RSI

[Ace844]

No, we don't treat the pain of being paralyzed, I've never heard of that to be honest. I always thaught we sedated for alert pt.'s so they don't go through being paralyzed alert and oriented and/or remember that experience.

we are able to stray away from our protocols when ever we feel necessary I will research the practice of giving opiates during RSI, and if it's a bennifit by all means I may adapt it, and will speak to my medical director. If you have a link to a good site let me know.

And about the Narcs thing, if you go to any pharmacy benzo's are controlled narcs, that's what they call them. At the hospital the call benzo's narcs, and in the back of an ambulance as well. I don't know when we stopped calling valium/versed a narc.

"AZCEP,"

As usual you hit the proverbial 'nail on the head'. That was exactly my point.[/font:1fa58b239c]

"FL_Medic,"

I am not arguing, my point was to cause you to do some research where you would most certainly find that IN FACT BENZODIAZEPINES ARE NOT NARCOTICS...They are sedatives. As far as your hospitals comment. Perhaps that is just in your area. In the NorthEast I spend ALOT of time in the hospital and in my experience here have yet to run into a single doc, anestheasiologist, etc... who doesn't know or understand the difference.

Here is a great book to help you with this subject and understand why this is important.[/font:1fa58b239c]

I have two.

Manual of Emergency Airway Management

by Ron M Walls, Robert C Luten, Michael F Murphy, Robert E Schneider

Paperback: 368 pages

Publisher: Lippincott Williams & Wilkins; 2nd edition (May 1, 2004)

Language: English

ISBN: 0781747643

This is a great airway book! It offers excellent review of anatomy, pharmacology and methods for everything from simple to difficult airways. Assessment methods are also discussed to help identify those potentially problematic airways.

The downside is that it's aimed more towards physician/in hospital airway management. However, the same methods and assessments that apply in hospital work prehospitally as well.

If you're looking for an airway book this is it.

Other sources and information can be found here by doing a search for ETI, RSI, andd individually for the various meds which make up the part of your sequence. Here's one to get you started: [/font:1fa58b239c] Teaching Points:::: Intubation-RSI

I think what you'll find here is part of what makes this site different from other EMS 'forums' is we expect a higher standard, and try to do our best to educate each other and learn as much as possible about EMS and medicine. Also, unofficially we have a sort of policy here where if one makes clinical or medicine related statements and purports it as fact; that we usually ask for independently cerifiable studies and literature which support your 'claims'. Like I said in my original post, based on your posts which I've read you seems to be a smart guy who wants to advance himself and EMS, thats why I asked for supporting information where if you had info. which no of us had perhaps we could all learn from it.

Out Here,

ACE844[/font:1fa58b239c]

[Ace844]

"FL_Medic,"

Here's a link to a 'paramedic RSI' protocol -rationale document where there are examples of this.

http://www.azdhs.gov/diro/admin_rules/guid...067-phs-ems.pdf

Anesthetics and Muscle Relaxants

For intravenous induction, a rapidly acting anesthetic is first administered. This is usually thiopental or propofol, but induction drugs include other rapidly acting barbiturates (e.g., methohexital, thiamylal), ketamine, benzodiazepines, narcotics (large doses if given alone), and etomidate. The details of the pharmacology of these drugs are described in the chapters on narcotics and nonnarcotic intravenous anesthetic agents. The choice of drug depends mainly on the status of the cardiovascular system but is also influenced by central nervous system effects, effects on bronchomotor tone, presence of an allergy, pharmacokinetic differences, side effects, and the experience of the clinician. Intubation may be accomplished with intravenous or inhalational anesthetics without relaxant, but this approach also possesses difficulties such as the potential for laryngospasm and a lesser degree of muscle relaxation to improve laryngoscopic conditions. In practice, most clinicians employ muscle relaxants to facilitate intubation.

Special Considerations

Laryngoscopy and intubation are powerful noxious stimuli, and the response may have deleterious respiratory, neurologic, or cardiovascular effects. Deeper levels of anesthesia are required to blunt the response to laryngoscopy and intubation than the response to surgical incision. When planning the anesthetic induction, these effects must be blunted to whatever degree is possible, especially if the patient is in a high-risk population (e.g., with coronary artery disease, asthma, elevated intracranial pressure, cerebral aneurysm).

SEDATION.

Narcotic analgesics are the key to facilitating conscious intubation. They afford mild sedation, analgesia, and reduction of airway reactivity that may result in cough and bronchospasm. Any narcotic may be used, but the overall characteristics of fentanyl have made it the most useful in such procedures. A lag in onset (i.e., hysteresis) of about 5 minutes for the full effect of fentanyl should be kept in mind as incremental doses of the drug are administered. Dose requirements also vary greatly between individuals (25 to 500 µg), and the drug should be administered slowly in small increments. The effect (or lack thereof) may not be apparent until the laryngoscope is inserted. Perhaps the greatest advantage of narcotics, especially fentanyl, is the ease of reversibility by naloxone if an undesired degree of respiratory depression results. Such patients may need to be reminded to breathe to ventilate adequately. If awake intubation is being performed because of a severe risk of aspiration, narcotics (and other intravenous sedatives) must be used sparingly.

To afford more sedation than a moderate dose of narcotics provides, a second drug is usually given. Droperidol (Inapsine) is a butyrophenone that supplies adequate sedation without adding to narcotic-induced respiratory depression. The drug is contraindicated in patients with Parkinson's disease because it blocks dopamine receptors and may produce a dystonic reaction. Doses of 1.25 to 5.0 mg given intravenously are usually adequate, although doses up to 10 mg have been used. The higher doses may be associated with bizarre side effects such as akathisia, dysphoria, and a prolonged state of sedation (up to 24 hours). To maximize the patient's comfort, it is best to administer a small dose of fentanyl before droperidol is given.

Other clinicians prefer to add a benzodiazepine to the narcotic effect. Midazolam (Versed), diazepam (Valium), or lorazepam (Ativan) may all be used, but midazolam is probably the most popular because of its relatively rapid onset and offset of action and the production of anterograde amnesia. The benzodiazepines should be administered slowly in small doses because their effect on consciousness, respiration, and cardiovascular status in individuals is unpredictable. Even 0.5 mg may produce adequate amnesia in some adults. Unlike droperidol, benzodiazepines result in increased respiratory depression in the presence of narcotics, which is usually manifest by apneic spells.[38] Flumazenil, a specific reversal agent, is available clinically. The principal disadvantage of using benzodiazepines may be the profound decreased level of consciousness that results in loss of verbal contact with the patient, who in such situations must be able to respond to commands, especially to breathe. In the frail elderly patient, intravenous diphenhydramine (Benadryl) in doses of 12.5 mg may provide good supplemental sedation to narcotics without excessive respiratory depression or adverse mental effects.

Out here,

ACE844

[AZCEP]

I won't discuss why you should or shouldn't use an opioid narcotic to assist with intubation. That is a matter entirely for your system to deal with.

A suggestion would be to try using some Morphine/Fentanyl in combination with the other agents, and you might find you get better results. The issue is one of patient comfort. Muscle groups that can't flex/extend periodically become extremely sore after a short time.

[chbare]

I have seen this confusion occur many times. People have a bad habit of grouping all controlled substances together an calling them narcotics. However, a narcotic is just that, a narcotic substance. While a benzo is a controlled substance, it is not a narcotic. We are talking about two different substances with completely different mechanisms of action.

Take care,

chbare.

[Ace844]

Hello Everyone,

Here's an interesting article on succs vs Roc. in RSI with an even more interesting reply...

HTH,

ACE844

(© 2005 by International Anesthesia Research Society. Volume 101(5) @ November 2005, pp 1356-1361

Rocuronium Versus Succinylcholine for Rapid Sequence Induction of Anesthesia and Endotracheal Intubation: A Prospective, Randomized Trial in Emergent Cases

[Anesthetic Pharmacology)

Sluga, Mathias MD; Ummenhofer, Wolfgang MD; Studer, Wolfgang MD; Siegemund, Martin MD; Marsch, Stephan C. MD, DPhil

Department of Anesthesia, Krankenhaus Thusis, Switzerland

Accepted for publication April 21, 2005.

Address correspondence to Stephan Marsch, MD, DPhil, Medizinische Intensivstation, Kantonsspital, 4031 Basel, Switzerland. Address e-mail to smarsch@uhbs.ch.]

Abstract

When anesthesia is induced with propofol in elective cases, endotracheal intubation conditions are not different between succinylcholine and rocuronium approximately 60 s after the injection of the neuromuscular relaxant. In the present study, we investigated whether, in emergent cases, endotracheal intubation conditions obtained at the actual moment of intubation under succinylcholine differ from those obtained 60 s after the injection of rocuronium. One-hundred-eighty adult patients requiring rapid sequence induction of anesthesia for emergent surgery received propofol (1.5 mg/kg) and either rocuronium (0.6 mg/kg; endotracheal intubation 60 s after injection) or succinylcholine (1 mg/kg; endotracheal intubation as soon as possible). The time from beginning of the induction until completion of the intubation was shorter after the administration of succinylcholine than after rocuronium (median time 95 s versus 130 s; P < 0.0001). Endotracheal intubation conditions, rated with a 9-point scale, were better after succinylcholine administration than after rocuronium (8.6 ± 1.1 versus 8.0 ± 1.5; P < 0.001). There was no significant difference in patients with poor intubation conditions (7 versus 12) or in patients with failed first intubation attempt (4 versus 5) between the groups. We conclude that during rapid sequence induction of anesthesia in emergent cases, succinylcholine allows for a more rapid endotracheal intubation sequence and creates superior intubation conditions compared with rocuronium.

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A rapid sequence induction of anesthesia and endotracheal intubation are indicated in emergency situations in the presence of a full stomach or other conditions with an increased risk of aspiration. Traditionally, succinylcholine has been the neuromuscular blocking drug of choice for rapid sequence induction of anesthesia. However, as a result of its depolarizing effect, succinylcholine can have serious side effects and is contraindicated in many conditions. Rocuronium has the most rapid onset of the currently available nondepolarizing neuromuscular blocking drugs. Therefore, many studies have investigated whether rocuronium may be a suitable alternative to succinylcholine. A meta-analysis of the Cochrane collaboration concluded that when propofol is used to rapidly induce anesthesia, endotracheal intubation conditions are not statistically different between succinylcholine and rocuronium (1). Before applying this evidence in daily practice, some important limitations of the Cochrane Review have to be recognized: (a) most of the patients receiving propofol were elective cases; ( only a small number of emergent cases actually underwent a rapid sequence induction of anesthesia and endotracheal intubation with propofol and rocuronium; and © in most studies included in the meta-analysis, tracheas were intubated approximately 60 s after the injection of the neuromuscular blocking drug, yet clinical practice may allow intubation sooner than 60 s after the injection of succinylcholine. It is currently not known whether endotracheal intubation conditions obtained at the actual moment of intubation under succinylcholine differ from those obtained 60 s after the injection of rocuronium.

Accordingly, the aim of the present study was to compare rocuronium with the current practice of the use of succinylcholine (i.e., endotracheal intubation as soon as possible) in patients requiring rapid sequence induction of anesthesia and endotracheal intubation for emergent surgery. The hypotheses to be tested were that (a) succinylcholine would allow for an earlier completion of the endotracheal intubation sequence and ( succinylcholine would create superior intubation conditions at the actual time of intubation.

Methods

The study took place in the Hospital of Thusis, a rural Level III center. All adult (age, >=18 yr) patients undergoing emergent surgery under general anesthesia were eligible. Indications for emergent surgery were mainly trauma (the hospital is located in a tourist region with skiing accidents in winter and climbing accidents in summer) and laparotomies. Exclusion criteria were hyperkalemia, neurologic disorders, burns, familial history of malignant hyperthermia, cesarean delivery, complications during birth before delivery, known or anticipated difficult endotracheal intubation warranting awake fiberoptic intubation, contraindication against the use of propofol (e.g., shock) and allergy to rocuronium. The study was approved by the regional Ethics Committee, and written informed consent was obtained during the preoperative visit. The primary outcomes of the study were the duration of the endotracheal intubation sequence and intubation conditions. Using a 9-point grading system for intubation conditions (Table 1), a difference of at least 1.0 points was considered to be of clinical relevance. A power analysis revealed that 85 patients were required for each study group to detect that difference with a power of 0.9 and a two-sided [alpha] of 0.05. To account for protocol violations related to an emergent procedure, we planned to enroll 90 patients per group.

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[Email Jumpstart To Image] Table 1. Scoring System for Endotracheal Intubation Conditions

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Patients were randomly allocated (sealed envelopes) to receive either 0.6 mg/kg of rocuronium (Esmeron™, Organon, Switzerland) or 1.0 mg/kg of succinylcholine (Lystenon™, Nycomed, Switzerland) as the neuromuscular blocking drug. No premedication was administered. Upon arrival in the operating room, a 18-gauge cannula was inserted in a forearm vein. Routine monitoring was used. End-tidal carbon dioxide was measured using the side-stream method (Cardiocap, Datex, Finland). Electrodes of a nerve stimulator (Healthcare NS 272; Fisher & Paykel, New Zealand) were placed over the left ulnar nerve.

One of three experienced staff anesthesiologists (MS, WU, or SM), assisted by a registered anesthetic nurse and a scrub nurse, was present throughout the whole procedure, guided the injection of drugs, and performed the endotracheal intubation. The staff anesthesiologist was not blinded to the neuromuscular blocking drug used, and the management of difficulties and complications, if any, was left to his discretion. To minimize bias, intubations were performed by three different anesthesiologists who had no personal preference for one of the two neuromuscular blocking drugs.

The endotracheal intubation sequence was defined as time interval between the injection of propofol and the first appearance of end-tidal carbon dioxide on the screen of the monitor. After 3 min of the administration of oxygen, cricoid pressure was applied, and anesthesia was induced with fentanyl 2 µg/kg and propofol 1.5 mg/kg. The neuromuscular blocking drug was injected as soon as the eyelid reflex had disappeared, and the nerve stimulator was switched to the single-twitch mode (rate, one twitch per second). Laryngoscopy was started either after the cessation of fasciculations in the lower extremities (2), if any, the cessation of a visible motor response to continuous single-twitch nerve stimulation, or after 50 s (anticipated time of intubation 60 s after the injection of the neuromuscular blocking drug), whichever was earlier. Endotracheal intubations were performed using a Macintosh size 3 blade and a tracheal tube (Mallinckrodt Hi-Contour, Mallinckrodt, Ireland) with an internal diameter of 7.5 cm in women and of 8.5 cm in men. The timing of events was performed by the anesthetic nurse.

Intubation conditions are usually evaluated using the following factors: (a) ease of laryngoscopy, ( position and movement of the vocal cords, and © response to intubation of the airway and the limbs (3). However, previous studies differ in that either a numerical (1) or a qualitative (4) score was derived from these factors. To allow for a comparison with both types of scoring systems previously used, we provide both a numerical and a qualitative rating. Both ratings are based on a scoring system proposed for good clinical research practice in studies of neuromuscular blocking drugs (3). The intubating anesthesiologist rated the ease of laryngoscopy, the movement and position of the vocal cords, and the reaction to intubation, as demonstrated in Table 1.

Desaturation was defined as either a saturation <=90% or a decrease in saturation of >=5% occurring at any time between the start of the induction sequence and 3 min after the completion of the intubation.

Data, presented as mean ± sd unless otherwise stated, were analyzed using SPSS 12.0 for Windows, a commercially available statistical software (SPSS, Chicago, IL). Two-way analysis of variance, unpaired Student’s t-test, Mann-Whitney test, Fisher’s exact test, and the logrank test were applied, as appropriate. General linear modeling was used to assess differences among the 3 intubating anesthesiologists with regard to scoring of the intubation conditions. A P < 0.05 was considered to represent statistical significance.

Results

During the study period ending with the completion of the protocol in the 180th patient, 234 consecutive patients underwent emergency surgery under general anesthesia. Five had to be excluded because of predefined exclusion criteria (2 cesarean delivery, 2 hemorrhagic shock, and 1 hyperkalemia), 16 refused to participate, and the enrollment of 33 was missed, mainly because of high workload. One-hundred-eighty patients were randomized, received the allocated treatment, and were included in the analysis (Table 2).

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[Email Jumpstart To Image] Table 2. Patient Demographics

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The median time interval between the beginning of the administration of propofol and the disappearance of the eyelid reflex was 30 s (interquartile range, 18.5 s) in the succinylcholine group and 26 s (interquartile range, 20 s) in the rocuronium group (P = 1.0). Figure 1 depicts the time interval from injection of the neuromuscular blocking drug to the cessation of a visible motor response to continuous single-twitch nerve stimulation of the ulnar nerve. This time interval was significantly shorter (P < 0.0001) in the succinylcholine group (median time, 40 s) compared with the rocuronium group (median time, 70 s). Figure 2 depicts the time interval between the beginning of the administration of propofol and the first appearance of end-tidal carbon dioxide after endotracheal intubation, which was significantly shorter (P < 0.0001) in the succinylcholine group (median time, 95 s) compared with the rocuronium group (median time, 130 s).

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[Email Jumpstart To Image] Figure 1. Kaplan-Meyer curve of the probability of the disappearance of a visible motor response to a continuous single-twitch stimulation of the ulnar nerve after injection of succinylcholine or rocuronium. Time 0 denotes the injection of the neuromuscular blocking drug. Curves differ significantly (P = < 0.0001; logrank test).

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[Email Jumpstart To Image] Figure 2. Kaplan-Meyer curve of the probability of the completion of the endotracheal intubation sequence including succinylcholine or rocuronium as the neuromuscular blocking drug. Time 0 denotes the beginning of the injection of the induction drug propofol. The endotracheal intubation sequence was defined to be completed upon the first appearance of end-tidal carbon dioxide after intubation. Curves differ significantly (P < 0.0001; logrank test).

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Scores for endotracheal intubation conditions were significantly higher in the succinylcholine group than in the rocuronium group (8.6 ± 1.1 versus 8.0 ± 1.5; P < 0.001). This difference resulted almost exclusively from a difference in the subscore rating the response to intubation (2.8 ± 0.5 versus 2.3 ± 1.0; P < 0.0001), whereas there was no difference in the subscores for laryngoscopy (2.9 ± 0.3 versus 2.9 ± 0.3; P = 0.91) and vocal cords (2.9 ± 0.4 versus 2.8 ± 0.6; P = 0.23). Figure 3 depicts the scores for intubating conditions. Note that compared with the rocuronium group, there were significantly more excellent intubation conditions in the succinylcholine group (Fig. 3). However, there was no difference in patients with poor intubation conditions between the groups (7 versus 12; P = 0.33). General linear modeling showed (a) no significant difference among the 3 intubating anesthesiologists with regard to the rating of the intubation conditions (F2,168 = 0.21; P = 0.81), ( no significant interaction of the 2 between-subject factors intubating anesthesiologist and neuromuscular blocking drug (F2,168 = 1.47; P = 0.23), and © no significant interaction of the between-subject factor intubating anesthesiologist and the within-subject factor subscores of intubation conditions (F4,336 = 0.87; P = 0.48). This indicates that there was no systematic difference in scoring among the 3 intubating anesthesiologists.

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[Email Jumpstart To Image] Figure 3. Endotracheal intubation conditions during rapid sequence induction of anesthesia and endotracheal intubation with succinylcholine or rocuronium as the neuromuscular blocking drug. The scoring system is explained in Table 1. *P < 0.05 between the 2 neuromuscular blocking drugs (Fisher’s exact test).

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Eighty-six of 90 patients in the succinylcholine group and 85 of 90 patients in the rocuronium group were intubated during the first attempt (P = 1.0). All remaining nine patients were successfully endotracheally intubated in the second attempt. The reasons for the four failures of the first intubation attempt in the succinylcholine group were one poor intubation condition (numerical score 3), one esophageal intubation (intubation score excellent), and two “difficult anatomy” (intubation scores excellent and good, respectively) that could be mastered in the second attempt by mounting the tube on a stylet. The reasons for the five failures of the first intubation attempt in the rocuronium group were one poor intubation condition (numerical score 4), two esophageal intubations (intubation scores excellent and good, respectively), and two “difficult anatomy” (intubation score excellent in both cases) that could be mastered in the second attempt by mounting the tube on a stylet. Thus, poor intubation conditions were observed in only two of the nine patients (one in each group) not intubated in the first attempt.

A desaturation occurred in 5 of 90 patients in the succinylcholine group and in 9 of 90 patients of the rocuronium group (P = 0.40). Poor endotracheal intubation conditions were observed in only 2 of the 14 patients (one in each group) with desaturation, whereas 8 of 14 desaturations were associated with an excellent intubation score. Four of 14 desaturations (2 in each group) occurred in patients with a second intubation attempt. Compared with the patients without desaturation, the time interval from the beginning of the administration of propofol and the completion of the intubation was longer in patients with desaturation (134 ± 9 s versus 116 ± 3 s; P = 0.047).

Discussion

In the present study, we compared rocuronium with the current practice of the use of succinylcholine (i.e., endotracheal intubation as soon as possible) in patients requiring rapid sequence induction of anesthesia and endotracheal intubation for emergent surgery. When succinylcholine was used as the neuromuscular blocking drug for rapid sequence induction of anesthesia, the median intubation sequence was 35 s shorter than when rocuronium was used. Succinylcholine created excellent intubation conditions more often than rocuronium, and there was a statistically significant difference of 0.5 points on a 9-point grading scale of intubation conditions in favor of succinylcholine. However, as far as clinically acceptable intubating conditions and failed intubation attempts are concerned, the two relaxants were not statistically different.

Analyzing the available evidence up to the year 2000, a Cochrane Review concluded that for rapid sequence induction of anesthesia, succinylcholine created superior endotracheal intubation conditions to rocuronium when comparing excellent intubation conditions. Using the less stringent clinically acceptable intubation conditions, the two drugs were not statistically different (1). Moreover, based on a subgroup analysis, the Cochrane Review concluded that intubation conditions did not statistically differ between the administration of succinylcholine and rocuronium when propofol was used as the drug to induce anesthesia (1). Several potential limitations of these conclusions are noteworthy. Only 24 of the 1606 patients included in the Cochrane Review were emergent cases that actually underwent a true rapid sequence induction of anesthesia and endotracheal intubation with both propofol and rocuronium. All 24 patients were part of a single study and received 1 mg/kg of rocuronium (4). Moreover, only 47 of the 640 patients included in the subgroup using propofol as the induction drug (4–12) were emergency cases undergoing a true rapid sequence induction of anesthesia and endotracheal intubation. From the remaining 593 elective cases, approximately 50% (n = 290) did not undergo a true rapid sequence induction of anesthesia. Most previous studies comparing succinylcholine and rocuronium assessed endotracheal intubation conditions approximately 60 seconds after the injection of the neuromuscular blocking drug (1). Whereas this is an appropriate time interval for rocuronium, a delay between injection of succinylcholine and start of laryngoscopy of 50 seconds or more does not reflect current practice; most, if not all, anesthesiologists choosing succinylcholine for rapid sequence induction of anesthesia and endotracheal intubation take advantage of its rapid onset of action and start laryngoscopy as quickly as possible, i.e., after the cessation of fasciculations. Indeed, 50 seconds after the injection of the neuromuscular blocking drug, i.e., the time of the beginning of the laryngoscopy in previous studies, the intubation sequence was already completed in more than one-third of the patients in the succinylcholine group of the present study.

Based on current evidence, the induction of anesthesia sequence of the present study was chosen to achieve the best possible endotracheal intubation conditions for the rocuronium group. Propofol was used as the induction drug because this anesthetic seems to be superior to all other drugs with regard to intubating conditions after rocuronium injection (1). Fentanyl (2 µg/kg) was added to the induction sequence because opioids, in doses equivalent to alfentanil 20 µg/kg, were found to significantly improve intubating conditions after rocuronium administration (13). Intubation was attempted 60 seconds after the injection of rocuronium because this seemed to be the earliest moment when acceptable intubation conditions can be reliably achieved (1). Rocuronium was used in a dose of 0.6 mg/kg because there seemed to be no benefit of larger rocuronium doses on intubation conditions when propofol was used as the induction drug (1). Previous work demonstrated a dose-dependent effect of rocuronium on both onset and duration of neuromuscular block (14). Thus, there is the possibility that larger doses of rocuronium would allow for an earlier intubation. However, all studies comparing intubation conditions after different doses of rocuronium did so after a predefined time interval (usually 60 seconds after the injection of rocuronium). Thus, it is unknown whether the earlier onset of neuromuscular block associated with doses larger than 0.6 mg/kg of rocuronium would translate into a clinical advantage, i.e., the possibility for an earlier intubation with at least the same intubation conditions that are achievable at 60 seconds.

An important limitation of our study is the lack of a double-blind design. Concealing the effects of drugs that have visible effects such as fasciculations is inherently difficult. Moreover, because the two neuromuscular blocking drugs studied differ in onset time, awareness of the time of the injection of the drug results in unblinding. Thus, a perfect double-blind design implies that the intubating anesthesiologist is not able to see or overhear the patient and the team performing the induction sequence and is immediately available to intubate the patient’s trachea after the cessation of fasciculations. A rapid sequence induction of anesthesia is a high-risk procedure requiring the full attention of an appropriately trained anesthesiologist. Because, in our settings, the simultaneous achievement of perfect blinding and optimal patient safety was not feasible, we opted for a single-blind study design. The statistical analysis of the effects and interactions of neuromuscular blocking drugs and the intubation scores revealed a homogenous rating with no systematic differences among the anesthesiologists performing the intubations.

The power of the present study was too small to allow reliable conclusions on the incidence of complications. These issues should be addressed in large multicenter trials. Interestingly, in the present study, only a minority of failed first endotracheal intubation attempts and desaturations were associated with a low score of intubation conditions. If confirmed in further trials, these findings may lead to a modification of the scoring system presently used.

What are the practical implications of our findings? Choosing rocuronium instead of succinylcholine for rapid sequence induction of anesthesia prolongs the time of unprotected airway, i.e., the time interval from beginning of the induction until completion of endotracheal intubation, from a median time of 95 seconds to a median time of 130 seconds. The additional risk of aspiration and desaturation resulting from a prolongation of the intubation sequence by a median time of 35 seconds is unknown, but it is most likely very small in most patients. However, patients with an especially high risk for aspiration or a desaturation may benefit from a more rapid intubation. Choosing rocuronium instead of succinylcholine for rapid sequence induction of anesthesia results in less optimal intubating conditions. However, the difference between the two relaxants is small and mainly results from lower ratings in the subscore addressing the reaction to intubation, i.e., coughing or bucking. Because the reaction to intubation occurs after the placement of the tube, the relevance for patients’ safety is marginal. Until more data on complications are available, we suggest that anesthesiologists select the best treatment for their patients undergoing a rapid sequence induction of anesthesia on an individual basis by balancing intubation conditions and duration of the intubation sequence against potential side effects.

Compared with the subgroup of patients receiving propofol included in the recent Cochrane Review on rapid sequence induction (1), in the present study, we observed significantly more poor intubation conditions after both neuromuscular blocking drugs (19 of 180 versus 27 of 640 poor intubation conditions; P = 0.007). Because most patients included in the Cochrane Review were elective cases not undergoing a true rapid sequence induction of anesthesia, this difference is most likely explained by differences in the patient population and the procedure. Although elective cases are valuable models for investigating the effects of neuromuscular blocking drugs, findings obtained in this setting may thus not be necessarily extrapolated to emergency situations.

In conclusion, in the context of a rapid sequence induction of anesthesia with propofol and fentanyl in emergent cases, succinylcholine allowed for a more rapid endotracheal intubation sequence and created superior intubation conditions than rocuronium. Presently, practitioners have to balance the quality of intubation conditions and the duration of the intubation sequence against the potential for side effects. Large-scale trials are required to address important safety issues such as failed intubation attempts and desaturations associated with the use of succinylcholine or rocuronium.

References

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2. Ummenhofer WC, Kindler C, Tschaler G, et al. Propofol reduces succinylcholine induced increase of masseter muscle tone. Can J Anaesth 1998;45:417–23. SFX Bibliographic Links Library Holdings [Context Link]

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4. Andrews JI, Kumar N, Van Den Brom RHG, et al. A large simple randomized trial of rocuronium versus succinylcholine in rapid-sequence induction of anaesthesia along with propofol. Acta Anaesthesiol Scand 1999;43:4–8. SFX Bibliographic Links Library Holdings [Context Link]

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6. Chiu CL, Jaais F, Wang CY. Effect of rocuronium compared with succinylcholine on intraocular pressure during rapid sequence induction of anaesthesia. Br J Anaesth 1999;82:757–60. SFX Bibliographic Links Library Holdings [Context Link]

7. Latorre F, Stanek A, Gervais HW, Kleemann PP. Intubation requirements after rocuronium and succinylcholine. Anasthesiol Intensivmed Notfallmed Schmerzther 1996;31:470–3. SFX Bibliographic Links Library Holdings [Context Link]

8. Le Corre F, Plaud B, Benhamou E, Debaene B. Visual estimation of onset time at the orbicularis oculi after five muscle relaxants: application to clinical monitoring of tracheal intubation. Anesth Analg 1999;89:1305–10. Ovid Full Text Bibliographic Links Library Holdings [Context Link]

9. Naguib M, Samarkandi AH, Ammar A, Turkistani A. Comparison of suxamethonium and different combinations of rocuronium and mivacurium for rapid tracheal intubation in children. Br J Anaesth 1997;79:450–5. SFX Bibliographic Links Library Holdings [Context Link]

10. Puhringer FK, Khuenl-Brady KS, Koller J, Mitterschiffthaler G. Evaluation of the endotracheal intubating conditions of rocuronium (ORG 9426) and succinylcholine in outpatient surgery. Anesth Analg 1992;75:37–40. SFX Bibliographic Links Library Holdings [Context Link]

11. Vinik HR. Intraocular pressure changes during rapid sequence induction and intubation: a comparison of rocuronium, atracurium, and succinylcholine. J Clin Anesth 1999;11:95–100. SFX Bibliographic Links Library Holdings [Context Link]

12. Stoddart PA, Mather SJ. Onset of neuromuscular blockade and intubating conditions one minute after the administration of rocuronium in children. Paediatr Anaesth 1998;8:37–40. [Context Link]

13. Sparr HJ, Giesinger S, Ulmer H, et al. Influence of induction technique on intubating conditions after rocuronium in adults: comparison with rapid-sequence induction using thiopentone and suxamethonium. Br J Anaesth 1996;77:339–42. SFX Bibliographic Links Library Holdings [Context Link]

14. Wright PM, Caldwell JE, Miller RD. Onset and duration of rocuronium and succinylcholine at the adductor pollicis and laryngeal adductor muscles in anesthetized humans. Anesthesiology 1994;81:1110–5. SFX Bibliographic Links Library Holdings [Context Link]

(Rocuronium in Emergent Intubation

[Letters to the Editor)

Chamorro, C MD; Romera, M A. MD; Valdivia, M MD

Intensive Care Unit; Hospital Universitario Puerta de Hierro; Madrid, Spain; cchamorro.hpth@salud.madrid.org

Dr. Marsch does not wish to respond.]

To the Editor:

The interesting study published by Sluga et al. (1) could be misinterpreted concerning the use of succinylcholine and rocuronium for emergency tracheal intubation. For surgical emergencies (unscheduled emergency operations), there is typically time to obtain serum electrolytes, a medical history, and written informed consent, as happened in Sluga et al.’s study. However, during emergency tracheal intubations in other settings (e.g., shock, trauma) there is no time to assess renal function status, potassium levels, previous neurologic disorders, or whether the patient has had a long period of immobilization. We reviewed the medical records of all patients who required emergency tracheal intubation in our intensive care unit over the course of 1 yr. Thirty-five percent had at least one condition that potentially contraindicated the use of succinylcholine (2). In several cases, succinylcholine may have precipitated the subsequent cardiac arrest. As Sluga et al. observe, rocuronium results in less optimal, but good, intubating conditions compared with succinylcholine. Other authors have reached the same conclusion (3,4). For these reasons we have replaced succinylcholine with rocuronium for emergency tracheal intubation outside of the operating room. In our view, succinylcholine is an obsolete (5) and potentially dangerous drug for intubating patients in settings where one cannot eliminate well-established contraindications to its use.

C. Chamorro, MD

M. A. Romera, MD

M. Valdivia, MD

Intensive Care Unit

Hospital Universitario Puerta de Hierro

Madrid, Spain

cchamorro.hpth@salud.madrid.org

[FL_Medic]

This is a link to our treatment guidelines. Just in case your interested. Thanks for all your resources.

http://internet.lee-ems.com/intranet/publi..._guidelines.pdf

[Ace844]

"FL_Medic, and Everyone,"

In addition to the material already posted above. Here is a great article which covers the assessment of analgesia under anesthesia. The majority of the study discusses 'perioperative' conditions, yet i am sure that we all know this info can be extarpolated to both the CCT-flight environment S/P RSI in the setting of contuing paralysis and sedation as well as initally.

Hope This Helps,

ACE844 [/font:e8cbdcc9fb]

[quote=Best Practice & Research Clinical Anaesthesiology

Volume 20, Issue 1 , March 2006, Pages 161-180

Monitoring Consciousness

doi:10.1016/j.bpa.2005.09.002

Copyright © 2005 Elsevier Ltd All rights reserved.

14

Monitoring analgesia

Bruno Guignard MD,

Département d'Anesthésie Réanimation, Hôpital Ambroise Paré, 9 avenue du général de Gaulle, 92100 Boulogne Billancourt, France

Available online 17 March 2006.]

Analgesia (pain relief) amnesia (loss of memory) and immobilisation are the three major components of anaesthesia. The perception of pain, and therefore, the need for analgesia, is individual, and the monitoring of analgesia is indirect and, in essence, of the moment. Under general anaesthesia, analgesia is continually influenced by external stimuli and the administration of analgesic drugs, and cannot be really separated from anaesthesia: the interaction between analgesia and anaesthesia is inescapable. Autonomic reactions, such as tachycardia, hypertension, sweating and lacrimation, although non-specific, are always regarded as signs of nociception or inadequate analgesia. Autonomic monitoring techniques, such as the analysis of heart rate variability, laser Doppler flowmetry, phlethysmographically derived indices and the pupillary light reflex, may help to quantitate reactions of the autonomic nervous system. For the past few years, automated electroencephalographic analysis has been of great interest in monitoring anaesthesia and could be useful in adapting the peroperative administration of opioids. A range of information collected from the electroencephalogram, haemodynamic readings and pulse plethysmography might be necessary for monitoring the level of nociception during anaesthesia. Information theory, multimodal monitoring, and signal processing and integration are the basis of future monitoring.

Monitoring analgesia

Definitions

Anaesthesia is a state of unconsciousness induced by a drug. The three components of anaesthesia are analgesia (pain relief), amnesia (loss of memory) and immobilisation, even though some authors have tried to reduced anaesthesia to a lack of perception or recall of noxious stimulation.1 The drugs used to achieve anaesthesia usually have varying effects in each of these areas. Some drugs may be used individually to achieve all three targets, whereas others have only analgesic or sedative properties and may be used individually for these purposes or in combination with other drugs to achieve full anaesthesia. Physiological methods of monitoring must be used to assess anaesthetic depth as normal reflex methods will not be reliable. The major problem is to define what anaesthesia and analgesia really are. In this regard combinations of anaesthetics and analgesics, known as ‘balanced anaesthesia’, do not help to provide a practical understanding of the concept of depth of anaesthesia paradigm.2

Pain is one of the most unpleasant sensations in existence, and even in fetal life noxious stimulation causes detectable stress responses. The prevention and treatment of pain are a basic human right, so a better comprehension of the detailed action of analgesics on pain relief is a challenge for the future.3 There have been many reports on pain research from various fields of medical science, for example physiology, pharmacology, biochemistry and immunology, and the knowledge acquired of the mechanisms of pain perception in the human brain can be directly related to the treatment of pain and the monitoring of pain relief.

Pain is a more complicated sensation than other somatosensory modalities such as touch and vibration, as the degree of feeling can be easily changed by a change in mental state, pain being, by its very nature, subjective. In conscious subjects, pain is greatly affected by the amount of attention paid to and distraction from a noxious stimulus, but this is not the case under sedation or general anaesthesia. Human, as well as animal, studies on pain perception are necessary, but only a relatively small number of the former have been carried out because such studies must be non-invasive. Recently, non-invasive techniques have been developed, such as electroencephalography (EEG), magnetoencephalography, positron emission tomography, functional magnetic resonance imaging and transcranial magnetic stimulation, and the number of reports on pain perception using these techniques has progressively increased over the past 10 years.4, 5, 6 and 7

Analgesia is defined by the relief of pain, in other words by absence of pain in response to stimulation that would normally be painful. This definition is subjective because pain is defined by the International Association for Study of Pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”. Pain is a subjective sensation because of this individuality and is also difficult to assess because of the inability to communicate directly about the sensation of pain. Instead, indirect clinical signs of pain are used during anaesthesia. Because of the difficulty in determining when pain is present during general anaesthesia, it is assumed that something that is painful involves reactions of the body that are visible by clinical observation or by monitoring. Analgesia could also be defined by the combination of a stable state and the absence of pain—if the subject were conscious—during and immediately after a painful stimulus.

One of the great paradoxes of analgesia is that, by its very nature, it cannot be predicted because of the perpetual interaction between variations in stimulation and variations in the patient's anaesthetized state. Like anaesthesia, analgesia is a continuum between a perceived absence of pain and maximum pain. Analgesia can be partial and incomplete, and the notion of a threshold of analgesia depends on the state of the patient and is continually under influence of external stimuli.

Which parameters should be used to monitor analgesia?

Individual perception of pain

This chapter does not aim to consider the auto-evaluation of pain: a discussion of quantitative sensory testing of the nociceptive system in conscious subjects can be found in an article by Dotson.8 Instead, we will look at methods that could be used in unconscious patients; elucidating the mechanisms underlying pain perception in unconscious subjects could help us to understand analgesia.

There is a relationship between the pain system and the motor, sensory and autonomic systems. Alterations to these systems, for example in a child with a significant neurological impairment, can have a profound and unique impact on the pain experience and analgesia.9 Likewise, hypoalgesia in borderline personality disorders may primarily be due to altered intracortical processing similar to that seen in certain meditative states: there is no general impairment of the sensory-discriminative component of pain, no hyperactive descending inhibition, and no attention deficits revealed by laser evoked potentials.10 There are also gender differences in pain perception11, 12 and 13, which might be of clinical relevance in morphine titration.14 These differences could be explained by a more pronounced descending inhibitory control.15 Nevertheless, there is no difference in desflurane minimum alveolar concentration (MAC) between young men and women.16

Clinical variation in the perception of analgesia

Both the Ramsay Sedation Score and the Observer's Assessment of Alertness/Sedation Scale include response to pain in their graduated scales, reflecting an abolition of conscious pain perception.17 and 18 The Cardiac Analgesic Assessment Scale is a postoperative pain evaluation instrument used in children after cardiac surgery, providing more information than a visual analogue scale completed by an observer.19 Studies performed with anaesthetic personnel show that no variable was considered entirely specific for either intraoperative pain or depth of anaesthesia. Changes in breathing rate and volume, blood pressure, heart rate and lacrimation, as well as the presence of moist and sticky skin, were given higher scoring values as indicators of pain than as indicators of depth of anaesthesia.20

Movement and minimum anaesthetic concentration

Under general anaesthesia, movement in response to painful stimulation is the end-point classically used to assess the potency of anaesthetic agents. Withdrawal reflexes are tailored to produce the most appropriate movement according the site at which the noxious stimulus is applied, as flexors or extensors could act as the primary movers. Areas from which a reflex can be sensitised closely match those from which the reflex itself can be evoked, providing the spinal cord is intact.21 The principal site of response to nociceptive stimulation is spinal22, and the interaction between analgesia and anaesthesia is inescapable.

Interconnection between haemodynamics and nociception

Somatosympathetic reflexes have been characterised for more than 30 years23, but the exact interaction between systems is still being researched because relationships are complexes.24 and 25

Some neurones from the rostral ventrolateral medulla have spinally projecting axons, and their responses to noxious mechanical, thermal and/or electrical stimulation have been shown to be accompanied by increases in arterial pressure in anaesthetised rats. In humans with spinal cord transection above vertebral level T5, profound elevations in systolic blood pressure and pulse pressure were induced by bladder distension: the authors noticed a decrease in heart rate in three of seven patients.26 A baroreflex mechanism may explain hypertensive hypoalgesia. At rest, arterial baroreceptors are stimulated during the systolic upstroke of the pressure pulse wave. Stimulation of the baroreceptors by natural increases in blood pressure during the systolic phase of the cardiac cycle was associated with dampened nociception.

There are also interactions between angiotensin and pain perception. Untreated hypertensive subjects showed a reduced perception to painful stimuli when compared with normotensive individuals. A significant reduction in both pain threshold and tolerance was observed during enalapril or losartan treatment.27 Hypertension diminishes pain perception, and the electrical stimulation of vagal afferent nerves (cardiopulmonary baroreceptors) suppresses nociceptive responses. In addition, both a pharmacological elevation of blood pressure and vascular volume expansion produce anti-nociception.28

Autonomic reactions

Autonomic reactions, such as tachycardia, hypertension, sweating and lacrimation, have usually been regarded as signs of nociception or inadequate analgesia, heart rate being less consistent than blood pressure response. Isoflurane used as a sole agent is unable to suppress haemodynamic reactions (blood pressure and heart rate) to painful stimuli.

The lack of motor response is not an accurate predictor of the ability of an agent to depress haemodynamic reactions29, but haemodynamic responses after noxious stimulation such as laryngoscopy or tracheal intubation are still considered to be the responses which are easiest to interpret during anaesthesia.30 Motor or haemodynamic responses to nociceptive stimuli could, a posteriori, serve to adapt the dosage of hypnotic or analgesic agents, and heart rate variations have been used to automatically amend remifentanil target-controlled infusion during general anaesthesia.31 Tentative measures for standardisation have been proposed by Evans, using the PRST (blood Pressure, heart Rate, Sweating, Tears) score of responsiveness (Table 1).

Table 1.

Evans' PRST score. Clinical signs Conditions Score

Systolic arterial pressure (mmHg) <Control+15 0

<Control+30 1

>Control+30 2

Heart rate (beats per minute) <Control+15 0

<Control+30 1

>Control+30 2

Sweating None 0

Skin moist to touch 1

Visible beads of sweat 2

Tears No excess of tears in open eye 0

Excess of tears in open eye 1

Tears overflow closed eye 2

Stimulation of the sympathetic system in response to noxious stimulus is, however, not always the case. Parasympathetic stimulation can occur, with opposite responses (Table 2).

Table 2.

Responses of major organs to autonomic nerve impulses. Organ Sympathetic stimulation Parasympathetic stimulation

Heart Increased heart rate β1 (and β2) Decreased heart rate

Increased force of contraction β1 (and β2) Decreased force of contraction

Increased conduction velocity Decreased conduction velocity

Arteries Constriction (α1) Dilatation

Dilatation (β2)

Veins Constriction (α1)

Dilatation (β2)

Lungs Bronchial muscle relaxation (β2) Bronchial muscle contraction

Increased bronchial gland secretions

Eye Dilatation of pupil (α) Constriction of pupil

Contraction of sphincters (α) Increased lacrimal gland secretions

Liver Glycogenolysis (β2 and α) Glycogen synthesis

Gluconeogenesis (β2 and α)

Lipolysis (β2 and α)

Kidney Renin secretion (β2)

Bladder Detrusor relaxation (β2) Detrusor contraction

Contraction of sphincter (α) Relaxation of sphincter

Uterus Contraction of pregnant uterus (α)

Relaxation of pregnant and non-pregnant uterus (β2)

Submandibular and parotid glands Viscous salivary secretions (α) Watery salivary secretions

Different types of pain can lead to particular reactions. For example, the mesenteric Pacinian corpuscle is the baroreceptor that probably initiates the vasomotor reflexes in skin and muscle32 during abdominal pain.

Chronotropic and inotropic responses to the noxious stimulation caused by laryngoscopy or surgical stimulation can be effectively suppressed by beta-receptor blockade33, and esmolol leads to analgesia and a reduction in cardiovascular responses to pain in the non-sedated rat.34 Esmolol does not attenuate the heart rate response to sternotomy but does attenuate the increase in blood pressure in patients receiving chronic beta-blocker therapy.35 Perioperative esmolol administration during anaesthesia reduced the intraoperative use of isoflurane and fentanyl by 25%, decreased haemodynamic responses and reduced morphine consumption by 30% for the first 3 postoperative days in patients undergoing a hysterectomy.36

Vagal afferent nerves are thought to mediate autonomic responses evoked by noxious mechanical or chemical oesophageal stimuli, and participate in the perception of pain originating from the oesophagus. The fibres involved in this mechanism include both A and C fibres.37 Sesay et al have evaluated electrocardiographic (ECG) spectral analysis during surgery on the cerebellopontine angle. Vagal reactions were defined as a decrease in heart rate or an increase in HF of more than 10% of the pre-stimulus value. This monitoring permits the detection of intraoperative vagal reactions earlier than is allowed by the conventional monitoring of heart rate38, as could be seen during a study of hysteroscopy.39 The vagus nerves supply the guinea-pig oesophagus with nociceptors in addition to tension mechanoreceptors.37 Susceptibility to vasovagal reactions after a noxious stimulus may be associated with individual differences in baroreflex sensitivity.40

Monitoring the cardiac autonomic system: heart rate variability

Cardiac autonomic function is estimated by heart rate variability measures and is expressed in the time domain as the mean of R–R intervals for normal heart beats and the standard deviation of all normal R–R intervals. The spectral analysis of heart rate variability allows a continuous, non-invasive quantification of cardiac autonomic function, pure vagal activity being assessed by high-frequency power (0.15–0.4 Hz). Low-frequency power (0.04–0.15 Hz) reflects both parasympathetic and sympathetic control.

Numerous studies of ischaemic heart disease have used this method, demonstrating the clinical significance of heart rate variability analysis. An acute noxious stimulus appears to produce an increase in respiratory-related sympathetic heart rate control and a significant decrease in respiratory-related parasympathetic control in adults and infants. Stressful events during the heel-prick procedure in newborn infants41 or painful stimuli in children42 could be evaluated by this method. With increasing age, the sympathetic and parasympathetic changes appear to be less intense but more sustained.43 Limitations of this method are artefact detection and the necessity for a long enough period of signal sampling. Wavelet analysis could be helpful with this indication.44

Skin vasomotor reflexes

Testing the skin vasomotor reflexes (SVmR) by laser Doppler flowmetry is a recognised method of measuring peripheral dysautonomia and can detect an impairment of the reflex control of fingertip blood flow in both diabetes mellitus and leprosy.45 The reflex control of fingertip blood flow is assessed by measuring the reduction in laser Doppler flowmetry induced by a deep inspiratory gasp, a cold challenge of immersing the contralateral hand in cold water or electrostimulation of the ulnar nerve. Patients with diabetic neuropathy had resting laser Doppler flowmetry levels significantly lower than those of the uncomplicated group and showed a substantial impairment of both the inspiratory gasp and cold challenge reflexes.46

A sympathetic vasoconstrictor reflex is induced by noxious stimulation: laryngoscopy alone and intubation with laryngoscopy significantly reduced skin blood flow.47 Shimoda et al evaluated SVmR in response to laryngoscopy. A decrease in SVmR amplitude to less than 0.1 u before laryngoscopy is associated with blood pressure stability. SVmR amplitude and systolic blood pressure changes showed a significant linear correlation.48

SVmR is also useful to estimate objectively the level of somatosensory block induced by regional anaesthesia.49 and 50 Shimoda et al demonstrated that the level of current that induced the SVmR was proportional to the depth of anaesthesia induced by sevoflurane, and that the duration of electrostimulation (i.e. painful increase) was correlated to the magnitude of the SVmR.51 Thus, the SVmR could be helpful in the objective assessment of nociception and anti-nociceptive effects in individual cases. These authors also investigated the SVmR and haemodynamic responses to the insertion of an intubating laryngeal mask airway and found that the most stressful period was removal of the airway.52

Nakahara et al determined the MAC of anaesthetic that blocked the SVmR to surgical incision (MACBVR) for sevoflurane in 37 patients.53 They found that the MACBVR contribution to the total anaesthetic MAC multiple was 1.75 MAC for sevoflurane alone and 1.43 MAC when 50% nitrous oxide was used. There was no relationship between the amplitude of the reduction in skin blood flow and any changes in haemodynamic variables. Owing to its resistance to chronic ischaemia, the SVmR is preserved in chronically ischaemic limbs with non-diabetic, atherosclerotic peripheral arterial disease.54

Neuropeptide Y participates in sympathetically mediated cutaneous vasoconstriction.55 Owing, however, to the cost of the device to measure its level, this technique is used only in research.

Plethysmography

Plethysmogram amplitude

Sustained pinching of the interdigital webs of the hands of human volunteers induced a tonic reflex vasoconstriction in the stimulated hand with a rather slow adaptation rate and no signs of habituation between trials. Step increases in the pinching force in the course of a stimulus were reflected by a decrease in amplitude of the plethysmogram.56 This reflex occurred at a spinal level but could be inhibited by the cerebral hemispheres.57 Skin incision is followed by a clear sympathetic vasoconstrictor response in the plethysmographic signal, and suppression of the photoplethysmographic pulse wave reflex to a nociceptive stimulus has also been found to predict a reduced haemodynamic response to tracheal intubation.58

The pulse wave reflex may be a better predictor than other variables. In another study, the best variables for logistic regression classification in movers versus non-movers at incision appeared to be response entropy, instant RR and plethysmogram notch amplitude. Plethysmogram notch amplitude was measured as the distance from the baseline to the lowest value of the notch (Figure 1).59 Nevertheless, arterial pressure was not incorporated into the variables studied.

(20K)

Figure 1. Parameters measured from the pulse plethysmography waveform.

Pulse transit time

PTT was originally measured by recording the time interval between the passage of the arterial pulse wave at two consecutive sites. More recently, for ease of measurement, the electrocardiographic R or Q wave has been used as the starting point as it approximately corresponds to the opening of the aortic valve. This ‘new’ pulse transit time (rPTT), the interval between ventricular electrical activity and the arrival of a peripheral pulse waveform, has been used to detect changes in autonomic tone and in inspiratory effort. Noxious stimulation can affect this parameter: during anaesthesia, rPTT decreased by an average of 43±25 ms in response to endotracheal intubation but did not vary in response to the insertion of laryngeal mask airway or to a surgical stimulus.60 This measure does not seem suitable, but further studies are needed.

The major problem with SVmR and plethysmography-derived measures is that skin blood flow is profoundly influenced by not only pathological states, but also thermoregulatory state, age and emotional stress.61, 62 and 63

Pupil

Iris activity reflects physiological reactions to different sensory stimuli, resulting in a variation in pupil size. As such, pupillometry is a method that can provide valuable data concerning the functioning of the autonomous nervous system.64 Pupil size reflects the interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system and can be used to evaluate brainstem function in comatose patients.65 Noxious stimulation and the cold pressure test dilate the pupil—pupillary reflex dilatation (PRD)—in both unanaesthetised and anaesthetised humans.66 In the absence of anaesthesia, dilatation is primarily mediated by the sympathetic nervous system. In contrast, under anaesthesia, pupillary dilatation in response to noxious stimulation or desflurane step-up is mediated principally by inhibition of the midbrain parasympathetic nucleus, although the exact mechanism remains unknown.67 PRD is not present in organ donors (Yang). In addition, esmolol does not block PRD in anaesthetised volunteers.68

Pupillary size and reactivity have long been a critical component of the clinical assessment of patients with or without neurological disorders.69 Neuromuscular blocking drugs do not alter the pupillary light reflex.70 Infrared pupillary scans have been used extensively as an objective measure of pupillary reflexes during pharmacological studies on human subjects.71 Women show greater pupillary dilatation than men, this gender difference in pain perception being beyond voluntary control and reflecting low-level sensory and/or affective components of pain.11 Pupillometry has served to assess the bioavailability of rectal and oral methadone in healthy subjects72, as well as, for example, the influence of age or cytochrome P4503A activity on the acute disposition and effects of oral transmucosal fentanyl citrate.73 and 74 Pupillometry is also able to quantify the extent and time course of the effects of morphine-6-glucuronide.75 Similarly, the pharmacodynamics of epidural alfentanil, fentanyl and sufentanil have been studied with this method.76 and 77

Dynamic pupillometry with automatic recording has recently been developed.78 and 79 PRD is measured using an ophthalmic ultrasound biomicroscope (Oasis Colvard Pupillometer) or video-based pupillometer (Procyon video pupillometer, FIT 2000, videoalgoscan). The pupillary response to noxious stimulation induced by electrical fingertip stimulation was investigated in volunteers by Chapman et al.80 These authors found that PRD began at 0.33 seconds and peaked at 1.25 seconds after the stimulus. PRD increased significantly in peak amplitude as the intensity of the stimulus increased.

Larson et al showed that alfentanil exponentially impaired the PRD, decreasing the maximum response amplitude from 5 mm at 0 ng/ml, to 1.0 mm at 50 ng/ml, and to 0.2 mm at 100 ng/ml.81 In contrast, alfentanil administration had no effect on the pupillary light reflex. Dilatation of the pupil in response to a noxious stimulus is a measure of opioid effect, and this stimulus-induced pupillary dilatation may be used to evaluate the analgesic component of a combined volatile and opioid anaesthetic. The relative variations of PRD (+233%) are more sensitive than those of heart rate (+19%) or arterial pressure (+13%) after an electrical stimulus (65–70 mA, 100 Hz) has been applied to the skin of the abdominal wall.68 During anaesthesia, PRD allows an estimation of the sensory level during combined general/epidural anaesthesia in adults.82 The supraspinal effects of epidural fentanyl can be assessed during general anaesthesia using infrared pupillometry, maximum suppression being 70±15% for the epidural route and 96±3% for the intravenous route.83 In children, a PRD of 0.2 mm is sensitive to the loss of analgesia.84 PRD during anaesthesia is not initiated by slowly conducting C fibres, and fentanyl at 3 μg/kg depresses the reflex.85 During propofol anaesthesia in healthy patients, the fall in PRD is a better measure of the progressive increase in effect of a remifentanil concentration up to 5 ng/ml than are haemodynamic measures or the bispectral index (BIS). Pupil dilatation in response to 100 Hz tetanic stimulation decreased progressively from 1.55 (0.72) to 0.01 (0.03) mm as remifentanil concentration increases.86 Similar responses have been found also in children by Constant et al.87

Quantitative pupillary measurements can be reliably obtained during anaesthesia with newer pupillometers. Continuous improvements are seen in the flexibility and recording capacity of pupillometers, and they are used in an increasing number of medical fields, including anaesthesiology.

The limitations of this method are that droperidol and metoclopramide constrict the pupil and block the pupillary dilatation brought about by nociceptive stimuli, whereas ondansetron does not. Larson recommends that when pupillary diameter measurements are used to gauge opioid levels during experimental conditions or during surgical anaesthesia, antiemetic medication acting on the dopamine D2 receptor should be avoided.88 Clonidine also modifies the central norepinephric control of pupillary function.89 Autonomic neuropathies and spinocerebellar degeneration syndromes are strongly associated with pupillary abnormality, both at rest and in tonic conditions, and may disturb monitoring.

Ocular microtremor

Ocular microtremor is a physiological tremor whose frequency is related to the functional status of the brainstem. It is suppressed by propofol and sevoflurane in a dose-dependent manner. Sevoflurane and ocular microtremor accurately predict response to verbal command.90 Ocular microtremor may be a useful monitor of depth of hypnosis, but further studies are needed despite encouraging results in the evaluation of preoperative analgesia.91

Spontaneous EEG

The effects of noxious stimulation on the EEG have long been studied to monitor cerebral function.92 The basic EEG responses to noxious surgical stimulation have not been clearly defined, which has been a major factor limiting the clinical use of the EEG to monitor anaesthesia.

Bispectral index

The BIS is a statistical index involving the weighted average of three subparameters that analyse the phase and frequency relations between the component frequencies in the EEG.93 It changes with increasing concentration of anaesthetic agents and is correlated with sedation scales. The BIS correlates well with the hypnotic component of anaesthesia but predicts movement in response to surgical stimulation less reliably, especially when different combinations of hypnotic and analgesic drugs are used. Use of the BIS has been shown to prevent awareness in at-risk patients.94

Early studies with the BIS show that it could be a useful predictor of whether patients will move in response to skin incision during anaesthesia with isoflurane/oxygen or propofol/nitrous oxide and no opioid.95 and 96 Leslie et al97 have compared several parameters in 10 propofol-anaesthetised volunteers and determined their prediction probability of movement. The BIS (PK=0.86), 95% spectral edge frequency (PK=0.81), pupillary reflex amplitude (PK=0.74) and systolic arterial blood pressure (PK=0.78) did not differ significantly from those of a modelled propofol effect-site concentration (PK=0.76). In a study of 60 unpremedicated adults98, a BIS of 60 separated patients responding to laryngeal mask airway insertion from non-responders (P=0.006), with a sensitivity of 68% and a specificity of 70%. Movement response was not predicted by cardiovascular changes. Sebel et al, in a multicentre study, pointed out that, when opioid analgesics were used, the correlation to patient movement became much less significant, so that patients with apparently ‘light’ EEG profiles could not move or otherwise respond to incision. Therefore, the adjunctive use of opioid analgesics confounds the use of BIS as a measure of anaesthetic adequacy when movement responses to skin incision99 or to another noxious test100 are used.

BIS and sevoflurane end-tidal concentration are reliable guides to the depth of sedation, with prediction probability values of 0.966 and 0.945, respectively, but not to the adequacy of anaesthesia for preventing movement.101 In a same way, Doi et al102 have shown that the auditory evoked potential (AEP) index discriminated between movers and non-movers with a prediction probability of 0.872. BIS, spectral edge frequency and median frequency could not predict movement at laryngeal mask airway insertion in patients anaesthetised with propofol and alfentanil. The addition of remifentanil to propofol affected the BIS only when a painful stimulus was applied.103 Moreover, remifentanil attenuated or abolished increases in BIS and MAP after tracheal intubation in a comparable dose-dependent fashion.

In another study with sevoflurane104, the prediction probability values for AEP index, BIS and sevoflurane concentration for sedation score were 0.820, 0.805 and 0.870, respectively, indicating a high predictive performance for depth of sedation. AEP index and sevoflurane concentration successfully predicted movement after skin (prediction probability 0.910 and 0.857, respectively), whereas BIS did not (prediction probability 0.537). Despite these limitations, BIS might be a useful clinical monitor for predicting patient movement to command during the intraoperative wake-up test in scoliosis surgery105, particularly when controlled hypotension is used and haemodynamic responses to the emergence of anaesthesia are blunted.

There are, however, various limitations of the BIS. Vivien et al pointed out the fact that the fall in BIS following the administration of myorelaxant was significantly correlated to the BIS.106 During fentanyl-induced muscular rigidity, BIS recordings reflect EMG variations. When assessing BIS in the absence of neuromuscular blockade, it is necessary to evaluate the effect of the electromyelogram (EMG) on the BIS before making conclusions about depth of sedation. Fentanyl-induced rigidity appears to be a dose-related phenomenon that an EMG variable of BIS 3.4 is able to quantify.107 It must be borne in mind that BIS is primarily a sedation monitor.

Entropy

Entropy is a quantitative measure used to determine the disorder or randomness in a closed system, in the sense of thermodynamic/metabolic processes or the increasing molecular disorder in a structure, according to Boltzmann's definition of entropy (S) S=k ln(Ω). The second law of thermodynamics states that the entropy (and disorder) increases as time moves forward. Shannon has extended this concept to information theory and defines entropy in terms of a discrete random event x, with possible states 1,…,n as:

H(x)=−Sumi(p(i)log(p(i)).

There are multiple ways in which to compute the entropy of a signal: in a time domain, as approximate entropy108 and 109 or as Shannon entropy.110 In the frequency domain, spectral entropy may be computed; this is the case for the Datex-Ohmeda Entropy Module, a new EEG monitor designed to measure depth of anaesthesia.111 The monitor calculates a ‘state entropy’, computed over the frequency range 0.8–32 Hz, and a ‘response entropy’, computed over the frequency range 0.8–47 Hz. The difference between the response and state entropies is a reflection of the high-frequency activity of the EEG, and includes by nature some EMG-frequency components.

Some studies with this monitor have now been published. It appears that it has the same lack of sensibility as the BIS when analgesics drugs are used, for example with ketamine112 or nitrous oxide.113 An elevated difference between response entropy and state entropy is related to a significant increase in state entropy, blood pressure and heart rate, response entropy during painful stimulation is seen more often in patients anaesthetised with 0.8% compared with 1.4% isoflurane. Response entropy more probably reflects the frontal EMG and may be useful to identify inadequate anaesthesia and patient arousal during painful stimulation.114

Vanluchene et al115 compared state entropy, response entropy and BIS when measuring loss of response to verbal command (LOR(verbal)) and noxious stimulation (LOR(noxious)) during propofol infusion with and without remifentanil. BIS, state entropy and response entropy all detected LOR(verbal) accurately, but BIS performed better at 100% sensitivity. The sensitivity/specificity for the detection of LOR(verbal) decreased for all methods with increasing Ce(REMI). LOR(noxious) was poorly described by all measures. Future studies are needed to elucidate the role of response entropy in terms of analgesia monitoring.

Evoked EEG

Animal and human cerebral evoked potentials have been employed for years in pain research to describe pain perception physiology and to test the effectiveness of various analgesics.116 and 117 More recently, positron emission tomography has revealed significant changes in pain-evoked activity within multiple cerebral regions, particularly the anterior cingulate cortex.118 Subdivision of the anterior cingulate cortex into an anterior non-specific attention/arousal system and a posterior pain system explain the interaction between alertness and pain.119

Mid-latency AEPs are small changes noted on the EEG that are caused by discrete auditory stimuli. AEPs are more sensitive to pain stimuli than are spectral features of the spontaneous EEG120 or BIS.102 The A-Line Auditory Evoked Index (AAI) is a unique device commercially available for depth of anaesthesia monitoring. Values of the index range between 0 and 100, but there is a wide variation in the awake values and a considerable overlap of AAI values between consciousness and unconsciousness, suggesting that further improvement of the AAI system is required.121 and 122

Unlike AEPs, because of the variability in latency and the difficulties of repeating stimulation, somatosensory evoked cerebral potentials are analysed by calculating the spectral power in selected frequency bands and frequency percentiles from the spontaneous EEG segment preceding each somatosensory stimulus. Late cortical somatosensory evoked potentials response parameters are calculated from the respective post-stimulus EEG segments.

Spectral analysis of the late cerebral (later than 80 milliseconds) components of the potential evoked by painful somatosensory stimuli reveals a stimulus-induced increase of power in the low frequencies—delta and theta. The pre-stimulus:post-stimulus relationship of the delta waves was found to be the most sensitive measure for monitoring the cerebral bioavailability of meperidine.123 Under halothane anaesthesia, late somatosensory evoked potentials and haemodynamic responses in response to painful electrical stimuli are abolished by fentanyl.124 The same authors showed that the analgesic effect of low-dose ketamine (0.25 and 0.5 mg/kg) could be quantified by somatosensory evoked potentials, especially by a dose-dependent decrease of the long-latency N150-P250 somatosensory-evoked late cortical response.125

Laser-evoked potentials are nociceptive-related brain responses to activation of the cutaneous nociceptors by laser radiant heat stimuli. The cost of the technique is the major limitation to its development.

Monitoring analgesic administration

The computer administration of opioids by target-controlled infusion contributes to the monitoring of analgesia.126 and 127 Real-time displays of intravenous anaesthetic concentrations and effects could significantly enhance intraoperative clinical decision-making by a visualisation of pharmacodynamic relationship between hypnotics and analgesics.128

Titration of opioids during noxious events

The majority of clinical studies have focused on the BIS. Brocas et al showed that an alfentanil bolus of 15 μg/kg markedly reduced the increase in BIS values, blood pressure and heart rate observed immediately after tracheal suction, whereas there are differences in Ramsay scores.129 Godet et al showed that maintenance of anaesthesia predominantly with propofol and a low dose of remifentanil, administered in accordance to the BIS, was associated with a greater stability in perioperative haemodynamics.130 Likewise, sufentanil effect-site concentrations adjusted on BIS values and variations could achieve good haemodynamic tolerance.127 In cardiac patients, titration of propofol using the BIS allows a significant reduction in propofol consumption, with only minor effects on the stress response in these conditions.131

Considerations of stability

Analgesia is a stable state seen both during and after a noxious stimulus. One of the questions of importance here is the definition of stability. For example, a system is stable if it can maintain equilibrium after stimulation, and adequate analgesia could be defined in terms of resistance to change. In control theory, stability characterises the reaction of a dynamic system to external influences. Likewise, haemodynamic stability is often defined by a lack of variation between 20% under or upper reference heart rate or arterial pressure. This percentage is guided by experience and can be changed if a more stable state is required. Absolute or relative percentages of variation, coefficients of variation, standard deviations and ranges are parameters available to describe stability. Variations in statistical significance are not always of great clinical use. Analgesia is a temporal state and must always be topped up against a background of duration and intensity of stimulation.

Conclusion

If information collected from the EEG response entropy, heart rate and pulse plethysmography of anaesthetised patients is combined, a significantly improved classification performance (96%) between movers and non-movers to skin incision is achieved compared with discrimination using any single variable alone. This suggests that a combination of information from different sources may be necessary for monitoring the level of nociception during anaesthesia.59

Pupillometry seems to be a promising generalised tool, but we must aware of being too enthusiastic towards it because there are commercially available analgesia monitors who no longer still exist.132 Many candidate signs are available for analgesia monitoring (Table 3). But whatever the latest monitors are like133 and 134, they will never be able to predict whether the depth of analgesia is sufficient for the next painful surgical stimulus: they can only monitor the anaesthetic state at the time of measurement, and the balance between excitation and responsiveness. Anaesthetists must always consider their experience ahead of any technique for monitoring the depth of analgesia.

Table 3.

Different parameters available for monitoring analgesia. Parameter to be monitored

Clinical scales PRST score

Sedation scores

Effect of pain

Sympathetic system Direct microneurography

Heart rate variability

Spectral analysis of heart rate

Low-frequency/high-frequency power ratio

Arterial blood pressure

Skin vasomotor reflexes: laser Doppler flowmetry

Plethysmogram amplitude, notch amplitude

Pulse transit time

Ventilation Respiratory rate

Pupil Pupillary reflex dilatation

Brainstem Ocular microtremor

Spinal Movement

Cerebral Response entropy

Auditory evoked potentials

Somatosensory evoked potentials

Spectral analysis of late cerebral potential components

Bispectral index

Action of analgesics Plasma concentration

Theoretical concentrations with target-controlled infusions

Secondary effects: heart rate, respiratory rate

Action of anaesthetics End-tidal concentrations of inhaled anaesthetics

Theoretical concentrations of intravenous drug

Multiparametric approaches are probably the best way to deal with monitoring analgesia.135 Like Kutas and Federmeier136, we could say that a combination of measures—old and new, central and peripheral—will ultimately provide the greatest power to resolve the questions we hope to answer, using all the physiological measures at our disposal, in our quest to understand the nature of the relationship between mind and body, between analgesia and anaesthesia.(Box 1)

Research agenda

• characterise the mechanisms of pain perception

• characterise the mode of action of analgesics

• characterise individual variations in and intervariability of events related to noxious stimuli

• develop plethysmography-derived and pupillary reflex indices

• include the pharmacodynamics of hypnotics/analgesics in EEG automated depth of anaesthesia systems

• develop data-fusion systems and multimodal monitoring of analgesia

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[Spock]

chbare has hit the nail right on the head. A narcotic is an opioid of either natural or synthetic manufacture and is a controlled substance. Benzodiazepines are not narcotics but are controlled substances. Some hospital pharmacy's will also consider sodium thiopental and propofol as controlled substances.

I would agree that the use of an opioid for RSI is desirable but not essential. Myalgia caused by muscle fasciculations secondary to succinylcholine administration are seen hours to days afterwards and will not be mitigated by fentanyl/morphine. Use of a defasciculating dose of a non-depolarizing neuromuscular blocking agent will obviate myalgia (either 1mg of vecuronium or 5mg of rocuronium will do the trick).

If you have any compassion at all for your patient you will give as much versed and fentanyl as their blood pressure will stand after paralyzing them.

Live long and prosper.

Spock

[mdparamedic]

For those of you that think RSI is a big deal I'm here to yell you it is but when used properly it is the best tool for the PT and yourself. we use it at my agency for medical and trauma Pt's. When i say use it properly I mean when the person really can't control there own airway and when you use it the best thing to do is have everything that you need or think you might need ready for example all your meds drawn up tube ready laryngascope ready and working bvm and O2 on and your secondary device ready ( we use a combitub). be confidant but not cocky and you will do just fine..

[AZCEP]

Good points mdparamedic, and welcome to the City.

RSI has somehow developed into a sordid "merit badge" for those that get to use it. It also has become a device to compare different systems, and how progressive/restrictive they are. I'm sure we've all seen/heard it, "We use RSI, but you don't? We must have a better system."

There are many that have used medication-assisted intubation quite frequently, with great success. This same group is the most hesitant to upgrade to RSI.

Let's all step back for just a moment and try to remember that RSI is a tool. That is all it is. The process for using this tool can be quite complex, but it is a tool designed to make the first intubation attempt easier. Ideally, it will make first attempt placement much easier. Hopefully success rates will bear this out.

The most important tool in any intubation attempt is the one holding the laryngoscope.