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Abstract

Background:

Mechanical power (MP) applied to the respiratory system (MP_RS) is associated with ventilator-induced lung injury (VILI) and ARDS mortality. Absent automated ventilator MP_RS measurements, the alternative is clinically unwieldy equations. However, simplified surrogate formulas are now available and accurately reflect values produced by airway pressure-volume curves. This retrospective, observational study examined whether the surrogate pressure -control equation alone could accurately assess mortality risk in subjects with ARDS managed almost exclusively with volume control (VC) ventilation.

Methods:

Nine hundred and forty-eight subjects were studied in whom invasive mechanical ventilation and implementation of ARDS Network ventilator protocols commenced ≤ 24 h after ARDS onset and who survived > 24 h. MP_RS was calculated as 0.098 x breathing frequency x tidal volume x (PEEP + driving pressure). MP_RS was assessed as a risk factor for hospital mortality and compared between non-survivors and survivors across Berlin definition classifications. In addition, mortality was compared across 4 MP_RS thresholds associated with VILI or mortality (ie, 15, 20, 25, and 30 J/min).

Results:

MP_RS was associated with increased mortality risk: odds ratio (95% CI) of 1.06 (1.04–1.07) J/min (P < .001). Median MP_RS differentiated non-survivors from survivors in mild (24.7 J/min vs 18.5 J/min, respectively, P = .034), moderate (25.7 J/min vs 21.3 J/min, respectively, P < .001), and severe ARDS (28.7 J/min vs 23.5 J/min, respectively, P < .001). Across 4 MP_RS thresholds, mortality increased from 23–29% when MP_RS was ≤ threshold versus 38–51% when MP_RS was > threshold (P < .001). In the > cohort, the odds ratio (95% CI) increased from 2.03 (1.34–3.12) to 2.51 (1.87–3.33).

Conclusion:

The pressure control surrogate formula is sufficiently accurate to assess mortality in ARDS, even when using VC ventilation. In our subjects when MP_RS exceeds established cutoff values for VILI or mortality risk, we found mortality risk consistently increased by a factor of > 2.0.

Introduction

Mechanical power (MP) represents energy over time that, when applied to the respiratory system (lungs and chest wall: MP_RS), is linked to both ventilator-induced lung injury (VILI) and ARDS mortality.^1

–4 In the absence of ventilators calculating MP_RS directly from airway pressure (P_aw)–volume curves (ie, “geometric” measurements once provided by the Bicore pulmonary mechanics monitor), mathematical formulas are needed. However, estimating MP_RS by formula is complex and unwieldy, as it includes the variables minute ventilation, peak P_aw, PEEP, and inspiratory flow in order to approximate the accepted standard (geometric area within P_aw-volume curve).

In an attempt to address this obstacle, Chiumello et al⁵ devised simplified (“surrogate”) formulas to calculate MP_RS during either volume control (VC) or pressure control (PC) continuous mechanical ventilation (CMV) modes. They found both surrogate equations were highly correlated with direct (geometric) measurements of MP_RS. Surrogate MP_RS values averaged 0.8 J/min greater than direct, geometric measurements (8.64 ± 2.62 vs 7.84 ± 2.62, respectively, P = .01).⁵

In this retrospective, observational study, we assessed whether reliance on the PC surrogate formula alone could accurately assess hospital mortality risk in subjects with ARDS managed with lung-protective ventilation (LPV) and when VC-CMV was used almost exclusively. The basis for doing so was that we recorded plateau pressure (P_plat) and driving pressure (P_DR) as part of our quality assurance monitoring, not peak P_aw and inspiratory flow. The justification for applying the PC surrogate formula in subjects managed with VC-CMV is described below in the Methods section (see Design Rationale).

Essentially this study asked whether the fraction of MP applied by the ventilator needed to overcome flow resistance properties of the ventilator-patient system is essential to assess mortality risk in ARDS from excessive MP_RS. We approached answering this question by assessing (1) the association between PC surrogate MP_RS and mortality, (2) whether MP_RS increased correspondingly with increasing ARDS severity (ie, Berlin classifications) and its associated mortality risk, and (3) whether mortality differed at-or-below versus above MP_RS thresholds previously association either with VILI or mortality as reported in other studies.^3,4,6,7

QUICK LOOK

Current knowledge

Mechanical power (MP) applied to the respiratory system (MP_RS) is associated with ventilator-induced lung injury (VILI) and ARDS mortality. Because power is energy transferred to lungs (and is a composite of all variables known to cause and perpetuate lung injury), it is widely considered the most important variable to monitor in mechanically ventilated patients. Because ventilators currently don’t calculate power from the airway pressure–volume loops, cumbersome mathematical formulas are used to estimate power. However, simplified surrogate formulas accurately estimate power and can be used to assess mortality risk at the bedside.

What this paper contributes to our knowledge

The current study demonstrates that estimating MP_RS using only the pressure control surrogate equation (even in subjects managed with volume control ventilation) discriminates survivors from non-survivors across both ARDS severity classifications, as well as MP threshold levels associated with increased VILI and mortality risk. This indicates complex equations accounting for the resistive components of MP are not necessary to assess the mortality risk from MP in ARDS.

Methods

Design rationale

The PC surrogate formula (ie, MP_RS = 0.098 × tidal volume [V_T] × breathing frequency × (PEEP + P_DR)⁵ was used to assess mortality risk, without distinguishing CMV modes (ie, P_DR = P_plat−PEEP vs peak P_aw−PEEP, and excluding the corresponding inspiratory flow). The rationale for applying this simplified equation to both VC-CMV and PC-CMV is as follows: 1.

P_plat not peak P_aw reflects the stress applied to the lungs and chest wall at end inspiration. In contrast, peak P_aw and inspiratory flow largely reflect endotracheal tube resistance. Even when tube deformation and lumen occlusion (which occurs clinically) are absent, its frictional resistance approximates that of lung resistance in early ARDS (∼10 cm H₂O).^8,9 Moreover, in terms of VILI risk, the relevance of accounting for frictional resistive forces is controversial.^2,10

In ARDS, the primary source of VILI is the uneven distribution of lung strain and stress during inspiration. Uneven lung strain-stress is reflected in measure of viscoelastic resistance: a phenomenon that only can be captured during a 2–5 s end-inspiratory pause when gases redistribute and lung pressures equilibrate (see Supplementary Data S1).^11
–13

Clinically, we used a 0.5-s pause time per ARDS Network (ARDSNet) ventilator protocols.¹⁴ Therefore, P_plat measured at 0.5 s likely reflects some portion of the mechanical unevenness believed to cause VILI.

MP_RS also reflects the energy needed to overcome the elastic, viscoelastic, and resistive properties of the chest wall, as well as its inertial properties.¹⁵ In the presence of morbid obesity or abdominal compartment syndrome, chest-wall elastance is markedly increased,¹⁶ and inertial forces are no longer negligible.¹⁷ In light of these factors, as well as the absence of esophageal manometry (to isolate the pulmonary component), all MP_RS techniques are crude approximations for estimating its impact on VILI and ARDS mortality. Likewise, similar limitations apply when trying to separate artificial airway frictional resistance from that of the pulmonary airways.

Subjects

The 1,995 subjects in our ARDS LPV quality assurance database (2002–2017) have been described previously.^18,19 In this study, a subset (948 subjects) was selected based on the following criteria: (1) having met the Berlin definition of ARDS,²⁰ (2) both CMV and ARDSNet protocols^21,22 were initiated within 24 h of ARDS onset, and (3) subjects having survived > 24 h after protocol initiation (Fig. 1).

Fig. 1.

Subject selection flow chart. ARDSNet, ARDS Network.

The justification for these criteria are, first, those mechanically ventilated prior to ARDS onset may have been exposed to VILI. Second, our focus was the impact of MP_RS on mortality in the exudative phase of ARDS. After ∼48 h, lung injury begins to transition to a proliferative or fibrotic stage,²³ therefore possibly producing changes in lung mechanics and MP_RS. Thus, excluding subjects in whom ARDS onset preceded ARDSNet protocol initiation would introduce interpretive ambiguity by mixing subjects at different stages of ARDS evolution. Third, evaluating subjects who survived beyond the day of ARDS onset allowed time for potential optimization of LPV. Fourth, excluding those who died on the day of ARDS onset eliminated additional ambiguity because whatever MP moribund subjects were exposed to over a matter of hours prior to death cannot reasonably be attributed to mortality risk.

Our sample consisted of 108 subjects with mild (11%), 440 with moderate (46%), and 400 with severe ARDS (42%). During the study period, subjects were managed almost exclusively with VC-CMV, as stipulated by the ARDSNet protocols.^21,22 Approval to use our quality assurance data was granted by the University of California, San Francisco Institutional Review Board (approval reference number: 268589).

Measurements and calculations

Lung and chest wall subcomponents of MP_RS (MP_L and MP_CW, respectively) were estimated using respiratory system elastance (E_RS) data and its lung (E_L) and chest wall (E_CW) subcomponents in ARDS subjects from our previous study:²⁴ E_L/E_RS (0.74), E_CW/E_RS (0.26). These values were consistent with other studies (Supplementary Data S2). Other calculations included comparing MP_RS to normal resting power (MP_RS ratio)²⁵ using a value of 4 J/min,²⁶ MP_RS index adjusted power to predicted body weight,²⁷ and Δ MP_RS as the change in power ∼24 h after protocol initiation (ie, a signifier for LPV optimization).

Assessments

MP_RS and its subcomponents were assessed from several perspectives: (1) the overall mortality risk for sample population; (2) mortality differences between non-survivors and survivors across Berlin definition classifications; (3) changes in MP_RS from initiation of LPV to the first full day of ARDSNet protocol management between non-survivors and survivors; and (4) mortality risk between subjects falling at-or-below versus above MP_RS thresholds of 15, 20, 25, 30 J/min. These corresponded with estimated MP_L thresholds of 11, 14, 18, and 22 J/min, respectively.

We tested threshold values that approximated those of preclinical studies of VILI induced in normal lungs and a clinical study of ARDS. One preclinical study found an MP_RS threshold of 25 J/min (MP_L of 13 J/min) was associated with greater lung damage.²⁸ In their subsequent study, MP_RS thresholds of 15 J/min and 30 J/min produced morphologic and histologic injury.⁶ In another preclinical study, an MP_L 15 J/min (MP_RS of 18 J/min) produced whole lung edema.⁷ The clinical study found that an MP_RS threshold of 19 J/min was associated with increased mortality risk.⁴

Statistical analysis

Data are expressed as median and (25-75%) interquartile range, as all variables failed a normality test (D’Agostoni and Pearson method). Direct comparisons between non-survivors and survivors were analyzed by Mann-Whitney test. Cross-group comparisons were done by Kruskal-Wallis and Dunn post test. The Fisher exact test was used to assess mortality risk above and below the aforementioned thresholds. Univariate logistic regression was used to assess the mortality risk of each MP-associated variable (eg, MP_RS, MP_L, MP_CW). Alpha was set at 0.05.

Results

Achieving LPV goals

Regarding traditional pulmonary mechanics measured ∼24 h after ARDSNet protocol initiation, the most salient findings (for both non-survivors and survivors) were 75% of P_plat and V_T values met protocol goals (Supplementary Table S1). Respiratory system compliance was significantly lower, and P_DR was significantly higher among non-survivors.

Mortality and MP

Hospital mortality was 35.6%, and all MP variables were significant predictors of mortality risk (Table 1). For every 1 J/min increase in MP_RS, mortality risk increased by 6%. The MP_RS ratio of 5.8 (4.4–7.8) was ∼6-fold greater than normal (ie, ∼4 J/min). MP_CW was associated with a higher mortality risk than MP_L. MP_RS index appeared to carry a more pronounced mortality risk.

Table 1.

Mortality risk for various aspects of mechanical power in ARDS

	Odds ratio (95% CI)*	Area under receiver operating curve (95% CI)
MP_RS, J/min	1.06 (1.04–1.07)	0.650 (0.613–0.686)
MP_L, J/min	1.08 (1.06–1.10)	0.650 (0.613–0.687)
MP_CW, J/min	1.22 (1.17–1.29)	0.649 (0.613–0.686)
MP_RS ratio	1.25 (1.18–1.32)	0.649 (0.612–0.686)
MP_RS index, J/min/kg	44.1 (18.9–106.9)	0.666 (0.630–0.703)
Δ MP_RS, J/min	1.02 (1.01–1.04)	0.584 (0.544–0.623)

All tested variables P < .001.

MP_RS, power applied to the respiratory system; MP_L, power applied to the lungs; MP_CW, power applied to the chest wall; MP_RS ratio, applied power relative to power transfer under normal physiologic conditions at rest (ie, 4 J/min); MP_RS index, power normalized to predicted body weight; Δ MP_RS, change in applied power 1 d following initiation of lung-protective ventilation.

Mechanical power characteristics across Berlin definition ARDS classifications

All MP measures increased significantly with increasing ARDS intensity: moderate versus mild (P = .02), severe versus moderate (P < .001), and severe versus mild (P < .001) (Fig. 2). The median increase in MP_RS was 113% between mild to moderate ARDS, 116% between moderate and severe ARDS, and 131% between mild and severe ARDS. Likewise, MP_RS index increased with ARDS intensity: 0.30 J/min/kg predicted body weight, 0.36 J/min/kg predicted body weight, and 0.42 J/min/kg predicted body weight for mild, moderate, and severe ARDS, respectively, with the same proportional increases and associated P values described above.

Fig. 2.

Respiratory system mechanical power and its lung and chest-wall subcomponents across Berlin definition classifications. ^* P < .001 compared to severe ARDS. ^† P = .02 compared to moderate ARDS.

Mortality and changes in MP from ARDS onset to the following day

Particularly noteworthy was that from ARDSNet protocol initiation to the following day MP_RS among all subjects decreased by −0.9 (−4.2 to 2.4) J/min from 24.7 (18.5–32.7) J/min to 23.3 (17.6–31.3) J/min (P = .02). However, non-survivors had an increase in MP_RS of 0.9 (–5.1 to 6.8) J/min, whereas in survivors MP_RS decreased by –1.5 (–5.9 to 2.5) J/min (P < .001). The corresponding change in MP_L among non-survivors and survivors was 0.7 (–3.7 to 4.9) J/min versus –1.1 (–4.3 to 1.8) J/min (P < .001). In other words, by ∼24 h into ARDS a difference in MP_RS of 2.4 J/min (MP_L of 1.8 J/min) had already separated non-survivors from survivors.

Differences in MP and mortality between Berlin classifications

When differences in MP_RS and its subcomponents were compared between non-survivors and survivors across Berlin classifications, median MP_RS among non-survivors always exceeded 24 J/min in contrast to survivors (< 24 J/min) irrespective of ARDS severity (Table 2). Extrapolating these findings to corresponding estimates of MP_L, the median values among non-survivors always exceeded 17 J/min regardless of ARDS severity. Likewise, MP_RS ratio was > 6 times normal values in non-survivors and < 6 in survivors. Mortality rates observed with increasing ARDS severity were consistent with previous findings.²⁰

Table 2.

Power distribution across Berlin definition categories between non-survivors and survivors

	Non-survivors	Survivors	Mortality %
Mild
n	28	80	26
MP_RS, J/min	24.7 (14.1–33.2)	18.5 (14.6–25.0)*
MP_L, J/min	17.8 (10.1–23.9)	13.3 (10.5–18.0)^†
MP_CW, J/min	6.9 (4.0–9.3)	5.2 (4.1–7.0)^‡
MP_RS ratio	6.2 (3.5–8.3)	4.6 (3.7–6.3)^‡
MP_RS index, J/min/kg	0.37 (0.29–0.50)	0.29 (0.23–0.38)^†
Moderate
n	142	298	32
MP_RS, J/min	25.7 (19.5–34.5)	21.3 (16.6–27.2)^†
MP_L, J/min	18.5 (14.1–24.9)	15.4 (12.0–19.6)^†
MP_CW, J/min	7.2 (5.5–9.7)	4.6 (3.7–6.3)^†
MP_RS ratio	6.4 (4.9–8.6)	5.3 (4.2–6.8)^†
MP_RS index, J/min/kg	0.43 (0.33–0.55)	0.34 (0.27–0.44)^†
Severe
N	168	232	42
MP_RS, J/min	28.7 (21.6–38.7)	23.5 (18.1–31.8)^†
MP_L, J/min	20.6 (15.6–27.9)	16.9 (13.0–22.9)^†
MP_CW, J/min	8.0 (6.1–10.8)	6.6 (5.0–8.9)^†
MP_RS ratio	7.2 (5.4–9.7)	5.9 (4.5–8.9)^†
MP_RS index, J/min/kg	0.49 (0.35–0.63)	0.38 (0.30–0.50)^†

P = .034.

†

P < .001.

‡

P = .033.

MP_RS, power applied to the respiratory system; MP_L, power applied to the lungs; MP_CW, power applied to the chest wall; MP_RS ratio, applied power relative to that at rest under normal physiologic conditions (ie, 4 J/min); MP_RS index, power normalized to predicted body weight.

MP thresholds and mortality risk

Across the 4 MP_RS and corresponding MP_L thresholds, mortality steadily increased for both at-or-below and above cohorts at each threshold level. However, mortality in the above cohort was consistently and substantially greater: its associated risk factor always exceeded 2.0 (Table 3). The absolute cumulative mortality increased by 6% (23−29%) in the at-or-below cohort compared to 14% (38–51%) in the above cohort. This translated into total mortality rate increases of 126% versus 134%, respectively. The highest separation in mortality between cohorts (Δ22%) occurred at the MP_RS (MP_L) threshold of 30 (22) J/min, with a mortality of 51% (Fig. 3).

Fig. 3.

Mortality across 4 respiratory system mechanical power thresholds. Percentages listed above the bars reflect the difference in mortality between the above-threshold cohort versus the at-or-below threshold cohort. ^* P < .001 for mortality comparisons between cohorts measured at each threshold.

Table 3.

Mortality rates and risk for subjects with ARDS above and below mechanical power thresholds

MP_RS (MP_L) thresholds J/min	Mortality at/below, %	Odds ratio (95% CI)	Mortality* Above, %	Odds ratio (95% CI)	% Sample > threshold
15 (11)	23	0.49 (0.32–0.75)	38	2.03 (1.34–3.12)	85
20 (14)	24	0.43 (0.32–0.58)	42	2.33 (1.72–3.16)	65
25 (18)	27	0.43 (0.33–0.56)	47	2.34 (1.77–3.07)	43
30 (22)	29	0.40 (0.30–0.54)	51	2.51 (1.87–3.33)	29

P < .001 for all mortality differences between each power threshold.

MP_RS, mechanical power applied to the respiratory system; MP_L, mechanical power applied to the lung.

Discussion

Our main finding was the PC surrogate MP_RS equation⁵ was strongly associated with mortality across all ARDS severity classifications. This despite subjects managed almost exclusively with VC-CMV. Eighty-five percent of our subjects had MP_RS levels > 15 J/min (associated with VILI in animals with normal lungs),⁶ and 65% had MP_RS levels above 20 J/min that exceeded a mortality threshold found in subjects with various etiologies of acute respiratory failure (Table 3).⁴

Interestingly, 34% of subjects who met ARDSNet study mortality risk–exclusion criteria with corresponding MP_RS ≤ 25 J/min had similar mortality to 3 ARDSNet trials that occurred during our data collection period (24–27% vs 25–28%, respectively).^22,29,30 Yet, a particularly worrisome finding was mortality exceeding 50% in those whose MP_RS exceeded 30 J/min (MP_L > 22 J/min): a mortality rate associated with late 20th century ventilator management prior to the adoption of LPV.^31,32

Elevated levels of MP_RS associated with VILI also were observed in our subjects. This has practical implications for achieving safer threshold levels (ie, MP_RS < 15 J/min, MP_L < 12 J/min) proposed by others.³³ Our results suggest the likelihood of achieving these stringent threshold (without liberalizing sedation usage or dosing) is improbable. Moreover, in severe ARDS, such thresholds might require extracorporeal membrane oxygenation in cases that otherwise wouldn’t meet salvage criteria. The vast majority of survivors across ARDS severity classes were managed with MP_RS > 15 J/min: 74% (mild), 81% (moderate), and 87% (severe). Overall, 59% of our survivors required MP_RS > 20 J/min (MP_L > 14 J/min).

Our results support our hypothesis accounting for resistive work is unnecessary for clinical purposes. It also supports our reasoning that the major sources of VILI are elastic and viscoelastic properties of a heterogeneously injured lung: a substantial portion of which might be captured with a brief pause time (0.5 s) that we adopted by adhering to the ARDSNet protocols.³⁴

In reviewing the literature, a nettlesome problem became apparent: How should MP_RS be targeted since studies have used different equations with varying complexity? Among surrogate formulas relevant to our study, some excluded PEEP (ie, static MP) but included 50% of peak P_aw multiplied by P_DR.² Others included PEEP and used 50% of P_DR. Although not explained, a 50% correction factor is an attempt to estimate the absorption of pressure (energy) across the lung parenchyma.^2,3

Of particular interest to us were studies done by Xie et al¹⁰ and Costa et al² who used a 50% correction factor as a means of estimating “elastic power” (EP) (Supplementary Data S3): Xie and colleagues¹⁰ found EP was highly accurate in identifying severe ARDS (threshold of 14.6 J/min). Costa and colleagues² parsed EP into its static and dynamic subcomponents (as well as a resistive subcomponent) to estimate total MP. Their relevance to our study was that only the dynamic EP (and not the resistive subcomponent) was associated with mortality risk: odds ratio (95% CI) of 1.31 (1.19–1.45).²

These 2 studies are directly related to our estimates of MP_L (0.74 correction factor) compared with their estimates of EP (0.5 correction factor).^10,2 In our post hoc analysis, we found that our MP_L and EP using their equations produced the same results (Supplementary Data S3). However, because the equations differ, the conversion factors are not interchangeable. Ours requires a conversion factor more reflective of the E_L/E_RS relationship reported in ARDS.

We also compared our mortality to that found by Wu et al³⁵ who used the same surrogate formula as we used. They also observed elevated levels of mean MP_RS at baseline ∼28 J/min (V_T 8.4 mL/kg predicted body weight) compared to our baseline measurements (when expressed as mean) of ∼27 J/min (V_T 7.1 mL/kg predicted body weight). A similar finding was that after 2 d of LPV they reported average MP_RS had decreased in survivors and increased in non-survivors (mean total difference of Δ 5.1 J/min). In our subjects, the total difference between non-survivors and survivors after ∼1 d was Δ 2.5 J/min.

We feel compelled to comment upon two of our other findings. First, that MP_CW carried a greater mortality risk than MP_L was baffling (being a derived variable not directly relevant to VILI). The only cogent explanation we can offer is that MP_CW was a latent signifier for subjects with intra-abdominal hypertension and, therefore, associated with heightened mortality risk.³⁶ Unfortunately, our database lacked supporting information. Second, the higher mortality risk associated with MP_RS index is concerning. We speculate that E_CW was lower in smaller stature, leaner subjects so that a higher fraction of MP_RS was applied to the lungs, thereby increasing VILI risk.

The limitations of our study were its retrospective nature and the limitations of our quality assurance data. Most vexing was the potential contribution of subject effort to MP_RS during assisted CMV. Our sedation practice (Particularly during the first days after ARDS onset was to promote synchrony while maintaining V_T and P_plat targets). Passive ventilation was pharmacologically induced when asynchrony interfered with LPV goals and gas exchange stabilization. This practice was followed with particular fidelity during the initial days after implementing ARDSNet protocols.

Conclusions

In summary, for bedside management in the absence of automated ventilator measurements of MP_RS, the PC-CMV surrogate formula is a reasonable method to estimate MP_RS even when using VC-CMV. Despite the ambiguities and limitations described above, surrogate estimates of MP_RS are strongly associated with mortality risk across threshold values and degrees of ARDS severity. Our data suggest that exceeding an MP_RS threshold of 30 J/min (MP_L of 22 J/min) greatly increases mortality risk when it occurs early in the exudative phase of ARDS. Prospective trials are needed to examine varying MP_RS safety thresholds across both different severity classifications and pathological stages ARDS. Of equal importance, it would behoove such studies to assess the impact of MP_RS thresholds on competing needs such as its impact on sedation requirements and the related issues of duration of mechanical ventilation and ventilator-associated events.

Footnotes

Author Disclosure Statement

Mr. Kallet discloses a relationship with ContinuED. Dr. Lipnick has disclosed no conflicts of interest.

Elements of this paper were published as abstracts in Respiratory Care October 2023;68(Suppl 10):3934725 (14, 25, 49, 76, and 95).

Supplementary Material

Supplementary Data S1

Supplementary Data S2

Supplementary Data S3

Supplementary Table S1

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Supplementary Material

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Pressure Control Surrogate Formula for Estimating Mechanical Power in ARDS Is Associated With Mortality

Abstract

Background:

Methods:

Results:

Conclusion:

Introduction

QUICK LOOK

Current knowledge

What this paper contributes to our knowledge

Methods

Design rationale

Subjects

Measurements and calculations

Assessments

Statistical analysis

Results

Achieving LPV goals

Mortality and MP

Mechanical power characteristics across Berlin definition ARDS classifications

Mortality and changes in MP from ARDS onset to the following day

Differences in MP and mortality between Berlin classifications

MP thresholds and mortality risk

Discussion

Conclusions

Footnotes

Author Disclosure Statement

Supplementary Material

References

Supplementary Material