2. Introduction
RSI describes a coordinated, sequential process of preparation, sedation, and paralysis to facilitate safe, emergency
tracheal intubation.
Pharmacologic sedation and paralysis are induced in rapid succession to quickly and effectively perform
laryngoscopy and tracheal intubation.
The goal of RSI is to intubate patients quickly and safely using sedation and paralysis.
RSI is generally recommended because it is more successful and safer than intubation without sedation and
paralysis for patients with varying levels of consciousness, active protective airway reflexes, and/or a full stomach.
Sedation and paralysis are unnecessary prior to intubation for some patients, such as those who are in cardiac arrest
or already deeply comatose.
3. INDICATION OF INTUBATION IN ED
Indication of intubation in ED
Airway protection
Failure to oxygenate
Failure to ventilate
Anticipate deterioration
Others eg cerebral resuscitation/transport purpose
4. Predicting Difficult airway
• Difficult airway can mean
difficulty at various levels:
• Difficult for laryngoscopy
• Difficult to bag (BMV)
• Difficult for extra-glottic
devices
• Difficult to
critcothyroidotomy
7. Definition of rsi, dsi, crashed intubation
• Rapid sequence intubation (RSI) is an airway management
technique that produces inducing immediate unresponsiveness
(induction agent) and muscular relaxation (neuromuscular
blocking agent) and is the fastest and most effective means of
controlling the emergency airway
• Delayed sequence intubation (DSI) is a procedural sedation, with
the procedure being preoxygenation, after which the patient can
be paralyzed and intubated
• Crashed airway refers to patients in cardiopulmonary arrest,
deep coma or near death, who can't maintain ventilation and
oxygenation
9. Preparation
Patient : airway assessment and back up plan
to manage unanticipated problems with
intubation
Equipment
• M : Mask, Medications
• A : Airway adjunct, Ambu Bag
• L : Laryngoscope and blade
• E : Endotracheal tube
• Male : 7.5-8.0mm
• Female : 7-7.5mm
• Paeds : (Age/4)+4 (uncuffed), (Age/4)+3.5
(cuffed)
• S : Suction, Syringe, Stylet,
Stethoscope
Personnel
11. Protection and positioning :
• Maintain manual cervical spine
immobilization during intubation in the
trauma patient.
• If cervical spine injury is not potentially
present, put the patient in the "sniffing
position" (ie, head forward so that the
external auditory canal is anterior to the
shoulder and the nose and mouth point to
the ceiling).
• Utilize external laryngeal manipulation or,
in infants, gentle cricoid pressure to
optimize the view of the glottis during
direct laryngoscopy if the initial view is
suboptimal or inadequate despite correct
laryngoscope blade positioning.
12. Preoxygenation
• Process of denitrogenation by simply breathing
spontaneously O2 rich to replace N2 volume of
the individual FRC
• It increases O2 reserves in the lungs, blood and
other tissues preventing anticipated
hypoxaemia during the subsequent apnea
following muscle paralysis (especially if
endotracheal intubation proves to be difficult)
• Method :
1. Administer high flow 100% oxygen via a tight
fitting non rebreather mask or anaesthesia
face mask applied for 3-5 minutes with a
spontaneously breathing patient
2. If time is an issue (dire emergency)
preoxygenation maybe sufficient after 8 vital
capacity breath <60 seconds (requires patient
cooperation)
13. Pre treatment
Administration of certain medication in order to counter or minimize the adverse effects of
laryngoscopy and tracheal intubation
Example:
1. Atropine 20 mcg/kg blunts vagal stimulation in infant less than one year old – no longer a
routine
2. Lignocaine 1-1.5 mg/kg blunts sympathetic effects
3. Fentanyl 1-2 mcg/kg blunts CVS effects and increase in ICP
14. Paralysis with induction
Usage of a rapidly acting induction agent and a NMB
agent (paralytic) to achieve an immediate
unconsciousness and motor paralysis
15. INDUCTION AGENTS
Drugs Mechanism of action Onset Duration of action Contraindications Advantages Side effects
Thiopental (2-5mg/kg) Facilitate GABA
inhibitory
neurotransmission at
GABA receptors and
inhibit excitatory
neurotransmission
30-40s 20-30 min • Airway
obstruction
• Porphyrias
• Status
asthmaticus
• Cardiovascular
instability
• Rapid onset
• Potent
anticonvulsant
• No nausea and
vomiting
• Respiratory
depression
• Shivering
• Hypotension
• Tissue necrosis
• Allergic reaction
Ketamine (1-2mg/kg) NMDA receptor
antagonists
- Impaired glutamate
release
(neurotransmitter)
1-5 mins Approx 20 mins • Active psychotics
symptoms
• Uncontrolled HPT
• Increase ICP
• CCF or coronary
artery disease
• Provide
analgesia,
amnesia and
sedation
• Does not
decrease
respiratory drive
• Emesis
• Laryngospasm
• Emergence
reaction
•
Propofol ( 1-2mg/kg) Activate GABA
receptors
15-20s 3-10 mins • Hypersenstivity to
soybean, egg or
egg products
• Obstetrics
procedures
• Children below
3y/o
• Rapid and
smooth recovery
• Complete
elimination in 4H
• Anti-emetic
• Hypotension
• Propofol related
infusion
syndrome (PRIS)
Etomidate (0.1-
0.3mg/kg)
Activate GABA
receptors
30-60s 3-5 mins • Marked
hypotension
• Severe asthma
• Known
hypersensitivity
• Injection site pain
• Respiratory
depression
• Skeletal muscle
movement
• Nausea and
vomiting
• Headache
16. Drugs Mechanism of action Onset Duration of action Contraindications Advantages Side effects
Midazolam (0.15-
0.3mg/kg)
Short acting
benzodiazepines
Potentiate action of
GABA at GABA-a
receptors
1-3mins 10-20 min • Known
hypersensitivity
• Narrow angle
glaucoma
• Hypotension or
head injury
• Rapid onset
• Amnesia
• Anticonvulsant
• Respiratory
depression
17. Drugs Mechanism of
action
Onset Duration of action Contraindications Advantages Side effects
Vecuronium
(0.1mg/kg)
Nicotinic receptors
anatagonist hence
block binding of
acaetylcholine and
potential for muscle
depolarisation
3-5mins 30-60 mins • Myopathy
• Neuromuscular
disease such as
myasthenia
gravis, lambert-
eaton syndrome
• Safe in cardiac
patient
• Rapid excretion
by biliary system
• Prolonged
paralysis
Pancuronium
(0.1mg/kg)
Nicotinic receptors
anatagonist hence
block binding of
acaetylcholine and
potential for muscle
depolarisation
3-5 mins 45-90 mins • Known
hypersensitivity
• Use with cautious
in severe renal
Impairment
patient (mainly
eliminate by
kidney)
• Long acting • Hypertension
• Tachycardia
• Allergic reaction
• Arrythmia
Mivacurium (0.15-
0.3mg/kg)
Nicotinic receptors
anatagonist hence
block binding of
acaetylcholine and
potential for muscle
depolarisation
30-60s 15-20 mins • Known allergy
• Myasthenia
gravis
• Short acting • Histamine
release
• Acute myopathy
Rocuronium (0.8-1.0
mg/kg)
Nicotinic receptors
anatagonist hence
block binding of
acaetylcholine and
potential for muscle
depolarisation
30-60s 20-35 mins • Marked
hypotension
• Severe asthma
• Known
hypersensitivity
• Eliminated
primarily by liver
• Injection site pain
• Respiratory
depression
• Skeletal muscle
movement
• Nausea and
vomiting
• Headache
NEUROMUSCULAR BLOCKING AGENTS
18. Drugs Mechanism of
action
Onset Duration of action Contraindications Advantages Side effects
Atracurium (0.4-0.5
mg/kg)
Nicotinic receptors
anatagonist hence
block binding of
acaetylcholine and
potential for muscle
depolarisation
2-3mins 15-35mins • Known
hypersensitivity
• - • Hypotension
• Bronchospasm
• Tachycardia
Cisatracurium (0.15-
0.2mg/kg)
Nicotinic receptors
anatagonist hence
block binding of
acaetylcholine and
potential for muscle
depolarisation
3-4 mins 50-60 mins • Known
hypersensitivity
• Myasthenia
gravis
• 3x more potent
than atracurium
• Release less
histamine than
atracurium
• Hypertension
• Tachycardia
• Allergic reaction
• Arrythmia
Succinylcholine (1-
1.5mg/kg)
Resemble
acetylcholine at Ach
receptor agonist
Cause end plate
depolarisation lead to
muscle relaxation
30-60s 5-10 mins • Neuromuscular
disease
• Burns
• Renal failure
• Allergy
• Head injury
• Rapid onset
• Most commonly
use for intubation
• Muscle
fasciculation
• Increase IOP, ICP
• Malignant
hyperthermia
• Hyperkalemia
20. Placement with proof
• Direct visualization of ET through the
vocal cords
• Auscultation of the lungs
• Symmetrical chest movement on each
PPV
• Capnograph or ETCO2 tracing
• Vapor (mist) on internal side of ETT
during exhalation
22. Post intubation management
• SPO2 monitoring
• CXR
• - Assess placement of ETT, desired
position of an ETT is 5 +- 2cm above
carina or T2-T4
• ABG post intubation
• Maintenance of sedation and NMB
• NG tube
• Stress ulcer prophylaxis
• CBD
24. Consumption • Increased Oxygen Consumption
• Paediatric patients, sepsis, acute respiratory distress syndrome (ARDS), or other
high-demand states such as excited delirium, thyrotoxicosis, and pregnancy all
increase the consumption of oxygen
• These patients may exhibit a normal saturation during preoxygenation; however, the
increased peripheral consumption may still result in rapid desaturation
• Intervention: Optimize preoxygenation, utilise apneic oxygenation, and anticipate
shorter (safe) apnea time
Right
Ventricular
Failure
• The right ventricle has very little reserve to overcome increased afterload. As
dilation and regurgitant flow across the tricuspid valve worsen eventually impairs left
ventricular diastolic filling.
• Cardiac output is only maintained by tachycardia at this point, and any further
increase in RV afterload, or further volume loading of the right ventricle, can push
the right ventricle too far and result in cardiac arrest.
• Intervention: Optimize preoxygenation, inhaled pulmonary vasodilators, choice of
induction agents, early use of vasopressors .Cardiac ultrasound can help identify a
failing RV and guide judicious fluid resuscitation.
25. Acidosis • Severe metabolic acidemia increases risk by further decreasing the pH with any
interruption of compensatory ventilation during intubation or unmatched alveolar
ventilation requirement after intubation
• Apneic phase of greater than 60 seconds caused statistically significant changes in
pH and PaCO2 by 0.15 and 12.5 respectively
• Intervention: Correct the underlying issues; avoid mechanical ventilation if possible;
minimize apnea time; consider awake intubation, maintain increase minute ventilation
Saturation • Critically ill patients with airspace disease such as ARDS have limitations in the ability
to preoxygenate to provide an adequate safe apnea duration
• Intervention: Optimize preoxygenation
Hypotension • Intervention:
Intravenous fluid
ROCKETamine (rocuronium then ketamine), dose induction agents low and paralytic
agents high
Push dose epinephrine
Peripheral vasopressors prior to intubation
If time permits, perform the awake intubation
