Editing Rapid sequence induction (section)

=== 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"/>