Asma 6

1/7/2021 Invasive mechanical ventilation in adults with acute exacerbations of asthma - UpToDate
Official reprint from UpToDate®

www.uptodate.com © 2021 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
Invasive mechanical ventilation in adults with acute

exacerbations of asthma
Authors: Carey C Thomson, MD, MPH, Kohei Hasegawa, MD, MPH
Section Editor: Scott Manaker, MD, PhD
Deputy Editor: Helen Hollingsworth, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2021. | This topic last updated: Aug 14, 2020.
INTRODUCTION
Intensive therapy with inhaled bronchodilators and systemic glucocorticoids is usually sufficient
to reduce airflow obstruction and ameliorate symptoms in patients with acute asthma
exacerbations. However, 3 to 5 percent of all patients hospitalized for acute asthma
exacerbation develop respiratory failure and require invasive mechanical ventilation [1-4].
Although potentially life-saving, mechanical ventilation and its associated interventions (eg,
sedatives, paralytics) can also cause morbidity and mortality [5-9].
In this topic review, the indications, management, and adverse effects of invasive mechanical
ventilation in patients with severe acute asthma exacerbation will be reviewed. The
pharmacologic treatment of acute exacerbations of asthma and the role of noninvasive positive
pressure ventilation are discussed separately. (See "Acute exacerbations of asthma in adults:
Home and office management" and "Noninvasive ventilation in adults with acute respiratory
failure: Benefits and contraindications".)
INDICATIONS
The primary indication for mechanical ventilation in an acute asthma exacerbation is acute
respiratory failure (ie, insufficient oxygenation or alveolar ventilation). The decision to initiate
mechanical ventilation should be based on serial clinical evaluations that consider the severity
of airflow limitation (eg, peak expiratory flow), degree of respiratory difficulty (eg, respiratory
https://www.uptodate.com/contents/invasive-mechanical-ventilation-in-adults-with-acute-exacerbations-of-asthma/print 1/25
rate >40/minute, inability to talk), clinical findings (eg, accessory muscle use, intercostal
retractions, fatigue, somnolence), hypoxemia, hypercapnia (elevated arterial tension of carbon
dioxide [PaCO2]), and response to therapy [10,11]. Bronchoconstriction can worsen abruptly
after placement of an endotracheal tube, so the need for ventilatory support must be weighed
against the potential for initial worsening of ventilation. Nonetheless, intubation and
mechanical ventilation should not be delayed until the need becomes emergent.
Generally, acute asthma exacerbations are associated with mild hyperventilation and a low
PaCO2. However, with worsening airflow limitation, the high work of breathing leads to fatigue,
a resultant decrease in the minute ventilation, and an increase in PaCO2. Thus, during an acute
asthma exacerbation, a PaCO2 of 42 mmHg or greater, while technically "normal," may suggest
incipient respiratory failure. On the other hand, hypercapnia alone is not an indication for
mechanical ventilation in the absence of decreased mental status or exhaustion.
NONINVASIVE VENTILATION
The optimal role of noninvasive ventilation (NIV, also called noninvasive positive pressure
ventilation [NPPV]), including biphasic positive airway pressure and continuous positive airway
pressure ventilation, in acute asthma exacerbations is unclear [3,12-17]. However, a brief trial of
NIV may be reasonable in selected patients with impending respiratory failure with careful
attention to comorbid conditions [3,17-20]. Failure of NIV to improve oxygenation would be an
indication for invasive mechanical ventilation. (See "Noninvasive ventilation in adults with acute
respiratory failure: Benefits and contraindications", section on 'Asthma exacerbation'.)
GENERAL APPROACH
The goals of mechanical ventilation during an acute asthma exacerbation are to maintain
adequate oxygenation, reduce the work of breathing, and prevent barotrauma due to
airtrapping, while waiting for bronchodilator and glucocorticoid medications to reverse the
airway edema, inflammation, and bronchoconstriction. While maintenance of a normal arterial
tension of carbon dioxide (PaCO2) is generally a goal of mechanical ventilation, this is not
always desirable or achievable in respiratory failure due to asthma, as the amount of ventilation
needed to normalize PaCO2 may contribute to hyperinflation and barotrauma.
Intubation — Intubation should be approached cautiously in patients with severe acute

asthma exacerbations because manipulation of the airway can cause laryngospasm and
worsening of bronchoconstriction [10]. Venous access and noninvasive monitoring should be in
place prior to intubation. The clinician most experienced with airway management should
intubate the patient, preferably with a large-bore (≥8 mm) endotracheal tube to minimize
airway resistance and enable suctioning [18,21]. Oral intubation is preferred over nasal
intubation. Issues related to preoxygenation and patient positioning are discussed separately.
(See "Emergency airway management in acute severe asthma" and "The decision to intubate"
and "Direct laryngoscopy and endotracheal intubation in adults".)
Resolution of wheezing and absence of an elevated airway pressure immediately after

intubation are clues to an upper airway cause of respiratory failure. Patients with severe asthma
exacerbation typically have increased airway pressures; the absence of elevated airway
pressures after intubation suggests that upper airway obstruction (eg, vocal cord dysfunction,
laryngeal malignancy) may have been contributing to wheezing and respiratory distress. (See
"Evaluation of wheezing illnesses other than asthma in adults".)
Induction agents — Once the decision has been made to proceed with intubation, most
patients receive rapid sequence induction [22,23]. The most commonly used agents are
etomidate, ketamine, and propofol. Etomidate is least likely to cause hemodynamic instability,
while ketamine and propofol have more bronchodilating characteristics; however, the optimal
agent has not been determined. Most patients will also receive a neuromuscular blocking agent
(eg, succinylcholine or rocuronium), unless they have a contraindication [22,23]. The use of
induction agents in patients with asthma and general considerations for rapid sequence
induction are discussed separately. (See "Emergency airway management in acute severe
asthma", section on 'Rapid sequence intubation' and "Rapid sequence intubation for adults
outside the operating room" and "Pretreatment medications for rapid sequence intubation in
adults outside the operating room" and "Induction agents for rapid sequence intubation in
adults outside the operating room" and "Neuromuscular blocking agents (NMBAs) for rapid
sequence intubation in adults outside of the operating room".)
Opiate medications are avoided due to the risk of histamine release exacerbating
bronchoconstriction.
Ventilator mode — Volume-limited modes of ventilation are commonly used for patients with
respiratory failure due to acute asthma exacerbation, although the optimal mode is not known
and may vary from one patient to another and over the course of a single patient's illness. We
typically select one of the following volume-limited modes: assist control ventilation (ACV),
synchronized intermittent mandatory ventilation (SIMV), or SIMV with pressure support
ventilation (SIMV/PSV) and adjust as needed to achieve synchrony between the patient and the
ventilator. Pressure support and pressure-limited modes are less suitable for patients with
airflow limitation. If a pressure-limited mode is employed, careful attention must be paid to
tidal volume and gas exchange, as the volume delivered varies with airway resistance and lung
compliance. (See "Modes of mechanical ventilation" and "Invasive mechanical ventilation in
acute respiratory failure complicating chronic obstructive pulmonary disease", section on
'Ventilator modes'.)
Initial ventilator settings — The following are reasonable initial ventilator settings for adults
with acute severe asthma [21-25]:
● Respiratory rate: 10 to 12 breaths/min
● Tidal volume: 6 to 8 mL/kg (ideal body weight) (calculator 1)
● Minute ventilation (respiratory rate multiplied by tidal volume): less than 115 mL/kg/min
● Inspiratory flow: We advise an initial inspiratory flow of 60 L/min, which can be increased if
needed to decrease inspiratory time and prolong expiratory time in patients with more
severe airflow obstruction. We use 75 L/min as an upper limit. Given the possibility of
increased bronchoconstriction at increased flow rates, the impact of changes in flow rate
on ventilation should be carefully monitored.
● Allow increased expiratory time by decreasing I:E ratio (1:3 or 1:4 up to 1:5)
● Extrinsic positive end-expiratory pressure (extrinsic PEEP, also known as applied PEEP) less
than 80 percent of the intrinsic PEEP, or 5 cm H2O if intrinsic PEEP is <10 cm H2O (see
'Adding extrinsic PEEP to offset intrinsic PEEP' below)
● Set the fraction of inspired oxygen (FIO2) at 100 percent initially and then titrate downwards
as tolerated to maintain the pulse oxygen saturation (SpO2) above 90 percent or the arterial
oxygen tension (PaO2) above 60 mmHg
● Set the sensitivity for triggering a ventilator-assisted breath at -2 L/min
The sensitivity setting determines the inspiratory effort (inspiratory air flow) that the patient
needs to generate to trigger a machine-assisted breath. We typically use flow triggering of
ventilator-assisted breaths for patients on SIMV, as this appears to decrease the work of
breathing compared with pressure triggering. Greater sensitivity of the trigger (eg, -1 cm H2O)
can lead to over-ventilation; lower sensitivity (eg -3 cm H2O) can increase work of breathing.
Continuing medical management — Administration of inhaled bronchodilator medication (eg,

albuterol, levalbuterol, ipratropium) remains an important therapeutic modality during
mechanical ventilation. Inhaled medications can be delivered via the ventilator tubing using
either a metered dose inhaler (MDI) with a specialized adaptor or a jet or mesh nebulizer.
Methods for delivery of inhaled medication during mechanical ventilation and the medical
management of acute asthma exacerbations are discussed separately. Pretreatment with
bronchodilators prior to intubation can mitigate the increase in airway resistance often seen in
asthmatics after tracheal intubation [11]. (See "Delivery of inhaled medication in adults", section
on 'Mechanically ventilated patients' and "Acute exacerbations of asthma in adults: Emergency
department and inpatient management", section on 'Inhaled beta agonists'.)
Other interventions to treat acute asthma, such as intravenous magnesium and glucocorticoids,
should continue during ventilatory support. (See "Acute exacerbations of asthma in adults:
Emergency department and inpatient management".)
TROUBLESHOOTING HIGH PEAK PRESSURES
For patients requiring mechanical ventilation for a severe asthma exacerbation, several
processes can cause high peak pressures (eg, >30 cm H2O), which in turn can increase the risk
of barotrauma. Causes of high peak pressure include airway obstruction, decreased
lung/pleural elasticity (eg, hyperinflation, pneumonia, pneumothorax), and patient-ventilator
asynchrony.
Differentiating airway and lung parenchymal causes of high pressures — Mechanical

ventilators normally display the peak pressure (Ppeak), which is the highest airway pressure
measured during each respiratory cycle and reflects the sum of resistive pressure of airways +
elastic pressure of lungs + positive end-expiratory pressure (PEEP). The plateau pressure (Pplat)
is measured at end-inspiration and represents the pressure in the small airways and alveoli
after flow has ceased. To measure Pplat, an inspiratory hold (0.5 to 1 second) is applied at end-
inspiration and the airway pressure displayed by the ventilator drops from the peak pressure to
the plateau pressure.
● An increase in both Ppeak and Pplat (with less than a 5 cm H2O difference between them),
suggests a lung parenchymal, pleural, or chest wall/diaphragmatic process (eg, asynchrony,
hyperinflation, pneumonia, pleural effusion, pneumothorax).
● A large difference between Ppeak and Pplat indicates more airway resistance (eg,
bronchoconstriction, airway mucus, endotracheal tube obstruction).
Dyssynchrony — Patient-ventilator dyssynchrony exists if the phases of breath delivered by the

ventilator do not match those of the patient (eg, machine breath on top of patient-directed
inspiration or machine breath before exhalation complete) and is manifest by agitation,
tachypnea, tachycardia, use of accessory muscles, uncoordinated thoracic wall or abdominal

movement, or deterioration in gas exchange. Common causes among patients with asthma
include ineffective triggering of machine-assisted breaths (eg, due to insufficient trigger
sensitivity or auto-PEEP as described below) ( figure 1), intolerance of a slow inspiratory flow
rate, and cough. (See "Overview of initiating invasive mechanical ventilation in adults in the
intensive care unit", section on 'Follow-up' and "Ventilator management strategies for adults
with acute respiratory distress syndrome", section on 'Treat dyssynchrony'.)
Sedation (eg, with a combination of propofol and fentanyl) may help the patient to breathe in
synchrony with the ventilator, but some patients are unable to breathe in synchrony with the
ventilator even with sedation. Paralytic agents may be necessary in this setting. Adequate
sedation and analgesia must be maintained if paralysis is used [21]. Neuromuscular blockade in
patients receiving high-dose glucocorticoids increases the risk of post-paralytic myopathy and
should be used sparingly [26,27]. (See "Neuromuscular blocking agents in critically ill patients:
Use, agent selection, administration, and adverse effects" and "Neuromuscular weakness
related to critical illness", section on 'Critical illness myopathy'.)
Dynamic hyperinflation — Dynamic hyperinflation occurs when the expiratory time is

insufficient to completely exhale and inadequate emptying of the lungs between breaths
causes progressive hyperinflation and increases Pplat ( figure 2). Dynamic hyperinflation is a
common problem in patients who require mechanical ventilation for severe asthma
exacerbations. Bronchospasm, airway inflammation, airway edema, and mucus plugging
dramatically decrease expiratory flow and prolong the time needed to complete exhalation
prior to the onset of the next breath. (See "Invasive mechanical ventilation in acute respiratory
failure complicating chronic obstructive pulmonary disease", section on 'Dynamic
hyperinflation'.)
Assessment — When assessing whether an individual patient has excessively high

intrathoracic pressures due to dynamic hyperinflation, use of Pplat (at end-inspiration) is
preferred to use of Ppeak. A high Ppeak is not a reliable indicator of lung overdistension since
Ppeak can be elevated due to increased airway resistance or high inspiratory flow rates, even in
the absence of overdistension. A safe upper limit of Pplat has not been established; however,
most clinicians aim for a Pplat below 30 cm H2O [23] and an intrinsic PEEP under 10 cm H2O.
Adverse effects of dynamic hyperinflation — Dynamic hyperinflation, which can be

induced or exacerbated by mechanical ventilation, is common in patients with severe asthma
exacerbation and its consequences can be devastating. Sequelae of dynamic hyperinflation
include cardiovascular collapse, barotrauma, and increased work of breathing [28,29]. There are
numerous other adverse effects associated with mechanical ventilation that are discussed in
detail separately. (See "Physiologic and pathophysiologic consequences of mechanical

ventilation".)
● Cardiovascular collapse – Hyperinflation increases intrathoracic pressure, which increases

pulmonary vascular resistance and decreases venous return. The net effect is reduced
cardiac output. Progressive cardiovascular collapse culminating in cardiac arrest with
pulseless electrical activity may ensue if not treated quickly [30]. Intravascular volume
depletion and sedatives can accelerate the deterioration. Successful treatment requires
volume resuscitation and alleviation of the hyperinflation, usually by temporarily
disconnecting the ventilator circuit from the endotracheal tube [31].
Pneumothorax is in the differential and should be excluded by examining the patient (eg,
for subcutaneous emphysema, unilateral decrease in breath sounds, deviation of the
trachea), using a bedside ultrasound, and/or obtaining a portable chest radiograph. (See
"Bedside pleural ultrasonography: Equipment, technique, and the identification of pleural
effusion and pneumothorax".)
● Barotrauma and pneumothorax – Barotrauma refers to alveolar rupture due to elevated

transalveolar pressure and is caused by progressive hyperinflation with overdistension of
alveoli and subsequent loss of alveolar structural integrity. Interstitial emphysema,
pneumothorax, pneumomediastinum, subcutaneous emphysema, and/or
pneumoperitoneum can result. A pneumothorax in patients receiving positive pressure
ventilation usually requires evacuation via tube thoracostomy. Unrecognized, it can rapidly
increase in size, impair venous return, and lead to refractory hypotension ("tension
pneumothorax") complicated by cardiac arrest due to pulseless electrical activity [32,33].
(See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive
mechanical ventilation in adults", section on 'Ventilator management' and "Thoracostomy
tubes and catheters: Indications and tube selection in adults and children".)
● Increased work of breathing – Dynamic hyperinflation creates intrinsic PEEP, which

increases the magnitude of the drop in airway pressure that the patient must generate to
trigger a breath ( figure 3), thereby increasing the patient's workload. Careful application
of extrinsic PEEP at levels less than the intrinsic PEEP will reduce this gradient and the work
of breathing [28]. Extrinsic PEEP should not exceed 80 percent of the measured intrinsic
PEEP in order to avoid worsening the dynamic hyperinflation [25]. (See 'Adding extrinsic
PEEP to offset intrinsic PEEP' below and "Positive end-expiratory pressure (PEEP)".)
Adjustments to decrease dynamic hyperinflation — Dynamic hyperinflation creates

intrinsic PEEP and elevates the Pplat, which can lead to cardiovascular collapse and barotrauma,
as well as increase the work of breathing.
Initial steps — Adjustments of the ventilator settings should aim for an inspiratory Pplat
less than 30 cm H2O and an intrinsic PEEP less than 10 cm H2O. The following adjustments may
help achieve these goals with the most important adjustments aiming to decrease minute
ventilation [10,22,34]:
● Decreasing the tidal volume allows a shorter inspiratory time and decreases the volume
that the patient needs to exhale prior to the next breath.
● Decreasing the respiratory rate also increases the expiratory time, allowing the patient
more time to exhale.
● Ensuring that the trigger for machine supported breaths is not overly sensitive decreases
potential breath-stacking due to extra machine breaths.
● Increasing the inspiratory flow will shorten the inspiratory time and allow the patient more
time in the expiratory phase to fully exhale (assuming respiratory rate remains unchanged).
However, increased inspiratory flow may trigger bronchoconstriction in patients with
bronchial hyperresponsiveness.
Of note, some evidence suggests that increasing the inspiratory flow rate has less of an
ameliorative effect on dynamic hyperinflation at lower levels of minute ventilation (eg, <10
L/min) [34]. Also, increasing inspiratory flow may lead to an increase in the spontaneous
respiratory rate and thus not achieve a decrease in dynamic hyperinflation [22].
Adding extrinsic PEEP to offset intrinsic PEEP — Increased intrinsic positive end-
expiratory pressure (also known as auto-PEEP) is a manifestation of breath-stacking and
dynamic hyperinflation. Normally, the end-expiratory pressure is zero or equal to any extrinsic
PEEP (also known as applied PEEP) delivered by the ventilator. One consequence of intrinsic
PEEP is that initiation of the next breath by the patient requires sufficient negative pressure to
overcome the intrinsic PEEP and trigger the ventilator. (See "Positive end-expiratory pressure
(PEEP)", section on 'Auto (intrinsic) PEEP'.)
Intrinsic PEEP can be detected by using ventilator-generated flow versus time graphs to
determine whether inspiratory flow begins before expiratory flow reaches zero ( figure 4). To
obtain a numeric value for intrinsic PEEP, the extrinsic PEEP is subtracted from airway pressure
measured during a breath-hold at end-expiration ( waveform 1). Ideally, the intrinsic PEEP
should be <10 cm H2O. (See "Positive end-expiratory pressure (PEEP)", section on 'Assessment'.)
A small amount of applied PEEP (3 to 5 cm H2O) is used in most mechanically ventilated patients
to mitigate end-expiratory alveolar collapse. Increasing the extrinsic PEEP (eg, up to 80 percent
of the intrinsic PEEP) can offset the adverse effects of intrinsic PEEP and reduce the effort
necessary to trigger inspiration during patient-initiated breaths. However, the amount of
intrinsic PEEP must be measured accurately to avoid administering excess extrinsic PEEP and
exacerbating air-trapping and high inspiratory pressures. The following are examples of clinical
scenarios in which the measurement of auto-PEEP may be inaccurate:
● During severe asthma exacerbations, widespread airway closure due to luminal secretions
and airway edema/inflammation can impede measurement of end-expiratory alveolar
pressure, resulting in a falsely low intrinsic PEEP measurement [35]. As a consequence,
marked hyperinflation may be unrecognized.
● Persistent expiratory muscle activity at end-expiration can also cause a falsely high
measurement of intrinsic PEEP by the ventilator. This is recognized at the bedside by
observing expiratory muscle activity during the breath-hold at end-expiration. In this
situation, addition of extrinsic PEEP could be deleterious and lead to increased work of
breathing. (See "Positive end-expiratory pressure (PEEP)", section on 'Assessment'.)
The patient's airway pressures and gas exchange should be monitored closely after addition of
extrinsic PEEP. (See "Positive end-expiratory pressure (PEEP)".)
Additional methods to decrease intrinsic PEEP include prolonging the expiratory phase,
reducing minute ventilation, and administering medications to promote bronchodilation. (See
'Adjustments to decrease dynamic hyperinflation' above.)
Permissive hypercapnia — The strategies of decreasing the respiratory rate and tidal
volume to prevent barotrauma can lead to an increase in the arterial tension of carbon dioxide
(PaCO2). Permissive hypercapnia refers to the acceptance of the elevated PaCO2 and associated
respiratory acidosis. The effects of respiratory acidosis are generally better tolerated than the
consequences of barotrauma, such as pneumothorax. The indications, contraindications, and
technique of permissive hypercapnia are discussed separately. (See "Permissive hypercapnia
during mechanical ventilation in adults".)
TROUBLESHOOTING HYPOXEMIA
In patients with acute asthma exacerbations, adequate oxygenation is usually achieved without
difficulty (eg, with an FIO2 ≤50 percent) after intubation, as the main problem is typically failure
of the patient to maintain the necessary work for ventilation. However, some patients develop
hypoxemia due to processes such as mucus plugging, atelectasis, air trapping,

ventilation/perfusion (V/Q) mismatch, pneumonia, or pneumothorax.
The first step is to determine the cause of hypoxemia by examination at the bedside and review
of a chest radiograph and/or use of bedside ultrasound. Examination at the bedside should
include interrogation of the ventilator, looking for high peak (Ppeak) and plateau (Pplat) airway
pressures, and breath-stacking.
● Audible wheezing and higher peak pressures (with a gap between peak and plateau
pressures more than 5 cm H2O) can indicate that bronchoconstriction or airway secretions
are contributing to V/Q mismatch. Adequate dosing of inhaled bronchodilator and systemic
glucocorticoids should be ensured along with suctioning to remove secretions.
● Increasing extrinsic positive end-expiratory pressure (extrinsic PEEP), which is often helpful
for hypoxemia due to acute respiratory distress syndrome (ARDS), must be done cautiously
in an acute asthma exacerbation, because excess extrinsic PEEP (above 80 percent of
intrinsic PEEP) may contribute to air trapping and poor ventilation. Careful measurement of
intrinsic PEEP is needed to guide any addition of extrinsic PEEP. (See 'Adding extrinsic PEEP
to offset intrinsic PEEP' above.)
● Does the patient have a pneumonia or pneumothorax? Review chest radiograph and/or
ultrasound for features of pneumonia or pneumothorax (eg, asymmetric opacities on
imaging, deep sulcus sign, absence of "lung sliding" on ultrasound). (See "Bedside pleural
ultrasonography: Equipment, technique, and the identification of pleural effusion and
pneumothorax" and "Clinical presentation and diagnosis of pneumothorax", section on
'Diagnostic imaging'.)
● Consider adjunctive/experimental therapies to improve ventilation. (See 'Additional and

unconventional therapies' below.)
ADDITIONAL AND UNCONVENTIONAL THERAPIES
Rarely, airflow obstruction is so severe and refractory that sufficient ventilation cannot be
achieved despite maximal standard therapy, including deep sedation, paralysis, intravenous
glucocorticoids, and inhaled bronchodilators. In this circumstance, general anesthesia or heliox
may permit ventilation and extracorporeal life support may act as a substitute gas exchanger.
The routine use of these adjunctive therapies cannot be recommended on the basis of existing
clinical studies.
General anesthesia — Induction of general anesthesia, either by intravenous infusion (eg,

ketamine) or inhalation (eg, isoflurane), can reduce bronchospasm and airway resistance [36-
40]. This approach should not be undertaken lightly, due to the risk of profound hypotension
[41]. An anesthesiologist is required for the duration of the anesthesia and bronchoconstriction
may recur when anesthesia is withdrawn. The duration of general anesthesia typically ranges
from 2 to 12 hours. (See "Acute exacerbations of asthma in adults: Emergency department and
inpatient management", section on 'Anesthetic agents'.)
Heliox — Heliox is a blend of helium and oxygen that has a lower density than air. Heliox is
rarely necessary, but can reduce resistance to airflow, enhance delivery of nebulized
bronchodilators, and improve oxygenation compared with standard nitrogen-oxygen mixtures
[42-46]. However, it can also cause ventilator malfunction, including inaccurate measurement of
tidal volume and oxygen concentration [47]. (See "Physiology and clinical use of heliox".)
Extracorporeal life support — Oxygenation and carbon dioxide removal through an artificial
membrane may be beneficial as a temporizing measure for patients with severe asthma
exacerbation complicated by refractory respiratory acidosis, although evidence based on clinical
trials is lacking [48-53]. (See "Extracorporeal membrane oxygenation (ECMO) in adults".)
EXTUBATION
Patients who have been intubated for respiratory failure due to severe asthma exacerbation can
usually wean quickly once airway edema and inflammation and bronchoconstriction respond to
medical therapy. Specific weaning and extubation criteria have not been established for acute
asthma exacerbation. One approach is to perform a spontaneous breathing trial once the
patient is awake and has normal vital signs, minimal audible wheezes, a normal arterial tension
of carbon dioxide (PaCO2), intrinsic positive end-expiratory pressure (auto-PEEP) less than 10 cm
H2O, and no evidence of neuromuscular weakness. (See "Extubation management in the adult
intensive care unit".)
After extubation, observation in an intensive care unit is recommended for an additional 12 to

24 hours.
PROGNOSIS
Patients with severe asthma exacerbation who require mechanical ventilation have increased
in-hospital mortality compared with patients who do not require mechanical ventilation (7
versus 0.2 percent) [1,2]. Patients who survive to hospital discharge remain at high risk of
death; this excess risk is only beginning to be recognized and may be worse than some
malignancies. As an example, one study assessed the long-term outcome of 145 survivors of
severe asthma exacerbation who required mechanical ventilation [54]. The one-, three-, and six-
year mortality rates were 10, 14, and 23 percent, respectively. Most of the deaths were due to
recurrent asthma. Close medical follow-up may be a key to long-term survival ( table 1). (See
"Identifying patients at risk for fatal asthma".)
Poor perception of illness severity and depression can contribute to the risk of near-fatal
asthma episodes. Survivors of near death due to asthma often demonstrate a lot of denial
regarding their illness, and anxiety appears to be more common among close family members
than the patients themselves [55]. Denial is an understandable psychological mechanism for
dealing with fear. The challenge is to demonstrate to such patients that they can manage their
illness. This requires a coordinated team approach involving the inpatient and outpatient
medicine and nursing services, and the use of community resources like asthma support
groups. (See "Identifying patients at risk for fatal asthma", section on 'Identifying high-risk
patients' and "Identifying patients at risk for fatal asthma", section on 'Prevention'.)
Depression is strongly associated with an increased risk of asthma mortality, and suspicion of
depression in a survivor of a near-fatal asthma attack warrants formal evaluation and treatment
[56]. (See "Trigger control to enhance asthma management", section on 'Emotional factors' and
"Unipolar depression in adults: Assessment and diagnosis".)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Asthma in adolescents
and adults".)
SUMMARY AND RECOMMENDATIONS
● Among patients hospitalized for an acute severe asthma exacerbation, approximately 3 to 5

percent require mechanical ventilation. (See 'Introduction' above.)
● Acute respiratory failure (ie, insufficient oxygenation and/or alveolar ventilation) is the
primary indication for mechanical ventilation. The decision to initiate mechanical ventilation
should be based on clinical judgment that considers the entire clinical situation, including
clinical and physiologic derangements and clinical course. (See 'Indications' above.)
● The role of noninvasive ventilation (NIV), including biphasic positive airway pressure and
continuous positive airway pressure ventilation, in patients with acute asthma
exacerbations is not well-defined. However, a brief trial of NIV may be reasonable in
selected patients prior to intubation and mechanical ventilation. (See 'Noninvasive
ventilation' above.)
● Intubation should be approached cautiously in patients with severe asthma exacerbation

because manipulation of the airway can cause increased airflow obstruction due to
exaggerated bronchial responsiveness. While evaluating the need for intubation, the
patient's airway is examined for traits associated with potential difficulty. If a difficult
intubation is anticipated, the necessary assistance (personnel, equipment, airway devices)
for management of a difficult airway should be obtained in case intubation becomes
necessary. (See 'Intubation' above and "Direct laryngoscopy and endotracheal intubation in
adults" and "Approach to the anatomically difficult airway in adults outside the operating
room", section on 'Identifying the difficult airway'.)
● Once the decision has been made to intubate, the majority of patients are given rapid
sequence induction using sedation with etomidate, ketamine, or propofol and
neuromuscular blockade with succinylcholine or rocuronium. The optimal agent has not
been determined. The clinician most experienced with airway management should intubate
the patient, preferably with a large-bore (≥8 mm) endotracheal tube. (See 'Intubation' above
and 'Induction agents' above and "Emergency airway management in acute severe
asthma", section on 'Rapid sequence intubation'.)
● Reasonable initial ventilator settings include a respiratory rate from 10 to 12 breaths/min, a

tidal volume of 6 to 8 mL/kg, a minute ventilation less than 115 mL/kg, and an inspiratory
flow of 60 to 75 L/min. Positive end-expiratory pressure (PEEP) is usually initiated at 5 cm
H2O. (See 'Initial ventilator settings' above.)
● Dynamic hyperinflation is a common problem in patients with a severe asthma

exacerbation. It refers to progressive hyperinflation due to inadequate emptying between
breaths, a consequence of expiratory airflow limitation. Dynamic hyperinflation creates
intrinsic PEEP (auto-PEEP) and elevates the plateau pressure (Pplat), which places the
patient at risk for cardiovascular collapse, barotrauma, and increased work of breathing.
(See 'Dynamic hyperinflation' above.)
● To assess whether dynamic hyperinflation is occurring, measurement of Pplat is performed

during a brief breath-hold at end-inspiration. Pplat is felt to be a more accurate measure of
lung overdistension, than measurement of peak airway pressure (Ppeak). (See 'Assessment'
above.)
● Initial ventilator settings may need further adjustment to maintain Pplat less than 30 cm
H2O and intrinsic PEEP less than 10 cm H2O. Adjustments that may help achieve these goals
include increasing the inspiratory flow (to allow longer expiratory time), decreasing the tidal
volume, and/or decreasing the respiratory rate. Decreasing the tidal volume or respiratory
rate may require the acceptance of elevated arterial tension of carbon dioxide (PaCO2), a
strategy known as permissive hypercapnia. (See 'Adjustments to decrease dynamic
hyperinflation' above and "Permissive hypercapnia during mechanical ventilation in
adults".)
● Increased intrinsic-PEEP is a manifestation of breath-stacking and dynamic hyperinflation.

The intrinsic PEEP is equal to the airway pressure measured during a breath-hold at end-
expiration, minus the amount of extrinsic PEEP (also known as applied PEEP). Increasing the
amount of extrinsic PEEP (eg, up to 80 percent of the intrinsic PEEP) can offset the effects of
intrinsic PEEP and reduce the effort necessary to trigger inspiration during patient-initiated
breaths. The accurate measurement of intrinsic PEEP is essential to avoid adding excess
extrinsic PEEP. (See 'Adding extrinsic PEEP to offset intrinsic PEEP' above.)
● Hypotension due to dynamic hyperinflation and poor venous return is treated with fluid
resuscitation and prompt alleviation of hyperinflation, usually by temporarily disconnecting
the ventilator circuit from the endotracheal tube. Ventilator settings are adjusted to prevent
a recurrence when mechanical ventilation is resumed. (See 'Adverse effects of dynamic
hyperinflation' above.)
● Rarely, airflow obstruction is so severe that sufficient ventilation cannot be achieved despite
maximal standard therapy. Benefit has been reported with use of general anesthesia,
heliox, or extracorporeal life support in these circumstances, although formal study is
lacking. (See 'Additional and unconventional therapies' above.)
● Patients with severe asthma exacerbation who require mechanical ventilation have
increased in-hospital and long-term mortality. Vigorous efforts to improve asthma control
after discharge may help prevent recurrent episodes. (See 'Prognosis' above.)
ACKNOWLEDGMENT
The editorial staff at UpToDate would like to acknowledge Carlos Camargo, Jr, MD, DrPH, and
Jerry Krishnan, MD, PhD, who contributed to an earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Krishnan V, Diette GB, Rand CS, et al. Mortality in patients hospitalized for asthma
exacerbations in the United States. Am J Respir Crit Care Med 2006; 174:633.
2. Nanchal R, Kumar G, Majumdar T, et al. Utilization of mechanical ventilation for asthma
exacerbations: analysis of a national database. Respir Care 2014; 59:644.
3. Stefan MS, Nathanson BH, Lagu T, et al. Outcomes of Noninvasive and Invasive Ventilation
in Patients Hospitalized with Asthma Exacerbation. Ann Am Thorac Soc 2016; 13:1096.
4. Hasegawa K, Bittner JC, Nonas SA, et al. Children and Adults With Frequent Hospitalizations
for Asthma Exacerbation, 2012-2013: A Multicenter Observational Study. J Allergy Clin
Immunol Pract 2015; 3:751.
5. Scoggin CH, Sahn SA, Petty TL. Status asthmaticus. A nine-year experience. JAMA 1977;
238:1158.
6. Mansel JK, Stogner SW, Petrini MF, Norman JR. Mechanical ventilation in patients with acute
severe asthma. Am J Med 1990; 89:42.
7. Anzueto A, Frutos-Vivar F, Esteban A, et al. Incidence, risk factors and outcome of

barotrauma in mechanically ventilated patients. Intensive Care Med 2004; 30:612.
8. Hodder R, Lougheed MD, FitzGerald JM, et al. Management of acute asthma in adults in the
emergency department: assisted ventilation. CMAJ 2010; 182:265.
9. Schatz M, Kazzi AA, Brenner B, et al. Joint task force report: supplemental
recommendations for the management and follow-up of asthma exacerbations.
Introduction. J Allergy Clin Immunol 2009; 124:S1.
10. Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic
patient in respiratory failure. J Allergy Clin Immunol 2009; 124:S19.
11. Wu RS, Wu KC, Wong TK, et al. Effects of fenoterol and ipratropium on respiratory
resistance of asthmatics after tracheal intubation. Br J Anaesth 2000; 84:358.
12. Soroksky A, Stav D, Shpirer I. A pilot prospective, randomized, placebo-controlled trial of
bilevel positive airway pressure in acute asthmatic attack. Chest 2003; 123:1018.
13. Gupta D, Nath A, Agarwal R, Behera D. A prospective randomized controlled trial on the
efficacy of noninvasive ventilation in severe acute asthma. Respir Care 2010; 55:536.
14. Brandao DC, Lima VM, Filho VG, et al. Reversal of bronchial obstruction with bi-level
positive airway pressure and nebulization in patients with acute asthma. J Asthma 2009;
46:356.
15. Galindo-Filho VC, Brandão DC, Ferreira Rde C, et al. Noninvasive ventilation coupled with
nebulization during asthma crises: a randomized controlled trial. Respir Care 2013; 58:241.
16. Lim WJ, Mohammed Akram R, Carson KV, et al. Non-invasive positive pressure ventilation
for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane
Database Syst Rev 2012; 12:CD004360.
17. Bergin SP, Rackley CR. Managing Respiratory Failure in Obstructive Lung Disease. Clin
Chest Med 2016; 37:659.
18. Lavonas EJ, Drennan IR, Gabrielli A, et al. Part 10: Special Circumstances of Resuscitation:
2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care. Circulation 2015; 132:S501.
19. Global Strategy for Asthma Management and Prevention, Global Initiative for Asthma (GIN
A). www.ginasthma.org (Accessed on August 11, 2020).
20. Althoff MD, Holguin F, Yang F, et al. Noninvasive Ventilation Use in Critically Ill Patients with
Acute Asthma Exacerbations. Am J Respir Crit Care Med 2020; 202:1520.
21. Corbridge TC, Hall JB. The assessment and management of adults with status asthmaticus.
Am J Respir Crit Care Med 1995; 151:1296.
22. Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic
patient in respiratory failure. Proc Am Thorac Soc 2009; 6:371.
23. Mannam P, Siegel MD. Analytic review: management of life-threatening asthma in adults. J
Intensive Care Med 2010; 25:3.
24. Tuxen DV. Permissive hypercapnic ventilation. Am J Respir Crit Care Med 1994; 150:870.
25. Gladwin MT, Pierson DJ. Mechanical ventilation of the patient with severe chronic
obstructive pulmonary disease. Intensive Care Med 1998; 24:898.
26. Douglass JA, Tuxen DV, Horne M, et al. Myopathy in severe asthma. Am Rev Respir Dis 1992;
146:517.
27. Kupfer Y, Namba T, Kaldawi E, Tessler S. Prolonged weakness after long-term infusion of
vecuronium bromide. Ann Intern Med 1992; 117:484.
28. Smith TC, Marini JJ. Impact of PEEP on lung mechanics and work of breathing in severe
airflow obstruction. J Appl Physiol (1985) 1988; 65:1488.
29. Leatherman J. Mechanical ventilation for severe asthma. Chest 2015; 147:1671.
30. Rosengarten PL, Tuxen DV, Dziukas L, et al. Circulatory arrest induced by intermittent
positive pressure ventilation in a patient with severe asthma. Anaesth Intensive Care 1991;
19:118.
31. Kollef MH. Lung hyperinflation caused by inappropriate ventilation resulting in

electromechanical dissociation: a case report. Heart Lung 1992; 21:74.
32. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Part 8: advanced challenges in resuscitation: section 3: special challenges in ECC. The
American Heart Association in collaboration with the International Liaison Committee on
Resuscitation. Circulation 2000; 102:I229.
33. Perkins GD, Augré C, Rogers H, et al. CPREzy: an evaluation during simulated cardiac arrest
on a hospital bed. Resuscitation 2005; 64:103.
34. Leatherman JW, McArthur C, Shapiro RS. Effect of prolongation of expiratory time on
dynamic hyperinflation in mechanically ventilated patients with severe asthma. Crit Care
Med 2004; 32:1542.
35. Leatherman JW, Ravenscraft SA. Low measured auto-positive end-expiratory pressure
during mechanical ventilation of patients with severe asthma: hidden auto-positive end-
expiratory pressure. Crit Care Med 1996; 24:541.
36. Saulnier FF, Durocher AV, Deturck RA, et al. Respiratory and hemodynamic effects of
halothane in status asthmaticus. Intensive Care Med 1990; 16:104.
37. Johnston RG, Noseworthy TW, Friesen EG, et al. Isoflurane therapy for status asthmaticus in
children and adults. Chest 1990; 97:698.
38. Hemming A, MacKenzie I, Finfer S. Response to ketamine in status asthmaticus resistant to
maximal medical treatment. Thorax 1994; 49:90.
39. Maltais F, Sovilj M, Goldberg P, Gottfried SB. Respiratory mechanics in status asthmaticus.
Effects of inhalational anesthesia. Chest 1994; 106:1401.
40. Heshmati F, Zeinali MB, Noroozinia H, et al. Use of ketamine in severe status asthmaticus in
intensive care unit. Iran J Allergy Asthma Immunol 2003; 2:175.
41. Tobias JD. Inhalational anesthesia: basic pharmacology, end organ effects, and applications
in the treatment of status asthmaticus. J Intensive Care Med 2009; 24:361.
42. Gluck EH, Onorato DJ, Castriotta R. Helium-oxygen mixtures in intubated patients with
status asthmaticus and respiratory acidosis. Chest 1990; 98:693.
43. Manthous CA, Hall JB, Caputo MA, et al. Heliox improves pulsus paradoxus and peak
expiratory flow in nonintubated patients with severe asthma. Am J Respir Crit Care Med
1995; 151:310.
44. Kress JP, Noth I, Gehlbach BK, et al. The utility of albuterol nebulized with heliox during
acute asthma exacerbations. Am J Respir Crit Care Med 2002; 165:1317.
45. Schaeffer EM, Pohlman A, Morgan S, Hall JB. Oxygenation in status asthmaticus improves
during ventilation with helium-oxygen. Crit Care Med 1999; 27:2666.
46. Rodrigo G, Pollack C, Rodrigo C, Rowe BH. Heliox for nonintubated acute asthma patients.
Cochrane Database Syst Rev 2006; :CD002884.
47. Tassaux D, Jolliet P, Thouret JM, et al. Calibration of seven ICU ventilators for mechanical
ventilation with helium-oxygen mixtures. Am J Respir Crit Care Med 1999; 160:22.
48. Shapiro MB, Kleaveland AC, Bartlett RH. Extracorporeal life support for status asthmaticus.
Chest 1993; 103:1651.
49. Kukita I, Okamoto K, Sato T, et al. Emergency extracorporeal life support for patients with
near-fatal status asthmaticus. Am J Emerg Med 1997; 15:566.
50. Mikkelsen ME, Woo YJ, Sager JS, et al. Outcomes using extracorporeal life support for adult
respiratory failure due to status asthmaticus. ASAIO J 2009; 55:47.
51. Steinack C, Lenherr R, Hendra H, Franzen D. The use of life-saving extracorporeal

membrane oxygenation (ECMO) for pregnant woman with status asthmaticus. J Asthma
2017; 54:84.
52. Maqsood U, Patel N. Extracorporeal membrane oxygenation (ECMO) for near-fatal asthma
refractory to conventional ventilation. BMJ Case Rep 2018; 2018.
53. Di Lascio G, Prifti E, Messai E, et al. Extracorporeal membrane oxygenation support for life-
threatening acute severe status asthmaticus. Perfusion 2017; 32:157.
54. Marquette CH, Saulnier F, Leroy O, et al. Long-term prognosis of near-fatal asthma. A 6-
year follow-up study of 145 asthmatic patients who underwent mechanical ventilation for a
near-fatal attack of asthma. Am Rev Respir Dis 1992; 146:76.
55. Yellowlees PM, Ruffin RE. Psychological defenses and coping styles in patients following a
life-threatening attack of asthma. Chest 1989; 95:1298.
56. Global Initiative for Asthma. Global strategy for asthma management and prevention, revis
ed 2014. http://www.ginasthma.org/documents/4 (Accessed on January 06, 2015).
Topic 570 Version 17.0
GRAPHICS
Ventilator triggering in presence of intrinsic positive end-

expiratory pressure (PEEPi)
Recordings of tidal volume, flow, airway pressure (P aw ), and esophageal pressure (P es )

in a patient with chronic obstructive pulmonary disease receiving pressure support
ventilation. Approximately half of the patient's inspiratory efforts do not succeed in
triggering the ventilator. Triggering occurred only when the patient generated a P es
≤8 cm H 2 O (indicated by the horizontal line), which was equal in magnitude to the
opposing elastic recoil pressure.
Reproduced with permission from: Tobin MJ, Jubran A, Schweiz Med Wochenschr 1994; 124:2139.
Graphic 59751 Version 2.0
Dynamic hyperinflation during controlled ventilation in obstructive

lung disease
During resting ventilation of normal lungs or controlled ventilation of lungs with decreased
lung compliance (eg, ARDS), passive exhalation leads to a return to normal FRC at the end
of each breath. However, in patients with airway obstruction, such as asthma or COPD,
exhalation may not be complete at the time the next breath is initiated, leading to
increasing amounts of trapped air at end-exhalation, a process known as dynamic
hyperinflation. In this figure, the tidal volume curve in blue reflects ventilation of normal
lungs and shows a return to the normal FRC at the end of each exhalation. The tidal
volume curve in green shows the progressive increase in FRC in a patient with asthma or
COPD when successive breaths are initiated before complete exhalation. Dynamic
hyperinflation can occur in patients with airway obstruction during mechanical ventilation
or with exercise.
Dynamic hyperinflation is associated with increased intrathoracic pressure and potentially
decreased venous return to the heart. Dynamic hyperventilation is treated by decreasing
minute ventilation (ie, reducing tidal volume and/or respiratory rate) and sometimes by
shortening inspiratory time to enable adequate time for exhalation.
ARDS: acute respiratory distress syndrome; COPD: chronic obstructive pulmonary disease; FRC:
functional residual capacity; I: inspiration; E: expiration.
Adapted from: Tuxen DV. Permissive hypercapnic ventilation. Am J Respir Crit Care Med 1994; 150:870.
Extrinsic positive end-expiratory pressure (PEEP) reduces the work of

breathing in status asthmaticus
The figure compares three conditions: No intrinsic or extrinsic positive end-expiratory pressure
(PEEP), intrinsic PEEP only, and intrinsic plus extrinsic PEEP. When intrinsic PEEP exists, the addition
of extrinsic PEEP reduces inspiratory effort (shown in red) from -11 cm H 2 O to -3 cm H 2 O. Airflow
obstruction is inhomogenous, so levels of intrinsic PEEP are likely to vary from airway to airway.
Thus, as a general rule, extrinsic PEEP is usually set up to, but not exceeding, 80 percent of the
measured intrinsic PEEP in order to prevent regions of worsening dynamic hyperinflation.
Auto-PEEP: Time-flow graphic
Shown on the upper graphic is time versus flow for an individual mechanically ventilated patient. Expiratory flow should
normally reach zero before the onset of inspiration. However, when auto-PEEP is present, expiratory flow does not reach
zero before inspiration. The arrow indicates that inspiration for each breath begins before expiratory flow has reached
zero.
Auto-PEEP: Auto positive end-expiratory pressure; lpm: liters per minute.
Reproduced with permission: Negligan P. Auto-PEEP: Beware of auto-PEEP in pressure controlled ventilation. Critical Care Medicine
Tutorials. Available at: http://www.ccmtutorials.com/rs/mv/strategy/page17.htm (Accessed on October 15, 2014). Copyright © 2002
Patrick Neligan.
Intrinsic positive end-expiratory pressure (PEEPi)
Recordings of airway pressure (P aw ), flow, and volume in a patient receiving controlled

mechanical ventilation. After the third breath, the airway was occluded at end-
expiration using the end-expiratory hold function on the ventilator. During the period
of zero flow, pressure in the alveoli and ventilator circuit equilibrate, and the plateau
pressure reflects auto or intrinsic positive end-expiratory pressure (PEEPi), indicated by
the arrow.
Reproduced with permission from: Tobin MJ, Van de Graaff WB. Monitoring of lung mechanics and
work of breathing. In: Tobin MJ, ed. Principles and practice of mechanical ventilation. New York:
McGraw Hill, Inc, 1994: 967.
Steps to prevent fatal and nonfatal asthma exacerbations
Provide verbal and written education about trigger avoidance (eg, aeroallergens, aspirin, NSAIDs)
Educate about early warning signs of deterioration
Use objective measures of airflow limitation
Review prednisone based action plan at each visit
Arrange frequent visits to assess asthma control
Optimize controller therapy
Encourage adherence to medications
Encourage smoking cessation
Address illicit drug use
Provide annual influenza vaccination
Contributor Disclosures
Carey C Thomson, MD, MPH Nothing to disclose Kohei Hasegawa, MD, MPH Grant/Research/Clinical
Trial Support: Teva [Asthma]; Novartis [Asthma]; National Institutes of Health [Asthma]. Scott Manaker,
MD, PhD Consultant/Advisory Boards: Expert witness in workers' compensation and in medical negligence
matters [General pulmonary and critical care medicine]. Other Financial Interest: National Board for
Respiratory Care [Director]. Helen Hollingsworth, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

Asma 6

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Asma 6

Uploaded by

Copyright:

Available Formats

1/7/2021 Invasive mechanical ventilation in adults with acute exacerbations of asthma - UpToDate

Official reprint from UpToDate®

Invasive mechanical ventilation in adults with acute

Intubation — Intubation should be approached cautiously in patients with severe acute

Resolution of wheezing and absence of an elevated airway pressure immediately after

● Respiratory rate: 10 to 12 breaths/min

● Tidal volume: 6 to 8 mL/kg (ideal body weight) (calculator 1)

● Set the sensitivity for triggering a ventilator-assisted breath at -2 L/min

Continuing medical management — Administration of inhaled bronchodilator medication (eg,

TROUBLESHOOTING HIGH PEAK PRESSURES

Differentiating airway and lung parenchymal causes of high pressures — Mechanical

Dyssynchrony — Patient-ventilator dyssynchrony exists if the phases of breath delivered by the

tachypnea, tachycardia, use of accessory muscles, uncoordinated thoracic wall or abdominal

Dynamic hyperinflation — Dynamic hyperinflation occurs when the expiratory time is

Assessment — When assessing whether an individual patient has excessively high

Adverse effects of dynamic hyperinflation — Dynamic hyperinflation, which can be

detail separately. (See "Physiologic and pathophysiologic consequences of mechanical

● Cardiovascular collapse – Hyperinflation increases intrathoracic pressure, which increases

● Barotrauma and pneumothorax – Barotrauma refers to alveolar rupture due to elevated

● Increased work of breathing – Dynamic hyperinflation creates intrinsic PEEP, which

Adjustments to decrease dynamic hyperinflation — Dynamic hyperinflation creates

as well as increase the work of breathing.

hypoxemia due to processes such as mucus plugging, atelectasis, air trapping,

● Consider adjunctive/experimental therapies to improve ventilation. (See 'Additional and

ADDITIONAL AND UNCONVENTIONAL THERAPIES

General anesthesia — Induction of general anesthesia, either by intravenous infusion (eg,

After extubation, observation in an intensive care unit is recommended for an additional 12 to

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

● Among patients hospitalized for an acute severe asthma exacerbation, approximately 3 to 5

● Intubation should be approached cautiously in patients with severe asthma exacerbation

● Reasonable initial ventilator settings include a respiratory rate from 10 to 12 breaths/min, a

● Dynamic hyperinflation is a common problem in patients with a severe asthma

● To assess whether dynamic hyperinflation is occurring, measurement of Pplat is performed

● Increased intrinsic-PEEP is a manifestation of breath-stacking and dynamic hyperinflation.

Use of UpToDate is subject to the Subscription and License Agreement.

7. Anzueto A, Frutos-Vivar F, Esteban A, et al. Incidence, risk factors and outcome of

31. Kollef MH. Lung hyperinflation caused by inappropriate ventilation resulting in

51. Steinack C, Lenherr R, Hendra H, Franzen D. The use of life-saving extracorporeal

Ventilator triggering in presence of intrinsic positive end-

Recordings of tidal volume, flow, airway pressure (P aw ), and esophageal pressure (P es )

Graphic 59751 Version 2.0

Dynamic hyperinflation during controlled ventilation in obstructive

Graphic 78052 Version 6.0

Extrinsic positive end-expiratory pressure (PEEP) reduces the work of

Graphic 71369 Version 3.0

Auto-PEEP: Time-flow graphic

Auto-PEEP: Auto positive end-expiratory pressure; lpm: liters per minute.

Graphic 93546 Version 3.0

Intrinsic positive end-expiratory pressure (PEEPi)

Recordings of airway pressure (P aw ), flow, and volume in a patient receiving controlled

Graphic 57873 Version 4.0

Steps to prevent fatal and nonfatal asthma exacerbations

Educate about early warning signs of deterioration

Use objective measures of airflow limitation

Review prednisone based action plan at each visit

Arrange frequent visits to assess asthma control

Optimize controller therapy

Encourage adherence to medications

Encourage smoking cessation

Address illicit drug use

Provide annual influenza vaccination