5 – Anesthesia for Bronchoscopy




5 Anesthesia for Bronchoscopy



John Pawlowski



Introduction


Instrumentation of the airway is among the most noxious procedures physicians perform. Laryngoscopy and tracheal intubation require 1.3–2.8 times more inhalation anesthesia than does surgical incision. Physiologic responses to bronchoscopy include hypertension, tachycardia, increased cardiac output, laryngospasm, bronchospasm, retching, and vomiting. These hemodynamic and respiratory changes may be well tolerated by healthy individuals, but can lead to myocardial ischemia or respiratory compromise in others. To safely and effectively perform bronchoscopy and other airway procedures, pulmonary specialists must be able to adequately anesthetize the upper airway with local anesthetics, and safely administer moderate (conscious) sedation. This chapter will describe the methods used to anesthetize the oropharynx and upper airway, and the safe use of sedative hypnotics to minimize the frequency and severity of these complications.



Airway Anesthesia



Neuroanatomy of the Airway


Branches of the Vth, IXth, and Xth cranial nerves provide sensation to the airway. The nasal mucosa is innervated by the sphenopalatine plexus, composed of branches of the maxillary branch of the trigeminal nerve. These fibers lie just below the mucosa along the lateral wall of the nares, posterior to the middle turbinate. Sensation to the anterior 2/3 of the tongue is provided by fibers of the mandibular branch of cranial nerve V. The posterior 1/3 of the tongue and the pharyngeal mucosa to the vocal cords are innervated by the glossopharyngeal nerve through the pharyngeal plexus. The superior laryngeal and recurrent laryngeal branches of the vagus innervate the vocal cords, trachea, and bronchi.



Local Anesthetic Techniques


Many of the nerves of the airway can be directly anesthetized by injection or topical application of local anesthetics. Direct injection of the sphenopalatine plexus nerves can be accomplished by injecting 2–3 mL of local anesthetic below the nasal mucosa just posterior to the middle turbinate. However, this technique is impractical and runs the risk of intravascular injection. It also can lead to blood in the airway, obscuring fiber-optic visualization. More commonly, local anesthesia-soaked pledgets or cotton packing is pressed against the mucosa, anesthetizing the underlying nerves. A cotton swab is introduced into the nares and advanced along the turbinate all the way to the posterior wall of the nasal passage. A second swab is then advanced angled slightly more cephalad to the first along the middle turbinate. This swab is more likely to block the sphenopalatine plexus. These pledgets should be kept in place for 2–3 minutes to allow submucosal penetration of the local anesthetic. A 4 percent cocaine solution has traditionally been used for this procedure because of its vasoconstrictive properties, but lidocaine works as well.


The glossopharyngeal nerve can be similarly blocked by either injection or topical administration of local anesthetic at the base of the posterior tonsillar pillar (palatopharyngeal fold). After careful aspiration to prevent injection into the nearby carotid artery, approximately 5 mL of local anesthetic are injected into the submucosa. A 22-gauge, 9-cm needle is used, and the last 1 cm is bent to facilitate injection behind the pillar. Alternatively, cotton pledgets soaked in local anesthetics can be placed at the base of the posterior tonsillar pillar. Care must be taken not to inject too anteriorly, or the hypoglossal nerve can be blocked and motor function of the tongue impaired.


The internal branch of the superior laryngeal nerve can be blocked where it pierces the thyrohyoid membrane, halfway between the hyoid bone and the superior border of the thyroid cartilage. With the patient’s neck extended, the hyoid bone is moved laterally. The overlying skin is prepped with an alcohol wipe. A 25-gauge, 2.5-cm needle is advanced until it contacts the superior cornu of the hyoid bone, and is then walked off the cornu inferiorly. It is then advanced another 2–3 mm. As the needle passes through the thyrohyoid membrane, a loss of resistance or “pop” is felt. At that point, approximately 3 mL of local anesthetic are injected deep and superficial to the membrane. Alternatively, the needle can be advanced until air is aspirated and then withdrawn to the submucosal space and the medication injected. The procedure is then repeated on the contralateral side. Care must be taken to avoid intravascular injection into the carotid artery.


Finally, the trachea can be anesthetized by injection of lidocaine through the cricothyroid membrane. With the patient supine, the skin over the membrane is sanitized with an alcohol wipe, and a 22- or 20-gauge needle is used to puncture the membrane. Approximately 4 mL of 2 percent lidocaine is then quickly injected during maximal exhalation. Although this technique is simple and very effective, hemorrhage and even death have been reported because of laceration of small arteries in the cricothyroid membrane.


Although the nerve blocks and injections described earlier are all effective, they require multiple steps and can be unpleasant for the patient. Therefore, techniques that simply deliver the local anesthetics topically to the mucosa of the airway are more common. Several such techniques exist. First, the patient can be asked to gargle and “swish” a 2 percent viscous lidocaine solution. This technique can effectively anesthetize the tongue, mouth, and posterior pharynx. Alternatively, a nebulizer can be used to deliver aerosolized local anesthetic from the mouth to the lungs. Approximately 10 mL of 4 percent lidocaine is administered through a standard nebulizer. This technique is well tolerated, effective as the sole technique in 50 percent of patients, and may be associated with lower plasma levels compared with direct endobronchial administration; however, nebulized lidocaine may not decrease the amount of supplemental lidocaine needed by direct, endobronchial injection, and high serum levels have been described with this technique. Various sprays and atomizers can be used to directly spray the posterior pharynx. After the tongue has been sprayed, it can be grasped with gauze and the spray device inserted into the posterior pharynx. The patient is asked to take deep breaths, and local anesthetic is sprayed during inspiration. Commercially available products can be used to administer benzocaine, or a standard atomizer can be filled with lidocaine for this technique.


Finally, the bronchoscopist can simply use the “spray-as-you-go” method, administering the local anesthetic through the working port of the scope. Lidocaine (4 percent) is used most frequently above the vocal cords with this method, whereas 2 percent lidocaine is generally used below the cords. One report found this technique superior to nebulized lidocaine. All of the techniques described earlier for anesthetizing the airway are effective and safe when properly employed. Comparisons between them have not demonstrated that one is clearly superior to another.



Local Anesthetic Drugs and Their Complications


Several local anesthetics have been described for airway anesthesia, including lidocaine, tetracaine, benzocaine, and cocaine (see Table 5.1). Of these, 2 percent and 4 percent lidocaine are the most common. Irrespective of the technique used for airway anesthesia, the bronchoscopist must be vigilant in watching for signs and symptoms of local anesthetics toxicity. During a nerve block technique, the intra-arterial injection of even a small amount of local anesthetic into the carotid artery can cause seizures and other central nervous system (CNS) toxicity. Topical techniques can lead to the absorption of large quantities of the local anesthetic and to systemic toxicity. The signs and symptoms of local anesthetic toxicity are described in Table 5.2. When doses of 300–400 mg of lidocaine are used, serum lidocaine levels are generally well below toxic levels. The serum concentration is directly related to the dose of local anesthetic administered, and symptoms generally occur when the serum level is >5 mg/L. However, clinicians frequently administer more than the recommended doses without apparent complications, with doses exceeding 600 mg being published. The apparent relative safety of these larger doses is probably due to the fact that 88–92 percent of the drug administered by a nebulizer is wasted. Nonetheless, high serum lidocaine levels, seizures, and even death from local anesthetic toxicity have been described.




Table 5.1 Local Anesthetics
























Drug Maximum Dose Concerns
Lidocaine


  • 4–9 mg/kg (37,40)



  • 200–400 mg max dose (25,87)



  • <175 mg/m2 (20)




  • Seizures



  • Ventricular tachydysrhythmias



  • Sedation

Benzocaine 1–2 s spray of Cetacaine or Hurricaine (9)


  • Methemoglobinemia

Cocaine 1 mg/kg (4)


  • Hypertension



  • Tachycardia



  • Myocardial ischemia and infarction




Table 5.2 Signs and Symptoms of Local Anesthetic Toxicity

























Early Signs and Symptoms Late Signs and Symptoms
Metallic taste Somnolence
Tinnitus Sedation
Anxiety Seizure
Light-headedness Ventricular arrhythmia (V. Tach and V. Fib)
Cardiovascular collapse

The use of benzocaine spray or cocaine solution raises other specific concerns. Benzocaine metabolism in the blood can lead to the formation of methemoglobinemia. Although this is a relatively rare complication, severe cyanosis, arterial desaturation to levels below 40 percent, and death have been reported. Methemoglobin levels above 30 percent are common. Use of a benzocaine spray (compared with other gel or solution applications) increases the likelihood of methemoglobinemia, and might occur after only a single use. Treatment includes supplemental oxygen and intravenous (IV) methylene blue (1 mg/kg). Cocaine is frequently used for topical anesthesia of the nose. Its effects on the cardiovascular system are well-known. Myocardial ischemia and infarction have been described after topical cocaine administration to the airway.


The administration of anticholinergic agents, such as atropine or glycopyrrolate, is frequently recommended to decrease secretions, improve visibility, and enhance the efficacy of topical local anesthetics. Although this practice is not recommended prior to bronchoscopy, it remains common. Randomized trials have demonstrated that these medications do not improve the quality of airway anesthesia or bronchoscopic view. Higher serum lidocaine concentrations have been reported after the use of atropine. Clinicians should be wary of the potential complications from the tachycardia caused by these medications.



Moderate Sedation



Introduction


Adequate local anesthesia allows the clinician to perform flexible, bronchoscopy without the addition of sedatives or anxiolytics, and the concomitant administration of moderate (conscious) sedation during this procedure is controversial. Conflicting data exist as to whether sedation improves patient tolerance of the procedure. In addition, many of the complications associated with bronchoscopy, and up to half of the life-threatening events can be attributed to the sedation. Others have suggested that sedation should be routine for bronchoscopy. Irrespective of this controversy, a large majority of physicians routinely administer sedation during bronchoscopy. Thus, it is incumbent on the bronchoscopist to understand the regulatory requirements, risks, benefits, medication dosages, monitoring requirements, and impact of patient disease states to safely administer moderate sedation.



Definition and Oversight


Many local, state, and national agencies have published recommendations, guidelines, and standards for the administration of sedation. The clinician must become familiar with these regulations and any local hospital policies regulating the practice of sedation. The American Society of Anesthesiologists (ASA) has published guidelines for the administration of sedation and analgesia by nonanesthesiologists. These guidelines define a continuum of sedation depth, ranging from minimal sedation (anxiolysis) to general anesthesia, as described below.




  • Anxiolysis: A drug-induced state during which patients respond normally to verbal commands. Although cognitive function and coordination may be impaired, ventilator and cardiovascular functions are unaffected.



  • Moderate sedation/analgesia (previously called conscious sedation): A drug-induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained (withdrawal from a noxious stimulus is not purposeful movement).



  • Deep sedation: A drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully following repeated painful stimulation. The ability to independently maintain ventilatory function may be impaired. Patients may require assistance in maintaining a patent airway, and spontaneous ventilation may be inadequate. Cardiovascular function is usually maintained (withdrawal from a noxious stimulus is not purposeful movement).



  • General anesthesia: A drug-induced loss of consciousness during which patients are not awakened, even by painful stimuli.


The ASA guideline outlines recommendations for preprocedure patient evaluation, patient monitoring, equipment availability, training of personnel, drug administration, and the recovery and discharge of patients during moderate or deep sedation. A full review of these guidelines is beyond the scope of this chapter, but the pulmonary physician should be familiar with its contents. In addition, The Joint Commission has adopted many of the recommendations of the ASA guideline and uses the same definitions for moderate and deep sedation. Furthermore, nine Joint Commission standards apply directly to the administration of sedation. All clinicians who administer sedation for interventional pulmonary procedures in the United States must comply with these standards:




  • Moderate or deep sedation is provided by qualified personnel. This indicates that all personnel who administer sedation must be trained in and have privileges for the safe administration of the sedative medications. In addition, they must be trained to rescue the patient from a deeper than expected level of sedation. Advanced Cardiac Life Support (ACLS) training generally fulfills this requirement.



  • Sedation risks and options are discussed prior to administration. Clinicians frequently include informed consent for sedation on the form for the procedure.



  • A presedation assessment is performed. This includes a history and physical examination, evidence that the patient is NPO (nil per os, i.e., nothing by mouth) in accordance with guidelines, and specific comorbidities that might impact the safe conduct of the sedation are identified. It also includes a determination that the patient is an appropriate candidate for the procedure and sedation and an immediate preinduction reassessment.



  • Moderate or deep sedation is planned. Many clinicians create a set of sedation orders that they can complete prior to the procedure.



  • Each patient’s physiologic status is monitored during sedation. See section on monitoring.



  • Each patient’s postprocedure status is assessed on admission to and before discharge from the postsedation recovery area.



  • Patients are discharged from the postsedation recovery area by a licensed, independent practitioner (LIP) or according to criteria approved by the medical staff. Most institutions create specific, objective criteria for home discharge or to an inpatient unit for patients who receive sedation. These criteria should include an adult escort home and postsedation instructions (including 24-hour contact information). The clinician must be aware that he or she is still responsible for the safe discharge of the patient, even if the patient has been sent home by a nurse in accordance with hospital criteria.



  • Each patient’s physiologic status while undergoing moderate or deep sedation is collected and analyzed. Many institutions have created a form, much like an anesthesia record, for documenting the conduct of moderate or deep sedation.



  • Outcomes of patients undergoing moderate or deep sedation are collected and analyzed.


Many other organizations, including the American Association of Respiratory Care, the Association of Operating Room Nurses, the American College of Emergency Physicians, and others, have published guidelines and standards regarding sedation to which the pulmonary physician may be held.



Preprocedure Assessment


The ASA moderate sedation guidelines and The Joint Commission standards require that all patients undergoing moderate or deep sedation have a presedation medical assessment. In addition to a standard history and physical examination, this assessment should include information specific to the safe conduct of moderate sedation:




  • Evidence that the patient is NPO in accordance with recommended guidelines



  • Assessment of the airway (see below)



  • Determination of the ASA Physical Status score (see below)



  • Evaluation for abnormalities of any major organ system that could negatively impact the safe conduct of sedation



  • Determination that the patient has an adult escort home (for those undergoing an outpatient procedure)



  • History of adverse experience with sedation



  • Consent for sedation (this may be included in the procedural consent)


Assessment of the airway is important because it helps identify those patients in whom endotracheal intubation may be difficult or impossible if they were to become oversedated. The Mallampati classification is one way to identify patients who might be difficult to intubate. To perform this evaluation, ask the patient to open his or her mouth fully and extend the tongue without phonating. The classification is as follows:




  • Class I: The entire tonsillar pillars are visible, as is the posterior pharynx



  • Class II: The top half of the tonsillar pillars can be seen



  • Class III: The tonsillar pillars cannot be seen, but the base of the uvula is visible



  • Class IV: Only the hard palate can be seen


Other physical markers of a potentially difficult intubation include a receding mandible, limited mouth opening (<3.5 cm between upper and lower incisors), pronounced overbite of the maxillary incisors, a decreased thyromental distance, and a history of a difficult or failed intubation. Patients deemed to be at significantly increased risk for difficult intubation may benefit from having an anesthesiologist perform the procedural sedation.


The physician who administers moderate or deep sedation must also understand the impact that comorbid diseases may have on the safe conduct of the sedation. Although bronchoscopy with sedation has been performed on patients with significant comorbidities, including obesity, pregnancy, brain lesions, and coronary disease, having such concurrent medical conditions increases the likelihood of complications from the sedation. A full review of the impact of coexisting disease on sedation is beyond the scope of this chapter, but several points can be made. First, the ASA Physical Status should be determined for each patient receiving moderate or deep sedation (see Table 5.3). Perioperative and anesthesia-related mortality correlates well with increasing ASA class. Many institutions restrict the administration of sedation by nonanesthesiologists to patients who are ASA Class III or below. Furthermore, the Joint Commission may deem this an indication that the patient was assessed and found to be an appropriate candidate for the procedure and sedation. Second, those patients with significant comorbidities should have their disease processes maximally controlled prior to the administration of sedation. When appropriate, a multidisciplinary team approach should be employed, and consultation with an anesthesiologist should be considered. Finally, several disease processes place the patient at significant risk for complications from sedation (see Table 5.4). The pulmonary physician should use extreme caution when administering sedation to these patients.




Table 5.3 ASA Physical Status
































ASA class Definition Examples
Class I No organic, physiologic, biochemical, or physical disturbances. Process for which the procedure is being performed is localized Healthy patient
Class II Mild to moderate systemic disturbance caused either by the condition to be treated or other process Controlled hypertension, mild asthma, AODM, stable (mild) CAD
Class III Severe systemic disturbance from whatever cause. Impacts daily function CAD, COPD, compensated CHF, SLE
Class IV Life-threatening systemic disturbance Unstable CAD, end-stage renal failure, severe CHF/COPD, long-standing IDDM with end-organ involvement
Class V Moribund. Not expected to survive 24 h with or without therapy Ruptured AAA, gunshot wound, severe sepsis


Note: AODM, adult-onset diabetes mellitus; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CHF, congestive heart failure; SLE, systemic lupus erythematosus; IDDM, insulin-dependent diabetes mellitus; AAA, abdominal aortic aneurysm.




Table 5.4 Risk for Complications from Sedation


































Comorbidity Sedation Risk
Obesity/sleep apnea


  • Central sensitivity to sedatives



  • Rapid arterial desaturation



  • Difficulty with mask ventilation or intubation

Hypertension


  • Increased rate of hypertension



  • Exaggerated hypotension from vasodilating effect of medications

Systolic cardiac dysfunction


  • Slow circulatory time. Delayed effects of sedatives



  • Prone to pulmonary edema with IV fluids or hemodynamic consequences of bronchoscopy

Ischemic heart disease


  • Myocardial ischemia or infarction



  • Less when supplemental oxygen is used

Aortic valve stenosis


  • Limited ability in increase cardiac output in response to hypotension from medications



  • Increased myocardial oxygen demand from left ventricular hypertrophy. Demand ischemia from hypotension or tachycardia

Dementia


  • Increased sensitivity to sedatives



  • Delayed recovery



  • Paradoxical agitation is common (reversal agents may help)



  • Dose slowly and small

Pregnancy


  • Aortocaval compression at 20 wk. 15° left uterine displacement



  • Benzodiazepines were once thought to cause cleft lip/palate. Probably not true.



  • Uteroplacental circulation and fetal well-being

Chronic pain


  • Tolerance. May require very high narcotic dose



  • Naloxone contraindicated for oversedation



Equipment and Monitoring


Bronchoscopy and other interventional pulmonary procedures are highly technical and require advanced equipment. In addition, the safe conduct of moderate or deep sedation requires that specific equipment be readily available, irrespective of the degree of complexity of the medical procedure. Table 5.5 describes the recommended equipment needed specifically for sedation.




Table 5.5 Recommended Equipment






















Category Specific Equipment
Airway


  • Laryngoscopes: Multiple sizes



  • Endotracheal tubes: Multiple sizes with stylettes



  • Laryngeal airway mask



  • Oxygen source and appropriate tubing, masks, or nasal cannulae



  • Bag/mask ventilation device



  • Suction with appropriate suction device (Yankauer)



  • Oral and nasal airways: Multiple sizes

Monitoring


  • Noninvasive blood pressure device



  • Electrocardiograph



  • Pulse oximeter



  • Capnograph (required for intubated patients)

Emergency


  • Cardiac defibrillator



  • ACLS medications



  • Reversal agents (naloxone, flumazenil)

Intravenous access


  • Gloves



  • Tourniquets



  • Alcohol wipes



  • IV catheters: Multiple sizes



  • IV tubing with needleless access ports



  • Tape



  • Appropriate IV fluids



Note: Adapted from Godwin SA, Caro DA, Wolf SJ, et al.

Although the equipment outlined is important, the vigilance of a clinician monitoring the patient while under sedation is the most important factor influencing patient safety during moderate sedation. Inadequate monitoring of patients has been cited as both too common and a frequent cause of adverse events during bronchoscopy. The monitor, generally a nurse, should have no other significant clinical duties and must have the same training and privileging in the safe administration of sedation and rescue techniques as does the physician performing the procedure. The monitor should continuously evaluate the patient’s respiratory rate, cardiac rate and rhythm, blood pressure, oxygen saturation, level of consciousness, and skin condition. These parameters should be documented every 5 minutes on a flow sheet designed specifically for moderate sedation (this document can be incorporated into the procedural documentation). In addition, the monitor should document the timing, dose, and indication for all medications administered and the amount of IV fluid administered. Recent literature has suggested the use of expiratory CO2 monitoring as a way to objectively measure respiration.


Most of the physiologic parameters monitored during sedation are objective and relatively easy to measure. However, both the adequacy of respiration and the level of sedation can be more subjective and prone to error. Simply observing the rise and fall of the chest as a measure of respiration may be misleading as upper airway obstruction caused by oversedation does not prevent chest wall movement. Thus, a patient may have no alveolar ventilation despite apparently normal chest wall movement. Even observing the presence of condensation on the oxygen mask during exhalation does not adequately assess minute ventilation or the presence of oversedation. Furthermore, the use of a full face mask is impractical during bronchoscopy. Given these limitations, the use of expired CO2 monitors during moderate sedation has been recommended. This monitor identifies hypoventilation and patients at risk for hypoxemia before other clinical markers and with nearly 100 percent sensitivity. In one series, clinicians identified poor ventilation in only 3 percent of cases, whereas CO2 monitoring found that 56 percent of patients were hypoventilated. More important, active intervention based on early detection of mild hypoventilation as indicated by expiratory CO2 can effectively prevent subsequent hypoxia. Although measuring true end-tidal CO2 may be impossible during bronchoscopy in a nonintubated patient, nasal cannula devices with side-port CO2 detection may be used.


Monitoring the level of consciousness is fraught with subjectivity and inaccuracy. The definition of moderate sedation is that patients should respond to verbal commands, perhaps in conjunction with light touch. Furthermore, their protective reflexes should be intact. This standard is highly subjective, and is made more difficult when the protective airway reflexes are blunted by local anesthetics as is the case in bronchoscopy. Semiobjective scoring systems that monitor the patient’s response to reproducible stimuli are often advocated, including the Ramsay score, the Continuum of Depth of Sedation Scale (CDSS), and the Observers Assessment of Alertness/Sedation Scale (OAAS). Each of these is based on a point scale, ranging from alert/anxious to unconscious. More recently, some authors have advocated the use of electroencephalogram(EEG-) based physiologic monitoring to obtain more objective sedation data. This monitoring appears to correlate well with the Ramsay scale, OAAS, and CDSS. More importantly, it may allow clinicians to administer less medication and improve patient cooperation. More work needs to be done in this area before EEG-based monitors become standard sedation monitors.


Monitoring of the patient who has received moderate or deep sedation should continue in the postprocedure recovery area. Vital signs should be continually assessed and documented at regular intervals (generally every 1–30 minutes) while the patient is in the recovery area. Patients who received reversal agents (flumazenil or naloxone) should remain in the recovery area for at least two hours after the reversal is administered. For other patients, no predetermined recovery time should be required, but the patient should demonstrate objective evidence of recovery from the sedative medications prior to discharge to an inpatient unit or to home. Aldrete and Kroulik developed the postanesthesia recovery (PAR) scoring system, similar to the Apgar score for newborns, which helps to determine readiness for discharge. This includes assigning 0–2 points for activity level, respiration, circulation consciousness, and oxygen saturation. (The original scoring system evaluated skin color, but this was modified when pulse oximetry became readily available.) When the patients reach a PAR score of 9 or 10, they are ready for discharge to the inpatient unit. Patients with a PAR score of ten may still demonstrate significant impairment from the sedative medications, and thus a second level of assessment has been added to the PAR score to determine readiness for discharge home. This postanesthesia discharge (PAD) score includes assigning 0–2 points for the dressing, the level of pain, the ability to ambulate, the ability to drink liquids, and urine output. When the sum of the PAR and PAD scores is 18 or greater, the patient is ready for discharge. These scoring systems are used in dozens of countries and are accepted by The Joint Commission.


The medical center should develop specific discharge criteria based on the PAR and PAD score or other objective criteria. Independent licensed practitioners can then discharge patients in accordance with these criteria. Prior to final discharge home, patients and their families should be given verbal and written instructions regarding diet, level of activity and medications, and a 24-hour contact number in case of emergencies. All patients should be discharged in the presence of a responsible adult who will escort them home.



Medications



Introduction


Moderate sedation represents a middle ground between the responsive and cooperative conditions of the lightly sedated patient and the unconscious, anesthetized condition of the patient under general anesthesia. Light sedation can always be augmented by the effective use of topical local anesthesia to numb the oropharynx and blunt the airway reflexes. During optimal situations, moderate sedation allows the patient to be comfortable, sleepy, amnestic, and stable hemodynamically with a modicum of medications. During difficult times, the patient is agitated, semiconscious, uncooperative, and tachycardic. Choosing the anesthetic medications to achieve optimal results requires an understanding of the kinetics and effects of each agent with its potential side effects and the patience to deliver divided doses and to titrate to effect. This section will review some of the commonly used medications in the delivery of moderate sedation to patients who are to undergo airway procedures (See Table 5.6.).




Table 5.6 Common Medications Used in Sedation and Adult Dosing Schedules

















































Drug Dose Onset Duration
Bolus type
Midazolam .5–2 mg 2 min 30 min
Fentanyl 25–100 μg 5 min 30 min
Ketorolac 15–30 mg 30 min 4–6 h
Infusion type
Remifentanil .1–.3 μg/kg/min 1–2 min
Propofol 25–100 μg/kg/min 1–2 min


Benzodiazepines


Midazolam is the most appropriate and commonly used benzodiazepine medication for moderate sedation. The combination of amnesia, anxiolysis, and sedation make midazolam an ideal drug either alone or in combination for moderate sedation during procedures that are of short duration and without significant painful stimulation. Midazolam may be administered intravenously orally, intramuscularly, or rectally. Unlike the more lipid-soluble benzodiazepines lorazepam and diazepam, midazolam is not diluted in propylene glycol. This additive is associated with pain on injection and thrombophlebitis. In sedative doses, midazolam reaches peak effect in two minutes and produces sedation for 30 minutes. The rapid onset and short duration make midazolam a useful drug for moderate sedation by bolus injection or infusion.


All benzodiazepines act on the γ-aminobutyric acid (GABA) receptors by enhancing their affinity for GABA. The actions of GABA are to produce both sedation and anxiolysis [73]. Other drugs that act on GABA, such as barbiturates, etomidate, and propofol, can act synergistically to enhance the effects of the benzodiazepines. Other CNS depressants, such as opioids, anesthetic vapors, and α-2 agonists, also have synergistic effects when combined with a benzodiazepine.


Anterograde amnesia is an important component of all benzodiazepines. These agents produce amnestic effects that are out of proportion to the sedative effects. For example, patients may appear alert and conversant, but may remain amnestic for postoperative conversations and instructions. The condition is anterograde (not retrograde) amnesia, and this distinction is frequently misstated. Although the event that is forgotten has occurred in the past, the storage of that event in a patient’s memory happens after the administration of midazolam, and thus is properly termed anterograde amnesia. Benzodiazepine cannot reliably cause patients to forget events that occurred before the medication was administered.


Midazolam should be used with caution in elderly patients or in patients with impaired liver function. Midazolam is highly protein bound and is cleared by the liver; therefore, patients with decreased concentrations of serum albumin or with decreased cytochrome P-450 enzymatic activity will have exaggerated effects and duration of activity. Agents that either raise or lower the cytochrome P-450 activity will also affect the action of midazolam. Sedative doses should be administered in a divided fashion, leaving sufficient time to assess the clinical effect of each interval dose. Midazolam does have a reversal agent, flumazenil, which will be discussed later.



Opioids


Although the opioid class of drugs includes dozens of medications with natural and synthetic origins, the major differences consist of their potencies and their rates of equilibration. All opioids are μ-receptor agonists, and this action accounts for their analgesic properties. In addition to the desired analgesic and antitussive effects, all μ-agonists share the side effects of nausea, vomiting, itching, muscle rigidity, and respiratory depression. The use of preemptive antiemetics has been shown to prevent the nausea and vomiting caused by opioids. Fentanyl has been shown to cause chest wall muscular rigidity more often than other synthetic opioids. In some cases, the chest wall rigidity is so severe that it can compromise ventilation and can only be successfully treated with the administration of neuromuscular blocking agents (paralytics). To be effective for moderate sedation, opioids should have high potency and rapidly reach equilibration. Fentanyl and remifentanil possess these properties.


Fentanyl is highly protein bound, lipid soluble, and metabolized by the liver. The time to peak analgesic effect following a single IV bolus is five minutes. The lipid solubility facilitates the movement of fentanyl across the blood–brain barrier. A single dose will last 30 minutes. Much of the initial bolus is taken up by inactive tissue sites in the lung, fat, and skeletal muscle. As these tissue sites become saturated by either repeated doses or by a continuous infusion, the context-sensitive half-life becomes longer. With continued administration of fentanyl, the half-life approaches the elimination half-life of 3–4 hours. Therefore, the advantage of fentanyl as a short-acting agent is lessened as the duration of the procedure requires multiple repeated boluses or a continuous infusion. Specific opioid antagonists do exist and will be discussed later.


An alternative opioid to fentanyl that can be used for both brief procedures and those with varying duration is remifentanil. This opioid is used for general anesthesia only, as remifentanil will cause apnea. Remifentanil is a synthetic opioid with equivalent potency to fentanyl; both are about 100 times more potent than morphine. A rapid onset of analgesic effect occurs after an IV bolus of remifentanil, with peak effect within 1–1.5 minutes. Unlike the other synthetic opioids, remifentanil has a unique degradation, being metabolized by plasma esterases. The elimination half-life is 8–20 minutes and is independent of liver or kidney function. Repeated dosing or continuous infusions do not prolong the elimination half-life. For example, a 5-hour infusion of remifentanil produced return of breathing within 3–5 minutes following discontinuation. Rapid elimination of remifentanil means that it does not provide any residual analgesia in the postoperative period. Other analgesics need to be started in the recovery area.


It is important to realize that all opioids have the unique property of providing intense pain relief without loss of proprioception or consciousness. Although this property has brought comfort to millions, it also brings the possibility of awareness. Intraoperative awareness under general anesthesia is a recognized complication and one that is more common when opioids are used. Awareness during moderate sedation should be an expected condition, but often patients will complain of hearing and feeling portions of their procedure. It is essential that anyone who is planning to administer moderate sedation advise the patient that some degree of recall is to be expected.

Only gold members can continue reading. Log In or Register to continue

Sep 9, 2020 | Posted by in ANESTHESIA | Comments Off on 5 – Anesthesia for Bronchoscopy

Full access? Get Clinical Tree

Get Clinical Tree app for offline access