rapid sequence induction rapid sequence induction in advanced airway management, rapid sequence induction (rsi) – also referred to as rapid sequence intubation or as rapid sequence induction and intubation (rsii) or as crash induction – is a special process for endotracheal intubation that is used where the patient is at a high risk of pulmonary aspiration. it differs from other techniques for inducing general anesthesia in that several extra precautions are taken to minimize the time between giving the induction drugs and securing the tube, during which period the patient's airway is essentially unprotected. rapid sequence induction/intubationemedicine80222 one important difference between rsi and routine tracheal intubation is that the anesthesiologist does not typically manually assist the ventilation of the lungs after the onset of general anesthesia and cessation of breathing, until the trachea has been intubated and the cuff has been inflated. uses this procedure is used where general anesthesia must be induced before the patient has had time to fast long enough to empty the stomach; where the patient has a condition that makes aspiration more likely during induction of anesthesia, regardless of how long they have fasted (such as gastroesophageal reflux disease or advanced pregnancy); or where the patient has become unable to protect their own airway even before anesthesia (such as after a traumatic brain injury). contra-indications there are relatively few absolute contraindications to a rapid sequence induction. the most significant contraindications include facial trauma that significantly distorts upper airway anatomy or complete airway obstruction (i.e. oropharyngeal cancer, hematoma, etc). in these cases, airway management is secured via a surgical airway instead. risks/complications there are several complications related to rsi to be aware of. the most concerning complication is airway management in a paralyzed patient. as the sequence of rsi dictates that the patient is paralyzed prior to obtaining adequate airway access, there is the possibility that the patient is difficult to intubate. if unable to secure an airway access, the patient may be in a "cannot intubate, cannot ventilate" situation where the apneic period is prolonged and the patient does not receive oxygen. this prolonged period of apnea can lead to brain damage, cardiovascular collapse, and death. in this situation, one must consider the difficult airway algorithm with the possibility of waking the patient with paralytic reversal medications such as sugammadex. conversely, the induction drugs classically used for rsi have short durations of action, wearing off after only minutes. this confers a degree of fault tolerance on the procedure when it is used in elective or semi-elective settings: if intubation is unsuccessful, and if the clinical condition allows it, the procedure may be abandoned and the patient should regain the ability to protect their own airway sooner than would be the case under routine methods of induction. another possible complication is anaphylaxis in response to a neuromuscular blockade. neuromuscular blockade agents are considered one of the highest anaphylaxis inducing substances in the operating room, along with latex, penicillin, and chlorhexidine. in this case, the anesthesiologist must be able to treat the anaphylaxis and resulting complications in a compromised patient. upper airway anatomy the process of applying cricoid pressure during sellick's maneuver can introduce complications such as laryngeal distortion, failure to completely occlude the esophagus, and potential esophageal rupture if the patient is actively vomiting. technique 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. midazolam – it is a fast-acting and the most lipophilic of all benzodiazepine and rapidly crosses the blood–brain barrier. it is a gamma-aminobutyric acid (gaba) agonist. usual doses for midazolam are 1 mg to 2 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. when midazolam is used alone, it has few side effects, but can cause respiratory depression if being used together with fentanyl. 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. 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 neonates 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 0.01 mg/kg. it has quick onset of action, and common side effects are: increased heart rate, dry mouth, flushing, and urinary retention. 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 causes reduction in mean arterial pressure (map). the dosage is 1.5 mg/kg. this drug is metabolized by liver. the side effects are: hypotension, arrythmia (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. induction agents administration of induction agents followed by neuromuscular blockade agents helps to achieve optimal conditions for intubation. etomidate – it is an imidazole-derivative that stimulates gaba receptors. the dosage is between 0.2 and 0.6 mg/kg (commonly 20 to 50 mg doses). dose reduction may be required in those with hypotension. etomidate has minimal cardiovascular side effects, reduces intracerebral pressure (by reducing cerebral blood flow), and does not cause histamine release. it has quick onset of action, short duration of action, and undergoes hepatic elimination. myoclonus, pain at the site of the injection, post-operative nausea and vomiting are common. while common, the incidence and severity myoclonus can be reduced with pretreatment lidocaine without affecting hemodynamic stability of the patient. a rare but serious potential complication is that etomidate can also suppresses the production of cortisol and aldosterone. 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 mg/kg, usually given at 100 mg. ketamine is metabolized by liver and excreted through kidneys. the drug lessen the reuptake of the catecholamine, increases heart rate, blood pressure, and cardiac output, thus suitable for those with hypotension. however, it can worsen the cardiac depression and hypotension for those with depletion of catecholamines. thus, maximum dose of 1.5 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. ketamine also relieves bronchospasm by relaxing bronchiolar smooth muscles. however, it increases oral secretions during intubation. ketamine is associated with nightmares, delirium, and hallucinations. propofol – it is a highly lipid-soluble, gaba agonist. the dosage is 1.5 mg/kg (usually 100 to 200 mg). it has quick onset of action, can cross the blood-brain barrier, wide tissue distribution, and can be hepatically cleared by the body quickly. in the elderly, the rate of propofol clearance is low. therefore, lower doses of propofol (50 to 100 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. however, propofol can induce hypotension and bradycardia due to its calcium channel blocker and beta blocker properties. 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 or enlarged liver, and metabolic acidosis. pain during peripheral administration of propofol can be reduced by using pretreatment lidocaine or a large bore cannula. midazolam – apart as a premedication, midazolam can be used as an induction agent at the dose of 0.2 to 0.3 mg/kg. it has slow onset of action when used alone, but the onset can be improved when using together with an opioid. however, for those with hypotension, midazolam can further reduce the blood pressure and has cardiac depressive effects. therefore, dose reduction is required for the elderly, and for those with heart and liver failure. methohexital – this is a barbiturate drug that works as a gaba agonist, reducing the dissociation of gaba a from its receptors. the dosage is 1.5 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. this drug is commonly associated with pain when given through small peripheral veins. this can be prevented by dissolving the drug into a lipophilic mixture without reducing the potency of the drug. 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. 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. depolarizing blockers succinylcholine – this drug has rapid onset of action and fast duration. its dosages are between 1 and 2 mg/kg body weight with common dosage of 100 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 3.3 °c (37.9 °f) to 8.7 °c (47.7 °f). when the intravenous access is not obtainable, the 3 to 4 mg/kg of intramuscular doses can be given (usual dose of 300 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. there are many absolute contraindications to succinylcholine including recent stroke, hyperkalemia, burn patients, immobilized patients (i.e. wheelchair bound). this is due to the upregulation of neuromuscular junctions. additionally, cautions should be used in patients with reduced serum plasma cholinesterase, as this is how the drug removed from the body. in patients with decreased plasma cholinesterase, the paralysis from succinylcholine can increase significantly in duration. a common side effect of succinylcholine includes myalgias after neuromuscular induced fasciculations upon induction. non-depolarizing blockers rocuronium – the dosage of rocuronium is between 0.6 and 1.2 mg/kg. since rocuronium has longer duration of onset, caution should be taken for those who are difficult to bag-mask ventilate. while rare, anaphylactic reactions have been known to occur with rocuronium. 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. vecuronium – the dosage of this drug is between 0.08 and 0.1 mg/kg. vecuronium is only used when there is a shortage of drugs such as succinylcholine and rocuronium. reversal agents sugammadex – it is used as a reversal agent for rocuronium and vecuronium. it works by encapsulating the paralytic drug thus preventing it from acting on the binding sites. the dose of 16 mg/kg is used for immediate reversal after administration such as during rsi. doses of 2 mg/kg and 4 mg/kg are used if the patient has twitches evident on a twitch monitor and terminates the rocuronium action within 3 minutes. 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. neostigmine – it can be used to reverse nondepolarizing neuromuscular blocking agents which cannot be reversed with