Procedural Sedation


Jamie Collings, MD, Executive Director of Innovative Education, Associate Professor, Emergency Medicine, Northwestern University, Feinberg School of Medicine, Department of Emergency Medicine, Chicago, IL.

Peter Samuel, MD, Department of Emergency Medicine, Northwestern University, Feinberg School of Medicine, Chicago, IL.

Peer Reviewer:

Robert E. O'Connor, MD, MPH, Professor and Chair of Emergency Medicine, University of Virginia School of Medicine, Charlottesville.


Procedural sedation is an important skill for emergency physicians to possess to mitigate the patient's intense physical and emotional reactions to painful and threatening procedures.1-3 Sedation not only facilitates and expedites procedures, allowing for early recovery and discharge, but also improves overall patient satisfaction.4,5 The skill needed to manage the airway, institute resuscitation measures, and provide critical care monitoring uniquely gives emergency physicians the necessary training to achieve the goals of procedural sedation — maximizing analgesia, amnesia, and anxiolysis, all while controlling behavior and preserving patient safety.

The Spectrum of Sedation

Sedation is a continuum of progressive impairment of consciousness and inhibition of neuromuscular function that ranges from wakefulness to general anesthesia.6-8 (See Table 1.) Minimal sedation causes mild cognitive and coordination impairment (e.g., ptosis and slurred speech). Patients with moderate sedation are somnolent but easily aroused with a light touch or voice. Minimal and moderate sedation are appropriate for procedures requiring only anxiolysis and analgesia. Deep sedation puts patients in a more profound level of somnolence in which they still purposefully respond to painful stimuli. Importantly, withdrawal from painful stimuli is not considered a purposeful response. With general anesthesia, the patient is unarousable to repeated painful stimuli and will likely require assistance with ventilation and maintaining a patent airway.

Table 1: Levels of Sedation

Level of Sedation


Airway Patency

Respiratory Drive



Follows commands;

Impaired cognition and coordination



Single dose pain or anxiety medication dose


Purposeful response to light tactile stimuli

No intervention required

Spontaneous ventilations are adequate

"Conscious sedation" adequate pain control with light sedation such as for abscess incision and drainage or shoulder reduction


Purposeful response to repeated or painful stimuli

May require intervention

Ventilatory function may be impaired

Level required for dislocated hip reduction, for example

General Anesthesia

Not arousable, even by painful stimuli

Requires intervention

Ventilatory function often impaired

General anesthesia for procedure such as rapid sequence intubation

The dissociative agent ketamine is considered separately, as it causes a trancelike cataleptic state with profound amnesia and analgesia, all while preserving airway protective reflexes and respiratory drive.

Achieving the appropriate level of sedation creates a clinical challenge due to the wide variability in patient response to different agents. The divisions among the different levels of sedation are arbitrary, and individual patient reactions to sedation may not fit perfectly into one of the defined levels. Movement between levels of sedation can happen quickly and often at unexpected doses in some patients. As patients advance to deeper levels of sedation, they are at greater risk for cardiorespiratory compromise.9,10 The emergency physician must be prepared to provide the necessary resuscitative measures should the patient inadvertently progress to a level of sedation that is deeper than intended.

Inadequate Sedation

Ideally, all painful procedures can be facilitated by using some level of sedation. However, there is a wide practice variation in sedation strategies, and patients in the emergency department are often under-sedated for some of the most painful procedures. Shavit and colleagues surveyed pediatric emergency physicians and found that less experienced physicians were less likely to use sedation and preferred restraints alone for the hypothetical case of a 3-year-old with a facial laceration who had already failed to achieve analgesia and anxiolysis with LET and distraction.11 Inadequate use of analgesia has been identified in emergency medicine, especially when treating the most vulnerable of populations, namely children and the elderly.12,13 Intubated patients often receive inadequate sedation in the emergency department14 and are more likely to receive analgesics after being transferred early to an intensive care unit.15

Heath Care Policy, Quality Measures, Standards, and Guidelines

As the field of procedural sedation has expanded, regulating bodies have increased their oversight. The Joint Commission has set minimum standards for sedation, requiring consistent sedation policies within each individual institution, leaving the finer details of implementation to be determined at the individual hospital level.16 These minimum standards stipulate that deep procedural sedation be provided by practitioners qualified to resuscitate patients if necessary, a skill every emergency medicine physician should possess.

There have been attempts to limit the use of deep sedation by non-anesthesiologists, often restricting the use of propofol and etomidate. In 2006, the American Society of Anesthesiologists declared that deep sedation should be limited to anesthesiologists, with no clear evidence to support this broad statement.17 In 2009, the Center for Medicare and Medicaid Services (CMS) issued a statement stipulating that physicians administering deep sedation, namely propofol, not be involved in a simultaneous procedure. Fortunately, CMS later published a revised policy removing these restrictions and recognizing that propofol may be titrated to different levels of sedation. At least 27 sets of procedural sedation guidelines have been published since 1985,18 and the controversy surrounding the regulation of procedural sedation continues. Fortunately, emergency physicians have the airway and resuscitation skills necessary to safely provide deep sedation in the emergency department.19

Patient Evaluation

The emergency physician should carefully consider whether or not the individual patient is a candidate for sedation in the emergency department or if the patient would be better served in the operating room. The type and duration of procedure that is planned may also help determine the most appropriate location for the procedure. Patient characteristics associated with the greatest risk of complication from procedural sedation include extremes of age (< 2 years and > 65 years),20-24 significant airway abnormality, obstructive sleep apnea, morbid obesity,25,26 hepatic or renal insufficiency, and American Society of Anesthesiologists (ASA) physical status classification of 3 or higher (see Table 2).27 It is more challenging to appropriately dose sedative agents in groups with increased sensitivity to sedatives, altered pharmacokinetics, and/or skewed drug clearance.28,29 The physician should perform a pertinent history and physical prior to sedation (see Table 3).30 The emergency physician should also evaluate for potential difficulties with airway management. The mnemonics MOANS, SHORT, and LEMON (Tables 4-6) can be used evaluate the risks.31-34 The physician should consider the potential of a difficult airway when deciding whether or not the patient is best served by ED sedation.

Table 2: Suitability for Sedation

ASA Class

Physical Status


Suitability for Sedation

Adapted from Krauss B, Green SM. Sedation and analgesia for procedures in children. N Engl J Med 2000;342:938-945.


No disease outside of uncomplicated surgical procedure

A normal healthy patient



Systemic disease that is well controlled with no functional limitation

Mild or controlled asthma, diabetes, hypertension, anemia, epilepsy

Generally good


Severe systemic disease resulting in functional limitation

Moderate COPD, poorly controlled hypertension, diabetes with vascular complications, morbid obesity

Weigh benefits against risks


Severe systemic disease that is a constant life threat

History of angina, stroke, myocardial infarction or acute heart failure in the previous 6 months; sepsis; poorly controlled epilepsy

Benefits rarely outweigh the risks


Moribund patient who is not expected to survive without the operation

Septic shock, severe trauma

Extremely poor

Table 3: Pre-sedation Assessment


Past medical history, anesthesia history, history of snoring or sleep apnea, medications, allergies, fasting time, age, weight

Airway Exam

Mallampati score, obesity, neck size and mobility, micrognathia, edentulous, tonsillar hypertrophy (See Boxes 2-4)

Cardiovascular Exam

Heart rate, blood pressure, rhythm disturbances, distal pulses, carotid bruits

Respiratory Exam

Respiratory rate, pulse oximetry, obstructive lung disease, active upper respiratory infection

Table 4: MOANS: Difficult Bag Mask Ventilation

Mask seal: Beard, facial shape

Obesity: Increased upper airway tissue

Aged (> 55): Decreased upper airway muscle tone

No teeth: Difficult seal

Stiff lungs: COPD, asthma, CHF, and pulmonary fibrosis

Table 5: LEMON: Difficult Intubation

Look externally: Large teeth or tongue, short neck, small mandible

Evaluate 3-3-2 finger-breadths: Mouth opens 3, thyromental distance of 3, 2 from hyoid to thyroid cartilage

Mallampati score: Ability to visualize posterior oropharynx

Obstruction: Evidence of upper airway obstruction

Neck mobility: Immobilization due to cervical trauma or arthropathies

Table 6: SHORT: Risk for Difficult Cricothyrotomy

Surgery scar






The need for fasting prior to procedural sedation has been a topic of debate. The ASA recommends waiting two hours for clear liquids and six hours for solids before performing sedation; however, these recommendations are based on general anesthesia literature for elective cases in the operating room and not the emergency department setting.30 In a review of 4,657 patients who had not been fasting according to the ASA guidelines, only 17 cases of vomiting occurred during ED sedation, with no evidence of aspiration.35 Similarly, a prospective study enrolling 400 pediatric ED patients sedated with propofol, of which 282 had not fasted according to ASA standards, found only two patients with vomiting — one had fasted and one had not — and no episodes of aspiration.36 A consensus guideline written by a panel of emergency medicine experts recommends prudent clinical decision-making on a case-by-case basis.37

Preparing for Sedation

Adequate preparation can help to mitigate risk and prevent adverse events from becoming catastrophic (see Table 7). Almost half of all poor outcomes from procedural sedation are preventable, and standards and guidelines used for general anesthesia should be practiced for sedation care in any location.38-40 In addition, several studies have emphasized that a dedicated team of trained professionals performing the procedural sedation improves outcomes.20,41-43 Deep sedation may be accomplished either with the emergency physician monitoring the patient and a separate practitioner performing the procedure or by the same emergency physician both administering sedation and performing the procedure. Since ED procedures are typically brief and can be interrupted to address sedation concerns, it is common for deep sedation to be performed using a single emergency physician and an ED nurse. In these circumstances, the emergency physician will initiate effective sedation and, once stable sedation is established, the physician will perform the procedure while the nurse or other trained provider monitors the patient. The caveat is that the supervising practitioner performing sedation may also perform the procedure only if the procedure is of such a nature that it can be immediately halted should the patient suffer an adverse reaction that requires urgent attention or resuscitation.18,27,44

Table 7: Procedural Sedation Checklist

• Informed consent for procedure and sedation
• IV access with IV fluid
• High flow oxygen through non-rebreather mask
• End-tidal CO2 monitor and pulse oximeter
• Blood pressure cuff cycling every 5 minutes at least
• Continuous EKG or telemetry (especially if at risk for cardiac disease)
• Cardiac Arrest Cart including defibrillator
• Airway equipment

–Suction equipment
–Bag valve mask
–Oral and nasal airways with lubricant
–Intubation equipment with appropriate ET tube
–Airway adjuncts such as supraglottic airways, bougie, surgical airway

• Rescue medications

–Additional sedation agents

• Procedure timeout with sedation team, emphasizing roles in the sedation

Patient Monitoring

As the procedure progresses and the patient transitions between levels of sedation, close and continuous patient monitoring not only maintains patient safety but also guides repeat dosing. The designated professional responsible for patient monitoring must be able to clearly view the patient and assess for apnea, obstruction, emesis, or other problems. Monitoring is important during the procedure, and the same level of vigilance must be maintained until the patient has completely recovered. The period of time immediately following the procedure is often the most critical because of two factors. The first is the fact that once the painful stimulus is removed, many patients will slip into a deeper state of sedation. The second is that many times a medication will not reach its peak effect until after the procedure has been completed.

Supplemental Oxygen and Capnography

Despite research supporting the use of supplemental oxygen and capnography, there remains a practice gap in the utilization of these two techniques.45,46

Hypoxemia — one of the most significant complications of procedural sedation — can be prevented with supplemental oxygen. In healthy patients with normal cardiac output, the pulse oximeter oxygen saturation (SpO2) reflects oxygenation delayed by 20 to 30 seconds.47,48 In vasoconstrictive shock states, this lag extends up to 90 seconds.49 Delayed drops in oxygen saturation are typically seen in hypoventilatory states because of this lag. However, if supplemental oxygenation is provided, hypoxemia can be prevented even during hypoventilation,50 and it takes, on average, more than six minutes for a previously hyperoxygenated apneic adult to desaturate to below 90%.51

Thus, while oxygen supplementation prevents hypoxemia, it also obscures detection of severe hypoventilation, necessitating the use of continuous capnography. Capnography is more sensitive than clinical assessment or oxygen desaturation in detecting depressed ventilation.52-56 Anesthesia guidelines suggest that capnography should be used in the setting of procedural sedation for patients with suspected sleep apnea because of the increased risk of airway obstruction.57

Noninvasive Positive Pressure Ventilation

The use of noninvasive positive pressure ventilation during procedural sedation has not been well studied. A case report describing its use in a morbidly obese patient with a history of obstructive sleep apnea who received procedural sedation with propofol for electrical cardioversion58 suggests it may be a useful adjunct in patients at risk for upper airway obstruction.

Selecting Procedural Sedation Agents

When choosing sedation agents, match the desired depth and duration of sedation to the medication strategy. The depth chosen is specific to both the individual patient and the type of procedure. Patient factors include underlying illness, tolerance to medications, previous reactions to sedative agents, and idiosyncratic facets of pain. Moreover, different procedures involve different levels of painful stimuli.

The dynamic nature of procedural sedation can make achieving the appropriate level of sedation difficult. Some procedures involve an intense painful stimulus for a short period of time (e.g., shoulder relocation), followed by rapid-onset of relative pain relief. On the other hand, if the duration of the painful procedure exceeds the effective period of the sedative medication, the patient may become uncomfortable, increasing the risk of procedural failure and decreasing patient satisfaction and risking an unsuccessful procedure.

The ideal sedation agent should be easy to administer, predictable to titrate, fast in onset, short in duration, easily reversible, and inexpensive, all while maintaining cardiorespiratory stability and patient safety. Unfortunately, there is no perfect sedation agent or combination of agents for every patient or procedure. (See Table 8.) When sedation is administered, the practitioner should attend closely to the dose, as well as the onset, peak, and elimination times for each agent. Ideal analgesic administration is before the onset of noxious stimuli from the procedure to allow for equilibrium based on peak onset times. Lastly, avoid using deeper levels of sedation as compensation for inadequate analgesia, and, whenever possible, use local and regional anesthesia to attenuate the need for systemic sedatives.

Table 8: Medications












1 min IV
5 min IM

10-20 min

1-2 mg/kg IV; IV redose at 0.25-0.5 mg/kg every 5-10 min; 3-4 mg/kg IM

Preserves respiratory drive and airway reflexes

Sympathomimetic causes tachycardia and hypertension; Increases intracranial and intraocular pressure; emesis; Laryngospasm; Possible emergence reaction; Slightly increases secretions; Avoid in psychotic patients

Nitrous oxide

Mild analgesia


3-5 min

3-5 min

50-66% N2O/O2

Very short duration
Inhalation agent

Often requires second agent to achieve adequate sedation; emesis; Requires special apparatus; Occupational exposure associated with spontaneous abortions


Hypnosis Anxiolysis Some analgesia


2-5 min

~ 6 min

Load 1 mcg/kg/min over 5-10 minutes then 0.2-1 mcg/kg/hr infusion

Very short duration

Preserves respiratory drive and airway reflexes

Sedates patients who are insensitive to benzodiazepines



Hypnosis Some amnesia


< 1 min

5-15 min

0.1-0.2 mg/kg over 1 minute

Very short duration; minimal cardiovascular effects

Airway obstruction and respiratory depression; myoclonus; emesis; adrenal suppression

No analgesia


Some amnesia


< 1 min

3-10 min

0.5-1.0 mg/kg over 1-2 minutes or 0.5 mg/kg titrated in 20 mg aliquots to desired effect.

Short acting

Airway obstruction and respiratory depression; Hypotension (consider infusion rather than bolus); Pain at injection site; Allergy: soy and egg

No analgesia




< 1 min

15 min

0.75-1 mg/kg IV bolus and can be redosed at 0.5 mg/kg every 3-5 minutes; 25 mg/kg rectal

Shorter acting, inexpensive, can be given rectally for pediatric sedation

Airway obstruction and respiratory depression; Hypotension and cardiovascular depression; Laryngospasm; No analgesia




15-60 min

1-4 hours

Rectal:< 4 years: 3-6 mg/kg; >4 years: 1.5-3 mg/kg, max 100 mg; Adults 100 mg slow IV bolus; peds 2-5 mg/kg IV

Longer acting
Multiple routes of administration

Airway obstruction and respiratory depression

Prolonged duration

Slow recovery associated with agitation

No analgesia




Active metabolite excreted renally

5-10 min (rectal); 3-5 min IV

1-4 hrs (rectal); 15-45 min IV; 1-2 hr IM

0.05-0.1 mg/kg IV (30-50% less in combo with opioid); Age greater than 70 years, half dose

Age greater than 90 years, quarter dose

Reversal agent: flumazenil

Shorter onset and duration than other benzodiazepines; Can be given intranasally

Airway obstruction and respiratory depression; Paradoxical excitement and disinhibition; Some hypotension; No analgesia


Hypnosis at higher doses


Active metabolite excreted renally

1 min

30-60 min IV

3-10 mcg/kg

Very short duration; less potent fentanyl; Reversal agent: naloxone

Minimal sedative effect; hypotension; hypoxemia; apnea; vomiting



5-10 min

2-4 hrs IV

0.5-1 mg IV
(Adult dose)

May work if patients are tolerant to morphine or fentanyl

Reversal agent: naloxone

Histamine release



Active metabolite excreted renally

5-10 min

2-4 hrs IV

4-8 mg
(Adult dose)

Reversal agent: naloxone

Histamine release



1-2 min

30-60 min for single dose IV

0.5-1 mcg/kg every 1-2 min to effect

Less hypotension than other opiates; 100 times more potent than morphine; Reversal with naloxone

Minimal sedative effect; hypotension; hypoxemia; apnea; vomiting; chest rigidity when given fast


Benzodiazepine receptor antagonist

1-2 min

30-60 min IV

0.1-0.5 mg

Rare agitation upon awakening

Seizures, especially with chronic benzodiazepine users


Mu opioid receptor antagonist; reversal agent

1-2 min

20-40 min IV

0.04-0.5 mg


*Off-label use for procedural sedation

Dissociative Agent: Ketamine

Ketamine produces significant analgesia as well as a dissociative state characterized by unresponsiveness to nociceptive stimuli with cardiovascular stability as well as airway protection and respiratory drive.59 Rapid onset and short duration are seen with intravenous administration and only slightly less so when given intramuscularly.44 Emesis is more common with intramuscular as opposed to intravenous ketamine, but may be treated by premedication with ondansetron.60 Other important but rare side effects include transient blood pressure elevation and laryngospasm.44,61 Emergence reactions with ketamine are uncommon but may be associated with pre-procedural anxiety and can be treated and prevented with midazolam orally prior to the procedure.44,62 Ketamine should be considered when intravenous access is not an option because the intramuscular dose is reliable and effective and it has an excellent safety profile.


Nitrous Oxide. Inhaled nitrous oxide provides sedation, anxiolysis, and mild analgesia with rapid onset and short duration for mild to moderately painful procedures. This drug allows for the patient to stay awake and follow commands; however, it often must be combined with opioid or local analgesia to achieve adequate sedation.18 Vomiting is a common adverse effect of nitrous oxide, with no prevention by fasting.63 Adverse events are more common in patients younger than 1 year of age and when used in combination with other sedatives.22 The use of this agent requires special equipment, including a scavenger system to prevent occupational exposure, which is associated with infertility and spontaneous abortion.64,65 The risk of vomiting, monitoring requirements, and availability of other options make nitrous oxide a substandard sedation option.

Dexmedetomidine. Although primarily used as an adjunctive agent in the critical care and perioperative setting in both adults and children, dexmedetomidine may be considered for procedural sedation in the emergency department.66,67 Dexmedetomidine achieves hypnosis, anxiolysis, and analgesia as a potent alpha-2 antagonist (similar to clonidine) without causing respiratory depression.59 It is typically given as a loading dose over 10 minutes, followed by infusion.68 Onset is within minutes, with a very short duration due to rapid redistribution. Dexmedetomidine is most useful for quick emergent procedures, in patients with opiate tolerance, and in cases where respiratory depression would be unsafe. Because of its sympatholytic properties, dexmedetomidine's side effects include bradycardia and hypotension.

Etomidate. Etomidate is a short-acting agent that first was used for general anesthesia but has become useful for deep sedation at lower doses. Within seconds, it provides hypnosis, anxiolysis, and amnesia with a duration of 5 to 15 minutes.69 Etomidate does not have any analgesic effects and often must be combined with analgesia (fentanyl is an excellent option). Key adverse effects include respiratory depression and emesis.70 Myoclonus occurs in 20-45% of patients and is often mistakenly assumed to be seizure activity.71 Myoclonus can be treated with midazolam in severe cases. Etomidate's temporary suppression of adrenal function has not been shown to have clinical significance for most ED patients, but is of some concern in ICU patients.72

Propofol. Similar to etomidate, propofol's quick onset, short duration, and easy redosing are ideal for procedural sedation. It also has beneficial antiemetic properties. Similar to etomidate, propofol does not have analgesic properties, and the addition of an analgesic may be necessary. Multiple studies have shown that the use of propofol can shorten recovery time for orthopedic procedures, reducing overall ED length of stay.73,74 In addition, in a prospective randomized trial comparing propofol and etomidate, propofol had a greater rate of procedural success and less myoclonus.69 However, that same study also revealed a trend in which propofol caused more subclinical respiratory depression. Another common side effect is hypotension, which can be reversed with the short-acting alpha-1 agonist phenylephrine. Another adverse effect includes pain at the injection site. Nonetheless, propofol's positive attributes make it a very attractive option for many ED procedures.


Barbiturate use in procedural sedation has declined dramatically with the rising popularity of etomidate and propofol. Methohexital, the most commonly used barbiturate, has a quick onset and short duration; however, it can precipitate seizures in a small percentage of patients.18 Rectal use of methohexital is reliable and effective and may be an option in selected patients. Another attractive feature for methohexital is the extremely low cost compared to many other options. Pentobarbital is sometimes used for pediatric procedural sedation, but its long recovery time is associated with adverse effects, including agitation.61


When administered intravenously or intranasally, midazolam achieves hypnosis, anxiolysis, and amnesia within minutes and is usually eliminated within one hour.61 When given orally, onset and duration are unpredictably prolonged due to first pass metabolism.18 Midazolam can cause respiratory depression, hypotension, and paradoxical excitement.24 Its effects can be reversed with flumazenil. The main disadvantage of midazolam is the extreme variability in patient dosing and effect. In addition, many pediatric patients will have a paradoxical increased agitation at recommended doses. Midazolam also has no analgesic properties, so it must be combined with an analgesic.


Opioids are commonly used for sedation due to their analgesic properties as well as their ability to potentiate the effect of other sedatives. Fentanyl is the most commonly used opioid for procedural sedation because it has a short duration of action and less histamine release than either hydromorphone or morphine.61 Compared with other opiates, fentanyl causes less emesis, pruritus, and hypotension. Respiratory depression, bradycardia, and hypotension are key adverse effects. Remifentanil and alfentanil are even shorter acting than fentanyl and will likely be used more commonly for short procedures in the future.24 Naloxone reverses the effects of opiates.

Specific Combination Agents

Recent literature has called into question the broad use of midazolam with fentanyl.1 Midazolam's slower onset and long duration of action have been shown to delay recovery, discharge home, and return to daily living.75 Additionally, when combined with opiates, synergic hemodynamic and respiratory depression has been observed.40 Along those same lines, the combination of benzodiazepines and opiates is associated with a greater risk of respiratory compromise than midazolam alone or midazolam with ketamine.76 Lastly, multiple studies have provided further evidence emphasizing that the use of multiple sedative agents is associated with more frequent adverse events.20,21,41,77,78

Ketamine and Propofol. The combination of decreased doses of ketamine and propofol has become popular for procedural sedation. Theoretically, this combination agent should take advantage of the seemingly synergistic and complimentary effects of ketamine and propofol. Ketamine's association with the release of endogenous catecholamines should counterbalance the hypotension seen with propofol, and the antiemetic effects of propofol should prevent the emesis seen with ketamine.79 However, the literature has yet to show a significant outcomes benefit with this combination.80-85 Ketamine and propofol are typically combined as a 1:1 ratio (0.5 mg/kg each) in one syringe, but the ratio of the two drugs can be adjusted to target more sedation or dissociation.

Recovery and Discharge

Complications during procedural sedation are more likely to occur immediately after completion of the procedure and removal of the noxious stimulus. Observational studies of ED procedural sedation indicate that no adverse events were observed after 25 minutes had elapsed after the last sedative dose in children86 and 12 minutes in adults.87 Patient monitoring must continue until cardiorespiratory stability is ensured and the patient's mental status has returned to baseline.

Special Patient Populations

Pediatrics. Procedural sedation for children may be required prior to painless procedures such as diagnostic imaging. Controlling behavior becomes difficult in the face of heightened fear amplified by parental anxiety, strange environments, and the anticipation of pain. This fear, combined with the need to control behavior, often necessitates mild or moderate sedation.88 Because children are easily overpowered and cannot withdraw consent, adequate analgesia becomes even more important.89

Both the pharmacokinetics and pharmacodynamics of procedural sedation drugs may differ in children.61 Techniques such as desensitization (i.e., gradually increasing the painful stimulus over time), distraction (e.g., nonnutritive sucking with sucrose, playing a game, or watching a movie), and positive reinforcement from parents have all been shown to improve procedural sedation.90,91

Obesity. The anatomy and physiology of obese patients not only alters pharmacokinetics but also increases the risk of adverse events related to procedural sedation. Generally, obese patients have less total body water, larger adipose mass, relatively larger lean body mass, and greater glomerular filtration rates. This alters the pharmacokinetics of all drugs, especially lipophilic drugs such fentanyl and propofol with a greater volume of distribution. In addition, the greater redundant airway soft tissue of obese patients increases the risk of obstructive sleep apnea, which leads to obstruction during sedation.26 Obese patients, even without obstructive sleep apnea, suffer from a greater risk of hypoxemia and airway obstruction during sedation.92,93

Elderly. Although many experts believe elderly patients have greater risk of adverse sedation events, the limited amount of research available has not validated this assertion.94-95 It should be noted that elderly patients have increased sensitivity to all sedative drugs, especially opiates and benzodiazepines, and cautious titration is preferred.24


Patients should not be discharged until they are alert and oriented to their baseline. They should have stable vital signs (consistent with their baseline) and be able to ambulate at their baseline. A responsible adult should be present to drive the patient home and stay with him or her for 6-12 hours. Patients and caregivers must be instructed to avoid eating or drinking for two hours after discharge and then to advance the diet slowly, starting with liquids as tolerated. Patients must avoid any activity that requires normal balance, strength, and coordination for 12-24 hours. Patients should not drink alcohol for 24 hours.

Take-home Points

Many patients in the ED will require procedural sedation. The emergency physician must be comfortable with multiple drug regimens and be able to adapt them to a given situation. Preparation and planning are the keys to preventing adverse outcomes. If the physician is prepared to manage the patient's airway and resuscitate the patient, when necessary, prior to starting the procedure, almost all adverse outcomes can be avoided.


  1. Sacchetti A, Senula G, Strickland J, et al. Procedural Sedation in the Community Emergency Department: Initial Results of the ProSCED Registry. Acad Emerg Med 2007;14(1):41-46.
  2. Sacchetti A, Stander E, Ferguson N, et al. Pediatric procedural sedation in the community emergency department. Pediatr Emerg Care 2007;23(4):218-222.
  3. Results from the National Survey of Ambulatory Surgery (preliminary data), National Center for Health Statistics, Centers for Disease Control and Prevention. Web Database. Available at: Accessed May 20, 2012.
  4. Joshi GP. Efficiency in ambulatory surgery center. Curr Opin Anaesthesiology 2008;21(6):695-698.
  5. Fung D, Cohen MM, Stewart S, et al. What determines patient satisfaction with cataract care under topical local anesthesia and monitored sedation in a community hospital setting? Anesthesia & Analgesia 2005;100(6):1644-1650.
  6. Godwin SA, Caro DA, Wolf SJ, et al. Clinical policy: Procedural sedation and analgesia in the emergency department. Ann Emerg Med 2005;45(2):177-196.
  7. O'Connor RE, Sama A, Burton JH, et al. Procedural sedation and analgesia in the emergency department: Recommendations for physician credentialing, privileging, and practice. Ann Emerg Med 2011;58(4):365-370.
  8. The Joint Commission, Sedation and Anesthesia Care Standards. Accessed May 20, 2012.
  9. Ebert TJ. Sympathetic and hemodynamic effects of moderate and deep sedation with propofol in humans. Anesthesiology 2005;103(1):20-24.
  10. Win NN, Fukayama H, Kohase H, et al. The different effects of intravenous propofol and midazolam sedation on hemodynamic and heart rate variability. Anesth Analg 2005;101(1):97-102.
  11. Shavit I, Leder M, Cohen DM. Sedation provider practice variation. Pediatr Emerg Care 2010;26(10):742-747.
  12. Rupp T, Delaney KA. Inadequate analgesia in emergency medicine. Ann Emerg Med 2004;43(4):494-503.
  13. Selbst SM, Clark M. Analgesic use in the emergency department. Ann Emerg Med 1990;19(9):1010-1013.
  14. Bonomo JB, Butler AS, Lindsell CJ, et al. Inadequate provision of postintubation anxiolysis and analgesia in the ED. Am J Emerg Med 2008;26(4):469-472.
  15. Chao A, Huang CH, Pryor JP, et al. Analgesic use in intubated patients during acute resuscitation. J Trauma 2006;60(3):579-582.
  16. Hospital JCA. Comprehensive Accreditation Manual for Hospitals: CAMH: The Official Handbook. Joint Commission on; 2007.
  17. Rex DK, Rex D, Rex D, et al. Effect of the Centers for Medicare & Medicaid Services policy about deep sedation on use of propofol. Ann Intern Med 2011;154(9):622-626.
  18. Krauss B, Green SM. Procedural sedation and analgesia in children. Lancet 2006;367(9512):766-780.
  19. Denny MA, Manson R, Della-Giustina D. Propofol and etomidate are safe for deep sedation in the emergency department. West J Emerg Med 2011;12(4):399-403.
  20. Cravero JP, Beach ML, Blike GT, et al, Pediatric Sedation Research C. The incidence and nature of adverse events during pediatric sedation/anesthesia with propofol for procedures outside the operating room: a report from the Pediatric Sedation Research Consortium. Anesth Analg 2009;108(3):795-804.
  21. Green SM, Green SM, Roback MG, et al. Predictors of emesis and recovery agitation with emergency department ketamine sedation: An individual-patient data meta-analysis of 8,282 children. Ann Emerg Med 2009;54(2):171-180.e174.
  22. Gall O, Annequin D, Benoit G, et al. Adverse events of premixed nitrous oxide and oxygen for procedural sedation in children. Lancet 2001;358(9292):1514-1515.
  23. Malviya S, Voepel-Lewis T, Tait AR. Adverse events and risk factors associated with the sedation of children by nonanesthesiologists. Anesth Analg 1997;85(6):1207-1213.
  24. Ekstein M, Gavish D, Ezri T, et al. Monitored anaesthesia care in the elderly: Guidelines and recommendations. Drugs Aging 2008;25(6):477-500.
  25. Vargo JJ. Procedural sedation and obesity: Waters left uncharted. Gastrointest Endosc 2009;70(5):980-984.
  26. Welliver M, Bednarzyk M. Sedation considerations for the nonintubated obese patient in critical care. Crit Care Nurs Clin North Am 2009;21(3):341-352, vi.
  27. Krauss B, Green SM. Sedation and analgesia for procedures in children. N Engl J Med 2000;342(13):938-945.
  28. Qadeer MA, Rocio Lopez A, et al. Risk factors for hypoxemia during ambulatory gastrointestinal endoscopy in ASA I-II patients. Dig Dis Sci 2009;54(5):1035-1040.
  29. Hug CC, Jr. MAC should stand for Maximum Anesthesia Caution, not Minimal Anesthesiology Care. Anesthesiology 2006;104(2):221-223.
  30. American Society of Anesthesiologists Task Force on S, Analgesia by N-A. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology 2002;96(4):1004-1017.
  31. Stanwood PL. The laryngeal mask airway and the emergency airway. AANA J 1997;65(4):364-370.
  32. Parmet JL, Colonna-Romano P, Horrow JC, et al. The laryngeal mask airway reliably provides rescue ventilation in cases of unanticipated difficult tracheal intubation along with difficult mask ventilation. Anesth Analg 1998;87(3):661-665.
  33. Levitan RM, Ochroch EA, Stuart S, et al. Use of the intubating laryngeal mask airway by medical and nonmedical personnel. Am J Emerg Med 2000;18(1):12-16.
  34. Bair AE, Panacek EA, Wisner DH, et al. Cricothyrotomy: A 5-year experience at one institution. J Emerg Med 2003;24(2):151-156.
  35. Thorpe RJ, Benger J. Pre-procedural fasting in emergency sedation. Emerg Med J 2010;27(4):254-261.
  36. Bell A, Treston G, McNabb C, et al. Profiling adverse respiratory events and vomiting when using propofol for emergency department procedural sedation. Emerg Med Australas 2007;19(5):405-410.
  37. Green SM, Roback MG, Miner JR, et al. Fasting and emergency department procedural sedation and analgesia: A consensus-based clinical practice advisory. Ann Emerg Med 2007;49(4):454-461.
  38. Metzner J, Posner KL, Domino KB. The risk and safety of anesthesia at remote locations: The US closed claims analysis. Curr Opin Anaesthesiology 2009;22(4):502-508.
  39. Bhananker SM, Posner KL, Cheney FW, et al. Injury and liability associated with monitored anesthesia care: A closed claims analysis. Anesthesiology 2006;104(2):228-234.
  40. Hession PM, Joshi GP. Sedation: Not quite that simple. Anesthesiology Clinics 2010;28(2):281-294.
  41. Hoffman GM, Nowakowski R, Troshynski TJ, et al. Risk reduction in pediatric procedural sedation by application of an American Academy of Pediatrics/American Society of Anesthesiologists process model. Pediatrics 2002;109(2):236-243.
  42. Vespasiano M, Finkelstein M, Kurachek S. Propofol sedation: Intensivists' experience with 7304 cases in a children's hospital. Pediatrics 2007;120(6):e1411-1417.
  43. Barbi E, Gerarduzzi T, Marchetti F, et al. Deep sedation with propofol by nonanesthesiologists: A prospective pediatric experience. Arch Pediatr Adolesc Med 2003;157(11):1097-1103.
  44. Green SM, Roback MG, Kennedy RM, et al. Clinical Practice Guideline for Emergency Department Ketamine Dissociative Sedation: 2011 Update. Ann Emerg Med 2011;57(5):449-461.
  45. Cote CJ, Karl HW, Notterman DA, et al. Adverse sedation events in pediatrics: Analysis of medications used for sedation. Pediatrics 2000;106(4):633-644.
  46. Coté CJ, Notterman DA, Karl HW, et al. Adverse sedation events in pediatrics: A critical incident analysis of contributing factors. Pediatrics 2000;105(4 Pt 1).
  47. Foo JY, Wilson SJ, Dakin C, et al. Variability in time delay between two models of pulse oximeters for deriving the photoplethysmographic signals. Physiol Meas2005;26(4):531-544.
  48. Tobias JD. Cerebral oximetry monitoring with near infrared spectroscopy detects alterations in oxygenation before pulse oximetry. J Intensive Care Med 2008;23(6):384-388.
  49. Xue FS, Liao X, Tong SY, et al. Effect of epidural block on the lag time of pulse oximeter response. Anaesthesia 1996;51(12):1102-1105.
  50. Fu ES, Downs JB, Schweiger JW, et al. Supplemental oxygen impairs detection of hypoventilation by pulse oximetry. Chest 2004;126(5):1552-1558.
  51. Jense HG, Dubin SA, Silverstein PI, et al. Effect of obesity on safe duration of apnea in anesthetized humans. Anesth Analg 1991;72(1):89-93.
  52. Soto RG, Fu ES, Vila H, Jr., et al. Capnography accurately detects apnea during monitored anesthesia care. Anesth Analg 2004;99(2):379-382.
  53. Burton JH, Harrah JD, Germann CA, et al. Does end-tidal carbon dioxide monitoring detect respiratory events prior to current sedation monitoring practices? Acad Emerg Med 2006;13(5):500-504.
  54. Miner JR, Heegaard W, Plummer D. End-tidal carbon dioxide monitoring during procedural sedation. Acad Emerg Med 2002;9(4):275-280.
  55. Deitch K, Chudnofsky CR, Dominici P. The utility of supplemental oxygen during emergency department procedural sedation and analgesia with midazolam and fentanyl: A randomized, controlled trial. Ann Emerg Med 2007;49(1):1-8.
  56. Anderson JL, Junkins E, Pribble C, et al. Capnography and depth of sedation during propofol sedation in children. Ann Emerg Med 2007;49(1):9-13.
  57. Gross JB, Bachenberg KL, Benumof JL, et al. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: A report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Anesthesiology 2006;104(5):1081-1093; quiz 1117-1088.
  58. Remick J, Sacchetti A, Bages G, et al. Noninvasive positive pressure ventilation in procedural sedation. Am J Emerg Med 2010;28(6):750.e751-750.e753.
  59. Panzer O, Moitra V, Sladen RN. Pharmacology of sedative-analgesic agents: Dexmedetomidine, remifentanil, ketamine, volatile anesthetics, and the role of peripheral Mu antagonists. Anesthesiol Clin 2011;29(4):587-605, vii.
  60. Langston WT, Wathen JE, Roback MG, et al. Effect of ondansetron on the incidence of vomiting associated with ketamine sedation in children: A double-blind, randomized, placebo-controlled trial. Ann Emerg Med 2008;52(1):30-34.
  61. Sahyoun C, Krauss B. Clinical implications of pharmacokinetics and pharmacodynamics of procedural sedation agents in children. Curr Opin Pediatr 2012:1.
  62. Sener S, Eken C, Schultz CH, et al. Ketamine with and without midazolam for emergency department sedation in adults: A randomized controlled trial. Ann Emerg Med 2011;57(2):109-114.e102.
  63. Babl FE, Puspitadewi A, Barnett P, et al. Preprocedural fasting state and adverse events in children receiving nitrous oxide for procedural sedation and analgesia. Pediatr Emerg Care 2005;21(11):736-743.
  64. Rowland AS, Baird DD, Shore DL, et al. Nitrous oxide and spontaneous abortion in female dental assistants. Am J Epidemiol 1995;141(6):531-538.
  65. Rowland AS, Baird DD, Weinberg CR, et al. Reduced fertility among women employed as dental assistants exposed to high levels of nitrous oxide. N Engl J Med 1992;327(14):993-997.
  66. Jewett J, Phillips WJ. Dexmedetomidine for procedural sedation in the emergency department. Eur J Emerg Med 2010;17(1):60.
  67. McMorrow SP, Abramo TJ. Dexmedetomidine sedation. Pediatr Emerg Care 2012;28(3):292-296.
  68. Shukry M, Miller JA. Update on dexmedetomidine: Use in nonintubated patients requiring sedation for surgical procedures. Therapeutics Clin Risk Management2010;6:111-121.
  69. Miner JR, Danahy M, Moch A, et al. Randomized clinical trial of etomidate versus propofol for procedural sedation in the emergency department. Ann Emerg Med2007;49(1):15-22.
  70. Green SM. Research advances in procedural sedation and analgesia. Ann Emerg Med 2007;49(1):31-36.
  71. Falk J, Zed PJ. Etomidate for procedural sedation in the emergency department. Ann Pharmacother 2004;38(7-8):1272-1277.
  72. Schenarts CL, Burton JH, Riker RR. Adrenocortical dysfunction following etomidate induction in emergency department patients. Acad Emerg Med 2001;8(1):1-7.
  73. Uri O, Behrbalk E, Haim A, et al. Procedural sedation with propofol for painful orthopaedic manipulation in the emergency department expedites patient management compared with a midazolam/ketamine regimen: A randomized prospective study. J Bone Joint Surg (American) 2011;93(24):2255-2262.
  74. Lee Y, Chen C, Lin H, et al. Propofol for sedation can shorten the duration of ED stay in joints reductions. Am J Emerg Med 2012;30:1352-1356.
  75. Dunn T, Mossop D, Newton A, et al. Propofol for procedural sedation in the emergency department. Emerg Med J 2007;24(7):459-461.
  76. Leroy PL, Schipper DM, Knape HJ. Professional skills and competence for safe and effective procedural sedation in children: Recommendations based on a systematic review of the literature. International J Pediatrics 2010;2010:934298.
  77. Pitetti RD, Singh S, Pierce MC. Safe and efficacious use of procedural sedation and analgesia by nonanesthesiologists in a pediatric emergency department. Arch Pediatr Adolesc Med 2003;157(11):1090-1096.
  78. Sanborn PA, Michna E, Zurakowski D, et al. Adverse cardiovascular and respiratory events during sedation of pediatric patients for imaging examinations. Radiology 2005;237(1):288-294.
  79. Menchine M, Arora S, Schriger D. Procedural sedation: Is two better than one? Ann Emerg Med 2011;58(4): 383-394.
  80. Andolfatto G, Abu-Laban RB, Zed PJ, et al. Ketamine-propofol combination (ketofol) versus propofol alone for emergency department procedural sedation and analgesia: A randomized double-blind trial. Ann Emerg Med 2012;59(6):504-512 e502.
  81. Shah A, Mosdossy G, McLeod S, et al. A blinded, randomized controlled trial to evaluate ketamine/propofol versus ketamine alone for procedural sedation in children. Ann Emerg Med 2011;57(5):425-433.e422.
  82. Messenger DW, Murray HE, Dungey PE, et al. Subdissociative-dose ketamine versus fentanyl for analgesia during propofol procedural sedation: A randomized clinical trial. Acad Emerg Med 2008;15(10):877-886.
  83. Andolfatto G, Willman E. A prospective case series of pediatric procedural sedation and analgesia in the emergency department using single-syringe ketamine-propofol combination (Ketofol). Acad Emerg Med 2010;17(2):194-201.
  84. David H, Shipp J. A randomized controlled trial of ketamine/propofol versus propofol alone for emergency department procedural sedation. Ann Emerg Med2011;57(5):435-441.
  85. Andolfatto G, Willman E. A prospective case series of single-syringe ketamine-propofol (Ketofol) for emergency department procedural sedation and analgesia in adults. Acad Emerg Med 2011;18(3):237-245.
  86. Newman DH, Azer MM, Pitetti RD, et al. When is a patient safe for discharge after procedural sedation? The timing of adverse effect events in 1367 pediatric procedural sedations. Ann Emerg Med 2003;42(5):627-635.
  87. Bawden J, Villa-Roel C, Singh M, et al. Procedural sedation and analgesia in a Canadian ED: A time-in-motion study. Am J Emerg Med 2011;29(9):1083-1088.
  88. Yaster M, Cravero JP. The continuing conundrum of sedation for painful and nonpainful procedures. J Pediatr 2004;145(1):10-12.
  89. Zempsky WT, Cravero JP, American Academy of Pediatrics Committee on Pediatric Emergency M, Section on A, Pain M. Relief of pain and anxiety in pediatric patients in emergency medical systems. Pediatrics 2004;114(5):1348-1356.
  90. Cohen LL. Behavioral approaches to anxiety and pain management for pediatric venous access. Pediatrics 2008;122 Suppl 3:S134-139.
  91. Chen E, Joseph MH, Zeltzer LK. Behavioral and cognitive interventions in the treatment of pain in children. Pediatr Clin North Am 2000;47(3):513-525.
  92. Patil SP, Schneider H, Marx JJ, et al. Neuromechanical control of upper airway patency during sleep. J Appl Physiol 2007;102(2):547-556.
  93. Dhariwal A, Plevris JN, Lo NT, et al. Age, anemia, and obesity-associated oxygen desaturation during upper gastrointestinal endoscopy. Gastrointest Endosc1992;38(6):684-688.
  94. Cicero M, Graneto J. Etomidate for procedural sedation in the elderly: A retrospective comparison between age groups. Am J Emerg Med 2011;29(9):1111-1116.
  95. Weaver CS, Terrell KM, Bassett R, et al. ED procedural sedation of elderly patients: Is it safe? Am J Emerg Med 2011;29(5):541-544.