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Consecuencias fisiológicas y fisiopatológicas de la

ventilación mecánica.
Autor: Robert C Hyzy, MD
Editor de sección: Polly E Parsons, MD
Subdirector: Geraldine Finlay, MD

Todos los temas se actualizan a medida que hay nuevas pruebas disponibles y nuestro proceso de revisión por pares
está completo.

Revisión de literatura actualizada hasta: diciembre de 2019. | Última actualización de este tema: 02 de abril de
2018.

INTRODUCCIÓN

La ventilación mecánica se puede realizar usando presión positiva o presión negativa. La

ventilación a presión positiva es el tipo principal de ventilación mecánica que se usa hoy en día.
Durante la ventilación a presión positiva, el ventilador fuerza el aire hacia las vías respiratorias
centrales y el gradiente de presión resultante provoca el flujo de aire hacia las pequeñas vías
respiratorias y los alvéolos. (Consulte "Descripción general del inicio de la ventilación mecánica
invasiva en adultos en la unidad de cuidados intensivos" ).

Las consecuencias fisiológicas y fisiopatológicas de la ventilación con presión positiva se analizan

en esta revisión del tema. Dos consecuencias principales de la ventilación con presión positiva, el
barotrauma pulmonar y la lesión pulmonar asociada al ventilador, se revisan por separado. (Ver
"Diagnóstico, manejo y prevención del barotrauma pulmonar durante la ventilación mecánica
invasiva en adultos" y "Lesión pulmonar inducida por el ventilador" ).

EFECTOS PULMONARES

Barotrauma : el barotrauma pulmonar es una complicación bien conocida de la ventilación con

presión positiva. Las consecuencias incluyen neumotórax, enfisema subcutáneo,
neumomediastino y neumoperitoneo. El barotrauma pulmonar durante la ventilación mecánica se
analiza por separado. (Ver "Diagnóstico, manejo y prevención del barotrauma pulmonar durante la
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ventilación mecánica invasiva en adultos" ).

Lesión pulmonar asociada al ventilador : la lesión pulmonar asociada al ventilador (VALI) se

refiere a la lesión pulmonar aguda que ocurre durante la ventilación mecánica. Es clínicamente
indistinguible de lesión pulmonar aguda o síndrome de dificultad respiratoria aguda (ALI / ARDS)
debido a otras causas. VALI se discute por separado. (Ver "Lesión pulmonar inducida por el
ventilador" ).

Auto-PEEP : existe una presión de expiración final positiva (auto-PEEP, también llamada PEEP
intrínseca) cuando hay presión positiva en las vías respiratorias al final de la espiración debido a
una exhalación incompleta [ 1 ]. En otras palabras, la inspiración se inicia antes de que el flujo de
aire espiratorio de la respiración precedente haya cesado. (Consulte "Presión positiva al final de la
espiración (PEEP)" .)

Causas : existen numerosas razones por las cuales los pacientes que reciben ventilación con
presión positiva son susceptibles de desarrollar auto-PEEP ( tabla 1 ) [ 2 ]:

● High minute volume – High minute volume ventilation exists when there are large tidal
volumes (greater than the patient's functional residual capacity), a high respiratory rate, or
both. Large tidal volumes increase the volume that must be exhaled prior to the next breath.
High respiratory rates decrease the duration of expiration. In both situations, the next breath is
initiated prior to completion of the last exhalation. A high minute volume may be due to patient
factors (eg, fever, infection) or ventilator settings.

● Prolonged inspiratory time – Prolonging the inspiratory time can be used to improve
oxygenation in patients with refractory hypoxemia. When the inspiratory time is increased,
there is an obligatory decrease in the expiratory time. This can lead to incomplete exhalation
and auto-PEEP [3].

● Time-constant inequality – Patients whose lung units empty heterogeneously (eg, patients
with obstructive airways disease) are particularly susceptible to developing auto-PEEP during
positive pressure ventilation, even at relatively low minute ventilation.

● Expiratory flow resistance – Resistance to airflow (eg, narrow endotracheal tube, ventilator
tubing) can cause auto-PEEP by impairing exhalation.

● Expiratory flow limitation (eg, obstructive airways disease) and altered respiratory system
compliance (eg, expiratory muscle activity) similarly impede exhalation, causing auto-PEEP.
Altered respiratory system compliance may also interfere with accurate measurement of auto-
PEEP [4].

Detection — Auto-PEEP can be identified by applying an expiratory breath hold (usually 0.5 to
1 second) and then directly measuring the airway pressure at the end of the breath hold (figure 1).
It can also be identified when ventilator waveforms, auscultation, and/or palpation demonstrate
ti d i t i fl f th di b th h th t
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continued expiratory airflow from the preceding breath when the next breath is triggered. In a study

of 73 patients (503 observations), physical examination identified auto-PEEP with positive and
negative predictive values of 95 and 58 percent, respectively [5]. This indicates that physical
examination is useful for confirming auto-PEEP, but not for excluding auto-PEEP.

Consequences — Auto-PEEP exacerbates the hemodynamic effects of positive pressure

ventilation (discussed below), increases the risk of pulmonary barotrauma, and makes it more
difficult for the patient to trigger a ventilator-assisted breath (figure 2). In addition, auto-PEEP can
lead to incorrect estimation of the mean alveolar pressure and static lung compliance [6].

Treatment — Immediate intervention is necessary if significant auto-PEEP is detected (table 2):

● Change ventilator settings – The ventilator settings should be changed in an effort to reduce
or eliminate auto-PEEP. The most helpful maneuvers are those that increase the duration of
expiration: increasing the inspiratory flow rate, decreasing the respiratory rate, or both.
Decreasing the tidal volume or using applied PEEP to overcome auto-PEEP may also be
helpful. The use of applied PEEP in this setting is discussed separately. (See "Positive end-
expiratory pressure (PEEP)", section on 'Treatment'.)

● Reduce ventilatory demand – Ventilatory demand can be decreased by reducing carbohydrate

intake, anxiety, pain, or fever. This may decrease the minute volume, thereby reducing auto-
PEEP.

● Reduce expiratory flow resistance – Reduction of expiratory flow resistance by suctioning,

administration of bronchodilators, and use of a wide endotracheal tube can reduce auto-PEEP.

Heterogeneous ventilation — The distribution of positive pressure ventilation is never uniform

because the amount of ventilation is a function of three factors that vary from region to region
within the lungs: alveolar compliance, airway resistance, and dependency (upper versus lower lung
zones). Compliant, non-dependent regions with minimal airway resistance will be best ventilated.
In contrast, stiff, dependent regions with increased airway resistance will be least ventilated. The
heterogeneity of ventilation is accentuated in patients who have both airways disease and
parenchymal lung disease.

Ventilation/perfusion mismatch — Mechanical ventilation can alter two opposing forms of

ventilation/perfusion mismatch (V/Q mismatch), dead space (areas that are overventilated relative
to perfusion; V>Q) and shunt (areas that are underventilated relative to perfusion; V<Q). By
increasing ventilation (V), the institution of positive pressure ventilation will worsen dead space but
improve shunt.

Increased dead space — Dead space reflects the surface area within the lung that is not
involved in gas exchange. It is the sum of the anatomic plus alveolar dead space. Alveolar dead
space (also known as physiologic dead space) consists of alveoli that are not involved in gas
h d t i ffi i t f i (i til t d l ti t
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exchange due to insufficient perfusion (ie, overventilated relative to perfusion). Positive pressure

ventilation tends to increase alveolar dead space by increasing ventilation in alveoli that do not
have a corresponding increase in perfusion, thereby worsening V/Q mismatch and hypercapnia.

Reduced shunt — An intraparenchymal shunt exists where there is blood flow through
pulmonary parenchyma that is not involved in gas exchange because of insufficient alveolar
ventilation. Patients with respiratory failure frequently have increased intraparenchymal shunting
due to areas of focal atelectasis that continue to be perfused (ie, regions that are underventilated
relative to perfusion). Treating atelectasis with positive pressure ventilation can reduce
intraparenchymal shunting by improving alveolar ventilation, thereby improving V/Q matching and
oxygenation. This is particularly true if PEEP is added. (See "Positive end-expiratory pressure
(PEEP)" and "Oxygenation and mechanisms of hypoxemia", section on 'V/Q mismatch'.)

Diaphragm — Mechanical ventilation itself causes diaphragmatic muscle atrophy, a phenomenon

called ventilator induced diaphragmatic dysfunction (VIDD). Controlled mechanical ventilation may
lead to a very rapid type of disuse atrophy involving the diaphragmatic muscle fibers, which can
develop within the first day of mechanical ventilation. An observational study of 22 patients
compared the size of diaphragmatic muscle fibers from patients who received positive pressure
ventilation for more than 18 hours to those from patients who received positive pressure ventilation
for fewer than three hours [7]. The mean cross sectional area of both fast twitch diaphragmatic
muscle fibers (1871 versus 3949 micron2) and slow twitch diaphragmatic muscle fibers (2025
versus 4725 micron2) was significantly smaller among those patients who received positive
pressure ventilation for a longer duration. These findings were supported by a subsequent study
that found that diaphragmatic strength decreased progressively during mechanical ventilation and
that long-term mechanical ventilation (defined as >24 hours) was associated with diaphragmatic
muscle injury, atrophy, and proteolysis compared to short-term mechanical ventilation (defined as
two to three hours) [8]. VIDD appears to be mediated by oxidative stress. Diaphragmatic lipid
accumulation is seen in conjunction with mitochondrial biogenesis and content down regulation [9].
Speculation exists as to whether these events are triggered by metabolic oversupply. The optimal
approach to potentially obviate this phenomenon clinically is unknown [9].

Diaphragmatic atrophy during mechanical ventilation may be associated with prolonged

mechanical ventilation, difficulty weaning, prolonged ICU stay, and a higher risk of complications
[10]. (See "Management of the difficult-to-wean adult patient in the intensive care unit", section on
'Investigational strategies (respiratory muscle training)'.)

Respiratory muscles — Respiratory muscle atrophy can develop in patients undergoing positive
pressure ventilation. The mechanism of respiratory muscle weakness is probably similar to that of
general neuromuscular weakness in critically ill patients, which is discussed elsewhere. (See
"Neuromuscular weakness related to critical illness".)

Mucociliary motility — Positive pressure ventilation appears to impair mucociliary motility in the
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airways. In a series of 32 patients, bronchial mucus transport velocity was measured using

technetium 99m-labeled albumin microspheres during the first three days of mechanical ventilation
[11]. Bronchial mucus transport was frequently impaired and associated with retention of
secretions and pneumonia.

The administration of mucolytics is poorly studied and in general, is not routine. One randomized
trial of 922 patients receiving mechanical ventilation who were not expected to be extubated within
24 hours reported that routine, compared with as needed, nebulization of the mucolytic,
acetylcysteine, together with salbutamol did not reduce the number of ventilator-free days, length
of stay, or mortality but did result in more tachyarrhythmias and agitation [12]. Whether the
tachyarrhythmias were beta-2 agonist-related is unclear.

SYSTEMIC EFFECTS

Hemodynamics — Positive pressure ventilation frequently decreases cardiac output, which may
cause hypotension. There are several mechanisms that contribute to the fall in cardiac output:

● Decreased venous return – The amount of venous return is determined by the pressure
gradient from the extrathoracic systemic veins to the right atrium. Intrathoracic and right atrial
pressure increase during positive pressure ventilation, thereby reducing the gradient for
venous return. This effect is accentuated by auto-PEEP, applied PEEP, or intravascular
hypovolemia [13].

● Reduced right ventricular output – Alveolar inflation during positive pressure ventilation
compresses the pulmonary vascular bed. This increases pulmonary vascular resistance,
thereby reducing right ventricular output. In a study of 21 patients with acute respiratory
distress syndrome (ARDS), titrating the PEEP from 5 cm H2O to achieve a plateau pressure of
30 cm H2O was associated with a fall in cardiac output and an increase in right ventricular
afterload [14]. This effect was mitigated by increasing the central venous blood volume via a
passive leg raise maneuver.

● Reduced left ventricular output – Increased pulmonary vascular resistance can shift the
interventricular septum to the left, impair diastolic filling of the left ventricle, and reduce left
ventricular output.

In contrast to these adverse effects, positive pressure ventilation may be beneficial in patients with
left ventricular failure. Specifically, increased intrathoracic pressure can improve left ventricular
performance by decreasing both venous return and left ventricular afterload [15].

These hemodynamic effects are the result of positive airway pressure being transmitted to the
surrounding structures of the thorax. The extent to which this occurs varies according to chest wall
and lung compliance. Transmission of airway pressure is greatest when there is low chest wall
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compliance (eg, fibrothorax) or high lung compliance (eg, emphysema); it is least when there is
high chest wall compliance (eg, sternotomy) or low lung compliance (eg, ARDS, heart failure).

Monitoring — Another consequence of positive airway pressure being transmitted to

surrounding intrathoracic structures is that hemodynamic measurements may be artificially
elevated. PEEP plays a particularly prominent role because most hemodynamic measurements
are performed at the end of expiration when PEEP is the primary source of positive airway
pressure.

The effect of positive pressure ventilation on hemodynamic measures has been best studied using
the pulmonary capillary wedge pressure (PCWP), although it appears to have a similar impact on
the central venous pressure (CVP). The PCWP is measured by a pulmonary artery catheter
(Swan-Ganz catheter). When a patient is receiving positive pressure ventilation, the PCWP is
artificially elevated and not reflective of the true transmural filling pressure.

The true transmural filling pressure can be estimated by subtracting one-half of the PEEP level
from the PCWP if the lung compliance is normal, or one-quarter of the PEEP level if lung
compliance is reduced [16]. As an example, for a patient with normal lung compliance who is
receiving a PEEP of 12 cm H2O and whose PCWP is measured as 18 mmHg, the true PCWP is
estimated to be 12 mmHg.

A more precise way to estimate the true transmural PCWP in patients requiring positive pressure
ventilation utilizes the respiratory related variation of PCWP to estimate the transmission of
alveolar pressure to the pulmonary vessels [17]. This measure is called the index of transmission:

Index of transmission =

(end inspiratory PCWP - end expiratory PCWP) / (plateau airway pressure - total PEEP)

Measurement of the plateau airway pressure is described separately. (See "Diagnosis,

management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in
adults", section on 'Prevention'.)

Once the index of transmission is calculated, the true PCWP can be estimated:

Transmural PCWP =

end-expiratory PCWP - (index of transmission x total PEEP)

This estimate may be unreliable if the respiratory variation of the PCWP is greater than that of the
pulmonary arterial pressure tracing (figure 3) [18]. (See "Pulmonary artery catheterization:
Interpretation of hemodynamic values and waveforms in adults".)

Gastrointestinal — Positive pressure ventilation for greater than 48 hours is a risk factor for
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clinically important gastrointestinal bleeding due to stress ulceration. (See "Stress ulcers in the

intensive care unit: Diagnosis, management, and prevention".)

Positive airway pressure (especially PEEP) is also associated with decreased splanchnic perfusion
[19]. The mechanism underlying this association is unknown, but may be related to decreased
cardiac output [20]. Decreased splanchnic perfusion manifests as elevated plasma
aminotransferase and lactate dehydrogenase levels.

Other gastrointestinal complications seen in patients receiving positive pressure ventilation include
erosive esophagitis, diarrhea, acalculous cholecystitis, and hypomotility [21,22]. It is uncertain
whether these complications are due to mechanical ventilation or the critical illness. Hypomotility
usually manifests as intolerance to enteral feeding. Correction of electrolytic abnormalities and
avoidance of drugs that adversely affect gastric motility (eg, opiates) can improve gastrointestinal
motility.

Renal — Mechanical ventilation is associated with the development of acute renal failure. In a
prospective cohort study of 29,269 critically ill patients, positive pressure ventilation was an
independent risk factor for acute renal failure (odds ratio 2.11, 95% CI 1.58-2.82) [23]. The
mechanism for renal injury during positive pressure ventilation is unknown, but it is likely
multifactorial. Hypotheses include renal injury through the release of inflammatory mediators (eg,
interleukin-6) and impaired renal blood flow due to decreased cardiac output, increased
sympathetic tone, or activation of humoral pathways [24].

Central nervous system — Positive pressure ventilation increases intracranial pressure (ICP).
This is probably the result of elevated intrathoracic pressure impairing cerebral venous outflow. In
an animal model, mechanical ventilation was found to trigger hippocampal neuronal apoptosis. As
hippocampal changes are frequently seen in delirious patients undergoing autopsy, this finding
raises the possibility of a similar phenomenon in critically ill mechanically ventilated patients [25].

Weakness — Systemic muscular weakness is common among patients who undergo mechanical
ventilation. Potential causes include immobilization, prolonged use of sedatives, use of
neuromuscular blocking agents, and critical illness. It is unknown whether the mechanical
ventilation can cause systemic weakness independently.

Weakness is associated with long-term disability and the need for protracted rehabilitation [26].
However, early mobilization and exercise (ie, physical and occupational therapy) may increase the
likelihood that a patient will return to an independent functional status. This was best demonstrated
by a trial that randomly assigned 104 patients to either standard care or mobilization plus exercise
beginning within 72 hours of the initiation of mechanical ventilation [27]. Patients who received
mobilization and exercise were more likely to return to an independent functional status by hospital
discharge (59 versus 35 percent, odds ratio 2.7, 95% CI 1.2-6.1).

The causes, diagnosis, and management of systemic weakness in patients in the intensive care
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unit (ICU) are discussed in detail elsewhere. (See "Neuromuscular weakness related to critical

illness".)

Immune system — Positive pressure ventilation appears to induce inflammation. In a randomized

trial of 44 patients, patients who received positive pressure ventilation using large tidal volumes
and low PEEP had higher concentrations of inflammatory mediators in their blood and
bronchoalveolar lavage fluid than patients who received a smaller tidal volumes and high PEEP
[28].

Positive pressure ventilation may also promote translocation of tracheal bacteria into the
bloodstream, according to one animal study [29]. Translocation was most pronounced during
ventilation with large tidal volumes and low PEEP.

Sleep — Disordered sleep is common among patients in the ICU [30,31]. This was illustrated by a
prospective cohort study of 20 patients who were being mechanically ventilated for acute lung
injury [30]. None of the patients experienced normal sleep according to 24-hour polysomnography.
Conventional sleep staging isn't possible in up to a third of awake, unsedated mechanically
ventilated patients without delirium. Such patients lack typical sleep stage-2 markers and are felt to
have previously uncharacterized states of "atypical sleep" or "pathological wakefulness" with sleep
fragmentation and the absence of rapid eye movement (REM) [32].

Environmental, disease-related, and treatment-related factors have been proposed as possible

causes of the disordered sleep seen in critically ill patients. Among these factors, environmental
factors may be the least important. This was demonstrated by a study that assessed seven
mechanically ventilated patients and six healthy subjects in the intensive care unit using both 24-
hour polysomnography and time synchronized environmental monitoring [33]. Patient care
activities and noise accounted for less than 30 percent of arousals and awakenings.

The mode of mechanical ventilation may also influence sleep quality, particularly pressure support
ventilation [34,35]. Experts suggest avoiding PSV-induced hyperventilation in central apnea
especially in those with chronic respiratory and cardiac failure [36]. Similarly, guidelines from the
Society of Critical Care Medicine endorse the use of assist-controlled ventilation rather than
pressure support ventilation during the night in critically ill patients [37]. Although newer modes
such as proportional assist ventilation (PAV) and neurally-adjusted ventilation (NAVA), may
improve ventilator asynchrony, their effect on sleep is unknown. For those receiving noninvasive
ventilation, administering NIV via the NIV-dedicated ventilator or through the standard ICU-
ventilator is appropriate to improve sleep quality.

How to optimize sleep quality in the ICU is unknown since measuring sleep and classifying sleep
disordered breathing in ICU patients is difficult and the impact of altering factors such as reducing
sedatives, maintaining normal circadian rhythms, and limiting external stimulants are unknown.
Thus, such issues need to be addressed before strong recommendations can be made about
improving sleep in this population
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improving sleep in this population.

Other — Weakness is not the only consequence of prolonged bedrest. Prolonged bedrest has also
been associated with insulin resistance [38], venous thromboembolic disease, and joint
contractures [39]. During mechanical ventilation, the head of the bed is frequently raised to prevent
aspiration and ventilator-acquired pneumonia, which may increase the risk of sacral pressure
ulcers by increasing the pressure on the skin in the sacral region [40].

SUMMARY AND RECOMMENDATIONS

● Adverse pulmonary effects of positive pressure ventilation include pulmonary barotrauma,

ventilator-associated lung injury, intrinsic positive end expiratory pressure (auto-PEEP),
heterogeneous ventilation, altered ventilator/perfusion mismatch (increased dead space,
decreased shunt), diaphragmatic muscle atrophy, respiratory muscle weakness, and
diminished mucociliary motility. (See 'Pulmonary effects' above.)

● Auto-PEEP exists when there is positive airway pressure at the end of expiration due to
incomplete exhalation. It exacerbates the hemodynamic effects of positive pressure
ventilation, increases the risk of pulmonary barotrauma, and makes it more difficult for the
patient to trigger a ventilator-assisted breath. (See 'Auto-PEEP' above.)

● Detection of auto-PEEP should prompt immediate ventilator setting changes, efforts to reduce
ventilatory demand, and efforts to reduce expiratory flow resistance (table 2). The most helpful
maneuvers are those that increase the duration of expiration: increasing the inspiratory flow
rate, decreasing the respiratory rate, or both. Decreasing the tidal volume or using applied
PEEP to overcome auto-PEEP may also be helpful. (See 'Auto-PEEP' above and "Positive
end-expiratory pressure (PEEP)", section on 'Applied PEEP'.)

● Positive pressure ventilation may reduce cardiac output and impair hemodynamic monitoring.
In addition, it is associated with gastrointestinal stress ulceration, decreased splanchnic
perfusion, gastrointestinal hypomotility, fluid retention, acute renal failure, increased
intracranial pressure, weakness, inflammation, and disordered sleep. (See 'Systemic effects'
above.)

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32. Drouot X, Roche-Campo F, Thille AW, et al. A new classification for sleep analysis in critically
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33. Gabor JY, Cooper AB, Crombach SA, et al. Contribution of the intensive care unit
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34. Parthasarathy S, Tobin MJ. Effect of ventilator mode on sleep quality in critically ill patients.
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35. Cabello B, Thille AW, Drouot X, et al. Sleep quality in mechanically ventilated patients:
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36. Rittayamai N, Wilcox E, Drouot X, et al. Positive and negative effects of mechanical
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Management of Pain, Agitation/Sedation, Delirium, Immobility, and Sleep Disruption in Adult
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39. Clavet H, Hébert PC, Fergusson D, et al. Joint contracture following prolonged stay in the
intensive care unit. CMAJ 2008; 178:691.

40. Peterson M, Schwab W, McCutcheon K, et al. Effects of elevating the head of bed on
interface pressure in volunteers. Crit Care Med 2008; 36:3038.

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GRAPHICS

Determinants of dynamic pulmonary hyperinflation and auto-PEEP

Internal External
Respiratory mechanics Added flow resistance

Flow resistance Fine bore endotracheal tube

Expiratory flow limitation Ventilator tubing and devices

Respiratory system compliance Ventilator setting

Breathing pattern Frequency

Frequency of breathing I:E ratio

T I /T TOT Inflation volume

Tidal volume End-inspiratory pause

T I : inspiratory time, T TOT : total cycle time.

Adapted from Rossi, A, Polese, G, Brandi, G, et al, Intensive Care Med 1995; 21:522.

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Quantification of the auto-PEEP effect

During mechanical ventilation of the patient with airflow obstruction, expiratory flow is too slow
to allow complete deflation of the lung to its normal relaxed state before the ventilator delivers
another breath. Slow flow continues until interrupted by the next inflation. Upper panel:
Alveolar pressure remains positive at end exhalation (15 cmH2O) but is not measured by the
ventilator manometer (0 cmH2O) located downstream from the site of increased airway
resistance. Lower panel: Alveolar pressure at end-exhalation can be quantified by stopping flow
transiently at the end of a set exhalation period, thereby allowing equilibration of pressures.

Adapted from O'Quinn, R, Marini, JJ, Am Rev Respir Dis 1983; 128:319.

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Trigger threshold for auto-PEEP

Effect of auto-PEEP on elevation of the triggering threshold in a mechanically

ventilated patient with obstructive airways disease. This figure representation shows
airway pressure over time. The solid blue line demonstrates the circuit pressure as
measured by the ventilator manometer, and the dashed red line is the alveolar
pressure. In the absence of auto-PEEP, the sensitivity setting of -1 cm H 2 O would be
achieved by the patient making inspiratory efforts at the end of expiration, when
airway pressure is at its minimum. In the presence of auto-PEEP, alveolar pressure
remains positive. In this setting, the patient's inspiratory effort needs to decrease
airway pressure not only by the -1 cm H 2 O sensitivity set on the machine, but also
by the amount of positive alveolar pressure (auto-PEEP). In this figure, the patient's
inspiratory efforts are insufficient to trigger the ventilator, and the patient is "locked
out," being unable to get a breath because of an inability to overcome the elevated
effective triggering threshold rendered by auto-PEEP.

PEEP: positive end-expiratory pressure.

Adapted from Puritan-Bennett 1994, Form AA-1888.

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Treatment of auto-PEEP

Changes in ventilator setting

Increase expiratory duration

Decrease respiratory rate

Decrease tidal volume

Reduction in the ventilatory demand

Decrease carbohydrate intake

Reduce dead space

Reduce anxiety, pain, fever, shivering

Reduction of total flow resistance

Use of large bore endotracheal tubes

Frequent suctioning

Bronchodilators

Application of external PEEP nearly up to the level of initial PEEPi

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Effect of positive end-expiratory pressure (PEEP) on

pulmonary hemodynamics

Pressure tracings from the same patient recorded at different levels of positive
end-expiratory pressure (PEEP). The top panel shows 0 PEEP, the middle panel
PEEP = 15 cm H 2 O, and the bottom panel PEEP = 20 cm H 2 O. Pulmonary
artery pressure (P pa ) is shown at the left of the tracing. The right side of the
tracing shows wedge (pulmonary artery occlusion) pressure (P paO ). The red
bars indicate the degree of respiratory (or respirophasic) variation (I, E)
exhibited at each level of PEEP in pulmonary artery pressure and wedge
pressure. The ratio of respiratory variation in pulmonary artery pressure divided
by respiratory variation in the wedge pressure was close to 1 when PEEP = 0 or
15 cm H 2 O PEEP. This increased to 2.3 at a level of 20 cm H 2 O PEEP. This
suggests a shift from zone three to a non-zone three condition, where airway
pressure has exceeded intravascular pressure at the balloon occluded
pulmonary artery catheter tip. The end-expiratory wedge pressure value during
PEEP = 20 cm H 2 O is markedly higher than during PEEP = 15 cm H 2 O (18
versus 10 mmHg), a change that cannot solely be explained by the increase in
PEEP.

I: inspiration; E: expiration.

Original figure modified for this publication. Teboul JL, Besbes M, Andrivet P, et al. J
Crit Care 1992; 7:22. Illustration used with the permission of Elsevier Inc. All rights
reserved.

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Contributor Disclosures
Robert C Hyzy, MD No hay nada que revelar Polly E Parsons, MD No hay nada que revelar Geraldine
Finlay, MD Consultora / Juntas asesoras: Junta directiva de LAM, comité de revisión de subvenciones
científicas LAM para la Fundación LAM.

Las divulgaciones de los colaboradores son revisadas por conflictos de intereses por el grupo editorial.
Cuando se encuentran, se abordan examinando a través de un proceso de revisión multinivel y a través de
los requisitos para que se proporcionen referencias para respaldar el contenido. Se requiere el contenido de
referencia apropiado de todos los autores y debe cumplir con los estándares de evidencia de UpToDate.

Política de conflicto de intereses

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