Noninvasive Ventilation Handbook

NONINVASIVE
VENTILATION
MASTERCLASS
Michael G. Allison, MD
Table of contents
Abbreviation list 4
Modes of noninvasive ventilation

Mastering continuous positive airway pressure 6
Mastering bilevel positive airway pressure 8
Deciphering the acronyms 10
Physiologic effects of NIV

Improving oxygenation 14
Improving ventilation 16
Enhancing pulmonary physiology 18
Reducing preload 21
Decreasing afterload 24
Traditional applications
Managing obstructive sleep apnea 29
Applying CPAP in pulmonary edema 32
Applying BPAP in pulmonary edema 34
Using BPAP for chronic obstructive pulmonary disease (COPD) 36
Controversial uses
Treating pneumonia 39
Managing acute respiratory distress syndrome (ARDS) 42
Managing asthma 45
Addressing altered mental status 47
Situational applications
Preoxygenating with NIV 50
Applying NIV after extubation 52
Using NIV in palliative care 54
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Practical pearls for applying NIV
Choosing the right mask 57
Initiating NIV 59
Titrating NIV 61
High-flow nasal cannula

Appreciating high-flow nasal cannula (HFNC) 66
Addressing how HFNC works 68
Treating hypoxic patients 70
Extubating to HFNC 72
Predicting failure 74
Bonus lesson
Noninvasive ventilation for the support of COVID-19 pneumonia 77

Abbreviation list
ACPE – Acute cardiogenic pulmonary edema
AECOPD – Acute exacerbations of chronic obstructive pulmonary disease
AMS – Altered mental status
ARDS – Acute respiratory distress syndrome
BMI – Body mass index
BPAP – Bilevel positive airway pressure
BVM – Bag-valve-mask
COPD – Chronic obstructive pulmonary disease
CPAP – Continuous positive airway pressure
DNI – Do not intubate
EPAP – Expiratory positive airway pressure
FIO2 – Fraction of inhaled oxygen
FRC – Functional residual capacity
GCS – Glascow Coma Scale
HFNC – Hyphenate high-flow canula
ICU – Intensive care unit
IPAP – Inspiratory positive airway pressure
NIV – Noninvasive ventilation
NRB – Nonrebreather mask
OSA – Obstructive sleep apnea
PaCO2 – Partial pressure of arterial carbon dioxide
PaO2 – Partial pressure of arterial oxygen
PEEP – Positive end-expiratory pressure
PS – Pressure support
RR – Respiratory rate
V/Q matching – Ventilation-perfusion matching
VT – Tidal volume

Chapter X
1
ENTER
MODESNAME
OF
NONINVASIVE
VENTILATION
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Mastering continuous positive airway pressure
Continuous positive airway pressure (CPAP) is one of two cardinal modes of
noninvasive ventilation (bilevel positive airway pressure, or BPAP, is the other).
As the name suggests, CPAP provides continuous pressure throughout the respiratory
cycle.
Inspiration Expiration
Figure 1. Continuous positive airway pressure (CPAP)—one of two cardinal modes of noninvasive
ventilation—provides one continuous pressure throughout the respiratory cycle.
When a patient on CPAP breathes in, the ventilator machine will provide one constant
pressure during the inspiration. When the patient then breathes out, the ventilator
will continue that inward pressure during the entire expiration.
Figure 2. Continuous positive airway pressure (CPAP) is one of two cardinal modes of noninvasive ventilation.
It provides one continuous pressure throughout the respiratory cycle—the pressure is set to the same level
for inspiration and expiration.

Ventilator settings for CPAP
The ventilator settings for CPAP are the following:
• One single pressure, measured in cm of water (cmH2O)
• The fraction of inhaled oxygen (FIO2), set between 21% and 100%
Continuous pressure FIO2

(cmH2O) 21%—100%
Figure 3. The ventilator settings for continuous positive airway pressure (CPAP) as visual memory aide:
continuous pressure and fraction of inspired oxygen (FIO2) set at 21–100%.
Common clinical uses for CPAP

CPAP is commonly used for patients with the following respiratory disorders:
• Acute pulmonary edema
• Obstructive sleep apnea
• Obesity hypoventilation syndrome (Pickwickian syndrome)
Pulmonary edema Sleep apnea Pickwickian

syndrome
Figure 4. Visual representation of the common clinical uses for continuous positive airway pressure (CPAP): acute
pulmonary edema, obstructive sleep apnea, and obesity hypoventilation syndrome (Pickwickian syndrome).

Mastering bilevel positive airway pressure
Bilevel positive airway pressure (BPAP) is the second of two cardinal modes of
noninvasive ventilation (continuous positive airway pressure, or CPAP, is the other).
As the name suggests, BPAP provides two different pressures during the respiratory
cycle.
Inspiration Expiration
Figure 1. Bilevel positive airway pressure (BPAP)—one of two cardinal modes of noninvasive ventilation—
provides two different pressures throughout the respiratory cycle.
When a patient on BPAP breathes in, the ventilator will provide constant pressure
during the inspiration. When the patient then breathes out, the ventilator will provide
a different, lower pressure during expiration.
Figure 2. Bilevel positive airway pressure (BPAP) is one of two cardinal modes of noninvasive ventilation. It
provides two different pressures throughout the respiratory cycle—the pressure is higher for inspiration than
for expiration.

Ventilator settings for BPAP
The ventilator settings for BPAP are as follows:
• Inspiratory positive airway pressure (IPAP), measured in cmH2O
• Expiratory positive airway pressure (EPAP), measured in cmH2O
• The fraction of inhaled oxygen (FIO2), set between 21% and 100%
Bilevel pressure FIO2

IPAP and EPAP (cmH2O) 21%—100%
Figure 3. The ventilator settings for bilevel positive airway pressure (BPAP) as visual memory aide: bilevel
pressure and the fraction of inspired oxygen (FIO2) set at 21–100%.
Common clinical use for BPAP

The main clinical use for BPAP is in patients with acute exacerbation of chronic
obstructive pulmonary disease (AECOPD).
Acute exacerbation of chronic obstructive

pulmonary disease (AECOPD)
Figure 4. Visual representation of the main clinical use for bilevel positive airway pressure (BPAP): acute
exacerbation of chronic obstructive pulmonary disease (AECOPD).

Deciphering the acronyms
CPAP, BPAP, IPAP, EPAP, PEEP, PS...with all the acronyms, it’s easy to get lost in the
terminology of mechanical ventilation. To help you find your way, let’s take a look at
what these acronyms mean and how they relate to one another.
We’ve already covered continuous positive airway pressure (CPAP) and bilevel
positive airway pressure (BPAP): CPAP delivers a single pressure during the
respiratory cycle, and BPAP delivers two different pressures.
The others—IPAP (inspiratory positive airway pressure), EPAP (expiratory positive

airway pressure), PEEP (positive end-expiratory pressure), and PS (pressure
support)—are all variables on mechanical ventilators that need to be set by the user.
What is pressure support?
Pressure support (PS) is the variable that often causes initial confusion. It’s the
pressure that’s added to PEEP—and only during inspiration. Keep in mind IPAP does
not equal pressure support—IPAP is PEEP plus PS.
That said, there are generally two types of ventilator machines you need to watch out for:
• Those that require inspiratory positive airway pressure (IPAP) and expiratory
positive airway pressure (EPAP) to be entered (i.e., initial IPAP / EPAP).
• Those—typically in intensive care settings—that require positive end-expiratory
pressure (PEEP) and pressure support (PS) values to be set (i.e., initial PEEP / PS)
So let’s take a look at how you’ll set up CPAP and BPAP on these two types of
machines.

Continuous positive airway pressure ventilator
settings
Remember with continuous positive airway pressure (CPAP) ventilation, constant
pressure is delivered over time.
1. Initial IPAP / EPAP
In order to deliver the same pressure over time, IPAP and EPAP must be set to the
same value.
Figure 1. To set up a CPAP ventilator where initial IPAP / EPAP settings are required, IPAP and EPAP are set to
the same value in order to deliver the same pressure over time.
2. Initial PEEP / PS
To deliver CPAP when PEEP and PS are required, you want to set the PEEP to the
amount of continuous pressure desired. Pressure support (PS) is set at zero—since
you’re not adding any additional pressure during inspiration.
Figure 2. To set up a CPAP ventilator where initial PS / PEEP settings are required, PEEP is set to the amount
of continuous pressure (during inspiration and expiration) desired, and PS is set at zero.

Bilevel positive airway pressure ventilator
settings
With BPAP two different pressures are delivered, one during inspiration and one
during expiration.
1. Initial IPAP / EPAP
On ventilators that use IPAP and EPAP settings, you set IPAP to the inspiratory
pressure you desire and EPAP to the expiratory pressure you desire.
Figure 3. To set up a BPAP ventilator where initial IPAP / EPAP settings are required, IPAP and EPAP are
independently set to the desired values.
2. Initial PS / PEEP
Setting BPAP on ventilators that use PS and PEEP is different. The PEEP, in this
case, is equal to the EPAP and is set at the desired expiratory pressure. The IPAP is
equal to the sum of the PEEP plus PS. Therefore, to set the IPAP, you set the PS to a
pressure that will be added to the PEEP.
Figure 4. To set up a BPAP ventilator where initial PS / PEEP settings are required, first, PEEP is set to the
desired expiratory pressure (and equals EPAP). Then PS is set to a pressure to bring IPAP up to the desired
level above PEEP (EPAP).

Chapter 2
PHYSIOLOGIC
EFFECTS OF NIV
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Improving oxygenation
The first way noninvasive ventilation (NIV) can help patients with pulmonary disease
is through improvements in oxygenation (the other, is by improving ventilation).
There are three main ways by which NIV improves oxygenation:

1. Increases delivery of FIO2
2. Reduces entrainment of room air
3. Improves the ventilation-perfusion (V/Q) ratio or V/Q matching
1. NIV increases the delivery of FIO2

The NIV ventilator and interface allow for an increased, and more accurate, delivery
of FIO2 compared to a traditional oxygen mask.
2. NIV reduces entrainment of room air

With nasal cannulas and traditional oxygen masks, the loose fit allows patients to
breathe in ambient air. This means the amount of oxygen delivered is being diluted
by the presence of room air entrainment. The tight fit of the NIV mask prevents the
entrainment of room air into the breathing circuit.
Oxygen mask NIV
Figure 1. The masks used in noninvasive ventilation (NIV), compared to nasal cannulas or traditional oxygen
masks, prevent the entrainment of room air.

3. NIV improves ventilation-perfusion (V/Q) ratio
or V/Q matching
Patients with lung diseases may have atelectasis, or collapsed areas of the lung,
that don’t effectively participate in gas exchange. By providing a positive pressure to
the lungs, these areas can re-expand and allow oxygen from the airways to diffuse
into the pulmonary circulation.
Before NIV After NIV
Figure 2. The effects of noninvasive ventilation (NIV) on regions of atelectasis. Before NIV the alveoli are
collapsed and don’t participate in gas exchange. After NIV, these areas can expand and allow the diffusion of
oxygen into the pulmonary circulation.
This results in better ventilation and perfusion matching, also known as

ventilation-perfusion (V/Q) matching. Ventilation, V, is a measure of the amount of
air that reaches the alveoli, and perfusion, Q, is a measure of the amount of blood
within the capillaries surrounding the alveoli. After NIV, more air can reach the
alveoli, increasing the V/Q ratio.
By improving V/Q matching through recruiting atelectatic lung regions and allowing
a reliable delivery of set FIO2, NIV can improve the oxygenation of patients with
hypoxic respiratory failure (HRF).
Lung
capillary

Collapsed alveoli Recruited alveoli
Figure 3. The effects of noninvasive ventilation (NIV) on the ventilation-perfusion ratio (V/Q) in lung disease. NIV
increases the V/Q ratio (V/Q matching) of areas of atelectasis, resulting in increased oxygenation of the lungs.

Improving ventilation
In addition to improving oxygenation, noninvasive ventilation (NIV) can also improve
ventilation—the exchange of oxygen for carbon dioxide—in a variety of pulmonary diseases.
First, let’s review what ventilation, specifically minute ventilation is so that we can
understand how NIV might affect it.
What is minute ventilation?

The minute ventilation of the respiratory system is the amount of air moved in and
out by a patient in one minute. It is defined as the respiratory rate (RR) times the
tidal volume (VT).
The tidal volume is the volume of air inspired with each breath, and the respiratory
rate is the number of breaths taken per minute.
Minute ventilation = respiratory rate (RR) × tidal volume (VT)
Figure 1. Minute ventilation is the respiratory rate (RR) times the tidal volume (VT).
Ok, so with that out of the way, let’s now take a look at how NIV improves ventilation—
in one of two key ways:
1. Improves tidal volume (VT)
2. Counteracts intrinsic positive end-expiratory pressure (PEEP)
1. NIV improves tidal volume

We know that NIV improves a patient’s ventilation. But how? Noninvasive ventilation
is most commonly delivered as a spontaneous mode of ventilation. This means that
patients control their intrinsic respiratory rate and the ventilator does not provide a
minimum respiratory rate, outside of emergency backup modes. Since NIV does not
directly influence the respiratory rate, it must exert its effect on the tidal volume.

Noninvasive ventilation increases the efficiency of breathing, and the added pressure
during inspiration augments the volume of air that is inspired—the tidal volume—
and increases in tidal volume improve ventilation of the entire lung.
Without NIV With NIV
Figure 2. Noninvasive ventilation (NIV) improves ventilation due to its effects on the tidal volume (VT). The
added pressure during inspiration augments the air inspired, or VT , and the increased VT improves ventilation
of the entire lung.
2. NIV counteracts intrinsic PEEP
Another method of improving ventilation relates to the intrinsic pressure created by

the airways at the end of expiration, which is termed intrinsic positive end-expiratory
pressure, or intrinsic PEEP.
In some disease states, the airways may be constricted making it more difficult
for air (specifically carbon dioxide) to be released during expiration, resulting in
hyperinflated alveoli and high intrinsic pressure (PEEP). Noninvasive ventilation
can counteract this pressure to allow improved expiration, ventilation, and carbon
dioxide exchange.
Figure 3. Noninvasive ventilation (NIV) improves ventilation due to its effects on intrinsic positive end-
expiratory pressure (PEEP). By counteracting the intrinsic PEEP observed in some lung diseases, NIV reduces
hyperinflation of alveoli and improves expiration.

Enhancing pulmonary physiology
When we see patients in the emergency department, medical ward, or intensive
care unit who are tachypneic and using accessory muscles, we clinicians typically
comment that they have increased work of breathing. We see this extra effort as
work, and quickly plan on how to diagnose the problem and ease our patient’s
breathing. We reach for a tool like noninvasive ventilation (NIV) to improve our
patient’s oxygenation or ventilation, but, as a side-effect, NIV changes their
pulmonary physiology in a way that makes breathing easier and more efficient.
Let’s review the three ways NIV can change standard pulmonary physiology:
1. Improves functional residual capacity (FRC)
2. Improves lung compliance
3. Removes lung water
1. NIV improves functional residual capacity (FRC)

By providing positive pressure throughout the respiratory cycle, NIV improves the FRC.
Functional residual capacity is the volume of air left in the lung after the end of a
typical breath.
Typically, exhalation against atmospheric pressure is a passive process that allows

the lung to empty significantly. But by providing positive pressure during expiration,
the breath ends earlier due to the cessation of passive recoil at a pressure higher than
atmospheric pressure, therefore the FRC is greater.
Functional residual capacity (FRC)
Figure 1. Functional residual capacity (FRC) is the air left in the lung after the end of the typical breath.

An improved FRC will allow alveoli that were completely closed previously to remain
open and participate in gas exchange. And areas of the lungs that were well-
perfused before without adequate ventilation will have improved V/Q matching and
improved oxygenation.

Collapsed alveoli Recruited alveoli
Figure 2. Noninvasive ventilation (NIV) improves the functional residual capacity (FRC) of the lung thereby
recruiting previously closed alveoli to participate in gas exchange. This leads to improved V/Q matching and
enhanced oxygenation.
2. NIV improves lung compliance

A secondary benefit of the recruitment of more alveoli is improved lung compliance—
the change in volume of the lung due to a change in pressure.
Figure 3. Lung compliance curve and functional residual capacity (FRC).
Low FRC is associated with atelectatic (closed) alveoli. When alveoli remain open,
the lung remains on the ideal portion of the compliance curve. On this steep portion
of the curve, changes in volume can be achieved with smaller changes in pressure,
reducing pressure-related injury of the lung.
Warning: Increasing positive pressure too much can cause overdistension of alveoli.

3. NIV removes lung water
Another way in which NIV can help improve pulmonary physiology of the diseased
lung is through the removal of lung water.
Alveoli that were otherwise full of fluid, say in the case of pulmonary edema, have a
thicker interstitium which increases the distances gas must travel to the neighboring
blood vessel.
Positive pressure can redistribute fluid into the neighboring bronchial interstitium,
allowing for a shorter distance for diffusion between the alveolus and blood vessel.
Without NIV With NIV
Figure 4. Noninvasive ventilation (NIV) can redistribute excess fluid in the interstitial space, reducing the
distance between alveoli and lung capillaries, and enhancing the diffusion of gases.

Reducing preload
In addition to the changes to the respiratory system (e.g., improved oxygenation,
ventilation, and pulmonary physiology), the positive pressure associated with
noninvasive ventilation (NIV) also causes changes in the thoracic cavity that affect
cardiovascular physiology.
We’ll begin by discussing how positive pressure through a noninvasive mask will
affect venous return and preload, and later we’ll review the effect of NIV on afterload.
What is preload, or end-diastolic pressure?

Preload is defined as the pressure in the right heart at the end of filling. Using more
technical terms, preload is the end-diastolic pressure of the right ventricle.
Right ventricular preload
Figure 1. Right ventricular preload is defined as the pressure in the right heart at the end of filling.
Venous return and preload (or end-diastolic pressure) change during the respiratory
cycle. When venous return to the heart increases, the preload increases. When
venous return to the heart decreases, the preload decreases.
And how the preload changes depends on whether the patient is breathing
spontaneously (i.e., with negative-pressure breathing), or breathing with the
assistance of a ventilator, which uses positive pressure.

How do venous return and preload change during
spontaneous (i.e., negative-pressure) breathing?
First, during inspiration, intrathoracic pressure decreases as the lungs inflate (Fig.
2b). In response to this decrease in pressure, the extrathoracic venous system
allows an increased venous return to the right heart (Fig. 2c). Since the change in
intrathoracic pressure will increase the volume of blood returning to the heart, the
pressure of the right ventricle goes up and preload increases (Fig. 2d).
a) b)
c) d)
Figure 2. Changes in venous return and preload due to changes in intrathoracic pressure during a spontaneous
breathing cycle, a) end-expiration, b) inspiration and decreased thoracic pressure, c) increased venous return,
d) increased end-diastolic pressure (increased preload).
How does NIV (or positive-pressure breathing) affect

venous return and preload?
During inspiration on NIV, intrathoracic pressure is positive when the lungs inflate
(Fig. 3b). The venous return will decrease due to the higher pressure (Fig. 3c).
The decreased venous return decreases preload (Fig. 3d), and this decreased
blood volume is transmitted to the left ventricle when the blood flows through the
pulmonary circulation to the left atrium and ventricle.

a) b)
c) d)
Figure 3. Changes in venous return and preload due to changes in intrathoracic pressure during positive-
pressure breathing (with noninvasive ventilation, or NIV), a) end-expiration, b) inspiration, and increased
thoracic pressure, c) decreased venous return, d) decreased end-diastolic pressure (decreased preload).
How are NIV-induced changes in preload and venous return

important in the clinic?
The changes in venous return as a result of moving from negative-pressure breathing

to positive-pressure breathing can have substantial physiologic implications on
patients. Understanding these changes and predicting them in advance can allow
for optimal use of NIV.
Hypervolemic patients on NIV
In patients with relative hypervolemia (fluid overload), such as patients with acute
cardiogenic pulmonary edema, decreasing venous return and preload may decrease
pulmonary blood flow leading to improved pulmonary function.
Hypovolemic patients on NIV
On the contrary, when trialing NIV in patients with status asthmaticus, who may
present with relative hypovolemia (low blood volume / inadequate distribution of
blood volume) resulting from insensible volume losses due to tachypnea, the positive
pressure of NIV may cause further decreases in preload and possible hypotension.

Decreasing afterload
As we mentioned, in addition to the changes to the respiratory system (e.g.,
improved oxygenation, ventilation, and pulmonary physiology), the positive pressure
associated with noninvasive ventilation (NIV) also causes changes in the thoracic
cavity that affect cardiovascular physiology.
We began by discussing how positive pressure through a noninvasive ventilation

mask affects venous return and preload, and now we’ll turn our focus to the effect
of NIV on afterload.
What is afterload?
Afterload is the pressure against which the heart has to pump when ejecting blood
during systole.
Pressure changes in the thoracic cavity affect the afterload of the left ventricle
just as they cause changes in the preload of the right ventricle. An increase in
intrathoracic pressure will increase afterload, and a decrease in intrathoracic
pressure will decrease afterload.
Afterload
Figure 1. Afterload is the pressure against which the heart has to pump when ejecting blood during systole.

Changes in afterload during respiration
During inspiration, the intrathoracic pressure becomes more negative (Fig. 2b).
This may be 1–2 mmHg in magnitude. The healthy left ventricle, normally needing
to generate a pressure of about 90 mmHg to open the aortic valve (Fig. 2c), will
typically easily overcome this negative pressure of 1–2 mmHg (Fig. 2d).
a) b)
c) d)
Figure 2. Changes in afterload during breathing, a) before inspiration, b) at the end of inspiration pressure
in the intrathoracic cavity is decreased, c) in this lower pressure environment, a greater pressure in the left
ventricle is needed to open the aortic valve, d) increased pressure in the left ventricle is sufficient to overcome
the change in intrathoracic pressure due to inspiration and blood flows out of the heart.
Changes in afterload during respiration—with a

weakened heart
In the case of a patient with a weakened left ventricle with poor compliance, the
extra work of the left ventricle may be quite magnified (Fig. 3b). Pulmonary edema
may start to develop (Fig. 3c), and, as a result, the patient will take in larger and
deeper breaths, which can increase the negative intrathoracic pressure (Fig. 3d).
The weakened myocardium must generate greater pressure to overcome both the
intrathoracic pressure and the pressure needed to open the aortic valve. If cardiac
contractility is not up to the task, further pulmonary edema will develop, and the
cycle will continue (Fig. 3e).

a) b) c)
d) e)
Figure 3. Changes in afterload during breathing with a weakened heart, a) increase in pressure in left ventricle
needed to overcome the decrease in pressure due to inspiration, b) a weak left ventricle cannot generate the needed
pressure, c) pulmonary edema may start to develop, d) a larger inspiration (deeper breath) is taken as a result of
fluid buildup, which generates a further decrease in pressure and larger gradient to overcome, e) the weakened
left ventricle cannot generate even more pressure so further pulmonary edema develops and the cycle continues.
How does NIV help break the cycle?

With NIV, the positive intrathoracic pressure actually decreases the pressure against
which the left ventricle must pump (Fig. 4d). This assists, or offloads, the left
ventricle (Fig. 4e). A weak left ventricle with poor contractility may find it easier to
pump blood through the body in this situation (Fig. 4f).
a) b) c)
d) e) f)
Figure 4. Noninvasive ventilation (NIV) can break the cycle of increasing afterload, a) end-expiration, b)
decrease in intrathoracic pressure due to inspiration, c) a weak left ventricle cannot generate the needed
pressure to overcome the afterload, d) NIV increases the intrathoracic pressure thereby reducing the afterload,
e) the weakened ventricle doesn’t have to work as hard to overcome the afterload, f) the blood can flow.

The net result is that the left ventricle when assisted by positive-pressure ventilation,
can generate a greater stroke volume for the same preload, due to improved
contractility and decreased afterload—in other words, it can improve its compliance.
Figure 5. The left ventricle, when assisted by positive-pressure ventilation, can improve its compliance.
Positive-pressure ventilation (e.g., NIV) can move the curve up, allowing a greater stroke volume for the same
preload, due to its improved contractility and decreased afterload.
How is afterload important in the clinic?

Take a patient with pulmonary edema due to a weak heart, pumping against a high
cardiac afterload. Reducing cardiac afterload will lessen the stress on the heart and
help relieve pulmonary edema.
So, knowing how positive-pressure ventilation improves left ventricular function and
decreases afterload, we can use NIV to avoid the potential death spiral in patients
with pulmonary edema from high afterload or weak hearts. Yet another physiologic
win for NIV!
Return to table of contents.

Chapter 3
TRADITIONAL
APPLICATIONS
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Managing obstructive sleep apnea
What is the prevalence of obstructive sleep apnea?
Obstructive sleep apnea (OSA) is estimated to affect 3–10% of individuals under the
age of 50 and 9–17% of those older than 50 years of age—making this a common
problem clinicians will face.
≤ 50-years-old > 50-years-old

3—10% 9—17%
Figure 1. The prevalence of obstructive sleep apnea (OSA). It is estimated that 3–10% of individuals under the
age of 50 and 9–17% of those older than 50 years of age will be affected by OSA.
What are the risk factors for OSA?

There are eight main risk factors that would lead to an evaluation for OSA:
1. Snoring
2. Daytime somnolence
3. Unrefreshed sleep
4. Sedentary fatigue
5. Nocturia
6. Morning headaches
7. High body mass index (BMI)
8. Increased neck circumference

Snoring Daytime Unrefreshed Sedentary
somnolence sleep fatigue
Nocturia Morning High body Increased neck

headaches mass index circumference
Figure 2. The eight main risk factors for obstructive sleep apnea (OSA) are snoring, daytime somnolence,
unrefreshed sleep, sedentary fatigue, nocturia, morning headaches, a high body mass index (BMI), and
increased neck circumference.
How is OSA diagnosed?

The diagnosis of obstructive sleep apnea is made with polysomnography to
determine the number of apneas and hypopneas per hour.
How is OSA treated?

The collapse of the upper airway that causes obstruction and apnea during sleep
is reversed with the application of positive-pressure ventilation. This is most
commonly delivered as continuous positive airway pressure (CPAP)
How should I titrate CPAP for my patient with OSA?
Laboratory titration
Initial titration of CPAP is typically done in the laboratory setting (during sleep) and
is adjusted to reduce the number of obstructive events. Typically, CPAP is started at
4 cmH2O and can be adjusted in fixed increments to a maximum of 20 cmH2O.

4–20 cmH20
Figure 3. Continuous positive airway pressure (CPAP) ventilation treatment for obstructive sleep apnea (OSA)
is typically titrated in a sleep lab with settings starting at 4 cmH2O and increased incrementally to 20 cmH2O.
Automated titration
Newer evidence suggests that automated CPAP titration—where titration is done

by the machine itself—appears as effective as sleep lab titration for initiating CPAP.
Though typically sleep apnea is treated at home, patients with sleep apnea often
have other medical problems and may become hospitalized. CPAP should be
continued in the hospital for patients with sleep apnea, but a common problem is
that many patients don’t know or can’t recall what their home settings are. In these
situations, automated titration of CPAP is convenient and sets reliable pressures
to improve the patient’s apnea. So, if available on your hospital’s CPAP machines,
automated titration is the ideal choice.
What do you do if you don’t have an automated titrate CPAP

machine? Use BMI-based settings.
Setting a CPAP machine based on BMI has been evaluated and results in settings
similar to those set by polysomnography. Start with a pressure of 8 cmH2O for
patients with a BMI of less than 30. Use 10 cmH20 if the BMI is 30 through 35, and
12 cmH2O if the BMI is greater than 35.
BMI < 30 BMI 30–50 BMI > 35

8 cmH20 10 cmH20 12 cmH20
Figure 4. The initial pressure setting for continuous positive airway pressure (CPAP) ventilation treatment for
obstructive sleep apnea (OSA) can be determined according to the patient’s body mass index (BMI): 8 cmH2O
for BMI < 30, 10 cmH2O for BMI 30–35, and 12 cmH2O for BMI > 35.

Applying CPAP in pulmonary edema
What are the physiological changes seen in acute
cardiogenic pulmonary edema?
Cardiovascular changes
In acute cardiogenic pulmonary edema (ACPE), an increased left ventricular end-

diastolic pressure (Fig. 1a) causes the left atrium to pump against an increased
load (Fig. 1b). The atrium becomes overwhelmed, and an increased hydrostatic
pressure gradient is created (Fig. 1c). Eventually, the pulmonary interstitium becomes
overloaded, and the pulmonary veins widen, due to the accumulation of fluid (Fig. 1d).
a) b)
c) d)
Figure 1. The progress of physiological changes in the heart and central vessels in acute cardiogenic
pulmonary edema (ACPE), a) increased left ventricular end-diastolic pressure, b) increased pressure in the left
atrium, c) left atrium is overwhelmed and pressure gradient is created, d) widening of the pulmonary veins as
fluid backs up in the pulmonary interstitium.
Respiratory system changes
The cardiovascular changes and resulting fluid overload in the pulmonary interstitium
may cause both alveolar collapse and fluid accumulation in the alveoli.
Alveolar collapse Fluid accumulation

Figure 2. Physiological changes to the alveoli seen in acute cardiogenic pulmonary edema (ACPE). The fluid
overload in the pulmonary interstitium causes alveolar collapse and fluid accumulation.

What is the outcome of the physiological
changes associated with ACPE?
Both of these processes limit the amount of oxygen that can get into the bloodstream
such that, clinically, patients develop respiratory distress and hypoxic respiratory
failure. Acute cardiogenic pulmonary edema can happen very quickly and has the
possibility of high morbidity and even mortality. The in-hospital mortality rate can
be as high as 12%!
How do I treat my patients with ACPE?

Noninvasive ventilation (NIV) for ACPE was first evaluated in the 1930s but didn’t
receive widespread use until the 1970s. In contemporary practice, the use of
continuous positive airway pressure (CPAP) for acute pulmonary edema should
be considered early and often. Its use has been strongly recommended in clinical
practice guidelines with the following four aims:
1. Reducing cardiac preload
2. Reducing afterload
3. Removing excess volume
4. Recruiting areas of the lung with ventilation-perfusion (V/Q) mismatch
In fact, positive pressure NIV can address many of these issues at once and has
been shown to improve a variety of clinical outcomes:
• Decreases respiratory rate
• Shortens the length of intensive care unit (ICU) stay
• Decreases need for endotracheal intubation
• Lowers mortality rate
What are the CPAP settings for a patient with ACPE?

• When possible, start with low pressures and titrate up to help with compliance.
• CPAP from 8–12 cmH2O worked best for patients in most clinical studies.

Applying BPAP in pulmonary edema
In the last article, we stressed the early use of continuous positive airway pressure
(CPAP) in patients with acute pulmonary edema. You may have been wondering,
why the focus on CPAP? Couldn’t bilevel positive airway pressure (BPAP) work just
as well?
Continuous positive airway pressure creates benefit because the positive pressure
increases the intrathoracic pressure—thereby decreasing preload and afterload.
Bilevel positive airway pressure should do the same since it is positive pressure,
just given at two different levels. Right?
Decreased preload Decreased afterload
Figure 1. Decreases in preload and afterload are seen as a result of noninvasive positive-pressure ventilation—
whether continuous pressure (CPAP) or bilevel pressure (BPAP).
Is BPAP recommended for pulmonary edema?

One early study on the use of BPAP in cardiogenic pulmonary edema found that
there was an increase in the incidence of myocardial infarction within the group
randomized to BPAP. These results presented a reason to use CPAP instead of BPAP.
And, a Cochrane review of BPAP versus standard therapy did not find conclusive
evidence of benefit. So, the evidence seemed to be in the corner of CPAP.
However, another Cochrane review found that when CPAP was compared with BPAP
in the treatment of pulmonary edema, there was no difference between the two. Talk
about conflicting literature!

So, should I use CPAP and BPAP for pulmonary
edema?
If there is no suspicion for acute hypercapnia or elevated carbon dioxide (CO2) in
the blood, CPAP is a great choice based on the benefits we’ve discussed. However,
if there is suspicion or evidence of hypercapnia, go with the BPAP mode because of
the added benefit of improving ventilation along with oxygenation.
Hypercapnia
Yes No
BPAP CPAP
(Bilevel positive (Continous positive
airway pressure) airway pressure)
Figure 2. When choosing between bilevel positive airway pressure (BPAP) and continuous positive airway
pressure (CPAP), check first to see if hypercapnia is present. If hypercapnia is present, choose BPAP, if not,
choose CPAP.
And don’t worry about the previously mentioned association between BPAP and
myocardial infarction—it has not been replicated in any subsequent recent trials.

Using BPAP for chronic obstructive
pulmonary disease (COPD)
Aside from its use in pulmonary edema, noninvasive ventilation (NIV) has
demonstrated repeated benefit in the subset of patients with acute exacerbation of
chronic obstructive pulmonary disease (AECOPD).
Acute exacerbation of chronic obstructive

Figure 1. Patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) can benefit
from noninvasive ventilation (NIV).
The positive pressure works to reduce the collapse of small and medium-sized
airways during expiration. It also reduces the workload of the muscles of inspiration
and expiration, allowing for more efficient breathing in a time of distress.
How does positive pressure NIV benefit patients

with COPD?
Before the routine use of NIV in patients with COPD, or chronic obstructive pulmonary
disease, in-hospital mortality rates were quoted up to 33%. These patients were given
nebulizers, steroids, and antibiotics—and when those measures failed, patients were
intubated and heavily sedated.
With the adoption of NIV as a routine treatment for COPD, we see a range of benefits:
• Improved respiratory rate
• Improved PaCO2
• Improved pH
• Decreased in-hospital complications
• Decreased hospital stays
• Reduced rate of intubation
• Reduced mortality rate

Which ventilator mode should I choose for my
patients with COPD?
The primary mode of NIV used in patients with COPD is bilevel positive airway
pressure (BPAP).
Figure 2. Bilevel positive airway pressure (BPAP) is the primary mode of noninvasive ventilation (NIV) used
in patients with chronic obstructive pulmonary disease (COPD). PEEP, positive end-expiratory pressure; PS,
pressure support.
The positive end-expiratory pressure (PEEP) works to stent open airways during
expiration when the bronchi are most at risk of collapse and airflow obstruction. The
additional pressure support (PS) during inspiration allows larger volume breaths
that work to increase the minute ventilation. The PS also reduces the work done
by accessory muscles to take in breaths and allows greater efficiency of breathing.
Could I use CPAP instead of BPAP for my patients

with COPD?
In patients with COPD, continuous positive airway pressure (CPAP) can provide a
pressure that would stent open the airways in expiration, but since there is no added
pressure support, it doesn’t help with inspiratory work. Plus, this mode really has not
been well studied for use in COPD.
So, since the preponderance of literature supports the use of BPAP in acute COPD,
that’s what you need to reach for the next time you have a patient with COPD.

Chapter 4
CONTROVERSIAL USES
www.medmastery.com
Treating pneumonia
In the prior chapter we talked about two very common causes of respiratory failure—
pulmonary edema and acute exacerbations of chronic obstructive pulmonary
disease (AECOPD). But what about the most common cause of respiratory failure
treated in the hospital setting—pneumonia? Can we use noninvasive ventilation
(NIV) in patients with pneumonia?
Figure 1. Pneumonia is the most common cause of respiratory failure treated in the hospital setting.
You probably think that NIV must be able to replicate many of the findings of other
respiratory diseases. You’d think it could reduce intubations and improve length of
stay by decreasing the need for invasive ventilation.
You’d be right about one thing: there has been great interest in using NIV for
patients with pneumonia to avoid many of the complications of invasive mechanical
ventilation. Unfortunately, the evidence for using NIV in patients with pneumonia
has produced some mixed results that has left many questions unanswered.
Failure rates as high as 50% have been demonstrated when trying to use NIV to
treat pneumonias of varying severity. And when you come across studies that
demonstrate lower rates of intubation with NIV in pneumonia, you’ll find these
studies primarily included patients who had less severe pneumonia and had good
response to initial medical therapy.
50% failure rate
Figure 2. Failure rates as high as 50% have been demonstrated when trying to use noninvasive ventilation
(NIV) to treat pneumonia.

When should I avoid using NIV to treat pneumonia?
Trying to identify which patients are at higher risk of failure may lead to better
success rates—by avoiding NIV in those patients at risk of failure and utilizing NIV in
patients with characteristics that may be amenable to treatment.
There are three key factors that could predict failure:

1. Size of pneumonia (measured in number of quadrants involved on the x-ray)
2. Severity of patient illness (measured in one study using an APACHE score)
3. Presence of shock requiring treatment with vasopressors (e.g., norepinephrine)
Size of Severity of Presence of

pneumonia pneumonia shock requiring
vasopressors
Figure 3. The three factors that could predict failure of NIV to treat pneumonia are the size of the pneumonia,
the severity of the disease, and the presence of shock requiring treatment with vasopressors.
Just know that failure rates are higher in pneumonia than in other disease states
(such as chronic obstrucive pulmonary disease [COPD] and acute cardiogenic
pulmonary edema [ACPE]) and these patients should be monitored closely.
Is it ever better to use NIV, compared to invasive

measures, to treat pneumonia?
Patients without properly functioning immune systems, such as those with the
human immunodeficiency virus (HIV), those on chemotherapy, or those taking
immunosuppressive medications, have high rates of complications when invasive
mechanical ventilation has been used to treat pneumonia. The use of NIV in these
patients—to potentially avoid these complications—has been the focus of much
research.

Figure 4. Immunocompromised patients with pneumonia could benefit from treatment with noninvasive
ventilation (NIV) compared to invasive measures such as intubation. Early investigations have shown
improved oxygenation, decreased rates of intubation, and lowered mortality.
Early investigations into the use of NIV for patients with immunosuppression
showed improved measures of oxygenation, decreased rates of intubation, and
improved mortality figures. More contemporary studies failed to demonstrate this
benefit, but they did not demonstrate any increase in complications.
So, should I use NIV to treat pneumonia?

By carefully choosing patients, monitoring them closely, and moving to invasive
mechanical ventilation at early signs of worsening, you may consider using NIV in
select patients with pneumonia.

Managing acute respiratory distress
syndrome (ARDS)
What is acute respiratory distress syndrome?
Acute respiratory distress syndrome (ARDS) describes a constellation of findings in
patients with bilateral lung infiltrates due to severe illness. It is a disease that, when
severe, is associated with mortality of nearly 50%.
What are the features of ARDS?

ARDS is defined by five features:
• Acute onset
• Bilateral lung disease
• Hypoxia (as measured by a P/F ratio)
• Absence of pulmonary edema
• Need for positive-pressure ventilation
Acute Bilateral Hypoxia No pulmonary Need positive-

onset edema pressure
ventilation
Figure 1. The five features of acute respiratory distress syndrome (ARDS): acute onset, bilateral lung disease,
hypoxia, absence of pulmonary edema, and a need for positive-pressure ventilation.
Can I use NIV to treat patients with ARDS?
The use of ventilation strategies to protect the lung during ARDS has been researched
for the past 20 years, and attempts have been made to define the role of noninvasive
ventilation (NIV) and invasive ventilation in ARDS.
Use of NIV in ARDS could theoretically confer benefit to patients—it would be

associated with less sedation, avoidance of paralytics, and fewer complications
from endotracheal intubation and mechanical ventilation.

But despite these proposed benefits, national societies preach caution when using
NIV for ARDS. The lack of ability to control tidal volumes and the possible detriment
of causing a delay in intubation may lead to worse patient outcomes. In fact,
historically, failure rates of NIV in patients with ARDS were about 50%.
50% failure rate
Figure 2. Historically, the failure rate of noninvasive ventilation (NIV) for patients with acute respiratory
distress syndrome (ARDS) was 50%.
Using the P/F ratio to determine if NIV is appropriate for

your ARDS patient
More recent data indicates that the success of NIV in ARDS depends upon the
severity of the disease. ARDS is a form of severe hypoxic respiratory failure that is
graded as mild, moderate, or severe according to the ratio of PaO2 (partial pressure
of arterial oxygen) from a blood gas to the FIO2 (fractional concentration of inspired
oxygen) delivered. This ratio is more commonly referred to as the P/F ratio.
Whereas 40% or more of patients with moderate to severe disease can fail NIV, only
20% of patients with mild disease will fail NIV.
20% > 40%
Mild Moderate Severe
Figure 3. Failure rate of noninvasive ventilation (NIV) for acute respiratory distress syndrome (ARDS) depends
on the severity of the disease based on the P/F ratio. Those cases determined to have a mild disease have only
a 20% failure rate, while those with moderate or severe disease have a greater than 40% failure rate

What factors could contribute to failure of NIV?
Factors associated with failure of NIV at initiation of therapy
• Higher severity of illness scores

• Higher respiratory rates
Factors associated with failure of NIV after initiating therapy
• Worsening partial pressure of arterial carbon dioxide (PaCO2) levels

• Worsening P/F levels over the initial 24–48 hours
ARDS patients who fail NIV have a higher mortality rate, so these variables may lead
to more appropriate patient selection and earlier use of invasive ventilation when
patients are not improving with therapy.
ARDS remains a complicated disease to manage. We know from observational data

that NIV is used in approximately 15% of ARDS cases.

Managing asthma
Imagine during your next clinical shift you’re called to evaluate a patient with a his-
tory of asthma. She is in severe respiratory distress. Since you recently had good
success with using noninvasive ventilation (NIV) in a patient with chronic obstruc-
tive pulmonary disease (COPD), you consider using NIV in this patient with asthma.
Asthma is similar to COPD—in both, there is airway obstruction, particularly during

expiration. And while the obstruction is somewhat different in its pathology—asthma
has inflammation due to an accumulation of mucus and thickening of the bronchial
walls whereas COPD has the loss of elasticity to the walls—you wouldn’t be alone to
think that the treatment should provide similar beneficial results.
COPD Asthma
Figure 1. Both asthma and chronic obstructive pulmonary disease (COPD) are obstructive airway diseases,
however, the pathophysiology is different. In COPD the airway obstruction is caused by a loss of elasticity.
While in asthma the obstruction is due to an accumulation of mucus and thickening of the bronchial walls.
However, there is a lack of literature on the use of NIV in acute asthma exacerbations.
A 2011 clinical practice guideline from the Canadian Critical Care Trials Group
“make(s) no recommendation about the use of noninvasive positive-pressure
ventilation in patients who have an exacerbation of asthma, because of insufficient
evidence.” 1
In fact, no studies have demonstrated improved morbidity or mortality rates from

the use of NIV in patients with asthma.
For these same reasons, a 2012 Cochrane Review on NIV for acute asthma
exacerbations states that “this course of treatment remains controversial.” 2

Figure 2. Based on the literature, the treatment of asthma with noninvasive ventilation (NIV) remains
controversial.
No large randomized trial has evaluated the use of continuous positive airway
pressure (CPAP) in asthma patients. In the literature that exists, the small trials
looking at CPAP in asthma concluded there was no harm to its use, but reported
no conclusive mortality or intubation benefit. The physiologic benefits of improved
airflow and improved deposition of nebulized bronchodilators have not translated
into a measurable change in clinical outcomes.
So, despite the lack of support from guidelines and medical literature, I hope I have
still convinced you to consider a trial of NIV for your patient in asthma.

Addressing altered mental status
Conventional teaching states that altered mental status (AMS) is a contraindication
to use of noninvasive ventilation (NIV) due to three main concerns:
1. Patients with certain types of AMS have a risk of developing aspiration with
positive-pressure ventilation, or NIV.
2. Patients whose AMS results in agitated behavior may have reduced

cooperation with a tight-fitting NIV mask.
3. Due to the tight seal of the NIV mask, secretions cannot be cleared from their
mouth if needed.
But not all altered mental status is the same! The presence of AMS is not as
important as the type of AMS. For example, patients with coma are different from
patients with agitated delirium or patients with confusion.
Using NIV for patients with coma

Literature supports the use of NIV in patients with a low Glasgow Coma Scale (GCS)
score. In fact, NIV can be successful in patients with a GCS score of less than 8,
especially if the cause of the low GCS score is due to confusion from hypercapnia
such as in acute exacerbations of chronic obstructive pulmonary disease (AECOPD).
Similarly, mental status changes such as delirium due to an infection may also be
amenable to the use of NIV.
Figure 1. The literature supports the use of noninvasive ventilation (NIV) in a subset of patients with a low
Glasgow Coma Scale (GCS) score. NIV can be used for patients with confusion due to hypercapnia or delirium,
but it is not recommended for patients in a deep coma due to neurological injury such as seizure or stroke.

However, patients in a deep coma due to neurological injury, such as seizure, stroke
or similar diseases, would likely not be candidates since it would be atypical for
the altered mental status to be rapidly reversed or controlled with medications or
supportive care.

Chapter 5
SITUATIONAL
APPLICATIONS
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Preoxygenating with NIV
Noninvasive ventilation (NIV) has an excellent track record when used for chronic
obstructive pulmonary disease (COPD) and pulmonary edema; yet it has limited
success with other diseases, such as pneumonia, acute respiratory distress
syndrome (ARDS), and asthma. But, as you may guess, every patient responds
differently to treatment with NIV. And patients that do not improve on NIV, may need
endotracheal intubation and invasive mechanical ventilation.
Can I use NIV to preoxygenate before intubation?

When NIV should not be used
Noninvasive ventilation should not be used for preoxygenation before routine

intubations. In situations like elective surgeries or procedures, a nonrebreather
mask (NRB) or a bag-valve-mask (BVM) is typically used.
When NIV should be used
When patients who require endotracheal intubation have hypoxia despite the use of
greater than 6 L / min of oxygen, delivered via nasal cannula, consider the use of NIV
as a tool for preoxygenation. These patients have a much higher risk of developing
low oxygen levels during the process of intubation, compared with patients who are
not on oxygen. In these cases, NIV is the preferable preoxygenation choice.
Using NIV for preoxygenation will allow for longer periods of normal oxygen levels
during apnea—once the patient is sedated, the NIV mask will need to be removed to
perform laryngoscopy and insertion of the endotracheal tube.
NIV versus NRB
Using NIV in patients prior to intubation can optimize their oxygen saturation and
blood oxygen content. NIV can deliver a set pressure and fraction of inspired oxygen
(FIO2) to patients through the mask interface, neither of which is possible with an NRB.
The NIV mask is placed so that it is tight-fitting and minimizes leakage. Compared
to the NRB mask, this delivery of positive pressure can improve preoxygenation by
allowing a higher FIO2 to be delivered to the patient.

NIV versus BVM
Noninvasive ventilation also improves preoxygenation when compared with a BVM.

Rather than using manual application of the BVM to the face, the NIV mask interface
can be optimally positioned to deliver oxygenated gas with minimal leakage around
the mask. The NIV ventilator can deliver inspiratory and expiratory pressures at a
set FIO2.
What settings should one choose initially to allow

a successful preoxygenation?
Typical settings for preoxygenation using NIV are pressure support (PS) of 10
cmH2O, positive end-expiratory pressure (PEEP) of 5 cmH2O, and the fraction of
inspired oxygen (FIO2) at 100%.
• Pressure support (PS) 10 cmH20

• Positive end-expiratory pressure (PEEP) 5 cmH20
• Fraction of inspired oxygen (FIO2) 100%
Figure 1. Typical settings for preoxygenation using noninvasive ventilation (NIV) are pressure support (PS)
of 10 cmH2O, positive end-expiratory pressure (PEEP) of 5 cmH2O, and the fraction of inspired oxygen (FIO2)
at 100%.
The goal is to get the patient’s oxygen saturation as high as possible. If they continue
to have oxygen saturation < 95%, consider increasing your positive end-expiratory
pressure, or PEEP, to 8 or 10 cmH2O, as tolerated by the patient.
Time is precious during attempts at intubation! You don’t want to have a situation
where the patient’s oxygen levels are dropping before the endotracheal tube is
inserted. Preoxygenation with NIV gives you more time to successfully complete the
intubation procedure, avoiding the possibility of deadly complications.

Applying NIV after extubation
When removing patients from mechanical ventilation, physicians are faced with a
sobering fact—up to 15–20% of patients will require reintubation within 48 hours.
And, patients who are reintubated after an unsuccessful extubation have a worse
prognosis, even when controlling for the severity of their illness.
Noninvasive ventilation (NIV) can be used to try to treat post-extubation respiratory

failure—or be used to attempt to prevent post-extubation respiratory failure before
it occurs. Here, we’ll examine whether NIV is effective in each of these scenarios.
Can NIV be used to prevent post-extubation

respiratory failure?
There have been a few studies that have looked at routine extubation to NIV
compared with extubation to standard treatment, such as a nonrebreather mask.
There was no conclusive difference between these two groups in the rate of
reintubation, suggesting that NIV did not prevent the onset of post-extubation
respiratory failure, and provided no benefit when routinely used after extubation.
However, several studies have examined the effects of NIV in older patients with
cardiac or respiratory comorbidities who were at high-risk of failure of extubation.
Most showed improvements in the rates of respiratory failure, reintubation, and
mortality when NIV was applied.
Respiratory failure
Reintubation
Mortality
Figure 1. Noninvasive ventilation (NIV) can help lower reintubation, mortality, and respiratory failure in older
patients with cardiac or respiratory comorbidities.

One subset of patients with respiratory disease at high-risk for reintubation has
been looked at with greater frequency than other groups. Patients with acute
exacerbations of chronic obstructive pulmonary disease (AECOPD) can benefit
from the use of NIV when weaning from mechanical ventilation. Even when these
patients do not pass a spontaneous breathing trial (SBT), extubation to NIV can
result in improved mortality, decreased weaning failure, and decreased incidence of
ventilator-associated pneumonia (VAP).
Mortality
Reintubation
Ventilator-association pneumonia (VAP)
Figure 2. Noninvasive ventilation (NIV) can help lower mortality, reintubation, and ventilator-associated
pneumonia (VAP) in patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD).
Since treating all patients after extubation with NIV may only help some, you might
be wondering if you can wait until patients develop overt respiratory failure after
extubation before applying NIV?
Can NIV help treat post-extubation respiratory

failure?
Despite positive results from some early case-control studies, further investigation
found no improvement in patients when NIV was used after the development of
respiratory failure. In fact, in the largest trial, patients actually did worse when NIV
was applied—possibly because the use of NIV delayed endotracheal intubation.
Now you know that NIV does not have a role in the treatment of patients undergoing routine
extubation, and isn’t effective in treating patients with signs of respiratory failure. But to
improve liberation from mechanical ventilation, use NIV in patients with cardiorespiratory
comorbidities at a high-risk for reintubation or patients who have AECOPD.

Using NIV in palliative care
In certain situations, you may encounter a patient with respiratory failure who has
a Do Not Intubate (DNI) order. Or, perhaps, you may encounter someone with a
terminal disease, such as cancer, who develops severe dyspnea after deciding on
treatment with palliation only. Where does noninvasive ventilation (NIV) fit in with
the treatment of these subsets of patients, for whom intubation is not an option?
Can NIV be used for patients with a DNI order?

There is little in the way of quality evidence or guideline recommendations to provide
a comprehensive understanding regarding the use of NIV only in patients presenting
with respiratory failure and DNI orders.
There have been reports of patients with chronic obstructive pulmonary disease
(COPD) and congestive heart failure (CHF) being treated successfully with NIV in
approximately 50% of cases, in the setting of DNI orders.
~ 50%
Figure 1. Noninvasive ventilation (NIV) has been used successfully to treat chronic obstructive pulmonary
disease (COPD) and congestive heart failure (CHF) in 50% of patients with a Do Not Intubate (DNI) order.
In patients presenting with respiratory failure and a wish not to be intubated, a trial
of NIV should be conducted before attempting to transition to comfort measures
Can I use NIV to provide breathing comfort to

those at end of life?
At the end of life, breathlessness frequently worsens even if patients present with
non-respiratory illnesses. This can be a source of distress for the patient and family
members.

Medications such as opioids are often utilized at the end of life to treat
breathlessness, but can be associated with side effects such as itching, nausea,
and sedation. The use of NIV at the end of life can treat breathlessness and
dyspnea without the side effects of excessive sedation. Though generally seen
as an intervention with a high rate of intolerance, the use of NIV for palliation of
dyspnea has an adherence rate of about 60%. It can also decrease the feeling of
breathlessness and decrease the required dose of morphine.
~ 60%
Figure 2. Noninvasive ventilation (NIV) has a 60% adherence rate for the palliation of dyspnea.

Chapter 6
PRACTICAL PEARLS
FOR APPLYING NIV
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Choosing the right mask
For noninvasive ventilation (NIV) to be successful, patients must adhere to the
therapy you prescribe. In many cases, this has a lot to do with the mask interface that
is provided for the patient. Here, we’ll review the different types of mask interfaces
you can choose from.
There are many varieties of masks that are used for the delivery of NIV which can be
broadly categorized into nasal masks, facial masks (which can be partial or total),
and helmet masks. There is no lack of ingenuity of design, as a quick internet search
for NIV masks can result in dozens of varieties. Despite the myriad of options, the
selection of masks in the inpatient setting is limited: the most common masks are
the oronasal face mask, used in the majority of cases, followed by nasal masks, full
face masks (not shown), and helmets.
Nasal mask Face Mask Helmet
Figure 1. Three of the most common noninvasive ventilation (NIV) masks are nasal masks, (oronasal or
partial) face masks, and helmets.
Despite decades of research in NIV and frequent use of NIV in clinical settings, a
statement published in 1994 still rings true with regards to the choice and selection
of facial masks: “The optimal interface and ventilator design have not been
determined, and these may differ among patients.”
Face masks
Face masks are the most common interface used in acute respiratory failure. Due
to the inspiratory demand of patients with respiratory failure, many patients utilize
their mouths for inspiration to bypass nasal resistance. A face mask that covers the
mouth and nose, or less commonly one that covers the mouth, nose, and eyes, can
provide a comfortable fit while preventing pressure loss due to air leaking from the
perimeter of the mask.

Nasal masks
Nasal masks are most commonly used for long-term ventilation but can also be
used for acute hypoxic or hypercapnic respiratory failure. The two most common
varieties are nasal masks, which cover the nose, and nasal pillows, which support
tubing that inserts externally into the nares.
Both types allow for eating and drinking, patients can better tolerate coughing, and
there are fewer complaints of claustrophobia with this interface.
Helmets
Helmet interfaces are the least common but have recently shown the most promise
with regards to NIV.
They have a collar attached at the neck and shoulders and a hood that allows for
gas exchange. There are two ports into the helmet—one for gas entry and one for
exhalation of expired gases. A small study recently conducted in patients with acute
respiratory distress syndrome (ARDS) demonstrated good outcomes in patients
with helmet interface NIV.1
To allow patients the greatest benefit from NIV you may need to rotate between
the different mask interfaces. Due to the pressure placed by the tight fit of an
oronasal mask, allowing a break with a nasal pillow may allow for a longer duration
of prescribed therapy and reduce the potential complications of skin breakdown.

Initiating NIV
Meryl is a 72-year-old woman with a history of chronic obstructive pulmonary
disease (COPD) who presents to you with an acute exacerbation. She has increased
cough, sputum production, and a fever. She doesn’t use noninvasive ventilation
(NIV) at home.
Figure 1. Meryl, a 72-year-old woman with a history of chronic obstructive pulmonary disease (COPD) with
an acute exacerbation.
In the emergency department, she is wheezing, breathing at a rate of 26 breaths /

minute, and is using accessory muscles to exhale.
A blood gas sample is sent to the laboratory for analysis. The results show that she
has acute respiratory acidosis.
You deftly diagnose her as having an acute exacerbation of chronic obstructive

pulmonary disease (AECOPD) and decide to place her on NIV to decrease her
likelihood of intubation and death. After discussion with the respiratory therapist,
you choose a face mask to deliver NIV. You discuss the plan with Meryl who, upon
questioning, tells you she’s never had a tight-fitting mask before and is nervous to
have it applied.
So what do you do next?
You consider administering an anxiolytic to help with her adherence to the mask, but
you then consider the risks of sedation, worsening her hypercapnia, and potentially
leading to the need for endotracheal intubation. You wonder, are there any other tips
or tricks to help with applying the NIV interface to allow patients to adjust to this
form of breathing?

The key maneuver that will help you initiate
noninvasive ventilation
One key maneuver is to hand the patient the mask to hold up to their face lightly
before strapping it on. This can prevent a feeling of helplessness or claustrophobia
that some patients report. This allows the patient to have a level of control prior to
the initiation of this therapy.
Once the patient has gotten the feel for the mask, start out with 2–3 cmH2O of
continuous positive airway pressure (CPAP) to allow the patient to get used to this
level of positive pressure.
Continous positive
airway pressure (CPAP)
2—3 cmH20
Figure 2. Allowing the patient to hold a noninvasive ventilation (NIV) mask to their face with a low pressure
before strapping on can allow the patient to get used to the experience.
Once the patient is comfortable with this feeling, you or the respiratory therapist can
strap on the mask to ensure a proper fit. Allow the patient to adjust for a few more
minutes to this low-pressure setting before titrating up slowly.
The key here is to avoid the mistake of starting with too much pressure that will
make the patient intolerant from the start!
So remember, if time allows, coach your patients through the initiation of NIV to
improve their adherence. Allow them to try out the mask, start low, and go slow with
your titration.

Titrating NIV
Previously, you learned tips on initiating noninvasive ventilation (NIV): avoid the use
of sedative medications if possible, start with a single low pressure on the ventilator
(i.e., continuous positive airway pressure, or CPAP, mode), and allow patients to hold
the mask up to their face before tightly attaching the straps.
FigUre 1. When initiating noninvasive ventilation (NIV), avoid the use of sedative medications if possible, start
with a single low pressure on the ventilator, and allow patients to hold the mask up to their face before tightly
attaching straps.
The real benefit of NIV is achieved when you choose the right mode of ventilation
and adjust to the appropriate settings.
In order to get a handle on how to titrate NIV, let’s take a look at how to use NIV in
two different patients.
Titrating NIV in patients with acute exacerbations

of chronic obstructive pulmonary disease (AECOPD)
First, let’s take a look at Meryl, a 72-year-old woman with an acute exacerbation of
chronic obstructive pulmonary disease (AECOPD).
Figure 2. Case study image: a 72-year-old woman with acute exacerbations of chronic obstructive pulmonary
disease (AECOPD).

Choose the right mode
For Meryl, with her AECOPD, we will want to choose bilevel positive airway pressure
(BPAP) as our mode of NIV. Delivering two pressures, one during inspiration and one
during expiration, will assist with ventilation, offload her respiratory muscles, and
improve her airflow obstruction.
Meet the pressure goals
For Meryl to acclimate, we started with a continuous pressure of 2–3 cmH2O and
then titrated up to a pressure of 5 cmH2O. To provide her with an inspiratory and
expiratory pressure, we’ll want to add pressure support (PS) until we see a reduction
in respiratory rate. To do this, we’ll increase by 2 cmH2O every five minutes to end up
with a level between 7–10 cmH2O.
Figure 3. When using bilevel positive airway pressure (BPAP) to treat acute exacerbations of chronic
obstructive pulmonary disease (AECOPD), start with a continuous pressure of 2–3 cmH2O. Once your patient
has acclimatized, titrate up to 5 cmH2O. Add pressure support (PS) of 2 cmH2O every five minutes until a PS of
7–10 cmH2O is reached with a reduction in respiratory rate.
Monitor oxygen saturation
The fraction of inspired oxygen (FIO2) can be set anywhere between 21% and 100% to
meet the saturation goals of the patient. For Meryl, we’ll want her oxygen saturation
to be greater than 88%, and we’ll titrate the FIO2 to that goal.

Titrating NIV in patients with acute respiratory
failure
Now, let’s consider Tom, a 67-year-old male with acute respiratory failure, perhaps
from acute pulmonary edema.
Figure 4. Case study image: a 67-year-old man with acute pulmonary edema.
Choosing the right mode
For Tom, continuous positive airway pressure (CPAP) is the preferred treatment
option. Start with a low level of CPAP and increase the pressure by 2 cmH2O every
few minutes. Just like with BPAP, the FIO2 can be titrated between 21% and 100%
according to the patient’s saturation goals.
Meet the pressure goals
Studies of NIV on patients with pulmonary edema found a positive end-expiratory

pressure (PEEP) level of 8–12 cmH2O provided clinical benefit for most patients.
Figure 5. In patients with pulmonary edema, a positive end-expiratory pressure (PEEP) of 8–12 cmH2O is of
clinical benefit.

Monitor effects on increased inspiratory pressures
As you titrate upwards, be mindful of the effects of increased inspiratory pressures.
With high pressures it is easier for the interface to leak, undoing any benefit from
the increased pressure. Additionally, there is the risk of gastric insufflation as the
pressure of air overcomes the pressure of the lower esophageal sphincter. When
inspiratory pressure settings approach 25 cmH2O, one must consider intubation and
invasive mechanical ventilation.
But don’t forget about tidal volume (VT). Since we are setting pressure and not
volume, the VT will depend on the compliance of the patient’s lungs. High VT can
cause volutrauma to the lungs that may lead to worse outcomes. To reduce this
risk, adjust the inspiratory pressure and monitor the measured VT on the ventilator
to achieve between 6 and 8 mL / kg of predicted body weight.
Interface Gastric Volutrauma

leaking insufflation
Figure 6. When using noninvasive ventilation (NIV), high pressures can cause leaking at the mask interface,
increased risk of gastric insufflation, and volutrauma.

Chapter 7
HIGH-FLOW NASAL
CANNULA
www.medmastery.com
Appreciating high-flow nasal cannula (HFNC)
High-flow nasal cannula (HFNC), also referred to as nasal high flow, is a therapy that
has gained traction in the past decade and is sometimes lumped together with the
use of noninvasive ventilation (NIV). Since it differs from noninvasive ventilation, it
will be important to highlight differences between these two therapies.
Oxygen delivery with HFNC

Let’s take a moment to remember the traditional nasal cannula. When connected
to wall oxygen, this cannula can deliver oxygen at flow rates from 1 to 6 L / min
for extended periods of time. Higher flow rates are not well tolerated due to nasal
irritation and discomfort.
High-flow nasal cannula, or HFNC, is a system that allows oxygen to be delivered to

patients at very high flow rates. In adults, it can be titrated from 20 L / min up to 60
L / min! By using specialized nasal cannulas, heating the circuit to body temperature
and humidifying the air, these high rates can be delivered with very good patient
tolerance.
Like the flow rate, fraction of inspired oxygen (FIO2) can be precisely titrated as well.
An air-oxygen blender can take 100% wall oxygen, mix it with room air, and deliver a
FIO2 between 21 and 100%.
HFNC parameters
• FIO2 21—100%
• Flow 20—60 L / min
• Heat
• Humidity
Figure 1. High-flow nasal cannula (HFNC) systems use specialized nasal cannulas that allow oxygen to be
delivered at an FIO2 of 21–100% with high flow rates of 20–60 L / min. Heating the circuit to body temperature
and humidifying the air allows these high flow rates to be well tolerated by the patient.

How is HFNC like NIV?
HFNC is similar to NIV in that it reduces the entrainment of room air and allows a
more precise amount of oxygen to be delivered. It requires a specialized interface
that sits in the nose with larger bore openings. It can provide respiratory support to
patients with respiratory failure due to hypoxia.
How does HFNC differ from NIV?

HFNC differs to NIV in that it provides less ventilatory support. You set a flow
rate instead of setting inspiratory and expiratory pressures. Therefore, the
pressure produced from HFNC flow rates is much lower in comparison to NIV.
HFNC NIV
• Large bore nasal cannula • Mask interface
• Reduces room air entrapment • Reduces room air entrapment
• Set flow rate • Set pressures
• Less pressure produced • Greater ventilatory support
• Supports patients with hypoxia • Supports patients with hypoxia
Figure 2. Similar to noninvasive ventilation (NIV), high-flow nasal cannula (HFNC) reduces room air entrapment
to allow for more precise oxygen delivery, uses a specialized interface, and can provide respiratory support to
patients with hypoxia. Unlike NIV, in HFNC, flow rates are set and less pressure is produced from these flow rates.
When should I avoid use of HFNC?

Do not use high-flow nasal cannula, or HFNC, in patients with:
• Ventilatory failure
• Hypercapnia
Ventilatory failure Hypercapnia
Figure 3. High-flow nasal cannula (HFNC) should not be used for a patient with ventilatory failure and hypercapnia.

Addressing how HFNC works
High-flow nasal cannula (HFNC) is a heated and humidified system that allows
prescribed fraction of inspired oxygen (FIO2) levels to be delivered at very high flow
rates. Let’s now consider how HFNC can help our patients improve their respiratory
disease.
There are three main proposed benefits of HFNC:

1. Precise oxygen delivery
2. Functional residual capacity enhancement
3. Dead space washout
Precise oxygen delivery

Traditional nasal cannula delivers flow rates of 2–6 L / min. But patients with respiratory
distress can have much higher peak inspiratory flow rates. If the inspiratory flow rate
of the patient is greater than what is being provided by the cannula, the patient will
entrain room air into the lungs. This results in oxygen dilution, and the patient will not
be receiving the precise amount of oxygen that is desired.
When high-flow nasal cannula, or HFNC, is used to deliver oxygen, the flow rates are
much higher than can be achieved with traditional nasal cannula. This results in a
greater delivery of prescribed oxygen into the lungs, and less entrainment of room air.
The oxygen you want to deliver to your patients is not prone to the same effect of dilution!
Figure 1. Differences in oxygen delivery between traditional nasal cannula and high-flow nasal cannula
(HFNC). When using the traditional nasal cannula, if the inspiratory flow rate of the patient is greater than what
is being provided by the cannula, the patient will entrain room air into the lungs, resulting in oxygen dilution.
When using HFNC, inspiratory flow rates of oxygen are higher, resulting in greater delivery of prescribed
oxygen into the lungs, and less entrainment of room air.

Functional residual capacity enhancement
HFNC also exerts its effect by providing some variable positive pressure.
When measured with manometers in the posterior oropharynx with closed mouth
breathing, the pressures are modest, but the effect nearly goes away when patients
open their mouths.
Despite this discrepancy, studies show that the functional residual capacity (FRC)
increases by about 25% when HFNC is applied.
Figure 2. By providing variable positive pressure, use of high-flow nasal cannula (HFNC) increases functional
residual capacity (FRC) by about 25% compared to use of traditional nasal cannula.
Dead space washout

Lastly, when HFNC is applied, the constant high flow of oxygen provides a washout
of the anatomical dead space of the oropharynx and proximal tracheobronchial tree,
which results in more efficient breathing.
Figure 3. Compared to traditional nasal cannula, the use of high-flow nasal cannula (HFNC) results in more efficient
breathing due to a washout of anatomical dead space in the oropharynx and proximal tracheobronchial tree.

Treating hypoxic patients
Once you’ve gotten the hang of the inner workings of high-flow nasal cannula
(HFNC), you’re ready to make the jump to the clinical applications of this oxygen
therapy.
Remember that high-flow nasal cannula works by reducing oxygen dilution,

improving functional residual capacity (FRC), and creating more efficient breathing
through dead space washout.
For a moment, think about a patient you might see presenting with pneumonia.
You’ve astutely ordered a chest x-ray, confirmed the diagnoses, and started
antibiotics. But your patient’s oxygen saturations continue to drop even when you
place them on traditional nasal cannula.
Figure 1. Patients with pneumonia may have low blood oxygen levels (i.e., hypoxia) and therefore require more
oxygen than a traditional nasal cannula can deliver.
Your patient needs more oxygen, but how are you going to deliver it? Turn the regular
nasal cannula up? Place the patient on oxygen via facemask? How about a move to
noninvasive ventilation (NIV)?
Hopefully you’ve considered high-flow nasal cannula! HFNC has been most robustly
studied in patients with hypoxic respiratory failure.
In fact, when put head to head against both traditional oxygen therapy and
noninvasive ventilation in patients with hypoxic respiratory failure, HFNC was found
to reduce the need for intubation in the sickest patients, and was able to reduce
mortality at 90 days.

Figure 2. In patients with hypoxic respiratory failure, high-flow nasal cannula (HFNC) was found to reduce the
need for intubation in the sickest patients, and was able to reduce mortality at 90 days when compared to
traditional nasal cannula and noninvasive ventilation (NIV).
It is important to understand that these studies were carried out in patients without
a number of medical problems—notably heart failure and acute exacerbations of
chronic obstructive pulmonary disease (AECOPD). But these patients were very sick,
and many had bilateral pneumonias.

Extubating to HFNC
Despite the benefits of high-flow nasal cannula (HFNC) in reducing the need for
intubation in patients with moderate and severe lung injury, 30% of patients may end
up requiring intubation and mechanical ventilation. Since high-flow nasal cannula
can improve oxygen delivery, wash out upper airway dead space, and improve
the functional residual capacity, let’s evaluate HFNC for respiratory support after
extubation.
Consider a patient with pneumonia. Despite antibiotics and the use of high flow
oxygen for hypoxia, the patient worsens and requires mechanical ventilation.
After five days of excellent intensive care unit (ICU) care, the patient is passing a
spontaneous breathing trial (SBT) and ready for extubation.
Role of HFNC after extubation

Traditionally, patients would be extubated to a traditional nasal cannula. Noninvasive
ventilation (NIV) would be used for patients with continued hypercapnia during the
breathing trial or those considered high-risk for extubation failure.
HFNC has been found to reduce the need for reintubation after liberation from
mechanical ventilation. HFNC has been evaluated in patients with both a low-risk
for reintubation and a high-risk for reintubation.
HFNC use in patients at low-risk for reintubation
Patients who are low-risk for reintubation are generally young, have few
comorbidities, were not intubated very long and passed their first attempted SBT.
These are patients that most clinicians would predict would do very well after
extubation.
Remarkably, the use of high-flow nasal cannula in this low-risk cohort reduced the
risk of reintubation by 7% when compared to conventional oxygen given by nasal
cannula or face mask.

Figure 1. Patients at low-risk of reintubation are young, without many comorbidities, not intubated for very
long, and passed their first attempted spontaneous breathing trial (SBT). The use of high-flow nasal cannula
(HFNC) in these patients reduced the risk of reintubation by 7% when compared to conventional oxygen given
by nasal cannula or face mask.
HFNC use in patients at high-risk for reintubation
But, what role can HFNC play in patients at high-risk for reintubation?
Patients without the low-risk features previously discussed—those that are older, were
intubated longer, had congestive heart failure or chronic obstructive pulmonary disease
(COPD), and were hypercapnic—were studied to determine the need for reintubation.
In the high-risk cohort, there was no statistical difference in failure when extubating
to the HFNC compared to NIV mask, suggesting that HFNC is equally as effective in
patients at highest risk for reintubation.
Figure 2. Patients at high-risk of reintubation are older, have congestive heart failure (CHF) or chronic
obstructive pulmonary disease (COPD), intubated longer, and hypercapnic. For this patient group, there is
no statistical difference in failure rates between extubating to the high-flow nasal cannula (HFNC), and the
noninvasive ventilation (NIV) mask.
So, high-flow nasal cannula, or HFNC, can reduce the risk of reintubation in low or high-
risk patients by a value greater than or equal to that of conventional approaches.

Predicting failure
Just as with noninvasive ventilation (NIV), high-flow nasal cannula (HFNC) is not
100% successful and not indicated in all forms of respiratory disease. Let’s discuss
the choice of patients who receive HFNC and how monitoring their response can
predict the failure of therapy.
Patient selection
There are two key patient groups in which HFNC should generally be avoided.
1. Patients with acute exacerbations of COPD (AECOPD)
2. Intensive care unit (ICU) patients on vasoactive drips
Patients with acute exacerbations of chronic obstructive

These are patients that you know will receive benefit from the use of NIV. However,
the use of HFNC in these patients is much less studied.
Figure 1. In patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD), the benefit
of using noninvasive ventilation (NIV) is clear.
High-flow nasal cannula, or HFNC, can be attempted during breaks from NIV, but
shouldn’t be considered as a replacement for NIV.
Intensive care unit patients on vasoactive drips
The next group of patients in which HFNC should generally be avoided is patients
who are on vasoactive drips in the intensive care unit.

Patients who are in shock and require vasopressors have a much higher rate of
HFNC failure. Consideration should be made for earlier intubation in these patients.
Figure 2. High-flow nasal cannula (HFNC) should not be used on patients in the intensive care unit (ICU) with
vasoactive drips.
Patient monitoring
Now we need to consider the role of monitoring clinical variables after placing
patients on high-flow nasal cannula. Let’s say we’ve put our patient with pneumonia
on HFNC and they are requiring 50 L of flow and an FIO2 of 60%. How will we know if
our patient is likely to fail HFNC therapy?
Indications of possible high-flow nasal cannula (HFNC) failure:

1. Persistence of thoracoabdominal dyssynchrony
2. Increased respiratory rate
3. Increase in oxygen requirements

Chapter 8
BONUS LESSON
www.medmastery.com
Noninvasive ventilation for the support of
COVID-19 pneumonia
In a matter of weeks, a novel coronavirus named SARS-CoV-2, and the resulting
illness, COVID-19, has caused a worldwide pandemic. As countries around the world
ration supplies and national stockpiles of ventilators are being commissioned, it is
worth discussing the role of noninvasive ventilation (NIV) as it pertains to patients
with severe illness due to COVID-19.
Many guidelines are recommending against the use of noninvasive ventilation in

patients with COVID-19, for two reasons:
1. NIV can result in an increase risk to hospital staff.
2. NIV may not be helpful and may cause harm to patients.
Let’s talk about these points in a little more detail.
Can the use of NIV increase the risk of exposure

for staff?
Let’s first deal with staff safety and the risk of aerosol-based transmission to health
care workers.
Some reports have stated that SARS-CoV-2 can remain viable in aerosols for up to
three hours, and NIV has been grouped together with a variety of other respiratory
procedures that may cause aerosolization (e.g., intubation, extubation, nebulization,
and bronchoscopy). Given the risk of aerosol dispersion through or around the mask
interface, and the fact that certain interfaces contain asphyxiation valves or ports
that can leak out exhaled gases, certain guidelines suggest noninvasive ventilation
should be avoided completely. In addition, improper fit may cause leaking gas from
around the mask
Using smoke to simulate aerosols, studies have looked at the dispersion distance
with a variety of respiratory support devices.1 A traditional nasal cannula at 5 L / min
demonstrated a dispersion of 100 cm. When there’s a leak or a valve in a NIV mask,
on a bilevel setting (BPAP) with an inspiratory positive airway pressure (IPAP) of 18
cmH2O, maximal dispersion in a negative pressure room was measured at 92 cm.
Shorter distances were demonstrated with lower inspiratory pressures—but still,
NIV results in larger dispersion distances compared to other noninvasive support
methods.2

Figure 1. Maximal dispersion of simulated aerosols when there’s a leak or a valve in a noninvasive interface,
with an inspiratory positive airway pressure (IPAP) of 18 cmH2O, was measured at 92 cm. A dispersion of 100
cm was demonstrated when using a traditional nasal cannula at 5 L / min.
And, based on data from the original SARS outbreak, use of noninvasive ventilation,
or NIV, was associated with an increased risk of encountering respiratory secretions,
and an increased risk of transmission of SARS to health care workers. COVID-19
may act differently, but we may not have reliable data for weeks to months. So, until
we have a better understanding, it’s best to only use NIV for patients with COVID-19
with caution and by following the most up-to-date recommendations at the time.
Does NIV help or harm patients with COVID-19?

Another concern about the use of NIV in patients with COVID-19 is the potential that
it will be ineffectual.
COVID-19 may cause a severe viral pneumonia that meets the definition of the acute
respiratory distress syndrome (ARDS). But we must be cautious with the use of NIV
in pneumonia and ARDS. Historical failure rates are around 50%.
50% failure rate
Figure 2. The use of noninvasive ventilation (NIV) in patients with acute respiratory distress syndrome (ARDS)
has a failure rate of 50%.

Additionally, noninvasive ventilation may cause harm to patients through two
different mechanisms, leading to worsening patient outcomes:
1. The lack of ability to control tidal volumes
2. The possible delay in intubation and mechanical ventilation
Applying NIV in patients with COVID-19

So, what to do if noninvasive ventilation, or NIV, might be the only option or seems
like a reasonable thing to try? For example, if you have a patient with an acute
exacerbation of chronic obstructive pulmonary disease (AECOPD) with wheezing,
and you suspect COVID-19, NIV may be a reasonable choice.
There are 5 steps to follow when using using NIV to treat

patients with COVID-19:
1. Ensure that you are able to get a negative pressure room. If none are available,
obtain a single occupancy room and ensure the door is closed at all times.
2. Choose the best interface for the patient’s tolerance. When available, consider
a helmet or full-face mask interface to minimize particle dispersion. Ensure a
good seal, and make sure the mask does not have an anti-asphyxiation valve
or cord.
3. Use dual limb circuitry with a filter on the expiratory limb of a critical care
ventilator. This may decrease dispersion compared with single limb circuitry
portable devices.
4. Start with continuous positive airway pressure (CPAP) using the lowest effective
pressures, between 5 and 8 cmH2O. Early reports suggest most patients with
COVID-19 are not hypercapnic, so bilevel positive airway pressure (BPAP) may
result in increased inspiratory pressures without any added benefit.
5. Reevaluate patients within the first few hours of therapy. If patients are not
responding, consider intubation and mechanical ventilation.

Figure 4. The 5 steps to follow when applying noninvasive ventilation (NIV) in patients with COVID-19.

Headline
Text
APPENDIX
www.medmastery.com

References and recommended reading
References
Chapter 3: Traditional applications

1. Bott, J, Carroll, MP, Conway, JH, et al. 1993. Randomised controlled trial of nasal
ventilation in acute ventilatory failure due to chronic obstructive airways disease.
Lancet. 341: 1555–1557. PMID: 8099639
2. Brochard, L, Mancebo, J, Wysocki, M, et al. 1995. Noninvasive ventilation for

acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med.
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3. Ram, FSF, Picot, J, Lightowler, J, et al. 2004. Non-invasive positive pressure

ventilation for treatment of respiratory failure due to exacerbations of chronic
obstructive pulmonary disease. Cochrane Database Syst Rev. CD004104.
PMID: 15266518
Chapter 4: Controversial uses

1. Keenan, SP, Sinuff, T, Burns, KEA, et al. 2011. Clinical practice guidelines for the
use of noninvasive positive-pressure ventilation and noninvasive continuous
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Chapter 6: Practical pearls for applying NIV

1. Patel, BK, Wolfe, KS, Pohlman, AS, et al. 2016. Effect of noninvasive ventilation
delivered by helmet vs face mask on the rate of endotracheal intubation in
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JAMA. 315: 2435–2441. PMID: 27179847

Chapter 8: Bonus lesson
1. Hui, DS, Chow, BK, Lo, T, et al. 2015. Exhaled air dispersion during noninvasive
ventilation via helmets and a total facemask. Chest. 147: 1336–1343.
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Recommended reading
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Hillberg, RE and Johnson, DC. 1997. Noninvasive ventilation. N Engl J Med.

337: 1746–1752. PMID: 9392701
Chapter 2: Physiologic effects of NIV

Kallet, RH and Diaz, JV. 2009. The physiologic effects of noninvasive ventilation.
Respir Care. 54: 102–115. PMID: 19111110
Chapter 3: Traditional applications

Berbenetz, N, Wang, Y, Brown, J, et al. 2019. Non-invasive positive pressure
ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane
Database Syst Rev. 4: CD005351. PMID: 30950507
Bott, J, Carroll, MP, Conway, JH, et al. 1993. Randomised controlled trial of nasal
ventilation in acute ventilatory failure due to chronic obstructive airways disease.
Lancet. 341: 1555–1557. PMID: 8099639
Brochard, L, Mancebo, J, Wysocki, M, et al. 1995. Noninvasive ventilation for acute

exacerbations of chronic obstructive pulmonary disease. N Engl J Med.
333: 817–822. PMID: 7651472

Hukins, CA. 2005. Arbitrary-pressure continuous positive airway pressure for
obstructive sleep apnea syndrome. Am J Respir Crit Care Med. 171: 500–505.
PMID: 15563637
Ram, FSF, Picot, J, Lightowler, J, et al. 2004. Non-invasive positive pressure

ventilation for treatment of respiratory failure due to exacerbations of chronic
obstructive pulmonary disease. Cochrane Database Syst Rev. CD004104.
PMID: 15266518
Veasey, SC and Rosen, IM. 2019. Obstructive sleep apnea in adults. N Engl J Med.
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mortality for patients with acute respiratory distress syndrome in intensive care
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community-acquired pneumonia and severe acute respiratory failure. Intensive
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Ferrer, M, Esquinas, A, Leon, M, et al. 2003. Noninvasive ventilation in severe

hypoxemic respiratory failure: a randomized clinical trial. Am J Respir Crit Care
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ventilation for acute respiratory failure in patients with hematologic malignancies:
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immunosuppressed patients with pulmonary infiltrates, fever, and acute respiratory
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Holley, MT, Morrissey TK, Seaberg, DC, et al. 2001. Ethical dilemmas in a
randomized trial of asthma treatment: can Bayesian statistical analysis explain the
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ventilation vs oxygen therapy on mortality among immunocompromised patients
with acute respiratory failure: a randomized clinical trial. JAMA. 314: 1711–1719.
PMID: 26444879
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patients with acute lung injury: observational cohort study. Crit Care. 10: R79.
PMID: 16696863
Rodríguez, A, Ferri, C, Martin-Loeches, I, et al. 2017. Risk factors for noninvasive

ventilation failure in critically ill subjects with confirmed influenza infection. Respir
Care. 62: 1307–1315. PMID: 28698265
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ventilation in patients with acute exacerbations of COPD and varying levels of
consciousness. Chest. 128: 1657–1666. PMID: 16162772
Soma, T, Hino, M, Kida, K, et al. 2008. A prospective and randomized study for
improvement of acute asthma by non-invasive positive pressure ventilation
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controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest.
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hypoxemic respiratory failure: intubation rate and risk factors. Crit Care. 17: R269.
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Chapter 5: Situational applications

Baillard, C, Fosse, JP, Sebbane, M, et al. 2006. Noninvasive ventilation improves
preoxygenation before intubation of hypoxic patients. Am J Respir Crit Care Med.
174: 171–177. PMID: 16627862

Esteban, A, Frutos-Vivar, F, Ferguson, ND, et al. 2004. Noninvasive positive-
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extubation in hypercapnic patients with chronic respiratory disorders: randomised
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Chapter 6: Practical pearls for applying NIV

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Chapter 7: High-flow nasal cannula

Dysart, K, Miller, TL, Wolfson, MR, et al. 2009. Research in high flow therapy:
mechanisms of action. Respir Med. 103: 1400–1405. PMID: 19467849
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in acute hypoxemic respiratory failure. N Engl J Med. 372: 2185–2196.
PMID: 25981908
Hernández, G, Vaquero C, Colinas, L, et al. 2016. Effect of postextubation

high-flow nasal cannula vs noninvasive ventilation on reintubation and
postextubation respiratory failure in high-risk patients: a randomized
clinical trial. JAMA. 316: 1565–1574. PMID: 27706464

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Noninvasive Ventilation Handbook

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Noninvasive Ventilation Handbook

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NONINVASIVE

Modes of noninvasive ventilation

Physiologic effects of NIV

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High-flow nasal cannula

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AECOPD – Acute exacerbations of chronic obstructive pulmonary disease

AMS – Altered mental status

ARDS – Acute respiratory distress syndrome

BMI – Body mass index

BPAP – Bilevel positive airway pressure

COPD – Chronic obstructive pulmonary disease

CPAP – Continuous positive airway pressure

DNI – Do not intubate

EPAP – Expiratory positive airway pressure

FIO2 – Fraction of inhaled oxygen

FRC – Functional residual capacity

GCS – Glascow Coma Scale

HFNC – Hyphenate high-flow canula

ICU – Intensive care unit

IPAP – Inspiratory positive airway pressure

NIV – Noninvasive ventilation

NRB – Nonrebreather mask

OSA – Obstructive sleep apnea

PaCO2 – Partial pressure of arterial carbon dioxide

PaO2 – Partial pressure of arterial oxygen

PEEP – Positive end-expiratory pressure

V/Q matching – Ventilation-perfusion matching

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Continuous pressure FIO2

Common clinical uses for CPAP

Pulmonary edema Sleep apnea Pickwickian

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Bilevel pressure FIO2

Common clinical use for BPAP

Acute exacerbation of chronic obstructive

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The others—IPAP (inspiratory positive airway pressure), EPAP (expiratory positive

What is pressure support?

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1. Initial IPAP / EPAP

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1. Initial IPAP / EPAP

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There are three main ways by which NIV improves oxygenation:

1. NIV increases the delivery of FIO2

2. NIV reduces entrainment of room air

Oxygen mask NIV

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Before NIV After NIV

This results in better ventilation and perfusion matching, also known as

Before NIV After NIV

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What is minute ventilation?

Minute ventilation = respiratory rate (RR) × tidal volume (VT)

1. NIV improves tidal volume

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Without NIV With NIV

2. NIV counteracts intrinsic PEEP

Another method of improving ventilation relates to the intrinsic pressure created by