Rapid Sequence Intubation: Review of Medications



hi everybody my name is Megan and I wanted to share with you information on medication views for rapid sequence intubation as well as the role that our pharmacist plays in this very common emergency Department procedure by the end of this presentation I would like for you to be able to describe the process for rapid sequence intubation identified the drug of choice and different patient populations describe the role of the pharmacist in RSI and identify patients who would benefit from post intubation sedation let's start with the definition of RFI RFI is the technique of concurrently administrating a poem sedative agent and a neuromuscular blocking agent for the purpose of successful endotracheal intubation RSI is the cornerstone of emergency airway management the decision to intubate a patient is not always an easy decision but every patient who is intubated will have at least one of the five following indications they will be unable to maintain their own airway unable to protect their airway against aspiration unable to ventilate properly unable to oxygenate properly or their provider anticipates that the patient is currently on a worsening course that will eventually lead to respiratory failure since RSI is done in an emergency situation it is important to have a distinct set of steps to follow to ensure successful airway management the way this is done is by using the 7ps of RSI the preparation step is the very first step this is where all providers are ensuring that all needed equipment is gathered this is going to include equipments for backup plans this intubation was not achievable this is the step where as a pharmacist you would look into the patient's history end of their situation to come up with a plan on the best conduction in paralytic agent for that patient with the provider once the decision is made on agents being used you would calculate the dose and then draw them up this is also where you would start to think about pre treatment as well as post intubation sedation for your patient the next step is pre-oxygenation this step is important is really important for patients who present already severely hypoxic but it's also important for all patients this step builds a reserve of oxygen that allows providers time to place that endotracheal tube pre treatment is a step that is not done for all patients we will go into pre treatment options in the next following slide step four paralysis with induction this is where medications are going to be provided to the patient to put them in a state that makes intubation easier for the provider and more comfortable for the patients Step five is wear protection and positioning occur and that is when the provider is making sure the patient is in an optimal position for intubation step six is where the placement of the tube is done and then an x-ray is done to provide proof that the tube is in the correct location and final step or step seven is post-intubation management this is where you're thinking about sedation analgesia and paralysis as indicated as mentioned before pretreatment is another step where pharmacists can be involved not every patient is going to require this step the goal of pretreatment is to attenuate the negative pathophysiologic response that is caused during intubation the process of intubation stimulates both sympathetic and parasympathetic nerves that are located in the airway this causes a release is systemic catecholamines which can increase your heart rates by about 30 beats per minute your map by 26 25 millimeters of mercury as well as increase arterial wall shear stress the placement of the tube itself stimulates the upper airway reflexes this can include the coughed reflex and cause luring Joe spasms as well as lower airway bronchospasm it's important to remember that if it is decided a pretreatment medication will be used you must give it time to circulate in the body so you want to make sure that it's given at least 20 minutes before induction historically pneumonic has been used load that includes lidocaine opioids specifically fentanyl atropine and D fasciculation doses of neuromuscular blocking agents current evidence really only supports the use of lidocaine fentanyl and in very few instances atropine the first pretreatment medication that will discuss is lighting the light Akane's mechanism of action is that it's an amide anesthetic the dose that is used for pre treatments is one point five milligrams per kilogram possible benefits for lidocaine are a little controversial the first benefit is that it potentially can prevent rise in intracranial pressure so as we know coughing increases ICP and when placing an endotracheal tube the coughing reflux is potentially stimulated so the theory behind the use of lidocaine is that it blunts the coughing reflex which would prevent the increase of ICP as mentioned before the data behind if lidocaine actually does this is conflicting but for now lidocaine has been shown to be safe when suppressing the cough reflex which is why in patients who already have an elevated ICP like patients who have had head trauma lidocaine and still be an option for pretreatment other benefits include reducing bronchospasm in reactive airway disease the data is conflicting for this as well but it can still be used for pretreatment in RSI contraindications to the use of lidocaine includes severe bradycardia as well as severe heart block patient Sentinel is going to be the second pretreatment medication that we discussed its mechanism of action is that it is an opioid receptor agonist the pretreatment dose of fentanyl is 1 2 3 micrograms per kilogram over 30 to 60 seconds I know he has like a couple of possible benefits the first one being and it does provide some analgesic properties the second possible benefit is that it potentially can blunt the effects of catecholamine release so this is this primary role in pretreatment and this is to protect patients who would be adversely affected by the catecholamine release that occurs during intubation those who are at most risk include patients with an increased ICP patients who had ischemic heart disease intracranial hemorrhage cerebral or aortic aneurysms or patients with major vessels dissections contraindications to the use of fentanyl and pre treatments include patients who have compensated shots and patients who hemodynamically are just unstable lastly we will talk about atropine and D fasciculation doses of n MBAs so atropine historically has been used to prevent bradycardia and pediatric patients the theory is that succinylcholine when used for paralysis causes stimulation of muscarinic receptors this stimulation can cause bradycardia which seems to happen more frequently and more severely in pediatric populations that is why historically atropine was used as pretreatment for pediatric populations undergoing RSI with the use of Seconal choline there really isn't a whole lot of data to support the routine use of atropine but it can be considered if pediatric patients or adult patients are experiencing bradycardia during RSI heaps of circulating doses of n nba's historically have been used to decrease the side effects of fasciculation caused by neuromuscular blocking agents the theory is is that when giving a depolarizing and MBA like succinylcholine that initially will cause a spontaneous contraction of the muscles in the body this is thought to cause a rise in intracranial pressure and so the theory was to give 10% of the dose needed for paralysis using a nondepolarizing and MBA to prevent the fasciculations that would be caused by the paralytic dose of the depolarizing and MBA there really is not any data behind the use of this as pretreatment and it is no longer recommended during RSI when providers have gathered all necessary equipment all medications are drawn up appropriately and the patient is pre oxygenated so everybody is ready is to start RSI induction is the next step the goal of induction is to provide an amnestic state for the patients it's important to remember that when you give a paralytic the patient will essentially be frozen in their own body unable to move but able to hear and see everything going on around them it's also important to keep in mind that they're also able to feel pain in this state so an induction agent induces an amnestic state so the patient is not able to remember hearing seeing or feeling anything during intubation the pharmacist plays a significant role here not only assuring the right induction agent is being used and is dosed correctly but also making sure that the induction agent is being used first it is important to give an induction agent immediately before a paralyzing agent ideal agents would have the following properties they would provide rapid loss of consciousness provide amnesia provide analgesia as well as have a very stable hemodynamic profile accommodate is the gold standard for injunction agents its mechanism of action is that is GABA agonist gathers one of the bodies and Tibbett or neurotransmitters that is responsible for calming nerve impulses in the brain so by stimulating gaba you're producing a sleep-like state in patient the dose for induction is 0.3 of milligrams per kilogram typically though is a patient is greater than 70 kilos you can use a standard dose of 20 milligrams for the patient etomidate has the property of an amnestic so it does not provide any analgesia but it does provide that amnestic state its onset is very quick at 10 to 15 seconds and its duration is also pretty quick so it's 10 minutes etomidate is considered the gold standard because its effects on hemodynamics is neutral so this means that it does not cause swings in blood pressure and heart rate in either direction some common side effects though are monoclinic jerk some other things that you need to consider when choosing etomidate is that it has been shown to cause adrenal insufficiency and the effects could last up to 24 to 48 hours some clinicians will advise against using etomidate in septic patients for this reason however others will still use it and then supplements the patient with stress dose corticosteroids thus the use of etomidate for septic patients is provider dependent it also has been shown to increase EEG activity in an actively seizing patient there are some studies that show that it potentially could lower the seizure threshold for a patient with seizures history but it's not quite as important to consider if a patient just has a seizure history compared to a patient who is actively seizing in the trauma Bay ketamine is the next induction agent that can be used during RSI if mechanism of action is that as an NMDA antagonist MN PA is a glutamate receptor glutamate is the brains primary excitatory neurotransmitter which does the opposite of gaba by inhibiting glutamate from binding to NMDA you're producing the same effect as seen when you stimulate gaba the dose for induction is a range between 1 2 milligrams per kilogram the typical dose though is usually one point five milligrams per kilogram one significant benefit of ketamine is that in addition to its amnestic properties it also has analgesic properties it also has a rather quick onset of 30 seconds and a shortened separation of ten minutes if hemodynamic and respiratory effects are not as nice as etomidate so it can cause hypertension as well as some tachycardia in patients but one benefit is that it can cause bronchodilation this could be beneficial for patients with reactive airway disease some common side effects include next segment which is a wobbling or shaking of the eyes while a patient in the a message state unless this is another common side effect things to consider is that you want to avoid it in patients with cardiac conditions this is because ketamine increases blood pressure and heart rate which increases oxygen demand for the heart and also the sheer force at which it flows ketamine should be avoided in patients with cardiac conditions such as myocardial infarction as well as a or neck dissection ketamine can also cause hallucinations when wearing off this is called re-emergence syndrome midazolam is the third agent that can potentially be used for RSI its mechanism of action is that it is also a GABA agonist the dose for induction is a zero point two to zero point three milligrams per kilogram dose it has a couple unique properties compared to the other agents it provides amnesia as well as anxiolytic effect which means that it reduces anxiety and it also is a muscle relaxant the uncertain duration though make it not very favourable for an induction agents its onset is between 60 to 90 seconds so it's important to make sure your provider knows how long this will take as an induction agent and then the duration is much longer between 15 to 30 minutes depending on the patient's hemodynamic and respiratory effects also make it not a very useful agent for induction it can cause hypotension and tachycardia as well as cause premature respiratory depression which is not an ideal effect when trying to prepare a patient for intubation things to consider is that it's basically not commonly used for induction due to the longer on sort of action compared to other agents as well as as well as a PMO dynamic and respiratory effects propofol is the source and final agents that can be used for induction in RSI its mechanism of action is that it is a GABA agonist the dose for induction is a 1.5 to 2.5 milligrams per kilogram notes as far as action goes it only provides the amnestic properties oxidant durations all are pretty desirable when talking about propofol its onset is 10 to 15 seconds and its duration is 5 to 8 minutes what makes propofol undesirable for intubation is a Sima dynamic and respiratory effects it can cause severe hypotension so it's important to not use propofol in patients who are hemodynamically unstable or in patients who present with low blood pressure to begin with it also can cause respiratory suppression which as mentioned before with midazolam is not an ideal situation when you are trying to prepare a patient for intubation things to consider is that since it is a lipid formulation you want to make sure the patients do not have a soy or any egg allergies the following is just a summary slide of all of the induction agents it with the mechanism of action the doses for intubation its onset its duration as well as key points to remember about each ages neuromuscular blocking agents are the medications that really set the physician up for an ideal situation when performing RSI the goal of an NMDA it's to paralyze skeletal muscles by blocking impulse transmission at the neuromuscular Junction so basically what we're doing is we're plucking the muscles and neck from contracting and fighting the intubation process this is going to allow the provider to perform a smooth intubation an MBAs are given immediately after induction to facilitate ideal conditions for intubation as well as to minimize the risk of aspiration it's important not for delay the administration after induction agents this is because as mentioned before those induction agents only work for a short period of time so if your induction agent wears off you risk the patient becoming aware of the situation but still being paralyzed if there is a pause before giving your paralyzing agent it's important to keep in mind what time the induction agent was given so you can Bree bolus the induction agent if needed there are two different classes of NMBS depolarizing at NBA's such as succinylcholine stimuli to the acetylcholine receptors that allow depolarization to occur this allows voltage-gated sodium channels to open and then closed which then become inactivated in order to reactivate the sodium channels the membrane potential must be reset depolarizing NMDA is though are not metabolized by acetylcholine esterase so this causes prolonged activation of the acetylcholine receptor causing the sodium receptors to remain inactivated this then causes the muscles to become flaccid as mentioned in the pretreatment section speculations are often seen with these agents this is due to that initial depolarization state nondepolarizing and MBAs such as rocuronium antagonize the action of acetylcholine in a competitive manner at the postsynaptic nicotinic receptor which prevents depolarization from happening at all they don't produce a conformational change light in the receptor like the depolarizing and NBA's do succinylcholine is the gold standard when it comes to paralyzing agents in RSI but mentioned reforest mechanism of action is bad as depolarizing NMDA the dose for induction is a 2 milligram per kilogram post and its onset inspiration is actually what helps make its gold standard so onset is about 45 seconds so it's pretty rapid as well as its duration is shorter than the 15 minutes which matches pretty nicely with the duration of the induction agents that we previously talked about things that make it not quite as desirable are the facts that it can cause hypotension as well as bradycardia so it's important to consider these properties when deciding which paralytic agent to use for your patient other things to consider is that it can increase potassium typically this is only by about 25 mil equivalents per liter but in patients who are already at risk of hyperkalemia it can increased this up to 5 no equivalents per liter patients at high risk for hyperkalemia include patients who are coming in with a crushing trauma patients who are on chemo dialysis patients who have been in a long code and patients who are currently on staff epilepticus you also want to avoid it in patients with a history or family history of malignant hyperthermia rocky Rome iam is the second agents that can be considered for paralysis in patients undergoing RSI I've mentioned before its mechanism of action is it's a nondepolarizing a nun BA the typical dose is a 1 milligram per kilogram dose on certain duration are what make it a little less desirable in most patients onset to take of 60 seconds and the duration can last 40 to 60 minutes which does not match up nicely with the induction agents that we previously talked about one thing that is very important to consider with rocuronium is that you need to start thinking about post intubation sedation as soon as it's decided that this is the agent booked that is going to be used things that make it very desirable however or that it's hemodynamic and respiratory effects are neutral so with this some providers will prefer its use due to the lack of major adverse effects such as hyperkalemia and the malignant hyperthermia things to consider though as we mentioned before is that the duration is much longer than succinylcholine so it's important to start thinking about that in post intubation film for your patient this is just a summary slide on the differences between the two agents just like the induction slide so we have the mechanism of action the dose onset duration and key point for consideration when deciding which agents to use post-intubation predation is important for all patients the goal is to provide a continued sedation after intubation to prevent post intubation complications so RSI is being done in a very fast-paced environment and even though it is not an invasive surgery there's still the risk of damaging the airway during the process when your initial sedation and paralytic wear off the patient could be in pain from this procedure for their current injuries that they came in with the other thing to keep in mind is that the patient now has a tube in the throat which is not the most comfortable situation which can cause restlessness and evening fighting of the ventilator post intubation sedation keeps the patient in a calm state in which the ventilator can do its job of breathing for the patient's as well as provide the patient a level of comfort well in this situation post intubation sedation is most important in patients who receive a paralytic without induction and in patients who receive rocuronium but it's like I said before it's still important to consider in all intubated patients to maintain that level of comfort and avoid the risk of self extubation agents that can be used are your propofol so you want to make sure that the patient is pema dynamically stable enough to receive propofol and this was due to the side effects of hypotension propofol is a good option if neurologic functions needs to be assessed due to its very short duration of action typically you'll start a continuous infusion between 5 to 70 micrograms per kilogram per minute typically though most patients get started at a 20 to 30 micrograms per kilogram per minute dose unless they are a little more hemodynamically on stable and vijaya subpoenas are also good views in patience for post-intubation film and this is you'll typically use these when a patient cannot tolerate the propofol drip or in patients who you do not need to assess the neurological function quickly after intubation you want to make sure you're avoiding its use in patients with hepatic failure and in that case you would if you do have a patient with hepatic failure lorazepam is preferred over midazolam typically benzodiazepines are given as a bullish midazolam since it's a little bit shorter acting compared to lorazepam typically means about two bolus doses after receiving Rafi rhodium to keep the patient nice and calm during while that paralyzation is wearing off lorazepam is a little bit longer so typically in that same situation you only need about one bolus dose it is important though to remember potentially the patient might need more making sure that the provider has a correct order in so the patient can remain comfortable and allow the vent to work thank you for spending some time with me today to talk about rapid sequence intubation pharmacists play a very important role in ensuring the right medications are being chosen the right dose is being used as well as the right sequence of drug administration is being performed this process is typically in a very high-stress situation and it's important to be able to recall the subtle differences in these agents to ensure a smooth intubation process for all of your patients you

9 comments

  1. the thing is you cant say that propofol or etomidate do not have anxiolytic actions, since this depends on the dose. any GABAergic depressant drug in high doses creates unconsciousness and amnesia, in lower doses it just reduces anxiety. And midazolam is a positive allosteric modulator of GABAA receptors not a GABA agonist. Thank you for the video though, I learned a few things about the hemodynamic profiles of these drugs.

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