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Procedural sedation and analgesia (PSA) is the practice of administering sedative or dissociative agents to induce a depressed level of consciousness in order to facilitate painful but necessary procedures. As emergency practitioners are trained to manage airway issues through all levels of sedation, the Center for Medicaid and Medicare Services (CMS) [1] as well as the American College of Emergency Physicians (ACEP) has deemed them as being capable of safely performing PSA. [2]

These various levels of sedation can be targeted through drug choice (see below) to accomplish minimizing pain, discomfort and suffering during procedures. The following are the levels of sedation as defined by CMS: [1]

- Minimal Sedation

  • Near baseline level of alertness and responsiveness, although cognitive function and coordination might be impaired
  • Cardiovascular and respiratory function are preserved
  • Example: Usually used in the ED prior to the minor procedures (Ex: Giving fentanyl or versed to facilitate patient relaxation in the reduction of an inguinal hernia)

- Moderate Sedation

  • Depressed level of consciousness, but will still respond to verbal or light tactile stimulation
  • Amnesia during event common
  • Cardiovascular and respiratory function preserved
  • Example: Usually used in the ED prior to more lengthy and moderately painful procedures (Ex: Giving fentanyl/versed in combination to drain a large pilonidal abscess)

- Deep Sedation

  • Profoundly depressed level of consciousness, will only respond purposefully to repeated painful stimuli
  • Oropharyngeal relaxation and respiratory depression may necessitate assistance in maintaining airway patency and adequate ventilation, but cardiovascular status should be maintained
  • Example: Usually used in the ED for very painful procedures that require patient relaxation (Ex: Giving propofol, etomidate, or ketofol prior to a trimalleolar fracture/dislocation reduction)

- Dissociative Anesthesia

  1. A trance-like state with profound analgesia and amnesia achieved through the unique properties of the drug ketamine
  2. Airway reflexes and spontaneous ventilation maintained
  3. Example: Due to safety used for a variety of procedures, from simple procedures like pediatric laceration repair to complex distal radius fracture reductions.

- General Anesthesia

  • A depth of sedation characterized by unresponsiveness to all stimuli
  • Absence of protective airway reflexes. Rapid sequence intubation (RSI) or placement of an extraglottic device for positive pressure ventilation may be required if this level of sedation is achieved due to over-sedation during a procedure.
  • Example: Usually only used in the E.D. to facilitate Rapid Sequence Intubation (RSI).


Adequate preparation is key to providing safe, reliable delivery of PSA. Any sedation targeting moderate, deep, or dissociate sedation can have significant respiratory or cardiovascular effects, so preparation should be aimed at managing and minimizing these effects. A checklist is included as an adjunct to use in preparing to perform PSA. (Disclaimer: Checklist designed to reflect the common practices at UCMC ED. Always follow your own institutional guidelines when delivering PSA.) This should help gather equipment as well as perform a pre-procedure assessment of the patient.


As PSA can induce all levels of sedation, sometimes with significant airway compromise, emergency physicians must be vigilant and prepare for all levels of airway management. Therefore, the same mnemonic used to prepare for Rapid Sequence Intubation (SOAP-ME) can also be used to prepare for PSA, with minimal changes. 

  • S- Suction should be hooked up, functioning, with an easily accessible yankauer within it’s package prepared at bedside. 
  • O-Oxygen All levels of non-invasive oxygen delivery at bedside and readily available: 15L nasal cannula on patient for pre oxygenation, nonrebreather (NRB) at bedside within packaging, and bag valve mask (BVM) assembled within its package and hooked to oxygen.
  • A- Airway equipment. All interventions from simple maneuvers . Appropriately sized nasal trumpets, lubricant, oral airway should be at bedside. Appropriate laryngoscope blade, handle, ETT, stylet, and syringe should be at bedside. Appropriate extraglottic device should be at bedside within its package. Back-up airway equipment’s (bougie, VL, cric-kit) location should be verified and known. 
  • P- Preoxygenation Preoxygenation with 15LPM NC or NRB prior to PSA with ETCO2 monitoring.
  • M- Monitoring- Patient should routinely be on cardiac telemetry monitoring as well as blood pressure monitoring q5 minutes and PRN. Ensure BP cuff is not on same arm as pulse ox as this will obscure pulse oximetry wave form. 
  • M- Medications- Appropriate sedative should be drawn up and doses triple-checked. Paralytic and reversal vials at bedside. Dose for paralytic pre-calculated in case of emergent RSI. 
  • E- ETCO2- ETCO2 quantitative monitoring should be done on all patients receiving moderate sedation or above for early detection of hypoventilation.

1. Suction 2. ETCO2 monitoring w/ Pre-ox NC at 15LPM, 3. Nasal Trumpet w/ lubricant, 4. NRB, 5. BVM assembled, 6. Oral airway, 7. intubating equipment, 8. Extraglottic device w/ lubricant

Wait, patients should receive ETCO2 monitoring and pre oxygenation? Can’t I just monitor pulse oximetry?

In ACEP’s clinical policy on PSA, it is a level II recommendation that quantitative capnograph ” may be used as an adjunct to pulse oximetry and clinical assessment to detect hypoventilation and apnea earlier than pulse oximetry and/or clinical assessment alone in patients undergoing procedural sedation and analgesia in the ED.” [2]

This is because it has been shown that capnography does detect hypoventilation earlier than pulse oximetry alone in previous studies. One ED study of 60 patients demonstrated capnography detected respiratory depression before pulse oximetry alone in 70% of patients studied. [3] In another study, comparing physician’s ability to detect respiratory depression with and without capnography, physicians were able to detect 92% of the events of respiratory depression that capnography detected that led to hypoxia, but only 3.7% of events of respiratory depression that capnography detected that did not involve hypoxia. [4]

Additionally, ETCO2 monitoring has been shown to reduce the risk of hypoxia in the emergency department. One randomized controlled trial of 132 ED patients comparing using only pulse oximetry to pulse oximetry in addition to capnography during procedural sedations with propofol. This showed a absolute risk reduction of 17% [95% CI 1.3-33%] for hypoxic events. [5] However, while ETCO2 monitoring has been shown to reduce hypoxic events, it has not been adequately studied whether quantitative capnography reduces the amount of serious adverse events during procedural sedation.

And so, as capnography has not only been shown to improve the detection of hypoventilation, but also prevent hypoxia, it is a safe and easy adjunct to use during ED procedural sedations. Additionally, because it can detect hypoventilation with and without hypoxia, pre-oxygenation during during sedations can greatly increase a patient's safe apnea time.


Past Medical History

  • Any history that would cause cardiovascular or respiratory compromise?
  • Any history of difficulty with anesthesia/intubation. Even the best pre-sedation airway evaluation can fail to detect an extremely complicated and difficult intubation.
  • American Society of Anesthesiology (ASA) class can help guide who may be suitable for sedation in the emergency department vs. those who likely require sedation in the operating room. ASA classes III-VI may be more suitable for operating room sedation secondary to higher risk of complications and higher likelihood of prolonged sedation.
    • ASA I- A normal, healthy patient
    • ASA II- A patient with mild systemic disease
    • ASA III- A patient with severe systemic disease
    • ASA IV- A patient with severe systemic disease that is a constant threat to life
    • ASA V- A patient not suspected to survive without an operation
    • ASA VI- Brain dead patient

Difficult Airway Features Mnemonics

  1. BVM:  ROMAN (Radiation/Restriction; Obstruction/Obesity/OSA; Mask seal/Male/Mallampati; Aged; No teeth)
  2. Extraglottic Device: RODS (Restriction; Obstruction/Obesity; Distorted anatomy; Short thyromental distance)
  3. Direct Laryngoscopy: LEMON (Look externally; Evaluate 3-3-2; Mallampati; Obstruction/Obesity; Neck mobility)
  4. Cricothyrotomy: SMART (Surgery; Mass; Access/Anatomy; Radiation; Tumor)  


  • Ask about drug AND food  allergies as propofol is formulated with a lipid emulsion containing 10% soybean oil, 2.25% glycerol, and 1.2% egg lecithin.


  • Calculate appropriate dose of sedative.
  • Calculate appropriate dose of paralytic should patient require emergent RSI,
  • Calculate appropriate dose of reversal agent prior to sedation.

Patient Comfort

  • Patient should have adequate analgesia in their position of comfort prior to PSA to decrease necessary dose of sedative. Etomidate, propofol have no intrinsic analgesia.

Last Meal

  • ASA recommends for healthy patients undergoing elective sedation the following fasting guidelines:
    • 2 hrs prior- Clear liquids
    • 4 hrs prior- Breast milk
    • 6 hrs prior- Solids

So should we delay sedations in the ED if patients haven't adequately fasted?

The short answer is it depends, but for most cases no. ACEP has the following recommendation: “Do not delay procedural sedation in adults or pediatrics in the ED based on fasting time. Preprocedural fasting for any duration has not demonstrated a reduction in the risk of emesis or aspiration when administering procedural sedation and analgesia.” [2]

In a systematic review of the literature of emergency department sedations, it was found that out of 22,329 adult and pediatric patients, only a single event of aspiration occurred. [6] Additionally, in a review of four pediatric clinical trials and one adult clinical trial [2], no relationship could be found between fasting time and emesis/aspiration.

Despite this, fasting should be recorded in patients. In the pre-sedation evaluation, patient’s with gastric outlet obstruction or gastroparesis may be at significantly higher risk of emesis and aspiration. Additionally, it pre-sedation anti-emetics can be targeted to high risk patients.


- Etomidate


  • Fast acting sedative with profound sedation
  • Short duration of action for short procedures
  • Allows good muscle relaxation for orthopedic procedures
  • Hemodynamically stable


  • Suboptimal for longer procedures due to rapid elimination
  • No intrinsic analgesia
  • Adrenocortical suppression in higher doses, but this has not been shown to be consequential. [7]
  • Myoclonus observed in up to 20% of ED patients [8], but this rarely causes procedure failure or delay.
  • Post-procedure emesis

- Midazolam/Fentanyl


  • Prolonged duration of action for minor procedures requiring minimal sedation


  • Delayed onset of 3-5 minutes for respiratory depressive effects
  • Difficult to titrate for moderate or deep sedation- over sedation can occur when titrating during painful procedures
  • Delayed recovery from sedation can lead to prolonged monitoring
  • Synergistic respiratory depression between the two medications
  • Hypotension
  • Midazolam Category D in pregnancy

- Ketamine


  • Fast acting dissociative agent
  • Preserves spontaneous respiration and airway reflexes
  • Comparatively long duration of action allows for longer procedures
  • Option of intramuscular administration
  • Intrinsic analgesia


  • Emergence reaction (vivid hallucinations upon awakening from sedation). However, only 1-2% clinically significant, and can be well controlled with midazolam PRN [9]
  • HTN, tachycardia- caution in patients with CAD, CHF
  • Controversial on whether it has clinically significant effect on ICP, but likely not
  • Emesis
  • Hypersalivation, but shown to be clinically inconsequential. No pretreatment needed, suction PRN. [10]

- Propofol


  • Fast acting sedative
  • Short duration of action for short procedures
  • Allows for excellent muscle relaxation for orthopedic procedures
  • Anti-emetic
  • Decreases ICP


  • No intrinsic analgesia
  • Painful injection
  • Hypotension common among patients
  • Apnea can occur
  • Lipid emulsion makes it a relative contraidinication in those with soy or egg allergy

- Ketamine + Propofol a.k.a Ketofol

Ketofol is a mixture of Ketamine and Propofol. This mixture is most commonly 1:1 in ED studies, but other mixtures have been done. The theory behind it's use is that because Ketamine and Propofol have opposing side effect profiles, a mixture may be more hemodynamically stable and safe for the patient. Additionally, as Propofol has no analgesic properties, ketamine addition could be beneficial. Lastly, it is thought that the lower doses of both sedative agents used by employing the other may be safer for the patient to avoid effects such as respiratory depression and apnea.

Theoretical Advantages

  • Ketamine ↑ BP, Propofol ↓ BP, so effects cancel out
  • Ketamine ↑ Emesis, Propofol ↓ Emesis, so less emesis
  • Ketamine preserves respiratory drive, Propofol ↓ respiratory drive, so less apnea and respiratory depression
  • Ketamine has intrinsic analgesia to add to Propofol
  • So how does it stack up in the literature? Well, the two recent and expansive ED studies show the following comparing Ketofol head-to-head with Propofol or Ketamine alone.

Shah et. al 2012 [11]

This is the largest trial to date to directly compare Ketamine to Ketofol in ED patients. This double-blinded, randomized controlled trial of evaluated ketamine at 1mg/kg IV vs. ketofol 1:1 at 1mg/kg in 136 pediatric patients in a single emergency department during procedural sedation for orthopedic reductions. Primary endpoint was total sedation time, with secondary endpoints included time to recovery, adverse events, efficacy, and patient satisfaction scores.

Total sedation time was shorter for Ketofol (13 vs. 16 minutes so -3 minutes w/ 95% CI of -5 to -2 minutes). This was statistically but not clinically significant. There was also less vomiting in the Ketofol group (2% vs 14% so -12% w/ 95% CI -14% to -4%). However, there was no other significant difference in complications or efficacy. Satisfaction scores were higher in using ketofol.

Ferguson et. al 2016 [12]

Though several trials have compared Propofol, this is the largest to date to compare Propofol to Ketofol in ED patients. In this randomized, double-blind trial of 573 patients, patients were randomized to receive either propofol or 1:1: ketofol. Primary outcome was occurrence of respiratory adverse events (desaturation, apnea, hypoventilation). Secondary outcomes included hypotension and patient satisfaction.

There was no significant difference in respiratory adverse events (2% w/ 95% CI -2% to 5%). Patients receiving propofol had a higher percentage of hypotension (8% vs 1% so -7% w/95% CI -4 to -10%). Patients receiving ketofol had lower pain scores 30 minutes post procedure.

What does this all mean? First, more study is needed to directly compare the three in a three-arm trial. However, current research is promising and shows Ketofol has some advantages over both Ketamine and Propofol alone in the above trials.



As patient's experience deeper levels of sedation, relaxation of their pharyngeal muscles can cause partial or total airway obstruction Additionally, as mentioned above, many of the medications can cause respiratory depression. Therefore, most airway and breathing abnormalities secondary to PSA will be hypoventilation and/or obstruction eventually leading to hypoxia. However, detecting these early will prevent hypoxia, so recognizing how to is vital for safe delivery of PSA. The following are the two most common ways hypoventilation will be reflected with a capnograph: 

  1. ↑ ETCO2, ↓ RR- Here, bradypnea causes slowly rising ETCO2. As minute ventilation decreases, ETCO2 levels rise. 
  2. ↓ ETCO2, normal or ↓ RR- Here, due to obstruction or decreased respiratory drive, less CO2 is exhaled, so ETCO2 levels fall. However, were RR to be high, this would merely reflect hyperventilation with increased minute ventilation. 


The following are step-wise interventions that can be performed to intervene on hypoventilation with or without airway obstruction in order to ensure patients do not become hypoxic. RSI/EGD should be a last resort should these interventions fail. 

First, before any intervention, attempt to optimize positioning of the patient. 

  1. If possible, sit the patient up at 45 degrees in order to prevent decreased lung compliance secondary to weight of the chest wall. 
  2. Place the patient into the sniffing position with their head in the midline 
  3. Clear any excess secretions with suctioning. Be mindful of airway reflexes and emesis as patients undergoing PSA are not paralyzed. 
  4. If this fails, move down interventions in a stepwise fashion to attempt to eliminate hypoventilation. 

Jaw Thrust

Jaw Thrust

Jaw Thrust

  1. Rest thumbs on the patients maxilla in order to give you the ability to anchor. 
  2. With your fingers behind the angle of the mandible, pull directly forward until the mandible is displaced anterior giving the patient an overbite. 

Nasal Trumpet Insertion

Nasal Trumpet Insertion

  1. Appropriate size of the nasal airway is the device should extend from the outer nares to the angle of the jaw
  2. Insert a well lubricated nasal trumpet with the bevel towards the septum. Aim straight (not upward) back along the floor of the nose and insert until the trumpet is completely within the nasopharynx.

Bag Mask Ventilation

Bag Mask Ventilation

  1. Create a firm seal by stretching the mask outward and placing down on patient's face
  2. Firmly rest the thenar eminences of bilateral hands against the mask
  3. Grip the patients mandible and pull upward towards the ceiling rather than pushing downward. Have a second individual give breaths at 1 breath every 6 seconds, being careful not to give too much positive pressure and insufflate the stomach. 

Oral Airway Insertion

Oral airway insertion

  1. Appropriate size of oral airway is the device should extend from the lateral corner of the lip to the angle of the jaw
  2. Scissor open the jaw and insert the oral airway with the tip pointing superiorly. Once the tip contacts the soft palate, rotate 180 degrees with the flange resting against the lips.

post procedure evaluation

  • All patients undergoing PSA should have post-procedure documentation to document any adverse events or interventions
  • Patient should be monitored with ETCO2, telemetry, BP monitoring until responding appropriately to verbal stimuli, AOx3 
  • If reversal agents must be given, it is appropriate to monitor the patient in the ED for the duration of the reversal (most commonly 60-90 minutes with naloxone), as patient should be at baseline mental status without any reversal agent effect
  • Criteria for discharge include baseline mental status, baseline ability to ambulate, and ability to tolerate PO


  1. Centers for Medicare & Medicaid Services (CMS). Revised appendix A, interpretive guidelines for hospitals— state operations manual, anesthesia services. Effective December 2, 2011. Available at: http:// www.cms.gov/Regulations-and-Guidance/Guidance/Transmittals/ downloads/R74SOMA.pdf. Accessed: December 19, 2016. 
  2. Godwin SA, Burton JH, Gerardo CJ et al. Clinical policy: procedural sedation and analgesia in the emergency department. Ann Emerg Med. 2014;63:246-258. 
  3. 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;13:500-504. 
  4. Deitch K, Chudnofsky CR, Dominici P. The utility of supplemental oxygen during emergency department procedural sedation with propofol: a randomized controlled trial. Ann Emerg Med. 2008;52:1-8. 
  5. Deitch K, Miner J, Chudnofsky CR, et al. Does end tidal CO2 monitoring during emergency department procedural sedation and analgesia with propofol decrease the incidence of hypoxic events? A randomized, controlled trial. Ann Emerg Med. 2010;55:258-264
  6. Thorpe RJ, Benger J. Pre-procedural fasting in emergency sedation. Emerg Med J. 2010;27:254-261.
  7. Schenarts CL, Burton JH, Riker RR. Adrenocortical dysfunction following etomidate induction in emergency department patients. Acad Emerg Med. 2001;8:1–7
  8. Miner JR, Danahy M, Moch A, et al. Randomized clinical trial of etomidate versus propofol for procedural sedation in the emergency department. Ann Emerg Med. 2007;49:15-22.
  9. Strayer RJ, Nelson LS. Adverse events associated with ketamine for procedural sedation in adults. Am J Emerg Med. 2008;26:985-1028.
  10. Brown L, Christian-Kopp S, Sherwin TS, et al. Adjunctive atropine is unnecessary during ketamine sedation in children. Acad Emerg Med. 2008;15:314-318.
  11. Shah A, Mosdossy G, McLeod S, Lehnhardt K et al. A blinded, randomized controlled trial to evaluate ketamine/propofol versus ketamine alone for procedural sedation in children. Ann Emerg Med. 2011;57:425-433. 
  12. Ferguson I, Bell A, Treston G, et al. Propofol or Ketofol for Procedural Sedation and Analgesia in Emergency Medicine- The POKER Study: A Randomized Double-Blind Clinical Trial. Ann Emerg Med. 2016;68:574-582. 

Originally Written and Posted by: Isaac Shaw, MD 12/30/2016

Last edited: Jeffery Hill, MD MEd 1/3/2017


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