Tag Archives: rsi

RSI Drugs

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RSI Drugs Summary

Dr James French

 

  • REDUCE THE DOSE OF INDUCTION AGENTS IN HYPOTENSION or when Pulse Rate is greater than Systolic Blood Pressure.
  • INCREASE THE DOSE OF PARALYZING AGENTS IN HYPOTENSION.

 

Give the sedative first, followed by a flush, followed by the parlaying agent, followed by a small fluid bolus.

 

KETAMINE

Ketamine is a dissociating sedative that that can also be used in lower doses for procedural sedation ( i.v. 0.5 – 1.0mg/kg) and as a powerful analgesic (i.v. 0.3mg/Kg). When used for RSI the dose is 2.0 mg/Kg and is halved to 1.0 mg/kg in hypotension or a raised shock index (i.e. if the pulse is greater than the systolic blood pressure) . Ketamine causes hypertension, tachycardia and vomiting as its main side effects. When used for procedural sedation Ketamine causes less respiratory depression than other sedatives. Patients can misperceive stimuli during sedation and recovery and become agitated; this is called “emergence”.

Ketamine is available as 10mg/ml concentration for IV use and a 50 mg/ml concentration for IM use only – confusing the concentration being used can cause cardiac arrest. The 10mg/ml concentration is used neat for analgesia, sedation and RSI in adult patients.

 

 

ETOMIDATE

Etomidate is a sedative. It has no analgesic effect.

Etomidate’s chief side effect is hypotension, hypoventilation and adrenal suppression. When used for RSI iv the dose is 0.3. In hypotension or is the pulse rate us greater than the systolic blood pressure the dose of per Kg is halved from 0.3 to 0.15 mg/kg to prevent post induction hemodynamic instability.

Etomidate can cause a myoclonic jerk which are a single gross limb movements. It has a rapid onset of 45 seconds.

Etomidate is short acting – The sedation effect lasts about 5 minutes.

Etomidate is usually dispensed as a white liquid in a single 10ml ampoule, which has a concentration of 2mg/ml.

 

 

SUCCINYCHOLINE

Succinylcholine is a depolarizing muscle relaxant that acts on acetylcholine receptors. It works by binding non-competitively to the muscular acetylcholine receptor. This causes muscular relaxation by “burning out” the neuromuscular mechanism. This activation of the neuromuscular junction causes fasiculations.

Succinylcholine also acts on the acetylcholine receptors on the heart causing bradycardia as its primary side effect, particularly when giving a second dose. 5 mcg/kg of Atropine is therefor given before the second dose of Succinylcholine and in children under one year of age (who are more prone to bradycardia).

Succinylcholine works rapidly, with optimal relaxation in the jaw produced 10 seconds after fasciculations finish in the face.

The paralyzing effect wears off after about 6 – 9 minutes.

Succinylcholine provides no analgesic or sedative effect so it is essential that analgesia and sedation are given after anesthesia.

Succinylcholine is given neat. is a clear liquid and is supplied in one concentration of 20 mg/ml in a glass ampoule containing 100mg.

Succinylcholine dose in adults is 1.5 mg kg. The dose can be increased in severe shock to 2.0 mg/kg and in children. Do not “underdose” the paralyzing drugs so round up when doing drug calculations. Especially do not practice “ampoule based medicine” when using paralyzing agents in emergency situations.

Succinylcholine cannot be given to anybody with acute or chronic neuromuscular disease.

 

 

ROCURONIUM

Rocuronium is a non-depolarizing muscle relaxant. It does not activate the acetylcholine receptor but blocks the bodies own neurotransmitter. It therefore does not cause fasciculations.

Rocuronium also blocks the action of acetylcholine on the heart causing tachycardia as its primary side effect.

Rocuronium is fast onset proving intubating conditions in 60 seconds when given in the correct dose – it is essential that this period is timed after administration.

Rocuronium is long acting providing muscular parlays for about 45 minutes. It provides no analgesic or sedative effect so it is essential that analgesia and sedation are given after anesthesia.

Rocuronium is given as 1.5mg/kg, which is a dose increase, so does not need to be adjusted in severe hypotension.

Rocuronium is given neat and is supplied as a colourless liquid of 10 mg/ml concentration.

 

Lessons from Case Review and the Literature.

 

  1. REDUCE THE DOSE OF INDUCTION AGENTS IN HYPOTENSION.
  2. INCREASE THE DOSE OF PARALYZING AGENTS IN HYPOTENSION.
  3. Give the sedative first, followed by a flush, followed by the parlaying agent, followed by a small fluid bolus.
  4. Time from the moment the drugs are given to prevent the intubator from making the first attempt too early.
  5. When pushing the drugs make sure the IV line is blocked off to prevent the drugs from being pushed back into the giving set.
  6. Use IV access on the opposite side of the blood pressure cuff.
  7. Always follow RSI drugs with analgesia first after the tube is secured.
  8. Give the RSI drugs rapidly, fast IV push, sedative first, then the paralysing agent followed by a large flush or fluid bolus.
  9. Do not paralyze the hypoxic patient until every attempt to restore hypoxia has been corrected.
  10. Resuscitate the circulation with haemorrhage control and blood products, or fluid and vasopressors prior to RSI.

 

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ED Rounds – September 2016

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Report by Kraig Worrall

DMNB Clinical Clerk Med3

 

 

Pre-oxygenation for Intubation – Dr Jay Mekwan

Oxygenation is essential in the management of critically ill patients. Intubation in the emergency department is a critical skill in improving patient outcomes. When indicated, intubation should be performed by skilled personnel to minimize hypoxia. Desaturation in the peri-intubation period can happen quickly – particularly in pediatric, bariatric and critically ill patients. Today in rounds, Dr. Mekwan reviewed recent evidence in the realm of pre-oxygenation. Bag Valve Mask (BVM) pre-oxygenation alone outperforms: (1) BMV with concurrent nasal cannula, (2) non-rebreather mask, and (3) non-rebreather mask with concurrent nasal cannula. Using a nasal cannula together with BMV compromises the mask seal, which leads to inferior pre-oxygenation performance. A nasal cannula should be applied after BMV and before intubation and remain in place during the intubation process. Discussion in rounds centered around strategies to improve peri-intubation O­2 saturations, and ultimately improve outcomes in the Saint John Emergency Department. Finally, the use of ketamine in rapid sequence intubation was also discussed.

 

Reference:

http://www.sciencedirect.com/science/article/pii/S0196064411016672

 

 

Blunt chest trauma – Dr. Andrew Lohoar

Although blunt chest traumas can present to the emergency department from a variety of etiologies, motor vehicle collisions and falls account for the majority of cases. This statistic holds true in Saint John, for which Dr. Lohoar presented some recent data (see slides). Several important conditions arising from blunt chest trauma were discussed, including lung contusion, hemothorax (HTX), cardiac tamponade and pneumothorax (PTX). In particular, discussion was centered around decisions surrounding chest tube placement for PTX and HTX. Emergency chest tube insertion is the definitive initial management for either of these potentially deadly presentations. The decision to place a chest tube in a hemodynamically stable patient with radiological evidence of PTX following blunt trauma is influenced by a number of factors. Today in rounds, we discussed how experience is paramount to successful chest tube placement. The balance between practitioner experience and patient’s need for urgent decompression must be considered. Complications from improperly placed chest tube can contribute significant morbidity. Initial observation of an otherwise stable patient can certainly be the right choice for emergency room staff with limited chest tube experience. The same can be true for patients requiring hospital transfer.

Additional teaching points included: the use of POCUS as part of the primary survey, the role of CT and CT-decision rules, the disposition of blunt chest trauma patients, and, finally, strategies to reduce complications when placing chest tubes.

 

 

Managing violent patients – Dr. Jo-Ann Talbot

For many patients, emergency departments are the gateway into medical care. This includes violent patients, who, despite their behaviour, are sick and in need of care. This presentation, by Dr. Talbot, described strategies for managing violent patients. Strategies when faced with a violent patient include; (1) Calling for help, (2) controlling the scene, (3) de-escalating the situation. Fundamental to de-escalation is recognizing signs of an impending crisis. As with other aspects of medicine, prevention is better than reaction. Recognizing a patient’s needs can prevent a violent episode, for example, a simple gesture of food, nicotine replacement, or medication can calm a tense situation, develop a therapeutic trust with the patient, and prevent physical violence.

When a situation moves beyond prevention, physical and chemical restraints become viable options to reduce harm to the patient, staff, and assets. When physical restraints are used, it requires a team of 5 trained individuals. If possible, the treating physician should not participate in restraining the patient, as this can be deleterious to the therapeutic relationship. Agents, dosing, and strategies for chemical restraint are reviewed in the attached presentation.

Finally, Dr. Talbot emphasized the need for a centre/region-wide protocol for violence in the ED that is understood and implemented by all staff.

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