Optional, Paramedic

Objectives1.1. Describe the indications, contraindications,

advantages, disadvantages, complications, and equipment for rapid sequence intubation with neuromuscular blockade.

1.2. Evaluate a patient who requires intubation and predict the difficulty of the intubation based on the patients’ physical findings.

1.3. Identify neuromuscular blocking drugs and other agents used in rapid sequence intubation.

Objectives1.4. Describe the indications,

contraindications, advantages, disadvantages, complications, and equipment for sedation during intubation.

1.5. Identify sedative agents used in airway management.

1.6. Differentiate between Neuromuscular blocking Agents and their uses.

Objectives1.7. Explain the pathophysiology of the

agents used in RSI.1.8. Correctly calculate drug dosages of

agents used in RSI.1.9. List the steps in Rapid Sequence

Intubation.

ScenarioYour Pt. is a 65 yo male with COPD who has been

nebulizing at home while watching football for the last 6 hours without much success. He is tri-poding as you enter the room, his skin is pale, cool, and clammy, respirations at 42 and shallow. He can only say one word at a time, ascultation reveals wheezing with minimal breath sounds, the patient shows signs of air trapping. He shakes his head yes when asked have you been intubated before and do you want it again.

What would you do?What would your next step be?

What is the pathophysiology of this patient?

The patient gets your attention points at his airway and colapses, apneic, what will you do?

When you attempt laryngoscopy without RSI the patients mandible is clenched with trismus. What are your options?

What medications and what doses would you give?

Evaluate the difficult airwayHistory

Deviated septum from Nasal fractures will make nasal tracheal intubation more difficult.

Neck Scars indicating potential changes to anatomical landmarks.

Physical SignsShort muscular neckReceding ChinsOverbite Limited Mobility of the mandibleOral Cavity - Malimapatti signs Flexion and extension of the neckExternal Larynx

MandibleOne way to measure

depth and mobility is to check the amount of available mandible.

More mandible will make visualizing the vocal cords easier.

Can the patient open their mouth far enough for 3 fingers

Mandible mobilityCan the patient

position his lower teeth outside his upper teeth.

Visualizing the anterior airway

Why Rapid Sequence Intubation RSI is a technique that allows the

Paramedic to control the airway of a patient that:

Can’t protect their own airway or otherwise requires paralysis to provide appropriate treatment.

Emergency intubation is warranted The patient has a “full” stomach Intubation is predicted to be successful If intubation fails, ventilation is predicted to be

successful

Pharmacological AdjunctsSedation

TranquilizersBarbituratesBenzodiazepinesNarcotics

Antianxiety and Sedative-Hypnotic Agents

Antianxiety agents are used to reduce feelings of apprehension, nervousness, worry, or fearfulness

Sedatives and hypnotics are drugs that depress the CNS, produce a calming effect, and help induce sleep

The major difference between a sedative and a hypnotic is the degree of CNS depression induced by the agent. For example, a small dose to calm a patient is called a sedative; a large dose of the same agent sufficient to induce sleep would be called a hypnotic. Therefore an agent may be both a sedative and a hypnotic, depending on the dose used.

Reticular formation Reticular formation consists of groups of

nuclei scattered through the brain stem Reticular formation and its neural pathways

constitute a system known as the reticular activating system (RAS)

Involved with the sleep-awake cycle Through these pathways incoming signals from

the senses and viscera are collected, processed, and passed to the higher brain centers

RAS determines the level of awareness to the environment and governs actions and responses to it

Antianxiety and sedative-hypnotic agents and alcohol act by depressing the RAS

Classifications Benzodiazepines: drug class most

commonly used today to treat anxiety and insomnia

Barbiturates: older drug class with many uses, from sedation to anesthesia

Benzodiazepines Benzodiazepines were introduced in the

1960s as antianxiety drugs; today they are among the most widely prescribed drugs in clinical medicine. This popularity results in part from their very high therapeutic index. Overdoses of 1,000 times the therapeutic dose have been reported not to result in death unless taken in conjunction with other central nervous system depressants (e.g., alcohol)

Benzo functions and binding

Thought to work by binding to specific receptors in the cerebral cortex and limbic system (a major integrating system that governs emotional behavior)

Highly lipid-soluble and widely distributed in the body tissues

Highly bound to plasma protein (usually more than 80%)

ActionsFour actions:

Anxiety-reducingSedative-hypnoticMuscle-relaxingAnticonvulsantAll benzodiazepines are schedule IV drugs

because of their potential for abuse

Common BenzodiazepinesFlumazenil (Romazicon) is a specific

benzodiazepine receptor antagonist and has been shown to be effective in reversing benzodiazepine-induced sedation and coma.

Alprazolam (Xanax) Chlordiazepoxide (Librium) Clorazepate (Tranxene) Diazepam (Valium) Flurazepam (Dalmane) Prazepam (Centrax) Midazolam (Versed) Lorazepam (Ativan) Triazolam (Halcion)

Barbiturates Once the most commonly prescribed class

of medications for sedative-hypnotic effects, but they have been virtually replaced by benzodiazepines

Divided into four classes according to their duration of action:

Ultra-short-acting Short-acting Intermediate-acting Long-acting

Ultra-short-acting barbituratesDifferences in onset and duration of action

depend on their lipid-solubility and protein-binding propertiesUltra-short-acting barbiturates

Used as intravenous anesthetics Act rapidly and can produce a state of anesthesia in

a few seconds Example: thiopental sodium (Pentothal)

Short acting barbiturates Short-acting barbiturates

Produce an effect in a relatively short time (10–15 minutes) and peak over a relatively short period (3–4 hours)

Rarely used to treat insomnia More commonly used for preanesthesia

sedation and in combination with other drugs for psychosomatic disorders

Examples include the following: Pentobarbital (Nembutal) Secobarbital (Seconal)

Intermediate-acting barbiturates

Have an onset of 45 to 60 minutes and peak in 6 to 8 hours

Short-acting and intermediate-acting agents have similar patient responses in the clinical setting

Examples include the following: Amobarbital (Amytal) Butabarbital (Butisol)

Long-acting barbiturates Require over 60 minutes for onset and peak

over a period of 10 to 12 hours Used to treat epilepsy and other chronic

neurological disorders and to sedate patients with severe anxiety

Examples include the following: Mephobarbital (Mebaral) Phenobarbital (Luminal)

Miscellaneous sedative-hypnotic drugs

Agents that are not benzodiazepines or barbiturates

More similar to barbiturates than benzodiazepines

Examples include the following: Etomidate (Amidate) Chloral hydrate (Noctec) Ethchlorzynol (Placidyl)

Some antihistamines have pronounced sedative effects:

Hydroxyzine hydrochloride (Vistaril, Atarax)

Pharmacological AdjunctsParalytic agents used for intubation

Depolarizing agents Can lead to fasciculations Succinylcholine (Anectine)

Nondepolarizing agents Vecuronium (Norcuron) Pancuronium (Pavulon)

Neuromuscular Blockers Neuromuscular blockers produce skeletal

muscle paralysis by binding to the nicotinic receptor for acetylcholine (ACh) at the neuromuscular junction The neuromuscular junction is the point of contact

between the nerve ending and the muscle fiber When nerve impulse pass through this junction,

ACh and other chemicals are released, causing the muscle to contract

Two types of neuromuscular blocking drugs: Depolarizing agents Nondepolarizing agents

Depolarizing Agents Substitute themselves into the

neuromuscular junction and bind to receptors for ACh

Because these drugs produce depolarization of the muscular membrane they often lead to fasciculations (uncontrollable muscle twitching) and some muscular contractions

Duration Depolarizing agents block additional

stimulation of the muscle fiber by remaining attached to the neuromuscular junction.

Complete muscle relaxation occurs in 30 seconds to 1 minute

Lasts for 2 to 3 minutes Dissipates within 10 minutes. This medication should be used cautiously

in children because it may cause severe bradycardia or cardiac arrest. (Particularly in children with known neuromuscular disorders)

Succinylcholine Rapid onset of action and briefest duration

of action of all neuromuscular blocking drugs, making it the drug of choice for emergency endotracheal intubation.

Standard dose: 1 to 1.5 mg/kg

Nondepolarizing agents Bind to receptors for ACh and block the

uptake of ACh at the neuromuscular junction, without initiating depolarization of the muscle membrane

Longer onset and duration than depolarizing agents

Examples Vecuronium Rapid onset—2 minutes Short duration—45 minutes Pancuronium Rapid onset—3 to 5 minutes Longer duration—1 hour

Dosing of Non-depolarizing AgentsVecuronium

Adult Pediatric

Pancuronium Adult – 0.04-0.1 mg/kg slow IV; repeat q 30-60 min

prn Pediatric – 0.04-0.1 mg/kg slow IV Newborn – 0.02 mg/kg/dose

Contraindications-Myasthenia Gravis

ImportantIt is important to note that paralytic agents

do not affect consciousness. It is vital to the patients continued health and psychological welfare that we sedate the patient continuously while they remain paralyzed.

Additionally remember that a patient in seizure remains in seizure despite the outward appearance induced by the paralysis. Adequate treatment via local protocol with an anti seizure agent such as Diazepam should be maintained despite paralysis.

Premedicating Because these blocking agents produce

complete paralysis, ventilatory support must be provided and the efficacy of ventilation and oxygenation closely monitored.

Atropine - (.02 mg/kg) should be strongly considered, to prevent vagus nerve stimulation potentially causing unwanted bradycardias.

Lidocaine - (1 to 1.5 mg/kg) may blunt any increase in intracranial pressure associated with intubation. Allow to circulate for 1 minute.

Rapid Sequence IntubationIndications

Emergency intubation neededFull stomachIntubation likely to be successfulIf intubation fails, ventilation possible

Six “Ps” of RSIPreparationPreoxygenationPretreatmentParalysis (with induction)Placement of the tubePostintubation management

PreparationStart an IVInitiate cardiac monitoringPrepare your equipment

Suction.ET Tube checked for leaks place stylet, attach 10 to 15 cc

syringe.Laryngoscope blade checked size and light.Set out ET Tube verification devices.

Prepare your medications and syringesBe sure to label any medications you pull up in an

unlabeled container (syringe)Set out your cricothyrotomy kit as a backup.

PreoxygenationAttempt pre-oxygenation of your patient with

an increased FIO2 to achieve a PAO2 as high as possible.

PretreatmentBegin your RSI with Pretreatment such as

Atropine or Lidocaine. Allow time for the medication to take effect.

Pretreat with your sedative agent. Allow time for the sedative hypnotic to take effect.

Paralysis (with induction)Administer your paralytic agent and allow

time for the induction to occur usually less than 15 to 30 seconds.

If utilizing succinylcholine observe the abdomen for fasciculation's.

Placement of the tubeOnce you observe the paralysis of your

patient open the airway manually and begin your intubation.

If the patients PAO2 drops below 80 or your PACO2 begins to elevate above accepted levels via your local protocol stop intubation and ventilate your patient via BVM and increased FIO2 until with accepted limits.

Attempt intubation again.

Postintubation managementOnce the tube has been placed confirm

placement via visualization of thee cords, auscultation of bilateral breath sounds and ETCO2 detector or continuous CO2 wave form.

Secure the tube in place and ventilate.Prepare to administer additional sedatives

and/or longer acting paralytic agents depending on your local protocol.

What IfWhat if I can’t get the tube?

Ventilate via BVM and increased FIO2.What if I can’t ventilate via BVM?

First of all then don’t paralyze, if you have no choice then this is a good time to perform cricothyrotomy.

What if my patient starts waking up during intubation attempts?Go back to your pre-medication point and sedate

the patient further then administer additional paralytic per local protocol.

Aspiration by InhalationInhalation of food, foreign body, or fluid into airway

Suspect in patients with decreased level of responsiveness

Aspiration is commonly lethal and will most likely be life changing if not lethal.The introduction of an acidic substance into the lungs

will cause destruction of alveoli and permanently change the lung parenchyma.

In response the body will constrict the post capillary sphincters in the effected tissues causing increased hydrostatic pressure and pulmonary edema.

It is our job to prevent aspiration by controlling the airway of the patient who cannot control their own. .

SummaryRapid Sequence Intubation is a technique to

enable a Paramedic to control a patients airway.

Proper assessment of your patient and assessment of the potential risk to intubation can prevent unexpected complications.

Prepare your equipment and medications.Utilize a device that ensures patency of the Et

tube.Remember to sedate your patient before the

last sedative has worn of.Aspiration and Apnea kill patients it is our job

to maintain the airway.