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The Airway Jedi

Tips and tricks on intubation, airway management, anesthesia and safe patient care

Pediatric Airway Risks: Inefficient

Mechanics of Breathing
Posted on February 25, 2019

Inefficient mechanics of breathing is one major risk factor for infants and young children because it
increases work of breathing. In many ways pediatric anatomy and physiology predisposes a child to
respiratory distress and respiratory failure.

(Illustrations copyright Whitten, Pediatric Airway Management: A Step By Step Guide)

Mechanics of Normal Breathing

Normal quiet breathing is effortless. The rate is neither too fast nor too slow, however, rate varies greatly
depending on age and metabolic rate. The chest rises and falls easily and symmetrically. Air flows into and
out of the lungs through the open airway based on changes in air pressure.

Adult Chest Cavity Anatomy Makes Breathing Efficient

Let’s start by reviewing the adult mechanics of breathing. The angulation and rigidity of the ribs during the
breathing cycle maximizes efficiency in the adult. The lungs are housed in a skeletal cage formed by the
ribs. In order to initiate airflow into the lungs, pressure in the lungs must drop below atmospheric pressure.
The body accomplishes this by expanding the airtight chest cavity, thereby decreasing the pressure inside.
Two motions are involved:

expansion of the rib cage by contraction of intercostal muscles

contraction and descent of the diaphragm

The ribs form three functional groupings. The first rib attaches rigidly to the sternum to anchor the rib cage.
It hardly moves during respiration.

The 8th through 12th ribs expand mostly laterally during inhalation. This effectively increases intra-
abdominal space for organs pushed downward by the diaphragm. The motion is like a bucket handle,
swinging up and down toward the side away from the centerline and expanding the width of the chest

The 2nd to 7th ribs flexibly expand mostly anterior-posterior with a little lateral motion. This motion is like a
pump handle — mostly up and down in the front of the chest, expanding the depth of the chest cavity.

— a. Ribs 8-12 expand mostly laterally, like a bucket handle. b. Ribs 2-7 expand mostly anteriorly, like
a pump handle.

Diaphragmatic Contaction Is The Bellows

The diaphragms are two large dome-shaped sheets of muscle separating the thoracic cavities from the
abdominal cavity. As the diaphragms contract with each inhalation, they act like a bellows. During inhalation
the bellows descends and flattens, increasing intrathoracic volume and decreasing intrathoracic pressure.
This pulls air into the lungs as they inflate.

During exhalation, the diaphragm and intercostals relax. As a result, the diaphragms rise and become dome
shaped again, decreasing intrathoracic volume and raising intrathoracic pressure. Lungs deflate. The patient
exhales. Unless there is obstruction, exhalation is passive, requiring little energy.

Full contraction of the intercostals and the diaphragm allows for much greater expansion of the chest cavity
and produces a larger breath, assuming that air is free to flow into the lungs..
— The diaphragm contracts and relaxes during breathing, expanding and contracting the volume of
the thoracic cage. The associated air pressure changes inside the thoracic cavity cause the lungs to
expand (a) and to deflate (b).

What Factors Affect Ease of Air Flow?

A variety of factors affect how easily that air flows:

breathing rate
too rapid or too slow a rate impairs air movement
inspired tidal volume
ventilating close to dead space volume causes CO2 levels to rise
airway resistance
smaller airways have higher resistance than larger airways
increased resistance impairs airflow
tissue resistance
increased frictional resistance of lung tissues and chest wall increases work of breathing and
limits tidal volume
elastic recoil
with weaker elastic recoil, airways tend to remain partially collapsed on exhalation rather than
passively reinflate to baseline
poor compliance makes it harder to distend the lungs, limiting air movement and increasing the
work of breathing

Changes in any of these parameters can significantly affect adequacy of respiration and how hard it is to
take a breath.
Anatomical Features That Increase Pediatric Work of Breathing

When the patient works hard to take a breath, for example against an obstruction, he generates a more
negative pressure inside the chest cavity.  The intercostal muscles more fully contract. Retractions, noisy
breathing, and a rocking chest wall motion are common. As respiratory failure progresses, the pattern of
respiration becomes more and more inefficient and ineffective. Work of breathing increases.

In the patient exhausted to the point of respiratory collapse, or in the patient with respiratory depression due
to altered mental status, there may be little effort to breathe. Hypoventilation worsens hypoxia, hypercarbia,
and respiratory acidosis. Level of sedation increases, further depressing respiratory drive.

Normal infants and small children have significant anatomic predispositions to serious disruption of their
mechanics of breathing if they become sick or injured.

— The differences in the mechanics of breathing of small children compared to adults places them at
much higher risk of respiratory failure.

Evaluating the degree of respiratory compromise is a judgment call. Mild or potential obstruction may have
no signs or symptoms at all. In certain patients such as facial burn victims or patients having a severe
allergic reaction, mild airway obstruction can convert to total obstruction quickly as edema forms. Constant
reassessment is important so that you may intervene early if necessary — before the airway is lost.

The Infant’s Chest Wall Increases The Work Of Breathing

In the infant or small child, the chest wall is more box-like in shape compared to the adult’s. The ribs are
more at right angles to the vertebral column and won’t be angulated like an adult until age 10 years. This
makes the pediatric chest wall mechanically less efficient and limits potential lung expansion.

— The shape and flexibility of the infant chest, and the shape and immaturity of the diaphragmatic
muscle both increase the risk of respiratory failure when the child is ill.

Babies “belly breathe”. To take a deep breath, the infant’s chest therefore expands a little and the abdomen
rises a lot as the diaphragm descends, pushing abdominal contents down and out of the way.  Anything that
interferes with descent of the diaphragm, such as a stomach or intestines distended with air or liquid, can
seriously impair an infant’s breathing.

The infant’s chest wall is also more compliant than an adult’s, with an elastic recoil close to zero because of
the lack of rib cage ossification. When the infant takes a breath against resistance, such as with airway
obstruction or poor pulmonary compliance from pneumonia, the chest wall actually moves inward as the
belly moves outward. The inward movement of the chest wall decreases the amount of air that enters. A
rocking chest wall motion is very common in children with even partial airway obstruction.
— The inefficient mechanics of infant/toddler breathing increases the risk of respiratory failure.

Because chest wall structure and “belly breathing” limit the ability to increase tidal volume, the baby must
rely on respiratory rate increases to compensate for stress. The harder a child tries to breathe, the less
efficient and more labored breathing becomes.

You can see video of a toddler with croup and the signs of airway obstruction described above here.

Monitor Your Pediatric Patient Carefully

Watch for signs of airway obstruction.

Infants and toddlers tire easily when they have airway or respiratory compromise. Respiratory distress can
easily progress to respiratory failure. Assess your patients carefully and monitor for change. Always ask
yourself: “How well is my patient breathing?” Follow the link below for discussions and video of recognizing
and treating airway obstruction.

Recognizing Airway Obstruction May Save Your Patient’s Life

Click here see a video clip comparing the signs of airway obstruction in a pediatric patient with a
more normal breathing pattern once the obstruction is relieved.

May The Force Be With You

Christine E Whitten MD, author:
Anyone Can Intubate: A Step By Step Guide
Pediatric Airway Management: A Step By Step Guide


Click on the covers to preview books at amazon.com


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Posted in Airway obstruction, Pediatric anesthesia, Respiratory physiology | Tagged airway obstruction,
differences pediatric airway anatomy, mechanics of breathing, pediatric airway obstruction, pediatric
mechanics of breathing, pediatric risk of respiratory failure, risks of respiratory failure in children, signs
of airway obstruction | Leave a reply

ETCO2: Valuable Vital Sign To Assess

Posted on January 24, 2019

Like pulse oximetry before it alerting us to changes in oxygenation, end-tidal CO2 monitoring, or ETCO2, is
rapidly becoming an additional vital sign. We routinely use ETCO2 to provide information on ventilation. But
ETCO2 can also provide valuable information on the adequacy of cardiac perfusion. It can be an essential
tool in ensuring optimal, high quality chest compressions during cardiac resuscitation.

Some Physiology

Ventilation and oxygenation are different. Ventilation exchanges air between the lungs and the atmosphere
so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of
oxygen to the body. Under normal circumstances, hyperventilation with room air will lower your arterial
carbon dioxide content (PaCO2) significantly, but not change your oxygen levels much at all. On the other
hand, if you breathe a high concentration of oxygen without changing your respiratory rate, your arterial
oxygen content (PaO2) will greatly increase. However, your PaCO2 won’t change.

Oxygenation changes PaO2. Ventilation changes PaCO2.

Some History Of Old Fashioned Monitors

When I started my anesthesia training in 1980, we monitored the patient with a manual blood pressure cuff,
EKG, pulse, and temperature. Pulse oximetry and capnography were not yet in clinical use. If we wanted to
determine PaO2, or PaCO2, we needed to draw a blood gas. Frequent blood gas determinations, or the need
to monitor continuous perfusion pressures, often necessitated placement of an arterial line.

To provide an indirect indicator of perfusion, we used a precordial stethoscope attached to an earpiece to

continuously listen to heart sounds. An attentive anesthesiologist could use changes in the loudness or
crispness of the heart tones to alert him or her to changes in cardiac output. As the patient got lighter or if
the blood pressure rose, heart tones got louder and sharper. Low blood pressure brought muffled, faint heart
tones independent of heart rate. We were essentially using our ears in place of the plethysmograph
waveform that pulse oximetry would eventually provide.

Pulse Oximetry

Pulse oximetry revolutionized anesthetic safety. Pulse oximetry was a non-invasive way of measuring
oxygen saturation. Oxygen saturation  is the percent of Hemoglobin (Hgb) binding sites in the blood that are
carrying oxygen. Hemoglobin is a chemical molecule in the red blood cell (RBC) that carries oxygen on
specific binding sites. Each Hgb molecule, if fully saturated, can bind four oxygen molecules. Depending on
conditions, Hgb releases some percentage of the oxygen molecules to the tissues when the RBC passes
through the capillaries.  We can measure how many of these binding sites are combined, or saturated, with
oxygen. This number, given as a percentage, is called the oxygen saturation or simply O2 Sat, commonly
pronounced “Oh Two SAT”. it is also referred to as SPO2. When all the Hgb binding sites are filled, Hgb is
100% saturated.

Oxygen saturation and PaO2 are NOT equivalent, and they have significant clinical differences that you can
read about here.

What’s The Difference Between Oxygen Saturation And PaO2?

However, with pulse oximetry we could now measure oxygen saturation. We could immediately see in real
time if our patient was hypoxemic or hypoxic and, if so, diagnose the cause and treat it before harm was

Watching the quality of the waveform, along with the oxygen saturation, told us valuable information about
perfusion. The higher the amplitude of the wave, the stronger the pulse was. The more damped out the
waveform appeared, the weaker the pulse.

With this new tool, and with the OR environment becoming increasingly noisy, use of the precordial
stethoscope has largely faded away. Pulse oximetry quickly spread to ICUs, on wards, and clinics to monitor
patients at risk. Pulse oximetry has become a fifth vital sign.

I believe we are seeing the same transition with end-tidal CO2 monitoring.

END TIDAL CO2 Has Many Uses

What Is ETCO2?

Capnography refers to the process of measuring the partial pressure of end-tidal CO2 in each expired
breath. Providers measure the value of ETCO2 in each exhaled breath with a very thin tube inserted into the
breathing circuit or the patients oxygen mask or nasal prongs.

The waveform (capnogram) that you then see on the capnography monitor provides a real time recording of
the patient’s respiratory rate, pattern and depth of breathing, and of course the value of CO2 exhaled. These
measurements help the provider evaluate adequacy of ventilation.
— The author looks at the capnography waveforms during an anesthetic to evaluate end-tidal CO2
(ETCO2) values and the adequacy of ventilation.

ETCO2 Helps Assess Adequacy of Ventilation

We routinely measure ETCO2 for every patient in the operating room. We use it increasingly for conscious
sedation provided in treatment rooms and on the wards. ETCO2 and PaCO2 are not the same value. PaCO2
is the concentration of CO2 in arterial blood. ETCO2 is the concentration of CO2 in the exhaled breath, and is
close to alveolar CO2. ETCO2 is usually about 5 mmHg below PaCO2. This makes sense. If the
concentration of CO2 in the alveoli were higher than in the blood stream, CO2 could not enter the lungs and
would not be exhaled.

ETCO2 offers a valuable trending tool to monitor and control ventilation. It alerts us immediately if the
patient hyperventilates, hypoventilates, or becomes apneic.

A normal trace appears as a series of rectangular waves in sequence, with a numeric reading
(capnometry) that shows the value of exhaled CO2. “Normal” ETCO2 is in the range of 35 to 45 mmHg.
In hyperventilation, the CO2 waveform becomes smaller and more frequent, and the numeric reading
falls below the normal range.
In hypoventilation), the waveform becomes taller and less frequent, and the numeric reading rises
above the normal range.
Fattening of the waveform indicates an airway obstruction.
If the series of rectangular waves become a flat line, the patient is not breathing.
Use ETCO2 In The Perioperative Areas

I believe we should increase our use of ETCO2 in our perioperative areas and procedure rooms. Patients
receiving conscious sedation on the ward or recovering from anesthesia are arguably at more risk of airway
compromise than patients in the operation room. They are often under more intermittent observation. I
encourage my recovery room nurses to use end-tidal CO2 monitoring when they are caring for patients at
risk of hypovention or obstruction such as those:

exhibiting prolonged sedation,

with opioid induced respiratory depression,
history of sleep apnea,
any cardiovascular instability
any time they are worried about a particular patient.

For clinical examples of how ETCO2 can change during clinical care and how we can use ETCO2 to guide
our treatment, read more here.

How Does Hypoventilation Cause Hypoxemia?

Anatomic Dead Space Affects Hypoventilation

Don’t Withhold Oxygen From That CO2 Retainer

ETCO2 Helps Verify Intubation

Esophageal intubation or accidental extubation are always risks.  Monitoring ETCO2 increases safety. The
continued presence of CO2 in the exhaled breath can only mean placement of the tube in the trachea. Loss
of the ETCO2 trace indicates extubation or disconnection from the circuit the ETCO2.

The shape of the capnography waveform can also indicate the severity of problems such as bronchospasm
or other cause of increased resistance to breathing or exhalation.

ETCO2 Is An Early Sign Of Poor Perfusion or Cardiac Arrest

Oxygen delivery and carbon dioxide removal depend on three systems: lungs, blood and circulation. It’s
important to remember that adequate oxygen absorption and delivery depends on the interaction between
lung function and circulation. As soon as cardiac output starts to fall, blood perfusion through the lungs
falls. CO2 now has more difficulty being carried to the lungs for exhalation. This leads to a rise in PaCO2 in
the blood stream and a fall in ETCO2.
— Oxygen delivery and CO2 removal from the lungs depend on lung function, blood hemoglobin
concentration, and circulation. Disturbance in any of these risks respiratory distress or failure. If
lung function and Hgb are stable, then changes in ETCO2 imply changes in perfusion.

In the operating room, I often see a drop in ETCO2 even before blood pressure itself starts to fall. As long as
there is some circulation, there will be some ETCO2 present, even if you can’t feel a weakened peripheral
pulse. ETCO2 can therefore be an early warning of developing shock, or pulmonary embolus.

If ETCO2 drops to zero, then the heart has stopped. This is true even for patients who are continuing to
receive manual ventilation, because although air is moving into and out of the lungs, there is no CO2 being
delivered to exhale. Loss of ETCO2 can also be the first sign of cardiac arrest. A patient may still have an
EKG trace in pulseless electrical activity, but not have circulation and therefore will not have a measurable

Here is a simplified flow chart for using ETCO2 to alert you to perfusion or ventilation problems.
— ETCO2 is a valuable tool for early recognition of poor perfusion and cardiac arrest.

Adequacy Of Chest Compressions

Good quality CPR depends on high quality chest compressions. When I practice with my staff during Critical
Event Training, failure to perform adequate chest compressions is common, a fact that reinforces the need
to routinely practice.

During one particular exercise, one diminutive RN was having trouble making her compressions meet the 2-
2.5 inch depth, 100 compressions per minute on the manikin (as measured by our test device). The rest of
the team encouraged her until she got it correct. The following weekend her Dad suffered a cardiac arrest in
her living room. She went into action delivering chest compressions while the family dialed 911. Her father
made a full recovery, and she gave credit to the training she had just received.

Good quality compressions can save lives. ETCO2 is one valuable tool we have to tell us that good quality
compressions are being delivered. The higher the ETCO2 measured during compressions, the better the
perfusion being supplied by CPR. The goal should be to maintain ETCO2 no lower than 10-20 mmHg. An
ETCO2 below 10 mmHg is associated with poor outcome.
Good quality chest compressions will also generate a waveform on the ETCO2 capnograph that allows you
to estimate the rate of compressions.

Return of Spontaneous Circulation

Return Of Spontaneous Circulation (ROSC) is accompanied by a sharp rise in ETCO2, usually within a range
higher of 35-45 mmHg or higher as CO2 is now delivered to the lungs and then exhaled. This is often
accompanied by a palpable pulse and a rising blood pressure.

Good news. However, the next 10 minutes are a very dangerous time for your patient. The heart is still
stunned and cardiac output may still be poor. Current consensus guidelines for cardiopulmonary
resuscitation (CPR) recommend that chest compressions resume immediately after defibrillation attempts
and that rhythm and pulse checks be deferred until completion of 5 compression:ventilation cycles or
minimally for 2min.

One study showed that perfusion remained poor for greater than 2 minutes in 25% of patients successfully
defibrillated [1]. Continue to monitor that ETCO2! This is now your powerful tool to see if perfusion is
adequate and being maintained. Assuming ventilation is consistent, a drop in ETCO2 during this period can
indicate failing circulation. A loss in ETCO2 can mean re-arrest.

Check to make sure your endotracheal tube is still properly positioned, check a pulse, and decide your
appropriate actions.

Prognosis During CPR Efforts

ETCO2 below 10 mmHg can be caused by poor compression technique.  It can also be caused by low
perfusion and metabolism from prolonged shock despite good compressions — in other words the cardiac
pump is damaged and failing. If high quality compressions are being delivered, and an advanced airway is in
place allowing accurate ETCO2 measurements, then an ETCO2 persistently below 10mmHg after 20 minute
of resuscitation is a poor prognostic sign. It can be used as an indication to consider terminating
resuscitation efforts.

On the other hand if ETCO2 is above 15mmHg, or it continues to rise, that is one indication that
resuscitation efforts should continue, as the brain and heart are being perfused. There are case reports of
patients surviving prolonged CPR with higher ETCO2 readings.

We’ve come a long way since I had to depend on a precordial stethoscope, skin color and finger on the pulse
to supplement blood pressure and EKG to assess perfusion in my patients. Capnography and pulse
oximetry are powerful tools. However, don’t forget that in the absence of either, you can still look at your
patient and be vigilant. Without vigilance, all the tools in the world will not protect your patient.

May The Force BeWith You

Christine E Whitten MD, author
Anyone Can Intubate: A Step By Step Guide
Pediatric Intubation: A Step By Step Guide
1. Pierce AE, Roppolo LP, Owens PC, Pepe PE, Idris AH. The need to resume chest compressions
immediately after defibrillation attempts: an analysis of post-shock rhythms and duration of pulselessness
following out-of-hospital cardiac arrest. Resuscitation. 2015 Apr;89:162-8. doi:
10.1016/j.resuscitation.2014.12.023. Epub 2015 Jan 15.


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Posted in Anesthesia, Respiratory physiology, Safety | Tagged capnography, end-tidal CO2 monitoring,
ETCO2, ETCO2 and perfusion, ETCO2 and ROSC, ETCO2 monitoring, ETCO2 vital sign | Leave a reply

# 1 Review Article for Anesthesiology News

2018: 10 Rules for Approaching Difficult
Intubation by Christine Whitten
Posted on January 3, 2019

And the numbers are in, my review article for Anesthesiology News was actually THE MOST viewed article
on the site for the whole year!

I’m afraid working overtime over the holidays and family trips have gotten in the way of posting this
December but I’m already hard at work for 2019, including a new article for Anesthesiology News.
In the meantime please enjoy this review on the “10 Rules for Approaching Difficult Intubation: Always
Prepare for Failure.”

I have included the longer formal link below in case the short link above fails to connect.


May The Force Be With You!

Christine E. Whitten MD
Anyone Can Intubate: A Step By Step Guide, 5th Edition
Pediatric Airway Management: A Step Be Step Guide

Please click on the covers to preview at amazon.com


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Posted in Anesthesia | Leave a reply

Conscious Sedation: Is Your Patient

Posted on December 17, 2018

Change in mental status can occur from conscious sedation or opioid administration, hypotension, sepsis,
head trauma, acid-base imbalance, alcohol, drugs, or toxins. Change in level of consciousness often affects
breathing, sometimes to the point of causing severe hypoxia, arrythmias and cardiac arrest. Let me repeat
that. Anything that alters consciousness can alter respiration, which can lead to the vicious cycle of
hypoventilation, hypercarbia, and hypoxia. If you don’t recognize inadequate respiration —and treat it— the
patient can suffer injury or die. Let’s look at a common clinical example of altered consciousness —
conscious sedation.

Everyday, in all of our practices, we purposefully try to alter our patient’s level of consciousness in order to
tolerate a procedure. We often take the safety of procedural conscious sedation for granted. After all, we’re
only giving a little sedation to make the patient relaxed, calm and more comfortable. Although problems are
rare, patients can become hypoxic, hypercarbic, and apneic with conscious sedation, and some have died.
The deaths of the celebrities Michael Jackson in 2009, and Joan Rivers in 2014 were related to hypoxia
from loss of the airway under deep sedation. Respiratory depression represents the principal potential risk
introduced with conscious sedation. If left unrecognized and untreated, it can be the cause of serious

Sleep and Sedation Affect Respiration

To understand why mental status change increases respiratory risk, let’s start with the respiratory effects of

Janet Smith is a 44 year-old healthy patient who is scheduled for correction of a trigger finger with
ambulatory surgery under conscious sedation tomorrow at the surgicenter. She’s worried, so it takes her a
long while to fall asleep. When she finally does sleep, her respiratory drive begins to change.

Does oxygen saturation change with normal sleep? For healthy young people between 19-25 years of age,
there appears to be no change in oxygen saturation with sleep (1). Other studies looking at a more varied
population up to age 64 did find up to an 11% drop in oxygen saturation(2,3,4). Adding a comorbidity such
as chronic bronchitis is also associated with saturation drops of about 10%. So the answer seems to
depend on age, presence of comorbidities and how ventilation changes with sleep for that particular person
due to such things as snoring.

With normal non-REM sleep, PaCO2 rises about 3-7 mmHg as the body’s response to increased CO2, or
hypercarbia, is blunted. Tidal volume and respiratory rate decrease. Pharyngeal muscles as well as muscles
of the tracheobronchial tree relax, increasing airway resistance and predisposing to potential obstruction,
such as snoring.

Although some of us sleep more deeply than others, we usually awaken easily if someone talks to us, or the
alarm goes off. If we obstruct our airway and begin to snore, we typically rouse ourselves enough to take a
deep breath and turn over. When we don’t easily rouse from sleep induced airway obstruction then we may
have sleep apnea. Now, let’s look at how giving sedation to a patient like Janet Smith interferes with her
ability to rouse.

Conscious Sedation

When Janet gets to the preop area, she’s nervous and tells her nurse that she didn’t sleep much the night
before. Her anesthesia provider gives her 1 mg of midazolam IV to relax her. Her care team then takes her to
the OR.

With light conscious sedation she will continue to respond to verbal commands. Cognitive function and
coordination may be impaired. She can still carry on a conversation, although she may not remember details
of it.  Cardiac and ventilatory function are usually not altered a lot. Like natural sleep, it’s common for the
patient’s respiratory rate and tidal volume to decrease slightly. She’ll lie comfortably on the OR bed while
we’re attaching her monitors and going through the final safety checks.

Moderate Sedation

Of course, many patients like to nap during their surgical procedure and in this case the anesthesiologist
starts a background infusion of propofol at a low rate of 25 mcg/kg/hr to induce a moderate level of
conscious sedation while things are being set up. Using this technique, the level of propofol in Janet’s
bloodstream builds slowly and she will get progressively sleepier until she’s moderately sedated.

With moderate sedation, a patient still responds to commands, but she might require a tap on the shoulder
to rouse and answer a question. She still shouldn’t require any help holding her airway open, but there may
be more of a tendency to snore, especially if the patient has a history of snoring. Snoring is a sign of airway
obstruction and is a warning sign that the patient needs to be monitored more closely.

Injecting local anesthetic can be a bit painful. As the surgeon gets ready to inject the local anesthetic the
anesthesiologist will often give just a little more sedation so that the patient does not remember the
injection. This could be more midazolam, or a short acting opioid like fentanyl. However, in this case Janet is
given a small bolus of 50 mg of propofol IV. The strategy behind this technique is to temporarily induce a
deeper level of sedation during the local anesthetic injection itself. Sedation from a Propofol bolus wears off
in a few minutes, allowing Janet’s level of consciousness to return back to the prior moderate level of
sedation for the rest of the procedure.

Deep Sedation

With deep sedation the patient is not easily arousable, but will still respond with repeated or painful
stimulation. The deeply sedated patient might occasionally require help holding her airway open and
spontaneous ventilation might become inadequate. Cardiovascular stability is usually maintained.
Janet tolerates the injection well and appears to be sleeping. However, after the injection is finished, the
anesthesiologist notices that Janet is no longer breathing well. Her airway is obstructed. He tips her chin
back and lifts her jaw to open her airway and she takes a deep breath. He has to periodically shake her
shoulder for the next few minutes to remind her to take deep breaths. After about 2 minutes she starts
breathing well again on her own.

Unconsciousness: General Anesthesia

What just happened? It can be easy to take a patient from deep sedation to general anesthesia. With general
anesthesia the patient is completely unresponsive and airway support of some type is often required, even
when the patient is breathing spontaneously. Cardiovascular changes are common. After the extra Propofol
bolus was given, Janet continued to breathe well — as long as she was being stimulated by the pain of the
injection. After that stimulus stopped, she slipped into an even deeper plane of sedation. The same scenario
can happen postoperatively upon arrival in the recovery room when stimulation ceases (see prior

Perhaps Janet was just more sensitive to sedatives than some patients. Perhaps it was because she was
sleep deprived from her insomnia the night before. Maybe it was the speed with which she got repeated
doses of medications in such a short time that added up to too much sedation.

In our case, the anesthesiologist was watching carefully and noticed immediately that he needed to assist
Janet’s breathing. Janet’s level of sedation could have eventually become light enough, or her CO2 levels
high enough, to allow her to start breathing again on her own. The question is whether she would start
breathing again quickly enough — before she became hypoxic or extremely hypercarbic. Prolonged hypoxia
and hypercarbia can cause complications, including potential cardiac arrest. And hypoxia and hypercarbia
both depress mental status, which, if severe enough can further depress respiration, making complications
more likely.

Sedation Is A Continuum

All four stages of sedation are a continuum. At any point with just a little more sedation or a little less
stimulation, your patient can stop breathing well. In my job as an anesthesiologist, I see on a daily basis how
easy it is to overshoot and cause a patient to become apneic using moderate to deep sedation. And if the
patient is frail or sick, or extremely old or young, sometimes even a small dose of sedative or opioid, — one
that would normally induce just light sedation — can cause apnea and hypoxia. Sedation, and its effect on
respiration, are not just dose related, they depend on the status of the patient receiving that dose and what
else is happening to that patient at that time. Be vigilant.


Opioid Induced Respiratory Depression: A Balance In The Force

Codeine Risk in Children, Especially Those With Sleep Apnea

May The Force Be With You

Christine Whitten MD, author
Anyone Can Intubate: A Step By Step Guide
Pediatric Airway Management: A Step By Step Guide
Click the cover to preview or purchase book at Amazon.com

1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC459897/pdf/thorax00225-0033.pdf
2. Gimeno F, Peset R. Changes in oxygen saturation and heart frequency during sleep in young normal
subjects. Thorax 1984;39(9):673-675.
3. Block AJ, Boysen PG, Wynne JW, Hunt LA. Sleep apnea, hypopnea and oxygen desaturation in normal
subjects. A strong male predominance. N Engl J Med. 1979 Mar 8;300(10):513–517. [PubMed]
4. Douglas NJ, Calverley PM, Leggett RJ, Brash HM, Flenley DC, Brezinova V. Transient hypoxaemia
during sleep in chronic bronchitis and emphysema. Lancet. 1979 Jan 6;1(8106):1–4. [PubMed]


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Posted in Anesthesia, Respiratory physiology | Tagged anesthesia and mental status changes, conscious
sedation, sedation, sedation and apnea, sedation and mental status changes, sedation and respiration,
sedation and respiratory arrest | Leave a reply

The MAC Blade, The Vallecula, and the

Hyoepiglottic Ligament
Posted on October 22, 2018
Correct placement of the tip of the MacIntosh , or MAC, blade is critical to successful intubation. When
learning to intubate, novice intubators often prefer the MAC blade because:

curved shape makes it easier to insert under the upper teeth,

wide area makes it easier to balance the head on the blade during the lift,
easier to control the tongue with the side flange.

However, if you don’t have the tip of the blade positioned properly in the vallecula, you wil not lift the
epiglottis and you will have a poorly view of the larynx. Why is this?

How The MacIntosh (MAC) Blade Works

A quick review of the anatomy is warranted. The vallecula is the mucosa covered dip between the back of
the tongue and the epiglottis. The hyoepiglottic ligament runs under the vallecular mucosa and connects the
hyoid bone to the back of the epiglottis.

— The hyoepiglttic ligament connects the hyoid bone to the back of the epiglottis
— Lateral Xray clearly showing the hyoid bone, the epiglottis and the
vallecula connecting them

The curved MAC blade is designed to match the curve of the tongue and to put point pressure on the
hyoepiglottic ligament. With pressure in the vallecula on this ligament, the epiglottis is pulled upward. The
curved blade can then pull the tongue and soft tissue under the tongue forward, bringing the glottis into
— The tip of the curved blade presses on the vallecula, allowing you to lift the epiglottis by pulling on
the folds at its base. The glottis is revealed with the epiglottis hanging above it.

In this video, posted on YouTube by AIMEairway.ca, you can see that if you lift too early, when the blade is
not placed far enough into the vallecula to engage the ligament, then pressure from the blade tip does not
lift the epiglottis. Advancing a little farther, placing the tip in the vallecula does lift the epiglottis.

If you advance the blade tip too far into the vallecula, it will press on the base of the vallecula and force the
epiglottis down, obscuring your view of the glottis. The difference between lifting too early or too late (by
placing the blade tip too shallow and too deep respectively) can be just a mm or two.
Valleculoscopy using a curved direct laryngoscope blade

Size of the MAC Blade matters

MAC blades come in different sizes to match your patient. However, you must choose the correct size to
apply the correct point pressure on the hyoepiglottic ligament. The correct size blade must be long enough
to reach into the vallecula. You can estimate the correct size by holding the blade adjacent to the patient’s
lower jaw and measuring it against the projected location of the vallecula.

— Laryngoscope blades come in different sizes and you should choose the optimal size if you can.

Blade Too Short

If the blade is so short that it doesn’t reach the vallecula, then lifting the blade will not lift the epiglottis (see
video above). Indeed may fold it downward over the glottis.

Blade Too Long

On the other hand, you can use a longer MAC blade. The key to success with a longer blade is to avoid
inserting the blade too deep, and covering the larynx. You must restrain yourself and insert only to a depth
sufficient to place the blade tip in the vallecula. You will know if you have placed the blade too deep because
the larynx will be hidden under the blade.

— If you insert your blade too deep you will hide the larynx underneath, as on the left. This action
also tents the esophagus and can made it mimic the glottic opening if you are not careful.

When using a longer blade in a small patient, you will find that you will have a fair amount of blade outside
the mouth. In this case you must be especially careful to avoid lips and teeth.

Altering the Angle Of The MAC Blade To Optimize View

As you can imagine from the above anatomical relationships, a very small change in angle at the handle will
markedly alter the angle, location and point pressure of the tip. Any angulation of the blade must be done
carefully to avoid damaging the teeth.

Insertion: Always Protect Those Lips and Teeth

Insertion of the blade should always be delicate and deliberate With the mouth open as wide as you can,
insert the blade slightly to the right of the tongue. Don’t hit the teeth as you insert. If necessary, you can tilt
the top of the handle slightly to insert the blade into the mouth, then rotate the blade back, scooping it
around the right side of the tongue as you do so.

Avoid catching the lips between the blade and the teeth. I use my right index finger to sweep the lips out of
the way of the blade as I insert it. You may need to angle a curved blade slightly to pass the teeth and then
return the blade to a more neutral position once it has entered the mouth.

How To Know You’re In The Vallecula

With experience, you will develop good instincts on how deep to insert the blade. Always look for the tip of
the epiglottis as you insert the blade. Once you see it, continue to advance the blade — usually close to its
maximum depth if it’s the correct size. Simultaneously sweep the tongue to the left as you advance. Once
you see the full epiglottis you can now start to transfer the weight of the patient’s head onto the blade as
you lift. Again, watch for the lips. Leave your blade toward the left side of the mouth with the tongue pushed
out of the way. Continue to advance until

As you lift, the pressure from the tip should lift the epiglottis. If it doesn’t, carefully slide the tip a little deeper
into the vallecula to engage the ligament and try again.

The list of posts below leads to other articles on intubation technique.

May The Force Be With You

Christine E Whitten MD
Author of Anyone Can Intubate— a Step By Step Guide
Pediatric Airway Management— a Step By Step Guide

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Posted in Anesthesia, Intubation | Tagged hyoepiglottic ligament intubation, learning intubation, vallecula
intubation | Leave a reply

Learning Intubation: Head Position Effects

Laryngeal View
Posted on September 20, 2018

When first learning intubation,  a beginner often concentrates on memorizing the key laryngeal anatomy.
This is important of course. If you can’t recognize the vocal cords, you will not be able to successfully
intubate. However, even more important to learning intubation is understanding how the larynx relates to the
other structures in the head and neck. In order to intubate you must manipulate those other structures to
bring the larynx into view.

A prior post, When Learning Intubation Is Hard, described in detail some of the most common barriers to
learning to intubate. Here I will concentrate on helping you see how head position effects your ability to see
the larynx.

Larynx Location In The Neck

To feel your own larynx, place your hand on the front of your neck, with thumb and forefinger on either side
of the firm, roughly cylindrical shape in the midline.
— Relationships thyroid and cricoid cartilage to cricothyroid membrane

The adult larynx lies opposite the 5th, 6th cervical vertebrae, as opposed to the infant larynx that lies
opposite the 2nd, 3rd and 4th. The fact that the infant larynx is higher in the neck leads to greater risk of
airway obstruction and a need to slightly alter technique during pediatric intubation. A link to how to intubate
the pediatric patient is located at the end of this article. Here we will concentrate on the adult.

The larynx is located in front of the esophagus in the neck. The opening to the larynx, called the glottis, and
the opening to the esophagus are immediately adjacent to each other. Misidentification of the esophagus as
the glottic can lead to esophageal intubation.
— It’s very easy  to insert the laryngoscope blade too deep, as in the right picture. If too deep you will
not see recognizable anatomy because you are looking down the esophagus and hiding the larynx.

— If you insert your blade too deep you will hide the larynx underneath. This action also tents the
esophagus and can made it mimic the glottic opening if you are not careful.

How The Larynx Relates To Other Structures

Look at this lateral Xray  of a head in neutral position. The outline of the epiglottis, the hyoid bone, the thyroid
cartilage and the cricoid cartilage are easily identified. Notice the relationship of the larynx to the
esophagus. The larynx lies in front of the esophagus but the opening to the larynx (the glottis) and the
esophagus are right next to each other. Accidental esophageal intubation is a risk with every intubation.

— Lateral view Xray showing the distinct outlines of the parts of the larynx and their
relationship to the jaw, tongue and cervical spine.

Now imagine yourself intubating this patient. what would you have to do to bring the larynx into view? How
deep would you have to insert a Macintosh blade to  place the tip in the vallecula? How deep would you
need to insert a Miller blade to lift the epiglottis?

Here is a CT scan of another adult patient. Notice that in this second patient the larynx is located higher in
the neck.
— Normal CT side view showing relationship of laryngeal structures to external

Whereas the epiglottis in the first patient is low behind the tongue, this patient’s epiglottis is higher. The
depth of insertion and the strategy to lift the epiglottis will change from patient to patient. Straight blades
often work better in patients with a larynx higher in he neck and this may be one of those patients.

How Does Neck Position Affect The Larynx During Intubation

Let’s look at a lateral Xray of our first patient, but now with his head tilted all the way back in full extension.
Patients with respiratory distress, will often tilt their heads back. You can see that this position more fully
opens the airway and decreases resistance to breathing.
— Lateral Xray of the neck in full extension showing how the relationship
of the larynx changes with respect to the rest of the neck structures.
Extension without placing the patient in the sniffing position will hide
the larynx behind the tongue, or a so-called anterior larynx.

During intubation, we need to tilt the head back to bring the axis of the oral and pharyngeal axes into
alignment. But if the patient is not in a good sniffing position,  with the head moved slightly forward  in
addition to being tilted, the larynx may remain hidden behind the tongue during laryngoscopy.

Let me rotate this image to show you what I mean.

— Lateral neck Xray showing how extreme head extension, without the sniffing position, can
make visualization of the larynx difficult.

You can now see how anterior that larynx would look during laryngoscopy. Pushing down on the cricoid
cartilage might help rescue a difficult intubation in a situation like this, but optimal head and neck
positioning from the beginning would work better.

When getting ready to intubate, always glance at the side of your patient and assess whether the head and
neck are in an optimal position before you start. If it’s not optimal, try to fix it. That several seconds can save
you, and your patient, potential trauma.

Head Position Also Affects Laryngeal Opening

As long as we are looking at X-rays, let’s look at our first patient with his head flexed fully forward. When the
head is flexed forward, the structures in the posterior pharynx and the tongue tend to obstruct the airway.
You can test this by flexing your head forward as far onto your chest as you can. It becomes much harder to
take a breath.
— With the head flexed fully forward onto the chest, the airway is almost
fully obstructed. Visualization of the larynx would be impossible.

While no one would position a patient’s head this way for intubation, it’s common for novices to place too
many pillows under the head trying to obtain a good sniffing position. If the head is too high, the patient, and
the intubator, will not be able to tilt the head back.  In other words, our novice intubator, trying to maximize
sniffing position, sabotages himself. Again, prior to intubation take a look to the side of your patient. Try to
tilt the head back (or have the patient tilt their head back).

When learning to intubate, learn the anatomical relationships, not just laryngeal anatomy.  A good intubator
understands that knowledge of how those structures move in relationship to each other gives you the power
to manipulate that anatomy to give you the best possible view during intubation.

Please share with your fellow students. I’ve included a list with links below to previous posts on learning
intubation to help you perfect your skills. Feel free to ask questions. Let me know if there are any topics that
you would find helpful.









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Posted in Anesthesia, Intubation | Tagged airway anatomy, intubation anatomy, laryngeal anatomy,
learning intubation, teaching airway management, Teaching intubation | Leave a reply

Announcing My Latest Article Has Been

Published: “10 Rules for Approaching
Difficult Intubation”
Posted on August 27, 2018

I’m excited. My latest article, titled, “10 Rules for Approaching Difficult Intubation,
Always Prepare for Failure” has just been released in the journal supplement Airway Management, published
by Anesthesiology News.

Managing the difficult airway is one of the most challenging, risk ridden, and downright scary clinical
problems in anesthesia. The article makes the point that although we all know that a “can’t intubate, can’t
ventilate” scenario can happen to anyone at anytime, many of us practice as though it will never happen to
us. We must always prepare for failure. In the article, I’ve provided practical information from my 38 years of
experience on how to recognize, manage, and protect our patients with challenging airways.

While there is a lot of information for the novice, there are also clinical pearls for the experienced intubator.
I’m hoping you will find this information helpful to you, and to your trainees.

You can find the article on-line here, where you can also download a pdf version to share:


In addition to my article, please read the others as well. This issue is full of helpful, well written submissions.
I have always found Anesthesiology News to provide interesting and timely updates and well written
reviews, and this issue is no exception.







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Posted in Anesthesia | Leave a reply

Bilateral Tension Pneumothorax: Harder To

Posted on August 18, 2018

Tension pneumothorax is a life-threatening emergency. We all know the signs of tension pneumothorax:

unilateral breath sounds (breath sounds absent on affected side),

thorax may be hyperresonant,
jugular venous distention,
tracheal deviation to the opposite side,
maximum heart sounds shifted to the opposite side, and often

However diagnosis is more difficult if the patient is suffering from bilateral tension pneumothoraces. We
think about bilateral tension pneumothorax occurring with trauma cases. Yet the three cases I’ve seen in my
career were complications of intubation and emergency airway management. Continue reading →


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Posted in Anesthesia, Complications, complications of intubation, Patient Safety | Tagged bilateral

tension pneumothorax, iatrogenic tension pneumothorax, pneumothorax, tension pneumothorax | 3

PostObstructive Pulmonary Edema

Posted on July 23, 2018

Patients with postobstructive pulmonary edema (or P.O.P.E.) develop sudden, unexpected and potentially
life-threatening pulmonary edema after relief of airway obstruction.  It can be mild or severe. My first
experience with it was in 1983.

The Case

In 1983, we didn’t have pulse oximetry, end-tidal carbon dioxide monitoring or even automated blood
pressure cuffs. The patient was a healthy 6’3” tall and 250 lbs , 20 year old man. All muscle and clearly in
great shape. He had just had knee surgery under general anesthesia and was on the verge of waking up.

He was coughing vigorously on the endotracheal tube. Four people held him down. My resident, fearful he
night hurt himself or the team, extubated him while he was still coughing and before he was following
commands. Unfortunately the patient was still in stage 2, when the airway reflexes are hyperdynamic.

Within seconds the patient went into laryngospasm, intense spasmodic closure of the vocal cords and other
laryngeal muscles. There followed several minutes of struggling to re-establish an open airway. Finally the
spasm broke with the use of positive pressure and the patient awoke.

However the mood in the room quickly turned from relief to concern. Our patient started to panic, claiming
that he couldn’t breathe. His color was poor. He was wheezing badly, with pink frothy sputum bubbling out
of his mouth. He was awake enough to communicate with us but so panicked that he started to fight the
team of caregivers. Continue reading →

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Posted in Anesthesia, Complications, complications of intubation, Emergency airway management |

Tagged laryngospasm, negative pressure pulmonary edema, P.O.P.E type 2, P.O.P.E. type 1, POPE type 1,
POPE type 2, postextubation pulmonary edema, postobstructive pulmonary edema | Leave a reply

Anatomic Dead Space Affects

Posted on July 5, 2018

Understanding anatomic dead space is important to recognizing subtle hypoventilation. Hypoventilation

from sedation, pain medications, anesthesia in the immediate postoperative period is common. The most
obvious sign is slowing of the rate of breathing. A more subtle sign is that tidal volume becomes shallower.
Having a tidal volume close to, or smaller than the patient’s dead space can lead to significant hypercarbia,
hypoxia, and respiratory failure. This article discusses the concept of dead space and it’s clinical use in
recognizing hypoventilation and preventing hypoxia and hypercarbia. Continue reading →


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Posted in Airway Management, Anesthesia, Patient Safety, Respiratory physiology | Tagged alveolar gas
equation, anatomic dead space, dead space, dead space and hypoventilation, equipment dead space,
hypoventilation, physiologic dead space | Leave a reply

GlideScope Technique For Intubation In

Small Mouths
Posted on June 26, 2018
The GlideScope Video Laryngoscope (GVL) is an extremely useful tool for managing challenging intubations,
but it can be more difficult to use if your patient has a small mouth and a high arched, narrow palate. The
problem: once the GlideScope is in place in a small mouth, maneuvering the endotracheal tube around it and
into the posterior pharynx can be challenging. If you can pass the endotracheal tube (ETT) at all, the cuff
tends to scrape against the teeth, risking rupture. However, there is a modified GlideScope technique you
can use in those situations. Continue reading →


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Posted in Anesthesia, Difficult Intubation, Glidescope | Tagged Difficult Glidescope Intubation,

Glidescope, Glidescope intubation, intubation small mouth | 4 Replies

Difficult Intubation In A Newborn

Posted on June 4, 2018

Difficult neonatal intubation can occur unexpectedly. We’re ready to perform neonatal resuscitation in the
delivery room. We may be less ready to have to deal with a difficult neonatal airway at the same time.
Recently I, and my colleagues, had to manage an unanticipated difficult neonatal intubation in labor and

The Case

The baby was born extremely edematous, and in respiratory distress. Although it was easy to ventilate the
baby using the NeoPuff, airway swelling prevented the neonatologist  from identifying the epiglottis and
vocal cords. The anatomy was too distorted. Following protocol when faced with a difficult intubation, the
neonatologist called a “Code White”, an overhead page that in my hospital summons help from anesthesia,
nursing, respiratory care and pharmacy to assist with either a emergency pediatric cardiac arrest or
emergency intubation.

As a responding anesthesiologist, I too was unable to see landmarks during laryngoscopy.

Continue reading →


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Posted in Anesthesia, can’t intubate can’t ventilate, Difficult Intubation, pediatric intubation, Ventilation
With Bag-Valve-Mask | Tagged difficult intubation baby, difficult newborn intubation, difficult ventilation
baby, difficult ventilation newborn, midwife neonatal resuscitation, neonatal resuscitation, newborn
intubation | Leave a reply

Announcing My New Book: Pediatric Airway

Management: A Step-by-Step Guide
Posted on May 14, 2018

At long last, after two years of writing (and rewriting),  illustrating, and  filming  on-line videos, I’m excited to
announce the publication of my new book Pediatric Airway Management: A Step-by-Step Guide, by
Christine E. Whitten MD.

— Click to look inside at Amazon.com

Anyone who rarely cares for children tends to be anxious when faced with a small child’s airway. This is true
even if they are comfortable with adult airway management.

My goal for this book is to demystify basic pediatric airway management. I want to give you the skills you
need to recognize when a child is in trouble and act quickly to safeguard that child, including helping them
breathe if necessary. Continue reading →

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Posted in Airway Management, Emergency airway management, pediatric intubation, Teaching Airway
Management | Tagged books by Christine Whitten, Pediatric Airway Management Book | Leave a reply


Posted on April 8, 2018

When I was training, we used nitrous oxide on just about every anesthetic. It was easy to use. It was
inexpensive. It didn’t tend to effect hemodynamics so it was useful in less stable patients when combined
with an opioid. It helped speed induction through the second gas effect. It was not metabolized so renal and
liver insufficiency were of less concern.

However, with all of the more recent investigation into reasons for cognitive dysfunction or decline in infants
and the elderly following anesthesia, a lot more is now known about the pharmacologic disadvantages of
nitrous oxide (1, 2, 3). Continue reading →


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Posted in Anesthesia, Patient Safety | Tagged nitrous oxide and B12 pathway, nitrous oxide and climate
change, nitrous oxide and folate pathway, nitrous oxide and greenhouse gas, nitrous oxide and local
warming, nitrous oxide and patient safety | Leave a reply

Intubation During Cardiac Resuscitation

Posted on February 8, 2018

Intubation during cardiac resuscitation is often challenging because of the circumstances surrounding the
intubation. Excitement and apprehension accompany this life saving effort. If you don’t intubate often, you’re
likely to be nervous. Even experienced intubators get excited in emergency situations, but we control our
excitement and let the adrenaline work for us, rather than against us.
Step one, therefore, is to remain in control of your own sense of alarm. The leaders, which includes the
person in control of the airway, must stay calm. If you appear panicked, the rest of your team will follow your

Step two is to quickly assess the situation. Is the patient being ventilated? Ventilation takes priority over
intubation. Is there suction available? Without suction you many not be able to see the glottis, and you won’t
be able to manage emesis. What help do you have? The intubator almost always needs some assistance in
having someone hand equipment, or assist with cricoid pressure, among other tasks. As I tell my students,
intubation is a team sport.

Finally you need to assess what position the patient is in, and how can you optimize that position. The
patient is often in a less than optimal position while chest compressions are in progress. You usually find
the patient in one of two awkward positions: on the ground or in a bed. This article discusses techniques to
better manage intubation during cardiac resuscitation, especially with the patient in an awkward position.
Illustrations are copyright from Anyone Can Intubate, 5th Edition.  Continue reading →


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Posted in Anesthesia, Difficult Intubation, Emergency airway management, Intubation | Tagged Difficult
Intubation, intubation during cardiac arrest, intubation during cardiac rsuscitation, intubation during
chest compressions, intubation with the patient the ground | 5 Replies

When Learning Intubation Is Hard

Posted on January 15, 2018

Learning to intubate is easier for some people than for others. Sometimes, no matter how knowledgeable
you are about the theory of the intubation technique, the novice can still struggle to bring it all together to
pass the endotracheal tube. The anatomy can be confusing. Understanding how to place the laryngoscope
blade and manipulate that anatomy can be challenging. And all the while you must be ever vigilant to protect
those precious front teeth, avoid hypertension and tachycardia, and breathe for the patient at regular

I believe there are 4 chief barriers that inhibit learning how to intubate:

1. Failure to visualize how the outside anatomy links with the inside anatomy makes it hard to predict
how deeply to insert the blade.
2. A mistaken belief that placing the laryngoscope blade itself is all that is needed to align the axes of the
airway and reveal the larynx.
3. Failure to grasp the dynamic nature of the larynx, and the need to actively manipulate it during
4. A lack of understanding that intubation is not a sequence of isolated steps, but is instead a complex
dance of interacting steps, each setting the stage for the next.

This discussion is going to assume some knowledge of the basic intubation technique. If you’d like to review
those basics you can find links for multiple prior in depth discussions at the end of this article. (Illustrations
and animation from Anyone Can Intubate, 5th edition, C Whitten MD.) Continue reading →


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Posted in Anesthesia, Difficult Intubation, Intubation, Teaching Airway Management | Tagged intubation
curved blade, intubation straight blade, intubation technique, laryngeal anatomy, Teaching intubation | 4

Not All Airway Emergencies Need

Posted on December 17, 2017

An emergency department physician I met the other day shared with me an experience from her hospital
 that offers a good example of the fact that there are many different ways of managing an airway
emergency in a child that don’t involve intubation. Medical management can sometimes avoid some of the
risks of losing the airway that intubation might impose.

The Case

The child was an 18 month old girl whose older brother had been playing with laundry detergent pods. He
had offered a pod to his little sister, who promptly put it in her mouth and chewed it, releasing the liquid. Her
mother had brought her to the emergency room with respiratory distress. The child had severe stridor and
was breathing at 40 times a minute. Oxygen saturation was 92%. She was awake and alert but anxious.

The ED doctor recognized significant airway obstruction and was concerned that the obstruction could
worsen if the edema got worse. She immediately called for an anesthesiologist and a Head and Neck
surgeon to come to the Emergency Department to evaluate the child. While waiting, she gave 10 mg of IM
decadron and treated the child with nebulized racemic epinephrine. She attached a pulse oximeter and left
the child sitting on her mother’s lap and otherwise did not disturb the child, trying to avoid making her cry. By
the time the anesthesiologist and surgeon arrived the stridor, although still present, sounded better.

The question was what to do now? Continue reading →


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Posted in Airway obstruction, Emergency airway management, Percutaneous Jet Ventilation | Tagged jet
ventilation, pediatric airway obstruction, percutaneous transtracheal ventilation | 1 Reply

Remember That Respiratory Failure Is Not

Always Due to Lung Failure
Posted on December 3, 2017

There are many causes of respiratory failure. Some causes of respiratory failure result from disease or
damage to the respiratory system. However disease or injury to other organ systems such as the central
nervous system, the musculoskeletal system, or the presence of cardiac or septic shock can also cause
respiratory dysfunction.

While final diagnosis will certainly affect treatment, assessing and managing the patient’s ability to breathe
will not change with diagnosis.  However, once the airway is secure, you then have to diagnose and treat the
real problem in order to resolve the respiratory failure.

The Case

In this case, I was an anesthesia resident doing my pediatric rotation at a children’s hospital. It was my turn
to be on call for the weekend. At this particular hospital back in 1982, the anesthesia department managed
the airway emergencies in the Emergency Department so when I got the page to go to the ED, I ran.

Inside the triage cubicle a 6 year-old girl was clearly unresponsive. She had been sick with fever, nausea,
vomiting and diarrhea for several days according to her mother, who was crying in the corner. She hadn’t
been able to hold down any food or fluids for over 24 hours. Her temperature was 102F. She was breathing
rapidly but very shallowly. We did not as yet have pulse oximetry, but her color was dusky blue. Her blood
pressure was 60/40 and her pulse was 150. She looked septic.
I placed an oral airway and assisted her breathing. She didn’t react at all to the oral airway — no gag reflex.
We decided to intubate.

My colleagues quickly placed an IV and I decided to intubate without induction agent or muscle relaxant. If
she didn’t need those agents then I didn’t want to potentially compromise her status by giving them. Had
she reacted at all when I started to perform direct laryngoscopy I would have aborted and changed the plan.

She didn’t respond at all as I slid the endotracheal tube into the trachea.

We gave her two boluses of 20ml/kg of normal saline. Her color improved, her pulse came down to 110 and
her blood pressure rose to 80/50, appropriate for her age. But she still hadn’t woken up.

Ten minutes later the first blood test results returned. Her blood glucose was 10, extremely low. We gave her
2 ml/kg of D25W. Within two minutes she woke up and started fighting the endotracheal tube. As her other
vital signs looked much improved and she was now awake and protecting her airway, we elected to extubate

The child was admitted to the pediatric ward, was treated for gastroenterits and she did well.

Learnings: Hypovolemia and Hypoglycemia Can Cause Respiratory Failure

This was the first experience that I remember seeing in my career that demonstrated that hypovolemic
shock and hypoglycemia can cause profound respiratory failure without lung pathology.  It’s important to
remember that respiratory failure can result from a variety of other systemic problems, not just dysfunction
of the respiratory system.
— Respiratory distress or respiratory failure can come from many causes.

While assisting ventilation and protecting the airway are first priorities to stabilize a patient, treating the
cause of the respiratory failure may require more than just ventilation and/or intubation. In fact, treating the
cause can sometimes help you avoid the progression of respiratory distress to respiratory failure. If you
don’t consider a potential problem or cause, you’re not going to be able to diagnosis it.

May The Force Be With You

Christine Whitten MD
Author of Anyone Can Intubate: a Step by Step Guide, 5th Edition
Pediatric Airway Management: a Step by Step Guide


Please click on the covers to preview at amazon,com



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Posted in Emergency airway management, Respiratory physiology | Tagged respiratory failure and
hypoglycemia | 1 Reply
Exhaling During Manual Ventilation Is As
Important As Inhaling
Posted on November 26, 2017

Exhalation during manual ventilation is as important as inhalation. One of my readers recently asked a very
important question about ventilating a patient with a bag-valve-mask device: “Is there an outlet for the
expired air of the patient?” The answer is yes. When ventilating a patient we are concentrating, and rightfully
so, on watching the lungs expand and verifying that we hear breath sounds. It is just as important to verify
that your patient can exhale. All ventilation devices have a built in pressure relief valve, also called a pop-off
valve, which allows you to balance the force needed to expand the lungs with the ability to the patient to
passively exhale. Failure to allow exhalation can lead to patient injury from barotrauma.

— Common parts for bag-valve-mask devices, In this case a self-inflating style bag. The reservoir bag,
when present, allows near 100% inspired oxygen if allowed to fill.

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Posted in Ventilation, Ventilation With Bag-Valve-Mask | Tagged bag-valve-mask, pop off valve,
Ventilation | 2 Replies