Editing Rapid sequence induction (section)

== Technique ==

=== Common medications ===

==== Premedication ====
Premedication is used to reduce anxiety of those who are going to be intubated and to reduce the anticipated physiological response of the patient during intubation.<ref name="Joanna 2014"/>
* [[Midazolam]] – It is a fast-acting and the most [[lipophilicity|lipophilic]] of all [[benzodiazepine]] and rapidly crosses the [[blood–brain barrier]]. It is a [[gamma-aminobutyric acid]] (GABA) [[agonist]].<ref name=":3">{{cite book | vauthors = Lingamchetty TN, Hosseini SA, Saadabadi A |title=Midazolam |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK537321/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30726006 |access-date=2022-11-02 }}</ref> Usual doses for midazolam are 1&nbsp;mg to 2&nbsp;mg where the older people receive smaller doses and [[obese]] people receive higher doses. Midazolam is metabolized in the liver and is excreted through the kidneys.<ref name=":3" /> When midazolam is used alone, it has few side effects, but can cause respiratory depression if being used together with [[fentanyl]].<ref name="Joanna 2014">{{cite journal | vauthors = Stollings JL, Diedrich DA, Oyen LJ, Brown DR | title = Rapid-sequence intubation: a review of the process and considerations when choosing medications | journal = The Annals of Pharmacotherapy | volume = 48 | issue = 1 | pages = 62–76 | date = January 2014 | pmid = 24259635 | doi = 10.1177/1060028013510488 | s2cid = 8797670 }}</ref>
* [[Fentanyl]] – It is a synthetic, centrally-acting [[opioid]]. It suppresses pain and sympathetic stimulation. Sympathetic stimulation can cause further injury to those with heart disease, [[aortic dissection]], and [[aortic aneurysm]]. Fentanyl is ideal because of its rapid onset, lack of [[histamine]] release, high lipophilicity, and short duration of action. The dosage is between 1 and 3 μg/kg. It is metabolized by liver. The most significant side effect is respiratory depression.<ref name="Joanna 2014"/>
* [[Atropine]] – The process of intubation can cause massive stimulation to [[vagus nerve]], causing [[bradycardia]] (low heart rate). The people who are at increased risk of bradycardia are [[neonate]]s and children. This does not happen in adults because sympathetic stimulation overpowers the vagal response. However, for those adults who have received drugs such as [[beta blocker]], [[calcium channel blocker]], and [[digoxin]] have an increased risk of developing bradycardia. Atropine is a muscarinic receptor [[antagonist]], thus blocking the vagal response. The dose is 10&nbsp;mcg/kg. It has quick onset of action, and common side effects are: increased heart rate, dry mouth, flushing, and urinary retention.<ref name="Joanna 2014"/>
* [[Lidocaine]] – It is used to reduce the sympathetic response in those who have suspected raised [[intracranial pressure]] (ICP) or those who received [[succinylcholine]] which also causes increase ICP or those with underlying asthma that have [[bronchospasm]]. Administration of lidocaine can cause reduction in [[mean arterial pressure]] (MAP). The dosage is 1.5&nbsp;mg/kg. This drug is metabolized by liver. The side effects are: hypotension, [[arrhythmia]] (irregular heart beat). Lidocaine can further interact with other drugs such as [[amiodarone]] and [[monoamine oxidase inhibitor]] to cause hypotension, and [[dronedarone]] to cause arrhythmia.<ref name="Joanna 2014"/>

==== Induction agents ====
Administration of induction agents followed by neuromuscular blockade agents helps to achieve optimal conditions for intubation.<ref name="Joanna 2014"/>
* [[Etomidate]] – It is an [[imidazole]]-derivative that stimulates GABA receptors. The dosage is between 0.2 and 0.6&nbsp;mg/kg (commonly 20 to 50&nbsp;mg doses). Dose reduction may be required in those with [[hypotension]].<ref name=":4">{{cite journal | vauthors = Arteaga Velásquez J, Rodríguez JJ, Higuita-Gutiérrez LF, Montoya Vergara ME | title = A systematic review and meta-analysis of the hemodynamic effects of etomidate versus other sedatives in patients undergoing rapid sequence intubation | journal = Revista Espanola de Anestesiologia y Reanimacion | pages = 663–673 | date = October 2022 | volume = 69 | issue = 10 | pmid = 36241514 | doi = 10.1016/j.redare.2021.05.020 | s2cid = 252857226 }}</ref> Etomidate has minimal cardiovascular side effects, reduces intracerebral pressure (by reducing cerebral blood flow), and does not cause histamine release.<ref name=":4" /> It has quick onset of action, short duration of action, and undergoes hepatic elimination.<ref>{{cite book | vauthors = Williams LM, Boyd KL, Fitzgerald BM | chapter = Etomidate |date=2022 | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK535364/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30570985 }}</ref> [[Myoclonus]], pain at the site of the injection, post-operative nausea and vomiting are common.<ref name=":5">{{cite journal | vauthors = Lang B, Zhang L, Yang C, Lin Y, Zhang W, Li F | title = Pretreatment with lidocaine reduces both incidence and severity of etomidate-induced myoclonus: a meta-analysis of randomized controlled trials | language = English | journal = Drug Design, Development and Therapy | volume = 12 | pages = 3311–3319 | date = 2018-10-04 | pmid = 30323563 | pmc = 6174893 | doi = 10.2147/DDDT.S174057 | doi-access = free }}</ref> While common, the incidence and severity myoclonus can be reduced with pretreatment lidocaine without affecting hemodynamic stability of the patient.<ref name=":5" /> A rare but serious potential complication is that etomidate can also suppresses the production of [[cortisol]] and [[aldosterone]].<ref name="Joanna 2014"/>
* [[Ketamine]] – It is highly lipophilic and crosses the blood-brain barrier. It inhibits the binding of [[glutamine]] to [[N-Methyl-D-aspartic acid]] (NMDA) receptors in [[Thalamocortical radiations]] and [[limbic system]], causing [[amnesia]]. Through the same blockade of NMDA receptor, ketamine is also effective as a painkiller. The dosage is 1 to 2&nbsp;mg/kg, usually given at 100&nbsp;mg. Ketamine is metabolized by liver and excreted through kidneys.<ref>{{cite book | vauthors = Rosenbaum SB, Gupta V, Patel P, Palacios JL | chapter = Ketamine |date=2022 | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK470357/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=29262083 |access-date=2022-11-02 }}</ref> The drug lessen the reuptake of the [[catecholamine]], increases heart rate, blood pressure, and cardiac output, thus suitable for those with hypotension.<ref name=":6">{{cite journal | vauthors = Baekgaard JS, Eskesen TG, Sillesen M, Rasmussen LS, Steinmetz J | title = Ketamine as a Rapid Sequence Induction Agent in the Trauma Population: A Systematic Review | journal = Anesthesia and Analgesia | volume = 128 | issue = 3 | pages = 504–510 | date = March 2019 | pmid = 29944524 | doi = 10.1213/ANE.0000000000003568 | s2cid = 49427767 | doi-access = free }}</ref> However, it can worsen the cardiac depression and hypotension for those with depletion of catecholamines.<ref name=":6" /> Thus, maximum dose of 1.5&nbsp;mg/kg is need for this situation. For those with head injuries, ketamine does not appear to increase intracranial pressure, while able to maintain the mean arterial pressure.<ref name=":6" /> Ketamine also relieves bronchospasm by relaxing bronchiolar smooth muscles. However, it increases oral secretions during intubation. Ketamine is associated with nightmares, delirium, and hallucinations.<ref name="Joanna 2014"/>
* [[Propofol]] – It is a highly lipid-soluble, [[Γ-Aminobutyric acid|GABA]] agonist.<ref name=":7">{{cite book  | vauthors = Folino TB, Muco E, Safadi AO, Parks LJ | chapter = Propofol |date=2022 | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK430884/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=28613634 |access-date=2022-11-02 }}</ref> The dosage is 1.5&nbsp;mg/kg (usually 100 to 200&nbsp;mg). It has quick onset of action, can cross the [[Blood–brain barrier|blood-brain barrier]], wide tissue distribution, and can be hepatically cleared by the body quickly.<ref name=":7" /> In  the elderly, the rate of Propofol clearance is low. Therefore, lower doses of Propofol (50 to 100&nbsp;mg) should be given. It is suitable in those with kidney or liver impairment and decreases intra-cranial pressure. For those with bronchospasm, Propofol also has mild bronchodilating effect.<ref name=":7" /> However, Propofol can induce hypotension and bradycardia due to its [[calcium channel blocker]] and [[beta blocker]] properties.<ref name=":7" /> At prolonged high Propofol dosages, it can induce [[Propofol infusion syndrome]], characterized by acute refractory [[bradycardia]] leading to [[asystole]] accompanied by one of the following: [[rhabdomyolysis]], acute [[Fatty liver disease|fatty liver]] or enlarged liver, and [[metabolic acidosis]].<ref>{{cite journal | vauthors = Kam PC, Cardone D | title = Propofol infusion syndrome | journal = Anaesthesia | volume = 62 | issue = 7 | pages = 690–701 | date = July 2007 | pmid = 17567345 | doi = 10.1111/j.1365-2044.2007.05055.x | s2cid = 16370071 }}</ref> Pain during peripheral administration of Propofol can be reduced by using pretreatment lidocaine or a large bore [[peripheral venous catheter|cannula]].<ref name="Joanna 2014"/>
* [[Midazolam]] – Apart as a premedication, midazolam can be used as an induction agent at the dose of 0.2 to 0.3&nbsp;mg/kg.<ref name=":3" /> It has slow onset of action when used alone, but the onset can be improved when using together with an opioid.<ref name=":3" /> However, for those with hypotension, midazolam can further reduce the blood pressure and has cardiac depressive effects.<ref name=":6" /> Therefore, dose reduction is required for the elderly, and for those with heart and liver failure.<ref name="Joanna 2014"/>
* [[Methohexital]] – This is a barbiturate drug that works as a GABA agonist, reducing the dissociation of GABA A from its receptors.<ref name=":8">{{Citation |last1=Syed |first1=Qaisar |title=Methohexital |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK544291/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=31335011 |access-date=2022-11-10 |last2=Kohli |first2=Arpan}}</ref> The dosage is 1.5&nbsp;mg/kg. It is metabolized in liver. However, methohexital can cause respiratory depression, laryngospasm, venodilatation, myocardial depression, and hypotension. Additionally, it can also cause reduced cerebral blood flow and histamine release. It can cause distal thrombosis and tissue necrosis if given into the arterial system.<ref name="Joanna 2014"/> This drug is commonly associated with pain when given through small peripheral veins.<ref name=":8" /> This can be prevented by dissolving the drug into a lipophilic mixture without reducing the potency of the drug.<ref name=":8" />

==== Paralytics ====
Paralytics are also known as [[neuromuscular-blocking drugs]] (NMB). NMB can reduce the complication rates of rapid sequence induction such as inadequate oxygenation of the blood, airway complications, and instability of the cardiovascular system. NMB can be divided into two types: depolarising and non-depolarizing blockers.<ref name=":9">{{Citation |last1=Cook |first1=Danielle |title=Neuromuscular Blockade |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK538301/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30855885 |access-date=2022-11-10 |last2=Simons |first2=David J.}}</ref> Depolarizing blockers resembles the [[acetylcholine]] and activates the motor end-plate of the [[neuromuscular junction]] (NMJ). Meanwhile, non-depolarizing blockers competitively blocks the NMJ without activating the motor end plate.<ref name="Joanna 2014" />

===== Depolarizing blockers =====
* [[Suxamethonium|Succinylcholine]] – This drug has rapid onset of action and fast duration. Its dosages are between 1 and 2&nbsp;mg/kg body weight with common dosage of 100&nbsp;mg. The drug can only be kept under room temperature for 14 days. Therefore, for longer shelf life, it has to be kept under temperatures from {{convert|3.3|C|F}} to {{convert|8.7|C|F}}.  When the intravenous access is not obtainable, the 3 to 4&nbsp;mg/kg of intramuscular doses can be given (usual dose of 300&nbsp;mg). However, duration of onset will be delayed to 3 to 4 minutes. Repetitive dosages of succinylcholine are discouraged to prevent vagal stimulation which leads to bradycardia.<ref name="Joanna 2014"/> There are many absolute contraindications to succinylcholine including recent [[stroke]], [[hyperkalemia]], [[burn]] patients, immobilized patients (i.e. wheelchair bound).<ref>{{Citation |last1=Cook |first1=Danielle |title=Neuromuscular Blockade |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK538301/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30855885 |access-date=2022-11-10 |last2=Simons |first2=David J.}}</ref> This is due to the upregulation of [[Neuromuscular junction|neuromuscular junctions]].<ref name=":9" /> Additionally, cautions should be used in patients with reduced serum [[Butyrylcholinesterase|plasma cholinesterase]], as this is how the drug removed from the body.<ref name=":10">{{Citation |last1=Hager |first1=Heather H. |title=Succinylcholine Chloride |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK499984/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=29763160 |access-date=2022-11-10 |last2=Burns |first2=Bracken}}</ref> In patients with decreased [[Butyrylcholinesterase|plasma cholinesterase]], the paralysis from succinylcholine can increase significantly in duration.<ref name=":10" /> A common side effect of succinylcholine includes [[Myalgia|myalgias]] after neuromuscular induced [[Fasciculation|fasciculations]] upon induction.<ref name=":10" />

===== Non-depolarizing blockers =====
* [[Rocuronium]] – The dosage of rocuronium is between 0.6 and 1.2&nbsp;mg/kg. Since rocuronium has longer duration of onset, caution should be taken for those who are difficult to bag-mask ventilate.<ref name="Joanna 2014"/> While rare, [[Anaphylaxis|anaphylactic]] reactions have been known to occur with rocuronium.<ref>{{Cite journal |last1=Reddy |first1=Jeffrey I. |last2=Cooke |first2=Peter J. |last3=van Schalkwyk |first3=Johan M. |last4=Hannam |first4=Jacqueline A. |last5=Fitzharris |first5=Penny |last6=Mitchell |first6=Simon J. |date=2015-01-01 |title=Anaphylaxis Is More Common with Rocuronium and Succinylcholine than with Atracurium |journal=Anesthesiology |volume=122 |issue=1 |pages=39–45 |doi=10.1097/aln.0000000000000512 |pmid=25405395 |s2cid=9596238 |issn=0003-3022|doi-access=free }}</ref> While historically this was not the paralytic of choice in RSI due to the longer duration of action, with the recent approval of [[Sugammadex]] as a reversal agent the concern for a long duration of paralysis is reduced.<ref>{{Citation |last1=Jain |first1=Ankit |title=Rocuronium |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK539888/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30969710 |access-date=2022-11-10 |last2=Wermuth |first2=Harrison R. |last3=Dua |first3=Anterpreet |last4=Singh |first4=Karampal |last5=Maani |first5=Christopher V.}}</ref>
* [[Vecuronium bromide|Vecuronium]] – The dosage of this drug is between 0.08 and 0.1&nbsp;mg/kg. Vecuronium is only used when there is a shortage of drugs such as succinylcholine and rocuronium.<ref name="Joanna 2014"/>

===== Reversal agents =====
* [[Sugammadex]] – It is used as a reversal agent for [[rocuronium]] and [[Vecuronium bromide|vecuronium]]. It works by encapsulating the paralytic drug thus preventing it from acting on the binding sites.<ref name=":11">{{Cite journal |last1=Schaller |first1=Stefan Josef |last2=Fink |first2=Heidrun |date=2013 |title=Sugammadex as a reversal agent for neuromuscular block: an evidence-based review |journal=Core Evidence |volume=8 |pages=57–67 |doi=10.2147/CE.S35675 |issn=1555-1741 |pmc=3789633 |pmid=24098155 |doi-access=free }}</ref> The dose of 16&nbsp;mg/kg is used for immediate reversal after administration such as during RSI.<ref name=":11" /> Doses of 2&nbsp;mg/kg and 4&nbsp;mg/kg are used if the patient has twitches evident on a [[Neuromuscular monitoring|twitch monitor]] and terminates the rocuronium action within 3 minutes.<ref>{{Cite journal |last1=Otomo |first1=Shigeaki |last2=Iwasaki |first2=Hajime |last3=Takahoko |first3=Kenichi |last4=Onodera |first4=Yoshiko |last5=Sasakawa |first5=Tomoki |last6=Kunisawa |first6=Takayuki |last7=Iwasaki |first7=Hiroshi |date=2014 |title=Prediction of Optimal Reversal Dose of Sugammadex after Rocuronium Administration in Adult Surgical Patients |journal=Anesthesiology Research and Practice |volume=2014 |pages=848051 |doi=10.1155/2014/848051 |issn=1687-6962 |pmc=3942288 |pmid=24672542|doi-access=free }}</ref> The FDA initially did not approve Sugammadex due to concerns over potential allergic reactions, however it was subsequently approved on December 15, 2015, for use in the United States.<ref>{{Cite journal |last1=Cada |first1=Dennis J. |last2=Levien |first2=Terri L. |last3=Baker |first3=Danial E. |date=July 2016 |title=Sugammadex |journal=Hospital Pharmacy |volume=51 |issue=7 |pages=585–596 |doi=10.1310/hpj5107-585 |issn=0018-5787 |pmc=4981107 |pmid=27559192}}</ref>
* [[Neostigmine]] – It can be used to reverse nondepolarizing neuromuscular blocking agents which cannot be reversed with Sugammadex, although its onset is much slower. It works by competitively inhibiting [[acetylcholinesterase]], an enzyme that breaks down acetylcholine.<ref name=":12">{{Cite journal |last1=Neely |first1=Grant A. |last2=Sabir |first2=Sarah |last3=Kohli |first3=Arpan |date=2022-08-15 |title=Neostigmine |publisher=StatPearls |pmid=29261883 |url=https://www.ncbi.nlm.nih.gov/books/NBK470596/#:~:text=Neostigmine%20is%20water-soluble,%20an,neuromuscular%20blocking%20agents%20after%20surgery. |language=en}}</ref> This results in an accumulation of acetylcholine present in the neuromuscular junction, effectively reversing the paralysis of the patient.<ref name=":12" /> The dosage is between 0.03 and 0.07&nbsp;mg/kg. A common side effect of this drug is [[bradycardia]].<ref name=":12" /> Therefore, [[glycopyrrolate]], an [[anticholinergic]] drug, should be given immediately prior to neostigmine to prevent bradycardia.<ref name="Joanna 2014"/>

==== Other medications ====
* [[Thiopental]]
* [[Metaraminol]] or [[ephedrine]], where [[hypotension]] may occur secondary to the sedating drugs.
* [[Phenylephrine]] – This drug is administered to those with hypotension post intubation as a result of lidocaine, midazolam, fentanyl, Propofol, and ketamine. The dosages range from 50 to 200 μg in adults. It has quick onset and quick elimination. The common side effect is [[reflex bradycardia]].<ref name="Joanna 2014"/>

=== Pre-Intubation Steps ===
Rapid sequence intubation refers to the pharmacologically induced [[sedation]] and neuromuscular [[paralysis]] prior to intubation of the trachea. The technique is a quicker form of the process normally used to induce [[general anesthesia]]. A useful framework for describing the technique of RSI is the "seven Ps".<ref>{{cite web|vauthors=Cooper A|title=Rapid Sequence Intubation – A guide for assistants|url=http://www.scottishintensivecare.org.uk/education/RSI%20brochure.pdf|work=Scottish Intensive Care Society Education|publisher=NHS – Education for Scotland|access-date=31 March 2013|archive-date=24 January 2013|archive-url=https://web.archive.org/web/20130124225751/http://www.scottishintensivecare.org.uk/education/RSI%20brochure.pdf|url-status=dead}}</ref>
[[File:Prehospital RSI training.jpg|thumb|Prehospital RSI training using a checklist]]

==== Preparation ====
The patient is assessed to predict the difficulty of intubation. Continuous physiological monitoring such as [[Electrocardiogram|ECG]] and [[pulse oximetry]] is put on the patient. The equipment and drugs for the intubation are planned, including the endotracheal tube size, the laryngoscope size, and drug dosage. Drugs are prepared in syringes. [[Intravenous]] access is obtained to deliver the drugs, usually by placing one or two IV [[cannulae]].<ref>{{Citation |last1=Schrader |first1=Matthew |title=Tracheal Rapid Sequence Intubation |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK560592/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32809427 |access-date=2022-11-10 |last2=Urits |first2=Ivan}}</ref>

==== Preoxygenation ====
The aim of preoxygenation is to replace the nitrogen that forms the majority of the [[functional residual capacity]] with oxygen. This provides an oxygen reservoir in the lungs that will delay the depletion of oxygen in the absence of ventilation (after paralysis). For a healthy adult, this can lead to maintaining a blood [[oxygen saturation]] of at least 90% for up to 8 minutes.<ref>{{cite journal | vauthors = Benumof JL, Dagg R, Benumof R | title = Critical hemoglobin desaturation will occur before return to an unparalyzed state following 1 mg/kg intravenous succinylcholine | journal = Anesthesiology | volume = 87 | issue = 4 | pages = 979–982 | date = October 1997 | pmid = 9357902 | doi = 10.1097/00000542-199710000-00034 | s2cid = 27271368 | doi-access = free }}</ref> This time will be significantly reduced in obese patients, ill patients and children. Preoxygenation is usually performed by giving 100% oxygen via a tightly fitting face mask. Preoxygenation or a maximum of eight deep breaths over 60 seconds resulting in blood oxygenation is not different from that of quiet breathing volume for 3 minutes.<ref>{{Cite web | url=http://anesthesiageneral.com/preoxygenation/ | title=Preoxygenation| date=2010-10-04}}</ref>

Newer methods of preoxygenation include the use of a nasal cannula placed on the patient at 15 LPM at least 5 minutes prior to the administration of the sedation and paralytic drugs. High flow nasal oxygen has been shown to flush the nasopharynx with oxygen, and then when patients inspire they inhale a higher percentage of inspired oxygen. Small changes in FiO2 create dramatic changes in the availability of oxygen at the alveolus, and these increases result in marked expansion of the oxygen reservoir in the lungs prior to the induction of apnea. After apnea created by RSI the same high flow nasal cannula will help maintain oxygen saturation during efforts securing the tube (oral intubation).<ref name="pmid28684195">{{cite journal | vauthors = Binks MJ, Holyoak RS, Melhuish TM, Vlok R, Bond E, White LD | title = Apneic oxygenation during intubation in the emergency department and during retrieval: A systematic review and meta-analysis | journal = The American Journal of Emergency Medicine | volume = 35 | issue = 10 | pages = 1542–1546 | date = October 2017 | pmid = 28684195 | doi = 10.1016/j.ajem.2017.06.046 | s2cid = 8624609 }}</ref><ref name="pmid28647137">{{cite journal | vauthors = Pavlov I, Medrano S, Weingart S | title = Apneic oxygenation reduces the incidence of hypoxemia during emergency intubation: A systematic review and meta-analysis | journal = The American Journal of Emergency Medicine | volume = 35 | issue = 8 | pages = 1184–1189 | date = August 2017 | pmid = 28647137 | doi = 10.1016/j.ajem.2017.06.029 | s2cid = 2383170 }}</ref> The use of nasal oxygen during pre-oxygenation and continued during apnea can prevent hypoxia before and during intubation, even in extreme clinical cases.<ref>{{Cite web | vauthors = Levitan R | url=http://www.epmonthly.com/archives/features/no-desat-/ | title=No Desat! | work = Emergency Physicians Monthly | date=9 December 2010 }}</ref>

==== Pretreatment ====
Pretreatment consists of the medications given to specific groups of high-risk patients 3 minutes before the paralysis stage with the aim of protecting the patient from the adverse effects of introducing the laryngoscope and endotracheal tube. Intubation causes increased [[Sympathetic nervous system|sympathetic]] activity, an increase in [[intracranial pressure]] and bronchospasm. Patients with [[reactive airway disease]], increased intracranial pressure, or cardiovascular disease may benefit from pretreatment. Two common medications used in the pretreatment of RSI include Lidocaine and Atropine. Lidocaine has the ability to suppress the cough reflex which in turn may mitigate increased intracranial pressure. For this reason Lidocaine is commonly used as a pretreatment for trauma patients who are suspected of already having an increase in intracranial pressure. Although there is not yet definitive evidence to support this, if proper dosing is used it is safe. The typical dose is 1.5&nbsp;mg/kg IV given three minutes prior to intubation.<ref name="pmid21719592">{{cite journal | vauthors = Hampton JP | title = Rapid-sequence intubation and the role of the emergency department pharmacist | journal = American Journal of Health-System Pharmacy | volume = 68 | issue = 14 | pages = 1320–30 | date = July 2011 | pmid = 21719592 | doi = 10.2146/ajhp100437 }}</ref> Atropine may also be used as a premedication agent in pediatrics to prevent bradycardia caused by hypoxia, laryngoscopy, and succinylcholine. Atropine is a parasympathetic blocker. The common premedication dose for atropine is 0.01–0.02&nbsp;mg/kg.

==== Paralysis with induction ====
With standard intravenous induction of general anesthesia, the patient typically receives an [[opioid]], and then a hypnotic medication. Generally the patient will be manually ventilated for a short period of time before a [[neuromuscular block]]ing agent is administered and the patient is intubated. During rapid sequence induction, the person still receives an IV opioid. However, the difference lies in the fact that the induction drug and neuromuscular blocking agent are administered in rapid succession with no time allowed for manual ventilation.{{citation needed|date=January 2022}}

Commonly used hypnotics include [[Sodium thiopental|thiopental]], [[Propofol]] and [[etomidate]]. The [[Neuromuscular-blocking drug|neuromuscular blocking agents]] paralyze all of the [[Skeletal striated muscle|skeletal muscles]], most notably and importantly in the [[oropharynx]], [[larynx]], and [[Thoracic diaphragm|diaphragm]]. [[Opioid]]s such as [[fentanyl]] may be given to attenuate the responses to the intubation process ([[tachycardia|accelerated heart rate]] and increased [[intracranial pressure]]). This is supposed to have advantages in patients with [[Ischaemic heart disease|ischemic heart disease]] and those with [[brain injury]] (e.g. after [[traumatic brain injury]] or [[stroke]]). [[Lidocaine]] is also theorized to blunt a rise in intracranial pressure during laryngoscopy, although this remains controversial and its use varies greatly. Atropine may be used to prevent a reflex bradycardia from vagal stimulation during laryngoscopy, especially in young children and infants. Despite their common use, such adjunctive medications have not been demonstrated to improve outcomes.<ref name=Neilipovitz2007>{{cite journal | vauthors = Neilipovitz DT, Crosby ET | title = No evidence for decreased incidence of aspiration after rapid sequence induction | journal = Canadian Journal of Anaesthesia | volume = 54 | issue = 9 | pages = 748–764 | date = September 2007 | pmid = 17766743 | doi = 10.1007/BF03026872 | doi-access = free }}</ref>

==== Positioning ====
Positioning involves bringing the axes of the mouth, pharynx, and larynx into alignment, leading to what's called the "sniffing" position.  The sniffing position can be achieved by placing a rolled towel underneath the head and neck, effectively extending the head and flexing the neck. You are at proper alignment when the ear is inline with the sternum.<ref>{{cite book|title=Nancy Caroline: Emergency Care in the Streets 7th Ed.|year=2013|publisher=Jones & Bartlett Learning|pages=780}}</ref>

As described by [[Brian Arthur Sellick]] in 1961, [[cricoid pressure]] (alternatively known as Sellick's maneuver) may be used to occlude the esophagus with the goal of preventing aspiration.

==== Placement of tube ====
During this stage, [[laryngoscopy]] is performed to visualize the [[glottis]]. Modern practice involves the passing of a "Bougie", a thin tube, past the [[Vocal folds|vocal cords]] and over which the endotracheal tube is then passed.  The bougie is then removed and an inbuilt cuff at the end of the tube is inflated, (via a thin secondary tube and a syringe), to hold it in place and prevent aspiration of stomach contents.

The position of the tube in the trachea can be confirmed in a number of ways, including observing increasing end tidal carbon dioxide, auscultation of both lungs and stomach, chest movement, and misting of the tube.

==== Postintubation management ====
Mispositioning of the [[Tracheal tube|endotracheal tube]] (in a bronchus, above the glottis, or in the esophagus) should be excluded by confirmation of end tidal {{CO2}}, auscultation, fogging of the endotracheal tube, and observation of bilateral chest rise.