Principles of Anesthesia and Pain Management
Providing an anesthetic for the trauma victim is among the greatest challenges for an anesthesiologist. In many cases, care must be rendered to a patient about whom one knows very little, who may be physiologically unstable, who may possess obvious comorbidities that increase anesthetic risk, and for whom one has very little time to prepare. Additionally, necessity may demand that an anesthetic be provided with nothing more than basic monitoring modalities, using the simplest of anesthetic techniques. Consequently, it is helpful for the surgical practitioner to possess a basic working knowledge of anesthetic principles and practice.
AN OVERVIEW OF THE ANESTHETIC PLAN
The anesthetic plan must encompass preoperative, intraoperative, and postoperative care. During the preoperative phase, the fitness of the patient for the intended anesthetic and surgical procedure is determined; the urgency of surgery determines much of the time devoted to this phase. The postoperative period includes monitoring the recovery of the patient from the anesthetic, maintaining an attitude of vigilance in respect to the development of postoperative complications and managing postoperative pain. The American Society of Anesthesiologists has published specific guidelines that outline the provision of care during these periods, which can be modified as circumstances demand. The responsibility for the preoperative and postoperative care of a patient is shared by nursing personnel, surgeons, and anesthesiologists, who work together for the benefit of their patient. In contrast, the intraoperative phase of the anesthetic care plan is the realm of the anesthesia professional. It has three components: induction, maintenance, and emergence. An anesthetic plan of action arises from the needs of the patient, the experience of the anesthesiologist and the constraints placed upon both by the proposed surgical procedure. In particular, a trauma anesthetic needs to be dynamic and responsive to rapid changes in patient condition. The design of such a plan is aided through the employment of a decision tree, which is constructed by answering three questions: “why,” “what else,” and “what if.”
The “Why?” Question One seeks the answers to any number of questions, from “How did the injury occur?” to “Why are these lab values abnormal?” to “Is my plan still what this patient needs—and if not, why not?”
The “What else?” Question Questions posed include, but are not limited to, those such as “If general anesthesia is not an option, what else can I do” or “If succinylcholine is contraindicated, what else can I use?” or “If my patient gets nauseated when he gets opiates, what else can I do for his pain?”
The “What if?” Question Of course, the classic question is “What if I can’t intubate the patient?”, and there are innumerable others, including “What if my block fails,” “What if he arrests when the aortic clamp comes off,” and “What if he develops malignant hyperthermia?”
The successful execution of the plan requires vigilance, adaptability, and a thorough understanding of the basic principles pharmacology, physiology, and monitoring modalities, as applied to the victim of trauma.
BASIC ANESTHETIC PHARMACOLOGY
The goals of an anesthetic plan may include some or all of the following: anxiolysis, analgesia, amnesia, unconsciousness, control of sympathetic reflexes, maintenance of homeostasis, and muscle relaxation. The anesthesia professional achieves these goals through pharmacologic manipulation of basic physiologic processes. The drugs employed to accomplish are divided into two general categories: anesthetic agents and anesthetic adjuvants. Anesthetic agents include general and local anesthetic agents; anesthetic adjuvants include sedatives, narcotics, and muscle relaxants.
General Anesthetic Agents These include volatile inhalational (halothane, enflurane, isoflurane, sevoflurane, desflurane) and intravenous (thiopental, methohexital, propofol, etomidate, ketamine) agents. The volatile agents possess simple halogenated alkane or ether structures. Nitrous oxide is usually considered an adjuvant to general inhalational techniques because it can produce surgical anesthesia only under hyperbaric conditions. All of these drugs share the ability to inhibit spinal and supraspinal neural transmission through either the activation or the inhibition of specific receptors. With the exception of ketamine, they are able to produce suppression of cortical electrical activity and inhibition of spinal reflexes. Burst suppression on the electroencephalogram may be achieved in clinically useful doses, and isoelectricity (and cardiovascular depression) may result if these doses are exceeded.
The effects of these drugs usually dissipate following their metabolism and excretion. In the case of volatile inhalational agents, this is very rapid because they are, in general, metabolically inert and are removed by reversing their concentration gradients. The majority of intravenous anesthetic agents follow time-dependent pathways of metabolism through the liver and kidneys. The mechanism of action of general anesthetic agents is not uniform and is the subject of intense study.1,2 Pertinent physicochemical characteristics are summarized in Tables 17-1 and 17-2.
TABLE 17-1 General Anesthetic Agents Delivered by Inhalation
TABLE 17-2 General Anesthetic Agents Administered Intravenously
Local Anesthetic Agents These include the amino-amide (lidocaine, mepivacaine, bupivacaine, ropivacaine) and amino-ester (cocaine, tetracaine, benzocaine) local anesthetic agents. They are used to produce topical anesthesia of mucous membranes, infiltration anesthesia of superficial skin wounds, blockade of the neuraxis using the spinal or epidural approach, and peripheral nerve blockade. Appropriately administered neuraxial or peripheral nerve blockade generally produces surgical anesthesia to the target dermatomes. Their mechanism of action is thought to involve inhibition of sodium conductance in excitable membranes, which suppresses the transmission of neural impulses. Amino-amide local anesthetic agents are metabolized in the liver and excreted by the kidneys; amino-ester agents are inactivated by plasma cholinesterase.
Unintentional intravenous injection or overdosage generally results in seizure activity, cardiovascular collapse and, in the case of bupivacaine or ropivacaine, a particularly malignant form of torsade de pointes. Intravenous intralipid administration may be helpful in treating this dysrhythmia, should it occur in the setting of toxicity involving these two agents.3,4 Excessive doses of benzocaine are well known to produce methemoglobinemia, a side effect that may be avoided through careful attention to dosing requirements. Cocaine inhibits the reuptake of catecholamines at noradrenergic nerve terminals; therefore, adrenergic agents must be administered with caution in its presence. Interestingly, the concept of regional anesthesia is expanding outside the immediate intraoperative period to include techniques suitable for postoperative pain control. This is a particularly attractive concept for many trauma patients. Pertinent physicochemical characteristics are summarized in Table 17-3.
TABLE 17-3 Local Anesthetic Agents
Sedative-Hypnotic Agents Although almost any intravenous or inhalational agent may be administered in very low doses to produce sedation or hypnosis, it is the benzodiazepine class of minor tranquilizers that are most commonly used for this purpose. They produce reliable amnesia and anxiolysis; they have no analgesic potency. In combination with an opiate, benzodiazepines (most commonly midazolam) are the linchpins of the technique of conscious sedation. Intense amnesia can be achieved with the co-administration of small doses of a benzodiazepine and ketamine, with the ketamine providing additional, substantial analgesia. These drugs are reliable anticonvulsants and should be at hand whenever local anesthetic agents are being administered. Midazolam has a relatively short duration of action, although its effects can be prolonged in the presence of hepatorenal impairment or systemic acidosis. In large doses, it is possible to achieve a plane of relatively deep general anesthesia with benzodiazepines.
Flumazenil is considered to be a specific benzodiazepine antagonist; its duration of activity, however, is much shorter than that of most benzodiazepines and it should be administered with careful attention to this limitation.
Neuromuscular Blocking Agents There are two broad categories of muscle relaxants: those that produce competitive inhibition of impulse transmission at the junctional endplate and those that do not. Competitive inhibitors of neuromuscular transmission are further subdivided into two groups, which are distinguished by their chemical structures. These groups are the benzylisoquinoline curariform alkaloids (curare, atracurium, mivacurium, cis-atracurium) and the 4-aminosterol compounds (pancuronium, vercuronium, rocuronium). The sole noncompetitive inhibitor of neuromuscular transmission in contemporary clinical use is succinylcholine. All of these drugs are generally used to facilitate endotracheal intubation and to enhance the muscle relaxation produced by general anesthetics.
Plasma cholinesterase rapidly cleaves the succinylcholine molecule and terminates its activity; its duration of action may be prolonged in the rare patient who possesses a genetic deficiency of this enzyme. Terminating the activity of competitive neuromuscular blocking agents is more complex. Curare and each of the 4-amino sterol compounds must first be displaced from the junctional endplate by acetylcholine and then be transported in the plasma to the liver for metabolism and excretion, usually by the kidneys. Plasma cholinesterase assists in terminating the activity of mivacurium. A complex, pH-dependent process known as “Hoffmann degradation” assists the inactivation of atracurium and its isomer cis-atracurium. No similar assistive processes exist for terminating the activity of the 4-aminosterol compounds.
With competitive inhibitors, these time-dependent processes of inactivation may be hastened by transiently increasing the concentration of acetylcholine at the junctional endplate, which through mass effect displaces a greater amount of relaxant and makes it available for metabolism and excretion. This displacement is usually produced by the simultaneous administration of a cholinesterase inhibitor and an anticholinergic agent; neostigmine and glycopyrrolate are generally used to accomplish this objective. This practice is commonly known as “reversal,” which is a misleading term, because it is more precisely an example of time-dependent pharmacologic antagonism. The duration of activity of most cholinesterase inhibitors is relatively brief and their effect may dissipate prior to complete termination of a profound neuromuscular block. If this should occur, re-paralysis of the patient may ensue.
The mechanism of action of sugammadex represents a novel approach to the concept of antagonism; however, its efficacy is greatest only for rocuronium, and it is currently not available in the United States.5,6 Neuromuscular blockade monitors (“twitch monitors”) are routinely used to assess the depth of paralysis and the efficacy of antagonism. It should be clear by now that these complex drugs are potentially lethal and that their effects must be carefully monitored. Pertinent physicochemical characteristics are summarized in Table 17-4.
TABLE 17-4 Neuromuscular Blocking Agents
Analgesic Agents Drugs commonly employed to facilitate analgesia fall into two general categories: those that stimulate inhibitory opiate receptors and those that block excitatory N-methyl-D-aspartate (NMDA) receptors. Nonsteroidal anti-inflammatory drugs are also used, as are nerve blocks produced by local anesthetics. Stimulation of the inhibitory, G-protein–linked opiate receptor is accomplished with agents possessing either a morphinan nucleus (morphine, codeine, hydromorphone, hydrocodone, oxycodone) or a phenylpiperidine nucleus (meperidine, fentanyl, sufentanil). Blockade of the excitatory NMDA receptor is achieved with ketamine, dextromethorphan, or nitrous oxide. Methadone constitutes a special case: broadly speaking, it is a phenylpiperidine derivative and its racemic mixture has activity at both opiate and NMDA receptors. Its potency and duration of activity make it a very useful analgesic; however, recent reports of its association with a drug-induced prolonged QT syndrome are troubling.7–10
Most analgesic agents are dependent upon hepatic metabolism and renal excretion for the termination of their effects; dosages must be adjusted for the extremes of age or in the presence of hepatorenal impairment. Morphine and meperidine may also accumulate potent active metabolites in the presence of renal insufficiency. Opiate agonists are notorious for producing an array of side effects, such as meiosis, respiratory depression, constipation, dysphoria, urinary retention, and generalized pruritus. The side effects of the NMDA antagonist ketamine include agitation, hallucinosis, hypersalivation, and sympathetic stimulation. There is a “ceiling effect” to the analgesia produced by both classes of drugs, and there is no point in their further administration if side effects are developing. Smaller doses of both classes of drugs, for example morphine and ketamine, may be given together to provide a synergistic response characterized by intense analgesia with less frequent side effects.11,12
Naloxone produces reliable antagonism of the narcosis and respiratory depression produced by opiate agonists. However, it is a very short-acting drug and care must be taken not to antagonize the analgesic effects of the opiate agonist. A massive sympathetic discharge producing cardiac arrest may ensue if a patient abruptly awakens from an opiate-induced narcosis and has the sudden perception of extreme pain. There is no reliable antagonist for ketamine.
AN INTRODUCTION TO ANESTHESIA MACHINES AND MONITORS
Anesthesia Machines
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