Epidural Anesthesia for Coronary Artery Bypass Surgery

Compared with General Anesthesia Alone Does Not Reduce

Biochemical Markers of Myocardial Damage
Michael J. Barrington, FANZCA, Roman Kluger, FANZCA, Robert Watson,
David A. Scott, FANZCA, and Karen J. Harris, RN

FANZCA,

Department of Anaesthesia, St. Vincents Hospital, Melbourne, Australia

High thoracic epidural anesthesia/analgesia (HTEA)

for coronary artery bypass grafting (CABG) surgery
may have myocardial protective effects. In this prospective randomized controlled study, we investigated
the effect of HTEA for elective CABG surgery on the
release of troponin I, time to tracheal extubation, and
analgesia. One-hundred-twenty patients were randomized to a general anesthesia (GA) group or a GA
plus HTEA group. The GA group received fentanyl
(715 g/kg) and a morphine infusion. The HTEA
group received fentanyl (57 g/kg) and an epidural
infusion of ropivacaine 0.2% and fentanyl 2 g/mL until postoperative Day 3. There were no differences in

igh thoracic epidural anesthesia/analgesia

(HTEA) for coronary artery bypass graft
(CABG) surgery promotes effective analgesia
and sympatholysis and attenuates the stress response
to surgery (1,2). In experimental conditions, HTEA
reduces myocardial infarct size (3), possibly by improving myocardial oxygen balance. HTEA provides
effective pain relief for patients with unstable angina
and myocardial infarction; it reduces the major determinants of myocardial oxygen demand while maintaining coronary artery perfusion pressure (4,5). Balancing these potential benefits of HTEA is concern
regarding epidural hematoma and permanent spinal

This study received grants from the Australian Society of Anaesthetists and the Australian and New Zealand College of Anaesthetists.
Presented in part at the annual meeting of the Australian and
New Zealand College of Anaesthetists, Brisbane, Australia, May 12,
2002, and at the Australian Society of Anaesthetists National Scientific Conference, Adelaide, Australia, October 26, 2002.
Accepted for publication September 14, 2004.
Address correspondence and reprint requests to Michael J. Barrington, FANZCA, Department of Anaesthesia, St. Vincents Hospital, Melbourne, PO Box 2900, Fitzroy, Victoria 3065, Australia.
Address e-mail to Michael.Barrington@svhm.org.au.
DOI: 10.1213/01.ANE.0000146437.88485.47
2005 by the International Anesthesia Research Society
0003-2999/05

troponin I levels between study groups. The time to tracheal extubation [median (interquartile range)] in the
HTEA group was 15 min (10 320 min), compared with
430 min (284 590 min) in the GA group (P 0.0001).
Analgesia was improved in the HTEA group compared
with the GA group. Mean arterial blood pressure poststernotomy and systemic vascular resistance in the intensive care unit were lower in the HTEA group. We
conclude that HTEA for CABG surgery had no effect on
troponin release but improved postoperative analgesia
and was associated with a reduced time to extubation.
(Anesth Analg 2005;100:9218)

cord damage with neuraxial block in patients who are

fully heparinized for surgery.
Most randomized controlled studies in this area
have focused on hemodynamic effects and the stress
response to surgery. Studies assessing the important
issue of potential cardioprotective effects of HTEA
have yielded conflicting results. The release of cardiac
troponin I (cTnI) has been shown to be a sensitive and
specific marker of myocardial cell necrosis, with significant prognostic importance after cardiac surgery
(6,7). Priestley et al. (8) found no difference in troponin
levels between general anesthesia (GA) alone and GA
plus HTEA groups, yet Loick et al. (9) found significantly reduced troponin T levels in their HTEA group.
The aim of this prospective randomized study was to
investigate the effect of HTEA for elective CABG surgery on postoperative release of biochemical markers
and electrocardiograph (ECG) changes of myocardial
ischemia/infarction. Although the time to tracheal extubation has been reduced by the use of HTEA in
many studies, it can be influenced by multiple factors
and varies greatly among institutions (10). Therefore,
a secondary aim of this study was to assess the effect
of HTEA on time to tracheal extubation in our institution. In addition, although HTEA has been shown in
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a number of studies to improve postoperative analgesia (1,8,11), analgesic regimens and their efficacy are
also institution specific, and thus a third aim of our
study was to assess the effect of HTEA on the quality
of postoperative analgesia.

Methods
The St. Vincents Hospital human research ethics
committee approved this prospective randomized
controlled trial, and written informed consent was
obtained from all patients. All patients scheduled
for elective CABG surgery (using cardiopulmonary
bypass (CPB)) were eligible. Exclusion criteria were
emergency or repeat CABG surgery, combined
valve and CABG surgery, aspirin ingestion within
6 days of surgery, a platelet count 150 109/L, an
international normalized ratio 1.1, active neurological disease, and cutaneous disorders at the epidural insertion site. Patients were randomized the
day before surgery to the GA group or the combined
GA and HTEA group. The random-allocation sequence was computer-generated in permuted blocks
of four and enclosed in sequentially numbered
opaque sealed envelopes.
Patients randomized to the HTEA group had an
epidural catheter (20-gauge; Portex, Hythe, Kent, UK)
inserted the day before surgery at T1-2 or T2-3 by
using a midline approach and loss-of-resistance-tosaline technique. Epidural catheters were inserted
with patients sitting, by using an 18-gauge needle with
the bevel directed cephalad, advanced into the epidural space 4 cm, and flushed with saline. Patients
received their usual cardiac medications on the day of
surgery. Premedication consisted of temazepam 20 mg
and ranitidine 150 mg orally and morphine 0.10
0.15 mg/kg IM 2 h before anesthetic induction.
After initiation of ECG monitoring (leads II and V5
monitored) and insertion of invasive monitoring (radial artery cannula and pulmonary artery catheter),
epidural block was established with 5 mL of ropivacaine 1% and fentanyl 50 g. The block was assessed
20 min later by using loss of temperature sensation to
ice, with success defined as a block over the T1 to
T6 dermatomes. If required, the block was extended
with 2 mL of ropivacaine 1%.
GA was induced with midazolam (0.05 0.1 mg/kg),
fentanyl (715 g/kg for the GA group and 57 g/kg
for the HTEA group), propofol (20-mg increments as
required), and rocuronium (0.6 mg/kg). GA was
maintained with propofol 3 6 mg kg1 h1. Further
doses of rocuronium 10 mg were given only for overt
patient movement, with no additional rocuronium
given after CPB. Intraoperative hemodynamic management was standardized although, to represent routine practice, anesthesiologists defined acceptable limits to optimize individual patient management.

ANESTH ANALG
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Hypotension was treated with volume, metaraminol,

or ephedrine; hypertension was treated with propofol
0.251 mg/kg, additional fentanyl, a volatile drug, or
glyceryl trinitrate; tachycardia was treated with
propofol 0.251 mg/kg or a -adrenoceptor blocker;
and bradycardia was treated with ephedrine. All patients received heparin (300 IU/kg and 10,000 IU in
the pump prime) and -aminocaproic acid (5 g before
CPB and 5 g in the pump prime). Further heparin (100
IU/kg) was administered to maintain an activated
clotting time more than 450 s at all times during CPB.
CPB was performed with a noncoated circuit, membrane oxygenator, and nonpulsatile flow via a roller
pump at 2.0 2.4 L min1 m2. Myocardial protection consisted of an initial dose of antegrade and retrograde blood cardioplegia (composition: potassium
20 mmol, aspartate 14 mmol, glutamate 14 mmol,
magnesium 5 mmol, bicarbonate 15 mmol, and lidocaine 100 mg). Maintenance of arrest was achieved
with intermittent retrograde blood cardioplegia (composition: potassium 8 12 mmol, aspartate 7 mmol,
and bicarbonate 10 mmol) at the completion of each
anastomosis. Cardioplegia was delivered at 25C
30C, with no crystalloid added. Phenylephrine 0.25
0.5 mg or isoflurane was used to maintain mean arterial blood pressure (MAP) between 65 and 90 mm Hg.
Patients were separated from CPB after completion of
grafting and rewarming to at least 36.5C. Heparin
was reversed with protamine 3 mg/kg. Further protamine (0.51 mg/kg) was given to return the activated clotting time to baseline or as initial management of bleeding.
Samples of blood for cTnI and creatine kinase myocardial fraction (CK-MB%) were collected preinduction and 12 and 24 h after aortic cross-clamp release,
consistent with published recommendations (7,1215).
cTnI was measured by using the Abbott AxSYM analyzer (Abbott Laboratories, North Chicago, IL; reference value for cTnI, 0.6 g/L; upper limit of measurement, 50 g/L). The reference value for CK-MB%
was 8. Twelve-lead ECGs were recorded before surgery and on postoperative Days 1 and 5 and were
assessed by 2 observers blinded to group allocation
and postoperative clinical course. Observers were specifically asked to note new persistent Q waves 0.04 s
and new ST segment depression or elevation (0.1
mV at 0.08 s after the J point) in at least 2 contiguous
leads of the same vascular territory. Transmural infarction was defined as new Q waves and cTnI 15
g/L at 24 h1 (13).

1
Martin B, Murphy F, Levy T, et al. Cardiac isoform of troponin-I
(c-TnI): a sensitive marker of perioperative myocardial infarction
(PMI) in CABG surgery [abstract]. Br J Anaesth 1999;82:A10.

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Hemodynamic measurements were recorded immediately before induction, 5 min after tracheal intubation, 12 min poststernotomy, and 10 min after separation from CPB. Measurements consisted of heart
rate, MAP, mean pulmonary arterial pressure, central
venous pressure, pulmonary artery occlusion pressure
(PAOP), cardiac index (mean of three determinations
by thermodilution), and systemic vascular resistance
(SVR). Baseline left ventricular (LV) function was
scored after induction by using transesophageal echocardiography based on a 16-segment model (16). Segments were scored as 1, normal; 2, mild hypokinesis;
3, severe hypokinesis; 4, akinesis; 5, dyskinesis; and 6,
aneurysmal. An LV score was calculated by totaling
the scores of the 16 segments. After CPB, the LV was
assessed for new segmental wall motion abnormalities
(SWMAs). Intraoperative and postoperative vasoactive drug requirements were recorded.
To facilitate early tracheal extubation, the propofol
infusion was ceased at sternal closure, and minute
ventilation was reduced to stimulate spontaneous
ventilation. The time to tracheal extubation was measured from the time of surgical dressings. The anesthesiologist tracheally extubated patients in the operating
room if extubation criteriarespiratory rate 10 20
breaths/min, responsiveness to voice, end-tidal CO2
50 mm Hg, Sao2 94% with a fraction of inspired
oxygen of 1.0, hemodynamic stability, minimal chest
drain output (not requiring transfusion or consideration for surgical reexploration) and temperature
35.9Cwere achieved within 30 min. For patients
not extubated in the operating room, postoperative
management of ventilation and extubation followed
existing unit guidelines (17). Patients were required to
respond appropriately to voice, have an acceptable
ventilatory pattern and arterial blood gas analysis,
and be hemodynamically stable. The first postextubation arterial blood gas (at approximately 30 min), complications, chest tube drainage, and day of discharge
were recorded. Hemodynamic measurements were repeated in the intensive care unit (ICU) at two or more
time points.
The GA group received an initial loading dose of
morphine 0.1 0.2 mg/kg after separation from CPB
and infiltration of ropivacaine 3 mg/kg into chest
drain sites. Pain management in the ICU followed
existing guidelines (17), including titration of morphine increments (1 mg) and commencement of a
morphine infusion (after tracheal extubation) that continued until the morning of postoperative Day 2. In
the HTEA group, an epidural infusion (ropivacaine
0.2% and fentanyl 2 g/mL) was commenced 1 h after
the induction of GA at an hourly rate equal to the
required initial loading volume and was continued
until the morning of postoperative day 3. If epidural
analgesia was inadequate, the infusion was increased
by 2 mL/h after a bolus of 2 mL. All patients received

923

acetaminophen 1 g rectally at the completion of surgery. Pain rescue medication for both groups consisted of indomethacin 100 mg/12 h and oxycodone
5 mg/6 h. HTEA patients with a failed block received
a morphine infusion as was used in the GA group.
Pain scores were measured with a visual analog
scale (VAS) of 0 100 mm at 4 time points (separated
by 4 6 h) during the first 24 h after tracheal extubation and at 2 time points (separated by 8 12 h) in the
second and third 24-h periods after surgery. VAS pain
scores were measured at rest and with coughing. Side
effects and complications of analgesia were recorded
at each analgesia assessment. Sedation was graded as
0, fully alert; 1, mildly drowsy; 2, moderately drowsy,
easily rousable; 3, very drowsy but rousable; and 4,
difficult to rouse or unrousable. Nausea was graded as
0, no nausea; 1, nausea but no vomiting; and 2, nausea
and vomiting. Motor and sensory block were recorded
in the HTEA group. Motor block in the upper limb
was graded as 0, none; 1, mild hand weakness; 2,
elbow weakness; and 3, weakness involving the shoulder. A research nurse or investigator usually performed these assessments. After hours, some of the
assessments were performed by appropriately briefed
ICU nurses and anesthesiology residents.
A formal sample size determination based on cTnI
was not possible because cTnI data after CABG surgery with the Abbott AxSYM analyzer were not available at the time of study inception. The confidence
interval for differences in median cTnI levels between
groups was calculated to assess the precision of our
data and, hence, the adequacy of our sample size.
Nonparametric confidence intervals were calculated
using Confidence Interval Analysis software (BMJ
Books, London, UK).
For our secondary end-point, sample size was calculated by using a mean time to tracheal extubation of
240 min, with an sd of 200 min (17). A clinically
significant difference was determined to be a 50%
reduction; this required a sample size of 45 in each
group. Between-group analyses were performed with
the Mann-Whitney U-test or Students t-test, depending on the distribution and character of the data. Bonferronis correction was used for multiple comparisons for hemodynamic data. Categorical data were
compared by using Fishers exact test. Time to tracheal
extubation was analyzed with Kaplan-Meier survival
curves and log-rank tests for differences between
groups. The level of significance was taken as 0.05.
Data were analyzed with StatView 4 (Abacus Concepts, Berkeley, CA) and Stata Version 7.0 (Stata
Corporation, College Station, TX).

Results
One-hundred-twenty patients were randomized to 2
groups of 60 from December 1999 to March 2002. All

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Table 1. Patient and Surgical Characteristics

Variable
Sex (male/female)
Age (yr)
Body mass index (kg/m2)
Hypertension (treated with medication)
Family history (first-order relative)
Diabetes
Cigarette smokingcurrent
Cigarette smokingex-smokera
Peripheral vascular disease
Cerebrovascular disease
-Adrenoceptor blockers
Calcium channel blockers
ACE inhibitors
Nitrates
Statins
NYHA angina score
LV score
Aortic cross-clamp time (min)
Antegrade cardioplegia (mL)
Retrograde cardioplegia (mL)b
CPB time (min)
Time of surgery (min)
Minimum temperature on CPB (C)
Temperature at end of surgery (C)
No. coronary grafts

GA group
(n 60)

HTEA group
(n 60)

P value

53/7
62 (10)
27.7 (4)
39
35
4
20
24
2
1
38
24
21
21
44
3 (23)
17 (1619)
83 (25)
576 (202)
1166 (400)
105 (31)
266 (57)
32.5 (0.9)
36.3 (0.4)
3 (34)

51/9
63 (9)
27.1 (4)
36
25
8
20
27
11
12
32
15
21
22
41
2 (2 3)
17 (1619)
77 (22)
537 (116)
1082 (293)
98 (25)
258 (47)
32.5 (0.9)
36.3 (0.3)
3 (34)

NS
NS
NS
NS
NS
NS
NS
0.016
0.002
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS

GA general anesthesia; HTEA high thoracic epidural anesthesia; NS not significant; NYHA New York Heart Association; LV score cumulative
score based on 16 segment model; ACE angiotensin-converting enzyme; CPB cardiopulmonary bypass.
Data are n, mean (sd), or median (interquartile range).
a
A patient who claimed to have ceased smoking for 2 mo before surgery.
b
Total volume given.

patients were included in the analysis. Patient and

surgical characteristics are listed in Table 1. There was
a more frequent prevalence of cerebrovascular and
peripheral vascular disease in the HTEA group (Table
1). Epidural blockade was successful in 58 of 60 patients. The two patients with nonfunctional epidural
catheters were analyzed as being in the epidural
group (i.e., intention to treat) but received analgesia
with a morphine infusion as if in the GA group. All
patients had baseline cTnI levels 0.3 g/L.
Epidural blockade required a median initial loading
dose of 7 mL of ropivacaine, resulting in median upper and lower levels of sensory block of C5 (range, C3
to T1) and T10 (range, T3 to L3), respectively. The
HTEA group had a significantly reduced MAP (78 vs
94 mm Hg) and SVR (994 vs 1261 dynes s cm5)
preinduction and had reduced MAP poststernotomy
(83 vs 97 mm Hg) compared with the GA group. There
were no other significant intraoperative hemodynamic
differences between groups, nor were requirements
for metaraminol and ephedrine different (Table 2).
The fentanyl dosage (based on protocol) was significantly smaller in the HTEA group [median (interquartile range; IQR), 5.2 g/kg (4.4 6.1 g/kg)] than in
the GA group [12.0 g/kg (10.113.8 g/kg)]. The
intraoperative midazolam dosage was significantly

smaller in the HTEA group [0.044 mg/kg (0.026

0.058 mg/kg)] than in the GA group [0.056 mg/kg
(0.035 0.068 mg/kg)]. The intraoperative propofol
dosage was not significantly different between
groups: HTEA group, 16.3 mg/kg (13.4 18.4 mg/kg);
GA group, 17.3 mg/kg (14.6 21.5 mg/kg). The
GA group received morphine 0.12 mg/kg (0.1
0.12 mg/kg) after CPB. There were 21 patients with
new SWMAs. Fifteen SWMAs had resolved by the
completion of surgery. The distribution of SWMAs
(persistent and resolving) was not different between
groups.
Time to tracheal extubation was significantly less in
the HTEA group [15 min (10 320 min)] than in the GA
group [430 min (284 590 min); log-rank test; P
0.0001]. Sixty percent of HTEA patients were extubated within 30 min of the completion of surgery (in
the operating room), compared with 5% of GA patients (Fig. 1). However, of those patients who remained intubated on arrival in the ICU, there were no
differences in time to tracheal extubation: HTEA
group, 458 min (230 594 min); GA group, 450 min
(300 605 min). Within the HTEA group, patients extubated in the operating room were more likely to be
male (97% vs 67%; P 0.002) and to receive a smaller

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Table 2. Vasoactive Drug Use

GA (n 60)
Variable
Intraoperative
Metaraminol
Ephedrine
Postoperative
Epinephrine
Norepinephrine
GTN

HTEA (n 60)

Dose (mg)

Dose (mg)

P value

2.0 (1.03.3)
10 (5.018)

53
30

2.0 (1.03.5)
6.0 (6.012.8)

45
37

NS
NS

1.0 (0.124.7)
2.0 (0.280.2)
21 (4.071.1)

8
13
58

1.0 (0.22.8)
2.0 (0.59.4)
16 (3.818.8)

6
21
51

NS
NS
0.01a

GA general anesthesia; HTEA high thoracic epidural anesthesia; NS, not significant; GTN glyceryl trinitrate.
Data are expressed as median (interquartile range) or n (number of patients requiring treatment).
a
For dosage only.

Figure 1. Kaplan-Meier survival plot for time to extubation. F

high thoracic epidural anesthesia (HTEA) group; general anesthesia (GA) group (P 0.0001).

propofol dosage (median, 14.8 vs 17.6 mg/kg; P

0.025).
There was no difference in postoperative epinephrine
and norepinephrine use (Table 2) between groups, although the GA group required more glyceryl trinitrate
for vasodilation compared with the HTEA group (P
0.02). The HTEA group had higher Paco2, lower lactate
levels, and reduced postoperative SVR compared with
the GA group (Table 3). HTEA patients tracheally
extubated in the operating room had a higher Paco2
than HTEA patients extubated in the ICU (54 vs
48 mm Hg; P 0.003).
The cTnI levels were increased in both groups at 12
and 24 h, but there were no significant differences between groups (Table 4). The distribution of cTnI levels
was not different in the two groups, and the nonparametric 95% confidence interval for the difference in median cTnI levels between groups was 2.1 to 2.4 g/L.
Eight (6.7%) patients developed new persistent Q waves
by Day 5 (GA group, n 5; HTEA group, n 3).
However, with combined ECG and cTnI criteria, only 3
(2.5%) patients had a transmural myocardial infarction
(GA group, n 2, HTEA group, n 1) (Table 4). There

was no difference between groups in the incidence of

myocardial ischemia or infarction based on any of the
following ECG or biochemical criteria: CK-MB% 8 at
12 and 24 h, Q wave and increased CK-MB%, ST increases, and cTnI or CK-MB increases.
In the HTEA group, pain scores were significantly
reduced compared with those in the GA group at all
measurement times in the 72 h after surgery, both at rest
and with coughing. The VAS results with coughing are
shown in Figure 2. On average at rest, the VAS results
were 28 mm less in the GA group and 9 mm less in the
HTEA group compared with scores during coughing. In
the GA group, the morphine dosage and duration of
infusion (measured from the completion of surgery)
were 46.5 mg (33 66 mg) and 41 h (3351 h), respectively. Only the two patients with nonfunctioning epidurals required morphine in the HTEA group. The duration of epidural infusion was 70.5 h (6773 h) at an
average infusion rate of 8.1 mL/h, with median upper
and lower limits of sensory block of C6 to T9 on Day 1,
C7 to T6 on Day 2, and C8 to T6 on Day 3. Indomethacin
was required in 25 GA patients and 24 HTEA patients;
however, the median dosage in the GA group was
100 mg, compared with 200 mg in the HTEA group (P
0.02). Oxycodone was required more frequently in the
GA group (21 patients) compared with the HTEA group
(9 patients). There were no differences in sedation or
nausea scores between groups. Motor block in the upper
limbs (mild hand weakness) occurred in 16% and 9% of
patients on postoperative Days 1 and 2, respectively, and
in all cases improved with reduction or temporary cessation of epidural infusion. There were no major complications due to epidural anesthesia or to other analgesic techniques.
The HTEA group had one patient who required tracheal reintubation (for agitation) in the ICU. The GA
group had two patients who required reintubation (one
before reoperation for hemorrhage and one who required a tracheostomy for respiratory failure). There
were two deaths in the GA group: one due to uncontrolled postoperative bleeding and one from postoperative stroke. There were no deaths in the HTEA group.

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Table 3. Intensive Care Unit Pao2, Paco2, Lactate, and Hemodynamic Variables
Variable
a

Pao2 (mm Hg)

Paco2 (mm Hg)a
Lactate (mmol/L)
Cardiac index (L min1 m2)
SVR (dynes cm s1)
Minimum SVR (dynes cm s1)b

GA, median (IQR)

HTEA, median (IQR)

P value

112 (94146)
48 (4450)
1.8 (1.42.5)
2.8 (2.53.2)
1008 (8311146)
784 (613940)

121 (98157)
51 (4657)
1.4 (1.21.9)
2.9 (2.63.31)
861 (7611072)
694 (600821)

NS
0.006
0.005
NS
0.03
0.07

GA general anesthesia; HTEA high thoracic epidural anesthesia; IQR interquartile range; NS not significant; SVR systemic vascular resistance.
a
First postextubation arterial blood gas.
b
Mean of the lowest SVR calculated in the intensive care unit.

Table 4. Troponin Results (n 60)

Variable
Continuous data, median (IQR)
Troponin I 12 h (g/L)
Troponin I 24 h (g/L)
Categorical data (n)
Troponin I 12 15 (g/L)
Troponin I 24 15 (g/L)
Q wave/troponin I 24 15 (g/L)

GA

HTEA

17.2 (10.726.4)
9.1 (4.925.9)

17.0 (10.427.9)
9.1 (6.021.0)

32
19
2

35
20
1

GA general anesthesia; HTEA high thoracic epidural anesthesia; IQR interquartile range; troponin I 12 and 24 h samples taken 12 and 24 h after release
of aortic cross-clamp; Q wave new persistent Q wave on Day 5.

Figure 2. Visual analog scale scores for pain with coughing for the
first 72 h. Boxes represent median and interquartile range; horizontal bars represent 5th and 95th percentiles. Shaded boxes high
thoracic epidural anesthesia group; open boxes general anesthesia group. P 0.0001 at all time points.

There were no differences between the HTEA and GA

groups in median total chest tube drainage (1460 vs
1510 mL, respectively), incidence of new postoperative
atrial fibrillation (AF) (16 of 60 vs 20 of 60, respectively;
P 0.55), or median day of discharge [6.0 days (6
8 days) versus 6.5 days (6 8 days), respectively].

Discussion
In this prospective randomized study, HTEA for elective CABG surgery had no effect on biochemical or
ECG markers of myocardial ischemia or infarction.

However, HTEA improved analgesia and facilitated

earlier tracheal extubation.
cTnI is a sensitive and specific marker of perioperative myocardial infarction (1215,18 20) and is an
independent predictor of short- and long-term morbidity and mortality after CABG surgery (6,7). Reported levels of cTnI indicating perioperative myocardial infarction range from 11.6 to 40 g/L (1214,21),
and although we used a threshold of 15 g/L, our
analysis showed no difference between groups regardless of the threshold used. A threshold of 15 g/L
at 24 hours would result in an incidence of infarction
(Q or non-Q wave) of 32% and 33% in the HTEA and
GA groups, respectively. This is consistent with the
30% incidence of non-Q wave infarction after CABG
surgery found with sensitive tests such as technetium
pyrophosphate scanning (22). Our sample size was
adequate to exclude any clinically relevant difference
in cTnI levels between groups, because the narrow
95% confidence intervals for cTnI indicate that any
difference between groups would probably be 2.4
g/L. Clearly this study was not powered to detect a
difference in Q-wave infarction between groups; such
a study would require several thousand patients.
The lack of an effect of HTEA on cTnI levels is in
agreement with one study (8), but in contrast, Loick et al.
(9) reported reduced troponin T release with HTEA.
Differences between the study of Loick et al. and ours
include fewer patients than this study, different cardioplegia techniques, different times to tracheal extubation,
and a longer aortic cross-clamp period in our study (80
vs 49 minutes). Perhaps our infusion of ropivacaine 0.2%

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EPIDURAL ANESTHESIA FOR CORONARY ARTERY BYPASS SURGERY

did not maintain a dense sympathetic block, compared

with bupivacaine 0.75% in the study of Loick et al. However, Priestley et al. (8) used ropivacaine 1% and also
found no effect on troponin levels with HTEA.
One limitation of our cTnI results is the more frequent prevalence of peripheral and cerebrovascular
disease in the HTEA group. However, patients with
and without these conditions had identical cTnI levels.
Another potential limitation is that we measured cTnI
only within 24 hours; therefore, we may have missed
later events. However, a single 24-hour cTnI measurement has been shown to be reliable in detecting
perioperative myocardial infarction (12) and predicting poor outcome (7). Despite the theoretical advantages of HTEA, factors such as technical difficulty in
grafting and myocardial protection during the ischemic period may have a more significant effect than
epidural anesthesia on troponin release.
Although the time to tracheal extubation in the HTEA
group was significantly reduced, group allocation was
not masked; therefore, bias toward early extubation in
the HTEA group cannot be excluded (even though extubation criteria were standardized). A further limitation
was a protocol requirement for reduced fentanyl dosage
in the HTEA group, thus favoring earlier tracheal
extubation. However, the investigators considered the
prescribed fentanyl and morphine dosages necessary
to facilitate hemodynamic stability and postoperative
analgesia while retaining the capability to extubate
early. Our finding of reduced extubation times with
HTEA is in agreement with that of similar randomized
controlled studies (1,8,9,11,23) with median extubation times ranging from 1.6 to 10 hours. It is important
to note that nonepidural anesthesia techniques, such
as remifentanil (24) and small-dose opioid (25,26) techniques, have been used to facilitate tracheal extubation
in the operating room after off-pump surgery; however, these findings may not be applicable to on-pump
CABG surgery with long CPB durations (as in our
study).
Analgesia was improved in the HTEA group in the
72 hours after surgery, which is consistent with other
reports (1,8,11). The longer duration of epidural infusion compared with that of the morphine infusion
may have contributed to lower VAS scores on postoperative Days 2 and 3 in the HTEA group and increased
oxycodone requirements in the GA group. However,
it was decided to continue the existing unit practice
and stop the morphine infusion on postoperative Day
2. The optimal duration of epidural analgesia after
CABG surgery is not clear. Our decision to continue
the infusion to postoperative Day 3 was strongly influenced by the general observation that post-CABG
platelet counts were lowest on postoperative Days
12.
After anesthesia induction there were no significant
hemodynamic differences between groups, except that

927

poststernotomy MAP and SVR in the ICU were lower in

the HTEA group. Apart from decreased postoperative
glyceryl trinitrate use in the HTEA group, there was no
significant difference in requirements for vasoactive
drugs, which is consistent with other studies (27).
There was no difference in the incidence of AF
between groups, consistent with two studies (8,28) but
in contrast with a large study by Scott et al. (23), who
found a significantly reduced incidence of AF with the
use of HTEA. In the study of Scott et al., the epidural
infusion included clonidine, which may have contributed to the less frequent incidence of AF.
There were no complications related to the epidural
technique. The risk of epidural hematoma after epidural
anesthesia in cardiac surgical patients has been estimated to be between 1 in 1,500 and 1 in 150,000 (29). This
broad confidence interval is of limited value in our practice, where informed consent regarding risk is of paramount importance. There have been no case reports of
epidural hematoma due to epidural anesthesia in fully
anticoagulated patients having cardiac surgery. Heparin
has no fibrinolytic effects, but cardiac surgery and CPB
result in fibrinolysis and platelet dysfunction. Patients
routinely received -aminocaproic acid during this
study, but its contribution to the safety of neuraxial
blockade in this population has not been determined.
Inserting the epidural catheter the day before surgery
was a conservative approach that has been the practice
in most studies using HTEA for CABG surgery. However, admitting patients the day before surgery in a
health care system in which day-of-surgery admission is
routine may offset any economic advantage of earlier
tracheal extubation. Although the combination of early
tracheal extubation, cardiac sympathetic blockade, stress
response attenuation, and excellent analgesia are unique
to HTEA, its attendant complexity and potential for epidural hematoma cause its use to remain controversial.
In conclusion, in this study, the use of HTEA for
CABG surgery had no effect on the release of cTnI as
a marker of myocardial ischemia/infarction. However, HTEA improved postoperative analgesia and
was associated with a reduced time to tracheal
extubation.
The authors acknowledge the assistance of the staff of the Open
Heart Surgical Unit and Intensive Care Unit and Dr. Simon McPherson, St. Vincents Hospital, Melbourne.

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