Indications for Intubation (In Order of Urgency)
Greenfield – July 10
Rapid Sequence Intubation
Indications for Intubation (in order of urgency)
- to obtain or maintain the airway
- correct abnormalities of gas exchange (oxygen the priority)
- protect the airway
- predicted clinical deterioration (to one of the above three situations)
Approach
no difficulty cooperative = awake or RSI
no difficulty uncooperative = RSI
difficulty cooperative = awake
difficulty uncooperative no difficulty predicted with BMV or extraglottic devices = RSI
difficulty uncooperative difficulty predicted with BMV or extraglottic devices = other options (defer, get help, get more info, sedative facilitated awake, blind nasal, RSI with double setup)
Definition of Rapid Sequence Intubation
a process that involves pharmacologically inducing unconsciousness and paralyzing the patient in a manner that facilitates tracheal intubation, while minimizing the risk of aspiration using application of cricoid pressure (traditional definition included this last point)
“rapid sequence” refers to the fact that the induction agent and the neuromuscular blocker are given in quick succession, and are not titrated to effect
Contraindications to RSI (relative)
inadequate clinician skills
arrested patient
anticipated difficult airway if also predicted problems with BMV or rescue extraglottic device (LMA)
9Ps
Preparation (SOAPME)
suction, oxygen, airway equipment and assessment, pharmacological agents, monitors, end tidal CO2
Preoxygenate and Preload with fluid
Position
sniffing position / line up external auditory meatus with sternal notch
Premedicate (“LOADE”)
lidocaine, opiate (fentanyl), atropine, defasciculating dose of nondepolarizing agent, esmolol
evidence lacking but may be beneficial in certain patient populations
Paralysis with Induction (“KEPT”)
Induction Agents: ketamine, etomidate, propofol, thiopental
Paralytic Agents: depolarizing (succinylcholine) or nondepolarizing (rocuronium)
Pressure (cricoid); controversial – probably should not be routinely done
Pass tube
Position (check position with end tidal CO2, EDD)
Post tube care and postintubation management
treat post intubation hypotension with fluids, ephedrine/phenylephrine (have drawn up if predicted post intubation hypotension)
Premedication
pretty good review in Robert’s procedure text 2009
“no convincing data exist proving an ultimate or clinically consequential beneficial effect of multiple commonly used interventions”
Lidocaine – used in asthma (reactive bronchospasm), head injured (may attenuate cough reflex in non-paralyzed, may attenuate hypertensive response and may attenuate increased ICP associated with intubation)
Opiate (fentanyl) – blunts the pressor (hypertensive) response
Atropine – falling out of favour – should be used if needed, ie. if develop significant bradycardia or secretions but probably not routinely as a pretreatment
Defasciculating dose of non-depolarizing agent (rocuronium) – one tenth the intubating dose (0.1mg/kg) 2 minutes before induction – may block the fasciculations seen with succinylcholine use and may blunt any increased ICP seen with these fasciculations
Esmolol – very short acting, blunts the pressor response
Pharmacology of Induction Agents
Key Point
preservation of oxygenation and blood pressure often takes priority over attenuation of undesirable reflexes; in the head injured, hypoxia or hypotension can be devastating
Ketamine
produces “dissociative amnesia” (refers to dissociation occurring between the thalamocortical and limbic systems on EEG)
amnestic and analgesic
centrally stimulating effect on sympathetic nervous system by decreasing catecholamine reuptake (increased HR and BP – inotropic and chronotropic effects)
potent bronchodilator
tends to preserve respiratory drive but can see apnea in large, rapidly administered boluses
possibly associated with laryngospasm (probably through increased secretions) when paralytic not used (probably more common in infants)
hemodynamic effects due to sympathetic nervous system stimulation but intrinsically is a myocardial depressant so could theoretically lower BP in patients who are maximally sympathetically stimulated
increases ICP therefore theoretically bad for head injured, this now being questioned as may be helpful in the hypotense/head injured patient as may preserve CPP
Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension – decreased intracranial pressure and increased cerebral perfusion pressure in intubated children with intracranial hypertension; conclude that it is safe in ventilation-treated patients with intracranial hypertension- it actually decreased ICP without lowering blood pressure and CPP, conclude that it could possibly be used safely in trauma emergency situations J Neurosurg Pediatr. 2009 Jul;4(1):40-6.
Rosen 2009: “in the hypotensive head trauma patient ketamine is a reasonable choice for induction”
indicated in severe bronchospasm, unstable hemodynamics
can get “emergence phenomenon” (benzos attenuate this)
dose 1-2 mg/kg IV or 5-10 mg/kg IM, reduce in severe shock, increase if bronchodilation is goal
onset in 1 min, lasts about 15-20 min
consider pretreatment with atropine to decrease secretions (practically rarely done)
consider using smaller doses as a sedative for awake intubation or awake look laryngoscopy (divided doses of 0.25-0.5 mg/kg)
“ketafol” can be drawn up in a single syringe
Etomidate
sedative-hypnotic, no analgesic properties, MOA probably involves GABA receptors
spontaneous ventilation better preserved compared with propofol or thiopental but apnea still common
with usual dose usually see no significant change in HR or BP and does not effect myocardial contractility
can see changes in HR/BP if preexisting severe hypovolemia, hypotension (use lower dose)
does not release histamine so maybe useful in asthmatics but ketamine agent of choice currently in that patient subgroup
does not block pressor response to intubation (may see hypertension especially if no premedication)
cerebroprotective - lowers ICP, cerebral blood flow and cerebral metabolic rate without adversely affecting systemic MAP and CPP
inhibits adrenocortical function with continuous infusion and now shown to do same with single bolus dose – may lead to relative adrenocortical insufficiency (Malerba et al. Intensive Care Medicine 2005; 31: 388-92); more recently however: Etomidate versus ketamine for rapid sequence intubation in acutely ill patients: a multicentre randomized controlled trial Lancet 2009 – no clinical difference in outcomes but did see some adrenal suppression based on cortisol levels and ACTH stim tests
myoclonus (brief), nausea and vomiting do occur, and seizure foci may be stimulated (controversial if actually does promote seizures – probably not)
indicated if unstable hemodynamics
possibly still avoid in septic patient (b/c of adrenal suppression)
dose 0.3 mg/kg, if hemodynamically unstable give lower dose – as low as 0.15mg/kg
onset within 30 sec and duration 5-10 min
Propofol
sedative/hypnotic that works primarily via GABA receptors
compared with the other induction agents probably supresses the laryngeal and pharyngeal reflexes the most
no intrinsic analgesic properties, but produces amnesia
respiratory depressant – can see apnea
myocardial depressant and peripheral vasodilator = decrease in BP (exaggerated in the hypovolemic patient)
decreases ICP
anticonvulsant and antiemetic properties
dose 1-3 mg/kg; decrease in elderly, hypovolemic, hypotense
supplied as an emulsion with soybean oil and purified egg phosphatide but allergic reactions exceedingly rare
Thiopental
short acting barbiturate sedative/hypnotic acts on GABA receptors
respiratory depressant – apnea the norm following induction dose
associated with histamine release so can see bronchospasm
can cause laryngospasm and rarely trismus
myocardial depressant and peripheral vasodilator = decrease in BP (exaggerated in the hypovolemic patient)
nay be best for head injured, stroke etc. (if not hypovolemic) because decrease ICP
dose 3-5 mg/kg; decrease in elderly
works in 30-60 sec and lasts 10-30 min
supplied as a powder, which must be dissolved in sterile water to produce a 2.5% solution (25 mg/mL)
Pharmacology Neuromuscular Blockers
Depolarizing (succinylcholine)
mimics effect of acetylcholine on receptors at neuromuscular junction (and throughout the body) causing membrane depolarization
remains bound preventing normal repolarization
majority of adverse reactions not dose dependent so err on higher side of dosing interval
can see transient rise in K (0.5mEq/L) thought to result from asynchronous depolarization of muscle cells and resulting cellular injury, exaggerated hyperkalemic response seen in those with extra acetylcholine receptors (major crush injuries, burns, stroke, spinal cord injuries, but probably need at least 5 days to form these extra receptors so generally not an issue in the acute presentation)
would be an issue in a patient with a chronic neuromuscular disorder (spinal cord injury, muscular dystrophy, ALS)
can increase IOP but probably not that clinically relevant
can increase ICP
known trigger for malignant hyperthermia….dantrolene
masseter muscle rigidity - rare
prolonged effects in those with abnormal pseudocholinesterase (this normally breaks sux down quickly resulting in its fast offset)
dose 1-2 mg/kg, onset less than 1 minute and duration 5-10 minutes
Nondepolarizing (rocuronium)
competitive antagonist to acetylcholine at the NMJ
only contraindication is predicted inability to BMV if intubation fails
dose is 1 mg/kg IV, onset 1-1.5 minutes, duration 45-80 minutes
Cochrane review (2003 and 2007) favoured intubating conditions seen with succinylcholine
Post intubation hypotension (short acting vasopressors)
Phenylephrine
direct acting alpha agonist, no beta effects, potent vasoconstrictor, increase in BP with no direct effect on HR but do see reflex slowing, supplied as 10mg/1mL vial, dose is 40-100ug q 1-2minutes, effects last 5-10 minutes
Ephedrine
acts indirectly on alpha-1 receptors by causing noradrenaline release, and directly, through action on beta adrenergic receptors, results in increase HR and BP, dose 5-10 mg IV, effects last 5-10 minutes, supplies as 50mg/1mL vial, dilute in 10 cc syringe to 50mg/10mL or 5mg/mL
Greenfield’s Final Take Home Points
1. oral airways – use them if you need them to accomplish a goal, maintaining the airway with positioning is generally safer with respect to pharyngeal stimulation and vomiting
2. get external auditory meatus lined up with sternal notch
3. hyoepiglottic ligament – engage this with your laryngoscope by putting the tip into the valeculla. This will lift the epiglottis.
4. External Laryngeal Manipulation – works, try it
5. Buy Kovacs and Law “Airway Management in Emergencies”
6. Use the approach discussed today but still always be ready for the unpredicted failed airway