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, 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 and potentially
unstable, 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.
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 and high airway pressures. 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.[3]
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 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.
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
(not TV) 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). 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 to be
beneficial for COPD, reducing the rate of tracheal intubations as well as
length of stay.[2] Their benefit increases with
increasing severity of disease. In patients with mild cases of COPD and CHF who
would not otherwise require ventilatory support do not benefit from noninvasive
positive-pressure ventilatory support. The use of noninvasive positive-pressure
ventilation has been less well studied in asthma, but, in one small randomized
trial, it reduced hospital admission rates.[4]
Adverse Consequences of Mechanical Ventilation
The
deterioration of intubated patients 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.[5] 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.[6]
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, saying that high airway pressures
result in alveolar overdistention (volutrauma) and accompanying increased
microvascular permeability and parenchymal injury might 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
decreased cardiac output from reduction in 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 always—and most appropriately—a 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 exists—for example, obtunded patients who
may be hypercarbic but might have a reversible metabolic or toxicological
etiology for their conditions—but 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
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
- 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
- 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.
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
PEEP has
several beneficial effects and may be clinically underutilized. Research
underway is examining the utility of high (>10 cm H2 O) PEEP in
disease states ranging from COPD/asthma to ARDS. PEEP has been found to reduce
the risk of atelectasis trauma and increase the number of "open"
alveoli participating in ventilation, thus minimizing V/Q mismatches. 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.
One obvious
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.
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
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.
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.
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.[7]
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. 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.[8] The National Heart, Lung, and Blood
Institute ARDS Clinical Trial Network, however, in a randomized comparison of
high and low PEEP among 549 patients with ARDS, found no statistical difference
in the outcomes of death rates and time spent intubated.[9]
Small,
nonrandomized studies have evaluated the effects of prone positioning and
kinetic therapy in ARDS/ALI. In a study of trauma and general surgery patients,
Davis et al demonstrated shorter durations of intubation and reduced mortality
among their kinetic prone therapy group, but this study was not randomized.[10]
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.[11] 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.[12]
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.
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.[13]
Ventilator Troubleshooting - Managing Complications in
the ED
The
complications most commonly encountered in the emergency department include
hypoxia, hypotension, high pressure alarms, and low exhaled volume alarms.
High
pressure alarms are triggered when resistance to ventilation is high. This may
occur secondary to reduced lung elasticity or airway obstruction, or extrinsic
compression. Thus, patients should be evaluated for pneumothorax, bronchospasm,
elevated abdominal pressure, mainstem intubation, tube plugs or kinks, tube
biting, dynamic hyperinflation/air trapping, psychomotor agitation, and
worsening pulmonary compliance secondary to progressive pulmonary disease. Tube
suctioning and adequate patient sedation are recommended after other causes of
obstruction are ruled out. Comparison of peak pressures with plateau pressures
may be helpful in identifying the location of resistance, especially if
graphical representation of airway pressures is available.
Plateau
pressure can be measured by applying a brief inspiratory pause after
ventilation. It better reflects the risk of barotrauma than peak inspiratory
pressure, but it is not in itself necessarily dangerous; if pleural pressure is
elevated secondary to a stiff chest wall or high abdominal pressure,
transpulmonary pressure (plateau pressure - pleural pressure) will be low,
minimizing the risk of bleb or alveolar rupture.
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.
