Presentation on theme: "Pharmacologic Management of Rapid Sequence Intubation (RSI)"— Presentation transcript:
1Pharmacologic Management of Rapid Sequence Intubation (RSI) James Gibson, PharmDPGY1 Pharmacy Practice Resident
2Learning Objectives List the six P’s of RSI. Discuss historical rationale for “LOADing” patients undergoing RSI.Understand the rationale for use of one induction agent over another.Identify the contraindications to succinylcholine administration and how to manage patients who are not candidates.
3Rapid Sequence Intubation (RSI) Induction of a patient using simultaneousSedativesRapid-acting paralytic agentGoal: to avoid assisted ventilation due to elevated risk of aspirationUn-fasted patientPharyngeal/laryngeal manipulation
4The Six P’s of RSI Preparation Pre-oxygenation Pretreatment and inductionParalysisPlacement of the tubePost-intubation management
5Preparation Assess patient—difficult airway? IV access Monitor (tele, pulse ox)Gather:Equipment for intubationPost-intubation medication(s)Pertinent patient historySupplies for surgical airway (just in case!!)Difficult airway: trauma, cervical collar, can you visualize the oral pharynx or just hard palate?; obstruction/obesity, neck mobility
6Pre-Oxygenation Goals: Methods: Establish O2 reservoir Maximize time for intubationPrevent need for bag-mask ventilationMethods:3-5 minutes of 100% O2 via face mask4 (or 8) vital capacity breaths on 100% O2100% O2 for 3 minutes = acceptable O2 sats for ~8 min4 vital capacity breaths = acceptable O2 sats for ~6 min
7Pre-OxygenationPre-oxygenation is complicated by comorbidities, body habitus (pregnancy), agitation or patient cooperation, and availability of equipment to deliver 100% oxygen.
8PretreatmentGoal:Mitigate adverse physiologic reactions to intubationSympathetic “pressor response”BronchospasmIncreased intracranial pressure (ICP)Muscle fasciculationBegins 2-3 minutes PRIOR to induction/paralysis“LOAD”Not routinely done in practicePressor response—manipulation of airway increase BP and HRsmall effect from succinylcholine administration
9Pretreatment Lidocaine Opioid Atropine Defasciculating agent Dose: 1.5 mg/kg IVTo prevent rise in ICP byPreventing coughBlunting pressor responseMay reduce reactive bronchospasm in asthmaLidocaine lowers ICP by:preventing coughing, andBlunts pressor response—though less effective than fentanylHowever, paralyzed patients cannot cough, so benefit is likely insignificantLidocaine may be added to albuterol to prevent bronchospasm in asthmatics—the added benefit of lidocaine is uncertain
11Pretreatment Lidocaine Opioid Atropine Defasciculating agent Dose: 0.02 mg/kgTo prevent bradycardia caused by airway manipulation and succinylcholineHistorically used in pediatricsMay be more beneficial with repeated doses of succinylcholine (i.e. OR setting)Laryngoscopy and intubation thought to cause vaso-vagal reflexbradycardiaReview found that bradycardia in RSI is usually clinically insignificant (i.e. with single doses of succinylcholine)Benefit was mostly described in case series involving the OR setting where multiple doses of succs were givenAtropine may predispose to arrhythmias (i.e. not benign drug)
12Pretreatment Lidocaine Opioid Atropine Defasciculating agent Fasciculations occur in >90% of patients given succinylcholineMuscle painIncrease intragastric pressure emesisIncrease ICP (?)PreventionHigher doses of succs (1.5 mg/kg vs 1 mg/kg)Non-depolarizing NMB (1/10th of paralytic dose)
13Induction Agent(s)Given as rapid IV push immediately before paralyzing agentIdeally provides:Rapid loss of consciousnessAnalgesiaAmnesiaStable hemodynamicsInduction agents also provide relaxation, which is additive to that of NMBA’s
14Induction Agents Drug Dose Thiopental 3-5 mg/kg IV Methohexital Fentanyl5-15 mcg/kg IVMidazolam0.1 mg/kg IVKetamine1-2 mg/kg IVEtomidate0.3 mg/kg IVPropofol2 mg/kg IV
15Induction Agents Etomidate Ultrashort-acting non-barbiturate hypnotic Rapid onset—30 to 60 secsHemodynamic stabilityHydrolyzed in liver and plasma ICP with minimal effects on cerebral perfusionNO analgesiaADE: Myoclonic jerks, cortisol productionMyoclonic jerks can be confused with seizure activity, but just disinhibition of subcoritcal activity.Prevented by NMB, thus rarely seen in RSI.No treatment needed; can use benzo if persistent.Infusions of etomidate have been associated with adrenal suppression and strongly linked to increased mortality in critically ill patients.Suppression after single dose has been inconsistently demonstrated, and significance of mild cortisol suppression in septic shock is uncertain.
16Induction Agents Fentanyl Short-acting, potent Minimal histamine releaseHemodynamically stableSedation is rate- AND dose-dependentCombined with other induction agents for analgesiaADE: muscle rigidity, grand mal seizures (rare)No histamine release = no hypotension or emesisChest wall rigidity difficult bag ventilation. But NMBA obviates clinical significance of this.
17Induction Agents Midazolam Sedative, amnestic, muscle relaxant NOT analgesicLess cardiorespiratory depression vs. other benzosBP; HRUse lower dose in hypovolemic, elderly, or traumatic brain injury patients (0.05 mg/kg)Does NOT contain propylene glycolPropylene glycol toxicity acute renal failure, lactic acidosis, osmol gapSolubilizing agent in lorazepam IV
18Induction Agents Ketamine NMDA-antagonist dissociative anesthesia Analgesic, amnestic, anestheticDissociation occurs at threshold of mg/kg IV4-5 mg/kg IM (more emesis)Catecholamine reuptake inhibition ( HR, BP, CO, ICP)Maintains respiration and airway reflexesADE: Emergence delirium (30%)—Premed: midazolam 0.07 mg/kgEmesis (highest in adolescents ~9yo)CI: schizophrenia (schizoaffective); <3 months(relative): Asthma exacerbation; CVDProduces a cataleptic-like state; dissociated from the surrounding environment by direct action on the thalamocortical and limbic systems.Noncompetitive NMDA receptor antagonist that blocks glutamate.Eyes often remain open, and patient may make spontaneous, non-purposeful movementsCV effects may make it useful in patients w/ hemorrhagic shock~1/3 of patient have emergence reaction. Less common in children + midaz does not seem to decrease incidence in children.Annals of Emergency Medicine (2011):
19Neuromuscular Blocking Agents (NMBAs) Quaternary ammonium compounds that mimic structure of AChDepolarizing vs non-depolarizingAllow complete airway controlHigher success (100% vs 82%)Less aspiration and airway traumaEnable lower doses of sedativeBetter hemodynamic stabilityAcetylcholineSuccinylcholineRoberts: Clinical Procedures in Emergency Medicine. 5th.Philadelphia, PA: Elsevier,
20Succinylcholine Depolarizing NMBA Paralysis in ~60 sec. DOA: 3-5 min Non-competitively binds ACh receptors initial membrane depolarizationLonger degradation time than AChParalysis in ~60 sec. DOA: 3-5 minProlonged in pseudocholinesterase deficiency (genetic, hepatic/renal failure, pregnancy, cocaine)Repeat doses prolong paralysisMay increase bradycardia/hypotensionDOC for RSIDuration varies by resource—some state up to 6-10 minutes.Pseudocholinesterase deficiency may prolong to 23 minutes in severe cases
21Succinylcholine Dose: 1.5 mg/kg IV (infants: 2 mg/kg IV) ADEs: Use ACTUAL body weightRapid bolus; follow w/ mL saline flushADEs:Muscle fasciculation myalgiasHyperkalemia, CPKBradycardia/hypotensionMild increase in ICPMalignant hyperthermiaMalignant hyperthermia: rare, hereditary complication—autosomal dominantFever, tacypnea, tachycardia, arrhythmias, acidosis, muscle rigidity, impaired coagulationTreat with cooling, volume repletion, and Dantrolene sodium (1-2 mg/kg IV)
22Succinylcholine Hyperkalemia Typical K+ increase < 0.5 mEq/L Up to a 5 mEq/L K+ increase in certain settings:Contraindicated in:Conditions with up-regulation of ACh-receptors (see table)Known/suspected hyperkalemiaPersonal/family hx of malignant hyperthermiaHyperkalemia is NOT prevented by defasciculating doses of non-depolarizing NMBAsClinically, safer to consider period of concern >72 hours (or 3 days)Myasthenia Gravis is NOT a contraindication—actually require higher doses of succinylcholine (2 mg/kg)
23Non-Depolarizing NMBAs Competitive antagonists of ACh at neuromuscular junctionsHigher doses = faster onset, longer durationReversibleAlternatives to succinylcholineLong-acting vs intermediate-actingAgentDose (mg/kg)Onset (min)Duration (min)Succinylcholine1.513-5Rocuronium1-1.530-110Vecuronium0.10.25330-3560-120Pancuronium2-5(60-100)Neostigmine: mg/kg IV; Max of 5 mg in adults (depending on reference)Will reverse NMBA’s action only after ~40% of effects have worn off (UpToDate)Give with atropine to block systemic cholinergic response (0.5-1mg)Sugammadex is an investigational agent for reversal of non-depolarizing agentsRoberts: Clinical Procedures in Emergency Medicine. 5th.Philadelphia, PA: Elsevier,
24Non-Depolarizing NMBAs PancuroniumLong time to onset HR and BP (vagolytic effect)Histamine release bronchospasm/anaphylaxisActive metabolitesAccumulatesRenal dosing requiredNOT recommended for RSIBinds muscarinic receptors in SA node and prevents uptakeRenally cleared, so accumulates with renal insufficiencyCrCl 10-50: 50% of doseCrCl <10: do not administer
25Non-Depolarizing NMBAs VecuroniumSlower onset than rocuroniumNon-vagolytic; no histamine releaseActive metabolitesOften requires “priming” dose0.01 mg/kg during pre-oxygenation phase, then1.5 mg/kg given 3 min later for paralysis
26Non-Depolarizing NMBAs RocuroniumOnset similar to succinylcholineNon-vagolytic; no histamine releaseNo active metabolitesPreferred alternative to succinylcholine in RSI
27Post-intubation Care After endotracheal tube is placed: Provide continued sedation/analgesiaPropofol drip (No analgesia)≤ 120 kg begin infusion at 20 mcg/kg/minkg begin infusion at 15 mcg/kg/min>151 kg begin infusion at 10 mcg/kg/minBolus fentanyl and midazolamFentanyl (analgesia):LD: mcg IV q15 min PRN (max 300 mcg in first hr)MD: mcg IV q30 min PRN (max 200 mcg/hr)Midazolam (sedation):LD: 1-4 mg IV q15 min PRN (max 16 mg in first hr)MD: 1-4 mg IV q1 hr PRNUWMC Form U2914
28ReferencesClaudius, C, LH Garvey, J Viby-Mogensen, et al. "The Undesirable Effects of Neuromuscular Blocking Drugs." Anaesthesia (2009): Print.Fleming, Bethany, Maureen McCollough, et al. "Myth: Atropine should be administered before succinylcholine for neonatal and pediatric intubation.." Can J Emerg Med. 7.2 (2005): Print.Green, Steven, Mark Roback, et al. "Clinical Practice Guidelines for Emergency Department Ketamine Dissociative Sedation: 2011 Update." Annals of Emergency Medicine (2011): Print.Hopson, Laura, and Richard Schwartz. Roberts: Clinical Procedures in Emergency Medicine. 5th. Philadelphia, PA: Elsevier, Print.Martyn, Jeevendra, and Martina Richtsfeld. "Succinylcholine-induced Hyperkalemia in Acquired Pathologic States." Anesthesiology (2006): Web. 8 MarWalls, Ron. Marx: Rosen's Emergency Medicine. 7th ed. Philadelphia, PA: Elsevier, Print.