Agreement between peak inspiratory pressure in decelerating-flow ventilation and plateau pressure in square-flow ventilation in pediatric acute respiratory distress syndrome

Abstract

Objective:

Acute respiratory distress syndrome guidelines suggest limiting plateau pressures to 28–30 cmH₂O. Plateau pressure is most accurately measured in square-flow modes, such as volume control. In children, decelerating-flow modes such as pressure-regulated volume control and pressure control are more common. Consequently, plateau pressures are rarely obtained and pressure limits are instead provided for peak inspiratory pressure. The degree to which peak inspiratory pressure in decelerating-flow overestimates plateau pressure is unknown. Therefore, we assessed the correlation and accuracy of peak inspiratory pressure in decelerating-flow ventilation for approximating plateau pressure during square-flow ventilation.

Design:

Prospective, observational study.

Setting:

Tertiary, academic pediatric intensive care unit.

Patients:

Fifty-two intubated children with acute respiratory distress syndrome enrolled between January 2020 and May 2021.

Interventions:

Measurement of peak inspiratory pressure in decelerating-flow ventilation and plateau pressure after transition to square-flow ventilation.

Measurements and main results:

Peak inspiratory pressure in decelerating-flow was highly correlated (r² = 0.99, p < 0.001) with plateau pressure in square-flow. Peak inspiratory pressure was 1.0 ± 0.6 cmH₂O higher than plateau pressure, with 96% of values within 2 cmH₂O. The single outlier had co-existent asthma and inspiratory flows which did not reach zero.

Conclusions:

Peak inspiratory pressure measured during decelerating-flow ventilation may be an adequate surrogate of plateau pressure in pediatric acute respiratory distress syndrome when inspiratory flow approaches zero. Practitioners should be aware that peak inspiratory pressures in decelerating-flow may not be substantially higher than plateau pressures.

INTRODUCTION

Ventilation with tidal volumes (V_T) approximating 6 mL/kg and plateau pressures (P_plat) ≤ 30 cmH₂O in adults with acute respiratory distress syndrome (ARDS) improved mortality compared to V_T of 12 mL/kg and P_plat ≤ 50 cmH₂O (1). The 2015 Pediatric Acute Lung Injury Consensus Conference (PALICC) recommended a P_plat ≤ 28 cmH₂O (2). Monitoring P_plat is therefore a key tenet of lung-protective ventilation. Re-analysis of adult trials associated lower driving pressure (ΔP = P_plat minus positive end-expiratory pressure [PEEP]) with increased survival (3), highlighting the significance of monitoring P_plat.

In pediatric ARDS (PARDS), providers more commonly use decelerating-flow modes, such as pressure-regulated volume control (PRVC) or pressure-control (PC), rather than the square-flow volume-control ventilation (4, 5). P_plat is less reliably measured in decelerating-flow; therefore, peak inspiratory pressure (PIP) is often substituted. However, resistive components of ventilation may make PIP an unreliable surrogate for lung stress. The degree to which PIP overestimates P_plat has not been quantified in either adults or children. Therefore, we aimed to assess the correlation and accuracy of PIP during decelerating-flow ventilation (PIP_decel) for approximating P_plat in PARDS. We hypothesized that PIP_decel would approximate P_plat in square-flow ventilation within 0.5 cmH₂O.

METHODS

Study design and patient selection

This prospective, observational study was approved by the Children’s Hospital of Philadelphia’s (CHOP) Institutional Review Board (IRB 20–017935) and the requirement for informed consent was waived. Patients were screened daily for study eligibility from January 1, 2020 to May 31, 2021 in the pediatric intensive care unit (PICU). Inclusion criteria included elements of both Berlin (6) and PALICC definitions (2): 1) acute respiratory failure requiring invasive ventilation, 2) age > 1 month without upper limit, 3) oxygenation index (OI) ≥ 4 or oxygen saturation index (OSI) ≥ 5 on two consecutive measurements ≥ 4 hours apart, and 4) bilateral parenchymal infiltrates on radiograph. Exclusion criteria were 1) respiratory failure primarily from cardiac failure, 2) exacerbation of underlying chronic respiratory disease, 3) chronic ventilator dependence, 4) mixing cyanotic heart disease, 5) ventilation for ≥ 7 days before meeting eligibility, and 6) PARDS established outside of CHOP.

Data collection and PARDS management

Demographics, ventilator settings, laboratory data, and medications were recorded. In the absence of a standardized ventilator protocol, our institutional practice is to initiate conventional ventilation (Evita XL, Draeger, Germany) with PEEP ≥ 5 cmH₂O with age-appropriate cuffed endotracheal tubes (ETTs) and active humidification. We exclusively use decelerating-flow (either PRVC or PC), and institutional practice ensures that both inspiratory and expiratory flows approach zero. Pressures are measured at the ventilator for V_T ≥ 100 mL; for V_T < 100 mL, we use a sensor at the ETT. Persistently elevated PIP (≥ 35 cmH₂O), ongoing hypercarbia (arterial pressure of carbon dioxide ≥ 80 mmHg), or oxygenation difficulties (inability to wean fractional inspired oxygen ≤ 0.60 despite increasing PEEP) prompt consideration for changing ventilation mode or escalating to extracorporeal support.

For this study, we recorded clinician-prescribed decelerating-flow ventilation settings within 24 hours of PARDS onset. We verified quiet breathing by ensuring measurements during either neuromuscular blockade or absence of spontaneous effort above the set respiratory rate. We recorded PIP_decel without adjustment of the set inspiratory time. Then, we switched the patient to square-flow volume control ventilation using the exhaled V_T. We allowed 30 to 60 seconds of ventilation, and then recorded P_plat and PIP in square-flow (PIP_square). P_plat was recorded after 0.5 seconds of inspiratory pause, with an inspiratory hold performed if the set inspiratory time did not have an intrinsic pause of 0.5 seconds.

OSI converted to OI for reporting. Shock severity was quantified using the vasopressor-inotrope score (7). The designation “immunocompromised” required an immunocompromising diagnosis (oncologic, immunologic, rheumatologic, transplant) and active immunosuppression or a congenital immunodeficiency.

Statistical analysis

Data are expressed as percentages, median (interquartile range [IQR]), or mean ± standard deviation (SD). Our primary analysis tested the equivalence of PIP_decel and P_plat. After the first 10 subjects, we calculated the SD of this difference to calculate a sample size. In an equivalence test of paired means, 45 subjects were required for 90% power at α = 0.05 to demonstrate a true difference (± SD) of 0 ± 1, with equivalence limits of −0.5 and 0.5. Pearson correlation and Bland Altman analyses were done to describe the agreement between PIP_decel and P_plat. Data were analyzed using GraphPad Prism 9.

RESULTS

Fifty-six subjects had PARDS, of whom four were on non-conventional modes and did not have pressures recorded. Thus, our cohort consisted of 52 subjects (Supplementary Table) with 8 non-survivors (15%) at day 28. Pneumonia (54%) and non-pulmonary sepsis (15%) accounted for the majority of PARDS. Most had comorbidities, including 14 (27%) who were immunocompromised, and 29 (56%) requiring vasopressors. Median OI was 15.7 and median PaO₂/FIO₂ 124. Forty-one patients (79%) were on PRVC and eleven (21%) on PC ventilation. PIP_decel ranged from 20 to 42 cmH₂O and inspiratory times from 0.4 and 1.3 seconds.

P_plat and PIP_decel were strongly correlated (Figure 1; r² = 0.99, p < 0.001). Bland-Altman analysis revealed that PIP_decel was greater than P_plat with a mean of 1.0 ± 0.6 cmH₂O with 95% limits of agreements (LOA) of −0.3 and 2.2. One (2%) patient was outside of the LOA, and only one patient had P_plat > PIP_decel. The one subject outside of the upper LOA had coexistent asthma with an inspiratory flow that prematurely terminated prior to reaching zero. In 50 patients (96%), PIP_decel exceeded P_plat by ≤ 2 cmH₂O.

Figure 1:

Correlation (left) and Bland-Altman analysis (right) comparing peak inspiratory pressure during decelerating flow (PIP_decel) with plateau pressure during square-flow (P_plat). PIP_decel and P_plat are strongly correlated (Pearson r² = 0.99), and PIP_decel overestimates P_plat by 1.0 ± 0.6 cmH₂O.

DISCUSSION

Imprecision in measuring PIP_decel has precluded widespread acceptance of it as a surrogate for P_plat. In our study, PIP_decel overestimated P_plat by 1.0 ± 0.6 cmH₂O, with 96% of patients having a PIP_decel within 2 cmH₂O of P_plat. PIP_decel measured during quiet breathing may be a reasonable surrogate for P_plat provided that inspiratory flow approaches zero, and may be used clinically to approximate P_plat and calculate ΔP.

In a multicenter PARDS cohort, the most common modes were PC and PRVC (65%); P_plat was reported in 2.9% of measurements (8), suggesting most providers relied on PIP. Elevated PIPs (9) and ΔP calculated by substituting PIP_decel for P_plat (10) were associated with worse outcomes, confirming utility of PIP_decel. Recently, a pre-clinical study concluded that PIP_decel overestimated P_plat when inspiratory time was decreased or airway resistance increased (11). Our study is in agreement as evidenced by the one patient with concurrent obstructive disease. In an adult study, PIP_decel was 25.1 ± 2.3 cmH₂O while P_plat (in square-flow) was 24.8 ± 2.5 cmH₂O, a minimal difference consistent with our results (12). We conclude that PIP_decel approximates P_plat when inspiratory flows reach zero. Providers should be cognizant that PIPs may not be much higher than P_plat. Our data may inform adherence to lung-protective guidelines among practitioners who do not record P_plat.

Our study has limitations. It was from a single center, which may limit generalizability, and had a small sample size. Results only apply to PARDS, and should not be extended to processes where resistance may be elevated such as obstructive conditions where it is more likely that inspiratory flows do not reach zero. Our cohort included only seven patients < 12 months and may not generalize to younger patients. However, PIP_decal was 1.0 ± 0.7 cmH₂O higher versus P_plat in these seven patients, similar to the entire cohort. We only measured P_plat after a 0.5 second pause as this is the suggested duration in adult trials; however, longer pauses may yield a more accurate P_plat. Finally, we chose to switch to square-flow volume control, rather than performing an inspiratory hold in decelerating-flow, because this represents the gold standard for measuring P_plat (1, 3) and because inconsistent V_T in PRVC make P_plat in that mode unreliable.

Conclusions

PIP_decel slightly overestimates P_plat in PARDS but may be a reasonable approximation when inspiratory flow approaches zero, without significant obstructive disease, and within the range of PIPs and inspiratory times reported.