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RSI Pharmacology. New Hampshire Division of Fire Standards & Training and Emergency Medical Services. RSI Medications. Protocol meds Oxygen Lidocaine Atropine Etomidate Succinylcholine Lorazepam Fentanyl Rocuronium Vecuronium. Medication Information Parameters. Class

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rsi pharmacology

RSI Pharmacology

New Hampshire

Division of Fire Standards & Training and

Emergency Medical Services

rsi medications
RSI Medications
  • Protocol meds
  • Oxygen
  • Lidocaine
  • Atropine
  • Etomidate
  • Succinylcholine
  • Lorazepam
  • Fentanyl
  • Rocuronium
  • Vecuronium
medication information parameters
Medication Information Parameters
  • Class
  • Pregnancy Risk Category
  • Preparation
  • Action
  • Onset
  • Duration
  • Drug Interactions
  • Side Effects
  • Reversal Agent(s)
lidocaine
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
lidocaine1
Lidocaine
  • Antidysrhythmic with anesthetic properties that blunt transient increases in ICP that result from laryngoscopy.
  • Also blunts cough/gag reflex during laryngoscopy
atropine
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
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
etomidate1
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 situation

Pediatrics – not approved for patients under 10 – however RSI protocol only for age 12 and above.

etomidate2
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
etomidate3
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
etomidate4
Etomidate
  • Indication: as an induction agent before the administration of a neuromuscular blockade agent.
  • Contraindications: Known hypersensativity
etomidate5
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
etomidate6
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
etomidate7
Etomidate
  • Drug Interactions
    • Sedatives and Hypnotics – increased effect
    • Opiates – increased effect
    • No interaction with any neuromuscular blocker
etomidate8
Etomidate
  • Side Effects
    • Elderly patients sensitive
    • Hypotensive patients sensitive
    • Pain at injection site
    • Muscle twitching
      • 30%
      • Myoclonic jerks
      • Variable, Facial
etomidate9
Etomidate
  • Side Effects
    • Decreased plasma cortisol concentrations
    • Last up to 8 hours after injections

“Legal Laundry List” –

hyper and hypoventilaiton

apnea (5-90 seconds)

laryngospasm

hiccups / snoring

hyper and hypotension

Nausea / Vomiting after emergence

etomidate10
Etomidate
  • Reversal Agents
    • NONE
neuromuscular blockers
Neuromuscular Blockers
  • HOW DO THEY WORK ????
  • WHAT DO THEY DO ?????
neuromuscular blockers1
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 blockers2
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
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
Motor Neuron

Dendrites

Neuron

Cell Body

Axon

Telondendria

acetylcholine
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
Anectine (Succinylcholine)SCh or “Succs”
  • The only depolarizing paralytic in clinical use
  • Benefits:
    • Rapid onset
    • Short duration

Will cause “fasciculations”

succinylcholine
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
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
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.
succinylcholine1
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
succinylcholine2
Succinylcholine
  • Action
    • Binds to nicotinic “M” receptors usually acted upon by Acetylcholine
    • Initial Depolarization of muscle membrane
    • Block further binding
succinylcholine3
Succinylcholine
  • Drug interactions
    • Potentiation of effects
      • Oxytocin, Beta Blockers, Organophosphate insecticides
    • Reduced duration of action
      • Diazepam
    • Other effects
      • Cardiac Glycosides – dysrhythmias
succinylcholine4
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!

Contraindications
succinylcholine5
Succinylcholine
  • Adverse Effects:
      • Fasciculations
      • Hyperkalemia
      • Bradycardia
      • Prolonged Neuromuscular Blockade
      • Malignant Hyperthermia
succinylcholine adverse effects
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 effects1
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
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
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
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
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/SlideShow_ENG_files/frame.htm
succinylcholine6
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

succinylcholine7
Succinylcholine
  • Onset
    • < 1 Minute
    • Slightly slower in hypotension
succinylcholine8
Succinylcholine
  • Duration
    • 5-10 minutes
    • Beware acetylcholinesterase deficiency
      • Rare
      • Prolonged action
succinylcholine9
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
succinylcholine10
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
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
Midazolam (Versed)
  • Dose: 0.05-0.1 mg/kg IVP
  • Rapid onset – 1-2 minutes
  • Single dose duration: 15-20 minutes
midazolam
Midazolam
  • Duration: 1-4 hours
  • Hepatic clearance
  • Decreased dose needed (longer half life)
    • Obese
    • Geriatric
    • CHF
    • Hepatic or renal insufficiency
lorazepam
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
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
lorazepam1
Lorazepam
  • Enhances GABA – the primary neuro-inhibitor
  • Amnesia, anxiolysis, central muscle relaxation, anticonvulsant effects, hypnosis
  • Doesn’t release histamine
  • Allergic reactions rare
lorazepam metabolism
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
Vecuronium & Rocuronium
  • Non-Depolarizing Paralytics
  • Provide paralysis, but NO sedation, amnesia, or analgesia properties
vecuronium norcuron
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 norcuron1
Vecuronium (Norcuron)
  • Dose: 0.1mg/kg IVP
  • Repeat/maintenance dose: 0.01 mg/kg
  • Onset: 2-3 minutes
  • Duration: approx. 20-30 minutes
vecuronium norcuron2
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
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 zemuron1
Rocuronium (Zemuron)
  • Competitive blockade of ACH
  • Reversed by ACHesterase inhibitors
  • Degradation, liver metabolism and bile/kidney excretion
  • Reversed by neostigmine
rocuronium zemuron2
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 zemuron3
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
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
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
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