ISSN NUMBER: 1938-7172
Issue 2.6

Michael A. Fiedler, PhD, CRNA

Contributing Editors:
Mary A. Golinski, PhD, CRNA
Alfred E. Lupien, PhD, CRNA

Guest Editors:
Penelope S. Benedik, PhD, CRNA, RRT
Terri M. Cahoon, MSN, CRNA
Gerard T. Hogan, Jr., DNSc., CRNA
Steven R. Wooden, MS, CRNA

Assistant Editor
Jessica Floyd, BS

A Publication of Lifelong Learning, LLC © Copyright 2008

New health information becomes available constantly. While we strive to provide accurate information, factual and typographical errors may occur. The authors, editors, publisher, and Lifelong Learning, LLC is/are not responsible for any errors or omissions in the information presented. We endeavor to provide accurate information helpful in your clinical practice. Remember, though, that there is a lot of information out there and we are only presenting some of it here. Also, the comments of contributors represent their personal views, colored by their knowledge, understanding, experience, and judgment which may differ from yours. Their comments are written without knowing details of the clinical situation in which you may apply the information. In the end, your clinical decisions should be based upon your best judgment for each specific patient situation. We do not accept responsibility for clinical decisions or outcomes.

Table of Contents














Ghai a, Saini S, Kiran S, Kamal K, Kad N, Bhawan P


Influence of lithotomy position on the heamodynamic changes in patients with coronary artery disease

J Anaesth Clin Pharmacol 2008;24:359-360

Ghai a, Saini S, Kiran S, Kamal K, Kad N, Bhawan P



Purpose            The purpose of this article was to emphasize the impact that the lithotomy position has on patients with depressed cardiac function.

Background            Placing a patient in the lithotomy position can auto transfuse as much as 1500 mL of blood from the lower extremities to the central circulation. Patients with depressed cardiac function may not tolerate this rapid increase in myocardial preload.

Methodology            A 78 year old male with a history of myocardial infarction five years prior to the procedure was scheduled for a cystoscopy. He had an uneventful transurethral prostatectomy two months earlier using a spinal anesthetic. His history reported good exercise tolerance, an ejection fraction of 63.5% and normal left ventricular function. His preoperative vital signs showed a pulse of 72 and blood pressure of 130/80. After preloading the patient with 500 mL of lactated ringers, spinal anesthesia was performed using 1.2 mL of 0.5% bupivacaine (6 mg). The patient was placed in the lithotomy position and surgery was started. After 10 minutes the patient complained of chest pain radiating to his left arm. EKG showed an increased heart rate of 100 beats per minute with ST segment elevation, while the blood pressure remained normal. Surgery was stopped and the patient placed in the supine position. He was given a sublingual nitrate and 5 mg of IV morphine. Within ten minutes the patient’s symptoms disappeared, vitals returned to normal, and it was decided to continue with the procedure.

After 15 minutes the patient again complained of chest pain but this time the blood pressure decreased to 86/56, the pulse slowed to 54, and the EKG showed ST depression. He was given IV ephedrine, placed in the supine position, and a 12 lead EKG was obtained. After 5 minutes the vital signs returned to normal and the 12 lead EKG showed changes consistent with inferolateral ischemia. The case was terminated and the patient transferred to the ICU. Within twelve hours the EKG returned to normal and the patient was discharged without further consequences.

Result            Both cardiac events were preceded by placing the patient in the lithotomy position. The first episode of chest pain was most likely associated with coronary artery spasm because the blood pressure remained normal and the EKG showed ST elevation. The second episode was a more serious imbalance between cardiac oxygen supply and demand. Although the bradycardia decreased the oxygen demand the hypotension reduced the oxygen supply more significantly. It is likely that the event which initiated both cardiac episodes was the rapid placement of the patient in a lithotomy position. This position change acutely increased the cardiac preload leading to increased cardiac workload and wall tension.

Conclusion            One of the basic challenges during anesthesia is to maintain the balance between myocardial oxygen supply and myocardial oxygen demand. Several events during an anesthetic conspire to disrupt that balance. They include tachycardia, hypertension, stress, and hypoxemia. In addition, position changes that disrupt the cardiac filling pressures can cause an already compromised myocardium to become ischemic. This case study emphasizes the potential problems faced when placing a patient in the lithotomy position and the importance of ST segment monitoring during surgery.



This case study did an excellent job reminding us of the potential problems with the lithotomy position in patients with preexisting cardiac depression. We often see patients with cardiac problems in the operating room for simple cases which require a lithotomy position. It is imperative that we recognize the risk and monitor the patient closely, no matter how simple the procedure is. I am aware of anesthesia providers that place patients in this position without monitors in place. I know that elderly patients with cardiac conditions are placed in the lithotomy position in the clinic without any monitors at all. What kind of stresses have we placed on the heart in these situations without even recognizing the results?

I often find operating room nurses and physicians who are unaware of the potential problem created by rapidly raising the patient’s legs into a lithotomy position. I frequently remind them. Early in my clinical career I had a patient become hypotensive after placing her in the lithotomy position. At the time I assumed that the problem was the result of the abdominal pressure created by bending the legs back in an exaggerated position. I slowly placed the patient in a modified lithotomy position and the problem of hypotension resolved itself. The problem certainly could have been the result of a rapid raise in preload and I did not recognize it at the time. Slowly raising the legs gave the cardiovascular system time to compensate and not raising the legs so high reduced the volume. Compression of the abdominal cavity could have been a factor, but looking back I believe now that increasing the preload was probably the primary factor in that case.

I continue to be amazed at the complexities of the cardiovascular system and our responsibility to maintain that important balance between myocardial oxygen supply and demand. The important cardiovascular monitoring tools we have at our disposal, including ST segment analysis should always be employed even for the simplest of cases.


Steven R. Wooden, MS, CRNA



© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008

Hogue CW, Fucetola R, Hershey T, et. al.


the role of postoperative neurocognitive dysfunction on quality of life for postmenopausal women 6 months aftr cardiac surgery

Anesth Analg 2008;107:21-28

Hogue CW, Fucetola R, Hershey T, et. al.



Purpose          The purpose of this study was to determine the influence of early postoperative cognitive dysfunction on quality of life in postmenopausal women undergoing cardiac surgery in which cardiopulmonary bypass was required. This was part of a larger study to determine whether preoperative treatment with 17β-estradiol impacted postoperative neurocognitive dysfunction

Background   Women are a growing proportion of patients undergoing cardiac surgery, yet most of the literature involving postoperative neurocognitive dysfunction revolves around men. Operative morbidity and mortality figures are higher for women than they are for men. As the surgical population ages, it is important to understand the impact of any invasive treatment that could impair post procedural quality of life. The initial study revolved around the effectiveness of 17β-estradiol for neuroprotection in females undergoing cardiopulmonary bypass. That study showed no improvement with that drug. Cognitive impairment has been shown to lower quality of life in patients with cardiac disease.

Methodology  After IRB approval, 174 postmenopausal women age ≥ 55 undergoing coronary artery bypass and/or cardiac valve replacement were enrolled in the study. The patients were prospectively randomized into a treatment group (those receiving 17β-estradiol) and a control group (those receiving a placebo). A standard body of neurocognitive tests were administered to all participants 1-2 days prior to surgery, 4-6 weeks after surgery, and then 6 months after surgery by trained personnel. All participants were given midazolam, opioids, and volatile anesthetics and underwent nonpulsatile cardiopulmonary bypass with a membrane oxygenator at a body temperature of 24°C to 32°C.

Result At the conclusion of the study, 15 of the original participants had died and 31 were unavailable for follow up. The study was completed by 128 patients. Complete quality of life data were available for 108 patients. There were no differences in psychometric test scores between the groups preoperatively, nor were there any differences in the demographic composition. After stepwise linear regression analysis, it was noted that those patients who self reported lower scores on the physical health summary were associated with a greater incidence of postoperative cognitive dysfunction.

Conclusion     Although 17β-estradiol showed promise in reducing the extent of ischemic injury in a variety of in vitro and animal model studies, the investigators found no difference between the control and treatment groups. Early studies showed an improvement in quality of life in general after cardiac surgery. The investigators found that this was not universally true. Women appear to be at increased risk for postoperative neurocognitive dysfunction than men. Less symptomatic relief and higher rates of depression and anxiety in women have been proposed as explanations for their poorer quality of life after surgery. The notable finding in this study was that preoperative assessments independently predicted lower post operative self-rated health status and that many aspects of quality of life in women were not amenable to improvement after cardiac surgery.



This study is significant because it helps shift our focus to the negative ramifications of cardiac surgery. Many of us have been led to believe that if the patient survives the surgery, their quality of life will improve. This is not always the case. Although a significant number of women in this study did improve, there was a direct correlation between lower self-rated health status before surgery and quality of life post surgery. This tells me that cardiac surgery on those patients who perceive themselves as a poor risk rarely see a significant improvement in their self perceived health status.


Gerard T. Hogan, Jr., DNSc., CRNA


Edwards FH, Carey JS, Grover FL, Bero JW, Hartz RS. Impact of gender on coronary bypass operative mortality. Ann Thorac Surg 1998;66:125-31

Welke KF, Stevens, JP, Schults WC, Nelson EC, Beggs VL, Nugent WC. Patient characteristics can predict improvement in functional health after elective coronary bypass grafting. Ann Thorac Surg 2003;75:1849-55


© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008

Equipment & Technology

Parikh BR, Simon AM, Kouvaras JN, Ciolino RB, Suthar TP, Dorian RS


influence of intermittent pneumatic compression devices on non-invasive blood pressure measurement of the ankle

J Clin Monit Comput 2007;21:381-6.

Parikh BR, Simon AM, Kouvaras JN, Ciolino RB, Suthar TP, Dorian RS



Purpose            This study evaluated the effect of intermittent compression devices on ankle noninvasive blood pressure measurement in healthy volunteers.

Background            In the perioperative period, high-risk patients are now routinely supplied with intermittent compression devices (ICD) as prophylaxis against the formation of deep vein thrombosis. High risk patients include those with such characteristics as age > 50 years, obesity, history of varicosity, cancer, chemotherapy, atrial fibrillation, stroke, diabetes, previous DVT, coagulation disorders, and smoking, although this list is not exhaustive. For a variety of reasons, including surgical site (upper extremity, axillary, A-V fistula surgery), surgical convenience (surgeon requiring arms “tucked” and then leaning on the cuff during surgery) or anatomic (obesity, abnormal upper extremity shape), blood pressure cuffs cannot always be placed on the upper extremity during operation. In many of these cases, the Non-Invasive Blood Pressure (NIBP) cuff will be placed on the ankle. It is appropriate to question the accuracy of blood pressure measurement on a site that is subjected to intermittent external compression by an ICD.

Methodology            Fifty healthy volunteers, aged 23 to 35 (mean age 27.8 years), were enrolled in the study. Data were collected with subjects in the supine position wearing a right ankle blood pressure cuff with the cuff bladder aligned over the posterior tibial artery. ICDs were placed over both lower extremities. NIBP measurements were taken at four times: 1) control with ICD in place over cuff but not inflated, 2) 15 seconds prior to ICD inflation, 3) at the same time as inflation of the ICD, and 4) 15 seconds after inflation of ICD. Each NIBP was measured three times; the average value of the mean, systolic, and diastolic BP in each category was compared to the control and the absolute value of the difference were determined. Repeated measures analysis of variance was used to assess the results.

Result            No significant difference was found between the control NIBP measurement and the NIBP at any point during the ICD inflation (∆ systolic BP P=0.872, ∆ diastolic BP P=0.645, ∆ mean BP P=0.522).

Conclusion            Inflation of an intermittent compression device had no effect on noninvasive blood pressure measurement on the ankle in healthy volunteers.



Although useful as a pilot study for future research, this study is self-limited and does not apply to the typical population of surgical patients. In fact, the study sample comprised subjects who are the least likely to require ICDs or an altered NIBP cuff position (healthy, lean and young). This is a serious limitation to the study and to our ability to generalize the results to our own patients.

Some methodological issues deserve mention. First, three BP measurements were averaged to determine each data point with no mention of how close the individual values were before averaging. In research measurement versus clinical practice, there is a higher standard for data collection. For example, in pulmonary function testing, it is standard practice to repeat measurements until the reported values are within 10% of each other and only these values are selected for averaging. Second, there was no discussion of the accuracy of NIBP measurement versus the gold standard, mercury sphygmomanometry. In fact, automated oscillometric NIBP devices accurately measure only mean BP and then estimate systolic and diastolic pressures. (Reference any NIBP operator’s manual.) Oscillometric techniques are unreliable in the presence of irregular heartbeats and in particular during blood pressure extremes (hypotension and its prevalence in the OR comes to mind). Because an ICD generally inflates to 40 mmHg during the compression cycle, the presence of hypotension may influence its effects. Unfortunately, by testing only healthy, thin, normotensive individuals, this study may not provide the certainty that ICDs do not affect ankle NIBP measurement in the OR.

Last, it is important to remind providers of the expected physiological differences between brachial and ankle blood pressures. Ankle pressures will demonstrate higher systolic and lower diastolic values and the decision tree for treatment of hypo- and hypertension must be adjusted accordingly.

Penelope S. Benedik, PhD, CRNA, RRT


Circulation 2005;111;697-716

© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008

Kikuchi T, Kamiya Y, Ohtsuka T, Miki T, Goto T


Randomized prospective study comparing the laryngeal tube suction II with the proseal laryngeal mask airway in anesthetized and paralyzed patients

Anesthesiology 2008;109:54-60

Kikuchi T, Kamiya Y, Ohtsuka T, Miki T, Goto T



Purpose          The purpose of this study was to compare the Laryngeal Tube Suction II (LTS II) to the ProSeal Laryngeal Mask Airway (PLMA) in regard to their ease of insertion, effectiveness, and stability in delivering positive pressure ventilation during controlled ventilation and general anesthesia.

Background   The LTS II is a supraglottic airway device similar to devices designed for out of hospital emergency airway management. The distal and proximal cuffs block the esophageal inlet and the pharyngeal space above the larynx while the holes between the cuffs allow ventilation. The LTS II also has an esophageal drainage tube which allows the passage of a gastric tube into the esophagus.

The PLMA is designed to fit over the larynx sealing the space between the larynx and the oral pharyngeal space with an inflatable cuff.

Methodology  One hundred male patients undergoing prostate surgery were enrolled in the study. Patients were excluded who had disease of the neck, increased risk of aspiration, a body mass index greater than 30 kg/m2, or a mouth opening of less than 3 cm. Patients were randomly allocated to an LTS II or the PLMA with 50 patients receiving each type of airway. Each patient was placed in a supine position with the head in a sniffing position. After general anesthesia was induced with fentanyl, propofol, and sevoflurane, the patient received 0.1mg/kg of vecuronium for paralysis.

Thirty five anesthetists, including residents, used the devices. Staff anesthesiologists were familiar with the PLMA but not the LTS II. They were given instruction on the LTS II and allowed to practice on mannequins prior to using the device. Prior to insertion of either device, a water soluble lubricant was applied. After insertion, the cuffs were inflated with air according to manufacturer’s instructions. After insertion, no adjustment of the airway or device was allowed. The number of attempts to place the device was recorded. Three unsuccessful attempts were recorded as a failure. After several cases of LTS II misplacement, the protocol was altered to use fluoroscopic verification of tube placement, or to determine how misplacement occurred. The positioning of the PLMA was not observed with fluoroscopic imaging because previous studies indicated that the cuff of the properly placed PLMA was always located at the level of the larynx.

Cuff pressure was monitored with a gauge. Positive pressure ventilation was maintained with a gas flow of 3 l/m restricting the maximum airway pressure to 40 cm H2O. The pressure that allowed gas leakage was identified by decreasing the cuff pressure in 5 cm increments. The primary aim of this study was to compare the seal pressures of the two devices considering a difference of 5 cm H2O to be significant.

Result Demographics between the two groups were not significantly different. Placement of the LTS II was accomplished by 16 residents and 9 staff anesthesiologists while the PLMA was placed by 8 residents and 10 anesthesiologists. The median number of years of anesthesia experience for both airway groups was 3 years. The success rate of insertion was significantly higher with the PLMA than with the LTS II. There were 48 successful PLMA placements compared to 37 successful LTS II placements. Median leak pressure was lower with the LTS II than with the PLMA. The PLMA leaked at 21 cm H2O while the LTS II leaked at 16 cm H2O. Reducing the cuff pressure and movement of the device shaft resulted in leakage in the LTS II more often than the PLMA. There were no differences in the incidence of traumatic insertion or postoperative complications between the two groups.

Conclusion     The LTS II was more difficult to insert and had a less reliable seal than did the PLMA. The LTS II entered the tracheal inlet instead of the esophagus in 10% of the patients but ventilation was still possible in four of those five patients, probably because the shape of the distal cuff allowed gas to leak into the trachea. The seal of the PLMA was more reliable than the LTS II. The PLMA cuff pushes against the cartilage of the larynx while the LTS II cuff pushes against the soft tissue wall of the upper esophagus. The tidal volume produced by the LTS II was lower than the PLMA probably because of the small ventilation holes in the LTS II tube. Although the incidence of post operative sore throat was twice as high with the PLMA as with the LTS II (9 vs. 4) this difference was not statistically significant. This study suggested that the placement and airway seal of the LTS II is less reliable than the PLMA.



I have used both the LTS II and PLMA and found them both easy to insert and maintain. It is interesting that another study found no significant difference in ease of insertion between the two devices.1 The difference in the two studies was that the providers inserting the LTS II in the second study had more experience in inserting the device. This is exactly why I have problems with studies using inexperienced providers and trying to indicate that a device is technically inferior just because an inexperienced person had trouble with it. The median years of experience in this study was 3 years. I have not found the LTS II to be technically difficult to insert. Sometimes it does require manipulation of the device in the airway in order to position it correctly, but so does the PLMA. I do like the easy access to the esophagus provided by the LTS II, and the fact in my practice that the LTS II results in fewer post operative sore throats which is suggested by this study. I have also not found that the cuff leakage as indicated in this study is clinically significant in my practice.

Both devices have their place, and as with most airway devices each provider finds unique aspects that meet their needs and builds experience with an individual device. I try to have multiple airway devices available and maintain my experience so that when the more difficult patients present themselves I have a choice of which device I might find more useful in the particular situation.


Steven R. Wooden, MS, CRNA


1. Genzwuerker HV, Altmayer S, Hinkelbein J, Gernoth C, Viergutz T, Ocker H: Prospective randomized comparison of the new Laryngeal Tube Suction LTSII and the LMA ProSeal for elective surgical interventions. Acta Anesthesiol Scand 2007;51:1373-7


© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008


Dirkmann D, Hanke AA, G?rlinger K, Peters J


Hypothermia and acidosis synergistically impair coagulation in human blood

Anesth Analg 2008;106:1627-1632

Dirkmann D, Hanke AA, Görlinger K, Peters J


Purpose            The purpose of this study was to investigate the effects of graded hypothermia and acidosis on whole blood coagulation and hemostasis in vitro.

Background            Hypothermia and acidosis have both been shown to influence coagulation in clinical settings. Massive hemorrhage in traumatized patients is a major cause of mortality. Not enough is known about the influences of acidosis in clinical coagulopathy. The authors evaluated whole blood to determine the effects of hypothermia, with and without acidosis, on hemostasis.

Methodology            A convenience sample of 10 healthy volunteers (2 female, 8 male) provided samples of their whole blood for evaluation. Specimens were drawn with a 12 gauge needle to avoid venous stasis. Volunteers were screened for bleeding diathesis and denied any use of anticoagulants or antiplatelet medications. All 10 specimens were incubated at 30, 33, 36, and 39°C and analyzed with the thromboelastomer system. To assess the effects of acidosis, hydrochloric acid was added to specimens in increasing molarity to achieve blood pH (measured at 37°C) of 7.37, 7.2, 7.1, and 7.0. Specimens were recalcified and tested. The researchers determined coagulation time, clot formation time, maximum clot firmness, and the clot lysis index. Results were analyzed using Analysis of Variance (ANOVA).

Result            Hypothermia consistently impaired coagulation in whole blood. All tested variables were significantly impaired at 30°C. Acidosis alone failed to exert any significant effect on coagulation under normothermic conditions. A 2-way ANOVA revealed that hypothermia and acidosis acted synergistically to impair coagulation. Clot lysis was not influenced by hypothermia or acidosis, but was slightly increased in hyperthermia.

Conclusion            Hypothermia and hypothermia with acidosis, but not acidosis alone, impaired coagulation in whole blood studied using the thromboelstomer system.


This study does bear some attention by nurse anesthetists, especially those who are involved in trauma and open heart procedures. Keeping a tight control on pH during operative care may help in decreasing the coagulopathies associated with major blood loss. Limitations of the study include having been done in vitro. Also, it did not take into consideration the expected dilution of clotting factors that can occur with massive fluid resuscitation. Up to a point, the dilutional effect of a crystalloid fluid resuscitation actually increases the coagulability of blood. It would be useful to see follow up studies done in vivo, but ethical issues would prevent that from occurring. The authors did mention that by using human blood in vivo they were able to exclude other physiologic responses that would alter coagulation. I would argue that the effects of tissue plasminogen activator, and other bodily mechanisms, could potentially change the results of their study. The information is useful, and can be applied to clinical Nurse Anesthesia practice.

Gerard T. Hogan, Jr., DNSc., CRNA

© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008

Cao CGL, Weineger MB, Slagle J et al.

Differences in day and night shift clinical performance in anesthesiology

Hum Factors 2008;50:276-90

Cao CGL, Weineger MB, Slagle J et al.


Purpose            To compare the clinical performance of physician anesthesiology residents between regular day shift and an extended night shift.

Background            Fatigue from sleep loss is a common complaint of medical personnel and has been associated with decreases in cognitive abilities, memory reliability, and vigilance; increases in aggressiveness and anxiety; negative mood; and difficulty in adjusting problem-solving strategies. After 24 hours without sleep, performance on a hand-eye coordination task is equivalent to a blood alcohol level of 0.10%. Although findings from initial investigations suggested that provider motivation prevented errors after one overnight shift without sleep, subsequent investigations have demonstrated decreased technical skills and lengthened time required to complete tasks. An Internet survey of approximately 3,000 interns found that fatigue-related errors and preventable adverse events occurred 7 times more frequently in months when the physicians worked more than 5 “extended duty shifts” compared to months without extended duty. Unfortunately, the generalizability of most study findings is limited because the investigations were conducted in non-clinical settings. The current investigation was designed to measure physician performance in actual clinical settings. It was hypothesized that night-shift work would result in decreases in resident perception, vigilance, and cognitive abilities.

Methodology            Thirteen physician anesthesiology residents with between 2 and 31 months experience were observed during the administration of two anesthetics. The first anesthetic was administered overnight on a call day that started between 6:30 a.m. and 10:00 a.m. Within the following month, the residents were assigned and observed during a daytime case matched prospectively for complexity and length of procedure. Measures included a questionnaire concerning sleep, activity, and consumption of drugs and caffeine in the previous 24 hours; the modified Profile of Mood States survey; behavioral task and workload density data collected in the operating room by a trained observer; and participant response time to detect a random light illumination as a secondary indicator of cognitive workload and vigilance. Data were analyzed using a variety of between- and within-subject techniques.

Result            During night cases, more time was allocated to “observing” behaviors such as looking at the patient, monitors, or surgical field during maintenance (40% versus 30%) and overall (36% versus 27%). The percentage of time allocated to “manual” behaviors including adjusting equipment, performing technical procedures, and administering medications was higher in day cases during the maintenance phase (22% versus 17%) and the overall case (31% versus 25%). There were no statistically significant differences in conversing (approximately 10%), recording (approximately 12%) or “other” (18%) behaviors between day and night cases during any phase of the anesthetics.

There were no statistically-significant differences in response time to light illumination, self-reported workload, or observer-assessed workload. Night case mood scores were significantly higher (indicating a more negative mood) both pre-case (6 versus 24) and post-case (5 versus 22). The slightly improved mood scores after case completion was not statistically significant

Conclusion            Differences in the distribution of manual and observing behaviors may have been the result of sleeplessness and fatigue. As the capacity to sustain attention decreases with sleep loss, allocating more time for information collection and verification offsets the effects of fatigue; however, the consequences of this activity redistribution potentially reduces the patient safety margin should an unanticipated event occur.

The lack of a statistically significant difference in detection of alarm light illumination was inconsistent with the investigators’ conceptual framework. This non-significant finding may be explained either because the workload increase imposed by this task was minimal or because imbedding the light within the patient monitoring system coincidentally facilitated detection when the amount of time observing the patient increased.

The finding of mood differences between day and night is consistent with previous investigations. The lack of change in mood scores from the beginning to the end of a case suggests that time of day affects mood more so than participation in care.

Overall, the results of this investigation confirm findings from some of the investigations conducted in non-clinical settings. This study’s approach using matched-case control may be beneficial in conditions with the use of a randomized control design is not achievable; however, conducting the study in a naturalistic setting also imposed limitations such as differences in the characteristics of the matched cases, resident maturation between the cases, an inability to control sleep debt prior to, and between cases, and the Hawthorne effect of participants knowing that their performance was being observed.



I have been a long-time admirer of co-author Dr. Weineger’s research. His studies are focused on an important topic: understanding how our characteristics as human systems affect the delivery of anesthesia care. His methodologies are described in detail, analysis is strong, and conclusions are drawn carefully from the evidence obtained. I have never discussed this issue with Dr. Weinger, but I imagine that he, like most other human factors researchers in anesthesia, is exploring our limits as providers to help define a set of performance specifications … specifications that, if met, should result in consistently safe practice and, if exceeded through conditions such as fatigue or production pressure, significantly increase the risk of failure. Viewed from that perspective, this investigation of Cao, Weineger, et al. provides good news for clinicians and our patients. There were no dramatic differences in the care provided by a small number of physician anesthesiology residents when comparing their performance during one night-time anesthetic followed a few weeks later by a day-time case with similar characteristics. The main difference detected was that residents allocated the highest percentage of their time to “manual” tasks during day cases whereas the highest percentage of night-case time was used for “observing” tasks. With our current level of understanding of provider performance, answering one research question leads to many more.

The authors suggest that the increase in observational activities may be a strategy employed to compensate for the reduced attentional capacity associated with fatigue and sleep loss. Other researchers have suggested that clinicians ‘create’ cognitive or physical tasks to sustain their attention above a minimal threshold. If the residents’ themselves were not being studied and their actions recorded, would they (we) have maintained alertness the same way, or by engaging in non-patient care activities such as extraneous conversation, reading, or Sudoku?  What were the consequences of decreased manual workload? Was there less “busy work” such as re-arranging syringes on the anesthesia cart or was quality of care potentially compromised through alterations in terms of medication dosing, repositioning the head or extremities, etc.?  Or, to what extent was the margin of safety for responding to unanticipated events such as resuscitation or complex differential diagnosis actually compromised because of the reallocation of workload?

That’s where we find ourselves at the end of this investigation. Human Factors is an exacting journal (of the Human Factors and Ergonomics Society) with high standards for publication. Cao, Weineger and colleagues used “their” pages well to inform us of a novel research design, offer some insight into diurnal variations in our practice patterns, and provide us with a new set of questions for follow-up investigations.

Alfred E. Lupien, Ph.D., CRNA

© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008


Hausman LM, Eisenkraft JB, Rosenblatt MA


The safety and efficacy of regional anesthesia in an office-based setting

J Clin Anesth 2008;22:271-275

Hausman LM, Eisenkraft JB, Rosenblatt MA



Purpose            The purpose of this report was to describe a one year experience with regional anesthesia in an office-based setting.

Background            About 20% of all surgical procedures performed in the USA are outpatient procedures and as many as 25% may be performed in on office. Office-based surgical procedures may result in significant savings and are becoming a larger portion of all surgical procedures performed in the USA. Regional anesthesia offers multiple advantages to both patients and institutions including: postoperative analgesia, reduced PONV, and faster eligibility for discharge. Nevertheless, a 2002 survey reported a reluctance among Society of Ambulatory Anesthesia members to use peripheral nerve blocks in an office-based setting.

Methodology            This was a retrospective chart review of anesthetics administered over a one year period in an orthopedic office.

Result            In all, 278 patients underwent procedures, 136 men and 142 women. Patients were fairly evenly split between ASA physical status I and II. About 4% were ASA III. All procedures were performed in a single operating room with standard anesthesia equipment including a crash cart and defibrillator. Anesthetics provided included Monitored Anesthesia Care (MAC) (140 cases, 50%), general anesthesia (17 cases, 6%), and regional anesthesia (125 cases, 44%). Regional anesthetics were broken down as follows:

  • Interscalene blocks 60 (48%)
  • Ankle blocks 21 (17%)
  • Femoral blocks (3-in-1) 16 (13%)
  • Popliteal blocks 11 (9%)
  • Axillary blocks 11 (9%)
  • Infraclavicular blocks 4 (3%)
  • Subarachnoid blocks (spinal) 2 (2%)

Axillary blocks were performed with a 23 gauge needle by the transarterial technique. Other peripheral blocks were performed with a 21 or 22 gauge insulated needle and peripheral nerve stimulation.

The average (median) time from anesthesia start to surgery start was as follows:

  • MAC 19 (20) minutes
  • Regional 29 (30) minutes
  • General 31 (30) minutes

The average (median) time from end of surgery to end of anesthesia was as follows:

  • MAC 9 (10) minutes
  • Regional 9 (10) minutes
  • General 12 (10) minutes

Two complications were observed related to regional anesthesia (1.6% incidence). One patient had a paresthesia in a finger lasting a week following an axillary block. One patient experienced femoral neuropathy for three months following a femoral nerve block.

Conclusion            Regional anesthesia can be used safely and efficiently in an office-based environment.



I have long thought that regional anesthesia was underused and, often, underappreciated. This report is worthwhile because, as a profession, our familiarity with regional anesthesia in an office-based surgery setting is so limited. It simply describes the experience with regional in one orthopedic office and, in doing so, provides testimony that regional can be used successfully in the office-based setting.

One statement the authors make is on shaky ground. They say that regional anesthesia in their office-based setting was not “associated with increased morbidity.” The question, of course, is “increased” compared to what? Complications following regional anesthesia are rare so getting a feel for the “real” incidence of temporary and permanent nerve damage is difficult. While their outcomes were good, with only two temporary complications, there are two reasons why I wouldn’t base my assessment of the safety of regional anesthesia in the office-based setting on this information alone. First, the number of patients who received regional anesthesia was small, only 125 over the course of a year, and, second, this was not a properly designed research study to assess “safety.” That said, their complication rate was lower than that reported in the literature1 and the lack of serious complications is, at least, reassuring. This makes sense, though, doesn’t it? Why should the incidence of complications following regional anesthesia be higher just because the block was performed in an office?

Using regional anesthesia safely in the office-based setting requires equipment, supplies, support personnel, and a skilled anesthesia provider. Clearly, the standards don’t change based upon location. Regional anesthesia can be used safely in a hospital operating room or an outpatient surgery center. So as long as standards for equipment and personnel are met, and there is an plan in place for dealing with emergencies and patients that unexpectedly require admission there is no reason to believe regional can’t be safely used in an office-based setting as well.

Recently, I’ve been doing some work in an office-based setting where subarachnoid blocks are used for some procedures and sedation for others. Spinals are perhaps the least used block in an outpatient setting; only 2 of the 125 regional blocks in this report were spinals. But now that we have small gauge Sprotte and Whitacre needles the incidence of Post Dural Puncture Headache is low. With proper technique and by avoiding epinephrine, which prolongs motor block, recovery room stays need not be long. Surgeons and patients are happy. With proper planning, equipment, personnel, and patient selection I see no reason why regional anesthesia can’t be more commonly used safely in an office-based environment.


Michael Fiedler, PhD, CRNA


1.            Brull R, McCartney CJ, Chan VW, El-Beheiry H. Neurological complications after regional anesthesia: contemporary estimates of risk. Anesth Analg 2007;104:965-74.


Other articles of interest from previous issues of Anesthesia Abstracts:

Disclosure of risks associated with regional anesthesia: a survey of academic regional anesthesiologists. Reg Anesth Pain Med 2007;32:7-11. Anesthesia Abstracts March 2007, volume 1, number 1.

A comparison of regional versus general anesthesia for ambulatory anesthesia: a meta-analysis of randomized controlled trials. Anesth Analg 2005;101:1634-42. Anesthesia Abstracts December 2007, volume 1, number 8.

© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008

Pediatric Anesthesia

Ong M, Chambers NA, Hullet B, Erb TO, von Ungern-Sternberg BS


Laryngeal mask airway and tracheal tube cuff pressures in children: are clinical endpoints valuable for guiding inflation?

Anaesthesia 2008;63:738-744

Ong M, Chambers NA, Hullet B, Erb TO, von Ungern-Sternberg BS



Purpose            The purpose of this study was to describe endotracheal tube and laryngeal mask airway cuff pressures in children when cuff inflation was guided by clinical endpoints.

Background            Excessive cuff pressure in endotracheal tubes (ETT) and laryngeal mask airways (LMA) can reduce or eliminate mucosal perfusion near the cuff. The relationship between LMA measured cuff pressure and the pressure exerted on pharyngeal mucosa is non-linear. Pressure on the mucosa is not the same as the measured cuff pressure. While LMA cuff pressure exerted on the mucosa in adults rarely exceeds mucosal perfusion pressure, it may in children. In adults high cuff pressures result in sore throat, hoarseness, laryngeal and tracheal lesions, vocal cord paralysis, hypoglossal and recurrent laryngeal nerve injury, and dislocation of arytenoid cartilages resulting in long term hoarseness. Pressure on adult tracheal mucosa in excess of 30 cm H2O has been shown to reduce mucosal perfusion and mucosal pressure above 50 cm H2O eliminates mucosal perfusion all together. Presumably, since a child’s airway is more easily damaged than an adult’s, the risk of reduced mucosal perfusion and airway complications with excessive cuff pressures is also higher and lower maximum mucosal pressures should be observed.

Methodology            This prospective, blinded study included a total of 640 children 0 years to 16 years old; 400 in the LMA group and 240 in the ETT group. All ETTs were cuffed. LMA sizes 1-4 were used. ETT sizes 3-7 mm Internal Diameter were used. Those inflating the cuffs were unaware of the study. The amount of air used to inflate cuffs was determined by clinical endpoints. Cuff pressure was measured at the beginning of the case immediately after inflation and before any nitrous oxide was used, and at the end of the case before airway removal. Cuff pressure was measured with a calibrated Portex Cuff Inflator Pressure Gauge (Portex Limited, Hythe, Kent, United Kingdom). Cuff pressure data was not normally distributed so a nonparametric test was used to compare cuff pressures.

Result            In almost all patients, measured cuff pressures exceeded recommendations in all sizes of both LMAs and ETTs immediately after placement and at the end of the case. Nitrous oxide was used in 44% of LMA cases and 38% of ETT cases. When nitrous was used cuff pressures increased from the start to the end of the case in both ETTs and LMAs (P<0.001). When nitrous was not used, cuff pressures did not increase. The smaller the ETT or LMA size, the higher the cuff pressures. No LMA patients had stridor in recovery. Three ETT patients had stridor in recovery. Each of these three children had ETT cuff pressures > 60 cm H2O.

Conclusion            Using clinical endpoints alone for inflating ETT and LMA cuffs in children was associated with excessive cuff pressures in almost all patients. Excessive cuff pressures, in turn, increase the risk of airway complications. Cuff pressures were more excessive in smaller size LMAs and ETTs and smaller sized airway devices are used in patients at greater risk for airway injury. Nitrous oxide uniformly increased cuff pressure. A cuff manometer should be used to monitor ETT and LMA cuff pressure.



This well designed study of commonly used practices in pediatric airway management provides sound evidence that changes should be made. Using clinical endpoints of an LMA rising slightly upon cuff inflation and loss of audible leak with ETT cuff inflation does not safeguard against excessive pressures in the cuffs being exerted on the mucosa. Both of the endpoints are basic criteria included in pediatric anesthesia literature and in clinical practice. This evidence shows that, even with the appropriate attention to detail, pediatric patients are likely exposed to dangerous levels of pressure on the subglottic area from ETT cuffs and on the supraglottic mucosa from LMA cuffs. Using the manufacturer’s recommended maximum intracuff pressure as a standard and even using less than the maximum inflation volume, the intracuff pressure exceeded the safety level of 60 cm H2O in most patients. In the smallest sizes, the pressure was almost doubled. The intracuff pressures of the ETTs well exceeded the recommended 30 cm H2O pressure and the suggested 20 cm H2O pressure. Again, in the smaller sizes the pressures were nearly triple the suggested pressure. The higher values for the smaller size LMAs and ETTs translates to greater risk for injury in patients with smaller airways to whom a small change in airway diameter could be catastrophic. Based upon this evidence, I would like to add a cuff manometer to my clinical tools to supplement the obviously inadequate clinical assessment.

Being the educator and lifelong learner, I also like this article as it discusses the debate of cuffed v. uncuffed ETTs in pediatric patients, especially under the age of eight. An anti-cuff proponent may argue that the results of this study show the value of using uncuffed ETTs. However, one must recall that the airway morbidity with cuffed ETTs is not increased significantly over uncuffed ETTs. Even in this study, only three of 240 intubated patients experienced stridor upon extubation. Each of these had intracuff pressures in excess of 60 cm H2O. So although pressures need to be monitored more closely and the potential for greater airway morbidity is proposed, does it really increase in pediatric patients as demonstrated in adult patients?


Terri M. Cahoon, MSN, CRNA

© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008


McDonnell C, Barlow R, Campisi P, Grant R, Malkin D


Fatal peri-operative acute tumour lysis syndrome precipitaed by dexamethasone

Anaesth 2008;63:651-655

McDonnell C, Barlow R, Campisi P, Grant R, Malkin D



Purpose            This case study reported the death of a 3 year-old male from acute tumor lysis syndrome that was precipitated by an antiemetic dose of dexamethasone given during operation.

Background            Acute tumor lysis syndrome may occur when a large, rapidly dividing tumor–often lymphoma or acute leukemia–is treated with cytotoxins. As the cancer cells are destroyed, there is a massive release of potassium, phosphate, uric acid, and lactate into the circulation with a corresponding hypocalcemia. If not identified rapidly and treated aggressively, death from cardiac and/or renal failure may result. Both tumor manipulation via biopsy or the administration of dexamethasone have been reported as triggers for tumor lysis syndrome.1

Methodology            A 3½ year-old, 16.7 kg boy presented on day of surgery for adenotonsillectomy indicated by tonsillar hypertrophy and clinical signs and symptoms of obstructive sleep apnea syndrome. He had a history of developmental delay, mild hypotonia and recurrent upper respiratory infection consistent with a previously identified genetic syndrome (Xq28 microduplication syndrome).2 He had received general anesthesia at the same site without incident for computed tomography and magnetic resonance imaging to evaluate hematologic disorders and splenomegaly within the last 2 years. Induction and anesthetic course were unremarkable; he received oxygen, nitrous oxide, sevoflurane, acetaminophen 650 mg PR, dexamethasone 0.25 mg/kg IV, and ondansetron 0.1 mg/kg IV intraoperatively.

Result            The first hour post-operative course was uneventful, followed by repeated episodes of desaturation, increased work of breathing, and ultimately cardiopulmonary collapse in the sixth post-operative hour. The resuscitation required extracorporeal membrane oxygenation (ECMO) initiated at 30 minutes post-arrest. Lab values obtained prior to ECMO revealed:

  • pH 6.76
  • Potassium 9.4 mmol/L
  • Lactate 16 mmol/L
  • Base deficit -24 mmol/L
  • Hemoglobin 2.5 gm/dL
  • Platelets 7,000 /µL
  • White count 180,000/µL

Acute tumor lysis syndrome was diagnosed and treated with rasburicase therapy, packed red blood cells, platelets, fresh frozen plasma, and supportive critical care.

Conclusion            Although the patient was successfully removed from ECMO, neurological testing revealed hypoxic encephalopathy and further therapy was withdrawn. He died on the third post-operative day.



Here is a case that we perform on a regular basis: a “sickly kid with a syndrome” for tonsillectomy. They all get dexamethasone for postoperative nausea and vomiting (PONV) prophylaxis. This one died, almost assuredly due to the administration of a prophylactic drug. This case illustrates the potential for tragedy that can occur when a seemingly benign drug becomes so ubiquitous that we no longer assess for its contraindications during routine practice. Although the mechanism of dexamethasone as an antiemetic remains unclear, it is well known that dexamethasone induces rapid cellular death in B cells including those that accumulate in certain lymphomas and leukemias. Doses of dexamethasone used for PONV prophylaxis may be equivalent to doses used for chemotherapy and are known to precipitate acute tumor lysis syndrome.

The authors rightly warn anesthetists to be cautious of the effects of dexamethasone and/or tumor manipulation when a patient presents with a high-grade hematological cancer. However, in this case, the leukemia was undiagnosed. Additionally, this patient was not seen prior to the day of surgery for anesthesia assessment; in the production pressure of the day case scenario, neither an extensive history nor a preoperative hemoglobin was performed. Either might possibly have saved this boy’s life.

No drug should be administered “routinely” and no drug is always safe. Administration of any drug deserves careful deliberation.


Post Script

In an extraordinary coincidence, the morning after I wrote this abstract my first case was a 3 year 8 month, 11.1 kg male for inguinal hernia repair. He had a history of reflux and vomiting and had received intravenous (IV) hydration in the emergency room 4 days prior to surgery for dehydration with a probable viral cause. Parents stated that he had “asthma” when he got sick, but was not currently being treated. Both parents smoked in the home. Although very small for age, he was mentally appropriate. He was afebrile, denied recent upper respiratory infection, and had bilaterally clear breath sounds with no cough or rhinorrhea. The only laboratory analysis available was a normal urinalysis.

Inhalation induction proceeded with oxygen, nitrous oxide, and sevoflurane. Patient coughed throughout induction with end-tidal sevoflurane 4%. After IV catheter insertion and propofol 25 mg IV, he was intubated easily. Lungs sounds revealed scattered loud expiratory wheezes in all fields requiring albuterol.  At this point, the surgeon revealed that the patient was being “worked up” due to his growth retardation, but the underlying problem remained unknown.

Does this patient get dexamethasone?

Penelope S. Benedik, PhD, CRNA, RRT


1) Chanimov M, Koren-Michowitz M, Cohen ML et al. Tumor lysis syndrome induced by dexamethasone. Anesthesiology 2006;105:633-4.

2) Friez MJ, Jones JR, Clarkson K et al. Recurrent infections, hypotonia, and mental retardation caused by duplication of MECP2 and adjacent region in Xq28. Pediatrics 2006;118:e1687-95.


© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008

Karapandzic VM, Vujisic-Tesic BD, Pesko PM, Nenadic BMBabic DD


The effect of metoprolol on perioperative outcome in coronary patients undergoing nonvascular abdominal surgery

J Clin Anesth 2008;20:284-289

Karapandzic VM, Vujisic-Tesic BD, Pesko PM, Nenadic BM

Babic DD



Purpose            The purpose of this study was to evaluate the effect of perioperative metoprolol on cardiovascular complications in patients with angiographically verified coronary artery disease undergoing open abdominal non-vascular surgery with general anesthesia.

Background            Beta blockade has been widely studied as a prophylactic treatment against cardiac morbidity and mortality in at risk surgical patients. Guidelines exist for perioperative ß-blockade in high risk patients. A metaanalyses including 866 patients showed significant reductions in intraoperative and postoperative myocardial ischemia, myocardial infarction, and cardiac death in patients receiving perioperative ß-blockers. A retrospective study including over 780,000 patients from over 300 hospitals showed a significant reduction in the death rate while in the hospital in high risk cardiac patients who underwent noncardiac surgery and received perioperative ß-blockers. Several other randomized controlled trials have failed to show any benefit of administering perioperative ß-blockers to cardiac patients undergoing noncardiac surgery. Sudden discontinuation or on again, off again administration of ß-blockers can result in BP and HR instability and an increased risk of myocardial ischemia or infarction.

Methodology            This prospective, observational study included 111 consecutive patients with angiographically verified coronary artery disease (CAD). The study group included patients in ASA physical status class II (25.2%), III (47.7%), and IV (27.0%). American Heart Association 2002 guidelines were used for preoperative risk assessment, preoperative preparation, postoperative care, and perioperative drug therapy.

Participants were divided into two groups, a ß-blocker group and a non-ß-blocker group. Editor’s note: this was an observational study so patients were not assigned to a group. Investigators simply observed the results in patient’s whose attending physician chose, for whatever reason, either to administer or not to administer ß-blockers. The ß-blocker group received metoprolol before surgery and for 30 days after surgery. Most (87%) patients in the ß-blocker group had been receiving metoprolol as one of their regular maintenance medications long before surgery. Preoperatively, ß-blocker patients received 25, 50, or 100 mg metoprolol PO per day in two divided doses, including the morning of surgery. Postoperatively, they received 5, 10, or 15 mg of metoprolol IV per day for one to four days. When IV dosing was no longer necessary they again received PO metoprolol through postoperative day 30. The dose of metoprolol administered was determined by the patient’s blood pressure (BP) and heart rate (HR). BP and HR were taken immediately before the twice a day metoprolol dosing and the dose adjusted based upon the vital signs.

Care provided to the non- ß-blocker group was the same in every way except that they did not receive ß-blockers.

Result            Metoprolol was administered to 75% of the participants while 25% of participants did not receive metoprolol. Patients who received metoprolol had a lower incidence of all cardiac complications than did patients in the non- ß-blocker group. The thirty day postoperative cardiac death rate was 1.2% (1 of 83 patients) in the ß-blocker group vs. 7.1% (2 of 28 patients) in the non- ß-blocker group (P<0.05). Causes of cardiac death were established by autopsy. Those that died had multiple risk factors predictive of increased rates of postoperative mortality. Perioperative hypertension (35% less), new arrhythmias (53% less), transient myocardial ischemia (57% less), and heart failure (83% less) were all less common in patients who received metoprolol (P<0.05). The incidence of perioperative myocardial infarction was 3.6% (3 of 83 patients) in the ß-blocker group and 7.1% (2 of 28 patients) in the non- ß-blocker group (P not significant). One patient receiving metoprolol experienced transient hypotension and complete heart block.

Conclusion            Noncardiac surgery patients with angiographically verified CAD who received metoprolol perioperatively and for 30 days postoperatively had a lower incidence of cardiac complications than those who did not. The lower incidence of side effects in this study compared to others may have been due to the daily adjustment of metoprolol dose based upon vital signs.



Early on, perioperative beta blockade looked like it might really reduce morbidity and mortality in cardiac patients undergoing noncardiac surgical procedures. But as more studies became available the picture became much less clear, much more confusing. Some studies showed improved outcomes, some showed not much of anything, and some showed poorer outcomes. One of the largest and best designed studies to date, the POISE study published in the Lancet, included over 8,000 patients. The POISE study reported a significant reduction in perioperative cardiovascular death in patients taking metoprolol. The trouble was, metoprolol patients also had more strokes and more deaths from sepsis and infection.

I think the study we are looking at here helps to clear the picture a little bit. We should be careful about giving too much weight to this study because it was observational and the group that did not receive metoprolol was small. We don’t know why patients did or did not receive metoprolol and something about that “why” may have biased the study results. But, that said, the POISE study gave a standard dose of metoprolol to everyone and didn’t adjust the dose based upon vital signs. It is interesting to note that most of the strokes in the POISE study were ischemic. Perhaps, and I’m speculating here, the strokes were caused by hypotension from too much metoprolol. In contrast, this study administered a variable dose of metoprolol based on daily vital signs, sort of a metoprolol “sliding scale.” It may be that the wild card in all the perioperative beta blockade studies is controlling beta blocker side effects. If so, this study may show us the way to gain the benefits of perioperative beta blockade while avoiding many of the risks.

If there is one thing to learn from this study, it is that patients with high cardiovascular risk that are most likely to benefit from perioperative beta blockade are hemodynamically vulnerable. They can be injured just as easily by low heart rates and blood pressure as they can be by high heart rates and blood pressure. Perioperative beta blockade must be carefully managed in these patients to achieve the benefits while avoiding the risk.


Michael Fiedler, PhD, CRNA


See “Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial” in Anesthesia Abstracts, Volume 2 Number 4, May 31, 2008.

© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008

Gueugniaud P-Y, David J-S, Chanzy D, et al


Vasopressin and epinephrine vs. epinephrine alone in cardiopulmonary resuscitation

N Engl J Med 2008;359:21-30

Gueugniaud P-Y, David J-S, Chanzy D, et al



Purpose            The purpose of this study was to determine whether the combination of vasopressin and epinephrine was superior to epinephrine alone, when used for pharmacologic intervention as part of advanced cardiac life support in those who experience cardiac arrest outside of the hospital setting. Superior was primarily defined as a positive response to the pharmacologic intervention, evidenced by a palpable pulse and measurable blood pressure when admitted to the hospital from the remote setting.

Background            More than 500,000 people continue to experience cardiac arrest and die each year as a result. Epinephrine remains the vasopressor of choice to use for cardiac arrest when clinically indicated (asystole, pulseless electrical activity, ventricular fibrillation); however, previous research discovered endogenous vasopressin levels to be significantly higher in successfully resuscitated patients compared with patients who had died. It has been suggested that the administration of vasopressin during cardiopulmonary resuscitation may therefore be beneficial. Animal studies have shown that vasopressin increases blood flow to the vital organs, increases cerebral oxygen delivery, and increases short term survival. Animal studies have also demonstrated positive neurologic outcomes compared with those treated with epinephrine. Many human studies however, have demonstrated that the effects of vasopressin and epinephrine were similar; one clinical trial did show that successive administration of vasopressin and epinephrine in a subgroup of patients with refractory cardiac arrest resulted in significantly higher rates of survival to hospital discharge when compared to those who received repeated injections of epinephrine alone. It is theorized that stimulating both catecholamine and vasopressin receptors will maximally improve perfusion to the vital organs during resuscitation, while decreasing any vasopressor-mediated adverse effects.

Methodology            This study, conducted as a randomized, controlled, clinical trial, involved adult patients who suffered a cardiac arrest outside of the hospital setting presenting with ventricular fibrillation, pulseless electrical activity (PEA), or asystole. Those individuals requiring vasopressor therapy during their resuscitation were included. When the resuscitation team arrived and depending on the presenting rhythm, patients received either one milligram of epinephrine and 40 IU (international units) of vasopressin, or one milligram of epinephrine and saline placebo in separate injections less than 10 seconds apart. If spontaneous circulation was not restored within 3 minutes after the study drugs were given, the same combination of drugs were administered again. If spontaneous circulation was still not restored within 3 more minutes, epinephrine was administered for all in an open label format. The primary end point, or outcome variable, was survival to hospital emergency room admission. As aforementioned, patients had to present with a pulse and a measurable blood pressure. Several secondary end points were assessed as follows:

  • Return of spontaneous circulation for at least one minute
  • Survival to hospital discharge
  • Good neurologic recovery
  • 1 year survival

Result            A total of 2,956 patients were randomized into one of two treatment groups. Of those, 2,894 met inclusion criteria and were enrolled in the study. All told, 1,442 patients received the vasopressin-epinephrine combination and 1,452 received epinephrine alone. There were no adverse events related to the study itself, from either group. Important to note, patients with “witnessed” cardiac arrest were more likely to survive and enter in to the hospital setting compared with those who had an unwitnessed cardiac arrest. Also statistically significant, if basic life support was carried out for less than 8 minutes, and advanced life support carried out less than 12 minutes, survival rate to hospital admission was higher compared with those who required a lengthier time of intervention. Further analysis demonstrated that rates of survival to hospital admission, return of spontaneous circulation, survival to hospital discharge, good neurologic recovery at discharge, and one year survival rates were similar between the groups. One post-hoc analysis showed a statistically significant difference for patients who presented with PEA. The epinephrine only group had a higher rate of survival to hospital discharge (P<0.05).

Conclusion            In 2005, the International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science (with Treatment Recommendations) concluded that there was not sufficient evidence to support or refute the use of vasopressin as an alternative to, or in combination with, epinephrine in any cardiac arrest rhythm. Because the animal studies had found the combination of both drugs effective in the treatment of asphyxial cardiac arrest, a hypothesis generated by researchers stated the two drugs would be more effective than epinephrine alone, in humans suffering a cardiac arrest. The present study showed no benefit of the addition of vasopressin to the standard treatment algorithm with epinephrine during cardiopulmonary resuscitation of adults with out-of-hospital cardiac arrest. In contrast, those who presented with PEA were found to have a significant improvement in survival to hospital discharge compared to the epinephrine only group.

As part of treatment and in a non- randomized fashion, some patients in this study received early hypothermia in the post resuscitation phase. It remains inconclusive whether or not this could have influenced the recovery of those who presented with PEA and received epinephrine only.



The most recent guidelines published by the American Heart Association state that vasopressin 40 U (one dose only) is an acceptable alternative to epinephrine in ventricular fibrillation / pulseless ventricular tachycardia. As the American Heart Association long ago moved to an evidence-based format, the reader is reminded that guidelines are graded according to the strength of the supporting evidence as being definitely effective (Class I), probably effective (IIa), possibly effective (IIb), not useful (III), or of indeterminate benefit (because of insufficient evidence). The use of vasopressin has been graded as possibly effective, IIb. Endogenous vasopressin is a peptide hormone formed in the hypothalamus and transported via axons to, and released from, the posterior pituitary. Vasopressin has two principle sites of action: the kidney and blood vessels. Within the blood vessels it binds to V1 receptors and causes vasoconstriction, which clearly increases the systemic vascular resistance and raises the blood pressure. Do remember that success of any resuscitation attempt is built on a strong base of high- quality CPR and defibrillation when required by the patient’s ECG rhythm. Vasopressors can only be given when intravenous or intraosseus access is available; CPR must be the first critical intervention until defibrillation is available, then the administration of vasopressors are warranted.

Mary A. Golinski, PhD, CRNA

© Copyright 2008 Anesthesia Abstracts · Volume 2 Number 6, July 31, 2008