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Overview of mechanical ventilation

Author Section Editor Deputy Editor

Shelley L Schmidt, MD Polly E Parsons, MD Kevin C Wilson, MD
Robert C Hyzy, MD

Last literature review for version 16.3: October 1, 2008 | This topic last updated:
September 12, 2008

INTRODUCTION — Mechanical ventilation is also called positive pressure ventilation. Air is

forced into the central airways, increasing central airway pressure. Air follows the pressure
gradient from the central airways to the alveoli, which inflates the lungs. As the lungs inflate
and the device stops forcing air into the central airways, the intraalveolar pressure increases
and central airway pressure decreases. Expiration occurs when the air follows the newly
reversed pressure gradient from the alveoli to the central airways. Mechanical ventilation can
fully or partially replace spontaneous breathing.

The types of mechanical ventilation, as well as its benefits, indications, and initiation are
discussed in this topic review. Potential complications are described separately. (See
"Ventilator-associated lung injury" and see "Pulmonary barotrauma during mechanical
ventilation" and see "Physiologic and pathophysiologic consequences of mechanical
ventilation").

INDICATIONS — Mechanical ventilation is indicated for acute or chronic respiratory failure,

defined as insufficient oxygenation, insufficient alveolar ventilation, or both. Some common
acute disorders for which mechanical ventilation may be required are listed in the table (show
table 1).

Mechanical ventilation should be considered early in the course of illness and should not be
delayed until the need becomes emergent. Physiologic derangements and clinical findings can
be helpful in assessing the severity of illness (show table 2); however, the decision to initiate
mechanical ventilation should be based on clinical judgment that considers the entire clinical
situation [1,2]. Some of the objectives of mechanical ventilation are listed in the table (show
table 3) [2].

BENEFITS — The principal benefits of mechanical ventilation during respiratory failure are
improved gas exchange and decreased work of breathing:

Mechanical ventilation improves gas exchange by improving ventilation-perfusion

(V/Q) matching. The improved V/Q matching is primarily a consequence of
decreased physiologic shunting. (See "Physiologic and pathophysiologic
consequences of mechanical ventilation", section on Physiologic shunt).

The work of breathing can increase due to altered lung mechanics (eg, increased
airways resistance, decreased compliance) or increased respiratory demand (eg,
metabolic acidemia). The effort required to maintain this elevated work of
breathing may result in respiratory muscle fatigue and respiratory failure [1,3,4].
Mechanical ventilation can assume some or all of the increased work of breathing,

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allowing the ventilatory muscles to recover from their fatigue.

TYPES — Mechanical ventilation is sometimes classified according to the mechanism used to

terminate inspiration. Specifically, mechanical ventilation can be volume-, pressure-, flow-, or
time-limited.

Volume-limited — Inspiration ends after delivery of a preset tidal volume if mechanical

ventilation is volume-limited. The airway pressure is variable and related to compliance,
airway resistance, and tubing resistance. Examples of modes of mechanical ventilation that
can be volume-limited include assist control and synchronized intermittent mandatory
ventilation. (See "Modes of mechanical ventilation").

Pressure-limited — Inspiration ends when a preset maximum airway pressure is reached if

mechanical ventilation is pressure-limited. The tidal volume is variable and related to
compliance, airway resistance, and tubing resistance. A consequence of the variable tidal
volume is that a specific minute ventilation cannot be guaranteed. Examples of modes of
mechanical ventilation that can be volume-limited include assist control and synchronized
intermittent mandatory ventilation. Pressure-limited ventilation is increasingly common
because it may lessen ventilator-associated lung injury [5]. (See "Modes of mechanical
ventilation" and see "Ventilator-associated lung injury").

Flow-limited — A preset airway pressure is delivered once the ventilator is triggered if

mechanical ventilation is flow-limited. Inspiration ends when the inspiratory flow decreases to
a predetermined percentage of its peak value (show figure 1). An example of a mode of
mechanical ventilation that is typically flow-limited is pressure support. (See "Modes of
mechanical ventilation", section on Pressure support).

Time-limited — Inspiration ends after a preset inspiratory duration if mechanical ventilation

is time-limited. Both the tidal volume and airway pressure vary from breath to breath as lung
mechanics change. Many home ventilators are time-limited.

INITIATION — Once it has been determined that a patient requires mechanical ventilation,
numerous decisions need to be made including whether invasive or noninvasive mechanical
ventilation is warranted, the mode of mechanical ventilation, the amount of support, and the
initial ventilator settings.

Invasive versus noninvasive — Mechanical ventilation can be delivered invasively or

noninvasively. Invasive positive pressure is sometimes referred to as conventional mechanical
ventilation or traditional mechanical ventilation. It is delivered via an endotracheal tube or
tracheostomy tube. In contrast, noninvasive positive pressure ventilation (NPPV) is delivered
through an alternative interface, usually a face mask.

The decision about whether to initiate invasive or noninvasive mechanical ventilation requires
that the entire clinical situation be considered, including the underlying disease, its severity,
its rate of progression, and patient comorbidities. Generally speaking, a trial of noninvasive
positive pressure ventilation (NPPV) is worthwhile in patients with acute cardiogenic
pulmonary edema or hypercapnic respiratory failure due to chronic obstructive pulmonary
disease (COPD) who do not require emergent intubation and do not have contraindications to
NPPV [6-8]. Invasive mechanical ventilation is appropriate for most other patients. Patient
selection for NPPV is discussed in detail separately. (See "Noninvasive positive pressure
ventilation in acute respiratory failure", section on Patient selection).

Mode — Common modes of mechanical ventilation include assist control, synchronized

intermittent mandatory ventilation, and pressure support, although numerous other modes

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also exist. Selection of the mode is usually based on clinician familiarity and institutional
preferences [9,10]. The modes of mechanical ventilation are discussed in detail separately.
(See "Modes of mechanical ventilation").

Level of support — The level of ventilatory support refers to the proportion of the patient's
ventilatory needs that are met by the ventilator. It is an important consideration because
insufficient ventilatory support does not provide adequate rest for fatigued ventilatory
muscles. In contrast, excessive ventilatory support permits ventilatory muscles to atrophy.
An optimal level of support provides enough rest for the ventilatory muscles to recover from
fatigue without allowing atrophy.

The level of ventilatory support is determined by the mode and other settings. Generally
speaking, assist control tends to provide the most support, synchronized intermittent
mandatory ventilation provides the widest range of support, and pressure support tends to
provide less support:

The majority of patient effort during assist control involves triggering

ventilator-delivered breaths. Patients who do not need to trigger any breaths are
receiving full ventilatory support, while patients who trigger some breaths are
receiving somewhat less than full ventilatory support. (See "Modes of mechanical
ventilation", section on AC).

The level of ventilatory support can vary over the widest range during synchronized
intermittent mandatory ventilation (show figure 2) [11]. Full ventilatory support is
provided when the set respiratory rate is high enough that the patient does not
trigger any ventilator-delivered breaths. At the opposite end of the spectrum, no
ventilatory support is provided when the set respiratory rate is zero and all breaths
are spontaneous. (See "Modes of mechanical ventilation", section on SIMV).

Pressure support can not provide full ventilatory support because patients must
exert some effort to trigger each breath. The amount of ventilatory support
provided during pressure support ventilation is directly proportional to the pressure
support level. (See "Modes of mechanical ventilation", section on Pressure
support).

Settings — There are numerous settings that need to be considered when mechanical
ventilation is initiated. These include the trigger mode and sensitivity, respiratory rate, tidal
volume, positive end-expiratory pressure, flow rate, flow pattern, and fraction of inspired
oxygen.

Trigger — There are two ways to initiate a ventilator-delivered breath: pressure triggering
or flow-by triggering. This section discusses each.

When pressure triggering is used, a ventilator-delivered breath is initiated if the demand

valve senses a negative airway pressure deflection (generated by the patient trying to initiate
a breath) greater than the trigger sensitivity. A trigger sensitivity of -1 to -3 cmH2O is
typically set.

The trigger sensitivity should allow the patient to trigger the ventilator easily. A trigger
sensitivity that is too sensitive may cause a breath to be delivered in response to patient
movement or subtle pressure deflections caused by water moving within the ventilator
tubing. In contrast, a trigger sensitivity that is not sensitive enough increases patient effort
and may cause a prolonged period between the initial effort and the ventilator breath.
Pressure triggering can be used with the assist control or synchronized intermittent
mandatory ventilation modes of mechanical ventilation. (See "Modes of mechanical

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ventilation", sections on AC and SIMV).

Auto-PEEP (intrinsic positive end-expiratory pressure) interferes with pressure triggering.

Auto-PEEP refers to end-expiratory pressure that is created when inspiration begins before
expiration is complete. The mechanism by which auto-PEEP interferes with pressure
triggering is discussed separately. (See "Positive end-expiratory pressure (PEEP)", section on
Sequelae).

When flow-by triggering is used, a continuous flow of gas through the ventilator circuit is
monitored. A ventilator-delivered breath is initiated when the return flow is less than the
delivered flow, a consequence of the patient's effort to initiate a breath (show figure 3).
Flow-by triggering has been shown to decrease inspiratory work during continuous positive
airway pressure and the spontaneous breaths of synchronized intermittent mandatory
ventilation [12-14]. (See "Modes of mechanical ventilation", sections on Continuous positive
airway pressure and SIMV).

Tidal volume — The tidal volume is the amount of air delivered with each breath. The
appropriate initial tidal volume depends on numerous factors, most notably the disease for
which the patient requires mechanical ventilation. As an example, randomized trials found
that mechanical ventilation using tidal volumes of ≤6 mL per kg of ideal body weight (IBW)
improved mortality in patients with acute lung injury or acute respiratory distress syndrome
(ALI/ARDS) [15]. This is referred to as low tidal volume ventilation, which is described in
detail separately. (See "Mechanical ventilation in acute respiratory distress syndrome",
section on Low tidal volume ventilation).

The optimal tidal volume for patients who are mechanically ventilated for reasons other than
ALI/ARDS is unknown. An initial tidal volume of approximately 8 mL per kg of IBW seems
reasonable, albeit unproven and based only on clinical experience. Rarely should 10 mL per
kg of IBW be exceeded. The tidal volume can then be increased or decreased incrementally to
achieve the desired pH and arterial carbon dioxide tension (PaCO2), while monitoring the
auto-PEEP and airway pressure. Return to the previous tidal volume is indicated if the patient
develops auto-PEEP >5 cmH2O or a plateau airway pressure >30 cmH2O following an
increase in the tidal volume. Large tidal volumes can cause barotrauma or increase the risk
for ventilator-associated lung injury [16,17]. (See "Ventilator-associated lung injury").

During volume-limited ventilation, the tidal volume is set by the clinician and remains
constant. During pressure-limited ventilation, the tidal volume is variable. It is directly
related to the inspiratory pressure level and compliance, but indirectly related to the
resistance of the ventilator tubing. The clinician typically changes the tidal volume by
adjusting the inspiratory pressure level. (See "Modes of mechanical ventilation", sections on
Volume-limited and Pressure-limited).

Respiratory rate — An optimal method for setting the respiratory rate has not been
established. For most patients, an initial respiratory rate between 12 and 16 breaths per
minute is reasonable, although it may be modified according to the mode:

For patients receiving assist control, the respiratory rate is typically set four
breaths per minute below the patient's native rate (see "Modes of mechanical
ventilation", section on AC)

For patients receiving synchronized intermittent mandatory ventilation, the rate is

set to ensure that at least 80 percent of the patient's total minute ventilation is
delivered by the ventilator (see "Modes of mechanical ventilation", section on
SIMV)

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Once the tidal volume has been established, the respiratory rate can be incrementally
increased or decreased to achieve the desired pH and PaCO2, while monitoring auto-PEEP.
Return to the previous respiratory rate is indicated if the patient develops auto-PEEP >5
cmH2O. Other approaches are equally acceptable.

For patients with ALI/ARDS, the required respiratory rate is higher (up to 35 breaths per
minute), in order to facilitate low tidal volume ventilation. Setting the respiratory rate during
low tidal volume ventilation is discussed separately. (See "Mechanical ventilation in acute
respiratory distress syndrome", section on Low tidal volume ventilation).

Monitoring for auto-PEEP as the respiratory rate is increased should not be overlooked. In an
observational study of 14 patients receiving low tidal volume ventilation, increasing the
respiratory rate was associated with development of a mean auto-PEEP of 6 cmH2O [18].
Increasing the inspiratory flow rate and the respiratory rate simultaneously may mitigate the
development of auto-PEEP.

Occasionally, patients may continue to have respiratory acidosis despite optimization of their
tidal volume and respiratory rate settings. In this situation, permissive hypercapnic
ventilation is appropriate. (See "Permissive hypercapnic ventilation").

PEEP — Applied PEEP (extrinsic positive end-expiratory pressure) is generally added to

mitigate end-expiratory alveolar collapse. A typical initial applied PEEP is 5 cmH2O. However,
up to 20 cmH2O may be used in patients undergoing low tidal volume ventilation for acute
respiratory distress syndrome (ARDS). (See "Mechanical ventilation in acute respiratory
distress syndrome", section on Low tidal volume ventilation).

Elevated levels of applied PEEP can have adverse consequences, such as reduced preload
(decreases cardiac output), elevated plateau airway pressure (increases risk of barotrauma),
and impaired cerebral venous outflow (increases intracranial pressure). (See "Positive
end-expiratory pressure (PEEP)", section on Contraindications).

Flow rate — The peak flow rate is the maximum flow delivered by the ventilator during
inspiration. Peak flow rates of 60 L per minute may be sufficient, although higher rates are
frequently necessary. An insufficient peak flow rate is characterized by dyspnea, spuriously
low peak inspiratory pressures, and scalloping of the inspiratory pressure tracing [19].

The need for a high peak flow rate is particularly common among patients who have
obstructive airways disease with acute respiratory acidosis. In such patients, a higher peak
flow rate shortens inspiratory time and increases expiratory time (ie, decreases the
inspiratory to expiratory [I:E] ratio). These alterations increase carbon dioxide elimination
and improve respiratory acidosis, while also decreasing the likelihood of dynamic
hyperinflation (auto-PEEP) [19]. (See "Positive end-expiratory pressure (PEEP)", section on
Auto (intrinsic) PEEP).

However, there are costs to increasing the peak flow rate. Increased peak flow rates can
increase the peak airway pressure [20]. In addition, the decreased inspiratory time lowers the
mean airway pressure, which can decrease oxygenation.

Flow pattern — Microprocessor-controlled mechanical ventilators can deliver several

inspiratory flow patterns, including a square wave (constant flow), a ramp wave (decelerating
flow), and a sinusoidal wave (show figure 4). The ramp wave may distribute ventilation more
evenly than other patterns of flow, particularly when airway obstruction is present [21]. This
decreases the peak airway pressure, physiologic dead space, and PaCO2, while leaving
oxygenation unaltered [22]. The effects of the different flow patterns on potential

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complications of mechanical ventilation (eg, hemodynamic impairment, pulmonary

barotrauma, ventilator-associated lung injury) are unpredictable.

Fraction of inspired oxygen — The lowest possible fraction of inspired oxygen (FiO2)
necessary to meet oxygenation goals should be used. This will decrease the likelihood that
adverse consequences of supplemental oxygen will develop, such as absorption atelectasis,
accentuation of hypercapnia, airway injury, and parenchymal injury. (See "Oxygen toxicity").

The oxygenation goal varies from patient to patient. As an example, a patient with ischemic
heart disease requires greater oxygenation than a patient with chronic hypoxemia due to lung
disease. Typical oxygenation goals include an arterial oxygen tension (PaO2) above 60 mmHg
and an oxyhemoglobin saturation (SpO2) above 90 percent. In patients with ALI/ARDS,
targeting a PaO2 of 55 to 80 mmHg and a SpO2 of 88 to 95 percent is acceptable when the
trade off would be higher plateau pressures and an increased risk of lung injury due to
alveolar overdistension (ie, volutrauma) [15,23]. (See "Ventilator-associated lung injury").

ASYNCHRONY — Patient-ventilatory asynchrony exists if the phases of breath delivered by

the ventilator do not match that of the patient. It is common during mechanical ventilation:
more than 10 percent of breaths are asynchronous in approximately 24 percent of
mechanically ventilated patients, according to one observational study [24].

Patient-ventilator asynchrony can cause dyspnea, increase the work of breathing, and prolong
the duration of mechanical ventilation [25,26]. It can be detected by careful observation of
the patient and examination of the ventilator waveforms [27]. Generally, the abnormality that
is most readily apparent is failure of the ventilator to trigger a breath when the patient makes
an inspiratory effort. There are several common causes of patient-ventilator asynchrony:

Ineffective triggering of a ventilator-delivered breath - This may occur in as many

as one-third of inspiratory efforts [28]. Ineffective triggering is accentuated by an
insensitive inspiratory trigger, higher levels of pressure support, higher tidal
volumes, and higher pH [24]. The problem can be lessened or eliminated by
increasing the duration between the end of inspiration and the beginning of
expiration with an end-inspiratory pause.

Double triggering ventilator-delivered breaths - When this occurs, the ventilator

delivers two breaths in rapid sequence. This can be lessened or eliminated by
decreasing the trigger sensitivity (eg, from -1 cmH2O to -3 cmH2O).

Prolonged inspiratory time - Inspiratory time is the tidal volume divided by the
inspiratory flow rate. Attempts to increase the minute ventilation by raising only
the tidal volume result in an increased inspiratory time, causing patient discomfort
and asynchrony [18,28]. This problem may be avoided by increasing the
inspiratory flow rate when the tidal volume is increased, so that the inspiratory
time remains constant [29].

Other causes of respiratory distress in a mechanically ventilated patient are discussed

separately. (See "Assessment of respiratory distress in the mechanically ventilated patient").

SUMMARY AND RECOMMENDATIONS

Mechanical ventilation is indicated for acute or chronic respiratory failure, defined

as insufficient oxygenation, insufficient alveolar ventilation, or both. The principal
benefits of mechanical ventilation are improved gas exchange and decreased work
of breathing. (See "Indications" above and see "Benefits" above).

Mechanical ventilation is sometimes classified according to the mechanism used to

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terminate inspiration. Specifically, mechanical ventilation can be volume-,

pressure-, flow-, or time-limited. (See "Types" above).

Once it has been determined that a patient requires mechanical ventilation,

numerous decisions need to be made including whether invasive or noninvasive
mechanical ventilation is warranted, the mode of mechanical ventilation, the
amount of support, and the initial ventilator settings:

- For many patients, typical initial settings include a tidal volume of 8 mL per kg of ideal
body weight (IBW), a respiratory rate of 12 to 16 breaths per minute, a positive
end-expiratory pressure (PEEP) of 5 to 10 cmH2O, a peak flow rate that creates an
inspiratory to expiratory (I:E) ratio of 1:2 to 1:3, and the lowest fraction of inspiratory
oxygen (FiO2) sufficient to meet oxygenation goals. (See "Initiation" above).

- For patients with acute lung injury or acute respiratory distress syndrome (ALI/ARDS),
initial ventilator settings typically include smaller tidal volumes (6 mL per kg of IBW) and a
higher respiratory rate than those described above. (See "Mechanical ventilation in acute
respiratory distress syndrome", section on low tidal volume ventilation).

Patient-ventilatory asynchrony exists if the phases of breath delivered by the

ventilator do not match that desired by the patient. It is common during
mechanical ventilation and can cause dyspnea, increase the work of breathing, and
prolong the duration of mechanical ventilation. (See "Asynchrony" above).

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REFERENCES

1. Cohen CA, Zagelbaum G, Gross D, et al. Clinical manifestations of inspiratory

muscle fatigue. Am J Med 1982; 73:308.
2. Slutsky, AS. Mechanical ventilation. American College of Chest
Physicians'Consensus Conference [published erratum appears in Chest 1994
Aug;106(2):656]. Chest 1993; 104:1833.
3. Gil, A, Carrizosa, F, Herrero, A, et al. Influence of mechanical ventilation on blood
lactate in patients with acute respiratory failure. Intensive Care Med 1998; 24:924.
4. Weinberger, SE, Schwartzstein, RM, Weiss, JW. Hypercapnia. N Engl J Med 1989;
321:1223.
5. Marcy, TW, Marini, JJ. Inverse ratio ventilation in ARDS: Rationale and
implementation. Chest 1991; 100:494.
6. Keenan SP, Kernerman, PD, Cook DJ, et al. Effect of noninvasive positive pressure
ventilation on mortality in patients admitted with acute respiratory failure: A
meta-analysis. Crit Care Med 1997; 25:1685.
7. Calfee, CS, Matthay, MA. Recent advances in mechanical ventilation. Am J Med
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8. Bersten, AD, Holt AW, Vedig AE. Treatment of severe cardiogenic pulmonary
edema with continuous positive airway pressure in acute pulmonary edema. N engl
J Med 1991; 325:1825.
9. Esteban, A, Anzueto, A, Alia, I, et al. How is mechanical ventilation employed in
the intensive care unit? An international review. Am J Respir Crit Care Med 2000;
161:1450.
10. Esteban A, Anzueto A, Frutos R, et al. Characteristics and outcomes in adult
patients receiving mechanical ventilation: A 28-day international study. JAMA
2002; 287:345.

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11. Marini, JJ, Smith, TC, Lamb, V. External work output and force generation during
synchronized intermittent mechanical ventilation: Effect of machine assistance on
breathing effort. Am Rev Respir Dis 1988; 138:1169.
12. Sassoon, CSH, Giron, AE, Ely, EA, et al. Inspiratory work of breathing on flow-by
and demand flow CPAP. Crit Care Med 1989; 17:1108.
13. Hill, LL, Pearl, RG. Flow triggering, pressure triggering, and autotriggering during
mechanical ventilation [editorial; comment]. Crit Care Med 2000; 28:579.
14. Sassoon, CSH, Del Rosario, N, Fei, R, et al. Influence of pressure- and
flow-triggered synchronous intermittent mandatory ventilation on inspiratory
muscle work. Crit Care Med 1994; 22:1933.
15. Ventilation with lower tidal volumes as compared with traditional tidal volumes for
acute lung injury and the acute respiratory distress syndrome. The Acute
Respiratory Distress Syndrome Network. N Engl J Med 2000; 342:1301.
16. Dreyfuss, D, Soler, P, Basset, G, Saumon, G. High inflation pressure pulmonary
edema. Respective effects of high airway pressure, high tidal volume, and positive
end-expiratory pressure. Am Rev Respir Dis 1988; 137:1159.
17. International consensus conferences in intensive care medicine:
Ventilator-associated Lung Injury in ARDS. This official conference report was
cosponsoredby the American Thoracic Society, The European Society of Intensive
Care Medicine, and The Societe de Reanimation de Langue Francaise, and was
approved by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med
1999; 160:2118.
18. Vieillard-Baron, A, Prin, S, Augarde, R, et al. Increasing respiratory rate to improve
CO2 clearance during mechanical ventilation is not a panacea in acute respiratory
failure. Crit Care Med 2002; 30:1407.
19. Tobin, MJ. Mechanical ventilation. N Engl J Med 1994; 330:1056.
20. Chiumello D, Pelosi P, Calvi E et al. Different modes of assisted ventilation in
patients with acute respiratory failure. Eur Respir J 2002; 20:925.
21. Al-Saady, N, Bennett, D. Decelerating inspiratory flow wave form improves lung
mechanics and gas exchange in patients on intermittent positive pressure
ventilation. Intensive Care Med 1985; 11:68.
22. Yang, SC, Yang, SP. Effects of inspiratory flow waveforms on lung mechanics, gas
exchange, and respiratory metabolism in COPD patients during mechanical
ventilation. Chest 2002; 122:2096.
23. Brower, RG, Lanken, PN, MacIntyre, N, et al. Higher versus lower positive
end-expiratory pressures in patients with the acute respiratory distress syndrome.
N Engl J Med 2004; 351:327.
24. Thille, AW, Rodriguez, P, Cabello, B, et al. Patient-ventilator asynchrony during
assisted mechanical ventilation. Intensive Care Med 2006; 32:1515.
25. Hansen-Flaschen, JH. Dyspnea in the ventilated patient: a call for patient-centered
mechanical ventilation. Respir Care 2000; 45:1460.
26. Georgopoulos, D, Prinianakis, G, Kondili, E. Bedside waveforms interpretation as a
tool to identify patient-ventilator asynchronies. Intensive Care Med 2006; 32:34.
27. Nilsestuen, JO, Hargett, KD. Using ventilator graphics to identify patient-ventilator
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28. Tobin, MJ, Jubran, A, Laghi, F. Patient-ventilator interaction. Am J Respir Crit Care
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GRAPHICS

Conditions often requiring mechanical ventilation

Acute pulmonary parenchymal disease
Pneumonitis - infectious, aspiration, inhalation injury
Acute respiratory distress syndrome
Cardiogenic pulmonary edema
Acute myocardial infarction
Cardiomyopathy
Intravascular volume overload of any cause
Airways disease
Exacerbation of chronic obstructive pulmonary disease
Acute, severe asthma
Primary ventilatory failure
Guillain-Barre syndrome
Myasthenia gravis
Drug overdose
Chest wall disease
Systemic illness
Shock
Sepsis
Miscellaneous
Intraoperative (general anesthesia)
Chest trauma

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Abnormalities suggestive of the need for mechanical ventilation

Parameter Value
Loss of ventilatory reserve
Respiratory rate >35 breaths/min
Tidal volume <5 mL/kg
Vital capacity <10 mL/kg
Negative inspiratory force Weaker than -25 cmH20
Minute ventilation <10 L/min
Rise in PCO2 >10 mmHg
Refractory hypoxemia
Alveolar-arterial gradient (FiO2 = 1.0) >450
PaO2/PAO2 <0.15
PaO2 with supplemental O2 <55 mmHg

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Objectives of mechanical ventilation

Physiologic objectives
Support pulmonary gas exchange based on alveolar ventilation and arterial oxygenation
Reduce the metabolic cost of breathing by unloading the ventilatory muscles
Minimize ventilator-induced lung injury
Clinical objectives
Reverse hypoxemia
Reverse acute respiratory acidosis
Relieve respiratory distress
Prevent or reverse atelectasis
Reverse ventilatory muscle fatigue
Permit sedation and/or neuromuscular blockade
Decrease systemic or myocardial oxygen consumption
Stabilize the chest wall
Adapted from Slutsky, AS, Chest 1993; 104:1833.

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Pressure support ventilation

Changes in airway pressure, flow, and volume as measured in the distal endotracheal
tube during unsupported and pressure-supported spontaneous breaths in intubated
patients. The unsupported patient (blue lines) must first generate an initial negative
pressure "spike" to open the ventilator demand valves and then must maintain a small
amount of negative pressure during inspiration to produce flow through the ventilator
circuitry. The addition of increasing levels of pressure support (green lines) provides
plateaus of positive pressure that augment the spontaneous tidal volume in accordance
with the patient's spontaneous respiratory flow demand and inspiratory time pattern.
Redrawn from Respir Care 1987; 32:447.

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Effect of decreased SIMV support in ARDS

Effects of decreasing synchronized intermittent mandatory ventilation

(SIMV) support on the work of breathing per liter of ventilation in patients
with acute respiratory distress syndrome. Inspiratory work per unit volume
(work per liter Wp/L) done by the patient is shown during assisted cycles
(blue bars) and spontaneous cycles (red bars). As machine support was
withdrawn, the patients performed an increasing amount of inspiratory
work per liter of ventilation. The increased work was significantly greater at
all levels of machine support less than or equal to 60 percent (p 0.01).
Spontaneous breaths required 25 percent more work per liter of ventilation
than assisted breaths at these levels of machine support. The
pressure-time index exceeded a fatiguing level of work at all levels of
machine support less than 80 percent. It was suggested that, when using
the SIMV mode, the back-up rate should result in at least 80 percent of the
minute ventilation coming from the machine in order to prevent fatigue.
Redrawn from Marini, JJ, Smith, TC, Lamb, V, Am Rev Respir Dis 1988;
138:1169.

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Flow-by triggering in mechanical ventilation

Flow-by triggering involves the monitoring of gas flow through the circuit as it is
passed by the patient. The machine is triggered once the return flow is less than
delivered flow, due to the patient's inspiratory effort. The ventilator monitors
return flow (left upper panel), which decreases as patient effort begins (left
middle panel). The airway pressure and inspiratory flow required by flow
triggering (red dashed arrows) are less than those required to trigger a demand
valve (black solid arrows). Once the return flow has diminished, the base flow
increases as the machine is triggered; increased gas flow is then delivered to
the patient as shown in the graph in the upper right Adapted from Puritan
Bennett 1994, Form AA-1495

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Ventilator flow and pressure waveforms

Airway pressure (Paw) and flow rate shown for constant, decelerating, and
sinusoidal inspiratory flow waveforms. Inspiratory time and tidal volume
were held constant. Peak inspiratory airway pressures are similar with all
waveforms, but mean airway pressure is highest with the decelerating
inspiratory flow wave. Redrawn from Banner, MJ, Lanpontang, S, In:
Current Respiratory Care, Kacmarek, RM, Stoller, JK (Eds), BC Decker,
Philadelphia, 1988.

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