Ventilator Management: Introduction to Ventilator Management, Modes of Mechanical Ventilation, Methods of Ventilatory Support 7/5/16, 6:49 PM

Ventilator Management
Author: Allon Amitai, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP more...

Updated: May 31, 2016

Introduction to Ventilator Management

Intubation, with subsequent mechanical ventilation, is a common life-saving
intervention in the emergency department (ED). Given the increasing length of stay
of ventilated patients in EDs, it is necessary for emergency practitioners to have a
good understanding of techniques to optimize mechanical ventilation and minimize
complications.

Many different strategies of positive-pressure ventilation are available; these are

based on various permutations of triggered volume-cycled and pressure-cycled
ventilations and are delivered at a range of rates, volumes, and pressures. Poor
ventilatory management can inflict serious pulmonary and extrapulmonary damage
that may not be immediately apparent.

Because many of the effects of ventilator-induced lung injury are delayed and not
seen while patients are in the ED, much of our understanding of the adverse
consequences of volutrauma, air-trapping, barotrauma, and oxygen toxicity has
come from the critical care literature. While the fundamental principles underlying
mechanical ventilatory support have changed little over the decades, much
progress has been made in our understanding of the secondary pathophysiologic
changes associated with positive-pressure ventilation.

Ventilatory strategies have been devised for different disease processes to protect
pulmonary parenchyma while maintaining adequate gas exchange, and they may
be responsible for the increased rates of survival for pathologies such as acute
respiratory distress syndrome (ARDS). Several recent clinical trials have
demonstrated that optimizing ventilatory parameters reduces overall duration of
mechanical ventilation and organ failure. Additionally, an upsurge in utilization of
noninvasive ventilation has permitted many patients to avoid the risks and
complications of tracheal intubation.[1, 2]

Modes of Mechanical Ventilation

Volume-cycled mode
Inhalation proceeds until a set tidal volume (TV) is delivered and is followed by
passive exhalation. A feature of this mode is that gas is delivered with a constant
inspiratory flow pattern, resulting in peak pressures applied to the airways higher
than that required for lung distension (plateau pressure). Since the volume
delivered is constant, applied airway pressures vary with changing pulmonary
compliance (plateau pressure) and airway resistance (peak pressure).

Because the volume-cycled mode ensures a constant minute ventilation despite

potentially abnormal lung compliance, it is a common choice as an initial ventilatory
mode in the ED. A major disadvantage is that high airway pressures may be
generated, potentially resulting in barotrauma. Close monitoring and use of
pressure limits are helpful in avoiding this problem. Note that ventilators set to
volume-cycled mode function well as monitors of patients' pulmonary compliance,
which will be decreased in physiological states such as worsening ARDS,
pneumothorax, right mainstem intubation, chest-wall rigidity, increased intra-
abdominal pressure, and psychomotor agitation ("fighting the vent"). These
pathophysiological states increase peak pressure and should be considered
whenever pressure alarms are sounded.

In pressure-cycled settings, by contrast, such states result only in reduced

delivered volumes and may not trigger alarms. Given that the airway resistance
and pulmonary compliance of the critical ED patient is unknown, the authors
recommend the volume-cycled mode for initial ventilation of most patients.

Pressure-cycled mode

A set peak inspiratory pressure (PIP) is applied, and the pressure difference
between the ventilator and the lungs results in inflation until the peak pressure is
attained and passive exhalation follows. The delivered volume with each
respiration is dependent on the pulmonary and thoracic compliance.

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A theoretical advantage of pressure-cycled modes is a decelerating inspiratory flow

pattern, in which inspiratory flow tapers off as the lung inflates. This usually results
in a more homogeneous gas distribution throughout the lungs. However, no
definite evidence exists that this results in a reduction of the rate of ventilator-
induced lung injury or overall mortality. Nevertheless, pressure-cycled ventilation
has achieved considerable popularity in the intensive care setting for management
of patients with ARDS, whose lungs are most likely to be characterized by a broad
range of alveolar dysfunction and are also most vulnerable to the effects of
barotrauma and volutrauma.

A major disadvantage is that dynamic changes in pulmonary mechanics may result

in varying tidal volumes. This necessitates close monitoring of minute ventilation
and limits the usefulness of this mode in many emergency department patients.
However, newer ventilators can provide volume-assured pressure-cycled
ventilation, which increase peak pressures as needed to deliver a preset minimum
tidal volume.

High-frequency oscillatory support

In this ventilatory strategy, ultra-high respiratory rates (180-900 breaths per minute)
are coupled with tiny tidal volumes (1-4 mL/kg) and high airway pressures (25-30
mm H2 O).[3] This is a commonly accepted ventilatory setting for premature infants
and has now also been used in small critical care unit studies on patients with
ARDS, with reports of improving oxygenation and lung recruitment.[4, 5]

While this setting cannot currently be recommended for routine ED use, it may in
the future be found appropriate for the management of patients with ARDS.

Types of support

Most ventilators can be set to apply the delivered tidal volume in a control mode or
a support mode.

Control mode

In control mode, the ventilator delivers the preset tidal volume once it is triggered
regardless of patient effort. If the patient is apneic or possesses limited respiratory
drive, control mode can ensure delivery of appropriate minute ventilation.

Support mode

In support mode, the ventilator provides inspiratory assistance through the use of
an assist pressure. The ventilator detects inspiration by the patient and supplies an
assist pressure during inspiration. It terminates the assist pressure upon detecting
onset of the expiratory phase. Support mode requires an adequate respiratory
drive. The amount of assist pressure can be dialed in.

Methods of Ventilatory Support

Continuous mandatory ventilation
Breaths are delivered at preset intervals, regardless of patient effort. This mode is
used most often in the paralyzed or apneic patient because it can increase the
work of breathing if respiratory effort is present. Continuous mandatory ventilation
(CMV) has given way to assist-control (A/C) mode because A/C with the apneic
patient is tantamount to CMV. Many ventilators do not have a true CMV mode and
offer A/C instead.

Assist-control ventilation
The ventilator delivers preset breaths in coordination with the respiratory effort of
the patient. With each inspiratory effort, the ventilator delivers a full assisted tidal
volume. Spontaneous breathing independent of the ventilator between A/C breaths
is not allowed. As might be expected, this mode is better tolerated than CMV in
patients with intact respiratory effort.

Intermittent mandatory ventilation

With intermittent mandatory ventilation (IMV), breaths are delivered at a preset
interval, and spontaneous breathing is allowed between ventilator-administered
breaths. Spontaneous breathing occurs against the resistance of the airway tubing
and ventilator valves, which may be formidable. This mode has given way to
synchronous intermittent mandatory ventilation (SIMV).

Synchronous intermittent mandatory ventilation

The ventilator delivers preset breaths in coordination with the respiratory effort of
the patient. Spontaneous breathing is allowed between breaths. Synchronization
between preset mandatory breaths and the patient's spontaneous breaths
attempts to limit barotrauma that may occur with IMV when a preset breath is
delivered to a patient who is already maximally inhaled (breath stacking) or is
forcefully exhaling. One disadvantage of SIMV is increased work of breathing,
though this may be mitigated by adding pressure support on top of spontaneous
breaths.

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The initial choice of ventilation mode (eg, SIMV, A/C) is institution and practitioner
dependent. A/C ventilation, as in CMV, is a full support mode in that the ventilator
performs most, if not all, of the work of breathing. These modes are beneficial for
patients who require a high minute ventilation. Full support reduces oxygen
consumption and CO2 production of the respiratory muscles. A potential drawback
of A/C ventilation in the patient with obstructive airway disease is worsening of air
trapping and breath stacking.

When full respiratory support is necessary for the paralyzed patient following
neuromuscular blockade, no difference exists in minute ventilation or airway
pressures with any of the above modes of ventilation. In the apneic patient, A/C
with a respiratory rate (RR) of 10 and a TV of 500 mL delivers the same minute
ventilation as SIMV with the same parameters.

Pressure support ventilation

For the spontaneously breathing patient, pressure support ventilation (PSV) has
been advocated to limit barotrauma and to decrease the work of breathing.
Pressure support differs from A/C and IMV in that a level of support pressure is set
to assist every spontaneous effort. Airway pressure support is maintained until the
patient's inspiratory flow falls below a certain cutoff (eg, 25% of peak flow). The
patient determines the tidal volume, respiratory rate, and flow rate.[3] With some
ventilators, there is the ability to set a back-up IMV rate should spontaneous
respirations cease.

PSV is frequently the mode of choice in patients whose respiratory failure is not
severe and who have an adequate respiratory drive. It can result in improved
patient comfort, reduced cardiovascular effects, reduced risk of barotrauma, and
improved distribution of gas.

Noninvasive ventilation
The application of mechanical ventilatory support through a mask in place of
endotracheal intubation is becoming increasingly accepted and used in the
emergency department. Considering this modality for patients with mild-to-
moderate respiratory failure is appropriate. The patient must be mentally alert
enough to follow commands. Clinical situations in which it has proven useful
include acute exacerbation of chronic obstructive pulmonary disease (COPD) or
asthma, decompensated congestive heart failure (CHF) with mild-to-moderate
pulmonary edema, and pulmonary edema from hypervolemia. It is most commonly
applied as continuous positive airway pressure (CPAP) and biphasic positive
airway pressure (BiPAP). BiPAP is commonly misunderstood to be a form of
pressure support ventilation triggered by patient breaths; in actuality, BiPAP is a
form of CPAP that alternates between high and low positive airway pressures,
permitting inspiration (and expiration) throughout.

Reviews of the literature have shown noninvasive positive-pressure ventilation

(NPPV) to be beneficial for COPD, reducing the rate of tracheal intubations and the
length of stay.[2] Recently developed clinical guidelines recommend that NPPV be
considered as an adjunct to standard medical therapy in patients with severe
COPD exacerbations (pH < 7.35 and relative hypercarbia), as well as in patients
with cardiogenic pulmonary edema and respiratory failure without shock or acute
coronary syndrome requiring urgent percutaneous coronary intervention.[6]

The use of NPPV has been less well studied in asthma, though a recent meta-
analysis found that NPPV improved secondary outcomes such as number of
hospital admissions, length of ICU stay, and length of hospital stay, as well as had
a favorable effects on certain lung function parameters such as peak expiratory
flow, forced vital capacity, and FEV1.[7] However, the study did not demonstrate a
definite benefit ofNPPV for mortality or intubation rates.

Adverse Consequences of Mechanical Ventilation

The deterioration of intubated patients due to multiorgan failure has been observed
for decades. In recent years, however, much progress delineating the adverse
effects of positive-pressure ventilation has been made.[8] In 1993, Tremblay et al
demonstrated increased cytokine and inflammatory mRNA expression in a high-
stress ventilatory model, showing that increasing volumes and reducing PEEP
resulted in higher tumor necrosis alpha serum concentrations. Further research
over the 1990s demonstrated a cascade of systemic inflammatory effects of
biochemical pulmonary injury contributing to distal organ dysfunction.[9]

Pulmonary effects
Barotrauma may result in pulmonary interstitial emphysema, pneumomediastinum,
pneumoperitoneum, pneumothorax, and/or tension pneumothorax. High peak
inflation pressures (>40 cm H2 O) are associated with an increased incidence of
barotrauma. However, note that separating barotrauma from volutrauma is difficult,
since increasing barometric pressure is usually accompanied by increasing
alveolar volume.

Experimental models of high peak inflation pressures in animals with high

extrathoracic pressures have not demonstrated direct alveolar damage from
increased pressure without increased volume as well. Thus, the statement that

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high airway pressures result in alveolar overdistention (volutrauma) and

accompanying increased microvascular permeability and parenchymal injury may
be more accurate. Alveolar cellular dysfunction occurs with high airway pressures.
The resultant surfactant depletion leads to atelectasis, which requires further
increases in airway pressure to maintain lung volumes.

High-inspired concentrations of oxygen (fraction of inspired oxygen [FiO2] >0.5)

result in free-radical formation and secondary cellular damage. These same high
concentrations of oxygen can lead to alveolar nitrogen washout and secondary
absorption atelectasis.

It has been theorized that pulmonary biophysical and biomechanical injury in the
presence of bacterial lung infections contributes to bacterial translocation and
bacteremia.

Cardiovascular effects

The heart, great vessels, and pulmonary vasculature lie within the chest cavity and
are subject to the increased intrathoracic pressures associated with mechanical
ventilation. The result is a decrease in cardiac output due to decreased venous
return to the right heart (dominant), right ventricular dysfunction, and altered left
ventricular distensibility.

The decrease in cardiac output from reduction of right ventricular preload is more
pronounced in the hypovolemic patient and in those with a low ejection fraction.

Exaggerated respiratory variation on the arterial pressure waveform is a clue that

positive-pressure ventilation is significantly affecting venous return and cardiac
output. In the absence of an arterial line, a good pulse oximetry waveform can be
equally instructive. A reduction in the variation after volume loading confirms this
effect. These effects will most frequently be seen in patients with preload-
dependent cardiac function (that is, operating on the right side of the Starling
curve) and in hypovolemic patients or in those with otherwise compromised venous
return.

Increased alveolar-capillary permeability secondary to pulmonary inflammatory

changes may, alternatively, contribute to increased cardiac output.

For patients with Swan-Ganz catheterization in place for whom cardiac output may
be measured (usually in the ICU setting), PEEP studies may be performed. This is
performed by adjusting PEEP, monitoring oxygenation by peripheral oxygen
saturation or arterial oxygen measurement via blood gas sampling, and measuring
the associated cardiac output. The process is repeated at various PEEP settings,
and the results are recorded. The practitioner can then review the results and
determine the optimal PEEP for that patient at that time. This procedure is not
generally performed in the ED but underlies the association of ventilation strategy
and cardiac output.

Renal, hepatic, and gastrointestinal effects

Positive-pressure ventilation is responsible for an overall decline in renal function
with decreased urine volume and sodium excretion.

Hepatic function is adversely affected by decreased cardiac output, increased

hepatic vascular resistance, and elevated bile duct pressure.

The gastric mucosa does not have autoregulatory capability. Thus, mucosal
ischemia and secondary bleeding may result from decreased cardiac output and
increased gastric venous pressure.

Indications For Mechanical Ventilation

The principal indications for mechanical ventilation are airway protection and
respiratory failure. A compromised airway, or an airway at risk of compromise, may
be identified by physical examination and ancillary testing.

Respiratory failure in the ED is almost alwaysand most appropriatelya clinical

diagnosis. The decision to intubate and mechanically ventilate or to institute
noninvasive ventilation support is generally made purely on clinical grounds
without delay for laboratory evaluation.

Respiratory failure may also be easily identified with laboratory or pulmonary

function data. Obtaining a PaCO2 is useful to confirm respiratory failure when a
broader differential diagnosis existsfor example, obtunded patients who may be
hypercarbic but might have a reversible metabolic or toxicological etiology for their
conditionsbut adequate stabilization and ventilation of these patients should not
be delayed to wait for laboratory results.

Mechanical ventilation is indicated for both hypercapnic respiratory failure and

hypoxemic respiratory failure. It is also indicated for treatment of certain critical
conditions such as correction of life-threatening acidemia in the setting of salicylate
intoxication, for intentional hyperventilation in the setting of major head injury with
elevated intracranial pressure, for suspicion of clinical brain herniation from any
cause, or for a patient in critical condition with cyclic antidepressant toxicity.

Laboratory criteria

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Table. Laboratory Criteria for Mechanical Ventilation (Open Table in a new window)

Laboratory Criteria for Mechanical Ventilation

Blood gases PaO2 < 55 mm Hg
PaCO2 >50 mm Hg and pH < 7.32
Pulmonary function tests Vital capacity < 10 mL/kg
Negative inspiratory force < 25 cm H2 O
FEV1 < 10 mL/kg

Clinical criteria

See the list below:

Apnea or hypopnea
Respiratory distress with altered mentation
Clinically apparent increasing work of breathing unrelieved by other
interventions
Obtundation and need for airway protection

Other criteria
See the list below:

Controlled hyperventilation (eg, in head injury).

Severe circulatory shock

No absolute contraindications exist to mechanical ventilation. The need for

mechanical ventilation is best made early on clinical grounds. A good rule of thumb
is if the practitioner is thinking that mechanical ventilation is needed, then it
probably is. Waiting for return of laboratory values can result in unnecessary
morbidity or mortality.

Guidelines for Ventilator Settings

See the image below for suggested initial settings.

Initial ventilator settings in various disease states.

Mode of ventilation
The mode of ventilation should be tailored to the needs of the patient. In the
emergent situation, the practitioner may need to order initial settings quickly. SIMV
and A/C are versatile modes that can be used for initial settings. In patients with a
good respiratory drive and mild-to-moderate respiratory failure, PSV is a good
initial choice.

Tidal volume

Observations of the adverse effects of barotrauma and volutrauma have led to

recommendations of lower tidal volumes than in years past, when tidal volumes of
10-15 mL/kg were routinely used.

An initial TV of 5-8 mL/kg of ideal body weight is generally indicated, with the
lowest values recommended in the presence of obstructive airway disease and
ARDS. The goal is to adjust the TV so that plateau pressures are less than 35 cm
H2 O.

Respiratory rate
A respiratory rate (RR) of 8-12 breaths per minute is recommended for patients not
requiring hyperventilation for the treatment of toxic or metabolic acidosis, or
intracranial injury. High rates allow less time for exhalation, increase mean airway
pressure, and cause air trapping in patients with obstructive airway disease. The
initial rate may be as low as 5-6 breaths per minute in asthmatic patients when
using a permissive hypercapnic technique.

Supplemental oxygen therapy

The lowest FiO2 that produces an arterial oxygen saturation (SaO2) greater than
90% and a PaO2 greater than 60 mm Hg is recommended. No data indicate that
prolonged use of an FiO2 less than 0.4 damages parenchymal cells.

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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). Use of inverse I/E
may be appropriate in certain patients with complex compliance problems in the
setting of ARDS.

Inspiratory flow rates

Inspiratory flow rates are a function of the TV, I/E ratio, and RR and may be
controlled internally by the ventilator via these other settings. If flow rates are set
explicitly, 60 L/min is typically used. This may be increased to 100 L/min to deliver
TVs quickly and allow for prolonged expiration in the presence of obstructive
airway disease.

Positive end-expiratory pressure

Positive end-expiratory pressure (PEEP) has several beneficial effects and, when
used at optimal levels in combination with low tidal volumes, may reduce the
incidence of ventilator-induced lung injury. In particular, there is a significant
amount of ongoing research evaluating the use of high levels of PEEP in acute
lung injury (ALI) and ARDS. PEEP has been found to reduce the risk of atelectasis
trauma by increasing the number of "open" alveoli participating in ventilation,
thereby minimizing trauma due to the cyclical collapse and reopening of alveoli.
However, note that in disease states such as ARDS, the degree to which alveoli
function has been compromised varies tremendously within the lungs and there is
no single ideal PEEP appropriate for all alveoli; rather, a compromise PEEP must
be selected.

In addition to alveolar recruitment, an additional beneficial effect of PEEP is to shift

lung water from the alveoli to the perivascular interstitial space. It does not
decrease the total amount of extravascular lung water. This is of clear benefit in
cases of cardiogenic as well as noncardiogenic pulmonary edema. An additional
benefit of PEEP in cases of CHF is to decrease venous return to the right side of
the heart by increasing intrathoracic pressure.

Applying physiologic PEEP of 3-5 cm H2 O is common to prevent decreases in

functional residual capacity in those with normal lungs. The reasoning for
increasing levels of PEEP in critically ill patients is to provide acceptable
oxygenation and to reduce the FiO2 to nontoxic levels (FiO2 < 0.5). The level of
PEEP must be balanced such that excessive intrathoracic pressure (with a
resultant decrease in venous return and risk of barotrauma) does not occur.

Sensitivity
With assisted ventilation, the sensitivity typically is set at -1 to -2 cm H2 O. The
development of iPEEP increases the difficulty in generating a negative inspiratory
force sufficient to overcome iPEEP and the set sensitivity. Newer ventilators offer
the ability to sense by inspiratory flow instead of negative force. Flow sensing, if
available, may lower the work of breathing associated with ventilator triggering.

Monitoring During Ventilatory Support

Cardiac monitor, blood pressure, and pulse oximetry (SaO2) are recommended.
The authors practice with stable patients is to titrate down FiO2 to the minimum
value necessary to maintain maximal SaO2. An arterial blood gas (ABG)
measurement is frequently obtained 10-15 minutes after the institution of
mechanical ventilation. The measured arterial PaO2 should verify the
transcutaneous pulse oximetry readings and direct the reduction of FiO2 to a value
less than 0.5. The measured PaCO2 can suggest adjustments of minute ventilation
but should be interpreted in light of the patient's overall acid-base status. For
example, full correction of PaCO2 in a chronically hypercarbic COPD patient will
lead to unopposed metabolic alkalosis.
Reasonable alternatives to arterial blood gas measurement in more stable patients
include measuring the venous blood gas, which will give values close to arterial pH
and PaCO2 or monitoring an end-tidal CO2. An additional advantage of end-tidal
CO 2 monitoring is that it can detect acute ventilator dysfunction such as
endotracheal tube obstruction or dislodgement.[10]

Peak inspiratory and plateau pressures should be assessed frequently, although it

should be recognized that both pressures will be increased by extrapulmonary
pressure, for example from stiff chest walls or a distended abdomen, and do not
reflect the true risk of barotrauma. In general, however, parameters may be altered
to limit pressures to less than 35 cm H2 O. Expiratory volume is checked initially
and periodically (continuously if ventilator is capable) to ensure that the set tidal
volume is delivered. Any indication of an air leak must prompt a search for
underinflated tube cuffs, open tubing ports, or worsening pneumothorax. In
patients with airway obstruction, monitor auto-PEEP.

Initial Ventilator Settings in Various Disease States

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In the ED setting, patients frequently require full respiratory support. For most ED
patients who are paralyzed as a component of rapid-sequence induction, CMV and
A/C are good choices as an initial ventilatory mode. SIMV may be better tolerated
in nonparalyzed patients with obstructive airway disease and an intact respiratory
effort. PSV can be used when respiratory effort is intact and respiratory failure is
not severe.[11]

Noninvasive ventilation (CPAP, BiPAP) can be used effectively in many cases of

severe COPD and CHF to avoid tracheal intubation. Initial ventilator settings are
guided by the patient's pulmonary pathophysiology and clinical status. Adjustments
can then be made to limit barotrauma, volutrauma, and oxygen toxicity. CPAP and
BiPAP require alert, cooperative patients capable of independently maintaining
their airways and are contraindicated in the presence of facial trauma.

Asthma and COPD

Hypoxia can generally be corrected through a high FiO2, but patients with airway
obstruction are at risk of high airway pressures, breath stacking leading to intrinsic
PEEP, barotrauma, and volutrauma. To minimize intrinsic PEEP, it is recommended
that expiratory flow time be increased as much as possible and that tidal volumes
and respiratory rates are set at low values.[12] Permissive hypercapnia enables a
low respiratory rate of 6-8 breaths per minute to be used, as well as an increased
I:E ratio of 1:1.5 or 1:2.

PEEP may benefit some asthmatic patients by reducing the work of breathing and
maintaining open airways during expiration, but its effects are difficult to predict
and must be carefully monitored. Patients with asthma and COPD are at particular
risk of barotraumatic progression to tension pneumothorax, a complication that can
initially appear similar to runaway intrinsic PEEP. These conditions may be
distinguished by temporary detachment of the patient from positive-pressure
ventilation; if exhalation results in a recovery of pulse or normal blood pressure, the
diagnosis is intrinsic PEEP.

CPAP and BiPAP will benefit some asthmatics and many patients with COPD.
These patients will require careful monitoring as they can easily deteriorate from
hypercarbia, intrinsic PEEP, or respiratory exhaustion. Nevertheless, a
CochraneDatabase Systematic Review analysis of trials including patients with
severe COPD exacerbations demonstrated that the use of noninvasive positive-
pressure ventilation absolutely reduced the rate of endotracheal intubation by 59%
(95% confidence interval [CI] of relative risk [RR]: 0.33-0.53), the length of hospital
stay by 3.24 days (95% CI: 2.06-4.44 days), and the risk of mortality by 48% (95%
CI of RR: 0.35-0.76).[2]

Acute respiratory distress syndrome

ARDS lungs are typically irregularly inflamed and highly vulnerable to atelectasis
as well as barotrauma and volutrauma. Their compliance is typically reduced, and
their dead space increased. The standard of care for the ventilatory management
of patients with ARDS changed dramatically in 2000 with the publication of a large
multicenter, randomized trial comparing patients with ARDS initially ventilated with
either the traditional tidal volume of 12 mL/kg or a lower TV of 6 mL/kg. This trial
was stopped early because the lower tidal volume was found to reduce mortality by
an absolute 8.8% (P=0.007). Intriguingly, plasma interleukin 6 concentrations
decreased in the low TV group relative to the high TV group (P < 0.001),
suggesting a decrease in lung inflammation.[13, 14, 15, 16]

The authors recommend initiating ventilation of patients with ARDS with A/C
ventilation at a tidal volume of 6 mL/kg, with a PEEP of 5 and initial ventilatory rate
of 12, titrated up to maintain a pH greater than 7.25. There is not yet adequate
evidence to routinely recommend PEEP greater than 5 cm H2 O, but, in
appropriately monitored circumstances, it may be attempted.[17] Intrinsic PEEP
may occur in patients with ARDS at high ventilatory rates and should be watched
for and treated by reducing the rate of ventilation under direct observation until
plateau pressures decrease. The authors recommend a target plateau pressure of
less than 30 cm H2 O. Once a patient has been stabilized with adequate tidal
volumes at a plateau pressure of less than 30 cm H2 O, considering a trial of
pressure-cycled ventilation is reasonable.

Several recruitment maneuvers have been devised to increase the proportion of

alveoli ventilated in ARDS. These techniques typically attempt short-term
increased PEEP or volume to open occluded or collapsed alveoli. Gattinoni et al,
for example, found that among ARDS patients undergoing whole-lung CT, applying
45 cm H2 O PEEP recruited a mean of 13% new lung tissue.[18]

A recent meta-analysis that compared high versus low levels of PEEP in patients
with ALI and ARDS found no difference in mortality before hospital discharge
amongst studies that used the same tidal volume in both control and intervention
arms.[17] In a subsequent subgroup analysis that assessed lung-protective
ventilation (low tidal volume, high PEEP) versus conventional mechanical
ventilation, the authors found a decrease in mortality with the use of a lung-
protective ventilation strategy. The same review also found that high levels of
PEEP do improve oxygenation in patients with ALI and ARDS.

In a recent prospective, randomized, controlled trial, Guerin et al examined

whether early prone positioning during mechanical ventilation can improve

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outcomes in patients with severe ARDS. The authors found that both the 28-day
and unadjusted 90-day mortalities in the prone group were significantly lower (16%
and 23.6%, respectively) than in the supine group (32.8% and 41%, respectively).
[19]
Although they found no difference between the groups with regard to duration
of invasive mechanical ventilation or length of stay in the ICU, they found a higher
incidence of cardiac arrest in the supine group (31% vs 16% in the prone group).

Permissive hypercapnia is a ventilatory strategy that has won particular favor in the
management of patients with ARDS and COPD/asthma who would otherwise
require dangerously high tidal volumes and airway pressures. In patients without
contraindications such as head injury, cerebrovascular accident (CVA), elevated
intracranial pressure, or cardiovascular instability, permissive hypercapnia has
permitted much decreased tidal volumes, airway pressures, and respiratory rates,
though evidence for a decrease in mortality rates is incomplete.[20] The typically
recommended target pH is 7.25.

Noninvasive ventilatory strategies have met with little success in the treatment of
patients with ARDS. The authors recommend great caution and close monitoring if
noninvasive positive pressure ventilation (NIPPV) is attempted among patients with
ARDS.

In trials of NIPPV among patients with undifferentiated hypoxemia, the presence of

pneumonia or ARDS was associated with significantly increased risk of failure.
Some subgroups of patients with ARDS may benefit from NIPPV; however,
Antonelli et al demonstrated greater success in applying noninvasive positive
pressure ventilation to patients with lower simplified acute physiology scores and
higher PaO2/FiO2 ratios.[21]

Congestive heart failure

CHF responds very well to positive-pressure ventilation, which serves the dual role
of opening alveoli and reducing preload. Many patients with CHF benefit from a
trial of noninvasive CPAP or BiPAP. Some of these patients will clinically improve
so rapidly that admitting services may request discontinuation of noninvasive
ventilatory support, but great caution must be maintained if this is attempted, as
fluid may unpredictably reaccumulate, resulting in hypoxia and respiratory failure.

Intubated patients usually manage to adequately oxygenate. PEEP can be

increased as tolerated to improve oxygenation and reduce preload. However, in
some patients, cardiac output can be particularly dependent on preload and such
patients may easily develop postintubation hypotension. Management of this
common complication includes a combination of fluid therapy, discontinuation of
nitroglycerin or other medical therapies, and, if necessary, medical or mechanical
hemodynamic support interventions.[22]

Traumatic brain injury

Hyperventilation was traditionally recommended in the management of severe

traumatic brain injury, but recent studies have demonstrated poor outcomes
thought to be secondary to excessive cerebral vasoconstriction and reduced
cerebral perfusion. However, retrospective data have demonstrated decreased
mortality among traumatic brain injury ventilated to PCO2 between 30 and 39 mm
Hg, though this has not been prospectively validated.[23, 24]

Ventilator Troubleshooting - Managing

Complications in the ED
The differential diagnosis of the clinically deteriorating, mechanically ventilated
patient is wide and includes endotracheal tube or ventilator dysfunction, improper
ventilator settings, pain, anxiety, and pulmonary or extrapulmonary disease
processes.[10] The complications most commonly encountered in the ED include
hypoxia, hypotension, high-pressure alarms, and low exhaledvolume alarms.

Intubated patients who develop hemodynamic instability with respiratory

compromise should immediately be disconnected from the ventilator and manually
ventilated with 100% FiO2.

One of the first diagnoses that should be considered in any hemodynamically

unstable patient undergoing positive-pressure ventilation is tension pneumothorax.
This is a clinical diagnosis and should be detected and treated with needle
decompression prior to obtaining a chest radiograph.

A second diagnosis to exclude, particularly in patients with asthma or COPD, is

intrinsic PEEP. As discussed, intrinsic PEEP occurs as a result of incomplete
exhalation, which subsequently leads to hyperinflation, increased intrathoracic
pressure, decreased venous return, and decreased preload. The diagnosis of
intrinsic PEEP may be made by performing an end-expiratory hold or by detecting
a non-zero end-expiratory flow on the ventilator. The treatment for intrinsic PEEP is
to allow for lung deflation, then to alter mechanical ventilation settings to allow for
longer expiratory times by decreasing the respiratory rate, decreasing the tidal
volume, or changing the inspiratory-to-expiratory ratio.

Other diagnoses to consider are an obstructed endotracheal tube and an

endotracheal tube cuff leak. In the case of endotracheal tube obstruction, attempts

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to manually ventilate the patient are met with a significant amount of resistance
and high-pressure alarms may sound. Endotracheal tube obstruction may be
caused by extrinsic compression; tube plugs with mucus, blood, or foreign bodies;
tube kinks; or tube biting. Tube suctioning and adequate patient sedation are
recommended after other causes of obstruction are ruled out.

Measurement of peak pressures and plateau pressures may be helpful in

identifying the location of resistance, especially if graphical representation of
airway pressures is available. Peak pressure, which reflects resistance to airflow, is
measured by the ventilator during inspiration. Plateau pressure is thought to reflect
pulmonary compliance and can be measured by applying a brief inspiratory pause
after ventilation. High peak pressure with normal plateau pressures indicates
increased resistance to flow, such as endotracheal tube obstruction or
bronchospasm. An increase in both peak and plateau pressures suggest
decreased lung compliance, which may be seen in disease states such as
pneumonia, ARDS, pulmonary edema, and abdominal distention.

Low exhaled volume alarms are triggered by air leaks. These are most frequently
secondary to ventilatory tubing disconnect from the patient's tracheal tube but will
also occur in the event of balloon deflation or tracheal tube dislodgement. Tube
placement, balloon inflation, and connection to the ventilator should be carefully
verified.

Hypoxia after intubation may occur secondary to hypoventilation, worsening

cardiac shunting, inadequate FiO2, mainstem intubation, aspiration, tube
dislodgement, or pulmonary edema. The causes of high airway pressures and low
exhaled volumes described above can result in hypoxia if they cause
hypoventilation. Despite the use of numerous safety precautions, cases are
occasionally documented of ventilators being connected to compressed air or
nitrous oxide rather than oxygen. Increasing FiO2 and adjusting ventilatory settings
to increase PEEP or respiratory rate are useful first steps after excluding
equipment failure and mechanical causes of hypoxia.

Hypotension after intubation is usually attributable to diminished central venous

blood return to the heart secondary to elevated intrathoracic pressures. This can
be treated with fluid infusions and/or adjustment of ventilatory settings to lower
intrathoracic pressure (reducing PEEP, tidal volume, and, if air trapping is
suspected, respiratory rate). Hypotension may also be secondary to vasovagal
reaction to intubation, rapid sequence induction, sedation, and tension
pneumothorax.

Supportive Care
While the role of the emergency physician has traditionally been limited to
intubation and initiation of mechanical ventilation, intubated patients are spending
a greater portion of their hospital stay in the ED secondary to decreased availability
of ICU beds. In this setting, it becomes important to initiate preventative measures
to decrease the incidence of the secondary complications of mechanical
ventilation, such as ventilator-associated pneumonia (VAP), venous
thromboembolism (VTE), and stress-related mucosal injury.

VAP is defined as pneumonia in a mechanically ventilated patient that is not

clinically present at the time of intubation.[25] The time frame for development of
VAP is typically 48 hours or more after intubation, as this is when the disease
typically manifests itself clinically. VAP has been implicated as the most common
infectious complication occurring in ICU patients and results in prolonged ICU and
hospital lengths of stay, prolonged duration of mechanical ventilation, and overall
increased cost of care.[10]

Evidence suggests that prehospital and ED intubation, in addition to ED length of

stay, are independent risk factors for the development of VAP.[10, 26] These
findings, when combined with the significant morbidity and mortality associated
with VAP, confer upon the ED physician a responsibility to implement measures to
reduce the risk of VAP in the ED. These interventions are aimed at reducing the
risk of aspiration and decreasing bacterial colonization.

The Centers for Disease Control and Prevention published Guidelines for
Preventing Health-Care Associated Pneumonia in 2003, in which they recommend
placing the patient in a semiupright position, with the head of the bed elevated 30-
45o, in order to reduce the risk of aspiration.[27] Other measures such as early
placement of a nasogastric tube and oral care with a soft toothbrush and
chlorhexidine rinses may also be considered.[25] Lastly, endotracheal cuff
pressures should be monitored initially after intubation and every 4 hours
thereafter, with goal pressures of 20-30 cm H2 O, as increased risk of pneumonia
has been associated with cuff pressures less than 20 cm H2 O.

In addition to VAP, mechanically ventilated ICU patients are also at high risk for
development of VTE and stress-related injury of the gastrointestinal mucosa. In
patients without contraindications, unfractionated or low-molecular-weight heparin
should be considered in these patients for VTE prophylaxis. As the incidence of
gastric mucosal erosions has been found to be greater than 75% in ICU patients
within 24 hours of admission, gastrointestinal prophylaxis with a proton pump
inhibitor, sucralfate, or histamine receptor antagonist should be considered in
patients who are at high risk of gastrointestinal hemorrhage.[10] These high-risk
patients have been identified as those with coagulopathy, history of gastrointestinal

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bleeding, history of gastritis or peptic ulcer, or mechanical ventilation for more than
48 hours.

Contributor Information and Disclosures

Author
Allon Amitai, MD International Emergency Medicine Fellow, Rhode Island Hospital; Consulting Staff, Memorial
Hospital of Rhode Island; Doctoring Preceptor, Brown University Medical School

Allon Amitai, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Coauthor(s)
Richard H Sinert, DO Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research
Director, State University of New York College of Medicine; Consulting Staff, Vice-Chair in Charge of Research,
Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians, Society
for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Allison Regan, MD Resident Physician, Department of Emergency Medicine, State University of New York
Downstate Medical Center, Kings County Hospital Center, Brooklyn

Allison Regan, MD is a member of the following medical societies: American College of Emergency Physicians,
American Medical Association, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Ashika Jain, MD Assistant Professor, Department of Emergency Medicine, State University of New York
Downstate College of Medicine; Surgical Intensivist, Department of Surgery, Division of Trauma Critical Care,
Kings County Hospital Center, Brooklyn

Ashika Jain, MD is a member of the following medical societies: American College of Emergency Physicians,
Society of Critical Care Medicine, American Association of Physicians of Indian Origin

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa
Medical Center

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of
Emergency Physicians, Arizona Medical Association, American College of Osteopathic Emergency Physicians,
American Medical Association

Disclosure: Nothing to disclose.

Chief Editor
Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine,
Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung
Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest
Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic
Society

Disclosure: Nothing to disclose.

Additional Contributors
Steven A Conrad, MD, PhD Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care
Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health
Sciences Center

Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest
Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American
College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical
Society, Shock Society, Society for Academic Emergency Medicine, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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Medscape Reference 2011 WebMD, LLC

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