Rapid Sequence Intubation Periprocedural Care

Updated: Apr 07, 2020
  • Author: Keith A Lafferty, MD; Chief Editor: Guy W Soo Hoo, MD, MPH  more...
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Periprocedural Care


Equipment includes the following:

  • Laryngoscope (see image below): Confirm that light source is functional prior to intubation. A 2010 study demonstrated that single-use metal laryngoscope blades resulted in a lower failed intubation rate than did reusable metal blades. [15]
  • Laryngoscope handle, No. 3 Macintosh (curved) blad Laryngoscope handle, No. 3 Macintosh (curved) blade, and No. 3 Miller (straight) blade.
  • Endotracheal (ET) tube
  • Stylet
  • Syringe, 10 mL (to inflate ET tube balloon)
  • Suction catheter (eg, Yankauer)
  • Carbon dioxide detector (eg, Easycap)
  • Oral and nasal airways
  • Ambu bag and mask attached to oxygen source
  • Nasal cannula


Rapid sequence intubation (RSI) is predicated on the administration of medications in a specific sequence. The two phases of medication administration are induction and paralysis. In general, preoxygenation is carried out while medications are being drawn up.


Preoxygenation with high-flow oxygen via a nonrebreather mask for 3-5 minutes leading up to intubation results in supersaturation of oxygen in the alveoli by way of displacement of nitrogen (nitrogen washout). This allows the patient to maintain blood oxygen saturation during the apneic period of paralysis and allows the physician more time to successfully intubate.

In healthy adult volunteers who have been preoxygenated for 3-5 minutes, the average time to desaturation (oxygen saturation < 90%) is approximately 8 minutes. This time is significantly shorter in patients who are critically ill and have a much higher metabolic demand for oxygen. [1]

Use the least assistance necessary to obtain good oxygen saturation and adequate preoxygenation (see Technique section below). High-flow oxygen via nonrebreather mask may be appropriate for a patient with good respiratory effort. High-flow oxygen via well-fitting bag-valve-mask (BVM) without additional positive pressure (ie, squeezing the bag) may be needed for those with more respiratory compromise. High-flow oxygen via BVM with positive pressure assistance (squeezing the bag) is used only when necessary.

Preoxygenation can also be accomplished with high-flow nasal cannula oxygen, which is very different from using a nonrebreather mask or increased nasal cannula oxygen. This is a modality of oxygen delivery that has had an increase in use, as both flow and oxygen levels can be adjusted. High flows translate to some positive airway pressures (much like CPAP), which can also help with airway patency.

Apneic oxygenation

Because pulmonary blood flow is still occurring during the apneic period of ETT placement, oxygen is continually being diffused out of the alveoli epithelium at 250 mL/min and into the capillary endothelium and attaching itself to circulating hemoglobin. Despite no ventilations (RSI dictates this in assuming full stomachs unless oxygen saturations are low) after the patient is paralyzed, there is actual flow and movement of oxygen down these concentration gradients as the alveoli are somewhat subatmospheric and a mass flow of gas (oxygen) flows from the airways into the alveoli. By applying an NC at 15 L/min (noxious and otherwise not tolerable in the awake patient) proximal airways can come close to a FiO2 of 1.0 and serve to replace the alveoli oxygen. [16] Taha et al have shown that apneic oxygenation via an NC during RSI in comparison to those without this technique desaturated in 6 minutes compared with 3.65 minutes. [17]


Pretreatment agents may be used to mitigate the physiologic response to laryngoscopy and induction and paralysis, which may be undesirable in certain clinical situations.  Note though clinical dogma has supported their use in the past, evidence in the literature is deficient in this area and because of this, these are mentioned from a historical perspective. 

Pretreatment medications are typically administered 2-3 minutes prior to induction and paralysis. These medications can be remembered by using the mnemonic LOAD (ie, Lidocaine, Opioid analgesic, Atropine, Defasciculating agents).

Lidocaine (1.5 mg/kg IV) may suppress the cough or gag reflex experienced during laryngoscopy and has been considered to play a role in blunting increases in mean arterial pressure (MAP), heart rate (HR), and intracranial pressure (ICP). For this reason, it is commonly administered to patients with suspected intracranial hemorrhage, tumor, or any other process that may result in increased ICP, and it may be considered as part of RSI for patients in whom increased MAP could be harmful (eg, leaking aortic aneurysm). However, studies do not consistently demonstrate the effectiveness of lidocaine for these indications in patients in the emergency department (ED), and, based on this lack of evidence, a statement regarding its absolute indication cannot be made. [8, 18, 19, 20, 21, 22, 23, 24, 25, 26]

Opioid analgesic (fentanyl 3 mcg/kg IV) mitigates the physiologic increase in sympathetic tone associated with direct laryngoscopy (ie, blunts increases in blood pressure, heart rate, and mean arterial pressure). One author recommends this in patients with suspected high ICP, [27, 28, 29] though some data also suggest that these agents may increase ICP. [30, 31, 32, 33, 34, 35] Opioid analgesics may also be useful in patients with an aortic emergency (eg, aortic dissection or leaking aortic aneurysm) in whom blood pressure spikes should be avoided. At this time, no conclusive evidence supports the use of opioids in RSI.

Atropine (0.02 mg/kg IV) may decrease the incidence of bradydysrhythmia associated with direct laryngoscopy (stimulation of parasympathetic receptors in the laryngopharynx) and administration of succinylcholine (direct stimulation of cardiac muscarinic receptors). Previous recommendations indicated that all children younger than 10 years receive atropine prior to intubation, but this has fallen out of favor because of the lack of supporting data. Even if bradydysrhythmias occur, they are usually self-limited and clinically nonrelevant. However, atropine should be available in case a clinically significant decrease in heart rate occurs. Because of the increase in cardiac vagal tone, atropine can be considered for use in children younger than 1 year and should at least be at the bedside in this age group. [36, 37] Some evidence indicates that bradycardia can occur equally with or without atropine during intubation. [36, 38] Atropine can also be used in adolescents and adults for symptomatic bradycardia.

A "defasciculating" dose of a nondepolarizing agent may reduce the duration and intensity of muscle fasciculations observed with the administration of succinylcholine (due to the stimulation of nicotinic acetylcholine receptors). The recommended dose is 10% of the paralyzing dose (eg, 0.01 mg/kg for vecuronium). Equivocal studies suggest such pretreatment may help reduce increases in intracranial pressure related to the procedure.

Some practitioners bypass the pretreatment phase and go straight to induction agents. The exception is that some still administer opioids, but in conjunction with the induction agent and not as pretreatment.

The crux of RSI is to take the awake patient, with an assumed full stomach, and very quickly induce a state of unconsciousness and paralysis and securing the airway. This is done without positive-pressure ventilation, if possible.


Induction agents provide a rapid loss of consciousness that facilitates ease of intubation and avoids psychic harm to the patient.

Etomidate (Amidate) (0.3 mg/kg IV) has a rapid onset, a short duration, is cerebroprotective, and is not associated with a significant drop in blood pressure. It is hemodynamically neutral compared with other agents, such as sodium thiopental. It induces a transient decrease in cortisol levels as high as 86% in some studies. However, properly powered prospective studies are needed to validate this more theoretical phenomenon. Note cortisol levels are affected by severe illness independently of the induction agent used. Critical illness‒related corticosteroid insufficiency occurs in 10-20% of critically ill medical patients and as high as 60% in severe sepsis and septic shock. [39, 40] It is the most common agent used in the United States.

Ketamine (Ketalar) (1-2 mg/kg IV) produces a "dissociative" state, has analgesic properties, is a bronchodilator, and may decrease rather than increase intracranial pressure. Consider it for patients with asthma or anaphylactic shock; possibly avoid it in patients with suspected or known aortic dissection or abdominal aortic aneurysm and in patients with acute myocardial infarction. The general teaching has also been to avoid use of ketamine in patients in whom increased ICP is a concern; in particular, trauma patients with evidence of head injury. However, a review of the literature supports its use in this scenario as the hemodynamic stimulation induced by ketamine may, in fact, improve cerebral perfusion and prevent secondary penumbra ischemia. Furthermore, in the laboratory, ketamine seems to have neuroprotective properties. [41, 42, 43] Because of its positive hemodynamic effects and etomidate’s known tendency to transiently decrease cortisol levels, ketamine is being used more frequently as an induction agent.

Propofol (Diprivan) (2 mg/kg IV) has a rapid onset, a short duration, and is cerebral protective. However, propofol is a myocardial depressant and it decreases systemic vascular resistance.

Midazolam (Versed) (0.3 mg/kg IV) has a slower onset (2-3 min without opioid pretreatment) and longer duration (up to several hours) than etomidate. A study by Sagarin et al from a national airway registry demonstrated that midazolam is usually underdosed when used for RSI, presumably because of the concern for hypotension. [3] Note that the induction dose is about 20 mg for a 70-kg person. Use of midazolam as an induction agent is not recommended because of its delayed time to induction, predilection for hypotension at induction doses, and prolonged duration of action.


Paralyzing agents provide neuromuscular blockade and are administered immediately after the induction agent.

Neuromuscular blockade does not provide sedation, analgesia, or amnesia; thus, administering a potent induction agent is important.

A depolarizing neuromuscular blocker (eg, succinylcholine [Anectine] at 2 mg/kg IV or 4 mg/kg IM) has a rapid onset (45-60 sec) and the shortest duration of action (8-10 min). It should be used with caution in patients with known or suspected hyperkalemia and those with chronic neuromuscular disease. Also use caution in patients with chronic renal failure or dialysis-dependent patients as they are prone to be hyperkalemic and this may be unsuspected. Zink's 1995 prospective study of 100 patients in the ED undergoing RSI did not find a change in serum potassium level from before to after RSI with succinylcholine. Exclusion criteria were minimal; a limitation was that postintubation potassium level was checked at only 1 time interval (5 min). [44]

A nondepolarizing neuromuscular blocker (NMB) (eg, rocuronium [Zemuron] at 1-1.2 mg/kg IV) has a slightly longer onset of action (60-75 sec) than succinylcholine and longer duration of action (30-60 min). Use with caution in patients in whom difficult intubation is possible. Does not result in muscle depolarization or defasciculation and does not exacerbate hyperkalemia. Sugammadex is a new NMB reversal agent that has been shown to be safe and effective for reversal of neuromuscular blockade induced by nondepolarizing agents. Reversal occurs at 1.5 minutes with a dose of 16 mg/kg and at 3 minutes with a dose of 4 mg/kg. It has been shown to induce full reversal of such agents faster than succinylcholine’s normal metabolic breakdown and for the first time in over 50 years offers a safe alternative and viable option for emergent RSI. [45]



In cases of trauma in which cervical spine injury is suspected and not yet ruled out, intubation must be performed without movement of the head. Immobilization is best provided by an experienced assistant. In cases in which cervical injury is not a concern, proper head positioning greatly improves visualization.

In the neutral position, the oral, pharyngeal, and laryngeal axes are not aligned to permit adequate visualization of the glottic opening (see images below).

Proper alignment of the axes for tracheal intubati Proper alignment of the axes for tracheal intubation.
Three-axis theory. OA is oral axis, PA is pharynge Three-axis theory. OA is oral axis, PA is pharyngeal axis, and LA is laryngeal axis. Used with permission from Springer Publishing Company.

Place the patient in the sniffing position for adequate visualization; flex the neck and extend the head. This position helps to align the axes and facilitates visualization of the glottic opening.

Studies have shown that simple head extension alone (without neck flexion) was as effective as the sniffing position in facilitating endotracheal intubation. [46]


Monitoring & Follow-up

Complications include the following:

  • Esophageal intubation

  • Iatrogenic induction of an obstructive airway

  • Right mainstem intubation

  • Dental trauma

  • Postintubation pneumonia

  • Vocal cord avulsion

  • Failure to intubate

  • Hypotension

  • Aspiration