of general anesthesia was only after the completion of study period.
The measurements of the variables were commenced soon after administration of epidural test dose. Failed epidural resulted in exclusion from the study.
Repeated-measures Analysis of Variance (ANOVA) has been used to find the changes in the study parameters during the study period after testing for sphericity within the data by Mauchly's test. Estimate of effect size by Partial Eta Square has been used to know the effect of changes in the study parameters during the study period. P≤0.05 was considered to be significant. The statistical software SPSS 11.0 and Systat 8.0 was used for the analysis of the data. All values are mentioned as mean ± standard deviation.
| Results|| |
A total of 25 patients participated in the study. The male-to-female ratio in our group was 2.125:1, mean age was 54±8.2 years, mean weight was 59±12.6 kg. Six patients had well-controlled diabetes mellitus, three patients developed hypotension after administration of TEA (which was treated with intravenous infusion of 5 μg/kg/min of dopamine) and one bradycardia, which was treated with intravenous injection of 0.6 mg of atropine. None of the patients had either respiratory difficulties or failed epidural anesthesia. Volume of lactated ringer's solution used in the study period was 75±55 ml.
Changes in the hemodynamic variables: After administration of the full dose of epidural local anesthetic agent, there were significant decreases in HR, MAP, and cardiac index with P values of 0.01, 0.001, and 0.05, respectively [Table 1]. There were statistically insignificant decreases in pO 2 with P=0.358 and SvO 2 with P=0.100 [Table 2]. Further, we observed a significant decline in DO 2 I with P value of 0.015 [Table 2] with a statistically insignificant decrease in oxygen consumption with P value of 0.289 [Table 2] and insignificant increase in oxygen extraction ratio with P value of 0.435 [Table 2].
|Table 1: Changes in heart rate, mean arterial pressure, and cardiac index|
Click here to view
| Discussion|| |
In this study, we observed a significant decrease in heart rate, MAP, and cardiac index after activation of the TEA. Three patients developed hypotension after administration of TEA (which was treated with intravenous infusion of fluids and dopamine at 5 μg/kg/min) and one had bradycardia, which was treated with intravenous injection of 0.6 mg atropine. With TEA, a small but significant reduction in heart rate can be observed in humans, either in healthy volunteers  or in surgical patients.  The reduction in heart rate can be due to an action through a decrease of β-receptor stimulation,  but an increased vagal activity by TEA cannot be excluded. 
A decrease in systolic and diastolic blood pressure after epidural anesthesia has been shown in healthy volunteers.  Hypotension is partly due to its cardiodepressant action and partly to arterial and venous vasodilatation. The control of peripheral vascular tone is mediated by α and β adrenergic receptors and indirectly by circulating catecholamines released from the adrenal medulla through the sympathetic outflow between segments T5 and L1. The potential range of depressant effect by a high epidural blockade is quite broad, depending on the extent of deafferentation of the spinal segments involved. In patients with severe coronary artery disease and unstable angina, high TEA, while relieving chest pain, was found to have beneficial effects on the major determinants of myocardial oxygen consumption by lowering arterial systolic blood pressure, heart rate, pulmonary artery, and PCWP, but with no significant changes in coronary perfusion pressure. 
The above-mentioned changes in hemodynamic parameters were also accompanied by a fall in cardiac output. The reduction in cardiac sympathetic outflow by TEA may affect myocardial contractility, although available data have yielded contradictory conclusions. Goertz et al. evaluated myocardial contractility by transesophageal echocardiography and demonstrated that TEA severely affects contractility even in subjects without any cardiac disease.  In healthy patients, Niimi and coworkers found a decrease in cardiac output, but not a reduction in left ventricular ejection and diastolic filling performance as assessed by transthoracic echocardiographic evaluation.  Furthermore, a significant improvement in left ventricular function and a reduction in ischemia were demonstrated in patients undergoing coronary artery bypass grafting,with greater beneficial effect in patients with low ejection fraction.  Ideally, in patients at risk of ischemia, TEA should dilate constricted coronary vessels, decrease heart rate and myocardial metabolism, and improve cardiac function by reducing preload and afterload and optimizing myocardial oxygen availability.  We believe that even though the cardiac output decreased, tissue perfusion did not suffer, which is demonstrated by the absence of a significant change in SvO 2 levels. Gastric pH indirectly reflects the adequacy of oxygen delivery to the splanchnic bed. This area is particularly vulnerable to insufficient cardiac output. In a study of 30 patients undergoing major abdominal surgery under thoracic epidural anesthesia placed between T5-T10 levels, it was demonstrated that TEA prevented the decrease of pH during major abdominal surgery as an effect of stable visceral perfusion. 
We observed a significant decrease in DO 2 I with a small but statistically insignificant dectrease in oxygen consumption index. The decrease in DiO 2 can be attributed to the fall in cardiac output, which occurred after TEA. The changes in VO 2 can be due to favorable myocardial oxygen demand-supply induced by TEA.  There was no significant change in the oxygen extraction ratio. Intraoperative surgical stress increases adrenergic nervous activity and plasma catecholamine concentrations, which cause peripheral vasoconstriction and decreased partial pressure of oxygen in tissues, possibly leading to tissue hypoxia. Thoracic epidural anesthesia blocks afferent nociceptive stimuli and inhibits efferent sympathetic outflow in response to painful stimuli. Kabon et al. demonstrated that supplemental thoracic epidural anesthesia during major abdominal surgery improves tissue perfusion and subcutaneous oxygen tension outside the area of the epidural block.  TEA also improves wound oxygen tension, as investigated by Buggy et al. 
The limitations of the present study are as follows: the use of volume and inotropes to maintain cardiac output will alter some of the hemodynamic changes, the effect of general anesthesia and surgery was not studied and no metabolic parameter was studied.
We conclude that tissue perfusion and oxygenation is not compromised due to the fall in cardiac output and DiO 2 , which occurs after TEA. This can be attributed to the vasodilation and fall in stress response due to TEA, accompanied by favorable effects on the major determinants of myocardial oxygen consumption. Further, we advise careful monitoring of hemodynamic and oxygenation parameters during a high TEA.
| References|| |
|1.||Liu S, Carpenter RL, Neal JM. Epidural anesthesia and analgesia, their role in postoperative outcome. Anesthesiology 1995;82:1474-506. |
|2.||Liem TH, Hasenbos MA, Booij LH, Gielen MJ. Coronary artery bypass grafting using two different anesthetic techniques: Part 2: Postoperative outcome. J Cardiothorac Vasc Anesth 1992;6:156-61. |
|3.||Moore CM, Cross MH, Desborough JP Burrin JM, Macdonald IA, Hall GM. Hormonal effects of thoracic extra-dural analgesia for cardiac surgery. Br J Anaesth 1995;75:387-93. |
|4.||Blomberg S, Emanuelsson H, Kvist H, Lamm C, Pontén J, Waagstein F, et al. Effects of thoracic epidural anesthesia on coronary arteries and arterioles in patients with coronary artery disease. Anesthesiology 1990;73:840-7. |
|5.||Royse C, Royse A, Soeding P, Blake D, Pang J. Prospective randomized trial of high thoracic epidural analgesia for coronary artery bypass surgery. AnnThorac Surg 2003;75:93-100. |
|6.||Stenseth R, Bjella L, Berg EM, Christensen O, Levang OW, Gisvold SE. Thoracic epidural analgesia in aortocoronary bypass surgery. I: Haemodynamic effects. Acta Anaesthesiol Scand 1994;38:826-33. |
|7.||HO AM, Chung DC, Joynt GM. Neuraxial blockade and hematoma in cardiac surgery: Estimating the risk of a rare adverse event that has not (yet) occurred. Chest 2000;117:551-5. |
|8.||Vandermuelen EP, Van Aken H, Vermylen J. Anigcoagulants and spinal epidural anesthesia. Anesth Analg 1994;79:1165-77. |
|9.||O'Connor CJ, Tuman KJ. Epidural anesthesia and analgesia for coronary artery bypass graft surgery: Still forbidden territory? Anesth Analg 2001;93:523-5. |
|10.||Rolf N, Van Aken H. Physiology and pathophysiology of thoracic sympathetic blockade. Bailliere's Clin Anaesthesiol 1999;13:1-7. |
|11.||Wattwil M, Sundberg A, Arvill A, Lennquist C. Circulatory changes during high thoracic epidural anaesthesia: Influence of sympathetic block and of systemic effect of the local anaesthetic. Acta Anaesthesiol Scand 1985;29:849-55. |
|12.||Loick HM, Schmidt C, Van Aken H, Junker R, Erren M, Berendes E, et al. High thoracic epidural anesthesia, but not clonidine, attenuates the perioperative stress response via sympatholysis and reduces the release of troponin T in patients undergoing coronary artery bypass grafting. Anesth Analg1999;88:701-9. |
|13.||Hotvedt R, Platou ES, Refsum H. Electrophysiological effects of thoracic epidural analgesia in the dog heart in situ. Cardiovasc Res 1983;17:259-66. |
|14.||Hotvedt R, Refsum H, Platou ES. Cardiac electrophysiological and hemodynamic effects of beta-adrenoceptor blockade and thoracic epidural analgesia in the dog. Anesth Analg 1984;63:817-24. |
|15.||Stanton-Hicks MA. Cardiovascular effects of extradural anaesthesia. Br J Anaesth 1975;47 suppl:253-61. |
|16.||Blomberg S, Emanuelsson H, Ricksten SE. Thoracic epidural anesthesia and central hemodynamics in patients with unstable angina pectoris. Anesth Analg1989;69:558-62. |
|17.||Goertz AW, Seeling W, Heinrich H, Lindner KH, Schirmer U. Influence of high thoracic epidural anaesthesia on left ventricular contractility assessed by using end-systolic pressure length relationship. Acta Anaesthesiol Scand 1993;37:38-44. |
|18.||Niimi Y, Ichinose F, Saegusa H, Nakata Y, Morita S. Echocardiographic evaluation of global left ventricular function during high thoracic epidural anesthesia. J Clin Anesth 1997;9:118-24. |
|19.||Kilickan L, Solak M, Bayindir O. Thoracic epidural anesthesia preserves myocardial function during intraoperative and postoperative period in coronary artery bypass grafting operation. J Cardiovasc Surg (Torino) 2005;46:559-67. |
|20.||Kapral S, Gollmann G, Bachmann D, Prohaska B, Likar R, Jandrasits O, et al. The effects of thoracic epidural anesthesia on intraoperative visceral perfusion and metabolism. Anesth Analg 1999;88:402-6. |
|21.||Kabon B, Fleischman E, Treschan T, Taguchi A, Kapral S, Kurz A. Thoracic epidural anesthesia increases tissue oxygenation during major abdominal surgery. Anesth Analg 2003;97:1812-7. |
|22.||Buggy DJ, Doherty WL, Hart EM, Pallett EJ. Postoperative wound oxygen tension with epidural or intravenous analgesia: A prospective, randomized, single-blind clinical trial. Anesthesiology 2002;97:952-8. |
Department of Anesthesia, Critical Care and Pain Relief, Fortis Hospitals, Bangalore
Source of Support: None, Conflict of Interest: None
[Table 1], [Table 2]
|This article has been cited by|
||Epidural catheterization in cardiac surgery: The 2012 risk assessment
| || Hemmerling, T.M., Cyr, S., Terrasini, N. |
| ||Source of the Document Annals of Cardiac Anaesthesia. 2013; |