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RSI PharmacologyRSI Pharmacology
New HampshireNew Hampshire
Division of Fire Standards & Training andDivision of Fire Standards & Training andEmergency Medical ServicesEmergency Medical Services
RSI Medications
Protocol meds Oxygen Lidocaine Atropine Etomidate Succinylcholine Lorazepam Fentanyl Rocuronium Vecuronium
Medication Information Parameters
Class Pregnancy Risk Category Preparation Action Onset Duration Drug Interactions Side Effects Reversal Agent(s)
Lidocaine
Dose: 1.5 mg/kg IVP When: At least 2 minutes
prior to intubation Why: May prevent a rise in
ICP in TBI patients Suspicion of increased ICP Patient in respiratory
distress with reactive airway disease or COPD
Lidocaine
Antidysrhythmic with anesthetic properties that blunt transient increases in ICP that result from laryngoscopy.
Also blunts cough/gag reflex during laryngoscopy
Atropine
Dose: 0.5 mg IVP When: Prior to intubation for
bradycardic adults Why: Given to prevent
worsening bradycardia From Succs, vagal stimulation
during direct visualization, and hypoxia
Etomidate
Class – sedative/hypnotic used for general anesthesia induction Dose dependent Rapid onset/offset Minimal hemodynamic and
respiratory effects compared to other induction agents
Imidazole derivative unrelated to any other agent
Etomidate
Pregnancy Risk Category – C No human studies and animal studies show
adverse effect Transmission to breast milk uncertain – likely –
but not a significant concern in an RSI situationPediatrics – not approved for patients under 10 –
however RSI protocol only for age 12 and above.
Etomidate
Preparation – 2 mg/ml 20 and 40 mg vials (10 and 20 cc) Propylene glycol 35% Single use ampules Abboject Shelf life – 1 year Does not need refrigeration
Etomidate
Action Enhances GABA, the principal inhibitory
neurotransmitter Action at the GABA-A receptor complex Able to produce light sleep to deep coma Dose dependent EEG changes in anesthesia similar to
barbiturates
Etomidate
Indication: as an induction agent before the administration of a neuromuscular blockade agent.
Contraindications: Known hypersensativity
Etomidate
Onset Rapid onset of loss of consciousness Within one arm-brain circulation time Rapid distribution to CNS Then rapid clearance from the CNS and
redistribution
Etomidate
Dose: 0.3 mg/kg IV (maximum 40 mg) Duration of action
With doses of 0.3 mg/kg Duration of hypnosis is 3-5 minutes Metabolized in liver to inactive metabolites Then metabolite excreted through urine Elimination half-life – 1.25-5 hours 75% excreted in urine within 24 hours 10% in bile and feces
Etomidate
Drug Interactions Sedatives and Hypnotics – increased effect Opiates – increased effect No interaction with any neuromuscular blocker
Etomidate
Side Effects Elderly patients sensitive Hypotensive patients sensitive Pain at injection site Muscle twitching
30% Myoclonic jerks Variable, Facial
Etomidate
Side Effects Decreased plasma cortisol concentrations Last up to 8 hours after injections“Legal Laundry List” –
hyper and hypoventilaitonapnea (5-90 seconds)laryngospasmhiccups / snoringhyper and hypotension
Nausea / Vomiting after emergence
Etomidate Reversal Agents
NONE
Neuromuscular Blockers
HOW DO THEY WORK ????
WHAT DO THEY DO ?????
Neuromuscular Blockers
Work by blocking the natural transmission of nerve impulses to skeletal muscles.
No direct effect on: Heart, Digestive system, Brain, Pupillary Response, Smooth Muscle or other organ systems.
No effect on level of consciousness or pain perception.
No direct effect on seizure activity.
Neuromuscular Blockers
Depolarizing Neuro Muscular Blockers Succinylcholine (Anectine, Quelicin)
Non-Depolarizing Neuro Muscular Blockers
Pancuronium (Pavulon), Vecuronium (Norcuron)
Classified depending upon the effect they have
on the neuromuscular endplate
Neural Transmission
When a nerve impulse arrives at the synaptic knob of the presynaptic neuron calcium flows in and causes the release of neurotransmitters. The neurotransmitters diffuse across the synaptic cleft and attach to the dendrites of the postsynaptic neuron. This allows the current to flow from one neuron to the next.
More than 30 neurotransmitter in the human body.
Neurotransmitter acetylcholine is essential to understanding the function NMB
Motor Neuron
Axon
Dendrites
Cell Body
Telondendria
Neuron
Acetylcholine
– Produced within neurons by combining molecules of acetylcoenzyme A and choline
– Rapidly broken down in the synaptic cleft into acetate and choline by the enzyme acetylcholinesterase which is found on the outer surface of the cell membranes.
– The broken down choline is taken up by the axon terminal and used in the synthesis of new acetylcholine
Anectine (Succinylcholine)SCh or “Succs”
The only depolarizing paralytic in clinical use
Benefits: Rapid onset Short duration
Will cause “fasciculations”
Succinylcholine
Class Depolarizing Neuromuscular Blocker
Pregnancy Risk Category – C: “Risk cannot be ruled out – Human studies are lacking and
animal studies are either positive for fetal risk or lacking as well. However potential benefits may justify the potential risk.”
Lactation - ?Safe Metabolism – in plasma Excretion - kidney
Succinylcholine Effect
2 phases to blocking The first block is due to the prolonged stimulation
of the acetylcholine receptor results first in disorganized muscle contractions (fasciclations), as the acetylcholine receptors are stimulated. On stimulation, the acetylcholine receptors becomes a general ion channel, so there is a high flux of potassium out of the cell, and of sodium into the cell, resulting in an endplate potential less than the action potential. So, after the initial firing, the celll remains refractory.
Succinylcholine Effect - continued
The 2nd Block Phase On continued stimulation, the
acetylcholine receptors become desensitized and close. This means that new acetylcholine signals do not cause an action potential; and the continued binding of sux is ignored. This is the principal paralytic effect of sux, and wears off as the sux is degraded and the acetylcholine receptors return to their normal configuration.
Succinylcholine Dose: 1.5mg/kg IV (maximum 150 mg) When: Immediately after Etomidate Onset: rapid, usually 30-90 secs Duration: short acting, 3-5 mins
Succinylcholine
Action Binds to nicotinic “M” receptors usually acted
upon by Acetylcholine Initial Depolarization of muscle membrane Block further binding
Succinylcholine
Drug interactions Potentiation of effects
Oxytocin, Beta Blockers, Organophosphate insecticides
Reduced duration of action Diazepam
Other effects Cardiac Glycosides – dysrhythmias
Succinylcholine
Indication: Immediate severe airway compromise in the context of trauma, drug overdose, status epilepticus, etc. where respiratory arrest is imminent.
Contraindications
Severe burns > 24 hours old
Massive crush injuries >8 hours old
Spinal cord injury >3 days old
Penetrating eye injuries Narrow angle glaucoma
Hx of malignant hyperthermia patient or family
Pseudocholinesterase deficiency
Neuromuscular disease patient or family
Hyperkalemia May precipitate fatal
hyperkalemia!
Succinylcholine
Adverse Effects: Fasciculations Hyperkalemia Bradycardia Prolonged Neuromuscular Blockade Malignant Hyperthermia
Succinylcholine – Adverse Effects
Fasciculations: Associated with increased ICP, IOP, IGP ICP only clinically important Cause and Effect – unknown If needed pre-treat with Lidocaine, and a
defasciculating dose of a non-depolarizing neuromuscular blocker –
Rocuronium 0.06 mg/kg
Succinylcholine – Adverse Effects
Hyperkalemia Normal rise in serum K+ is up to 0.5 meq/L Pathological rise may occur in
Rhabdomyolysis Receptor upregulation
May be life-threatening 4-5 days post injury most critical Any ongoing neuro/muscular process is at risk
Succinylcholine Adverse Effects - Hyperkalemia
Receptor upregulation in Burns – especially 5 days post burn Denervation or neuromuscular disorders Crush injuries Intra-abdominal infections Myopathies Renal failure – controversial
Use a non-depolarizer instead (Roc)
Succinylcholine Adverse Effects – Malignant Hyperthermia (MH)
Malignant Hyperthermia Very rare condition – 1:15,000 Patient experiences a rapid increase of
temperature, metabolic acidosis, rhabdomyolysis, and DIC
Treatment includes administration of Dantrolene and external means of temp. reduction
Succinylcholine Adverse Effects - MH
Absolute contraindication Acute loss of intracellular calcium control Results in:
Muscular rigidity (masseter) Autonomic instability Hypoxia Hypotension Hyperkalemia Myoglobinemeia DIC Elevated temperature a late finding
MH - Treatment If the diagnosis of MH is seriously being
considered – Contact medical control immediately and divert to the CLOSEST facility
Once in the hospital Dantrolen 2.5 mg/kg IV q 5 minutes until muscle relaxation or maximum dose of 10mg/kg.
www.mhaus.org http://medical.mhaus.org/NonFB/Slideshow_eng/
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Succinylcholine
Dose: 1.5 mg/kg IV (maximum 150 mg), following Emotidate
Administration of a neuromuscular blocker does not alter mentation or the ability to feel pain
Succinylcholine Onset
< 1 Minute Slightly slower in hypotension
Succinylcholine
Duration 5-10 minutes Beware acetylcholinesterase deficiency
Rare Prolonged action
Succinylcholine Reversal Agent
Neostigmine 0.5-2 mg IV This is given if the patient does not loose their
paralysis. This would not be given pre-hospital. +/- atropine 05.-1 mg IV to prevent side effects
such as bradycardia
Succinylcholine
Special Considerations Consider atropine in bradycardic adults Pre-medicate with Lidocaine because
fasciculations can lead to increased ICP LETHAL in the wrong hands
Constant attendance Have BVM ready to go before administering drug Has no effect on consciousness
Midazolam & Lorazepam
Benzodiazepines Provide sedation, amnesia, and
anticonvulsant properties No analgesia
•Midazolam: Faster onset, shorter duration than lorazepam•Lorazepam: may be the preferred agent due to its longer action duration
Pay close attention to the patient’s level of consciousness. Signs/symptoms of discomfort may include movement, increase heart rate, increased blood pressure.
Midazolam (Versed)
Dose: 0.05-0.1 mg/kg IVP Rapid onset – 1-2 minutes Single dose duration: 15-20 minutes
Midazolam Duration: 1-4 hours Hepatic clearance Decreased dose needed (longer half life)
Obese Geriatric CHF Hepatic or renal insufficiency
Lorazepam
Class – Benzodiazepine II (Intermediate Acting)
Pregnancy Risk Category – D (Positive evidence of human fetal risk. Maternal benefit
may outweigh fetal risk in serious or life-threatening situations)
Metabolism – liver Excretion - urine
Lorazepam (Ativan)
Dose: 1-2 mg IV every 15 minutes as needed for sedation (maximum 10 mg)
Onset: 5 minutes Duration: 6-8 hours, dose dependant
Lorazepam
Enhances GABA – the primary neuro-inhibitor
Amnesia, anxiolysis, central muscle relaxation, anticonvulsant effects, hypnosis
Doesn’t release histamine Allergic reactions rare
Lorazepam - Metabolism Similar for all BNZ Lipid soluble – brain penetration Rapid onset – 60-120 sec t ½ - 3-10 min
t ½ - 10-20 hours – 5 active metabolites
Vecuronium & Rocuronium Non-Depolarizing Paralytics Provide paralysis, but NO sedation,
amnesia, or analgesia properties
Vecuronium (Norcuron)
Considered safe without many contraindications
May be used in most patients including cardiovascular, pulmonary, and neurological emergencies
Must be reconstituted from powdered form
Vecuronium (Norcuron)
Dose: 0.1mg/kg IVP Repeat/maintenance dose: 0.01 mg/kg Onset: 2-3 minutes Duration: approx. 20-30 minutes
Vecuronium (Norcuron)
Metabolized by the liver and kidneys Use with caution in patients with liver
failure May have 2x the recovery time
Patients with renal or hepatic failure will need less medication to maintain paralysis
Does not cause hypotension or tachycardia
Rocuronium (Zemuron)
Very similar properties to Vecuronium Does not need to be mixed, can be stored
at room temp for 60 days Less vagolytic properties
Rocuronium (Zemuron)
Competitive blockade of ACH Reversed by ACHesterase inhibitors Degradation, liver metabolism and
bile/kidney excretion Reversed by neostigmine
Rocuronium (Zemuron)
No known contraindications Pregnancy class B
(Animal Studies show no risk or adverse fetal effects but controlled human 1st trimester studies not available/ do not confirm. No evidence of 2nd or 3rd trimester risk. Fetal harm possible but unlikely)
Lactation ?Safe “Back-up” paralytic agent.
Rocuronium (Zemuron)
Onset: 30-60 seconds Fastest onset of all non-depolarizing NMBs Dose related
Dose: 1 mg/kg IVP Duration: 20-75 minutes Repeat/maintenance dose is the same as
the initial dose
Prolonged Seizure Activity
Neuromuscular Blockers cease motor activity but DO NOT stop seizure
Anticonvulsant (diazepam) administration should precede neuromuscular blockers
Pregnant Patients and Neuromuscular Blockers
Pregnancy = weight gain Larger breast may increase resistance
during BVM Toxemia may cause edemotous airway Desaturate more rapidly due to reduced
functional residual capacity and increased oxygen consumption
Regurgitation more likely Decreased cardiac output Supine Hypotensive Syndrome
SummaryR a p id S e qu en ce In tu b a tion
L o raze p am IV O RM id a zo lam
V e curo n ium O RR e cu ro m ium
P e r M e d ica l C o n tro l O n ly
IN T U B A T E !
S u cc in ylch o line
S e llic ks M a n e u ver - B U R P
E to m id a te IV
L id oca ine IV if in d ica ted
P re -o xyg e na te p a tie n t1 0 0% O 2 fo r 5 m inu tes
N R M a sk o r B V M