MODERATE SEDATION COMPETENCY


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Procedural Sedation


There is a continuum from sedation to anesthesia. It is not always possible to predict exactly how an individual patient will respond to sedating medications. Administering medications to provide sedation/analgesia or anesthesia may result in cardiac or respiratory depression that must be rapidly recognized and appropriately managed to avoid the risk of hypoxic brain damage.

It is necessary that physicians administering sedation be able to rescue the patient from the next level of sedation.

Please review the definitions of the four levels of sedation as detailed in the Conscious Sedation Policy. All physicians requesting privileges in sedation must complete the course of study in sedation principles and practices and pass a test covering this material. This may also be accomplished on-line via the GV Intranet. ACLS or ATLS certification or equivalent is also required.

Introduction


Sedation and analgesia describe a state of reduced consciousness that allows patients to tolerate unpleasant procedures while maintaining adequate cardiorespiratory function and the ability to respond purposefully to verbal command and/or tactile stimulation. Sedation/analgesia provides two primary benefits: (1) During uncomfortable procedures (e.g. endoscopy, arteriography, dental procedures), sedation and analgesia minimize anxiety and discomfort, while they also reduce undesirable autonomic responses to painful stimuli, and (2) sedation may also help expedite procedures such as MRIs and CT scans which are not particularly uncomfortable, but which require that the patient remain still for extended periods of time. Excessive sedation/analgesia may result in cardiac or respiratory depression that must be rapidly recognized and appropriately managed to avoid the risk of hypoxic brain damage, cardiac arrest, or death.

Sedation and analgesia may be administered to adult and pediatric patients undergoing diagnostic or therapeutic procedures in a wide variety of clinical settings including practitioners’ offices, freestanding clinics, and hospitals. Regardless of the site of administration, the same safety precautions must be followed, and emergency equipment and appropriately trained personnel should be readily available according to the Conscious Sedation Policy (PC-08).

Pre-Procedure Evaluation


Anesthesia consultants strongly agree that appropriate pre-procedure evaluation of patients increased the likelihood of satisfactory sedation and decreased the likelihood of adverse outcomes for both moderate and deep sedation.

Information obtained during the pre-procedure evaluation may significantly affect the subsequent management of patients undergoing sedation/analgesia. Because sedative and analgesic medications tend to cause significant cardiovascular and respiratory depression, doses may need to be reduced in patients with preexisting cardiac or pulmonary disease. Hepatic or renal abnormalities may impair drug metabolism and excretion, thus causing sedation to last longer than expected. Smokers are at increased risk of developing bronchospasm, cough, or increased airway irritability during sedation, while alcohol or illicit substance abusers as well as patients on certain prescribed medications may require increased doses of sedatives and/or analgesics to obtain the required effect. Finally, patients who have previously experienced adverse outcomes with sedation or general anesthesia may be at increased risk for developing complications during subsequent administration of moderate or deep sedation/analgesia.

Respiratory depression and airway obstruction may occur during sedation/analgesia. Pre-procedure examinations of the airway may help to predict which patients are more likely to develop airway obstruction. It also helps predict which patients are likely to be difficult to manage if airway obstruction, hypoventilation, or apnea should occur. The risks, benefits, and alternatives to sedation and analgesia should be explained to patients (or legal guardians for pediatric patients) before the procedure begins.  A note in the patient record or a signed consent form can document this, provided the latter includes consent for the administration of sedation/analgesia.

In summary, recommended pre-procedure evaluation includes:


ASA Physical Status:
PS-1 Normal Healthy Patient
PS-2 Mild systemic disease with no functional limitation
PS-3 Severe systemic disease with functional limitation
PS-4 Severe systemic disease that is a constant threat to life
PS-5 Moribund patient not expected to survive with or without the
Procedure
PS-6 Organ harvest for a brain-dead patient
E – Modifier for emergency procedure

Patients presenting for sedation/analgesia should undergo a focused physical examination including (at least) vital signs, auscultation of the heart and lungs, and evaluation of the airway. (See Example I)

Pre-procedure laboratory testing should be guided by the patient’s underlying medical condition and the likelihood that the results will affect the management of sedation/analgesia. These evaluations should be confirmed immediately before sedation is initiated.
Example I: Airway Assessment Procedures for Sedation and Analgesia

Positive pressure ventilation, with or without tracheal intubation, may be necessary if respiratory compromise develops during sedation/analgesia. This may be more difficult in patients with atypical airway anatomy. Also, some airway abnormalities may increase the likelihood of airway obstruction during spontaneous ventilation. Some factors, which may be associated with difficulty in airway management, are:

History:

1. Previous problems with anesthesia or sedation


Physical Examination:


Pre-Procedure Fasting


Sedative and analgesic medications tend to impair airway reflexes in proportion to the degree of sedation achieved. Therefore, patients may be at increased risk of aspirating gastric contents should regurgitation occur. For elective procedures, allowing sufficient time for gastric emptying before the procedure begins may minimize this risk. To minimize the risk of dehydration in infants and small children, clear liquids should be administered until 2-3 hours before the time of the procedure.

Factors that may delay gastric emptying include intestinal obstruction, pain, anxiety, opioid administration, trauma, diabetes, and pregnancy. In urgent or emergency situations where gastric emptying may be incomplete, the potential for pulmonary aspiration of gastric contents should be considered in determining the timing of the procedure and the degree of sedation/analgesia to be achieved. (See Example II)

Example II: Summary of American Society of Anesthesiologists Pre-Procedure Fasting Guidelines

Ingested Material Minimum Fasting Period


Clear liquids 2h
Breast milk 4h
Infant formula 6h
Non-human milk 6h
Light meal 6h

These recommendations apply to healthy patients who are undergoing elective procedures. They are not intended for women in labor. Following the guideline does not guarantee a complete gastric emptying has occurred.

Anesthesia Department guidelines for NPO status are six hours for solid food and four hours for clear liquids. The longer NPO time for liquids allows a little more flexibility for schedule manipulations and is applied to our patient population of mostly adults.

Monitoring Level of Consciousness


Patients’ responses to verbal commands during a procedure performed with sedation/analgesia serve as a guide to their level of consciousness. An appropriate level of consciousness implies that patients will be able to control their own airways and take deep breaths, as necessary. Level of consciousness should be assessed frequently (1-minute intervals) during the onset of sedation, and whenever medications are being titrated. Once an appropriately safe level of sedation is established, patients may be aroused less frequently if this is necessary to avoid interfering with the diagnostic or therapeutic procedure. With administration of sedative/analgesic medications, patients’ responses to verbal commands are delayed and responses are frequently slowed or slurred. Light tactile stimulation may be required to get the patient’s attention. However, once aroused they should respond appropriately to verbal commands. In cases where verbal response is not possible, seek other indications of consciousness in response to verbal or tactile stimulation. Patients whose only response to verbal command is reflex withdrawal from painful stimuli are deeply sedated, approaching a state of general anesthesia. These patients require special care to ensure the adequacy of pulmonary ventilation and hemodynamic stability if this undesirable state is reached.

Anesthesia consultants feel that the primary cause of morbidity associated with sedation/analgesia is drug induced respiratory depression and airway obstruction.

Table 1: Continuum of Sedation as adopted by the ASA House of Delegates, October 13, 1999*


  Minimal Sedation Moderate Sedation/Analgesia Deep   General
    (Anxiolysis) (Conscious Sedation) Sedation/Analgesia   Anesthesia
             
Responsiveness   Normal response Purposeful* response Purposeful*response   Unarousable even
    to verbal stimulation to verbal or tactile following repeated or   with painful stimulus
      stimulation painful stimulation    
             
Airway   Unaffected No intervention Intervention may   Intervention often
      required be required   required
             
Spontaneous            
Ventilation   Unaffected Adequate May be inadequate   Frequently inadequate
             
Cardiovascular            
Function   Unaffected Usually maintained Usually maintained   May be impaired
*Reflex withdrawal from a painful stimulus is not considered a purposeful response.

Pulmonary Ventilation


Sedative and analgesic medications significantly depress both ventilatory drive and airway patency. Monitoring of pulmonary ventilation provides the earliest indication of inadequate air exchange, which subsequently leads to alveolar hypoventilation and hypoxemia. By appropriate intervention when airway obstruction, hypoventilation, or apnea is first observed, the risk of adverse outcomes may be significantly reduced. Ventilatory function usually can be monitored by observation of spontaneous respiratory activity or continuous auscultation of breath sounds. In many patients, stimulation and simple maneuvers such as a chin lift or jaw thrust are adequate to improve ventilation and airway patency.

Oxygenation


Hypoxemia is the “final common pathway” through which hypoventilation, apnea, and airway obstruction lead to adverse outcomes such as cerebral hypoxia, cardiac arrest, and death. Clinical detection of cyanosis is notoriously unreliable, especially when lighting is sub-optimal or patients are anemic. Pulse oximetry should be used on a continuous basis to provide the earliest warning of hypoxemia. There may be a delay of a minute or more between the onset of apnea and the first decrease in oximetry reading, particularly if patients are breathing supplemental oxygen. This emphasizes the importance of independently monitoring patients’ ventilatory status.

Medications administered during sedation/analgesia may directly depress cardiac function. In addition, they may impair the ability of the autonomic nervous system to compensate for hemodynamic changes. Thus, patients who are dependent upon activation of the sympathetic nervous system to maintain hemodynamic stability because of hypovolemia, (N.P.O. status, endoscopy preparation, etc.) or underlying cardiac disease may become hypotensive when sedatives/analgesics are administered. By monitoring blood pressure and heart rate at frequent intervals, especially during the onset of sedation/analgesia, these changes may be rapidly recognized and treated if necessary. If recognized early, hypotension may readily be treated with elevation of the legs, administration of intravenous fluids and, in some cases, administration of a short-acting vasoconstrictor.

Patients may be at increased risk for developing cardiac dysrhythmias during sedation/analgesia. Continuous electrocardiographic monitoring enables the practitioner to rapidly detect and diagnose dysrhythmias, so that any necessary intervention can be undertaken in a timely manner. This is especially important in patients with underlying cardiovascular disease and in those patients who are suspected of having dysrhythmias because of an irregular rhythm noted on the pulse oximeter or detected during auscultation of heart sounds. Continuous electrocardiographic monitoring is also important in those procedures that are associated with an increased risk of dysrhythmia (those involving gastrointestinal distention or cardiovascular manipulations such as angioplasty and endocardial ablation), or in procedures in which epinephrine is administered with local anesthetics.

For both moderate and deep sedation, anesthesia consultants agree that vital signs should be monitored at least at five-minute intervals once a stable level of sedation is established. They also agree that continuous EKG monitoring reduces risks during deep sedation. They are equivocal concerning continuous EKG monitoring during moderate sedation, but feel it should be used in patients with significant history of cardiovascular disease.

For both moderate and deep sedation, patients’ level of consciousness, ventilatory and oxygenation status, and hemodynamic variables should be assessed and recorded at a frequency which depends upon the type and amount of medication administered, the length of the procedure, and the general condition of the patient. At a minimum, this should be: (1) immediately before the beginning of the procedure; (2) following administration of sedative/analgesic agents; (3) at regular intervals during the procedure, (4) during initial recovery; and (5) just before discharge. Vital signs, O2 saturation, and EKG rhythm (if applicable) should be recorded every five minutes.

It is difficult for the individual performing a diagnostic or therapeutic procedure to be fully cognizant of the patient’s condition during sedation/analgesia. Therefore, a qualified individual, other than the person performing the procedure, should be available to continuously monitor the patient’s status. This individual should be trained to recognize clinical signs of hypoventilation as well as abnormal blood pressure and pulse oximeter readings.

Training of Personnel


Individuals responsible for ordering sedatives and/or analgesics must be familiar with the clinical pharmacology of these medications and their potential interactions. For example, both sedatives (i.e., benzodiazepines, barbiturates, propofol) and opioids significantly depress ventilatory drive; when combined, their respiratory depressant effects potentiate each other. In addition, it may take several minutes after intravenous injection for sedative/analgesic medications to reach their peak effect; when administered by other routes, onset times for these medications may be further delayed. It is important to allow an adequate time for peak drug effects to occur before deciding that the patient requires an additional dose. Otherwise, a cumulative overdose may occur.

The primary complications of sedation/analgesia are related to respiratory and/or cardiovascular depression. Individuals monitoring patients receiving sedation/analgesia should be able to recognize the associated complications. Because sedation/analgesia constitutes a continuum, practitioners administering moderate sedation need to provide for the rescue of patients entering a state of deep sedation. Those intending to administer deep sedation need to provide for rescue of patients who enter a state of general anesthesia. Therefore, at least one individual trained in basic life support skills and capable of establishing a patent airway and positive pressure ventilation should be present whenever sedation/analgesia is administered. It is further recommended that an individual with advanced life support skills be immediately available for moderate sedation and within the procedure room for deep sedation.

Supplemental Oxygen


Supplemental oxygen decreases the likelihood that patients will become hypoxemic during sedation/analgesia. Should apnea or airway obstruction occur, the additional reserve of oxygen in the lungs would delay the development of hypoxemia, providing an additional margin of safety. However, this advantage is lost if pulmonary ventilation is not being monitored independently. If hypoxemia develops during sedation in a patient breathing room air, supplemental oxygen should be administered following a determination that there is adequate gas exchange. If gas exchange is inadequate, supplemental oxygen, alone, will not be effective. If necessary, a patent airway should be established and positive pressure ventilation initiated.

Titration of Medications to Achieve Desired Effect


The respiratory and hemodynamic effects of sedation and analgesic medications are dose dependent. By administering small, incremental doses of these medications it is possible to achieve an appropriate degree of sedation while minimizing the likelihood of complications. To avoid the risk of a cumulative overdose, it is necessary to wait long enough to observe the peak effect of each of dose before administering a subsequent dose. With intravenous medications, this generally mandates a 2-4 minute dose interval; longer intervals are necessary with IM, oral, or rectal drug administration.

Sedative medications such as barbiturates and benzodiazepines help patients to relax, relieve anxiety, provide amnesia, and induce drowsiness. They do not provide analgesia, and in some cases may actually have an anti-analgesic effect. While high doses may abolish the response to painful interventions, this generally requires deep sedation, approaching a state of general anesthesia, with the accompanying risks of respiratory depression, airway obstruction, and abolition of protective reflexes.

In contrast, small doses of opioids provide effective analgesia while maintaining an acceptable level of consciousness. Practitioners must be aware that the respiratory depressant effects of opioids potentiate those of sedatives. Therefore, doses of sedatives and opioids must be appropriately modified when it is anticipated that the medications will be administered concurrently.

Anesthetic Induction Agents Used for Sedation


Methohexital and propofol have been used by anesthesiologists to induce satisfactory moderate or deep sedation. These agents can, however, produce rapid, profound decreases in level of consciousness and cardiorespiratory function, potentially culminating in a state of general anesthesia. Even if moderate sedation is intended, patients receiving propofol or methohexital by any route should receive care consistent with that required for deep sedation. Therefore, practitioners administering these drugs should be qualified to rescue patients from any level of sedation, including general anesthesia.

Reversal Agents


Specific antagonist agents are available for the opioids (naloxone) and benzodiazepines (flumazenil). These may be administered to improve spontaneous ventilatory efforts in patients who have received opioids or benzodiazepines. Respiratory depression should be initially treated with supplemental oxygen, airway support, and, if necessary, positive pressure ventilation by mask. These drugs may be helpful in cases where airway control and positive pressure ventilation are difficult.

Prior to, or concomitant with pharmacologic reversal, patients who become hypoxemic or apneic during sedation/analgesia should (1) be encouraged or stimulated to breathe deeply; (2) receive supplemental oxygen; (3) receive positive pressure ventilation if spontaneous ventilation is inadequate. Following pharmacologic reversal, patients should be observed long enough to ensure that sedation and cardiorespiratory depression does not recur once effect of the antagonist dissipates. The use of sedation regimens that include routine reversal of sedation or analgesic agents is discouraged.

Recovery Care


Patients may continue to be a significant risk for developing complications after their procedure is completed. Decreased procedural stimulation, delayed drug absorption following non-intravenous administration, and slow drug elimination, may contribute to residual sedation and cardiorespiratory depression during the recovery period.

Following sedation/analgesia, patients should be observed in an appropriately staffed and equipped area until they are near their baseline level of consciousness and are no longer at increased risk for cardiorespiratory depression. Oxygenation should be monitored periodically until patients are no longer at risk for hypoxemia. Ventilation, and circulation should be monitored at regular intervals until patients are suitable for discharge. Discharge criteria should be designed to minimize the risk of central nervous system or cardiorespiratory depression following discharge from observation by trained personnel.

Whenever possible, appropriate medical specialists should be consulted prior to administration of sedation to patients with significant underlying conditions. The choice of specialists depends on the nature of the underlying condition and the urgency of the situation. For severely compromised or medically unstable patients (e.g., anticipated difficult airway, severe obstructive pulmonary disease, coronary artery disease, or congestive heart failure), or if it is likely that sedation to the point of unresponsiveness will be necessary to obtain adequate conditions, practitioners who are not trained in the administration of general anesthesia should consult an anesthesiologist.

Pharmacology

NARCOTICS
Narcotics are naturally occurring or synthetic opioids that act to provide analgesia, sedation, and elevation of pain threshold. They may be classified as agonists, mixed agonist-antagonists, or partial agonists by their activity at the opioid receptor. Chemically dependent patients usually require higher than recommended doses of opioids. Agonist-antagonist opioids should not be used in patients who have been receiving opioids prior to a procedure because of potential to reverse analgesia and precipitate a withdrawal syndrome. Two examples of agonist-antagonist opioids are Nubain and Stadol. Large bolus doses of narcotics should be avoided.  Small incremental IV doses should be titrated at 2-4 minute intervals to achieve the desired response.  Major predictors of sedative drug dosing include age, weight, prior sedative drug administration, and physiologic status of the patient. Dose reductions may be necessary in patients with significant cardiac, pulmonary hepatic, or renal disease.

Morphine


Morphine is the prototype opioid agonist to which all other opioids are compared. It produces analgesia with sedation, and the analgesia is more prominent when it is given before the painful stimulus occurs. The peak analgesic effect of Morphine given IV occurs about 20 minutes after the dose is given and duration of action is about four hours. Quoted dosages may range from 0.07 to 0.15mg/kg (5-10 mg for a 70kg adult) and 2 mg IV increments are commonly used. It is not uncommon for an adult to receive 30-40 mg in a perioperative period of several hours with a painful surgery.

Demerol


Meperidine (Demerol) is a synthetic opioid agonist that is about one tenth as potent as Morphine with a slightly faster onset of action and a somewhat shorter duration (2-4 hours). Normeperidine may accumulate in elderly patients and those with renal insufficiency, especially after prolonged usage. This may potentially cause myoclonus, seizures, or delirium. Orthostatic hypotension after Demerol injections is more frequent and more profound than after comparable doses of Morphine. Large doses of Demerol may result in reductions in myocardial contractility, stroke volume, and elevation in cardiac filling pressures. This direct myocardial depressant effect is unique to Demerol among narcotics.

Demerol is contraindicated in patients receiving monoamine oxidase inhibitors due to potential for a hyperpyrexia syndrome which can include hypertension, hypotension, depression of ventilation, skeletal muscle rigidity, seizures, and coma. Although a similar response can occur with other opioids, it is much less likely. The best course of action in the rare case of a patient on an MAO inhibitor is to discontinue the MAOI for two weeks before a procedure and avoid Demerol. GV has made a recent commitment to reduce usage of Demerol due to its potential side effect profile.

Fentanyl


Fentanyl (Sublimaze) is a synthetic opioid agonist that is 75 to 125 times more potent than Morphine with a more rapid onset and shorter duration of action than Morphine or Demerol. (10mg Morphine = 100mcg Fentanyl). The time to peak suppression of sympathetic response to painful stimulus is still 4-5 minutes, however. Despite the clinical impression that Fentanyl has a short duration of action, its elimination half time is greater than that for Morphine. The short duration of a single dose reflects its rapid redistribution to inactive tissue sites with an associated decline in plasma concentration. With multiple or high dosages these inactive tissue sites may become saturated and the plasma concentration may remain elevated causing the prolonged duration of analgesia and respiratory depression. Respiratory depression can be more of a problem with Fentanyl. Fentanyl does cause less histamine release, less cardiac depression, less hypotension and less emesis than Morphine and Demerol. Fentanyl comes in a concentration of 50 mcg/cc. Dosages up to 1-2mcg/kg may be used for analgesia alone, less if in combination with benzodiazepines. A dose of 25mcg is probably a reasonable increment for tritration in most adults. Go slowly.

High doses of opioid agonists can cause an episode of skeletal muscle rigidity, especially in truncal areas. Anesthesiologists call this a “stiff chest”, and these patients can have significant respiratory compromise and be very difficult to ventilate without the use of muscle relaxants. This is more common with Fentanyl, even with lower doses, if given rapidly.

BENZODIAZEPINES


Benzodiazepines have anti-anxiety, anti-convulsant, sedative, muscle relaxing, and amnestic properties. They have no analgesic properties.

Although small doses of benzodiazepines produce minimal respiratory depression, larger doses or doses in combination with other central nervous system depressants, or given to patients with chronic lung disease may result in exaggerated or prolonged depression of ventilation.

Midazolam


Midazolam (Versed) is a short acting benzodiazepine that is 2-3 times as potent as diazepam. It has rapid onset and produces greater amnesia with less post procedure sedation than diazepam. It is common to give 1-2.5 mg IV to adults for sedation. Up to 0.1 mg/kg may be given in small increments with adequate time between doses.

As always, reduced dosages are needed if combined with opioids. Tests of mental function return to normal within four hours after the administration of Versed to healthy patients. This of course may be greatly prolonged in elderly patients and in those with significant organ system disease.

Valium


Diazepam (Valium) is rarely used for IV sedation due to the many advantages of Versed. It has slower onset and much longer duration than Versed. IM administration is very painful and IV administration very commonly causes at least some degree of venoirritation and phlebitis.

Anesthesia Induction Agents

Brevital
Methohexital (Brevital) is a barbiturate used for induction of anesthesia. It has a rapid onset (around 30 seconds) and allows for rapid awakening due to redistribution to inactive tissue sites in the absence of other sedating drugs. Small doses of barbiturates seem to lower the pain threshold, accounting for the perception that these drugs are antianalgesic. Brevital may also cause excitatory phenomena, such as involuntary skeletal muscle movements, including hiccough. This is reduced by the inclusion of opioids.

Dosage of methohexital for induction of anesthesia is 1-1.5 mg/kg. Unconsciousness is usually produced within 30 seconds. There is usually a mild and transient reduction in blood pressure that accompanies induction of anesthesia with barbiturates. This reflects peripheral vasodilitation due to depression of the medullary vasomotor center and decreased sympathetic nervous system outflow from the CNS. Generally, there is a compensatory tachycardia with unchanged myocardial contractility. In the absence of compensatory increases in peripheral sympathetic nervous system activity, a negative inotropic effect of barbiturates can be demonstrated, and direct myocardial depression may accompany overdoses.

Barbiturates also produce dose-dependent depression of ventilation. Apnea is especially likely in the presence of other depressant drugs.

Textbook doses of Brevital used for sedation are in the range of 0.25-1mg/kg IV, with a duration of 5-10 minutes. Obviously, there is some overlap with anesthetic induction doses and it is very likely that a state of deep sedation or general anesthesia will be produced. An intermittent bolus technique can be used but will likely produce very large fluctuations in effect. An infusion of a 0.2% solution could be used at 25-150 mcg/kg/min., but the potential for cumulative overdose must be strongly considered.

Propofol


Propofol is a substituted isopropylphenol that is a rapid-acting IV sedative-hypnotic agent for use in the induction and maintenance of anesthesia or sedation. It is solubilized in a white oil-in-water emulsion that contains soybean oil, glycerol, and egg lecithin.  The generic form contains a sulfite as a preservative.  IV injection of a therapeutic dose of propofol produces hypnosis rapidly, with minimal excitation, usually within 40 seconds. Usual dosage for induction of anesthesia in healthy adults is 2.5 mg/kg. Awakening after a single bolus dose occurs in 4-8 minutes and in contrast to barbiturates, there seems to be less post-procedure sedation. Dose dependent cardiovascular and ventilitory depression is similar to that produced by barbiturates such Brevital.  Apnea and hypotension are very likely with a rapid bolus dose.

A vial of propofol, once it has been opened or spiked, must be used or discarded within six hours because it is not an antimicrobially preserved product under USP standards.

Besides induction of anesthesia, propofol can be used for maintenance of anesthesia and for sedation during painful procedures. It can also be used as an infusion in the ICU to sedate intubated and mechanically ventilated patients.

Propofol does not possess analgesic properties. Side effects include: (1) pain on injection; (2) involuntary skeletal muscle movements; (3) coughing or sneezing; (4) hiccoughs.

Propofol may be used for sedation by infusion or intermittent bolus technique. For initiation of sedation in healthy adults less than 55 years of age, a slow infusion or slow injection technique is recommended to avoid apnea or hypotension. Most patients require an infusion of 100-150 mcg/kg/min. (6-9 mg/kg/hr.) for 3-5 minutes or a slow injection of 0.5mg/kg over 3-5 minutes, followed immediately by a maintenance infusion.

For maintenance, a variable rate infusion of 25-75 mcg/kg/min. (1.5 to 4.5 mg/kg/hr.) may be used, although as little as 10 mcg/kg/min. or as much as 150 mcg/kg/min. may be necessary. Less desirable is giving incremental bolus doses of 10-20 mg every 2-4 minutes. Large, rapid boluses are to be avoided. It is frighteningly easy to reach an undesirable state of very deep sedation or general anesthesia with this agent. Other factors which alter indicated drug dosage must always be considered.

Reversal Agents


Narcan


Naloxone (Narcan) is a pure opioid antagonist with no agonist activity.

It competes with and displaces opioid agonists from receptors, thus reversing the effect of the agonist. Naloxone 1-4 mcg/kg, administered IV reverses opioid induced respiratory depression, sedation, and analgesia. Cardiovascular stimulation following administration of naloxone manifests as increased sympathetic nervous system activity, presumably reflecting the abrupt reversal of analgesia. This can cause tachycardia, hypertension, pulmonary edema, CHF, cardiac dysrhythmia or stroke.  Nausea and vomiting may also occur, closely related to the dose and speed of injection. The duration of action is short (30-45 minutes) as is its elimination half time (64 minutes); so supplemental doses may be necessary to sustain antagonism of longer acting opioid agonists. Dosages of 0.1 to 0.2 mg every 2-3 minutes are reasonable.

Flumazenil (Romazicon)


Flumazenil is a specific benzodiazepine antagonist that competes for CNS receptor sites, thereby reducing or reversing agonist effects. IV Romazicon has been shown to antagonize sedation, impairment of recall, psychomotor impairment and ventilatory depression produced by benzodiazepines. Usual dosage is 0.1 to 0.2mg IV every two minutes until the desired effect is achieved or until 1mg is given. It may take 6-10 minutes for a single dose of Romazicon to reach full effect. The terminal half-life is 41-79 minutes with clinical effect lasting about an hour. Resedation can occur and close monitoring is recommended for at least two hours after Romazicon administration. Romazicon can precipitate seizures in patients who have been receiving benzodiazepines chronically. These patients, as well as patients with known seizure disorders, should be given this medication with extreme caution. Romazicon as well as Narcan should be avoided if at all possible.


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