Intravenous trimethaphan during epidural plus general anesthesia decreases the direct radial artery pressure lower than the brachial artery pressure

Intravenous trimethaphan during epidural plus general anesthesia decreases the direct radial artery pressure lower than the brachial artery pressure

ELSEVIER Intravenous Trimethaphan During Epidural Plus General Anesthesia Decreases the Direct Radial Artery Pressure Lower than the Brachial Artery ...

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ELSEVIER

Intravenous Trimethaphan During Epidural Plus General Anesthesia Decreases the Direct Radial Artery Pressure Lower than the Brachial Artery Pressure Naoto Nagata, MD, * Mayumi Takasaki, MD,? Shoichiro Ibusuki, MDJ Masahiko Taniguchi, Osamu Kondo, MD,§ Department

*Assistant Professor +Professor and Chairman IResident $Instructor Address reprint requests to Dr. Nag&a at the Department of Anesthesiology, Miyazaki Medical College, Kiyotake, Miyazaki 889-16, Japan. Supported by a Grant-in-Aid for Clinical Investigation from the Ministry of Education, Science, Sports and Culture of Japan. Presented in part at the Annual Meeting of the Japan Society of Anesthesiology, Fukuoka, April 9-11, 1992, and Morioka, April Z-24, 1993.

of Anesthesiology,

MDJ

Miyazaki Medical College, Miyazaki, Japan

Study Objective: To determine whether vasodilators such as sodium nitropmLsside (SNP) and tm’methaphan (TMP) produce a pressure difference between the radial artery and the brachial artery during @idural @us general anesthesia or simple general anesthesia. Design: Randomized study and prospective study. Setting: Operating rooms of two hospitals. Patients: 36 and 6 adult patients in thefirst and second studies, respectively, who received spherkal acetabular osteotnmy with induced hypotensiw anesthesia. Interventions: In the first study, I8 patients received @idural plus general anesthesia ($idural group) and 18 patients received general anesthesia alone (genwal group). All patients rectiyiuedthe hy/lotensiue drqgs ji)r more than 50 minutes each. In the second .study, 6 patients rec;piuedTMPindu~ed hypotension jtir 20 minutes under e$dural plus general ane,ythe.sia. Measurements and Main Results: In thr,first skdy, radial in&a-arterial blood pru.rsuw (RIBP) and tonomettir. blood pressure (TBP) calibrated with osrillometric blood pressure of the arm were compared. In the .srcond study, RIBP and the twnrhial intro-arte-rial blood pressure (BIBP) were comfxlwd. In the first study, the bias hetwern RIBP and THPjor .systolic, mean and diastolic blood pressure WUQ.rignijkantly IQSSduring TMP-induced hypotension in the upiduralCgroup [--Il.5 + 2.5 (mean + SD), -6.0 2 3.1, and -2.8 + 3.7 mmHg, respectively] than during SNP-induced hypotension in the e@ural
Received for publication June ‘22, 1994; revised manuscript accepted for publication May 3, 199.5.

Journal of Clinical Anesthesia 8:180-187, 1996 0 1996 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010

09.52.8180/96/$15.00

SSDI 09~~-~1~0(9Fi)0019y-l)

Keywords: Anesthetic

techniques: epidural, induced hypotension; measurement techniques: blood pressure, tonometry; pharmacology: nitroprusside, trimethaphan.

Introduction During induced hypotensive anesthesia, accurate and frequent measurement of arterial blood pressure is essential because a rapid and large decrease in systemic blood pressure is detrimental to organ perfusion. Therefore, invasive pressure monitoring of the radial artery is practiced widely in hypotensire anesthesia. However, the radial artery systolic pressure is commonly higher than the aortic and brachial artery pressures because of general change in form of the pressure wave as it passes distally.‘,’ On the contrary, during induced hypotension, the direct radial artery pressure may be lower than the auscultatory or oscillometric brachial artery pressure.” Continuous epidural anesthesia results in a more stable hemodynamic pattern for patients than general anesthesia, even if strong surgical stimuli are added. Therefore, it is easy to maintain induced hypotension with a vasodilator during epidural anesthesia. However, the measurements of the radial artery systolic pressure obtained directly by arterial cannula and the brachial artery systolic pressure obtained indirectly by oscillometric or auscultatorv cuff were different.* The present study was designed to estimate whether vasodilators such as sodium nitroprusside (SNP) and trimethaphan (TMP) produce a pressure difference between the radial artery and the brachial artery during epidural plus general anesthesia or general anesthesia alone.

Materials

and Methods

We compared blood pressures of the radial and brachial arteries using initial measurements of the intra-arterial blood pressure (IBP) via the radial artery cannula and the tonometric blood pressure (TBP), periodically calibrated with the oscillometric blood pressure (OBP) of the brachial artery during controlled hypotension: SNP-induced or TMP-induced hypotension during epidural plus general anesthesia or general anesthesia alone in the first part of the study. In the second part of the study, we directly compared the radial and brachial artery blood pressures during controlled hypotension, especially TMP-induced hypotension following epidural plus general anesthesia (n = 6) to confirm the results in the first part of the study. Part 1

qf the Study

This study was approved by the Miyazaki Medical College Institutional Human Investigation Committee, and written

*Nagata N, Kawano T, Tsuneyoshi Y, Shirasaka T, Takasaki M: Pressure discrepancy between direct radial and brachial artery pressures under controlled hypotension induced by trimethaphan [Abstract], Jpn ,I Anmthesiol 1993;42:S309.

informed consent was obtained from each patient. Thirtysix adult ASA physical status I and II patients, scheduled for spherical acetabular osteotomy with induced hypotensive anesthesia were studied. Patients were randomly divided into two groups: an epidural group of 18 patients received epidural and general anesthesia and a general group of 18 patients received general anesthesia alone. Each patient had 1,000 to 1,600 ml of autologous blood stored preoperatively to avoid homologous blood transfusion. There were no differences between the right and left arm blood pressures, and no cardiovascular abnormality as assessed by physical examination, ECG or chest radiograph, was seen. Patients were predmedicated with oral brotizolam 0.25 mg 2 hours before induction of anesthesia, and hydroxyzine 25 mg, pentazocine 15 mg, and atropine 0.5 mg intramuscularly 30 minutes before induction of anesthesia. Two intravenous (IV) cannulae were placed for fluid and drug administration or blood transfusion, and a central venous catheter was inserted via the internal jugular vein for measurement of central venous pressure (CVP). Lactated Ringer’s solution was infused at a rate of 10 ml/kg/ hr using an infusion pump (Term0 STC-503, Tokyo, Japan). The hand arteries were evaluated by Allen’s test. A 22-G nontapered Teflon cannula (Term0 Surflo, Tokyo, Japan) was inserted into the left radial artery, and radial IBP (RIBP) monitoring was begun. The monitoring system consisted of the cannula, a 120 cm long, 1.5 mm internal diameter, low-compliance pressure tubing, a continuous flush device, a disposable transducer dome (Spectramed TA1015, CA) and a Gould P23XL transducer. Air bubbles were carefully flushed from the system. The natural frequency and damping coefficient of the tubing and transducer system were calculated from the ringing after a pressure transient4. The transducer was zeroed prior to measurements at 5 cm below Louis’s angle. The patient was positioned supine on an operating table. TBP was monitored on the wrist over the right radial artery using a Colin CBM-7000 tonometric instrument (Colin Electronics, Komaki, Japan). OBP was monitored on the right brachial artery to calibrate TBP automatically at 2.5-minute intervals. Both the TBP and RIBP waveforms were displayed simultaneously on a Nihonkohden BSM8500 monitor (Nihonkohden, Tokyo, Japan) and recorded simultaneously on a Nihonkohden WS-800R thermal array recorder (Nihonkohden, Tokyo, Japan) at a scale of 5 mmHg/cm and at a speed of 2.5 cm/set. A catheter was inserted into the epidural space and advanced 2.5 cm upward at the Ls-I,, interspace. According to age and height, 10 to 15 ml of 2% mepivacaine solution without epinephrine was injected as an initial volume 5 minutes after injection of 3 ml of a test dose in the epidural group. The upper level of analgesia extended on average to Ts 15 minutes after the initial injection, as assessed by pin-prick. After this, 2% mepivacaine was infused continuously through the epidural catheter at a rate of 8 to 10 ml/hr using a syringe infusion pump (Termo STC525, Tokyo, Japan), to avoid fluctuation of blood pressures and excess elevation of the blood mepivacaine concentraJ. Clin. Anesth., vol. 8, Mav 1996

181

Table 1. Patient Characteristics in Part 1 of the Study Epidural group (n = 18)

General group (n = 18)

37k8 15:3 157 f 8 54&8

42fll 1.5:3 151 i 6 51 f6

Age W Gender (F:M) Height (cm) Weight (kg) Values are means i SD.

tion.” In the general group, an epidural catheter was used after this investigation for postoperative pain relief. General anesthesia was induced with thiamylal 5 mg/ kg, and vecuronium 0.15 mg/kg was given to facilitate tracheal intubation in all patients. Anesthesia was maintained with 67% nitrous oxide (NZO) in oxygen (0,) following IV injections of diazepam 10 mg and pentazocine 15 mg in the epidural group. In the general group, anesthesia was maintained with 1.5% to 2 % enflurane and 67Yo N,O in 0,. Ventilation was controlled using a volume-cycled ventilator (Ohmeda 7000, Ohmeda, Madison, WI) with a tidal volume of 6 ml/kg and an I/E ratio of 0.5 at a rate of 10 to 15/min, to maintain normocapnia as determined by capnography (Ohmeda 5200). ECG, heart rate, RIBP, TBP, CVP, hemoglobin oxygen saturation, and rectal temperature were monitored using a Nihonkohden BSM-8500, and urinary volume was measured every hour. Hypotension was started before surgery and continued until the end of surgery. Mean RIBP was reduced to 50 to 70 mmHg by continuous IV infusion of SNP (0.5 to 1.0 pg/kg/min) in nine patients of each group and in the other nine patients by continuous infusion of TMP (10 to 60 pg/kg/min) using a syringe infusion pump (Term0 STC-525, Tokyo, Japan), and it was maintained at this level for more than 50 minutes. Mean RIBP was returned to 75 to 85 mmHg by discontitruation of SNP or TMP, and then

oscillometric measurement

sl

G

2 5

3 5

%

the hypotensive drugs were exchanged for induction of hypotension for another 50 minutes. All patients received both hypotensive drugs. After induction of general anesthesia and at 5-minute intervals during SNP-induced and TMP-induced hypotension, systolic, mean, and diastolic RIBP and TBP were recorded simultaneously for 30 seconds immediately following oscillometric calibration of TBP, and measured with three consecutive beats of the pressure waveforms obtained from each record. Mean pressure was taken as the electronically integrated mean determined by the monitor. Comparisons of RIBP and TBP variables were made for each patient during the normotensive period immediately after induction of general anesthesia, and for the SNPinduced and TMP-induced hypotensive periods in each group. The bias and precision were calculated for systolic, mean, and diastolic pressures of RIBP, with TBP used for the reference values, and were averaged to give the mean bias and precision during each hypotension. The differences in bias and precision among the four hypotensive periods of the two groups were compared using one-way analysis of variance and, where appropriate, the TukeyKramer test. Comparisons of patient characteristics and others between the two groups were analyzed by Student’s t-test for unpaired data. A p-value less than 0.01 was COIIsidered statistically significant. Data were expressed as means * SD.

Part 2 of the Study After obtaining approval from the Clinical Investigation Committee of Nichinan Prefectural Hospital and written informed consent from each patient, 6 ASA physical status I patients (5 females and 1 male) scheduled for spherical acetabular osteotomy with induced hypotensive anesthesia were enrolled in the study. Patients with a history or sign of cardiovascular abnormality were excluded from the

waiting for calibration of

TBP

RIBP

z o-

o-

CVP

Figure 1. The radial intra-arterial blood pressure(RlBP) and tonometric blood pressure (TBP) tracings recorded at a scale of 25 mmHg/cm for publication. Top: after induction of epidural and general anesthesia. Bottom: during trimethaphan-induced hypotension under epidurdl and general anesthesia. 182

J. (Xn. Anesth., vol. 8, May 1996

Hood presswe during rontrobd hypotenrion: Nagata it al.

study. Each patient had 1,400 to 1,600 ml of autologous blood stored preoperatively. There was no difference between the right and left arm blood pressures. Before induction of anesthesia they received the same drugs as in the first part of the study. Epidural and general anesthesia was induced and maintained with the same procedures as in the first part of the study. The hand arteries were evaluated by Allen’s test. Two 22-G nontapered Teflon cannulae (Term0 Surflo, Tokyo, *Japan) were inserted into the left radial artery and the right brachial artery. The same monitoring system used in the first part of the study was used for measurements of RIBP and brachial IBP (BIBP). Both the RIBP and BIBP waveforms were displayed simultaneously on a Nihonkohden BSM-8500 monitor (Nihonkohden, Tokyo, Japan), and the digital values of systolic, mean, and diastolic RIBP and BIBP were continuously recorded in a computer (Epson PC386IS, Tokyo, .Japan) for 20 minutes during normotension and for 20 minutes during hypotension. After these recordings were taken, to increase peripheral vascular resistance in the hand, the fingers of the left hand that was used for RIBP measurement were doubled up by one of the investigators into a fist with a thumb folded inside, and the RIBP and BIBP waveforms were recorded simultaneously. Hypotension was induced by continuous intravenous infusion of TMP (10 to 60 pg/kg/min) using a syringe infusion pump (Term0 STC-525, Tokyo, Japan) and maintained at mean RIBP of 50 to 70 mmHg. ECG, heart rate, RIBP, BIBP, CVP, hemoglobin oxygen saturation, and rectal temperature were monitored, and urinar), volume was measured. The digital values of the pressure data were collected at lo-second intervals. The bias and precision were calculated for each patient for systolic, mean, and diastolic pressures of RIBP, with BIBP used for the reference values. Statistical comparisons between the normotensive and hypotensive periods were performed by Student’s t-test for unpaired data. A p-value less than 0.01 was considered statistically significant. Data were expressed as means T SD.

significant differences between the two groups in patient characteristics (‘li~hk 1). The infusion rate of TMP was significantly higher in the epidural group (155 + 77 pg/kg/min) than in the general group (18 f 17 pg/kg/ min; p < 0.001). The infusion rate of SNP was higher in the general group (1.36 + 1.47 pg/kg/min) than in the epidural group (0.48 f 0.33 pg/kg/min) but the difference was not significant. Mean RIBP during controlled hypotension induced by SNP and TMP in the epidural group were 55.2 f 6.3 mmHg and 56.2 * 6.2 mmHg, and in the general group were 59.3 i 6.2 and .57.7 f 6.0 mmHg, respectively. Fipw 1 shows typical tracings. As shown in the top tracing, the patient’s RIBP and TBP were similar after induction of epidural and general anesthesia. After TMPinduced hypotension, however, the patient’s RIBP was lower than TBP, as shown in the bottom tracing. During the normotensive period immediately after induction of general anesthesia, the mean bias between RIBP and TBP for systolic, mean, and diastolic pressures were 1.0 ? 2.9 mmHg, -0.6 * 2.3 mmHg, and -1.5 * 3.0 mmHg in the epidural group and -1.9 + 1.9 mmHg, -0.5 * 2.9 mmHg, and 0.2 f 4.4 mmHg in the general group, respectively. The mean precisions for systolic, mean, and diastolic pressures were 3.2 ? 1.4 mmHg, 3.2 f 1.6 mmHg, and 3.3 + 1.4 mmHg in the epidural group and 2.3 f 1.9 mmHg, 3.2 f 2.8 mmHg, and 2.4 f 1.7 mmHg in the general group, respectively. During the hypotensive periods, the mean bias for systolic, mean, and diastolic pressures were significantly less during TMP-induced hypotension in the epidural group than during SNP-induced hypotension in the epidural group and SNP- and TMP-induced hypotension in the general group (p < 0.01; 7i& 2). The differences in systolic, mean, and diastolic pressures between RIBP and TBP are shown in Fiff-lrrs 2, 3, rind 4, respectively. The mean precisions for systolic and mean pressure were significantly greater during TMP-induced hypotension in the epidural group than the other three hypotension groups (p < 0.01). no

Results Part I of thP Stu&

Part 2 of the Study

The natural frequency of the tubing system was 21.3 + 3.6 Hz and damping coefficient was 0.43 & 0.11. There were

The age of patients was 41 f 11 years. Weight and height were 49 + 4 kg and 155 f 3 cm, respectively. Hemoglobin

Table 2.

Bias aud Precision in Part 1 of the Study Epidural

Group

Nitroprwside

General Group Trimetbaphan

Nitroprusside

Trimethaphan

(n = 378)

(n = 378)

(n = 378)

(n = 378) Systolic

Mean

Diastolic

Systolic

Mean

Diastolic

Systolic

Mean

Diastolic

Systolic

Mean

Diastolic

Bias (nunHg) -2.3+2.2 -0.3+1.3 0.7+1.6 -11.5*2.:i* -(i.o+3.1* -2.8k3.7” -3.1 + 1.6 1.7+‘L.7 4.1 y4.7 -5.4*2,7 ().:2&2,‘3 “,,3*:3,4 Prrcision (~nrnHg) 3.7 * 1.8 2.8 f I .4 9.4 + 1.5 11.8 i- 2.Y’ 7.1 + 1.9” .5.6k 2.3 3.1 k 1.FJ 3.4 + 1.5 .‘.3 * 2.5 3.5 * 1.7 3.3 f 1.3 4.8 k 2.0 “/J < 0.01 rompared with other three hypotension groups. N’otr: Data nrr ulrar~s i SD. 183

Origkl

Contributions

%‘-3f)

50

I

I

I

I

60

70

80

90

1

100

110

50

systolic RIBP(mmHg)

60

70

60

!3’0

80

90

80

3

mean RIBP(mmHg) I

r: : 0 k ii -10 z g-a lz P-30 50

E 60

70

60

90

100

110

systolic RIBP(mmHg)

60

sys:oqic RlEZ(mmH”g~

0

! 40

50

60

70

mean RIBP(mmHg)

5;

u) -30 50

-30

100

10

‘E g -2oE -30 I 40

50

60

70

mean RIBP(mmHg) Figure 2. Scatterplots of systolic RIBP and RIBP-TBP in the first part of the study (RIBP =radial intra-arterial blood pressure, TBP =tonometric blood pressure). The solid horizontal line indicates zero. Top: nitroprusside-induced hypotension under epidural plus general anesthesia. Middle: trimethaphan-induced hypotension under epidural plus general anesthesia. Bottom: trimethaphan-induced hypotension under general anesthesia.

concentrations before surgery were more than 10 g/d1 in all patients. Mean RIBP during hypotension was 58.6 f 7.8 mmHg. The mean bias for systolic, mean, and diastolic pressures were significantly less (p < O.Ol), and the mean precisions for systolic, mean, and diastolic pressures were significantly greater during hypotension than during normotension (p < 0.01; Table 3). The differences between RIBP and BIBP are shown in Figure 5. Clenching patient’s fist increased systolic RIBP during TMP-induced hypotension, and then as shown in Figure 6 the pressure differences disappeared.

Discussion This study demonstrated that the direct radial artery systolic and mean pressures were lower than the brachial 184

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Figure 3. Scatterplots of mean RIBP and RIBP-TBP in the first part of the study (RIBP = radial intra-arterial blood pressure, TBP = tonometric blood pressure). The solid horizontal line indicates zero. Top: nitroprusside-induced hypotension under epidural plus general anesthesia. Middle: trimethaphan-induced hypotension under epidural plus general anesthesia. Bottom: trimethaphan-induced hypotension under general anesthesia. artery systolic and mean pressures during TMP-induced hypotension following epidural plus general anesthesia. The mean bias was negative and precisions were great during hypotension in the second part of the study, and the same results were observed during TMP-induced hypotension in the epidural group in the first part of the study. Arterial tonometry for noninvasive measurement of arterial blood pressure is not popular. The principle and instruments of arterial tonometry have been reviewed.’ TBP measured on the radial artery is calibrated using oscillometric measurements on the brachial artery. Using an arterial tonometer in a stable hemodynamic state, it would be possible to noninvasively obtain an accurate representation of the beat-to-beat brachial artery pressure without cannulation into the brachial artery. During normotension after induction of general anesthesia, the mean bias

E:: ?$

-5

g-15 5 -25 2 -35

40 diastoli%BP(m%ig)

30

70

80

I 70

I 80

925 E 15 E5 ? 2

-5

E-15 P 2 -25 5I -35

*O

1

I

30

i:;=j

,

30

40

I

,

,

50

60

70

g-10

1

0

3 5 -20

80

20

diastolic RIBP(mmHg) Figure 4. Scatterplots of diastolic RIBP and RIBP-TBP in the first part of the study (RIBP = radial inn-a-arterial blood pressure, TBP = tonometric blood pressure). The solid horizontal line indicates zero. Top: nitroprusside-induced hypotension under epidural plus general anesthesia. Middle: trimethaphan-induced hypotension under epidural plus general anesthesia. Bottom: trimethaphan-induced hypotension under general anesthesia.

for systolic pressure was 1.0 and -1.9 mmHg, and that for mean pressure was -0.6 and -0.5 mmHg, in the epidural and general groups, respectively. The differences between RIBP and TBP were very small. Kemmotsu et al.’ reported that the errors in absolute mean values of TBP in systolic,

Table 3.

30

40 50 60 diastolic RIBP(mmHg)

70

80

5. Scatterplots of RIBP and RIBP-BIBP in the second part of the study (RIBP = radial intraarterial blood pressure, BIBP = brachial intra-arterial blood pressure). Top: systolic pressure. Middle: mean pressure. Bottom: diastolic pressure.

Figure

mean, and diastolic measurements ranged from 3.9 to 6.6 mmHg compared with RIBP, which was used as a reference. In our results, there is doubt as to whether the small bias of -2.8 mmHg between RIBP and TBP in the diastolic pressure in the first part of the study are true or due to error in measurement. However, there is no doubt about the large bias of -11.5 and -6.0 mmHg in the systolic and mean pressures, respectively, during TMP-induced hypo-

Bias and Precision in Part 2 of the Study Hypotension (n = 720)

Nomotemion (n = 720)

Bias (mmHg) Precision (mmHg)

Systolic

Mean

-1.2 f 0.7 1.6*0.6

-2.4 k 0.4

1.6f0.6

Diastolic -2.1 k 0.5 2.2 f 0.6

systolic

Mean

Diastolic

-6.4 If: 1.8* 6.5 k 1.6*

-5.2 k 1.1* 5.1 + 1.1*

-3.4 f 0.9* 3.5 f 0.9*

*p < 0.01 compared with normotension. Note: Data are means f SD. J. Clin. Anesth., vol. 8, May 1996

185

Original Contributzons

O-

Figure 6. The radial and brachial intra-arterial blood pressure (RIBP and BIBP) tracings taken from a patient during trimethaphan-induced hypotension under epidural plus general anesthesia in the second part of the study. The increase in pulse pressure of RIBP shown in the middle of the figure corresponds to clenching a list.

tension in the epidural group in the first part of the study. We measured RIBP via the cannula placed in the left radial artery, TBP on the right radial artery, and BIBP via the cannula placed in the right brachial artery. No differences between right and left arm blood pressures were observed before commencing the study. Furthermore, after induction of general anesthesia in both parts of the study, no significant differences were found between the RIBP and TBP values, although there were small differences of 1 to 2 mmHg during normotension. Goh et al.” reported that the mean systolic value of RIBP via a radial artery cannula was 4.2 mmHg lower than that of OBP measured on the brachial artery during hypotension with systolic blood pressure below 90 mmHg. This difference is close to the result found in this study, except for the data obtained following TMP-induced hypotension in the epidural group. Recently, Kemmotsu et al.* studied the relation between RIBP and TBP during nitroglycerin-induced hypotension following general anesthesia. However, it is difficult to compare nitroglycerin-induced hypotension in their study with SNP- or TMP-induced hypotension in the general group of our study. The mechanism involved in pressure discrepancy between the radial and brachial arteries was not investigated in this study; however, we hypothesize the following mechanism. The peripheral circulation is controlled by a change in sympathetic tone that alters the vasoconstrictor tone.” The change in blood flow in the hand occurs mainly in skin, and that in the forearm occurs mainly in muscle.“’ The resting vasoconstrictor tone is high in the hand and low in the forearm.” The vasodilator response that releases the resting vasoconstrictor tone is large in regions where the vasoconstrictor tone is known to be high.” SNP directly dilates arteries and veins but TMP dilates blood vessels indirectly by blocking ganglions in the sympathetic nerarteriolar resistance devous system.’ ’ The peripheral creases largely in the hand with high vasoconstrictor tone compared with the low vasoconstrictor tone of the forearm. Clenching a fist increased peripheral vascular resistance, thus restoring the pressure discrepancy, as seen in the second part of our study. In the epidural group of this study, the level of sympa-

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thetic nerve block would be T,, because the level of analgesia was T,.” The sympathetic nerves to the upper extremities remained intact. Epidural anesthesia leads to blood pooling in the denervated lower extremities but leads to reflex-vasoconstriction in the innervated arm.“‘-‘5 Our study showed that TMP was used at larger doses in epidural plus general anesthesia than in simple general anesthesia. We hypothesized that a large amount of TMP was required to dilate blood vessels constricted by the overactivated sympathetic nerve, although tachyphylaxis of TMP was also considered. The vasodilator response would be strong at regions of high vasoconstrictor tone, as in the hand; therefore, the peripheral arteriolar resistance may decrease markedly in the hand compared with the forearm, and a large discrepancy between the direct radial and direct or oscillometric brachial artery pressures may occur with TMP-induced hypotension following epidural plus general anesthesia. However, in our study, no increase in the infusion rate of SNP and no large discrepancy between RIBP and TBP were observed during SNP-induced hypotension in the epidural group. We could not speculate as to the mechanism, but the difference between SNP and TMP in the epidural group would be due to direct and indirect actions of vasodilators. At the end of cardiopulmonary bypass (CPB), systolic and mean IBP are lower in the radial artery than in the aorta, femoral, or brachial hyartery. I’-” Our results obtained during TMP-induced potension following epidural plus general anesthesia may be similar to pressure discrepancy seen after CPB, as indicated by Pauca et nL” In this study, we induced controlled hypotension with epidural anesthesia with the analgesic level of T,. If the high level of sympathetic nerve block was produced by epidurdl anesthesia, induced hypotension would be easily maintained with a small dose of vasodilators. However, compensatory responses to hemorrhage are not enough during widespread epidural anesthesia.“’ Therefore, epi&u-al anesthesia should be limited segmentally to the field of surgery. III conclusion, in the patients who received epidural plus gerreral anesthesia, TMP markedly lowers the direct radial artery systolic and mean pressures compared with the brachial artery systolic and rnean pressures.

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