Review Article

Page 1 of 11

The basics of respiratory mechanics: ventilator-derived

parameters
Pedro Leme Silva, Patricia R. M. Rocco

Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
Contributions: (I) Conception and design: All authors; (II) Administrative support: None; (III) Provision of study materials or patients: None; (IV)
Collection and assembly of data: None; (V) Data analysis and interpretation: None; (VI) Manuscript writing: All authors; (VII) Final approval of
manuscript: All authors.
Correspondence to: Prof. Patricia R. M. Rocco, MD, PhD. Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal
University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G1-014, Ilha do Fundão, Rio de Janeiro, RJ
21941-902, Brazil. Email: [email protected].

Abstract: Mechanical ventilation is a life-support system used to maintain adequate lung function in
patients who are critically ill or undergoing general anesthesia. The benefits and harms of mechanical
ventilation depend not only on the operator’s setting of the machine (input), but also on their interpretation
of ventilator-derived parameters (outputs), which should guide ventilator strategies. Once the inputs—tidal
volume (VT), positive end-expiratory pressure (PEEP), respiratory rate (RR), and inspiratory airflow (V’)—
have been adjusted, the following outputs should be measured: intrinsic PEEP, peak (Ppeak) and plateau
(Pplat) pressures, driving pressure (ΔP), transpulmonary pressure (P L), mechanical energy, mechanical
power, and intensity. During assisted mechanical ventilation, in addition to these parameters, the pressure
generated 100 ms after onset of inspiratory effort (P0.1) and the pressure-time product per minute (PTP/min)
should also be evaluated. The aforementioned parameters should be seen as a set of outputs, all of which
need to be strictly monitored at bedside in order to develop a personalized, case-by-case approach to
mechanical ventilation. Additionally, more clinical research to evaluate the safe thresholds of each parameter
in injured and uninjured lungs is required.

Keywords: Mechanical ventilation; tidal volume; positive end-expiratory pressure (PEEP); respiratory rate;
inspiratory flow; plateau pressure; driving pressure; transpulmonary pressure; mechanical energy; mechanical power

Submitted Jan 31, 2018. Accepted for publication May 30, 2018.
doi: 10.21037/atm.2018.06.06
View this article at: http://dx.doi.org/10.21037/atm.2018.06.06

Introduction on lung structures during mechanical ventilation adjusted

by the operator and the lung and chest wall mechanics
Mechanical ventilation is a life-support system used to
of the patient (3). Once the inputs—tidal volume (VT),
maintain adequate lung function in patients who are positive end-expiratory pressure (PEEP), respiratory rate
critically ill or undergoing general anesthesia (1,2); however, (RR), and inspiratory airflow (V’)—have been adjusted, the
it may cause lung damage. The benefits and harms of information obtained from the mechanical ventilator (the
mechanical ventilation depend not only on the adjustment outputs or ventilator-derived parameters) can be examined.
of ventilator parameters, but also on the interpretation Regardless of ventilator mode, the following ventilator-
of ventilator-derived parameters, which should be used derived parameters should be measured in order to mitigate
to guide ventilatory strategies. The basis of this process harmful effects (2,4): intrinsic PEEP (PEEPi), peak (Ppeak)
relies on the interaction between physical forces acting and plateau (Pplat) pressures, driving pressure (ΔP), and

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Page 2 of 11 Silva and Rocco. Basics of respiratory mechanics

transpulmonary pressure (PL). During assisted mechanical both sex and height, has been used to set V T (15-17).
ventilation, in addition to these parameters, the pressure The following PBW equations have been used: men,
generated 100 ms after onset of inspiratory effort (P0.1) and 50.0+0.905× (height in cm) −152.4; women: 45.5+0.905×
pressure-time product per minute (PTP/min) should also (height in cm) −152.4. To mitigate the risk of ventilator
be evaluated. In this review, we will discuss the ventilator induced lung injury (VILI) in ARDS patients, the National
parameters adjusted by the operator (inputs) and ventilator Institute of Health ARDS Network protocol suggests the
parameters obtained after interaction with respiratory use of VT =6 mL/kg PBW and Pplat limited to 30 cmH2O.
system structures during mechanical ventilation (outputs). If Pplat exceeds 30 cmH2O with a VT of 6 mL/kg PBW, the
Moreover, new ventilator-derived parameters, such as protocol recommends a reduction in VT (to 4–5 mL/kg
mechanical energy, mechanical power, and intensity, will be PBW) if pHa >7.15. Since ARDS lungs present great
discussed in light of recent evidence (5-7). variability due to edema, atelectasis, and consolidation, VT
should probably be set according to aerated lung volume,
e.g., functional residual capacity (FRC) or total lung
Inputs: ventilator parameters set by the operator
capacity (TLC) (18-20).
Tidal volume (VT) Nevertheless, further studies are required to evaluate
the safe limit of FRC and TLC when used to set VT. In
In both uninjured and injured lungs, the use of low VT has this line, in patients with severe ARDS and very low lung
been preferred over high VT. compliance, even setting V T below 6 mL/kg PBW can
In patients under general anesthesia, no association has result in high strain (VT/FRC) (19). This scenario may be
been observed between VT and postoperative pulmonary considered unsafe; thus, rescue therapies are needed, such
complications (PPCs) (8). Additionally, pressure-controlled as extracorporeal support (21).
ventilation (PCV) has been compared to volume-controlled Additionally, VT should be set according to ΔP [Pplat-
ventilation (VCV), focusing on PPCs; this comparison is PEEP or VT/Crs (respiratory system compliance)]. Since
important to distinguish the potential role of strict control of VT Crs is directly related to lung size, ΔP reflects the level of
during VCV. The frequency of PPCs was higher in PCV than VT in relation to the aerated lung volume. However, in the
in VCV. This could be attributed to the difficulty in controlling presence of reduced chest wall mechanics, ΔP does not reflect
VT during PCV, thus highlighting the importance of VT. VT. In this line, considering the same ΔP, a patient with a stiff
In the emergency department, mechanically ventilated chest wall has less lung overinflation than one with a normal
patients with injured and uninjured lungs could also benefit chest wall (22). Therefore, transpulmonary driving pressure
from the use of low VTs (9). (ΔPL, the difference in transpulmonary pressure between
In the intensive care unit (ICU), even though two meta- end-expiration and end-inspiration) (23) should be evaluated,
analyses suggest that patients with uninjured lungs could and VT could be limited to keep ΔPL in a safe range (19,24).
benefit from ventilation with low VT (10,11), a prospective
study reported no association between VT and outcomes (12),
Positive end-expiratory pressure (PEEP)
which may be attributed to the fact that VT in this study
was much lower than in the aforementioned meta-analyses PEEP is the alveolar pressure above the atmospheric
(10,11). In out-of-hospital cardiac arrest, VT reduction has pressure at end-expiration. PEEP applied through
been associated with favorable neurocognitive outcome mechanical ventilation (i.e., extrinsic PEEP) allows delivery
and more ventilator-free days (13). In short, the benefit of of positive pressure at the end of expiration to prevent
reduced VT in ICU patients with uninjured lungs remains unstable lung units from collapsing. Low levels of PEEP
unclear. Two ongoing randomized clinical trials, Protective (3 to 5 cmH2O) are routinely used in patients on mechanical
Ventilation in patients without ARDS at start of ventilation ventilation. This practice is important to: (I) keep lungs
(PReVENT) (14) and Preventive Strategies in Acute open at the end of expiration, thus promoting alveolar
Respiratory Distress Syndrome (EPALI) (Clinicaltrials.org stabilization (25); (II) prevent opening and closing of distal
registration number: NCT02070666), may elucidate this small airways and alveolar units (26); and (III) increase
issue. lymphatic flow through the thoracic duct, which may
In patients with the acute respiratory distress syndrome facilitate drainage of lung edema (27). However, higher
(ARDS), predicted body weight (PBW), taking into account levels of PEEP may cause regional overdistension and

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Annals of Translational Medicine, Vol 6, No 19 October 2018 Page 3 of 11

impairment of cardiac performance (28). The pros and cons Respiratory rate
of PEEP depend on the degree of lung injury (29).
In patients under general anesthesia, intraoperative Respiratory rate must be adjusted during mechanical
mechanical ventilation with VT =8 mL/kg and high PEEP ventilation to maintain a minute volume appropriate to the
(12 cmH2O), when compared with low PEEP (2 cmH2O), patient’s metabolic demands. Although higher RR is often
does not prevent PPCs, as shown in the Protective needed to maintain CO2 levels within safe range (39), it
Ventilation using High versus Low positive end-expiratory can alter the inspiratory-to-expiratory ratio, thus leading to
pressure (PROVHILO) trial (30). Further research is intrinsic PEEP due to short expiratory time. In this context,
required to evaluate moderate levels of PEEP (5–8 cmH2O). Vieillard-Baron et al. compared two levels of RR—15
In the emergency department, the use of higher PEEP breaths per minute (bpm) vs. 30 bpm—while maintaining
levels was associated with improvement in ventilator- and lower Pplat (<25 cmH2O). No difference in PaCO2 due
hospital-free days in patients with ARDS (9) and uninjured to increased intrinsic PEEP or dead space ventilation was
lungs (31). observed between groups (40). Increased RR may also cause
In ICU patients with uninjured lungs, a meta-analysis lung damage due to cyclic recruitment/derecruitment.
reported that benefit from PEEP is lacking in terms of
duration of mechanical ventilation and mortality rate (32).
Inspiratory airflow
In ICU patients at risk of ARDS, higher PEEP levels are
required than in those without ARDS risk (12). More Inspiratory airflow must be adjusted during mechanical
recently, ICU patients after cardiac surgery were found ventilation, since it may also cause lung damage (41-43).
to exhibit fewer lung complications with high PEEP (33). The mechanism whereby inspiratory airflow contributes
Certainly, further studies are required to compare low vs. to lung injury seems to be influenced by the viscoelastic
high PEEP levels in ICU patients without ARDS. properties of lung tissue. High inspiratory airflow enhances
Three major studies have assessed high vs. low PEEP damage to the lung parenchyma because the viscoelastic
levels combined with low VT for ARDS patients (16,17,34). accommodation has no time to dissipate damaging forces
In the ALVEOLI trial (34), mortality did not differ between when inflation occurs rapidly. This type of mechanism of
low and high PEEP levels. High PEEP resulted in improved injury usually occurs in asymmetrical lungs.
oxygenation (17) as well as more ventilator-free days and High inspiratory airflow is an important determinant of
organ failure-free days (16); however, mortality rate did pulmonary stress, since it enhances the transmission of kinetic
not differ between PEEP arms. A meta-analysis that used energy to lung structures, increases shear stress parallel to the
the data from the aforementioned three trials found that surface of the airways and alveolar walls, leads to deformation
higher PEEP levels were associated with improved survival of the pulmonary parenchyma and bronchial epithelial cells,
in severe ARDS (35). In moderate ARDS, lower PEEP and releases pro-fibrogenic (43) and pro-inflammatory (44)
(<12 cmH2O), compared to higher PEEP, was associated mediators. Therefore, controlling inspiratory airflow might
with greater risk of hospital mortality (26%) (36). In a provide additional lung protection (43,44).
recent randomized clinical trial comparing individualized
PEEP titration after recruitment maneuvers (RMs) vs. low
Outputs: ventilator parameters obtained as a
PEEP without RMs in patients with moderate-to-severe
result of the interaction between mechanical
ARDS, an increase in 28-day mortality was observed in the
ventilator and respiratory system
recruited group (37).
Several strategies have been used to determine optimal During mechanical ventilation, several ventilator-derived
PEEP, such as: (I) evaluation of the lower inflection point parameters should be monitored: PEEPi, Ppeak, Pplat, ΔP, PL,
of the pressure-volume curve, which reflects the transition P0.1, PTP/min, mechanical energy, mechanical power, and
from low to high compliance, and application of PEEP intensity.
2 cmH2O greater than this point; (II) the use of algorithms
combining PEEP and fraction of inspired oxygen (FiO2);
Intrinsic PEEP
and (III) measurement of transpulmonary pressure with an
esophageal catheter (38). Certainly, the best approach is to Intrinsic PEEP (PEEPi) reflects the residual pressure
individualize PEEP for each patient. when the expiratory phase may not be completed to full

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Page 4 of 11 Silva and Rocco. Basics of respiratory mechanics

exhalation. This residual pressure is higher than the point of associated with VT ≤7 mL/kg PBW lead to reduced PPCs
equilibrium of the respiratory system’s elastic properties (45). and a trend toward increased survival (P=0.052) (11). In
One easy form to detect its presence is to perform an ARDS patients, Pplat <30 cmH2O was associated with lower
expiratory pause and check the end-expiratory pressure. mortality (15). An observational study with ARDS patients
PEEPi is usually associated with obstructive diseases (46), suggested that Pplat <28 cmH2O is more beneficial in those
but may be present during other conditions; therefore, it is with a large percentage of non-aerated lung tissue (53).
considered an important ventilator-derived parameter for More recently, in patients with severe ARDS, the LUNG
monitoring. For example, obese patients under mechanical SAFE study (36) reported that Pplat <25 cmH 2O was
ventilation are prone to developing PEEPi, mainly in not associated with decreased risk of hospital mortality.
the supine position. Both external PEEP application and However, patients with a median Pplat ≥23 cmH2O on day
changing position (beach-chair) may alter PEEPi (47). 1 of ARDS diagnosis had higher mortality.

Peak pressure Driving pressure

Peak pressure is the maximum pressure measured at Driving pressure is defined as Pplat-PEEP or VT normalized
end inspiration. Ppeak includes the elastic and resistive to Crs (23,54,55). During intraoperative ventilation, ΔP
components (airway, lung tissue, and equipment, e.g., seems to be an important parameter for the optimization of
endotracheal tube). At bedside, the difference between mechanical ventilation (8,12).
Ppeak and Pplat can be easily visualized during an In mechanically ventilated ICU patients without ARDS (55),
inspiratory pause in controlled mechanical ventilation with ΔP was not associated with hospital mortality. The authors
constant airflow. Immediately after the inspiratory pause, a attributed this result to the fact that Crs was not a major
rapid airway pressure decay, which represents the pressure risk factor for mortality in those patients without ARDS.
dissipated to overcome airway resistance, is observed. The Conversely, Tejerina et al. (56) showed that, in patients with
difference between Ppeak and Pplat divided by the airflow is brain injury but uninjured lungs, low ΔP resulted in a better
the airway resistance. In normal subjects, airway resistance outcome.
values do not exceed 15–20 cmH2O/L/s under controlled In a study of ARDS patients, ΔP was considered the
mechanical ventilation (48). Several factors can modify variable most strongly associated with survival, as opposed
Ppeak, such as endotracheal tube diameter (49,50), airflow to VT and PEEP (54). The authors observed that increasing
intensity, plugging, or bronchospasm. PEEP level for a short period could lead to different
During controlled mechanical ventilation, Ppeak depends changes in ΔP. If the increase in PEEP level leads to
on VT, RR, and airflow, whereas during assisted mechanical increased aeration of lung tissue through recruitment, a
ventilation, the patient’s effort also contributes to Ppeak. decrease in ΔP is expected. On the other hand, if PEEP
In a multicenter, prospective cohort study of 2,377 increases and does not recruit lung tissue, the lungs may
patients with severe respiratory failure, conducted in 459 become overstretched, and ΔP may remain unchanged or
ICUs from 50 countries across five continents (36), the even increase over time (Figure 1).
authors reported the importance of monitoring Ppeak The LUNG SAFE study (36) showed that ΔP
besides other ventilator-derived parameters. Higher Ppeak, <14 cmH2O was associated with decreased risk of hospital
especially above 40 cmH2O, is associated with increased mortality in patients with moderate-to-severe ARDS.
mortality rates (51).

Transpulmonary pressure
Plateau pressure
Transpulmonary pressure, by definition, is the difference
Plateau pressure can be measured during an inspiratory between airway pressure (Paw) and pleural pressure (Ppl).
pause when the respiratory muscles are relaxed and is equal In the clinical setting, esophageal manometry is the only
to alveolar pressure when airflow is zero. Pplat can be clinically available method to separate airway pressure
affected by changes in VT and Crs, but not by changes in applied to the respiratory system into its chest wall (i.e.,
airflow and airway resistance (52). Ppl) and lung component (PL) (57-59). PL measurement
In ICU patients without ARDS, lower Pplat values has been proposed because it can determine the pressure

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Annals of Translational Medicine, Vol 6, No 19 October 2018 Page 5 of 11

Patient with Reduced C,RS Patient with Reduced C,RS

Before PEEP

Driving Pressure (ΔP) Monitoring

Overdistension
Increased
Aeration
After PEEP

ΔP reduce ΔP increase

Consolidation Collapse Normal Overdistension

Figure 1 Schematic drawing showing two theoretical patients with comparable and reduced respiratory system compliance (C,RS) before and
after PEEP increment. As explained in the main text, the increase in PEEP level can lead to different responses that can be easily evaluated
at bedside through the interpretation of ΔP values.

required to keep the lungs open (38,60,61) and it can delivered. The use of ΔP L offers some advantages.
assess inspiratory effort (62,63). In influenza A(H1N1)- First, ΔP L removes the stress caused by PEEP, which
associated ARDS, Grasso et al. (61) observed that the does not necessarily contribute to lung injury and
pressure applied to the airways was not transmitted to sometimes can mitigate it (65). Second, ΔP L removes
the lung parenchyma but dissipated against a stiff chest the distending pressure taken by the chest wall (66).
wall, providing further evidence of the importance of Hence, it seems that ΔPL might be a better surrogate of
measuring PL. lung stress and may even be a better predictor of clinical
During assisted mechanical ventilation, the esophageal outcomes than ΔP (67). ΔPL is calculated as:
catheter may not cover the entire vertical gradient while
ΔPL = (PPLAT – PESO, end-insp) – (PEEPTOT − PESO, end-exp) [1]
respiratory muscle activity is present. In this context,
Yoshida et al. (64) showed that esophageal pressure variation In experimental ARDS, low PL did not increase lung
significantly underestimated pleural pressure variation in inflammation, despite leading to alveolar collapse.
dependent regions. In addition, directly measured swings Intermediate levels of ΔP L reduced alveolar collapse,
in pleural pressure (−14.9) were significantly greater in increased overdistension, and resulted in alveolar
dependent lung than swings in Pes (−7.1). Esophageal instability. At high P L levels, alveolar hyperinflation
pressure may underestimate the local pleural pressure, was detected, but no further lung inflammation was
especially in those areas near the diaphragm which present observed (23). This study highlighted the importance
higher degrees of PL. of permissive atelectasis to protect lung damage, as
recently published (68) and discussed in two editorials
Transpulmonary driving pressure (ΔPL) (69,70).
The transpulmonary driving pressure (ΔP L) is defined P L is also an important ventilator parameter to be
as the difference between P L at end-inspiration (P Lend- monitored during assisted mechanical ventilation. Bellani
insp ) and P L at end-expiration (P Lend-exp ). It reflects the et al. tested the hypothesis that, for a given inspired volume
distending pressure taken by the lungs when V T is and flow, and for the same mechanical properties (i.e.,

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Page 6 of 11 Silva and Rocco. Basics of respiratory mechanics

1,200 PEEP ΔP

1,000
nt nt
one

Tidal Volume
pone omp
800 Com eC
stic tiv
sis
Ela Re

Volume (mL)
600

400

PEEP Volume
200

0 10 20 30 40 50 60
Pressure (cmH2O)

Elastic Component Resistive Component PEEP Volume

2
Energy, RS ΔV × [(0.5 × E, RS RR × (1 + I:E)/60 × I:E ×Raw) ΔV × PEEP]

Figure 2 Pressure-volume curve of the respiratory system, depicting all components needed to calculate the mechanical energy transferred
from the mechanical ventilator to the respiratory system. The blue area depicts the elastic property of the respiratory system with the
respective fraction in the energy formula [ΔV2 × (0.5 × ERS)]. The white area represents the resistive property of the respiratory system,
which is associated with the respective fraction in the energy formula [RR × (1+ I:E)/60× I:E × Raw]. The orange area represents the PEEP
volume, depicted in the energy formula by ΔV × PEEP. Modified from Tonetti et al. (79).

compliance and resistance) of the lung, ΔPL during assisted Pressure-time product per minute
and controlled mechanical ventilation should not differ Pressure-time product is a measure of the mechanical work
within the same patient (71). They found no difference of breathing. By integrating the pressure developed by the
in ΔPL at comparable volumes and flows. However, the respiratory muscles over the duration of the contraction
authors pointed out that, if assisted breaths contributed (i.e., chest wall elastic recoil pressure), it is possible to
to lung damage, this would not be due solely to ΔP L; obtain the respiratory PTP. Field et al. (77) found that the
the vertical gradient leading to different local pleural oxygen consumption of the respiratory muscles is only
pressures and, ultimately, local ΔPL ranges should also be weakly correlated with the mechanical work of breathing
acknowledged (64,72). (the product ΔP·ΔV), whereas it is well reflected by the
PTP. PTP takes into account the isometric phase of
Esophageal pressure generated 100 ms after onset of muscle contraction, thus representing a good indicator
inspiratory effort (P0.1) of energy expenditure (78). A common way of expressing
The esophageal pressure generated 100 ms after the onset PTP is through standardization by the sample period of a
of an occluded inspiratory effort (P0.1) has been used as respiratory cycle (TTOT).
a measurement of respiratory drive (73), and it could be
used to optimize the level of pressure support in individual
patients (74). In a recent prospective, randomized, crossover New ventilator-derived parameters: markers of
physiologic study, P 0.1 was evaluated in the presence patient–machine interaction
of different degrees of inspiratory efforts in patients
Mechanical energy
recovering from acute respiratory failure (75). Inspiratory
effort was found to correlate strongly with P0.1. Therefore, The energy delivered per breath to the airways and lungs is
this parameter may have yet-unrecognized importance as a defined as the area between the inspiratory limb of pressure (x)
marker of respiratory drive during mechanical ventilation, vs. the volume axis (y), measured in joules (J) (79) (Figure 2).
and efforts should be made to increase awareness of its Two equations have been proposed to calculate
potential utility (76). mechanical energy: one simple (80) and another more

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Annals of Translational Medicine, Vol 6, No 19 October 2018 Page 7 of 11

complex (7). If properly adjusted, both should yield similar intensity may reduce or remain constant.
results. Nevertheless, some technical differences between
the two should be addressed.
Conclusions
Simple equation:
EnergyL = ΔPL2/EL [2] The benefits and harms of mechanical ventilation in
critically ill patients with uninjured or injured lungs, as well
where ΔPL is the transpulmonary driving pressure and EL is
as in patients undergoing general anesthesia, depend not
the lung elastance.
only on ventilator settings, but also on the interpretation of
Complex equation:
ventilator-derived parameters. Both parameters adjusted by
EnergyL = ΔV2 × [(0.5× ERS + RR × (1+ I:E)/60× I:E × the operator (VT, PEEP, RR, and V’) and ventilator-derived
Raw) + ΔV × PEEP] [3] parameters (PEEPi, Ppeak, Pplat, ΔP, P L, mechanical
energy, mechanical power, intensity, P0.1, and PTP) need to
where ΔV is the variation of tidal volume, E RS is the
be strictly monitored at bedside, in order to develop a case-
respiratory system elastance, I:E is the inspiratory to
by-case approach to mechanical ventilation. Furthermore,
expiratory ratio, and Raw is the airway resistance. additional clinical studies are required to ascertain the
The simplified equation can be easily used in the safe thresholds of each of these parameter in injured and
clinical setting (5,80,81). This equation computes the most uninjured lungs.
important component (driving mechanical power), without
taking into account resistive properties or the contribution
PEEP, unlike the equation proposed by Gattinoni et al. (7). Acknowledgements
However, it is difficult to directly link the mechanical The authors would like to express their gratitude to Mrs.
energy dissipated in the proximal airways to alveolar injury. Moira Elizabeth Schottler and Mr. Filippe Vasconcellos for
The addition of PEEP to the complex equation takes into their assistance in editing the manuscript.
account the contribution of static strain, which is associated Funding: This work was supported by grants from the
with potential energy storage within the elastic tissues of Carlos Chagas Filho Rio de Janeiro State Research
the respiratory system (81). Foundation (FAPERJ) (grant number E-26/103.118/2), Rio
de Janeiro, Brazil; and the Brazilian Council for Scientific
Mechanical power and intensity and Technological Development (CNPq) (grant number
471438/2012-0), Brasília, Brazil.
Mechanical power represents the mechanical energy
multiplied by the RR. In a previous study (6), different
mechanical power values were applied to the respiratory Footnote
system in healthy pigs by changing the RR while keeping Conflicts of Interest: The authors have no conflicts of interest
the VT and PL constant, aiming to identify a mechanical to declare.
power threshold for lung damage. The authors reported
development of edema only when the delivered
transpulmonary mechanical power exceeded 12.1 J/min. References
In the presence of lung damage, the ventilated lung area is 1. Slutsky AS, Ranieri VM. Ventilator-induced lung injury. N
reduced, thus requiring greater driving pressure and airflow. Engl J Med 2013;369:2126-36.
This, in turn, increases the mechanical power delivered 2. Silva PL, Pelosi P, Rocco PR. Optimal mechanical
without changes in VT. ventilation strategies to minimize ventilator-induced lung
The so-called intensity (i.e., mechanical power injury in non-injured and injured lungs. Expert Rev Respir
normalized to the lung tissue) should also be considered. Med 2016;10:1243-5.
Depending on the mechanical power, intensity may be 3. Plataki M, Hubmayr RD. The physical basis of
comparable in volutrauma and atelectrauma (5). If power ventilator-induced lung injury. Expert Rev Respir Med
increases without changes in lung surface area, the intensity 2010;4:373-85.
will be higher; on the other hand, if both power and lung 4. Silva PL, Negrini D, Rocco PR. Mechanisms of ventilator-
surface area increase (e.g., due to lung recruitment), the induced lung injury in healthy lungs. Best Pract Res Clin

© Annals of Translational Medicine. All rights reserved. atm.amegroups.com Ann Transl Med 2018;6(19):376
Page 8 of 11 Silva and Rocco. Basics of respiratory mechanics

Anaesthesiol 2015;29:301-13. Respiratory Distress Syndrome Network. N Engl J Med

5. Samary CS, Silva PL, Gama de Abreu M, et al. Ventilator- 2000;342:1301-8.
induced Lung Injury: Power to the Mechanical Power. 16. Mercat A, Richard JC, Vielle B, et al. Positive end-
Anesthesiology 2016;125:1070-1. expiratory pressure setting in adults with acute lung injury
6. Cressoni M, Gotti M, Chiurazzi C, et al. Mechanical and acute respiratory distress syndrome: a randomized
Power and Development of Ventilator-induced Lung controlled trial. JAMA 2008;299:646-55.
Injury. Anesthesiology 2016;124:1100-8. 17. Meade MO, Cook DJ, Guyatt GH, et al. Ventilation
7. Gattinoni L, Tonetti T, Cressoni M, et al. Ventilator- strategy using low tidal volumes, recruitment maneuvers,
related causes of lung injury: the mechanical power. and high positive end-expiratory pressure for acute
Intensive Care Med 2016;42:1567-75. lung injury and acute respiratory distress syndrome: a
8. Epidemiology, practice of ventilation and outcome for randomized controlled trial. JAMA 2008;299:637-45.
patients at increased risk of postoperative pulmonary 18. Gattinoni L, Marini JJ, Pesenti A, et al. The "baby lung"
complications: LAS VEGAS - an observational study in 29 became an adult. Intensive Care Med 2016;42:663-73.
countries. Eur J Anaesthesiol 2017;34:492-507. 19. Chiumello D, Carlesso E, Cadringher P, et al. Lung
9. Fuller BM, Ferguson IT, Mohr NM, et al. A Quasi- stress and strain during mechanical ventilation for acute
Experimental, Before-After Trial Examining the Impact respiratory distress syndrome. Am J Respir Crit Care Med
of an Emergency Department Mechanical Ventilator 2008;178:346-55.
Protocol on Clinical Outcomes and Lung-Protective 20. Brower RG, Hubmayr RD, Slutsky AS. Lung stress and
Ventilation in Acute Respiratory Distress Syndrome. Crit strain in acute respiratory distress syndrome: good ideas
Care Med 2017;45:645-52. for clinical management? Am J Respir Crit Care Med
10. Serpa Neto A, Simonis FD, Barbas CS, et al. Association 2008;178:323-4.
between tidal volume size, duration of ventilation, and 21. Kopp R, Dembinski R, Kuhlen R. Role of extracorporeal
sedation needs in patients without acute respiratory lung assist in the treatment of acute respiratory failure.
distress syndrome: an individual patient data meta-analysis. Minerva Anestesiol 2006;72:587-95.
Intensive Care Med 2014;40:950-7. 22. Sahetya SK, Mancebo J, Brower RG. Fifty Years of
11. Neto AS, Simonis FD, Barbas CS, et al. Lung-Protective Research in ARDS. Vt Selection in Acute Respiratory
Ventilation With Low Tidal Volumes and the Occurrence Distress Syndrome. Am J Respir Crit Care Med
of Pulmonary Complications in Patients Without Acute 2017;196:1519-25.
Respiratory Distress Syndrome: A Systematic Review 23. Samary CS, Santos RS, Santos CL, et al. Biological Impact
and Individual Patient Data Analysis. Crit Care Med of Transpulmonary Driving Pressure in Experimental
2015;43:2155-63. Acute Respiratory Distress Syndrome. Anesthesiology
12. Neto AS, Barbas CSV, Simonis FD, et al. Epidemiological 2015;123:423-33.
characteristics, practice of ventilation, and clinical outcome 24. Protti A, Cressoni M, Santini A, et al. Lung stress and
in patients at risk of acute respiratory distress syndrome strain during mechanical ventilation: any safe threshold?
in intensive care units from 16 countries (PRoVENT): Am J Respir Crit Care Med 2011;183:1354-62.
an international, multicentre, prospective study. Lancet 25. Albert RK. The role of ventilation-induced surfactant
Respir Med 2016;4:882-93. dysfunction and atelectasis in causing acute respiratory
13. Beitler JR, Ghafouri TB, Jinadasa SP, et al. Favorable distress syndrome. Am J Respir Crit Care Med
Neurocognitive Outcome with Low Tidal Volume 2012;185:702-8.
Ventilation after Cardiac Arrest. Am J Respir Crit Care 26. Slutsky AS, Villar J, Pesenti A. Happy 50th birthday
Med 2017;195:1198-206. ARDS! Intensive Care Med 2016;42:637-9.
14. Simonis FD, Binnekade JM, Braber A, et al. PReVENT- 27. Fernandez Mondejar E, Vazquez Mata G, Cardenas A,
-protective ventilation in patients without ARDS at start et al. Ventilation with positive end-expiratory pressure
of ventilation: study protocol for a randomized controlled reduces extravascular lung water and increases lymphatic
trial. Trials 2015;16:226. flow in hydrostatic pulmonary edema. Crit Care Med
15. Ventilation with lower tidal volumes as compared with 1996;24:1562-7.
traditional tidal volumes for acute lung injury and 28. Retamal J, Borges JB, Bruhn A, et al. Open lung approach
the acute respiratory distress syndrome. The Acute ventilation abolishes the negative effects of respiratory

© Annals of Translational Medicine. All rights reserved. atm.amegroups.com Ann Transl Med 2018;6(19):376
Annals of Translational Medicine, Vol 6, No 19 October 2018 Page 9 of 11

rate in experimental lung injury. Acta Anaesthesiol Scand syndrome: low-stretch ventilation improves survival. Cleve
2016;60:1131-41. Clin J Med 2000;67:435-40.
29. Passaro CP, Silva PL, Rzezinski AF, et al. Pulmonary lesion 40. Vieillard-Baron A, Prin S, Augarde R, et al. Increasing
induced by low and high positive end-expiratory pressure respiratory rate to improve CO2 clearance during
levels during protective ventilation in experimental acute mechanical ventilation is not a panacea in acute respiratory
lung injury. Crit Care Med 2009;37:1011-7. failure. Crit Care Med 2002;30:1407-12.
30. Hemmes SN, Gama de Abreu M, Pelosi P, et al. High 41. Rich PB, Reickert CA, Sawada S, et al. Effect of rate
versus low positive end-expiratory pressure during general and inspiratory flow on ventilator-induced lung injury. J
anaesthesia for open abdominal surgery (PROVHILO Trauma 2000;49:903-11.
trial): a multicentre randomised controlled trial. Lancet 42. Maeda Y, Fujino Y, Uchiyama A, et al. Effects of peak
2014;384:495-503. inspiratory flow on development of ventilator-induced
31. Fuller BM, Ferguson IT, Mohr NM, et al. Lung-Protective lung injury in rabbits. Anesthesiology 2004;101:722-8.
Ventilation Initiated in the Emergency Department (LOV- 43. Garcia CS, Abreu SC, Soares RM, et al. Pulmonary
ED): A Quasi-Experimental, Before-After Trial. Ann morphofunctional effects of mechanical ventilation with
Emerg Med 2017;70:406-18.e4. high inspiratory air flow. Crit Care Med 2008;36:232-9.
32. Serpa Neto A, Filho RR, Cherpanath T, et al. Associations 44. Kotani M, Kotani T, Li Z, et al. Reduced inspiratory flow
between positive end-expiratory pressure and outcome of attenuates IL-8 release and MAPK activation of lung
patients without ARDS at onset of ventilation: a systematic overstretch. Eur Respir J 2004;24:238-46.
review and meta-analysis of randomized controlled trials. 45. Marini JJ. Dynamic hyperinflation and auto-positive end-
Ann Intensive Care 2016;6:109. expiratory pressure: lessons learned over 30 years. Am J
33. Costa Leme A, Hajjar LA, Volpe MS, et al. Effect of Respir Crit Care Med 2011;184:756-62.
Intensive vs Moderate Alveolar Recruitment Strategies 46. Caramez MP, Borges JB, Tucci MR, et al. Paradoxical
Added to Lung-Protective Ventilation on Postoperative responses to positive end-expiratory pressure in patients
Pulmonary Complications: A Randomized Clinical Trial. with airway obstruction during controlled ventilation. Crit
JAMA 2017;317:1422-32. Care Med 2005;33:1519-28.
34. Brower RG, Lanken PN, MacIntyre N, et al. Higher 47. Lemyze M, Mallat J, Duhamel A, et al. Effects of sitting
versus lower positive end-expiratory pressures in patients position and applied positive end-expiratory pressure
with the acute respiratory distress syndrome. N Engl J on respiratory mechanics of critically ill obese patients
Med 2004;351:327-36. receiving mechanical ventilation. Crit Care Med
35. Briel M, Meade M, Mercat A, et al. Higher vs lower 2013;41:2592-9.
positive end-expiratory pressure in patients with acute lung 48. MacIntyre NR, Cook DJ, Ely EW, Jr., et al. Evidence-
injury and acute respiratory distress syndrome: systematic based guidelines for weaning and discontinuing ventilatory
review and meta-analysis. JAMA 2010;303:865-73. support: a collective task force facilitated by the American
36. Laffey JG, Bellani G, Pham T, et al. Potentially modifiable College of Chest Physicians; the American Association for
factors contributing to outcome from acute respiratory Respiratory Care; and the American College of Crit Care
distress syndrome: the LUNG SAFE study. Intensive Care Med. Chest 2001;120:375S-95S.
Med 2016;42:1865-76. 49. Bock KR, Silver P, Rom M, et al. Reduction in tracheal
37. Writing Group for the Alveolar Recruitment for Acute lumen due to endotracheal intubation and its calculated
Respiratory Distress Syndrome Trial I, Cavalcanti AB, clinical significance. Chest 2000;118:468-72.
Suzumura EA, et al. Effect of Lung Recruitment and 50. Rocco PR, Zin WA. Modelling the mechanical effects
Titrated Positive End-Expiratory Pressure (PEEP) vs Low of tracheal tubes in normal subjects. Eur Respir J
PEEP on Mortality in Patients With Acute Respiratory 1995;8:121-6.
Distress Syndrome: A Randomized Clinical Trial. JAMA 51. Kregenow DA, Rubenfeld GD, Hudson LD, et al.
2017;318:1335-45. Hypercapnic acidosis and mortality in acute lung injury.
38. Talmor D, Sarge T, Malhotra A, et al. Mechanical Crit Care Med 2006;34:1-7.
ventilation guided by esophageal pressure in acute lung 52. Lucangelo U, Bernabe F, Blanch L. Lung mechanics
injury. N Engl J Med 2008;359:2095-104. at the bedside: make it simple. Curr Opin Crit Care
39. Wiedemann HP, Arroliga AC. Acute respiratory distress 2007;13:64-72.

© Annals of Translational Medicine. All rights reserved. atm.amegroups.com Ann Transl Med 2018;6(19):376
Page 10 of 11 Silva and Rocco. Basics of respiratory mechanics

53. Terragni PP, Rosboch G, Tealdi A, et al. Tidal strain during mechanical ventilation: any difference
hyperinflation during low tidal volume ventilation in acute between statics and dynamics? Crit Care Med
respiratory distress syndrome. Am J Respir Crit Care Med 2013;41:1046-55.
2007;175:160-6. 66. Cortes-Puentes GA, Keenan JC, Adams AB, et al. Impact
54. Amato MB, Meade MO, Slutsky AS, et al. Driving pressure of Chest Wall Modifications and Lung Injury on the
and survival in the acute respiratory distress syndrome. N Correspondence Between Airway and Transpulmonary
Engl J Med 2015;372:747-55. Driving Pressures. Crit Care Med 2015;43:e287-95.
55. Schmidt MFS, Amaral A, Fan E, et al. Driving Pressure 67. Baedorf Kassis E, Loring SH, Talmor D. Mortality and
and Hospital Mortality in Patients Without ARDS: A pulmonary mechanics in relation to respiratory system and
Cohort Study. Chest 2018;153:46-54. transpulmonary driving pressures in ARDS. Intensive Care
56. Tejerina E, Pelosi P, Muriel A, et al. Association between Med 2016;42:1206-13.
ventilatory settings and development of acute respiratory 68. Guldner A, Braune A, Ball L, et al. The authors reply. Crit
distress syndrome in mechanically ventilated patients due Care Med 2017;45:e328-9.
to brain injury. J Crit Care 2017;38:341-5. 69. Sahetya SK, Brower RG. Lung Recruitment and Titrated
57. Staffieri F, Stripoli T, De Monte V, et al. Physiological PEEP in Moderate to Severe ARDS: Is the Door Closing
effects of an open lung ventilatory strategy titrated on on the Open Lung? JAMA 2017;318:1327-9.
elastance-derived end-inspiratory transpulmonary pressure: 70. Villar J, Suarez-Sipmann F, Kacmarek RM. Should
study in a pig model*. Crit Care Med 2012;40:2124-31. the ART trial change our practice? J Thorac Dis
58. Fumagalli J, Berra L, Zhang C, et al. Transpulmonary 2017;9:4871-7.
Pressure Describes Lung Morphology During 71. Bellani G, Grasselli G, Teggia-Droghi M, et al. Do
Decremental Positive End-Expiratory Pressure Trials in spontaneous and mechanical breathing have similar effects
Obesity. Crit Care Med 2017;45:1374-81. on average transpulmonary and alveolar pressure? A
59. Yoshida T, Amato MBP, Grieco DL, et al. Esophageal clinical crossover study. Crit Care 2016;20:142.
Manometry and Regional Transpulmonary Pressure 72. Yoshida T, Brochard L. Ten tips to facilitate understanding
in Lung Injury. Am J Respir Crit Care Med and clinical use of esophageal pressure manometry.
2018;197:1018-26. Intensive Care Med 2018;44:220-2.
60. Loring SH, Pecchiari M, Della Valle P, et al. Maintaining 73. Elliott MW, Mulvey DA, Green M, et al. An evaluation
end-expiratory transpulmonary pressure prevents of P0.1 measured in mouth and oesophagus, during
worsening of ventilator-induced lung injury caused by carbon dioxide rebreathing in COPD. Eur Respir J
chest wall constriction in surfactant-depleted rats. Crit 1993;6:1055-9.
Care Med 2010;38:2358-64. 74. Alberti A, Gallo F, Fongaro A, et al. P0.1 is a useful
61. Grasso S, Terragni P, Birocco A, et al. ECMO parameter in setting the level of pressure support
criteria for influenza A (H1N1)-associated ARDS: ventilation. Intensive Care Med 1995;21:547-53.
role of transpulmonary pressure. Intensive Care Med 75. Rittayamai N, Beloncle F, Goligher EC, et al. Effect of
2012;38:395-403. inspiratory synchronization during pressure-controlled
62. Yoshida T, Uchiyama A, Matsuura N, et al. Spontaneous ventilation on lung distension and inspiratory effort. Ann
breathing during lung-protective ventilation in Intensive Care 2017;7:100.
an experimental acute lung injury model: high 76. Telias I, Damiani F, Brochard L. The airway occlusion
transpulmonary pressure associated with strong pressure (P0.1) to monitor respiratory drive during
spontaneous breathing effort may worsen lung injury. Crit mechanical ventilation: increasing awareness of a not-so-
Care Med 2012;40:1578-85. new problem. Intensive Care Med 2018;44:1532-5.
63. Grieco DL, Chen L, Brochard L. Transpulmonary 77. Field S, Sanci S, Grassino A. Respiratory muscle oxygen
pressure: importance and limits. Ann Transl Med consumption estimated by the diaphragm pressure-
2017;5:285. time index. J Appl Physiol Respir Environ Exerc Physiol
64. Yoshida T, Torsani V, Gomes S, et al. Spontaneous effort 1984;57:44-51.
causes occult pendelluft during mechanical ventilation. Am 78. Sassoon CS, Mahutte CK. Work of breathing during
J Respir Crit Care Med 2013;188:1420-7. mechanical ventilation. In: Marini JJ SA, editor.
65. Protti A, Andreis DT, Monti M, et al. Lung stress and Physiological Basis of Ventilatory Support. New York:

© Annals of Translational Medicine. All rights reserved. atm.amegroups.com Ann Transl Med 2018;6(19):376
Annals of Translational Medicine, Vol 6, No 19 October 2018 Page 11 of 11

Marcel Dekker; 1998, p. 261-310. protective mechanical ventilation in two randomized

79. Tonetti T, Vasques F, Rapetti F, et al. Driving pressure and controlled trials. Critical Care 2016;20:384.
mechanical power: new targets for VILI prevention. Ann 81. Marini JJ, Jaber S. Dynamic predictors of VILI risk:
Transl Med 2017;5:286. beyond the driving pressure. Intensive Care Med
80. Guerin C, Papazian L, Reignier J, et al. Effect of driving 2016;42:1597-600.
pressure on mortality in ARDS patients during lung

Cite this article as: Silva PL, Rocco PR. The basics of
respiratory mechanics: ventilator-derived parameters. Ann
Transl Med 2018;6(19):376. doi: 10.21037/atm.2018.06.06

© Annals of Translational Medicine. All rights reserved. atm.amegroups.com Ann Transl Med 2018;6(19):376