Table 2 - uploaded by Robert L Chatburn
Content may be subject to copyright.
Source publication
As hospitals begin to implement electronic medical records, the inadequacies of legacy paper charting systems will become more evident. One area of particular concern for respiratory therapists is the charting of mechanical ventilator settings. Our profession's lack of a standardized and generally accepted taxonomy for mechanical ventilation leaves...
Contexts in source publication
Context 1
... in our experience in teaching and using ventilation modes, people who view bi-level ventilation in this way have difficulty recognizing that time-triggered and time-cycled changes in airway pressure are not only mandatory pressure-control breaths by definition, but are associated with substantial, sometimes alarmingly large tidal volumes. Table 2 summarizes the terms and definitions we pro- pose for standardizing documentation of ventilator settings for pressure-control modes. While our proposal is modest in scope, implementation of any change regarding hospital culture is a challenge. ...
Context 2
... 3 gives the simulation spreadsheet equations (not including the code for the waveform graphic). Note that the equations are considerably more complex than is sug- gested by Table 2, because of added error-trapping fea- tures. Table 4 gives the instructions for using the simula- tion. ...
Citations
... Caregivers versed in waveform descriptors and ventilation annotation schemes [36] may also have difficulty adopting complex parametric descriptions of lung deformation properties. Such ontological differences further limit the scope and effectiveness of translating patient-specific parameters into clinical and translational informatics (e.g., machine learning) domains for desirable applications such as LVS phenotyping and classifying dyssynchronous behaviors [19]. ...
Mechanical ventilation is an essential tool in the management of Acute Respiratory Distress Syndrome (ARDS), but it exposes patients to the risk of ventilator-induced lung injury (VILI). The human lung-ventilator system (LVS) involves the interaction of complex anatomy with a mechanical apparatus, which limits the ability of process-based models to provide individualized clinical support. This work proposes a hypothesis-driven strategy for LVS modeling in which robust personalization is achieved using a pre-defined parameter basis in a non-physiological model. Model inversion, here via windowed data assimilation, forges observed waveforms into interpretable parameter values that characterize the data rather than quantifying physiological processes. Accurate, model-based inference on human-ventilator data indicates model flexibility and utility over a variety of breath types, including those from dyssynchronous LVSs. Estimated parameters generate static characterizations of the data that are 50%-70% more accurate than breath-wise single-compartment model estimates. They also retain sufficient information to distinguish between the types of breath they represent. However, the fidelity and interpretability of model characterizations are tied to parameter definitions and model resolution. These additional factors must be considered in conjunction with the objectives of specific applications, such as identifying and tracking the development of human VILI.
... The dynamic driving pressure (ΔP) and mechanical power of ventilation (MP) were calculated using standard formulas [12,13], i.e., ΔP (in cm H 2 O) = peak pressure (P peak )positive end-expiratory pressure (PEEP); and MP (in J/min) = 0.098 * tidal volume (V T ) * respiratory rate (RR) * (Ppeak -0.5 * ΔP). ...
Purpose
We investigated changes in ARDS severity and associations with outcome in COVID–19 ARDS patients.
Methods
We compared outcomes in patients with ARDS classified as ‘mild’, ‘moderate’ or ‘severe’ at calendar day 1, and after reclassification at calendar day 2. The primary endpoint was 28–day mortality. We also identified which ventilatory parameters had an association with presence of severe ARDS at day 2. We repeated the analysis for reclassification at calendar day 4.
Results
Of 895 patients, 8.5%, 60.1% and 31.4% had mild, moderate and severe ARDS at day 1. These proportions were 13.5%, 72.6% and 13.9% at day 2. 28–day mortality was 25.3%, 31.3% and 32.0% in patients with mild, moderate and severe ARDS at day 1 (p = 0.537), compared to 28.6%, 29.2% and 44.3% in patients reclassified at day 2 (p = 0.005). No ventilatory parameter had an independent association with presence of severe ARDS at day 2. Findings were not different reclassifying at day 4.
Conclusions
In this cohort of COVID–19 patients, ARDS severity and mortality between severity classes changed substantially over the first 4 days of ventilation. These findings are important, as reclassification could help identify target patients that may benefit from alternative approaches.
... V T was expressed in ml/kg predicted bodyweight (PBW) [20]. ΔP was calculated by subtracting PEEP from the maximum airway pressure, as all patients were under pressure-controlled modes of ventilation and no plateau airway pressures were available [21,22]. ...
Background:
Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury.
Aims and methods:
This was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume (VT) and driving pressure (ΔP), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and VT and ΔP. Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia.
Results:
Seventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median VT and ΔP before BAL were 6.7 [IQR 6.1 to 7.6] ml/kg predicted bodyweight (PBW) and 15 [IQR 11 to 18] cm H2O, respectively. BALF levels of C5a, C3b/c and C4b/c were neither different between patients with or without ARDS, nor between patients with or without pneumonia. BALF levels of C5a, and also C3b/c and C4b/c, did not correlate with VT and ΔP. Median BALF levels of C5a, C3b/c, and C4b/c, and the effects of VT and ΔP on those levels, were not different between patients with or without ARDS, and in patients with or without pneumonia.
Conclusion:
In this cohort of critically ill patients under invasive ventilation, pulmonary levels of complement activation products were independent of the size of VT and the level of ΔP. The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation.
... The modified ΔP was calculated by subtracting PEEP from P max [22,24]. ...
... P peak is suggested to be used in the originally reported "power equation" [25]. As proposed before [22,24], for the present analysis P max instead of P peak was used, as in the participating ICUs pressure-controlled ventilation was exclusively used for assist ventilation. ...
... Because patients in here analyzed cohort were exclusively receiving pressure-controlled ventilation, the calculation of the modified ΔP had to be adapted, i.e., P max was used instead of P peak , as with pressure-controlled ventilation there is no P peak . Of note, P max was measured and reported at zero flow in patients without a spontaneous breathing effort [22,24]. Furthermore, and for the same reasons, also the "power equation" was adapted. ...
Outcome prediction in critically ill patients under invasive ventilation remains extremely challenging. The driving pressure (ΔP) and the mechanical power of ventilation (MP) are associated with patient-centered outcomes like mortality and duration of ventilation. The objective of this study was to assess the predictive validity for mortality of the ΔP and the MP at 24 h after start of invasive ventilation. This is a post hoc analysis of an observational study in intensive care unit patients, restricted to critically ill patients receiving invasive ventilation for at least 24 h. The two exposures of interest were the modified ΔP and the MP at 24 h after start of invasive ventilation. The primary outcome was 90-day mortality; secondary outcomes were ICU and hospital mortality. The predictive validity was measured as incremental 90-day mortality beyond that predicted by the Acute Physiology, Age and Chronic Health Evaluation (APACHE) IV score and the Simplified Acute Physiology Score (SAPS) II. The analysis included 839 patients with a 90-day mortality of 42%. The median modified ΔP at 24 h was 15 [interquartile range 12 to 19] cm H2O; the median MP at 24 h was 206 [interquartile range 145 to 298] 10−3 J/min/kg predicted body weight (PBW). Both parameters were associated with 90-day mortality (odds ratio (OR) for 1 cm H2O increase in the modified ΔP, 1.05 [95% confidence interval (CI) 1.03 to 1.08]; P < 0.001; OR for 100 10−3 J/min/kg PBW increase in the MP, 1.20 [95% CI 1.09 to 1.33]; P < 0.001). Area under the ROC for 90-day mortality of the modified ΔP and the MP were 0.70 [95% CI 0.66 to 0.74] and 0.69 [95% CI 0.65 to 0.73], which was neither different from that of the APACHE IV score nor that of the SAPS II. In adult patients under invasive ventilation, the modified ΔP and the MP at 24 h are associated with 90 day mortality. Neither the modified ΔP nor the MP at 24 h has predictive validity beyond the APACHE IV score and the SAPS II.
... Also, esophageal pressure measurements were not performed routinely, and therefore the pulmonary ΔP could not be calculated. Because patients were exclusively under pressure-controlled ventilation, P max instead of P plat was used, as suggested previously (33)(34)(35). Furthermore, severity of illness scores like APACHE scores and SAPS have robust prognostic capacities, and thus should be held in consideration when investigating the prognostic capacities of the parameters of interest in this study. ...
Background:
Outcome prediction in acute respiratory distress syndrome (ARDS) is challenging, especially in patients with severe hypoxemia. The aim of the current study was to determine the prognostic capacity of changes in PaO2/FiO2, dead space fraction (VD/VT) and respiratory system driving pressure (ΔPRS) induced by the first prone position (PP) session in patients with ARDS.
Methods:
This was a post hoc analysis of the conveniently-sized 'Molecular Diagnosis and Risk Stratification of Sepsis' study (MARS). The current analysis included ARDS patients who were placed in the PP. The primary endpoint was the prognostic capacity of the PP-induced changes in PaO2/FiO2, VD/VT, and ΔPRS for 28-day mortality. PaO2/FiO2, VD/VT, and ΔPRS was calculated using variables obtained in the supine position before and after completion of the first PP session. Receiving operator characteristic curves (ROC) were constructed, and sensitivity, specificity positive and negative predictive value were calculated based on the best cutoffs.
Results:
Ninety patients were included; 28-day mortality was 46%. PP-induced changes in PaO2/FiO2 and VD/VT were similar between survivors vs. non-survivors [+83 (+24 to +137) vs. +58 (+21 to +113) mmHg, and -0.06 (-0.17 to +0.05) vs. -0.08 (-0.16 to +0.08), respectively]. PP-induced changes in ΔPRS were different between survivors vs. non-survivors [-3 (-7 to 2) vs. 0 (-3 to +3) cmH2O; P=0.03]. The area under the ROC of PP-induced changes in ΔPRS for mortality, however, was low [0.63 (95% confidence interval (CI), 0.50 to 0.75]; PP-induced changes in ΔPRS had a sensitivity and specificity of 76% and 56%, and a positive and negative predictive value of 60% and 73%.
Conclusions:
Changes in PaO2/FiO2, VD/VT, and ΔPRS induced by the first PP session have poor prognostic capacities for 28-day mortality in ARDS patients.
... Confusion increases when talking about pressure control ventilation. 2 For example, from the ventilator's point of view, driving pressure (ie, the pressure associated with inflation) could be ⌬P elastic ϭ elastance ϫ ⌬volume, or ⌬P resistive ϭ resistance ϫ flow, or ⌬P total ϭ ⌬P elastic ϩ ⌬P resistive , where the ⌬ denotes a change in time for ⌬P elastic and ⌬P total, and a difference in space for ⌬P resistive . From the patient's point of view, driving pressure could be any form of pressure that is driving inspiration 3 or the pressure that is driving expiration. ...
... In APRV, T high is much longer than T low , and thus P aw will be higher for the same peak airway pressure when compared with conventional ventilation. 12 In APRV, the time spent at the higher pressure is generally 80 -90% of the respiratory cycle. The higher the P aw , within a reasonable range, the higher P aO 2 will be, due to alveolar recruitment. ...
Airway pressure release ventilation (APRV) was originally described as a mode to treat lunginjured patients with the goal to maintain a level of airway pressure that would not depress the cardiac function, deliver mechanical breaths without excessive airway pressure, and to allow unrestricted spontaneous ventilation. Indeed, based on its design, APRV has technological features that serve the goals of safety and comfort. Animal studies suggest that APRV leads to alveolar stability and recruitment which result in less lung injury. These features are sought in patients at risk for lung injury or with ARDS. APRV allows unrestricted spontaneous ventilation, which is welcome in the era of less sedation and increased patient mobility (the effects in terms of lung injury remain to be explored). However, we must highlight that the performance of APRV is dependent on the operator-selected settings and the ventilator’s performance. The clinician must select the appropriate settings in order to make effective the imputed benefits. This is a challenge when the ventilator’s performance is not uniform, and the outcomes depend on high precision settings (very short expiratory time), where small variations can lead to undesired outcomes (de-recruitment or large tidal volumes leading to lung injury). Finally, we do not have evidence that APRV (as originally described) improves relevant clinical outcomes of patients with ARDS. For APRV to become the primary mode of ventilation for ARDS, it will require development of sound protocols and technological enhancements to ensure its performance and safety. For now, APRV does have a greater potential for adversely affecting patient outcome than improving it; unless definitive data are forthcoming demonstrating outcome benefits from the use of APRV in ARDS, there is no reason to consider this approach to ventilatory support.
Peak Inspiratory Pressure (PIP).
Background:
The majority of critically ill patients do not suffer from acute respiratory distress syndrome (ARDS). To improve the treatment of these patients, we aimed to identify potentially modifiable factors associated with outcome of these patients.
Methods:
The PRoVENT was an international, multicenter, prospective cohort study of consecutive patients under invasive mechanical ventilatory support. A predefined secondary analysis was to examine factors associated with mortality. The primary endpoint was all-cause in-hospital mortality.
Results:
935 Patients were included. In-hospital mortality was 21%. Compared to patients who died, patients who survived had a lower risk of ARDS according to the 'Lung Injury Prediction Score' and received lower maximum airway pressure (Pmax), driving pressure (ΔP), positive end-expiratory pressure, and FiO2levels. Tidal volume size was similar between the groups. Higher Pmaxwas a potentially modifiable ventilatory variable associated with in-hospital mortality in multivariable analyses. ΔP was not independently associated with in-hospital mortality, but reliable values for ΔP were available for 343 patients only. Non-modifiable factors associated with in-hospital mortality were older age, presence of immunosuppression, higher non-pulmonary sequential organ failure assessment scores, lower pulse oximetry readings, higher heart rates, and functional dependence.
Conclusions:
Higher Pmaxwas independently associated with higher in-hospital mortality in mechanically ventilated critically ill patients under mechanical ventilatory support for reasons other than ARDS. Trial Registration ClinicalTrials.gov (NCT01868321).
Peak Inspiratory Pressure (PIP)
