Mechanical Ventilation.pdf

Mechanical Ventilation

Routine practice in mechanical
ventilation in cardiac surgery

Directed by
DR.Karar .A.Ali

department of cardiothoracic surgery
[email protected]

-check air compressor (or AIR supply)
-check O2
-Check Electrical Supplies
-Check circuit

-Check bar panal
ventilators require both air and oxygen in
the range of 2 to 6 bars
-Check humidifier

CARESCAPE R860
the number and value is
just example

This just example

Inappropriate Sensitivity Setting: An insensitive flow trigger level (e.g. > 5 L/min below
bias flow) will increase the time delay between the onset of patient effort and the onset of
the mechanical breath that often results in substantial increases in patient work of
breathing and respiratory drive and patient-ventilator asynchrony. As described above, a
too sensitive ventilator causes excessive triggering that can interfere with ventilation and
can increase the risk of hyperinflation, barotrauma, hemodynamic instability and
hyperventilation during assist-control or high levels of pressure support ventilation.

expiratory trigger sensitivity
A typical ETS setting in a patient with normal lung mechanics
undergoing NIV is 25%
With obstructive patients, for example, in a patient with
chronic obstructive pulmonary disease (COPD), ETS should be
set higher to increase the expiratory time and thus avoid air-
trapping and intrinsic PEEP.

.
flow triggers ranging from 0.7 to 2.0 L/min)

•Definition and Classification
•Definition
•Mode refers to the characteristics of mechanical ventilation
which mainly include trigger (how inspiration begins), cycle
(how inspiration ends), and limit (when inspiration should
be aborted). The most commonly used modes are assist
control ventilation (ACV), especially for initiating ventilation,
and synchronized intermittent mandatory ventilation (SIMV)
with pressure support, especially for maintaining patients
on and weaning them off ventilation.
•Ventilator mode is described based on 3 characteristics:
trigger, cycle, and limit.

•Trigger: The type of signal that initiates the inspiratory
phase by the ventilator.
–Patient-triggered: patient’s inspiratory effort triggers the
inspiratory phase by the ventilator.
–Time-triggered: a time interval set by the operator determines
when the ventilator initiates an inspiratory phase.
•Cycle: The type of signal that ends the inspiratory phase
delivered by the ventilator. Volume-cycled ventilation: the
inspiratory phase ends once a preset volume exits the
ventilator.
•Other types include time-cycled ventilation and pressure-
cycled ventilation.
•Limit: A value (e.g., pressure) that should not be exceeded
and which is specified by the operator to protect the lung.

•Classification (common modes)
•Controlled: Commonly used in critically ill patients
with a significantly suppressed or absent respiratory
drive. All spontaneous patient breaths sensed by the
ventilator are assisted with a preset volume (or less
commonly preset pressure) specified by the operator.
These modes are patient-/time-triggered and volume-
/pressure-cycled.
–Assist-control ventilation (ACV), also known as volume-
control (VC) ventilation (VCV): more commonly used
–Pressure-control (PC) ventilation (PCV)

•Spontaneous/Supported: Used after significant
improvement of the critical state in patients who are
able to breathe spontaneously and are being
considered for weaning. These modes are patient-
triggered and flow-cycled. Pressure support (PS): all
spontaneous patient breaths sensed by the ventilator
are supported with a preset pressure specified by the
operator.
•Continuous positive airway pressure (CPAP) ± PS:
ventilator provides a continuous circuit pressure ± PS

•Combined (controlled + spontaneous/supported):
commonly used in patients for maintenance on
ventilation and weaning. A preset number (not all)
of patient breaths are assisted by the ventilator, as
described for controlled + remaining spontaneous
patient breaths are supported as described for the
spontaneous/supported mode PS. Synchronized
intermittent mandatory ventilation (SIMV)-VC +
PS: more commonly used
•SIMV-PC + PS

•General Principles
•Basic modes of ventilation: One can determine how the ventilator initiates a breath
(triggering), how the breath is delivered, how patient-initiated breaths are supported,
and when to terminate the breath to allow expiration (cycling).
•Initiation of a breath: Triggering of a ventilator occurs after a period of time has
elapsed (time triggered) or when the patient has generated sufficient negative airway
pressure or inspiratory flow exceeding a predetermined threshold (patient triggered).
•Modes of ventilationAssist-control (AC) ventilation: Ventilator delivers a fully
supported breath  whether time or patient triggered. Primary mode of ventilation
used in respiratory failure.
•Synchronized intermittent mandatory ventilation (SIMV): Ventilator delivers a fully
supported breath when time triggered. However, when the breath is patient
triggered, the ventilator delivers a pressure-supported breath (at a level set by the
clinician). The size of the patient-triggered breath depends on lung compliance and
patient’s effort. This mode is commonly used in surgical patients.
•Pressure support ventilation (PSV): Spontaneous mode of ventilation without a set
respiratory rate. Delivers a clinician-determined inspiratory pressure during patient-
triggered breathing. No respiratory rate is set, so there is no guaranteed minute
ventilation

•Type of breath deliveredVolume control (VC): Ventilator
delivers a clinician-determined tidal volume (V
T) for each
breath regardless of whether the breath was time or patient
triggered. When predetermined V
T is delivered, airflow is
terminated and exhalation occurs.
•Pressure control (PC): Delivers a practitioner-determined
inspiratory pressure for each breath. When inspiratory time
has elapsed, inspiratory pressure is terminated and
exhalation occurs. The tidal volume varies based on lung
compliance. PC ventilation does not deliver a guaranteed
V
T or minute ventilation and may lead to hypoventilation.
However, PC may improve patient synchrony and comfort
while on the ventilator.

A, Pressure–
time curve for
one breath. B,
Flow–time curve
for volume
control
ventilation.
Pressure varies
throughout
inspiratory time,
depending on
lung compliance.

C, Pressure–time
curve for pressure
control ventilation.
Flow varies
throughout
inspiratory time,
depending on lung
compliance. D,
Pressure–time curve
demonstrating auto–
positive end-
expiratory pressure
(auto-PEEP).

Basic ventilator terminology

Minute ventilation: Defined as the product of V
T and
respiratory rate (V
T × RR). Normally between 5–
10 L/min in resting adults, but may be much higher
in high metabolic states, e.g., septic shock.
Minute ventilation, also known as total ventilation,
is a measurement of the amount of air that enters
the lungs per minute. It is the product of respiratory
rate and tidal volume. Alveolar ventilation, on the
other hand, takes physiological dead space into
account. Minute ventilation = tidal volume x
respiratory rate

Physiological significance of minute volume

Blood carbon dioxide (PaCO2) levels generally vary inversely with minute
volume.For example, a person with increased minute volume (e.g. due to
hyperventilation) should demonstrate a lower blood carbon dioxide level.
The healthy human body will alter minute volume in an attempt to maintain
physiologic homeostasis. A normal minute volume while resting is about 5–8
liters per minute in humans. Minute volume generally decreases when at
rest, and increases with exercise. For example, during light activities minute
volume may be around 12 litres. Riding a bicycle increases minute ventilation
by a factor of 2 to 4 depending on the level of exercise involved. Minute
ventilation during moderate exercise may be between 40 and 60 litres per
minute.
Hyperventilation is the term for having a minute ventilation higher than
physiologically appropriate. Hypoventilation describes a minute volume less
than physiologically appropriate.

•What is normal minute ventilation on ventilator?
•5-8 L/min
•Normal minute ventilation is 5-8 L/min. A patient
with a high minute ventilation has a high drive to
breathe (pain, sepsis, etc) and may not be ready
to breathe comfortably without the ventilator. If a
patient's minute ventilation is too low, they may
retained CO2 if not mechanically ventilated.

•What increases minute ventilation?
•Increasing respiratory rate or tidal volume will increase
minute ventilation. Dead space refers to airway volumes not
participating in gas exchange
•What does low minute ventilation mean?
•Low Minute Ventilation (Ve): This alarm will sound when the
amount of air taken in perminute drops below a set value. It
will act similar to a low pressure alarm and usually indicates
some kind of a leak or disconnect in the system. High pressure
alarm
•If minute ventilation exceeds or decreases below the target
level, the ventilator rate is reduced or increased respectively.

•Minute ventilation (V′
E) starts to increase
significantly (by up to 48%) during the first
trimester of gestation, due to higher tidal volume
(V
T) with unchanged respiratory rate. This
ventilatory pattern is then maintained
throughout the course of pregnancy

Peak airway pressure: Composed of
pressures necessary to overcome inspiratory airflow
resistance, chest wall recoil resistance, and alveolar
opening resistance. Does not reflect alveolar
pressure.

•

Elevated peak inspiratory pressures and mean airway
pressures have been implicated as being traumatic to the lung
parenchyma. High peak inspiratory pressures are associated
with pneumothorax, whereas elevated mean airway pressures
are associated with pneumothorax and reduction in cardiac
output. It is not clear whether high peak inspiratory pressures
are a primary or secondary phenomenon associated with the
generation of pneumothorax. It is possible that
nonhomogeneous lung ventilation (areas of poorly ventilated
and well-ventilated alveoli in close proximity) results in
pressure gradients across the interstitium and alveoli and the
potential for rupture. However, it is a common clinical strategy
to try to limit peak inspiratory pressure and mean airway
pressure as much as possible.

•What causes high inspiratory pressure?
•Some causes for high pressure alarms are:

Water in the ventilator circuit. Increased or
thicker mucus or other secretions blocking the
airway (caused by not enough humidity)
Bronchospasm. Coughing, gagging, or “fighting”
the ventilator breath

•What is PIP and PEEP?
•PEEP improves gas exchange by increasing the
functional residual capacity (((FRC), is the volume
remaining in the lungs after a normal, passive
exhalation. In a normal individual, this is about
3L, reduces the respiratory effort)), lowers
requirements for respiratory mixture oxygen, and
enables to decrease the peak inspiratory pressure
(PIP) without decreasing the mean airway
pressure.

Normal peak inspiratory pressure (PIP) is 25-30 cm
H2O. Peak inspiratory pressure (PIP) should be kept
below 20 to 25 cm H2O whenever positive-pressure
ventilation is required, especially if pneumothoraces, or
fresh bronchial or pulmonary suture lines, are present
Things that may increase PIP could be increased
secretions, bronchospasm, biting down on ventilation
tubing, and decreased lung compliance. PIP should
never be chronically higher than 40(cmH
2O) unless the
patient has acute respiratory distress syndrome

•Low Peak Pressure: Think Air Leak
•The ventilator alarm is alerting you “low peak pressure” (or
simply “low pressure”). There is a leak in the system and
the ventilator is not able to generate the peak or plateau
pressure necessary to oxygenate or ventilate the patient
•How do you increase peak inspiratory pressure?
•Peak inspiratory pressure increases with any airway
resistance. Things that may increase PIP could be increased
secretions, bronchospasm, biting down on ventilation
tubing, and decreased lung compliance. PIP should never
be chronically higher than 40(cmH
2O) unless the patient
has acute respiratory distress syndrome

The peak inspiratory pressure (PIP) is the sum of the
plateau pressure (Pplat) (pressure used to keep air
in the lungs) and pressure used to overcome airway
resistance (P resistance) to get the air into the lungs
(elastic recoil of the lungs and chest wall, friction,
etc.). In other words: Peak inspiratory pressure
(PIP) = Pplat + P resistance.

Pplat can never be more than peak inspiratory pressure (PIP),
because there’s always going to be intrinsic resistance which must
be overcome by P resistance. In mechanical ventilation the number
reflects a positive pressure in centimeters of water pressure (cm
H2O). Normal peak inspiratory pressure (PIP) is 25-30 cm H2O.
Peak inspiratory pressure (PIP) should be kept below 20 to 25 cm
H2O whenever positive-pressure ventilation is required, especially
if pneumothoraces, or fresh bronchial or pulmonary suture lines,
are present. The risk for barotrauma increases whenever the peak
pressures and plateau pressures become elevated to the same
degree
2
. Peak inspiratory pressure (PIP) increases with any airway
resistance. Things that may increase Peak inspiratory pressure (PIP)
could be increased secretions, bronchospasm, biting down on
ventilation tubing, and decreased lung compliance.

Plateau pressure (Pplat) (pressure used to keep air in the
lungs) is determined by an inspiratory hold maneuver in
which the patient is given a fixed volume of air. Peak
inspiratory pressure (PIP) is determined at the end of that
inspiration. The drop-off that occurs between peak inspiratory
pressure (PIP) and plateau pressure (Pplat) is airway
resistance which was overcome during the inspiratory phase
by pressure used to overcome airway resistance (P
resistance). The pressure that remains during the hold
maneuver is the plateau pressure (Pplat) and is a product of
the lung tissue itself. Decreased pulmonary compliance,
pulmonary edema, and interstitial lung disease can all affect
this.

Now how does this translate to a real world example?
Let’s say you walk into the room and see a peak
inspiratory pressure (PIP) of 60 cm H2O (normal is 25-
30 cm H2O). Let’s say you do an inspiratory hold
maneuver, and plateau pressure (Pplat) is only 20 cm
H2O. That means there’s a huge pressure overcoming
airway resistance (ie, a very high P resistance). Now
you’ll be thinking more about things which are
decreasing the radius of the airway pipe. For example,
the patient was biting his endotracheal tube and there’s
a huge kink in the tubing coming off the ventilator.

What if the peak inspiratory pressure (PIP) was 50
cm H2O and the plateau pressure (Pplat) was 45 cm
H2O?
The high plateau pressure (Pplat) points towards a
lung issue affecting the alveoli or small airways. Did
the patient develop a pneumothorax? Is his
pneumonia evolving?

Pulmonary barotrauma results from positive
pressure mechanical ventilation. Positive pressure
ventilation may lead to elevation of the trans-
alveolar pressure or the difference in pressure
between the alveolar pressure and the pressure in
the interstitial space. Elevation in the trans-alveolar
pressure may lead to alveolar rupture, which results
in leakage of air into the extra-alveolar tissue.

Specific disease processes, including chronic
obstructive pulmonary disease (COPD), asthma,
interstitial lung disease, pneumocystis jiroveci
pneumonia, and acute respiratory distress
syndrome (ARDS), may predispose individuals to
pulmonary barotrauma. These diseases are
associated with either dynamic hyperinflation or
poor lung compliance, both of which predispose
patients to increased alveolar pressure and
ultimately barotrauma

Patients with obstructive lung disease, COPD, and asthma are
at risk of dynamic hyperinflation. These patients have a
prolonged expiratory phase, and therefore have difficulty
exhaling the full volume before the ventilator delivers the
next breath. As a result, there is an increase in the intrinsic
positive end-expiratory pressure (PEEP), also known as auto-
PEEP. The hyperinflation is progressive and worsens with each
tidal volume delivered. It leads to overdistention of the alveoli
and increases the risk for barotrauma. Dynamic hyperinflation
can be managed by decreasing the respiratory rate,
decreasing the tidal volume, prolonging the expiratory time (n
a mechanically ventilated patient with a normal lung, RC
EXP is
normally between 0.5 and 0.7 s.) , and in some cases by
increasing the external PEEP on the ventilator

auto-PEEP
obtain the total PEEP, the external PEEP subtracted from the
total PEEP will equal the intrinsic PEEP or auto-PEEP. In many
cases, auto-PEEP results in ventilator asynchrony, which may
result in an increased risk of barotrauma. For a patient to be
able to trigger a breath on the ventilator and for the flow to
begin, the inspiratory muscles must overcome the recoil
pressure. When intrinsic PEEP is present, it imposes an
additional force that the inspiratory muscles have to
overcome to trigger a breath. In many instances, auto-PEEP
may lead to ventilator asynchrony, increased alveoli
distention, and ultimately barotrauma

•Why does auto PEEP occur?
•Auto-PEEP is the positive end-expiratory pressure
caused by the progressive accumulation of air
(air trapping), due to incomplete expiration prior
to the initiation of the next breath. This occurs
when expiration is limited by airway narrowing or
obstruction, or when expiratory time is limited

The difference between
PEEPtot and PEEPe
corresponds with the intrinsic
PEEP (PEEPi), and is also known
as AutoPEEP (1).
AutoPEEP may also be referred
to as air-trapping, breath
stacking, dynamic
hyperinflation, inadvertent
PEEP, or occult PEEP.
AutoPEEP is a common
phenomenon in mechanically
ventilated patients with long
expiratory time constants, for
example patients with chronic
obstructive pulmonary disease
or acute severe asthma.

AutoPEEP predisposes the patient to increased work
of breathing, barotrauma, hemodynamic instability
and difficulty in triggering the ventilator. Failure to
recognize the hemodynamic consequences of
AutoPEEP may lead to inappropriate fluid restriction
or unnecessary vasopressor therapy. AutoPEEP can
potentially interfere with weaning from mechanical
ventilation

the amount of air trapping increases with each breath
and consequently the intrathoracic pressure increases
pathologically, compressing the RA and decreasing VR
causing hypotension, as well as increasing plateau
pressure (intra-alveolar pressure) and causing
barotrauma. The increased air trapping also will make it
harder for the patient to bring new air in, increasing the
work of breathing, which increases oxygen
consumption and CO2 production, thereby increasing
the need for ventilation, increasing respiratory rate, and
worsening auto-PEEP in a vicious cycle.

•Factors leading to auto-PEEP
•Airway inflammation and mucus plugs generate dynamic airflow
obstruction as a forced expiratory effort will increase the pressure
around the airway leading to closure around the plugs or inflamed area
and trapping air in the alveoli that are dependent on that airway.
•High lung compliance as in chronic obstructive pulmonary disease
(COPD) works similarly, as the airways lack scaffolding to stay open
during forced exhalation, leading to dynamic airway collapse and air
trapping.
•High tidal volume ventilation, where the tidal volume may be too high to
be exhaled in a set amount of time, so air is retained by the time the next
breath is delivered.
•The high respiratory rate is generating a short exhalation time.
•Slow inspiratory flow generating a higher inspiratory to expiratory time
ratio (too much time taken during inhalation does not leave enough time
for a full exhalation).

•Two types of auto-PEEP
•Dynamic hyperinflation with intrinsic expiratory flow obstruction is the
most common cause of auto-PEEP in COPD patients in whom alveolar
collapse during expiration leads to air trapping. It has been stipulated
that low-level extrinsic PEEP can help decrease auto-PEEP in these
patients by splinting airways open, leading to the easier release of air
from the alveoli. Airway inflammation and mucus plugs also cause
dynamic hyperinflation in a similar fashion, although the use of extrinsic
PEEP in these patients has not been shown to be beneficial as in COPD.
•Dynamic hyperinflation without airflow obstruction occurs when not
enough time is given for the patient to exhale, for example in high
respiratory rate, low inspiratory flow, or high tidal volume in which there
may not be enough time for the air to leave the lungs before the next
respiratory cycle leading to air trapping. In cases like this application of
extrinsic PEEP would be detrimental as it would generate backpressure
preventing air to flow freely out of the lungs.

•When to suspect auto-PEEP
•Exhalation is still ongoing when the next respiratory cycle starts. This can
be easily checked by looking at the volume curve in the ventilator display.
If this curve fails to go back to zero, then it is a sign that air is being
trapped.
• Increasing plateau pressures on the ventilator.
•Active exhalation by the patient as seen by the use of accessory muscles
of respiration during exhalation.
•Drop-in blood pressure.
•Long expiratory times.
•Respiratory distress.
•Although there is a big differential for an intubated patient, who
develops respiratory distress, the presence of a volume curve that does
not go back to zero before the next breath is delivered is very highly
suggestive of auto-PEEP.

•Treating auto-PEEP
•It is important to minimize or prevent the development of auto-
PEEP in the ventilated population as its consequences may be
dire.
•In the most extreme case in which patients are in respiratory
distress and shock, disconnecting the patient from the ventilator
and allowing enough time for exhalation before manually
bagging the patient is a quick life-saving measure.
•For less dramatic cases, several measures can be taken to
reduce the amount and prevent the development of auto-PEEP.
•Assuring enough time for exhalation so that all the air in the
lungs can get out is the most important principle governing the
prevention of auto-PEEP. This may be achieved by multiple
methods

•Decreasing respiratory rate will increase the time between breaths and
decrease the inspiratory to expiratory (I:E) ratio to 1:3 to 1:5.
•Increasing the inspiratory rate to 60 to 100 L/min will assure fast delivery
of air during inspiration, lending more time for exhalation.
•Utilize a square waveform for ventilation delivery. This is uncomfortable
for the patient but speeds the inspiration process.
•Decrease tidal volume. When there is less air being pushed into the
lungs, there is less air needed to be pushed out and less time is required
to finish a full exhalation.
•Decrease respiratory demand by decreasing CO2 and lactate production
(minimize work of breathing, control fever and pain, ensure adequate
sedation, control anxiety, treat sepsis)

The use of extrinsic PEEP is tricky, and although it may be beneficial, it has to be
guided by good clinical sense. In cases of dynamic flow obstruction, especially in
COPD where there is alveolar collapse, (Note: This does not include asthma where
there is inflammation of the airway but not necessarily airway collapse.) the
application of extrinsic PEEP will splint the airways open, permitting this way for air
to be flushed from alveolar pouches and decreasing auto-PEEP. Extrinsic PEEP will
also decrease the work of breathing in the appropriate setting. Nevertheless, when
applied in the wrong setting, like in patients without dynamic airflow obstruction,
the application of extrinsic PEEP will generate back pressure that will prevent air
from getting out of the lungs, worsening air trapping. It is also important to
understand that the extrinsic PEEP initially will add to the auto-PEEP, increasing the
intrathoracic pressure. When used, it is recommended to maintain extrinsic PEEP
below 75% to 85% of the auto-PEEP. Again, the use of extrinsic PEEP to treat auto-
PEEP has to be driven by strong clinical sense as not all patients will benefit from it
and others will be harmed. A practical way to assess the effects of extrinsic PEEP in
auto-PEEP is to apply small increments of extrinsic PEEP and check the static
pressures in the lungs. If the static pressures do not increase, then applying
extrinsic PEEP may benefit the patient, but if the pressures increase, then it is time
to back down on this strategy

Auto-positive end expiratory pressure (auto-PEEP) is a
physiologic event that is common to mechanically
ventilated patients. Auto-PEEP is commonly found in
acute severe asthma, chronic obstructive pulmonary
disease, or patients receiving inverse ratio ventilation.
Factors predisposing to auto-PEEP include a reduction in
expiratory time by increasing the respiratory rate, tidal
volume or inspiratory time. Auto-PEEP predisposes the
patient to increased work of breathing, barotrauma,
hemodynamic instability and difficulty in triggering the
ventilator. Failure to recognize the hemodynamic
consequences of auto-PEEP may lead to inappropriate
fluid restriction or unnecessary vasopressor therapy

•Auto-PEEP can potentially interfere with weaning from mechanical
ventilation. Many methods have been described to measure the Auto-
PEEP. Although not apparent during normal ventilator operation, the
auto-PEEP effect can be detected and quantified by a simple bedside
maneuver: expiratory port occlusion at the end of the set exhalation
period. The measurement of static and dynamic auto-PEEP differs and
depends upon the heterogeneity of the airways. The work of breathing
can be decreased by providing external PEEP to 75-80% of auto-PEEP in
patients who are spontaneously breathing during mechanical ventilation
but there is no evidence such external PEEP would be useful during
controlled mechanical ventilation when there is no patient inspiratory
effort. Ventilator setting should aim for a prolonged expiratory time by
reducing the respiratory rate rather than increasing inspiratory flow.
Routine monitoring for auto-PEEP in patients receiving controlled
ventilation is recommended.

•Mean airway pressure
•stresses applied to the lung parenchyma during
ventilation

• Mean airway pressure: Mean pressures applied during the inspiratory cycle.
Approximates alveolar pressure until overdistention occurs.

•
Fig. 1. Flow prioritized 3P (Pmean, CVP, and PI) Circulation Protective Ventilation
Strategy. Gas accompanied by blood flow. If the Pmean increases >10 cmH
2O, the CVP
may increase to >10 mmHg based on the cardiopulmonary interaction. Then, the blood
flow will be disrupted, leading to perfusion injury based on PI < 1.4. ARDS: Acute
respiratory distress syndrome; CVP: Central venous pressure; ICU: Intensive care unit; PI:
Perfusion index.

•What factors affect mean airway pressure?
•During mechanical ventilation, mean airway
pressure (MAP) can be increased by a variety of
manoeuvres, for example increasing inspiratory
time or elevating the positive end expiratory
pressure (PEEP).

•What is the difference between mean airway
pressure and plateau pressure?
•Peak pressure applies when there is airflow in the
circuit, i.e. during inspiration. What determines
the peak pressure is the airway resistance in the
lungs. So it follows that if there is a problem with
the airways the peak pressure will rise. Plateau
pressure applies when there is not airflow in the
circuit

•Plateau pressure less than or equal
to 30 cm H2O.
The plateau pressure reflects the
pressure the alveoli and small airways of
the lung are exposed to during
mechanical ventilation. This is sometimes
referred to as the transpulmonary
pressure.
Excessively high plateau pressures may
put the patient at risk for barotrauma
and atelectotrauma during mechanical
ventilation

•plateau pressure.The plateau pressure is measured after a
breath has been delivered to the patient and before exhalation
begins. Exhalation is prevented by the ventilator for a brief
moment (0.5 to 1.5 s). To obtain this measurement, the
ventilator operator normally selects a control marked “inflation
hold” or “inspiratory pause.” Plateau pressure measurement is
similar to holding the breath at the end of inspiration. At the
point of breath holding, the pressures inside the alveoli and
mouth are equal (no gas flow). However, the relaxation of the
respiratory muscles and the elastic recoil of the lung tissues are
exerting force on the inflated lungs. This creates a positive
pressure, which can be read on the manometer as a positive
pressure. Because it occurs during a breath hold or pause, the
manometer reading remains stable and it “plateaus” at a
certain value

•What is the difference between peak inspiratory pressure and plateau
pressure?
• The peak inspiratory pressure (PIP) records the highest pressure that
occurs inside the lungs at peak inspiration. The PIP should always be
higher than the plateau pressure because of the effect airway resistance
has on the PIP as air flows through the lungs.
Airway secretions, inflammation, bronchoconstriction, and even a kinked
endotracheal tube can all increase airway resistance and increase the PIP
as a result.
Unlike the PIP, the plateau pressure records the pressure inside the lungs
when no air is moving by performing an inspiratory pause at peak
inspiration. As a result, the plateau pressure does not factor in airway
resistance. The plateau simply reflects the pressure it takes to hold a
given volume inside the lungs. This is the pressure the small airways and
alveoli are subjected to, also known as the trans pulmonary pressure

•What causes elevated plateau pressures?
•Lung conditions that stiffen the lungs, such as
ARDS or pulmonary fibrosis may cause high
plateau pressures during mechanical ventilation.

Inappropriate ventilator settings, particularly
excessively large tidal volumes used during volume
control ventilation can also increase the plateau
pressure.

•How do you reduce plateau pressure in
ventilation?
•Lower tidal volume (6 mL/kg per predicted body
weight) ventilation is a strategy to reduce plateau
pressure and driving pressure, roughly reflecting
the level of alveolar overdistension.

Mechanical Ventilation Alarms: High Airway
Pressure

The first thing to do is turn up the upper limit
on the alarm parameter to stop the alarm and
ensure that the patient receives the set breath
from the ventilator. Now the ventilator is not
alarming, allowing you to see the peak
inspiratory pressure is 45 cm H
2O (normal <30
cm H
2O).
Two things can be happening when the peak
inspiratory pressure is high
==Peak pressure is high with a normal plateau
pressure, indicating a problem with resistance
==Peak pressure is high with an elevated
plateau pressure (normal < 25 cm H
2O)
demonstrating that there is a problem with
lung and/or chest wall compliance

•Do an inspiratory hold to determine your plateau pressure. Once
you have your peak pressure and plateau pressure you can
determine a differential diagnosis.
• Resistance problems (high peak pressure with normal plateau
pressure)
•Kink in the circuit
•Fluid pooling in the circuit
•Biting the ETT
•A small ETT with biofilm forming
•High flow rate or tidal volume
•Ventilatory asynchrony
•Laryngospasm
•Bronchospasm
•Mucous plugging
•Foreign body

•Compliance problems (high peak pressures and high
plateau pressures)
•ETT in right mainstem
•Pneumothorax
•Pulmonary edema
•Air trapping (Auto PEEP)
•ARDS
•Pulmonary fibrosis, ILD
•Abdominal compartment syndrome
•Obesity

•What is Pmax on ventilator?
•• Pmax. − Maximum pressure the ventilator. will
use to deliver the set volume.

Pmax: In the volume-controlled mode this is the
maximum peak inspiratory pressure you wish the
ventilator to administer to reach target tidal
volumes. Usually set 5 cmH
2O higher than the
average PIP used to achieve the set tidal volume

Modes of mechanical ventilation
In CARESCAPE R860

Assist Control

AC ventilation is a volume-cycled mode of
ventilation. It works by setting a fixed tidal volume
(VT) that the ventilator will deliver at set intervals of
time or when the patient initiates a breath. The VT
delivered by the ventilator in AC always will be the
same regardless of compliance, peak, or plateau
pressures in the lungs.

•Assist Control
•The first breath in this cycle is one initiated by the ventilator. The
second breath is the patient triggered breath. There is a slight
dip at the beginning of the breath, which is the patient creating a
negative pressure.
•The ventilator senses this and delivers another breath. The user
can set what the trigger is, in litres per minute of flow for
example, to make it easier or harder for the patient to trigger the
breath.
•The ventilator will then deliver that breath to the set volume or
pressure depending on the parameters set by the user i.e. is it
pressure controlled or volume controlled ventilation.
•So the ventilator assists the patient by controlling the amount
of volume the patient receives

Assist-control (AC) ventilation: Ventilator delivers a fully
supported breath  whether time or patient triggered.
Primary mode of ventilation used in respiratory failure

AC ventilation is a volume-cycled mode of ventilation. It
works by setting a fixed tidal volume (VT) that the
ventilator will deliver at set intervals of time or when
the patient initiates a breath. The VT delivered by the
ventilator in AC always will be the same regardless of
compliance, peak, or plateau pressures in the lungs.

•ACV (VCV)
•Most commonly used initial mode of ventilation because it assists every sensed
inspiratory effort made by the patient and reduces work of breathing.
•Trigger:
–Time-triggered if patient’s inspiratory effort is not sensed: ventilator delivers a preset
number of mandatory breaths per minute.
–Patient-triggered if patient’s inspiratory effort is sensed: ALL inspiratory efforts are
assisted by the ventilator. (Image 1)
•Volume-cycled:
–Inspiratory phase ends when a preset volume exits the ventilator.
–Inspiratory volume is an independent variable because it is set by the operator and
does not vary between breaths
–Inspiratory pressure is a dependent variable because it is not set by the operator and
varies between breaths
•Pressure-limited: preset by the ventilator to abort the inspiratory phase if
dangerous levels of airway pressure are reached.

•Example: An intubated patient has 20 spontaneous breaths/min.
All breaths are efficient enough to be sensed by the ventilator.
On the ACV mode, all 20 breaths are assisted by the ventilator
immediately after initiation by the patient. So the ventilator
frequency is 20/min. If the patient’s spontaneous breaths
(respiratory rate) increases to 30/min, the ventilator frequency
becomes 30/min.
•An intubated patient has 4 spontaneous breaths per minute
while the ventilator is set to 12 breaths per minute. On the ACV
mode, the ventilator assists the patient’s 4 breaths and adds 8
more breaths/min to reach the minimum number set by the
operator. If the patient’s spontaneous breaths equal or exceed
the minimum number of 12/min, the ventilator assists all patient
breaths without adding any further breaths.

•Problems: Respiratory alkalemia: in patients with
tachypnea, especially due to anxiety, pain, or
airway irritation
•Auto-positive end-expiratory pressure (auto-
PEEP): dynamic hyperinflation of lungs when air
builds up due to insufficient expiratory time; this
limits venous return, decreases cardiac output,
and predisposes to barotrauma.

•PCV
•Less commonly used
•Appropriate when control of peak airway pressures is
important such as in patients with previous
barotrauma or after thoracic surgery
•Time-triggered, time-cycled, and pressure-limited
•Inspiratory pressure is an independent variable
because it is set by the operator and does not vary
between breaths.
•Inspiratory volume is a dependent variable because it
is not set by the operator and varies between breaths

•Assist Control (AC) Mode
•This is the most common ventilation mode used in
ICU. “Full support” mode means that every breath
is a positive pressure ventilator breath, but it can
be initiated by the machine or the patient. The
patient receives a mandatory rate (RR) and a
mandatory volume (TV).

•Benefit of AC Mode
•AC mode decreases the work of breathing. It can be used for
patients who have some spontaneous breathing and those
who don’t. It provides the set number of breaths every
minute, but also allows the patient to initiate breaths on
their own, decreasing anxiety.
•Disadvantage of AC Mode:
•Due to the low work of breathing, respiratory muscles
weaken, which can cause breath-stacking, where air never
fully exits the alveoli before another breath is taken. Every
breath is the same size and if patient wants larger breaths
than the set TV, it can cause anxiety, leading to tachypnea
and hyperventilation.

•Volume Assist/Control:
•If you choose a volume mode then the advantage is that you
will have more control over your patients minute
ventilation, as you will be able to set a target tidal volume
and a rate. In Assist Control, the patient can trigger the
ventilator (Assist Breath) and determine their own rate, but
once they trigger they will receive the tidal volume you set.
If the patient becomes apneic or you set the rate much
faster than the patient is breathing, then your patient will
get all control breaths. I use this mode in my severe
obstructive disease patients (Asthma & COPD) as we. It also
has the advantage to control tidal volume therefore
preventing volutrauma and assuring low tidal volume
ventilation.

•Disadvantages:
•The disadvantage of a volume mode is that the
inspiratory flow rate is a constant flow and not a
variable decelerating inspiratory flow that we see in
pressure breaths and our normal physiologic
breathing pattern. A variable decelerating flow
pattern, allows for a very fast inspiratory flow rate at
the start of the breath, then throughout the
remainder of inspiration, the flow decelerates.
Because of this constant inspiratory flow we use in
volume breaths, patients may become uncomfortable.

•We cannot exactly match the flow pattern, but a way to improve
a patients comfort is to increase their inspiratory flow rate. A
normal inspiratory flow rate can range between 60-90
liters/minute, and you can increase the flow rate to give a breath
faster thus trying to mimic our decelerating flow pattern. The
breath will still be a constant flow and won’t decelerate
throughout inspiration like a pressure breath or normal breath
would. However, setting an increased flow rate can help with
patient comfort.
•Another careful consideration in using a volume mode is that
you have control over the tidal volume but not the PIP. Your goal
is keep the PPlat <30 mm Hg to avoid barotrauma. Just keep in
mind that PIP is constantly displayed on the ventilator with each
breath, but to obtain a PPlat you have to do an end-inspiratory
pause to assure that the PPlat is less than 30 mm Hg.

•Pressure Assist/Control:
•If you choose a pressure mode, the advantage is
possibly patient comfort due to the variable
decelerating inspiratory flow that we discussed
above and also in. It also may give you the
advantage of improving oxygenation due to the
constant pressure waveform also discussed in. You
also can limit your pressure delivery therefore
prevent barotrauma.

•Disadvantage:
•Clearly the disadvantage is that you may loose some
control over the minute ventilation. You can set a rate,
but if this is an assist control mode the patient can
trigger the ventilator, but when they do, they will get
a set pressure. If your patient develops apnea or you
set a rate higher than the intrinsic rate, then they will
get all controlled breaths. You should pay close
attention to the tidal volume being delivered to make
sure that the volume is not too high or too low,
especially in the setting of someone with changing
lung compliance or bronchospasm.

•AC mode is an excellent method to assure good
ventilation. It is frequently used in cases of metabolic
or respiratory acidosis.
•AC was the mode used in the landmark study
“Ventilation with Lower Tidal Volumes as Compared
with Traditional Tidal Volumes for Acute Lung Injury
and the Acute Respiratory Distress Syndrome,” from
where the ARDSNET protocol came to be. For this
reason, it is the only proven mode with survival
benefit in patients with acute respiratory distress
syndrome (ARDS) and should be the mode of choice
to use as it allows for the operator to administer low
tidal volumes and adjust PEEP as necessary.

n important concept to understand in AC mode is that because
the system is volume-cycled and a set volume will always be
delivered, the pressure that will be generated in the system
will be determined by lung compliance. A very compliant lung
will generate low plateau pressures, while a stiff lung does not
distend well with the set volume and will generate a much
higher pressure (i.e., patients with pulmonary edema, ARDS,
pneumonia, or pulmonary fibrosis). It is important to
understand this to prevent ventilator-induced lung injury or
barotrauma. Peak pressure in the system is usually determined
by airway resistance and not by compliance, while plateau
pressure or the pressure in the system at the end of inspiration
is determined by compliance and volume delivered.

ventilator parameters
set by the operator

• Inspired Oxygen Concentration
•Initially select high FI02 and adjust when obtain ABGs after 20 min
•Aim for lowest FI02 that will achieve Pa02 of 60-70 mm Hg (or Sp02 of 92%)
•PEEP may be required to achieve a decrease in FI02
•Oxygen toxicity
–Exposure to FI02 of 1.0 up to 24 hr does not result in a significant clinical risk,
but beyond that time it is clearly toxic.
–An FI02 of 0.50 is generally considered safe for several weeks if required.
–For FI02 between 0.5 and 1.0, the duration of safe exposure prior to the onset
of toxicity in humans is unknown.
–When managing hypoxemic patients, there is more to fear from severe
hypoxemia than the potential threat of oxygen toxicity.

The Fraction of Inspired Oxygen
F
IO
2: It is reasonable to start at 100%, but FIO
2 should be
weaned down quickly to maintain SaO
2 >87% or PaO
2
>55 mm Hg. There is growing evidence that tolerating
hyperoxia after intubation may actually worsen patient
survival. FIO
2 can generally be quickly titrated down
based on pulse oximetry alone

The fraction of inspired oxygen, FiO2, is an estimation
of the oxygen content a person inhales and is thus
involved in gas exchange at the alveolar level

SELECTION OF FRACTIONAL CONCENTRATION
OF INSPIRED OXYGEN
The goal of selecting a specific FIO2 for a patient is
to achieve a clinically acceptable arterial oxygen
tension (e.g., 60 to 100 mm Hg). To accomplish this
goal, a baseline arterial blood gas (ABG) should be
performed. If a baseline ABG is not available, it is
advisable to select a high initial FIO2 setting (≥0.50)
for patients with presumed severe hypoxemia.

This can provide a way of restoring normal oxygenation and
replacing tissue oxygen storage when oxygen debt and lactic acid
accumulation have occurred. Many practitioners start with an FIO2
of 1.0 and then reduce it as quickly as possible.
Extended use of 100% O2 is not recommended because it can
quickly result in absorption atelectasis and, in the long term, can
lead to oxygen toxicity. It is important to state, however, that 100%
oxygen should not be withheld if the patient is seriously ill and
requires a high FIO2. Indeed, any procedure that places the patient
at risk of developing hypoxemia should be performed with the
patient breathing 100% O2. For example, administering 100% O2
before and after suctioning and also during bronchoscopy is a
common practice

Hyperoxemia in the ICU
Hyperoxemia can be defined as an increase in
arterial oxygen partial pressure (PaO2) to a level
greater than 120 mmHg (16 kPa). It is considered to
be moderate for levels ranging between 120 and 200
mmHg, and severe if PaO2 exceeds 200 mmHg (27
kPa). Hyperoxemia is caused by hyperoxia (an
increase in oxygen) and occurs in 22% to 50% of
mechanically ventilated patients in the ICU

•Take-away messages
•Hyperoxemia can be defined as an increase in arterial oxygen
partial pressure (PaO2) to a level greater than 120 mmHg (16
kPa) and may occur in up to 50% of mechanically ventilated
patients.
•Retrospective studies have reported hyperoxemia to be
associated with the duration of mechanical ventilation, the ICU
stay and the hospital stay, as well as with VAP.
•Avoiding hyperoxemia and targeting physiological ranges of SpO2
and PaO2 in ICU patients may be associated with improved
outcomes.
•A closed loop oxygenation controller may support this strategy in
mechanically ventilated patients, and also reduce the workload
for healthcare staff.

Retrospective studies have reported hyperoxemia to be associated
with the duration of mechanical ventilation, of the ICU stay and the
hospital stay, as well as with ventilator-associated pneumonia.
Evidence indicates that conservative management of oxygen using
pulse oximetry to target an oxygen saturation (SpO2) of between
90% and 92% is associated with decreased radiological evidence of
atelectasis.
Severe hyperoxemia and the time spent in hyperoxemia are
associated with a higher mortality rate and fewer ventilator-free
days. In a study focusing primarily on oxygenation during the first
24 hours of ICU admission for mechanically ventilated patients,
results showed hospital mortality to have a U-shaped relationship
with PaO2, whereby both the lower and higher PaO2 values were
associated with higher mortality

F
IO
2. Natural air includes 21% oxygen, which is
equivalent to F
IO
2 of 0.21. Oxygen-enriched air has a
higher F
IO
2 than 0.21; up to 1.00 which means 100%
oxygen. F
IO
2 is typically maintained below 0.5 even
with mechanical ventilation, to avoid oxygen toxicity

Tidal Volume and Rate
The normal spontaneous VT for a healthy adult is about 5 to 7 mL/
kg with a spontaneous respiratory rate of 12 to 18 breaths/min.

VE is about 100 mL/kg of ideal body weight (IBW).

When determining VT for ventilated patients, a range of 6 to
8 mL/kg of IBW is typically used for adults, and 4 to 8 mL/kg IBW
for infants and children.

Lower VT rates (e.g., 4 mL/kg IBW) have been successfully used to ventilate
the lungs of adult patients with acute respiratory distress syndrome (ARDS).
These lower VT rates are described as protective strategies that minimize the
damaging effects associated with overdistention of the alveoli.

It is important to understand that an adult’s lungs do
not get larger as he or she gains weight. For
example, a 5-foot 6-inch adult male weighing 100 kg
would require the same VT as a 5-foot 6-inch
adult male weighing 65 kg. Remember, however,
that a heavier patient would have a higher metabolic
rate and thus a higher V

Regardless of the method used for
selecting the VT for a
patient, it is important for clinicians to be
aware of four risks
during the setup of VT:
1. Overdistention of lung tissue
2. Repeated opening and closing
(recruitment/derecruitment) of alveoli
3. Atelectasis formation
4. Inadequate VT setting

How do you calculate tidal volume per kg?
•To determine the adequate tidal volume (Vt)
to deliver during protective ventilation, it is
necessary to calculate the patient's PBW. This
is accomplished by using the Devine's
formulas (
3
) adjusted by gender:
• Male: PBW = 50 + 0.91 × (height in cm–152.4) Kg.
•Female: PBW = 45.5 + 0.91 × (height in cm–152.4) Kg.

An alternative method for calculating initial VT
settings is to use predicted values for body weight
rather than calculations of IBW. The predicted body
weight of male patients can be calculated using the
following equation: 50 + 0.91 (centimeters of height
–152.4). For female patients the predicted body
weight can be determined using the following
equation: 45.5 + 0.91 (centimeters of
height × 152.4)

Recommended tidal volumes for ventilated patients
vary depending on the lung pathology. For patients
with normal lungs, such as patients with a drug
overdose or patients with the postoperative effects
of anesthesia, an initial VT of 6 to 8 mL/kg and a rate
of 10 to 20 breaths/min is generally accepted.3 In
patients with chronic obstructive pulmonary disease
(COPD) and asthma, in which airway obstruction and
resistance are high, an initial VT of 6 to 8 mL/kg with
a rate of 8 to 12 breaths/min is acceptable

In patients with chronic or acute restrictive disease, such as
pulmonary fibrosis or ARDS, an initial VT of 4 to 6 mL/kg with a rate
of 15 to 25 breaths/min is indicated.7 As suggested in restrictive
disease, lower VT and higher rates are used. However, high rates
may not provide sufficient time for exhalation (short TE), and air
can be trapped in the lungs at the end of exhalation, resulting in
intrinsic PEEP (auto-PEEP).15 The VT should be adjusted to
maintain plateau pressure less than 30 cm H2O and rates adjusted
to minimize auto-PEEP

A VT of more than 9 to 10 mL/kg is not recommended because
of the risk of high pressures and accompanying overdistention
and trauma to the lung, in addition to other complications. Low
volume settings (4 to 8 mL/kg) are beneficial in restrictive disease
and may help prevent high pressures and alveolar overdistention.
It is worth mentioning that using volumes as low as 4 mL/kg may
contribute to atelectasis. Using tidal volumes this low may require
a recruitment maneuver or sigh breaths to avoid atelectasis.
Use of lower VT may be especially important in patients receiving
PEEP therapy to avoid high pressures and overdistention.

Key Point 6-2 When setting tidal volume (VT) and
rate, the goal is not to focus so much on the exact VT
and rate, but to focus on using settings that
do not harm the patient. Maintaining plateau
pressure lower than 30 cm H2O is very important. In
some cases it may even be necessary to let PaCO2
rise and pH fall outside the patient’s normal values
to avoid lung injury.

The low-tidal-volume strategy, which uses 6 mL/kg of predicted body weight,
has become the standard of care for patients with ARDS, following the Acute
Respiratory Distress Syndrome Network (ARDS Network) publication in
2000.
12
The ARDS Network prospectively studied intubated patients with
acute lung injury (ALI) or ARDS to determine whether a low-tidal-volume
strategy, compared with a traditional-tidal-volume strategy, could improve
mortality and decrease the total number of ventilator days. The final analysis
showed a 23% reduction in all-cause mortality and a 9% absolute decrease in
mortality with the use of a tidal volume of 6 mL/kg of predicted body weight
and plateau pressures of 30 cm H
2O or less, compared with the usual
practice of 12 mL/kg of predicted body weight and plateau pressures of
50 cm H
2O or less. Low tidal volume or so-called lung protective ventilation is
recommended for all patients with ARDS. In patients without ARDS, a
retrospective review demonstrated the relationship between ALI and the use
of tidal volumes greater than 10 mL/kg of predicted body weight.
13

Considering the current evidence, tidal volumes greater than 10 mL/kg of
predicted body weight should not be routinely used in the care of the
mechanically ventilated patient

Recent studies have shown decreased mortality with
the use of lower tidal volume in patients with acute
lung disease. Therefore, patients with an acute lung
disease such as pneumonia, ARDS, fibrotic lung
disease, or COPD should be ventilated with tidal
volumes of 6–8 ml/kg.

The standard starting tidal volume (Vt) for most
infants is approximately 4 to 6 mL/kg, although
occasionally, levels as high as 8 to 10 mL/kg may be
needed. PIP maximum should initially be set at a
level of about 15 to 20 cm H
2O, and adjusted as
necessary.

•Did You Know?
•Low tidal volume ventilation (LTVV) is one of the interventions specifically
designed to prevent ventilator-associated conditions (VAC).
•For patients without acute respiratory distress syndrome (ARDS), target
the recommended tidal volume of 6–8 mL/kg predicted body weight
(PBW).
•For patients with ARDS, the recommended tidal volume target is between
4–6 mL/kg PBW.
•Emerging evidence links protective tidal ventilation to decreased
incidence of acute lung injury (ALI) and ARDS, as well as decreased time
on the ventilator.
•Use at least 5 cm H2O positive end expiratory pressure (PEEP).
•Why wait? Initiate LTVV on all patients to prevent ALI and ARDS.
Prevent the lung damage that can occur within a few hours of
mechanical ventilation at high tidal volume.

•What the Evidence Says
•Low tidal volume ventilation could shorten the duration of
mechanical ventilation in general; LTVV may therefore be an
effective strategy to lower ventilator-associated events
rates.
1

•In patients with healthy lungs, low tidal volume ventilation,
moderate PEEP, and repeated recruitment maneuvers can
markedly help improve postoperative outcome in patients
undergoing abdominal surgery.
2

•Low tidal volume ventilation can benefit patients with or
without ARDS.
3

•Low tidal volume can reduce ARDS progression in patients
without ARDS.
4

For patients without acute respiratory distress
syndrome (ARDS), target the recommended tidal
volume of 6–8 mL/kg predicted body weight (PBW).
For patients with ARDS, the recommended tidal
volume target is between 4–6 mL/kg PBW

•tidal volume in neonates
•4–6 ml/kg
•In neonates, the average tidal volume is thought
to be 4–6 ml/kg. Minute ventilation (V
E) is
calculated from tidal volume (V
T) in milliliters
multiplied by the number of inflations per minute
or respiratory frequency (f). It is approximately
0.2–0.3 L/min/kg in healthy neonates

Table 1 Suggested initial tidal volume and pressure limit settings for Volume Guarantee
ventilation. These are merely starting points and are mean values based on available
data. Individual patients may deviate from average values. The pressure limit should be
adjusted once the working pressure needed for an appropriate tidal volume has been
determined.

•Respiratory Rate:
•This is truly the main way we improve ventilation as we typically set up the tidal
volume at 6 mL/kg based on ideal body weight and try not to deviate too far
from this. As we discussed, if a patient has a severe metabolic acidosis, then we
will want a very high respiratory rate, and if a patient has obstructive physiology,
we will want a low rate. For both of these patients, you will want to check a
blood gas after 20-30 minutes, and then re-adjust your rate accordingly.
•Recall if your rate is too fast then you may develop auto-peep so you may have to
either decrease your rate or adjust your inspiratory time or inspiratory flow rate.
We discussed that the majority of patients tolerate permissive hypercapnea (or
submissive hypercapnea) with the exception of pregnant females, patients with
serious head injuries who have elevated ICP, and those with severe pulmonary
hypertension. These patients may need more sedation, as the effects of
hyperacapnia can be uncomfortable.
•When you intubate a pediatric patient they will require a higher respiratory rate,
which for them may be a normal respiratory rate

How does dead space affect arterial oxygenation?
Dead spaces can severely impact breathing, because they
reduce the surface area available for gas diffusion. As a result,
the amount of oxygen in the blood decreases, whereas the
carbon dioxide level increases. Dead space is created when
no ventilation and/or perfusion takes place

Increasing respiratory rate has recently been
proposed to improve CO2 clearance in patients with
acute respiratory failure who are receiving
mechanical ventilation. However, the efficacy of this
strategy may be limited by deadspace ventilation,
and it might induce adverse hemodynamic effects
related to dynamic hyperinflation.

Summary of interventions
available for the treatment
of hypercapnia

•Increasing minute ventilation
•Changes in delivery of conventional mechanical ventilation including optimising the
settings such as increasing respiratory rate (and minute ventilation) as recommended by
the ARDS network
3
may help in management of hypercapnic acidosis.
•Increasing respiratory rate and minute ventilation, however, involves a trade-off with
higher minute ventilation needing greater delivered power of mechanical ventilation.
Higher mechanical power has been associated with increased risk of in-hospital mortality
using data from two separate ICU databases.
13
Mechanical power can be measured using
dynamic pressure volume curve in volume targeted ventilation mode, recorded during
tidal ventilation.
14
Mechanical power can be calculated at the bedside and comprises of all
the ventilator related variables that contribute to ventilator induced lung injury (VILI)
(tidal volume, respiratory rate, driving pressure and airway resistance).
14
The increase in
respiratory rates may, however, be associated with dynamic hyperinflation and right
ventricular dysfunction without clearance of hypercapnia.
15
While increasing respiratory
rate, one must be mindful of the impact on other ventilatory variables (inspiratory flow
rate and expiratory time) as well as on mechanical power to achieve best possible balance
between restoring normocapnoea and potential for VILI.
16
Interpretation of ventilator
waveforms to adjust the respiratory rate may aid in avoiding ventilator associated lung
injury.
17

•Reducing dead space ventilation
•Dead space ventilation causes hypercapnia and was shown to be
associated with an increased mortality.
18
Techniques that could
reduce dead space include alteration in the ventilation circuit
and strategies to reduce physiological dead space are relatively
simple to implement in patients with hypercapnic respiratory
failure. Catheter mounts are routinely used to connect the Y-
piece to the endotracheal tube, mainly to prevent accidental
extubation. Modifications to the ventilator circuit such as
connecting Y-piece directly to the endotracheal tube to reduce
the dead space in ventilator circuit.
19
Changes to the circuit in
mechanical ventilation including removal of heat and moisture
exchanger and using heated humidifier was also shown to
reduce hypercapnia without the need for increase in the need
for increasing tidal volumes or the respiratory rate.

•Reduction in physiological dead space
•End-inspiratory pause prolongation was shown to increase
clearance of hypercapnia in ARDS patients.
20
By increasing end-
inspiratory pause prolongation from 0.1 to 0.7, Bermeo et al.
demonstrated a significant decrease in PaCO
2 from 54 ± 9 to
50 ± 8 mmHg.
20
They showed that the decrease in PCO
2 was due
to a reduction in physiological dead space.
20
The diffusion of CO
2
during respiration is time dependent. End inspiratory pause
prolongation increases the time available for alveolar gas
exchange of CO
2 and hence its elimination. It must, however, be
noted that end inspiratory prolongation may be associated with
potential adverse effects such as an increase in intrinsic positive
end expiratory pressure (PEEP) and inversion of inspiration to
expiration (I/E) ratio that can increase mean airway pressure and
cause dynamic hyperinflation.

•Lung recruitment and PEEP titration
•PEEP is aimed to maintain recruitment of the lung regions opened during
previous inspiration.
21
Optimum PEEP can reduce physiological dead
space by recruiting atelectatic lung tissue, while excessive PEEP can
increase dead space by over distension of the alveoli. With regional
heterogeneity in diseased lung both over distension and recruitment
could happen at the same time, requiring the clinician to strike a delicate
balance between the two phenomena units.
•However, deploying ‘open lung strategy’, lung recruitment manoeuvres
with PEEP titration intended to improve oxygenation and reduce VILI, are
shown to cause severe hypercapnia during the first 24 h of institution.
22

The strategy of lung recruitment manoeuvre and PEEP titration according
to the best respiratory–system compliance was recently investigated by
Cavalcanti et al. in a large multinational, multicentre randomised
controlled trial

This study showed a higher 28-day and 6-month all-
cause mortality in patients who were treated with lung
recruitment. Higher mortality noted with lung
recruitment was attributed to several factors including
changes in driving pressure and lung over distention,
breath stacking, need for neuromuscular blockade and
haemodynamic compromise.
22
It is important to note
that in the lung recruitment group, hypercapnia and
acidosis during the first hour of randomisation was
observed, which was shown to be associated with
higher mortality in mechanically ventilated patients.

•Buffers in the management of hypercapnic acidosis
•The use of buffers in the management of hypercapnic acidosis remains
controversial.
23
Sodium bicarbonate and Tris-hydroxymethyl aminomethane
(THAM) were both used in clinical practice to buffer hypercapnic acidosis.
3,24,25

Kallet et al.
25
demonstrated THAM in improving arterial pH and base deficit, with
a reduction in PCO
2 that could not be fully accounted for by ventilation. Weber
et al. investigated the use of THAM in ARDS patients where permissive
hypercapnia was implemented for 2 h aiming for a target PCO
2 of 80 mmHg. In
their randomised controlled trial of 12 patients with ARDS, the use of THAM
buffering attenuated depression of myocardial contractility and hemodynamic
alterations during rapid permissive hypercapnia institution.
24
The ARDS network
trial recommended the use of sodium bicarbonate when pH was lower than 7.1.
3

However, bicarbonate infusions should not be administered to patients who are
hypoxemic and or having lactic acidosis.
•Some patients with severe ARDS will be hypercapnic in spite of best possible
conventional ventilation. In such patients, other modalities in addition to
conventional ventilation may be required. These include APRV, prone position
ventilation and high frequency oscillatory ventilation

•Airway pressure release ventilation
•APRV entails continuous positive airway pressure at a high level, with
intermittent time cycled release, to maintain alveolar recruitment and
lung volume. Patients can breathe spontaneously, independent of the
phase of respiration, through a biphasic positive pressure circuit.
26
This
allows movement of posterior muscular part of the diaphragm increasing
distribution of ventilation to dependent posterior lung regions, improving
ventilation perfusion matching, as compared to movement of anterior
tendinous region of diaphragm during controlled mechanical ventilation.
APRV was initially described as a spontaneous mode of ventilation to
treat patients with acute lung injury with aim of maintaining lower airway
pressure and to allow unrestricted spontaneous ventilation. There are
some reports suggesting that APRV may prevent progression of acute
lung injury in high-risk trauma patients.
27
APRV was also shown to be
effective in reducing CO
2 as well as improving oxygenation without
increasing minute ventilation

in conjunction with a reduction in peak and mean airway
pressures. Improvement in gas exchange with APRV is related
to the reduction in dead space ventilation. The use of APRV,
however, is not widespread and this mode is not available in
all commercially available ventilators.
29
Furthermore, the
improvement in survival with this mode of ventilation remains
to be evaluated. Higher mean airway pressures and low
release time reduce the applicability of APRV in patients with
conditions such as bronchopleural fistulae, raised intracranial
pressure, right ventricular dysfunction and with prolonged
expiratory time constants. Patients who cannot breathe
spontaneously because of neuromuscular paralysis or
diaphragmatic weakness do not benefit from this mode either.

inspiration/expiration
(I/E) ratio

•

•I:E Ratio
•The I:E ratio denotes the proportions of each breath cycle devoted to the
inspiratory and expiratory phases. The duration of each phase will depend on this
ratio in conjunction with the overall respiratory rate. The total time of a
respiratory cycle is determined by dividing 60 seconds by the respiratory rate.
Inspiratory time and expiratory time are then determined by portioning the
respiratory cycle based on the set ratio. For instance, a patient with a respiratory
rate of 10 breaths per minute will have a breath cycle lasting 6 seconds. A typical
I:E ratio for most situations would be 1:2. If we apply this ratio to the patient
above, the 6-second breath cycle will break down to 2 seconds of inspiration and
4 seconds of expiration. Changing the I:E ratio to 1:3 will result in 1.5 seconds of
inspiration and 4.5 seconds of expiration. Thus, changing the I:E ratio from 1:2 to
1:3 results in less inspiratory time and more expiratory time for the same length
of the breath cycle.
•Standard Pressure Control ventilation modes typically use I:E ratio of 1:2 or as
high as 1:3 or 1:4 in specific populations. In these cases, the expiratory phase is
set longer than the inspiratory phase mimics normal physiology. Inverse Ratio
Ventilation instead uses I:E ratios of 2:1, 3:1, 4:1, and so on, sometimes as high
as 10:1, with inspiratory times that exceed expiratory times

•Inspiration/expiration ratio
•The normal inspiration/expiration (I/E) ratio to
start is 1:2. This is reduced to 1:4 or 1:5 in the
presence of obstructive airway disease in order to
avoid air-trapping (breath stacking) and auto-PEEP
or intrinsic PEEP (iPEEP).

•Inverse ratio ventilation
•Inverse ratio ventilation is a mode of ventilation designed to improve
oxygenation at a given level of inspired oxygen. Conventional ventilation
uses the times of inspiration and expiration at a ratio of 1 : 4 or 1 : 2,
giving a longer time for expiration, as it is generally a passive process.
Inverse ratio ventilation reverses this ratio to give a longer inspiratory
time (1 : 1 or 2 : 1) by using rapid inspiratory flow rates and decelerating
flow patterns during the inspiratory phase. The effect of inverse ratio
ventilation is to increase mean airway pressures and thus recruit alveoli in
an effect similar to PEEP. Secondly, in severe lung disease, ventilation in
the lung is unequal due to peribronchial narrowing. Thus, some
underventilated alveoli that are actually open are not able to exchange
gases efficiently, increasing the intrapulmonary shunt and reducing
arterial oxygenation. Inverse ratio ventilation can improve this by
selective air-trapping or intrinsic PEEP in these compromised air spaces.

some studies have showed no benefit of inverse
ratio ventilation compared to conventional volume
ventilation in terms of oxygenation.
24
These studies
did show some slight improvements in ventilation
(Paco
2). For this reason, inverse ratio ventilation
cannot be recommended except in the setting of
ARDS refractory to other therapies

Zavala et al (1998) used an inverse I:E ratio in ARDS,
and found that oxygenation actually worsened in the
short term– mainly because of the poorer
pulmonary blood flow. Markström et al (2010) used
I:E ratios ranging from 1:1 to a whopping 4:1 (thus,
minimal expiratory time) and found a significant
increase in intrinsic PEEP – so much so that they had
to decrease their ventilator PEEP so as to keep the
total PEEP stable. Predictably, this had an adverse
effect on cardiac output: the cardiac index fell from
5.0 L/m2 to around 3.8 L/m2

A COPD patient is mechanically ventilated at 15 breaths per minute, and you want to
increase their expiration time in order to avoid hyperinflation. How do you do this?

If your ventilator uses inspiratory time: decrease inspiratory time. As the
respiratory rate will be constant, this will increase expiratory time.
If your ventilator uses I:E ratio, change the I:E ratio from 1:2 to (for example) 1:4.
Note that this not only increases expiratory time, but also decreases inspiratory time.

positive end-expiratory pressure (PEEP)

Hypercapnic Respiratory Failure
The ventilatory pump comprises
the diaphragm and chest wall
muscles, as well as the
neural control of them. This is
responsible for ensuring
adequate alveolar ventilation.
Four aspects of the ventilatory
pump, either alone or in
combination, can result in
pump failure: weak muscles,
excessive load, impaired
neuromuscular transmission,
motor neuron disease, or
decreased respiratory drive
(Table 14- 1). Hypercapnic
respiratory failure results in an
elevated Paco2•

Hypoxemic Respiratory Failure
Failure of the lungs to maintain arterial oxygenation is
hypoxemic respiratory failure. Hypoxemic respiratory
failure usually does not result in carbon dioxide
retention unless acute or chronic pump failure is also
present. Hypoxemic respiratory failure can usually be
treated with oxygen, but mechanical ventilation may be
necessary in severe cases of acute respiratory distress
syndrome (ARDS), heart failure, or pneumonia

Positive end-expiratory pressure (PEEP) is used to
increase oxygen delivery by preventing end-
expiratory alveolar collapse. However, the associated
increased intrathoracic pressure can lead to an
increase in right atrial pressure, and a decrease in
venous return and cardiac output.

•How does PEEP affect blood pressure?
•Our study found that when PEEP was below 4 cm
H
2O in the both control and hypertension groups,
blood pressure was unaffected by PEEP. However,
when PEEP was above 4 cm H
2O, the increase in
PEEP led to decreased blood pressure and PEEP
was negatively correlated with blood pressure in
the hypertension group

P. insp = inspiration pressure. This equates to peak
airway pressure. What you set on the PINSP
means the airway pressure is the same. So if the
Pinsp is set at 24, the peak airway pressure (Peak
AP on the patient’s observation chart) will be 24.
Pressure control helps protect the lung from
rising pressures as the PINSP is fixed and kept ≤ 30.
5 To 25

Pressure regulated
volume control
(PRVC)

•How many liters per minute does a ventilator use?
•The typical pipe size to med surge patient rooms is
¾”. The ventilator flow capacity is typically set at
40 LPM to 60 LPM

Pressure Support Ventilation

•Introduction
•Pressure support ventilation (PSV) is a mode of positive pressure mechanical
ventilation in which the patient triggers every breath. PSV is deliverable with
invasive (through an endotracheal tube) or non-invasive (via full face or nasal
mask) mechanical ventilation. This ventilatory mode is the most comfortable for
patients and is a useful ventilator setting for weaning from invasive ventilation
and for providing supportive care with non-invasive ventilation.[1] Flow (L/min)
delivery is by setting a driving pressure (cmH2O). The flow delivered will be
dependent on the set driving pressure, airway resistance, lung compliance, and
inspiratory effort of the patient. The breath is flow-limited, meaning that the
driving pressure terminates when the flow decreases to a set percentage (usually
25%) of the peak flow. Tidal volume (mL) delivered is dependent on the flow and
the duration of the inspiratory phase. Settings for PSV mode include driving
pressure, positive end-expiratory pressure (PEEP), and the fraction of inspired
oxygen (FiO2). Minute ventilation (L/min) is dependent on the patient’s
respiratory rate, and the tidal volume delivered with each breath. No mandatory
breaths are given in PSV; thus, no minimum minute ventilation is ensured

•Indications
•Pressure support ventilation is used to deliver oxygen and
support ventilation in patients with hypoxemic, hypercapnic, and
mixed respiratory failure. It is also used to perform a
spontaneous breathing trial (SBT) to determine if an intubated
patient on control mode ventilation is ready for extubation. The
flow delivered by the driving pressure can provide a tidal volume
and minute ventilation higher than the patient could achieve
without ventilator support. This higher minute ventilation
improves oxygen delivery and carbon dioxide offloading. PEEP
improves oxygen delivery by keeping distal airways and alveolar
sacs open during the expiratory phase, improving
ventilation/perfusion (V/Q) matching in the lungs. Also, there is a
reduction in oxygen consumption by decreasing the work of
breathing

•Contraindications
•Pressure support ventilation is relatively contraindicated in
patients who have a depressed respiratory drive, very high
oxygen consumption, or elevated airway resistance. Because
no mandatory breaths are given in PSV mode, minimum
minute ventilation is not ensured. Patients with neurologic
injury, encephalopathy from critical illness, or those
receiving sedation may hypoventilate. Work of breathing
and thus oxygen consumption is higher in PSV than in
control modes of ventilation. Patients with shock or low
cardiac output may need more respiratory support. High
airway resistance in patients with obstructive lung disease
limits peak flow and can result in small tidal volumes

•Equipment
•A mechanical ventilator and an external oxygen
supply are required to deliver PSV. For invasive
ventilation, an endotracheal tube, ventilator
tubing, an endotracheal tube holder, and
equipment for monitoring telemetry, blood
pressure, and oxygen saturation are necessary. For
non-invasive ventilation, CPAP tubing and a well-
fitting full face or nasal mask are requirements.

•Technique
•The initial settings for PSV are dependent on the indication.
In a patient breathing at a consistent respiratory rate,
setting a higher driving pressure will result in higher peak
flow and a higher tidal volume. Minute ventilation will
depend on the patient’s respiratory rate and inspiratory
effort. After initiating PSV, the patient should be directly
observed for several minutes to ensure that the goals of
ventilation, oxygenation and patient comfort are met. Pulse
oximetry, vital signs, the patient’s subjective response to
therapy, and arterial blood gas (ABG) testing can be used to
determine the effectiveness of the PSV settings

•Non-invasive Ventilation in Patients with Acute
Respiratory Failure
•It is worth noting that many ventilators designed to
provide non-invasive ventilation set an inspiratory
positive airway pressure (IPAP) and expiratory positive
airway pressure (EPAP) rather than a driving pressure
and PEEP. Thus, the driving pressure is the IPAP minus
the EPAP. It is important to set the driving pressure at
a minimum of 5cmH2O to provide adequate tidal
volume.
• Initial settings for non-invasive PSV are as follows:
IPAP 10-15cmH20, EPAP 5-10cmH20, FiO2 100%

•Invasive Ventilation for Patients with Acute Respiratory Failure
•Mechanical ventilators designed to provide invasive ventilation set a driving
pressure, PEEP, and FiO2. PSV is not an initial mode of ventilation for intubated
patients due to respiratory depression following sedation given during
intubation. Patients on control modes of ventilation who are meeting ventilation
and oxygenation goals are candidates for PSV. Initial driving pressure should be
tailored to approximate the patient’s tidal volume on control mode. PEEP and
FiO2 settings should be at the same values as the previous control mode. For
example, a patient on pressure control ventilation with a respiratory rate of 12,
driving pressure of 15cmH20, PEEP of 8 cmH2O, and FiO2 of 40% would
transition to PSV mode with driving pressure of 15 cmH20, PEEP of 8 cmH2O,
and FiO2 of 40%.[5] Once on PSV, the patient requires direct observation with
attention to signs of distress, changes in vital signs, and changes in minute
ventilation. An automatic backup control mode ventilation should be set to
initiate in case of prolonged apnea. Ventilator alarms for high and low minute
ventilation, tidal volume, respiratory rate, and airway pressure should be in
place.

The advantage of PSV for intubated patients is an
improvement in comfort and ventilator synchrony.
As the patient has more control over flow delivery
and respiratory rate in PSV mode, there tends to be
less ventilator desynchrony from patient-triggered
breaths during inspiration or passive exhalation and
less voluntary movement of the diaphragm in
opposition to delivered breaths. Sedation can often
be decreased for patients breathing comfortably on
PSV mode, allowing for more awake interaction and
participation in physical therapy

•Complications
•Complications of PSV include hypoventilation, hypoxemia,
and the resultant changes in mental status and vital signs
associated with these. It is imperative that a patient on PSV
has adequate monitoring as described above to quickly
identify these complications and change PSV settings or to a
control mode of ventilation. Hypoventilation and hypoxemia
can develop due to changes in mental status, airway
resistance, and lung compliance. Conditions such as
sedation effect, acute bronchospasm, and pulmonary
edema are examples of physiologic changes in the patient
that can result in decreased respiratory rate, decreased
delivery of flow from the ventilator, or both

The pressure support level can be adjusted to provide
either full support (PS
max), delivering a full tidal volume,
or at a lower level to provide partial support. Remember
that the pressure support level is the pressure applied
above baseline (i.e., a patient receiving 4 cm H
2O PEEP
and 16 cm H
2O pressure support actually gets 20 cm
H
2O peak inspiratory pressure)
Rise time is the amount of time required to reach the
pressure support level at the beginning of inspiration.

This mode consists of spontaneous ventilation with all
of the patient’s spontaneous breaths supported or
augmented by the ventilator. In other words, a set
pressure is added to each spontaneous breath.
The initial pressure support level is determined by
measuring the patient’s airway resistance. The pressure
support level can range from around 5cm H2O up to
20cm H2O.
Weaning from Pressure Support Ventilation → Start the
PS level at 5 to 15 cm H2O – or as directed by
medical staff - and adjust it gradually until the agreed
target tidal volume is achieved

If the patient becomes tachypnoeic, it may be due to the level
of pressure support being set too low. This
is usually confirmed by a low tidal volume. If this occurs, the
level of pressure support should be increased
so that a larger tidal volume (bigger breath) can be given to
the patient and this in turn will help slow down
the patient’s respiratory rate
If the patient does not make any spontaneous respiratory
effort, then no assistance will be provided and
‘Apnoea ventilation’ will alarm. It may be that the patient
remains too sleepy or too weak and is not quite
ready for weaning. Apnoea Ventilation must always be
switched ON in spontaneous breathing modes

Figure 20-2 Pressure support ventilation (PSV). The delivered
tidal volume (V
T) is calculated by integrating the area under
the flow curve (shaded area). The inspiratory rise time defines
how fast the maximal airflow (100%) is achieved. Thereafter,
the inspiratory airflow continuously decreases because once
the pressure target is reached, maintaining this level requires
progressively less air to flow into the lungs. As soon as the
cycling-off air flow threshold (i.e., a preset percentage of
maximal air flow) is reached, the ventilator ceases to deliver
inspiratory flow, and the expiratory valve is opened to allow
passive exhalation. (From Spiro SG, Silvestri GA, Agustí A:
Clinical respiratory medicine, ed 4, Philadelphia, PA, 2012,
Saunders.)

Figure 20-3 Changes in the parameters of PSV result in characteristic changes of the
pressure and volume curves. Panels “A” to “D” demonstrate isolated changes of
parameters, assuming that all other ventilatory parameters and the mechanical
characteristics of the respiratory system remain unchanged. A, PSV breath with an
inspiratory rise time of 0.20 second. B, After reducing the inspiratory rise time to its
minimum, the peak inspiratory flow and consequently also the cycling-off air flow
threshold are both reached earlier. Decreasing the inspiratory rise time results in a
shorter inspiratory time, while the tidal volume (V
T) remains unchanged. Note that
although the inspiratory rise time is decreased to 0 seconds, the peak inspiratory
flow is reached with a small delay. C, Increasing the cycling-off air flow threshold
from 30% to 50% similarly shortens the inspiratory time; however, V
T decreased in
this case. D, A combination of a maximal decrease in the inspiratory time and a
moderate increase in the cycling-off air flow threshold shortens the inspiratory time,
whereas the loss of V
T is only minimal. Such an approach may be used to achieve a
prolongation of the expiratory time in patients at risk for dynamic hyperinflation
because of the expiratory flow limitation (e.g., patients with chronic obstructive
pulmonary disease [COPD]). (From Spiro SG, Silvestri GA, Agustí A: Clinical
respiratory medicine, ed 4, Philadelphia, PA, 2012, Saunders.)

Synchronized Intermittent Mandatory Ventilation

Synchronized intermittent mandatory ventilation (SIMV)
is a type of volume control mode of ventilation. With
this mode, the ventilator will deliver a mandatory (set)
number of breaths with a set volume while at the same
time allowing spontaneous breaths. Spontaneous
breaths are delivered when the airway pressure drops
below the end-expiratory pressure ( trigger). This
activity reviews SIMV, and highlights the role of the
interprofessional healthcare team in evaluating,
managing, and improving care for patients who are
treated with SIMV.

Synchronized intermittent mandatory ventilation (SIMV) is a type of volume
control mode of ventilation. With this mode, the ventilator will deliver a
mandatory (set) number of breaths with a set volume while at the same
time allowing spontaneous breaths. Spontaneous breaths are delivered
when the airway pressure drops below the end-expiratory pressure (trigger).
The ventilator attempts to synchronize the delivery of mandatory breaths
with the spontaneous efforts of the patient. In contrast, to assist control
ventilation (ACV), SIMV will deliver spontaneous volumes that are 100%
driven by patient effort. Pressure support (PS) may be added to enhance the
volumes of spontaneous breaths. SIMV was initially developed in the 1970s
as a method to wean patients who are dependent on mechanical
ventilation.[1] SIMV gained popularity and was the most widely used
ventilatory mode for weaning, with 90.2% of hospitals preferring SIMV in a
survey conducted in the 1980s

•Indications
•Synchronized intermittent mandatory ventilation is typically
used to help wean patients from the ventilator.[4] From a
physiologic standpoint, SIMV has the advantage of avoiding
acute respiratory alkalosis by allowing patients to achieve
normal alveolar ventilation through an intact ventilatory
drive.[5] One concern when using SIMV is that it can result
in an increased work of breathing. One way to counteract
this is by adding pressure support to the
SIMV.[6] Mechanical ventilation, in general, is indicated in
severe hypoxic and hypercapnic respiratory failure, often
after a failed trial of non-invasive ventilation

•Contraindications
•Synchronized intermittent mandatory ventilation
is a ventilator mode that enables partial
mechanical assistance. This ventilator mode will
provide a set number of breaths at a fixed tidal
volume, but a patient can trigger a spontaneous
breath with the volume determined by patient
effort.[8] The maximal benefits of SIMV may only
be realized by a patient who can take a
spontaneous breath.

•Technique
•Once the patient is ready to initiate the weaning process, it
requires the appropriate settings on the ventilator. The
parameters include tidal volume, respiratory rate, positive end-
expiratory pressure (PEEP), the fraction of inspired oxygen
(FiO2), and, if used, the pressure support setting. After the
initiation of mechanical ventilation, it is best practice to obtain
an arterial blood gas within 60 minutes and to titrate the
ventilator settings accordingly.[9]
•SIMV is rarely used for weaning. A survey of intensivists from
various geographic regions showed SIMV was used 0 to 6% for
weaning, depending on the region. More common methods of
weaning are pressure support with PEEP (regional range of 56.5
to 72.3%) and T-piece (regional range of 8.9 to 59.5).

•Complications
•Complications affecting patients undergoing mechanical ventilation
include ventilator-associated pneumonia (VAP), barotrauma, acute
respiratory distress syndrome (ARDS), pneumothorax, atelectasis, and
post-extubation stridor. VAP is generally defined as a new persistent
infiltrate on chest radiograph after a patient has been on mechanical
ventilation for at least 48 hours, with at least three of the following
associated symptoms: fever, leukopenia/leukocytosis, increased sputum
production, rales, cough, or worsening gas exchange. ARDS is generally
defined using the Berlin definition. The definition requires the
measurement of the partial pressure of oxygen on a blood gas compared
to the fraction of inspired oxygen the patient is currently receiving. There
are three stages of ARDS: mild with a PaO2/FiO2 ratio less than or equal
to 300 mm Hg, moderate with PaO2/FiO2 less than or equal to 200 mm
Hg, and severe with PaO2/FiO2 less than or equal to 100 mm Hg

•A study of pediatric patients in Egypt showed 39.9% of patients
experienced complications, which equates to 29.5 complications per 1000
ventilation days. The complications were broken down into VAPs (27.3%
or 20.19/1000 ventilator days), pneumothorax (10.6% or 7.82/1000
ventilator days), atelectasis (4.4% or 3.28/1000 ventilator days), and post-
extubation stridor (2.4% or 1.76/1000 ventilator days).[12]
•Asynchrony is another complication, defined as a mismatch between the
patient's demand and the ventilator supply of measures such as
ventilation rate, flow, volume, or pressure.[13] Studies of neonatal
patients show that a neurally adjusted ventilatory assist has significant
fewer asynchrony events that SIMV.[14] In adult patients with acute
respiratory distress syndrome, there was no significant difference in
ventilator asynchrony amongst patients in assist/control mode and SIMV.
Additionally, there was no difference in the duration of mechanical
ventilation or hospital length of stay

•Clinical Significance
•If the patient does not trigger a breath, only the scheduled
mandatory breaths will be delivered. Perceived benefits of SIMV
include improved patient comfort on the ventilator, reduced
work of breathing, reduction in ventilator dyssynchrony, and
ease of ventilator weaning. Clinical trials evaluating some of
these benefits have not overwhelmingly supported these
benefits. SIMV, and specifically SIMV-PS, continues to be a
commonly used ventilator mode in the many US intensive care
units and especially in surgical ICUs. One of the newer modes of
mechanical ventilation, airway pressure release ventilation
(APRV), is a variant of SIMV-PS. In APRV, the inspiratory time is
longer than the expiratory time, providing an inverse I to E ratio
to improve oxygenation

SIMV was a popular method of mechanical ventilation when it was initially invented.
Newer studies demonstrate that it may not be the most effective mode of
ventilation. A study of preterm infants shows that SIMV has significantly worse mean
airway pressure, duration of time from the onset of weaning to extubation, duration
of nasal continuous positive airway pressure support after extubation, and an
extubation failure rate when compared to pressure support ventilation with volume
guarantee.[16] In adult patients receiving coronary artery bypass grafting, adaptive
support ventilation showed statistically lower amounts of atelectasis, number of
changes in mechanical ventilator settings, number of ventilator alarms, and hospital
length of stay when compared to SIMV.[17] After placing a patient on mechanical
ventilation, many intensivists begin to plan their strategy to wean and ultimately
liberate the patient from mechanical ventilation. Studies have shown that SIMV is
the least efficient technique of weaning when compared to pressure support
ventilation and intermittent T-piece trials.[18] Patients with acute respiratory
distress syndrome also have shown increased ventilator weaning duration time with
SIMV.[19] Similarly, in patients who underwent orthotopic liver transplantation,
pressure support SIMV had a significantly higher number of modifications to
ventilator settings and duration of mechanical ventilation than patients in adaptive
support ventilation.

Continuous Positive
Airway Pressure

•What are the contraindications for Continuous Positive
Airway Pressure?
•Contraindications
•Uncooperative or extremely anxious patient.
•Reduced consciousness and inability to protect their airway.
•Unstable cardiorespiratory status or respiratory arrest.
•Trauma or burns involving the face.
•Facial, esophageal, or gastric surgery.
•Air leak syndrome (pneumothorax with bronchopleural
fistula)

Continuous positive airway pressure (CPAP) is a type of
positive airway pressure that is used to deliver a set
pressure to the airways that is maintained throughout
the respiratory cycle, during both inspiration and
expiration. The application of CPAP maintains PEEP, can
decrease atelectasis, increases the surface area of the
alveolus, improves V/Q matching, and hence, improves
oxygenation. This activity describes the mechanism of
action, indications, contraindications, and complications
of CPAP therapy and explains the role of the
interprofessional team in managing patients with
hypoxia that can benefit from CPAP therapy.

•Introduction
•Continuous positive airway pressure (CPAP) is a type of positive airway
pressure, where the air flow is introduced into the airways to maintain a
continuous pressure to constantly stent the airways open, in people who
are breathing spontaneously. Positive end-expiratory pressure (PEEP) is
the pressure in the alveoli above atmospheric pressure at the end of
expiration. CPAP is a way of delivering PEEP but also maintains the set
pressure throughout the respiratory cycle, during both inspiration and
expiration.[1] It is measured in centimeters of water pressure (cm H2O).
CPAP differs from bilevel positive airway pressure (BiPAP) where the
pressure delivered differs based on whether the patient is inhaling or
exhaling. These pressures are known as inspiratory positive airway
pressure (IPAP) and expiratory positive airway pressure (EPAP). In CPAP no
additional pressure above the set level is provided, and patients are
required to initiate all of their breaths

The application of CPAP maintains PEEP, can
decrease atelectasis, increases the surface area of
the alveolus, improves V/Q matching, and hence,
improves oxygenation. It can also indirectly aid in
ventilation, although CPAP alone is often inadequate
for supporting ventilation, which requires additional
pressure support during inspiration (IPAP on BiPAP)
for non-invasive ventilation.

•Indications
•Airway collapse can occur from various causes,
and CPAP is used to maintain airway patency in
many of these instances. Airway collapse is
typically seen in adults and children who have
breathing problems such as obstructive sleep
apnea (OSA), which is a cessation or pause in
breathing while asleep. OSA may arise from a
variety of causes such as obesity, hypotonia,
adenotonsillar hypertrophy, among others.

•CPAP may be used in the neonatal intensive care unit (NICU) to treat
preterm infants whose lungs have not yet fully developed and who may
have respiratory distress syndrome from surfactant deficiency. Physicians
may also use CPAP to treat hypoxia and decrease the work of breathing in
infants with acute infectious processes such as bronchiolitis and
pneumonia or for those with collapsible airways such as in
tracheomalacia.
•It is used in hypoxic respiratory failure associated with congestive heart
failure in which it augments the cardiac output and improves V/Q
matching.
•CPAP can aid oxygenation via PEEP prior to placement of an artificial
airway during endotracheal intubation.
•It is used to successfully extubate patients that might still benefit from
positive pressure but who may not need invasive ventilation, such as
obese patients with obstructive sleep apnea (OSA) or patients with
congestive heart failure

Equipment

CPAP therapy utilizes machines specifically designed to deliver a flow of constant pressure.[5]
Some CPAP machines have other features as well, such as heated humidifiers. Components of
a CPAP machine include an interface for delivering CPAP.

CPAP can be administered in several ways based on the mask interface used:

Nasal CPAP: Nasal prongs that fit directly into the nostrils or a small mask that fits over the
nose

Nasopharyngeal (NP) CPAP: Administered via a nasopharyngeal tube- an airway placed
through the nose whose tip terminates in the nasopharynx. This has the advantage of
bypassing the nasal cavity, and CPAP is delivered more distally.

CPAP via face mask: A full face mask is placed over the nose and mouth with a good seal. It
can be used for those that are mouth breathers, or for pre-oxygenation in spontaneously
breathing patients prior to intubation.

A CPAP machine also includes straps to position the mask, a hose or tube that
connects the mask to the machine’s motor, a motor that blows air into the tube, and
an air filter to purify the air entering the nose.

Bubble CPAP is a mode of delivering CPAP used in neonates and infants where the
pressure in the circuit is maintained by immersing the distal end of the expiratory
tubing in water.[6] The depth of the tubing in water determines the pressure (CPAP)
generated. Blended and humidified oxygen is delivered via nasal prongs or nasal
masks and as the gas flows through the system, it “bubbles” out the expiratory
tubing into the water, giving a characteristic sound. Pressures used are typically
between 5 to 10 cm H2O. It requires skilled nurses and respiratory therapists to
maintain effective and safe use of the bubble CPAP system.

For patients using CPAP in the outpatient setting at home, it is important to wear it
regularly while asleep overnight and during daytime naps. Some CPAP units also
come with a timed pressure “ramp” setting that starts the airflow at a low level and
slowly raises the pressure to the set level that may make it more comfortable and
easier to which to become accustomed.

bubble cpap

face-mask CPAP, in which a tight-fitting face mask is put in place
and the patient exhales against a device that maintains positive
airway pressure. This approach can be useful when less than 10 cm
H2O CPAP is required to improve oxygenation and when the work
of breathing is not excessive. Face-mask CPAP in patients with
cardiogenic pulmonary edema can result in early physiologic
improvement and reduce the need for intubation and mechanical
ventilation. Gaseous distention of the stomach with emesis and
aspiration are potential problems, and therefore face-mask CPAP
should not be used in obtunded patients. The mask must be
removed periodically to prevent pressure necrosis. Thus, prolonged
use for many days is usually impractical. There has been recent
interest in the use of nasal positive-pressure ventilation (NPPV) in
the setting of acute respiratory failure. However, its clinical value
has not been established.

The long-term administration of prophylactic nCPAP
following cardiac surgery improved arterial
oxygenation, reduced the incidence of pulmonary
complications including pneumonia and reintubation
rate, and reduced readmission rate to the ICU or
IMCU. Thus noninvasive respiratory support with
nCPAP is a useful tool to reduce pulmonary
morbidity following elective cardiac surgery.

•Complications
•The first few nights on CPAP may be difficult, while patients
acclimate. Many patients at first find the mask uncomfortable,
claustrophobic or embarrassing.
•Side effects of CPAP treatment may include congestion, runny
nose, dry mouth, or nosebleeds; humidification can often help
with these symptoms. Masks may cause irritation or redness of
the skin, and use of the right size mask and padding can
minimize pressure sores from tight contact with skin. The mask
and tube must be kept clean, regularly inspected and should be
replaced every 3 to 6 months. Abdominal distension or a
sensation of bloating might occur which rarely can lead to
nausea, vomiting and subsequently aspiration this can be
minimized by decreasing the pressure or gastric decompression
through a tube in hospitalized patients.

•Compliance
•In spite of several benefits of CPAP therapy, compliance remains a big problem both in the
inpatient and outpatient setting.
•Physicians should monitor for compliance and follow up with their patients closely
especially during initiation of CPAP therapy to ensure long-term success.[7] Patients must
disclose any adverse effects that may limit compliance which must then be addressed by
the physician. Patients also need long-term follow up with an annual office visit to check
equipment, titrate settings as needed, and to ensure ongoing mask and interface fit.
Continuing patient education on the importance of regular use and support groups help
patients obtain the maximum benefit of this therapy.
•There may arise rare instances of respiratory distress where a hospitalized patient would
greatly benefit from CPAP but does not tolerate the mask or is not complaint due to
delirium, agitation or factors such as very young age in children or the elderly. In such
scenarios, mild sedation with low dose fentanyl or dexmedetomidine can be used to
improve compliance, until the therapy is no longer indicated. As the use of any sedative or
anxiolytic agent can lead to decrease in consciousness and decrease in respiratory drive
these patients should be monitored very closely. If adequate minute ventilation and or
oxygenation cannot be achieved, then management should include escalation to BiPAP or
intubation with mechanical ventilation following the code status and goals of care.

Bilevel positive airway pressure (BiPAP)
Initial BiPAP Settings:
Common initial inspiratory positive airway pressure (IPAP)
is 10 cm H20 (larger patients may need 15 cm H20)
Expiratory positive airway pressure (EPAP) is 5 cm H20.
Adjust from there usually by 2-5 cm H20. Rate of 10-12
breaths per minute (can increase rate if needing to get rid
of more CO2)

Biphasic positive airway pressure (BiPAP) is a ventilatory mode in
which two pressure levels (higher (Phigh) and lower (Plow)) acting
as continuous positive airway pressure (CPAP) alternate at preset
time intervals.

•What is the main difference between CPAP and
BiPAP?
•While CPAP generally delivers a single pressure,
BiPAP delivers two: an inhale pressure and an
exhale pressure. These two pressures are known
as inhalation positive airway pressure (IPAP) and
exhalation positive airway pressure (EPAP)

•How long can you stay on a BiPAP machine?
•BiPAP cannot be continued without a break for too
long (>24-48 hours) without causing nutritional
problems and pressure necrosis of the nasal skin.
Thus, if the patient fails to improve on BiPAP for 1-
2 days, then a transition to HFNC or intubation is
needed

Sedation is an essential component of the management
of intensive care patients. It is required to relieve
the discomfort and anxiety caused by procedures
such as tracheal intubation, ventilation, suction
and physiotherapy. It can also minimise agitation
yet maximise rest and appropriate sleep. Analgesia
is an almost universal requirement for the intensive
care patient.

Adequate sedation and analgesia
ameliorates the metabolic response to surgery
and trauma. Too much or too little sedation and
analgesia can cause increased morbidity, for example
over sedation can cause hypotension, prolonged
recovery time, delayed weaning, gut ileus, DVT,
nausea and immunosuppression; under sedation can
cause hypertension, tachycardia, increased oxygen
consumption, myocardial ischaemia, atelectasis,
tracheal tube intolerance and infection

Regarding the treatment of established delirium, a study
comparing dexmedetomidine with haloperidol in
patients with hyperactive delirium, dexmedetomidine
was associated with a shortertime to extubation and
shorter ICU length of stay Therefore, currently available
guidelines suggest administering continuous IV infusions
of dexmedetomidine for sedation to reduce the
duration of delirium in adult ICU patients with delirium
unrelated to alcohol or benzodiazepine withdrawal

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