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Optional, Paramedic. Objectives 1.1. Describe the indications, contraindications, advantages, disadvantages, complications, and equipment for rapid sequence.

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Presentation on theme: "Optional, Paramedic. Objectives 1.1. Describe the indications, contraindications, advantages, disadvantages, complications, and equipment for rapid sequence."— Presentation transcript:

1 Optional, Paramedic

2 Objectives 1.1. Describe the indications, contraindications, advantages, disadvantages, complications, and equipment for rapid sequence intubation with neuromuscular blockade Evaluate a patient who requires intubation and predict the difficulty of the intubation based on the patients’ physical findings Identify neuromuscular blocking drugs and other agents used in rapid sequence intubation.

3 Objectives 1.4. Describe the indications, contraindications, advantages, disadvantages, complications, and equipment for sedation during intubation Identify sedative agents used in airway management Differentiate between Neuromuscular blocking Agents and their uses.

4 Objectives 1.7. Explain the pathophysiology of the agents used in RSI Correctly calculate drug dosages of agents used in RSI List the steps in Rapid Sequence Intubation.

5 Scenario Your 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.

6 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?

7 Evaluate the difficult airway History Deviated septum from Nasal fractures will make nasal tracheal intubation more difficult. Neck Scars indicating potential changes to anatomical landmarks. Physical Signs Short muscular neck Receding Chins Overbite Limited Mobility of the mandible Oral Cavity - Malimapatti signs Flexion and extension of the neck External Larynx

8 Mandible One way to measure depth and mobility is to check the amount of available mandible. More mandible will make visualizing the vocal cords easier.

9 Can the patient open their mouth far enough for 3 fingers

10 Mandible mobility Can the patient position his lower teeth outside his upper teeth.

11 Visualizing the anterior airway

12 Malimapatti signs

13 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

14 Pharmacological Adjuncts Sedation Tranquilizers Barbiturates Benzodiazepines Narcotics

15 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.

16 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

17 Classifications Benzodiazepines: drug class most commonly used today to treat anxiety and insomnia Barbiturates: older drug class with many uses, from sedation to anesthesia

18 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)

19 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%)

20 Actions Four actions: Anxiety-reducing Sedative-hypnotic Muscle-relaxing Anticonvulsant All benzodiazepines are schedule IV drugs because of their potential for abuse

21 Common Benzodiazepines Flumazenil (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)

22 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

23 Ultra-short-acting barbiturates Differences in onset and duration of action depend on their lipid-solubility and protein- binding properties Ultra-short-acting barbiturates Used as intravenous anesthetics Act rapidly and can produce a state of anesthesia in a few seconds Example: thiopental sodium (Pentothal)

24 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)

25 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)

26 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)

27 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)

28 Pharmacological Adjuncts Paralytic agents used for intubation Depolarizing agents Can lead to fasciculations Succinylcholine (Anectine) Nondepolarizing agents Vecuronium (Norcuron) Pancuronium (Pavulon)

29 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

30 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

31 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)

32 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

33 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

34 Dosing of Non-depolarizing Agents Vecuronium Adult Pediatric Pancuronium Adult – mg/kg slow IV; repeat q min prn Pediatric – mg/kg slow IV Newborn – 0.02 mg/kg/dose Contraindications- Myasthenia Gravis

35 Important It 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.

36 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.

37 Rapid Sequence Intubation Indications Emergency intubation needed Full stomach Intubation likely to be successful If intubation fails, ventilation possible

38 Six “Ps” of RSI P reparation P reoxygenation P retreatment P aralysis (with induction) P lacement of the tube P ostintubation management

39 P reparation Start an IV Initiate cardiac monitoring Prepare 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 syringes Be sure to label any medications you pull up in an unlabeled container (syringe) Set out your cricothyrotomy kit as a backup.

40 P reoxygenation Attempt pre-oxygenation of your patient with an increased FIO2 to achieve a PAO2 as high as possible.

41 P retreatment Begin 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.

42 P aralysis (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.

43 P lacement of the tube Once 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.

44 P ostintubation management Once 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.

45 What If What 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.

46 Aspiration by Inhalation Inhalation 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..

47 Summary Rapid 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.


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