INTUBATION

OUTSIDE
THE ICU
 Goals and Objectives

1. Review indications and decision tree for intubation.

2. Review the different approaches and protocols for
intubation dependent of the clinical scenario.
 The need for Intubation need not
correlate to your Heart Rate.
Intubation of the critically ill patient in the ER can be one of the
most challenging and anxiety provoking activities we encounter.
All of this can be lessened by 3 things.
1. Being prepared for intubation – plan for the worst.
2. Practice. We have a set of simulation mannequins that are
obliging to be practiced on 24/7. Avail yourself!
3. Become familiar and comfortable with the different scenarios of
critically ill patients that might need intubation and the best
choice of induction agents.
 The Decision to Intubate
3 Question Assessment
1. Is there failure of the patient to maintain and
protect their airway?
2. Is there failure of oxygenation or ventilation?
3. Is there an anticipated need for intubation?
Intubation Decision Algorithm

From Up to Date
 1. Is there failure of airway maintenance
or protection?

A patient who can talk and answer questions appropriately has

airway patency (airway tone), ventilation and cerebral perfusion.
The same level of alertness to maintain airway tone is needed to
maintain protective reflexes to prevent aspiration.
 1. Is there failure of airway maintenance
or protection?

In the past, the ‘presence of a gag reflex’ was considered

indicative of an intact protective reflex.
This is NOT TRUE.
Gag reflex is not part of laryngeal closure/protection.
As well, many people lack a gag reflex altogether.
The ability to speak and swallow secretions is a far more reliable
indicator or airway protection.
 1. Is there failure of airway maintenance
or protection?

Upper airway patency is maintained by the upper airway

musculature. Flaccid airway muscles will cause obstruction.
Basic airway maneuvers (jaw thrust, chin lift, repositioning the
head) can obviate obstruction, but if these are needed and if they
require an oral airway (and can tolerate it), then such patients
need intubation.
 2. Is there failure of oxygenation?

Assessment of oxygenation but also clinically assessment and

Oxygen Saturation, (SpO2 monitors).
Clinically: restless, agitated and if severe cyanotic, confused,
somnolence and obtundation can indicate hypoxia.
SpO2 (pulse oximetry) can give an estimate of oxygenation,
but if there is poor peripheral perfusion (ie shock,
hypothermia), it can be unreliable.
EtCO2 can also help evaluate ventilation status, particularly if
followed by the trend (ie rising EtCO2)
 2. Is there failure of oxygenation?

Non invasive Ventilation (NIV) can often enable patients to avoid

needing intubation, but it requires an alert, cooperative patient.
NIV should not be used for patients who are poorly oxygenating
and who you feel are not going to reverse quickly with NIV.
3. Is there an anticipated need for intubation?
Even though some patients will be alert, protecting their
airway and appear to be oxygenating adequately, if the known
natural progression of their disease process is such, early
intubation may avoid a bad outcome.
Often our very resuscitative measures can necessitate
intubation. i.e. giving large fluid volumes to septic patients
with known pulmonary disease or pre-existing CHF.
Try to avoid hurried, unplanned situations or the ‘emergency
salvage airway procedures’.
 Are all intubation procedures
the same?
Quick answer …
NO
In the past, most rural doctors would use a simple intubation
protocol using such drugs as Fentanyl, Midazolam and
Succinylcholine.
Although this can be a useful combination, as we shall see, there
are different clinical scenarios in which ‘better options’ exist.
In the simulations, we will be practicing some of these ‘options’.
 Some Types of Critically Ill
Patients Needing Intubation.
1. Hemodynamic and Neurologically Stable patient.
2. Hypotensive, Shock Patient.
3. Elevated Intracranial Pressure Patient.
4. Asthmatic Patient.
5. Massive Upper GI bleed Patient.
6. Acidotic Patient.
 But before we start !

Oh no…not pharmacology again!

 Remember the Cardiovascular effects of IV drugs
b1 b1 b1
Drug a1 Inotr Chron Dromo b2 V/C V/D

Ketamine _ + +
Fentanyl _

Morphine _ ++

Propofol ++

Midazolam
 Induction Agents
1. Propofol – can cause hypotension and has been shown to be
associated with increased mortality in Septic patients.
Dose: 1.5 – 3 mg/kg
2. Ketamine – less hypotension associated, helps with
bronchodilation in asthmatics.
Dose: 2 mg/kg
3. Midazolam – used less now as associated with hypotension.
Dose: 0.3 mg/kg
4. Ketofol: 1:1 combination of ketamine and Propofol. Has been
shown to not cause hypotension.
Dose: Ketamine 0.5 mg/kg, Propofol 0.5 mg/kg
 Paralytics
We stock 2 paralytics – both kept in separate
yellow plastic containers in the fridge, second from
the bottom, back of the shelf.
1. Succinylcholine
2. Rocuronium
 Succinylcholine
Produces depolarization of motor endplates, resulting in flaccid
paralysis.
Onset: IV 15 – 30 seconds. (IM 2-3 minutes)
Duration: IV 8 - 15 minutes. IM 10-30 minutes
Dosage: Adults RSI 1 – 2 mg/kg IV
Pediatric RSI 1 mg/kg IV
When used will cause ‘muscle fasciculation’.
 Succinylcholine Warnings/Precautions

1. Bradycardia (more frequent with second dose and in children)

2. Acute renal failure (rhabdomyolysis) – more common with
burns, multiple trauma/tissue injury)
3. Hyperkalemia (usually delayed, more common in burns,
infections, tumors, renal or hepatic dysfunction)
4. Excessive salivation.
5. Can cause malignant hyperthermia.
 Rocuronium
A Non depolarizing neuromuscular blocking agent.
Dosing: Adult RSI 0.9 – 1.2 mg/kg
Obese RSI 1.2 mg/kg based on IBW
Onset: 1 -2 minutes
Duration: ~ 30 - 60 minutes
 Rocuronium
Warnings/Precautions

Can increase peripheral vascular resistance and tachycardia.

Can increase pulmonary hypertension, worsening right heart
failure.
Some Rescue and Pre-treatment
Medications

Epinephrine
Lidocaine
Atropine
Fentanyl
 Epinephrine

Consider having a push dose of epinephrine or an

infusion set up and ready for most intubations, as one
of the most common side effects of induction agents is
hypotension.
Hypotension is BAD for patients.
 Mixing Push Dose Epinephrine
Epinephrine:
Take a 10 cc N/S syringe. Discard 1 cc.
Take a preloaded syringe of Epi 1:10,000 from the cardiac drawer.
Take the bottom stopper off the syringe.
With the 9 cc Saline syringe, draw out 1 cc Epi (1:10,000)
You now have 10 mls of Epinephrine 10 mcg/ml
Dose is 0.5 – 2 ml (5-20 mcg) q 2-5 min
Onset 1 minute, duration 2-5 minutes.
 Lidocaine
Lidocaine has been used for RSI in different scenarios.
Lidocaine was thought to prevent an increase in intra cranial pressure
from laryngoscopy, so was given for Traumatic Brain Injury intubation.
The evidence is very weak that it actually does help. Most authorities
suggest either not bothering, or if you do give it there is likely no harm.
The other indication is for asthmatics, as it may reduce bronchospasm.
The evidence is again weak. It may be even less effective in patients who
have already received adequate beta-2-agonists.
Dose is 1.5 mg/kg given 2 -3 minutes prior to intubation.
 Atropine
Atropine, when used in children can blunt the vagal response
during intubation, which causes bradycardia.
In adults, atropine can blunt the muscarinic stimulation and
possible bradycardia from succinylcholine if they get a second
dose. Evidence however is conflicting and some studies have
even suggested atropine may cause tachyarrhythmias.
Current recommendations are to NOT give it routinely, but
have it handy as a rescue medication in case the patient
develops bradycardia.
 Scopolamine
Consider use in hypotensive patients as it can blunt
bradycardia, is a good amnestic and can decrease
salivation making intubation a bit easier
Dose: 0.4 mg IV
 Fentanyl

Can be used as a pre medication for both sedative

effect and analgesia.
Although does not typically cause much hypotensive
effect, it can do so in already hypotensive patients, or
if given too quickly.
Dose: 3 mcg/kg IV prior to induction agent.
 Histamine release and Opioids
Most opioids cause release of histamines.
Normally this is not a problem, except in patients with asthma
and anaphylaxis.
Fentanyl has the least, if any, propensity to cause release of
histamine, so patients with asthma or anaphylaxis who need
analgesic, this is the preferred drug.
 Some Quick Points on Intubation and
Resuscitating Critically ill patients.
1. With the exception of anaphylactic patients, ALL patients should
likely be resuscitated with the head of the bed elevated 30 degrees.
2. Anaphylactic patients should be resuscitated recumbent with the
feet/legs elevated.
3. As a MINIMUM, for intubation, the ear lobes should be at least
horizontal with the sternal notch.
4. When inserting an ET tube, place the tube down to 23 cm at the
lips for males, and 21 cm at the lips for females. In most cases that
will put you just above the carina.
 Some quick words on Intubation and
Resuscitating Critically ill patients.
5. A CXR does NOT confirm ETT ‘placement’ – it confirms
depth and location relative to the carina. Use EtCO2 for
confirming tube placement.
6. Once a patient is intubated, if the head of the bed is not
elevated 30 degrees, it should be now.
7. Have a back up plan! If the intubation fails, have a ‘rescue’
airway ready (LMA). Then consider a Cricothryotomy.
 Some quick words on Intubation and
Resuscitating Critically ill patients.
Cricothryotomy:
This procedure is often thought of as ‘the last option’
and as such when encountered is met with fear and trepidation.
Perhaps a way to lessen this is for every patient you are
considering intubation, take a moment and look and feel their
neck. Can you palpate the cricoid cartilage and membrane?
Ask yourself, do I think I can successfully do a
Cricothryotomy on this patient? If the answer is yes, you have
the ‘final’ back up plan. If the answer is no, consider getting
help, or be very careful with your intubation!
Types of Critically Ill Patients
Needing Intubation.

1. Hemodynamic and Neurologically Stable patient.

2. Hypotensive, Shock Patient.
3. Increased Intracranial Pressure Patient.
4. Asthmatic Patient.
Hemodynamic
and
Neurologically
Stable Patient
 Hemodynamic and Neurologically
Stable Patient
This is the patient that is obtunded (i.e. overdose,
pneumonia ..) and is having difficulty maintaining
their airway and oxygenation.
There are many drug regimes that will work in
such a patient.
The ‘Standard’ RSI Protocol
1. Positioning
2. Preoxygenation
3. Cricoid pressure
4. Induction agents
5. Neuromuscular blocking agents
6. Choice of laryngoscope, stylet, bougie.
7. Post intubation medications
8. Ventilator settings.
 The ‘Standard’ RSI Protocol
1. Positioning. Sniffing position and ideally head of the bed up.
2. Preoxygenation. Ideally patients should be given 100%
oxygen to increase oxygen reserve. Can use bag mask with
flow 15 l/min, a non rebreather mask at 10-15 l/m or nasal
cannula (not as effective). Try to avoid bag mask with actually
‘bagging’ as this inflates the stomach which increases the
chance of regurgitation.
Consider using nasal cannula at 10 l/m during intubation,
which has been shown to delay time to O2 desaturation.
 The ‘Standard’ RSI Protocol
3. Cricoid Pressure. Although controversial, the general consensus
is that it is not harmful and may be beneficial.
If used, relieve pressure if the patient starts to vomit.
Should use ~ 2.5 lbs of pressure.
BURP – Backwards, Upwards, Rightwards Pressure
 The ‘Standard’ RSI Protocol
4. Induction agents.
(1) Ketamine 2 mg/kg TBW or
(2) Propofol 1.5 – 3 mg/kg TBW or
(3) Midazolam. Can be used as an induction agent usually in
doses of 0.2 – 0.3 mg/Kg.
Consider Fentanyl 3 mcg/Kg 2-3 minutes prior to induction.
Can reduce the sympathetic response to intubation.
 The ‘Standard’ RSI Protocol
5. Neuromuscular Blocking Agents (NMBAs)
Succinylcholine 1.5 – 2 mg/Kg. Onset 15 – 30 seconds (can
be indicated when fasciculations have stopped). Duration 8-
15 minutes.
or
Rocuronium 0.9 – 1.2 mg/Kg. 30 – 60 second onset, but
long duration of action : 45 - 60 minutes.
 The ‘Standard’ RSI Protocol
6. Laryngoscope, stylet and bougie.
Choice of laryngoscope (direct versus video) is operator
dependent. Use what you are most comfortable with.
Stylet. Can increase chance of trauma to airway. Remove
immediately once ETT passed through the vocal cords.
Bougie. Can help increase success rates of intubation for both DL
and VL.
 The ‘Standard’ RSI Protocol
7. Post intubation medications. (reviewed on ‘ventilator sedation
Power point located on LMHER.com)
Can use morphine or fentanyl infusion.
May also want to add sedation (Diazepam, Lorazepam)
 The ‘Standard’ RSI Protocol
8. Ventilator settings.
This will depend on the patient condition.
Before intubation, have someone get and hook up the ventilator.
Remember to put an in-line EtCO2 monitor on the circuit. If not
using in line EtCO2, then after 8 breaths with bag mask, or 8
ventilations with ventilator, use the colorimetric CO2 monitor to
confirm placement.
 Ventilator Settings for
‘Standard RSI’ Patient
Mode AC (assist control)
Tidal Volume 6-8 cc/kg IBW
Respiratory Rate 10- 14 bpm
PEEP 5 cm H2O
FiO2 100% initially
After 15-20 min do ABG, follow ARDSnet chart
Goal Pa2 55-85 mmHg or SaO2 90%
 Ideal Body Weight

Height 5 5’1 5’2 5’3 5’4 5'5 5’6 5’7” 5’8” 5’9” 5’10 5’11 6’ 6’1” 6’2” 6’3” 6’4”
” ”

Male 52 53 55 57 59 61 63 65 66 68 70 72 74 76 78 79 81
Kg

Female 49 50 52 54 55 57 59 60 62 64 65 67 68 70 72 75 77
Kg
 FiO2/PEEP - aka ARDSnet Chart

• FiO2/PEEP Chart
• FiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0
• PEEP 5 5 8 8 10 10 10 12 14 14 14 16 18 18-24
Hypotensive
Shock
Patients
 Hypotensive, Shock Patient

Some strange things happen pharmacokinetically and

pharmacodynamically in Hypotensive/Shock patients.
Many of the pretreatment and induction agents need to be
given in much smaller doses. This has ‘something’ to do with
cerebral perfusion of unbound drugs in shock.
Conversely, paralytics, which work on motor endplates,
usually require much higher doses and take much longer to
work. This is because of the slow and poor perfusion seen in
shock.
 Hypotensive, Shock Patient
The patient in context.
A trauma or hypovolemic patient is in a major state of ‘catecholamine
release’. These patients are fighting for life and using every molecule
of epinephrine, norepinephrine and cortisol they can muster.
Then we come along and give them an induction agent which tells the
brain that ‘all is well’ and thus takes away that catecholamine
response.
The result of induction agents is that these patients will usually have
a dramatic drop in their blood pressure.
You need to be prepared for this hypotensive response.
 Hypotensive, Shock Patient
The patient in context.
Having an episode of peri or post intubation hypotension in an already
shocked patient increases their hospital mortality rate by 30%.
Being hypotensive prior to intubation is the biggest predictor of cardiac
arrest during or immediately after intubation.
Remember – ALL induction agents will drop BP in a shock patient.
Also, prior to intubation, patients are using ‘negative pressure
ventilation’ which assists heart filling via venous return. After intubation,
whether they are bagged or put on a ventilator, they are now on ‘positive
pressure ventilation’, which inhibits venous blood return to the heart.
 Induction/Analgesic Agents
in Shock Patients
Anesth 2004; 101:567
In shock, the dose of Propofol is 10-15% that of a normotensive patient
In shock the dose of Fentanyl is 40-50% that of a normotensive patient.
There is no good data for Ketamine, but felt you need a lower dose.
Message for induction, if using:
Propofol, use 0.1 – 0.15mg/kg
Ketamine – use 0.25 – 0.5 mg/kg
Fentanyl – use 40 – 50% regular dose
 Induction/Analgesic Agents
in Shock Patients

Midazolam/Fentanyl combination probably NOT a good choice in

Shock patients as this has large tendency to drop BP 3-5 minutes after
they are given, even if using low dose Midazolam.
 Neuromuscular Blockade Agents
in Shock Patients

Due to poor peripheral perfusion you need MORE paralytics

than in normotensive patients.
Succ and Roc – use 1.5 times the usual dose.
These agents will also usually take much longer to take effect.
 Hypotensive, Shock Patient
Steps of Intubation:
1. Check patient cricoid – can you do a cric? and is LMA close by?
2. Have someone get and set up the ventilator.
3. Get an epinephrine or norepinephrine drip ready or running or a
syringe of push dose epinephrine. Try to get MAP >65
4. Pre-oxygenate with high flow Bag mask oxygen for 3 minutes
5. Scopolamine 0.4 mg (amnestic but doesn’t drop BP)
6. Ketamine 0.25 – 0.5 mg/kg or Propofol 0.1 -0.15 mg/kg
7. Succinylcholine 2 mg/kg or Rocuronium 1.6 mg/kg
 Hypotensive, Shock Patient
Steps of Intubation:
7. Intubate
8. Vent settings.
AC mode
Tidal volume 6 – 8 cc/kg,
FiO2 100%
RR 10-14
PEEP/EPAP 0 up to 5 cm H20 to maintain SpO2 >90%
Elevated
ICP
Patients
 Elevated ICP Patient
Causes of elevated ICP include:
stroke
trauma
infection.

Airway management is the same regardless of cause.

The goal is to minimize any increase/fluctuations of ICP
through use of certain medications and intubation techniques.
 Pathophysiology of ICP
Cerebral Perfusion Pressure (CPP) is auto regulated over a wide
range of mean arterial pressures (MAP)
CPP can usually be maintained through MAPs of 60 – 160 mm Hg.
With severe elevations of ICP, autoregulation is lost. If the patient
is hypotensive the result can be cerebral hypoperfusion and
hypoxemia, which then results in more cerebral edema and
increasing ICP.
As well, excessive systemic hypertension can increase ICP.
 Pathophysiology of ICP
The ‘goal’ MAP should be approximately 100 – 110 mm Hg.
MAPs above or below this can both lead to increasing ICP.
Many airway techniques increase ICP.
Reflex Sympathetic Response to Laryngoscopy (RSRL)
RSRL is stimulated by the sensory innervation of the
supraglottic larynx. Result is release of catecholamines.
RSRL is usually induced by laryngoscopy.
 Intubation of ICP Patients
General Goals and Principles:
Gentle intubation
Try to avoid prolonged intubation (> 45 seconds)
Ensure a pre intubation neuro assessment – patient’s ability to interact,
pupillary response, motor response.
Maintain oxygenation – consider nasal cannula use during intubation.
RSRL occurs in comatose patients as well, so use appropriate induction
and neuromuscular blocking agents during intubation.
 Rapid Sequence Intubation for
Increased ICP Patients
Pretreatment
It has been thought that lidocaine may blunt RSRL and
therefore has been proposed as a pretreatment. However most
current research suggests it is of little or no value.
Some authors also suggest giving Fentanyl with the lidocaine,
although NOT to hypotensive patients.
For pure elevated ICP and no systemic hypotension, beta
blockers (labetolol, Esmolol) have been advocated to reduce
reflex hypertension and tachycardia due to laryngoscopy.
 Rapid Sequence Intubation for
Increased ICP Patients
Induction Agents
Etomidate is considered first choice, but unavailable.
Ketamine 2 mg/kg is good second choice.
Ketamine stimulates catecholamine release which increases
MAP and cerebral blood flow. It is good for induction of
normotensive or hypotensive ICP patients.
For hypertensive patients, if using Ketamine, you may want
to have some IV beta blockers on hand (labetalol)
 Rapid Sequence Intubation for
Increased ICP Patients
Neuromuscular Blockade :
Succinylcholine 1.5 – 2 mg/kg
Historically concern was that Succ may cause a
temporary increase in ICP (animal studies). Human
studies have failed to describe this effect.
No benefit has been shown to using Rocuronium.
 Mechanical Ventilation in
Elevated ICP Patients
Ventilator Settings
AC Mode
Tidal Volume 6-8 cc/kg IBW
FiO2 100% initially
EPAP (PEEP) use if necessary to get 95% O2 Sats.
Respiratory Rate: start 10/min. Increase until EtCO2 35
mm Hg, then send blood gas.
Asthmatic
Patients
 Asthmatic Patient

Approximately 4% of asthma patients presenting to

the ER will need intubation.
Of those intubated, ~ 7% die.
Of survivors, the one and three year mortality from
future asthmatic attacks is 10 and 23% respectively.
 Asthmatic Patient

Fatalities from asthma: 2 groups:

Slow onset – (80%) have symptoms for at least 12
hours up to several weeks. Death is due to mucus
plugging.
Rapid onset – (20%) have symptoms from 2-6
hours prior to death. Death is due to bronchospasm.
 Pathophysiology of Severe Asthma
1. Increased work of breathing from airway resistance.
2. Depletion of catecholamines during prolonged
exacerbations.
3. Increased intrathoracic pressure from air trapping,
which in turn increases work of breathing,
decreases preload and increases afterload.
 Decision to Intubate the Asthmatic
Is purely a clinical decision.
Consider the patient who can’t speak in full sentences, has
decreasing mental status or who is clearly tiring out.
ABGs are NOT of value in decision making.
The problem is that by intubating an asthmatic you can
actually cause cardiac collapse and barotrauma
(pneumothorax). In other words, asthmatic intubations are
very high risk, fraught with complications and bad outcomes.
However not intubating can result in an even worse outcome.
 Decision to Intubate the Asthmatic
Clinical signs of immanent respiratory collapse in an asthmatic:
1. Brief, fragmented speech
2. Decreased mental status
3. Inability to lie supine
4. Rapid, shallow breathing (RR > 30 breaths/minute)
5. Accessory muscle use, chest wall contractions.
6. Agitation
7. Profound diaphoresis
Non Invasion Ventilation in Asthmatics
Can be worth a try as try to avoid intubation if possible.
Use IPAP 8 cm H2O, EPAP (PEEP) 0-3 cm H2O
However if there is no improvement with NIV, consider
intubation.
If the patient is only maintaining their oxygen saturations or
PCO2 levels on NIV, they will likely continue to tire out and
require intubation.
Non Invasion Ventilation in Asthmatics
If using NIV and patient worsening or if unable to tolerate
NIV at all then give:
Ketamine 1.5 mg/kg over 30 seconds, (if no IV 5 mg/kg IM)
then 1 mg/kg/hr. Titrate to effect.
If still worsening with this then they need intubation.
 Steps in Asthmatic Intubation
1. Check patients neck for possible cric. Have kit and LMA.
2. Call ICU doc (or at least on call Respiratory Tech)
3. Pre-oxygenate with bag mask free flow
4. Have patient somewhat upright.
5. Use large ETT (size 8)
6. If time permits, Lidocaine 1.5 mg/kg 3 minutes prior.
7. Ketamine 2 mg/kg
8. Succinylcholine 2 mg/kg or Rocuronium 0.6 – 1.2 mg/kg
 Steps in Asthmatic Intubation
Mechanical Ventilation
1. Asthmatics are hypercapnic and tachypnic.
2. They need deep sedation to prevent asynchrony with vent
and resultant dynamic hyperinflation.
3. Use non histamine releasing opioid – Fentanyl drip.
 Steps in Asthmatic Intubation
Mechanical Ventilation – Ventilator settings
AC mode
RR start at 6-10 breaths/min
Tidal Volume 7-8 ml/kg IBW
FiO2 100% initially
Inspiratory Time – set low 0.6 – 0.8 seconds. Allows for more
time for expiration. (or if using LTV 1000, set I:E ratio 1:4 – 1:5)
PEEP/IPAP 0- 2 initially.
Fentanyl drip or Propofol drip
 Steps in Asthmatic Intubation

Mechanical Ventilation – Ventilator settings

Once intubated, you have done nothing for the actual disease process.
Patients need continuous bronchodilators.
Dynamic Hyperinflation in Asthmatics

Dynamic hyperinflation occurs when the expiratory time is

insufficient to allow complete exhalation thus causing
progressive hyperinflation.
Bronchospasm, mucous plugging, airway edema and
inflammation all add to decreased expiratory flow and thus
hyperinflation (‘auto PEEP’).
 Dynamic Hyperinflation in Asthmatics
Result:
1. Cardiovascular collapse (PEA) – from increased
intrathoracic pressure, decreased venous return which in turn
causes CV collapse.
2. Barotrauma (pneumothorax)
3. Increased work of breathing (AutoPEEP)
 What to do if the asthmatic codes
on the Ventilator.
Disconnect the ventilator and bag the patient.
DOPES mnemonic:
D- displacement – of tube. Consider re-intubation.
O- obstruction of tube (try to pass suction catheter)
P- pneumothorax – use EDE to look for pneumo.
E- Equipment – check the vent settings.
S- Stacked breaths – AutoPEEP. You correct this by
disconnecting the vent.