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Canadian Journal of Anesthesia 53:139-145 (2006)
© Canadian Anesthesiologists' Society, 2006
Regional Anesthesia and Pain

Similar incidence of hypotension with combined spinal-epidural or epidural alone for knee arthroplasty

[L’anesthésie rachidienne et péridurale combinée, et péridurale seule, ont une incidence similaire d’hypotension lors de l’arthroplastie du genou]

Tiberiu Ezri, MD*,{dagger}, Islam Zahalka, MD{ddagger}, Deeb Zabeeda, MD*, Zeev Feldbrin, MD{ddagger}, Alexander Eidelman, MD{ddagger}, Reuven Zimlichman, MD§,¶, Benjamin Medalion, MD{square} and Shmuel Evron, MD*,{dagger}

* From the Departments of Anesthesia,
{ddagger} Orthopedics,
§ Internal Medicine,
Brunner Institute for Cardiovascular Research, and
{square} Cardiothoracic Surgery, the Edith Wolfson Medical Center, Holon, Affiliated to Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel; and the
{dagger} OUTCOMES RESEARCHTM Institute, University of Louisville, Kentucky, USA.

Address correspondence to: Dr. Tiberiu Ezri, Head, Department of Anesthesia, the Edith Wolfson Medical Center, Holon 58100, Israel. Phone: 972-3-5028229; Fax: 972-3-5028218; E-mail: tezri{at}netvision.net.il. On the world wide web: www.or.org.


   Abstract
TOP
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Background: We hypothesized that the incidence of hypotension during total knee replacement (TKR) surgery is lower in patients given combined spinal-epidural (CSE) anesthesia vs those receiving epidural anesthesia alone.

Methods: In a prospective study, 80 American Society of Anesthesiologists I–II patients (aged 40–80 yr), undergoing elective TKR surgery were randomly assigned to either CSE anesthesia (CSE, n = 40) or epidural anesthesia alone (Epidural, n = 40). Hemodynamic measurements included oscillometric mean arterial blood pressure (MAP), heart rate (HR), and cardiac index (CI) as determined by thoracic bioimpedance; systemic vascular resistance (SVR) was calculated. Our primary endpoint (outcome) was the number of hypotension episodes (defined as MAP < 70 mmHg).

Results: Using univariate analysis, we found no differences between the groups in regards to MAP, HR, CI, or SVR during the perioperative period. The incidence of hypotension was similar in both groups (two patients in each group), as was the incidence of bradycardia (12 patients in CSE, 7 in Epidural; P = 0.2). There were no differences between groups in other hemodynamic measurements including CI and calculated SVR. Analgesia supplementation with fentanyl was more frequently required in the Epidural group (20 vs 6 patients – P = 0.03).

Conclusion: Combined spinal-epidural anesthesia and epidural anesthesia alone during TKR surgery are associated with the same incidence of hypotension with statistically and clinically similar hemodynamic responses.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
NEURAXIAL anesthesia techniques for major lower extremity surgery include epidural anesthesia alone, spinal anesthesia alone, or the combination of spinal and epidural anesthesia. Analgesia and surgical conditions provided by spinal anesthesia alone or combined spinal-epidural (CSE) anesthesia are superior to those provided by epidural anesthesia alone.1,2 Combined spinal-epidural anesthesia compared to epidural or spinal anesthesia alone produces superior muscle relaxation, improved sensory block3,4 and also, fewer hypotensive episodes have been claimed for CSE.5

Patients undergoing total knee replacement (TKR) are usually elderly and they often have concomitant diseases which compromise cardiovascular stability. Regional anesthetic techniques are most commonly used for TKR. The cardiovascular effects of epidural anesthesia are complex and predominantly related to the level of analgesia and dose of local anesthetic. The pharmacological effect of systemically absorbed local anesthetic drugs, inclusion of epinephrine in the local anesthetic solution, extent of sympathetic denervation, autonomic system impairment, baseline blood volume, and preanesthetic cardiovascular function of the patient are also important factors.6,7 About 18% of patients develop hypotension during epidural anesthesia8 and 30% during spinal anesthesia.9

Previous studies reported that women undergoing Cesarean delivery under CSE anesthesia (targeting a T4 sensory level) suffered less hypotension than those receiving epidural or spinal anesthesia alone.3,5 We therefore tested the hypothesis that during TKR surgery the incidence of hypotension is lower in patients given CSE anesthesia than those receiving epidural anesthesia alone.


   Methods
TOP
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
With approval of our Institutional Review Board and written informed consent, we recruited 80 American Society of Anesthesiologists Physical Status I–II patients, aged 40–80 yr, scheduled for primary elective TKR. We excluded patients in whom regional anesthesia was contraindicated (coagulopathy, infection at the puncture site) and patients with a history of congestive heart failure and/or an ejection fraction < 50% (per echocardiography, if available). Medications that could have altered coagulation and/or hemostasis were stopped.

Protocol
No preoperative anxiolytic medication was administered, but patients continued their routine medications. Participating patients were randomly allocated to receive either CSE anesthesia (CSE group) or epidural (Epidural group). Randomization was based on computer-generated codes that were maintained in sequentially numbered opaque envelopes. Before starting anesthesia, all patients received lactated Ringer’s solution (500 mL over 20 min) heated to 37°C. Regional anesthesia was performed with patients in the sitting position at the L3–L4 or L2–L3 interspace. As per protocol, the first interspace chosen was L3– L4. If the attempt at this level failed, the L2–L3 level was the next choice.

The lumbar space was assessed by visual inspection. Epidural anesthesia was performed with an 18-G Tuohy needle and 20-G catheter (Braun, Melsungen AG, Germany). The CSE was performed with an 18-G epidural needle, 20-G multiport catheter, and a 27-G pencil point spinal needle (Braun, Melsungen AG, Germany). The needles were inserted with the aperture oriented cephalad. Epidural anesthesia was induced with 0.5% bupivacaine as a 5-mL bolus followed by 5 mL every five minutes for a total of 20 mL. Combined spinal-epidural anesthesia was induced with 2 mL isobaric spinal bupivacaine 0.5%, followed by an epidural supplemental dose of 5 mL of bupivacaine 0.5%, 15 min after the spinal injection. The doses of local anesthetics were chosen from previously published studies for both epidural10 and CSE.11 However in our study, the recommended spinal dose was reduced by a third (from 15 to 10 mg), as a lower block height was required.

In both groups, hypotension [mean arterial blood pressure (MAP) < 70 mmHg] was treated with a bolus of 200 mL of Lactated Ringer’s solution. If the hypotension persisted for > five minutes, 5 mg ephedrine was given intravenously. Bradycardia [heart rate (HR) < 50 beat·min–1] was treated with 0.5 mg iv atropine. Throughout surgery, fluids were given at a rate of 10 mL·kg–1·hr–1. Just before releasing the tourniquet, a 200-mL bolus of lactated Ringer’s solution was infused rapidly. Patients were warmed with forced-air and fluids were infused at 37°C. The urinary bladder was catheterized in every patient. Tourniquets [with inflation pressures individualized to systolic blood pressure (SBP) plus 100 mmHg] were used in all cases, and all prostheses were cemented.

The sensory level, measured with a pinprick, was assessed every five minutes during the first 30 min of anesthesia, and subsequently every 15 min. The highest sensory level was also recorded. With a two-segment sensory block regression, 5 mL of 0.5% bupivacaine was administered epidurally to patients in both groups. Patients who expressed discomfort because of the tourniquet, were given 50 µg iv fentanyl and 1 mg iv midazolam. Postoperative analgesia was provided by a continuous epidural infusion of 6 to 10 mL·hr–1 of 0.2% ropivacaine. The infusion of epidural ropivacaine for postoperative analgesia was started after the patient regained full motor strength as determined by a modified Bromage scale score of 0. Motor block was assessed using a modified Bromage scale (0 = no motor block, 1 = inability to raise extended legs, 2 = inability to flex knees, and 3 = inability to flex ankle joints).12

Measurements
Morphometric and demographic characteristics of the patients were recorded. Motor block level was recorded every five minutes after induction of anesthesia for the first 30 min, and then every 15 min during and after surgery until full motor strength was regained. The sensory level was assessed bilaterally, in the mid-clavicular line. We recorded the time to readiness for surgery (sensory level at T10 or higher), time to two-segment sensory regression, the duration of surgery, the duration of tourniquet inflation, and time from the end of surgery until the postoperative analgesic epidural infusion was begun. The number of patients who required top-ups, the total number of top-ups and the sensory level 15 min after top-up administration was also recorded.

Our primary endpoint (outcome) was episodes of hypotension, which we defined as MAP < 70 mmHg. A secondary endpoint was the number of bradycardic episodes, defined as HR < 50 beat·min–1. The rational for choosing our primary endpoint was the following: an MAP of < 70 mmHg was chosen as a primary endpoint since this pressure is the lower limit for brain autoregulation (this lower limit has nevertheless, a considerable interindividual variation).13 A HR < 50 beat·min–1 was taken as another endpoint, as this HR is considered a risk factor for the development of cardiac arrest during regional anesthesia.14

Mean arterial pressure, SBP, diastolic blood pressure and HR were measured oscillometrically (AS/5TM, Datex- Ohmeda Division, Anaesthesia Monitor, Instrumentarium Corp., Datex-Ohmeda, Helsinki, Finland). Cardiac index was determined using thoracic bioimpedance readings (BoMed® Medical MFG. Ltd, Model NCCOM3, Irvine, CA, USA). Blood pressure and HR were recorded before starting anesthesia (baseline) and at five-minute intervals throughout surgery. Cardiac index was measured before starting anesthesia (baseline), every five minutes after initiation of the block for the first 30 min, and every 30 min afterwards. In addition, hemodynamic values were recorded after the skin was being closed, before tourniquet release, ten minutes after tourniquet release, and one hour after arriving in the recovery room. Systemic vascular resistance (SVR) was calculated using the standard formula.15

The total amount of local anesthetic was recorded, as was the number of patients who required epidural top-up, atropine, or ephedrine. The amount of fluid and blood infused, urinary output, and the estimated blood loss were also recorded. Arrhythmias (defined as runs of ventricular tachycardia, ventricular fibrillation, paroxysmal supraventricular tachycardia, atrial fibrillation, or cardiac arrest) were recorded, as were cardiovascular complications (intraoperative ischemia and myocardial infarction). Intraoperative myocardial ischemia was defined as a new 2-mm segment (ST) depression or new 1-mm ST elevation on an automatic ST analyzer (AS/5TM, Datex- Ohmeda Division, Anaesthesia Monitor, Instrumentarium Corp., Datex-Ohmeda, Helsinki, Finland). The total number of patients who received fentanyl and midazolam and the total dose of fentanyl were also recorded. Investigators blinded to the anesthetic technique recorded all measurements.

Data analysis
Our hypothesis was that during TKR surgery the incidence of hypotension is lower in patients given CSE anesthesia than those receiving epidural anesthesia alone. Our primary endpoint for sample size calculation was the incidence of hypotension episodes (MAP < 70 mmHg). In a pilot study of 20 patients (ten per group) we found an incidence of hypotension (MAP < 70 mmHg) of 10% in the CSE group and 40% in the Epidural group (a difference of 30%). Therefore, we considered clinically significant any difference between the groups ≥ 30%. Based on this assumption we calculated that the sample size needed to achieve a power of 80% with a two-sided {alpha} of 0.05, using the binomial approximation to normal distribution, was 40 patients per group.

Data were evaluated for normal distribution using the Kolmogorov-Smirnov test. Continuous variables with normal distribution were compared with the Student’s t test and those with distribution significantly differing from normal were compared using the Mann-Whitney U or median tests. Categorical data were described using frequency counts and percentages and compared using Chi-square (with Yates correction) or Fisher’s exact tests, as appropriate. The two groups were compared with univariate analysis.

Data analysis was performed using the SPSS for Windows (SPSS Inc, Chicago, IL, USA). Results are presented as means ± standard deviations; P < 0.05 was considered statistically significant.


   Results
TOP
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
No patient required general anesthesia due to failure of neuraxial block and no patient was excluded at any stage of the study. Morphometric and demographic characteristics of the patients were similar in both groups (Table IGo). There were also no differences in the surgical management of the groups. Injection site was L3–L4 in 80% of the CSE group and in 75% of the Epidural group. Tourniquet time was 130 ± 20 min in the CSE group and 136 ± 15 min in the Epidural group. The time to two-segment regression was 120 ± 20 min and 132 ± 22 min in the CSE and Epidural groups, respectively. The time to start of the postoperative epidural infusion of local anesthetic (measured from the end of surgery) was 95 ± 10 min in the CSE and 70 ± 7 min in the Epidural group (P = 0.10). Blood loss (from the tourniquet release to the end of surgery) was 130 ± 30 mL and 150 ± 50 mL, in the CSE and Epidural groups, respectively. No patient required a blood transfusion during the study period.


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  		TABLE I Morphometric and demographic characteristics and anesthetic management
 
The modified Bromage scores were significantly greater in patients receiving CSE 15 min after induction, at the end of surgery, and one hour after surgery. Patients given CSE were ready for surgery faster than those given epidural anesthesia alone (Table IGo). The number of patients requiring top-ups, total number of top-ups and sensory levels following top-ups (in patients who received them) were similar.

There were no statistically significant or clinically important differences between the groups with regard to MAP, HR, cardiac index, or SVR (Table IIGo). More patients in the Epidural group required fentanyl boluses (P = 0.03, Table IIIGo), while the total mean dose of fentanyl was 300 ± 50 µg in the CSE group and 1000 ± 100 µg in the Epidural group. The number of patients who developed bradycardia (e.g., HR < 50 beat·min–1) did not differ significantly between the groups (Table IIIGo). Five patients in the CSE group and six in the Epidural group received ß-blockers pre-operatively. The number of patients requiring atropine was similar for both groups. Only two patients in each group had an episode of hypotension (MAP < 70 mmHg), (Table IIIGo). Tourniquet inflation and deflation had no statistically significant impact on any of the hemodynamic variables. There were no intraoperative or postoperative complications in either group.


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  		TABLE II Hemodynamic measurements
 

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  		TABLE III Principal result
 

   Discussion
TOP
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Contrary to our primary hypothesis, our results showed that CSE anesthesia and epidural only anesthesia during TKR surgery are associated with a comparable incidence of hypotension.

Our findings contrast with previous studies in women undergoing Cesarean delivery under CSE anesthesia who experienced less hypotension than those given epidural or spinal anesthesia alone.3–5 The results may have differed due to the absence of pregnancy-specific changes including aortocaval compression, and also due to the fact that the mean highest sensory block achieved in our patients was different from that required to achieve analgesia for Cesarean section (T4).

The absence of hemodynamic changes in both groups may be explained by the relatively low dose of plain bupivacaine used in the spinal phase of CSE, and by the gradual administration of local anesthetics in the Epidural group. The small amount of local anesthetic injected into the subarachnoid space of patients in the CSE group may have ameliorated the hemodynamic changes that are common with spinal anesthesia, secondary to rapid and extensive sympathetic block. Indeed, there were no statistically significant or clinically important differences in MAP between groups or within each group at different time points.

Major factors related to the level of spinal anesthetic block include baricity of the anesthetic solution, patient position, and the dose of local anesthetic.16 Considering that the extent of sympathetic blockade with the resultant hemodynamic changes is correlated with the sensory level of the block, and that with hyperbaric solutions this latter factor is not influenced by the dose of the local anesthetic,17 it would not be expected that changes in the dose of spinal hyperbaric anesthetic will affect the hemodynamic responses.3–5 However, this may not be true for isobaric local anesthetics, the type of solutions used in our study. Furthermore, Carpenter et al.18 demonstrated that a major determinant of spinal block is the volume of cerebrospinal fluid (CSF). With a given volume of CSF, the dose of local anesthetic injected within this CSF volume will influence the spinal block characteristics. Moreover, a change in the dose of epidurally administered local anesthetic would affect the sensory level, and therefore the extent of hemodynamic changes recorded. Further studies are warranted to investigate the hemodynamic effects with different doses of local anesthetics.

We used bioimpedance cardiography to investigate non-invasively the mechanisms of changes in MAP and HR with the two anesthetic techniques. Thoracic bio-impedance (impedance cardiography) is a non-invasive technique that measures changes in the transthoracic electrical impedance induced by ejection of blood into the thoracic ascending aorta.19 Bioimpedance is a useful technique for non-invasive hemodynamic monitoring in regional anesthesia.20,21 The bioimpedance method has been validated with the dye dilution technique during epidural or general anesthesia for Cesarean section. Milsom et al.22 showed that there was no significant difference between the mean changes in stroke volume determined by the two techniques during serial measurements. Impedance cardiography was found to be a safe, reliable, non-invasive technique for the measurement of changes in stroke volume during Cesarean section.

The number of episodes of bradycardia was similar in the two groups (Table IIIGo). The CSE group did not require more atropine than did the Epidural group. However, patients having spinal anesthesia tend to develop bradycardia and in rare cases - an incidence of 2.7 to 2.9 per 10,00023,24 - cardiac arrest, for several reasons. One of the possible mechanisms may be a reflex bradycardia, possibly associated with low right-sided cardiac filling pressures.25 Although this phenomenon may occur during both types of neuraxial anesthesia, it is possibly more common during spinal anesthesia.24,26–28 Predisposing conditions that increase the risk of bradycardia with regional anesthesia include low baseline HR and vagal predominance.29 Prompt augmentation of central venous filling with iv fluids, and potent {alpha}-agonists and positional change may improve organ perfusion28,29 and eventually prevent progression to cardiac arrest. We speculate that the reason for the lack of difference in the incidence of bradycardia in the CSE patients may have been the use of relatively low doses of local anesthetics.

Tourniquet release may lead to serious hemodynamic fluctuations. In one study, the blood pressure measured up to 30 min after release of a pneumatic thigh tourniquet was decreased.30 We found no significant changes in any hemodynamic variable upon the tourniquet release in either group. As we measured blood pressure non-invasively, it is possible that transient episodes of hypotension after tourniquet release were not documented. However, it is unlikely that such short episodes would be of any clinical concern.

Tourniquet pain occurs less frequently with intense regional anesthesia (i.e., spinal block), but the incidence may be up to 30% during epidural anesthesia with bupivacaine 0.5% with epinephrine.31 A greater number of Epidural patients experienced some pain or discomfort related to the tourniquet, and required more fentanyl administration (P = 0.03 when compared to CSE). Although half of the Epidural patients received iv fentanyl supplementation (a total dose of 1,000 µg) this probably did not contribute to the development of bradycardia in this group of patients, considering that CSE patients received less than a third of this fentanyl dose (300 µg).

We conclude that CSE anesthesia and epidural anesthesia alone are associated with a comparable incidence of hypotension during TKR, with statistically and clinically similar hemodynamic responses.


   Footnotes
 
Accepted for publication July 20, 2005. Revision accepted September 1, 2005.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
1 Rawal N, Holmstrom B, Crowhurst JA, Van Zundert A. The combined spinal epidural technique. Anesthesiol Clin North America 2000; 18: 267–95.[Medline]

2 Holmstrom B, Laugaland K, Rawal N, Hallberg S. Combined spinal epidural block versus spinal and epidural block for orthopaedic surgery. Can J Anaesth 1993; 40: 601–6.[Abstract/Free Full Text]

3 Rawal N, Schollin J, Wesstrom G. Epidural versus combined spinal epidural block for Cesarean section. Acta Anaesthesiol Scand 1988; 32: 61–6.[Medline]

4 Rawal N, Van Zundert A, Holmstrom B, Crowhurst JA. Combined spinal-epidural technique. Reg Anesth 1997; 22: 406–23.[Medline]

5 Thoren T, Holmstrom B, Rawal N, Schollin J, Lindeberg S, Skeppner G. Sequential combined spinal epidural block versus spinal block for cesarean section: effects on maternal hypotension and neurobehavioral function of the newborn. Anesth Analg 1994; 78: 1087–92.[Abstract/Free Full Text]

6 Bonica JJ, Berges PU, Morikawa K. Circulatory effects of peridural block: I. Effects of level of analgesia and dose of lidocaine. Anesthesiology 1970; 33: 619–26.[Medline]

7 Simon, MJ, Veering BT, Stienstra R, van Kleef JW, Burm AG. The effects of age on neural blockade and hemodynamic changes after epidural anesthesia with ropivacaine. Anesth Analg 2002; 94: 1325–30.[Abstract/Free Full Text]

8 Borghi B, Casati A, Iuorio S, et al. Frequency of hypotension and bradycardia during general anesthesia, epidural anesthesia, or integrated epidural-general anesthesia for total hip replacement. J Clin Anesth 2002; 14: 102–6.[Medline]

9 Carpenter RL, Caplan RA, Brown DL, Stephenson C, Wu R. Incidence and risk factors for side effects of spinal anesthesia. Anesthesiology 1992; 76: 906–16.[Medline]

10 McGlade DP, Kalpokas MV, Mooney PH, et al. Comparison of 0.5% ropivacaine and 0.5% bupivacaine in lumbar epidural anaesthesia for lower limb orthopaedic surgery. Anaesth Intensive Care 1997; 25: 262–6.[Medline]

11 Chambers WA, Edstrom HH, Scott DB. Effect of baricity on spinal anaesthesia with bupivacaine. Br J Anaesth 1981; 53: 279–82.[Abstract/Free Full Text]

12 McNamee DA, McClelland AM, Scott S, Milligan KR, Westman L, Gustafsson U. Spinal anaesthesia: comparison of plain ropivacaine 5 mg·mL–1 with bupivacaine 5 mg·mL–1 for major orthopaedic surgery. Br J Anaesth 2002; 89: 702–6.[Abstract/Free Full Text]

13 Patel PM, Drummond JC. Cerebral physiology and the effects of anesthetics and techniques. In: Miller RD (Ed.). Anesthesia, 6th ed. Philadelphia: Elsevier; 2005: 817.

14 Pollard JB. Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention. Anesth Analg 2001; 92: 252–6.[Free Full Text]

15 Ouzounian JG, Masaki DI, Abboud TK, Greenspoon JS. Systemic vascular resistance index determined by thoracic electrical bioimpedance predicts the risk for maternal hypotension during regional anesthesia for cesarean delivery. Am J Obstet Gynecol 1996; 174: 1019–25.[Medline]

16 Brown DL. Spinal, epidural, and caudal anesthesia. In: Miller’s Anesthesia, 6th ed. Philadelphia, Elsevier; 2005: 1665–7.

17 Whiteside JB, Burke D, Wildsmith JA. Spinal anaesthesia with ropivacaine 5 mg·mL–1 in glucose 10 mg·mL–1 or 50 mg·mL–1. Br J Anaesth 2001; 86: 241–4.[Abstract/Free Full Text]

18 Carpenter RL, Hogan QH, Liu SS, Crane B, Moore J. Lumbosacral cerebrospinal fluid volume is the primary determinant of sensory block extent and duration during spinal anesthesia. Anesthesiology 1998; 89: 24–9.[Medline]

19 Shoemaker WC. Invasive and noninvasive monitoring. In: Grenvik A, Ayres SM, Holbrook PR, Shoemaker WC (Eds). Textbook of Critical Care, 4nd ed. Philadelphia: W. B. Saunders Company; 2000: 88–9.

20 Steinbrook RA, Concepcion MA. Respiratory gas exchange and hemodynamics during lumbar epidural anesthesia: effects of lidocaine with and without epinephrine. Reg Anesth Pain Med 2000; 25: 380–4.[Medline]

21 Kerkkamp HE, Gielen MJ. Cardiovascular effects of epidural local anaesthetics. Comparison of 0.75% bupivacaine and 0.75% ropivacaine, both with adrenaline. Anaesthesia 1991; 46: 361–5.[Medline]

22 Milsom I, Forssman L, Biber B, Dottori O, Sivertsson R. Measurement of cardiac stroke volume during cesarean section: a comparison between impedance cardiography and the dye dilution technique. Acta Anaesthesiol Scand 1983; 27: 421–6.[Medline]

23 Auroy Y, Benhamou D, Bargues L, et al. Major complications of regional anesthesia in France: The SOS Regional Anesthesia Hotline Service. Anesthesiology 2002; 97: 1274–80.[Medline]

24 Kopp SL, Horlocker TT, WarnerME, et al. Cardiac arrest during neuraxial anesthesia: frequency and predisposing factors associated with survival. Anesth Analg 2005; 100: 855–65.[Abstract/Free Full Text]

25 Geffin B, Shapiro L. Sinus bradycardia and asystole during spinal and epidural anesthesia: a report of 13 cases. J Clin Anesth 1998; 10: 278–85.[Medline]

26 Lovstad RZ, Granhus G, Hetland S. Bradycardia and asystolic cardiac arrest during spinal anaesthesia: a report of five cases. Acta Anaesthesiol Scand 2000; 44: 48–52.[Medline]

27 Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988; 68: 5–11.[Medline]

28 Lesser JB, Sanborn KV, Valskys R, Kuroda M. Severe bradycardia during spinal and epidural anesthesia recorded by an anesthesia information management system. Anesthesiology 2003; 99: 859–66.[Medline]

29 Pollard JB. Common mechanisms and strategies for prevention and treatment of cardiac arrest during epidural anesthesia. J Clin Anesth 2002; 14: 52–6.[Medline]

30 Iwama H, Kaneko T, Ohmizo H, Furuta S, Ohmori S, Watanabe K. Circulatory, respiratory and metabolic changes after thigh tourniquet release in combined epidural-propofol anaesthesia with preservation of spontaneous respiration. Anaesthesia 2002; 57: 588–92.[Medline]

31 Rucci FS, Trafficante FG, Pippa P. Fentanyl and bupivacaine mixture for extradural blockade in orthopaedic surgery: effects on haemodynamic responses and pain related to the use of thigh tourniquet. Eur J Anaesthesiol 1987; 4: 167–74.[Medline]




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