08. Rapid Sequence Intubation

Background 

  • Rapid sequence intubation (RSI) is the specific technique of induction, sedation, neuromuscular blockade, and intubation often used in an emergency situation to secure an airway in an acutely unstable patient.  
  • The medication selection and simultaneous administration enables providers to intubate quickly.  
  • These patients are often non-fasting and are at a high risk of aspiration and precautions are made to minimize this risk during the procedure.  

Equipment and Setup 

  1. Telemetry, pulse oximetry, and NIBP. 
  • Consider arterial line if time allows and/or hemodynamic instability. 
  • Consider capnography. 
  1. At least one (preferably two) working IVs. 
  2. Bag-valve mask. 
  3. Working suction (check carefully!). 
  4. Working oxygen supply. 
  5. Laryngoscope with functioning light (test it) and multiple blades of varying sizes. 
  6. Multiple endotracheal tubes of varying sizes along with stylet (always check cuff prior to use). 
  7. Appropriate medications and dosages drawn in labeled syringes (sedation, NMBA, vasopressors). 
  8. Code cart nearby. 
  9. Alternative airway equipment (e.g. laryngeal mask airway, cricothyroidotomy kit). 

Precautions 

  • Anatomic assessment that predicts difficult intubation or impossible rescue oxygenation is a relative contraindication to RSI and alternative modes of intubation should be considered. 
  • Patients who cannot tolerate apnea due to severe metabolic acidosis or refractory hypoxemia are unlikely to tolerate NMB which removes their compensatory ventilatory drive. In these situations, awake intubation may be the preferred method. 
  • In patients who cannot augment cardiac output (e.g. aortic stenosis, pHTN), sedation and induction (in particular when rapidly administered as in RSI) may lead to cardiovascular collapse as these agents reduce vascular tone. Arterial line hemodynamic monitoring is preferred and correction or optimization of hemodynamic derangements is strongly advised prior to intubation.  

Pre-oxygenation 

  • Provides an intrapulmonary oxygen reserve to enable the patient to tolerate a period of apnea during intubation and delay hypoxemia during RSI. The amount of reserve depends on the patient’s co-morbidities and baseline cardiopulmonary status. 
  • Ideally provide the patient with 3 minutes of 100% FiO2 at highest flow rate available (40-60 LPM). 
    • Higher flows are needed to wash out room air and prevent mixing in order to achieve >90% FiO2 delivered to the patient.  
  • Common devices: non-rebreather (NRB), bag-valve mask (BVM), Jackson-Rees bag. 
    • When using BVM, gentle PPV should be attempted to reduce gastric insufflation; provider can place cricoid pressure to compress the esophagus and reduce gastric insufflation as well. 
  • During apnea period, provide passive oxygenation with NC at maximum flow (15 LPM) which is safe, inexpensive, and may extend the tolerated apnea period. 

Pre-intubation Hemodynamic Optimization  

  • In addition to hypoxemia, hypotension is another leading cause of peri-intubation cardiac arrest.  
  • Causes of hypotension are many including bleeding/hemorrhage, dehydration/hypovolemia, sepsis/septic shock, decompensated heart failure, among others.  
  • Patients with co-morbid aortic stenosis or pHTN are unable to augment their cardiac output under stress including decreased vascular tone and risk rapid clinical and hemodynamic decompensation peri-intubation with induction.  
  • Addressing the cause of these derangements in the peri-intubation period is crucial whether that is providing fluid for hypovolemia or sepsis or blood products for active bleeding.  
  • These patients will also often need vasopressor support during and after intubation which should be anticipated prior to the procedure. 

Medications 

  • Simultaneous IV administration of rapid acting induction agent + NMBA (paralytic).  
  • Goal is to achieve sedation and paralysis within 45-60 seconds of administration. 
  • No titration of medication: dose and medication selection is calculated prior to starting.  
  • Paralytic agents (NMBA) provide NO sedation or analgesia; paralysis without preceding administration of adequate sedation will enable the patient to be aware but unable to respond and should never occur. 
  • Dosing should be made on an individual patient level taking into account co-morbidities and patient-specific factors. A separate source should be consulted for the most accurate dosing instructions. Below is a guide for dosing only: 
Induction Agent (i.e. sedative) Typical Bolus Dose (IV) Pharmacokinetics Notes
Etomidate 0.3 mg/kg Class: imidazole derivative
MOA: GABA agonist
Onset: 45-60 sec
Duration: 3-5 min
Minimal hypotension
No histamine release
Reversible adrenal suppression
May cause brief, transient myoclonus during RSI
No analgesia
Propofol 2 mg/kg Class: alkylphenol derivative
MOA: GABA agonist
Onset: 30-60 sec
Duration: 5-10 min
Hypotension (dose-related)
No analgesia
Added benefit of bronchodilation
Midazolam (Versed) 1-4 mg Class: benzodiazepine
MOA: GABA agonist
Onset: 2-3 min
Duration: 2-4 hours
Hypotension (less than propofol)
Good amnestic properties
No analgesia
Anti-convulsant effects
Ketamine 1-2 mg/kg Class: dissociative anesthetic, phencyclidine derivative
MOA: NMDA antagonist among other effects
Onset: 45-60 sec
Duration: 10-20 min
Provides analgesia in addition to amnesia and sedation
Good choice for awake intubations
Hemodynamically neutral in most patients
Added benefit of bronchodilation
Caution with elevated ICP or systemic HTN

Note: fentanyl is the preferred opioid used to provide analgesia which is not provided by induction agents. Typical dose is IV push of 25-100mcg depending on a variety of patient factors with onset in 2-3 minutes and peak in 3-5 minutes providing fast onset analgesia.  

See section Critical Care: ICU Sedation for more details. 

Paralytic Typical Bolus Dose Pharmacokinetics Advantages Disadvantages
Succinylcholine (preferred agent in most circumstances) 0.6-1.5 mg/kg MOA: depolarizing agent, analog of ACh that binds to post-synaptic ACh receptors causing continuous stimulation
Onset: 30-60 sec
Duration: 8-12 min
Rapid onset
Short acting
Bradycardia (consider atropine)
Increases ICP (avoid in CVA, spinal cord and ocular injuries)
Contraindicated with personal or family hx of malignant hyperthermia
Avoid with rhabdo, burns, hyperkalemia, neuromuscular diseases
Rocuronium 0.6-1.2 mg/kg
Based on IBW
MOA: non-depolarizing agent, inhibits post-synaptic ACh receptors
Onset: 60-90 sec
Duration: 25-60 min&
Rapid onset, shorter than succinylcholine
Shorter duration of action
Minimal CV effects
Relatively long acting: caution in difficult airway; can be reversed with neostigmine

Note: succinylcholine has been rarely reported to cause acute rhabdomyolysis with hyperkalemia followed by ventricular dysrhythmias, cardiac arrest, and death (in children later noted to have muscular dystrophy). There are also rare reports of it causing malignant hyperthermia. Avoid in patients with hyperkalemia, ESRD, ongoing or potential rhabdomyolysis (including those with prolonged immobility >48-72hrs) or history of malignant hyperthermia. 

See section Critical Care: Paralytics for more details. 

Intubation 

  • Most commonly video-assisted (vs. direct visualization) endotracheal intubation. 
  • Visualize passage through the vocal cords. 
  • Advance ETT to desired level. 
  • Inflate cuff. 
  • Remove stylet. 
  • Secure ETT. 
  • If difficulty is encountered, do not repeatedly try with same blade, operator, etc.; call for help and try alternative approach and maintain mask ventilation with 100% oxygen. 
  • Confirm tube placement: use multiple methods including visualization of the vocal cords, end-tidal CO2 monitoring (wave-form capnography is the most accurate), auscultation of bilateral breath sounds, and CXR (to determine dept of placement).