Bedside Monitoring of Respiratory Effort in Patients Undergoing Assisted Mechanical Ventilation

• In ICU
• Tue, 14 Oct 2025

ICU Management & Practice, Volume 25 - Issue 4, 2025

This review explores bedside methods for monitoring respiratory effort in patients undergoing assisted mechanical ventilation. It highlights the risks of lung and diaphragm injury from excessive or insufficient patient effort, reviews invasive and non-invasive pressure-based techniques, and discusses their strengths, limitations, and proposed safety thresholds. The article emphasises integrating these tools into clinical practice to guide lung- and diaphragm-protective ventilation strategies.

Introduction

For many patients who experience acute respiratory failure (ARF), the use of mechanical ventilation is a life-saving intervention. While identifying and treating the underlying cause of ARF, the application of lung-protective ventilation is also key to avoiding the progression of lung injury (Brochard et al. 2017). It is well understood that damage to the lungs can occur during mandatory ventilation. However, what is less widely appreciated is the potential for lung injury during mechanical ventilation in assisted modes of ventilation (Yoshida et al. 2017). Moreover, monitoring respiratory effort is increasingly being viewed as a crucial step to implement lung- and diaphragm-protective ventilation during assisted ventilation (Goligher et al. 2020).

During each patient-triggered inspiratory effort, the volume of gas inflating the lungs is the result of the combined effects of the negative pleural pressure (P_pl) generated by inspiratory muscle activity and the positive airway pressure (P_aw) generated according to the pressure support level (P_supp) set by the clinician. The transpulmonary pressure (P_L), the effective pressure distending the lungs, represents the difference between P_aw and P_pl and is directly correlated with the mechanical stress exerted on the lung parenchyma (Akoumianaki et al. 2014). In controlled ventilation, P_L closely reflects P_aw, since the ventilator is the sole driver of lung inflation. In contrast, during assisted ventilation, an identical P_awmay correspond to widely varying P_L values due to the contribution of patient-generated inspiratory effort. This additional hidden pressure, resulting from patient effort, cannot be directly inferred from ventilator waveforms, posing a challenge for accurate assessment.

Therefore, unveiling the pressures generated by the patient’s effort of breathing in spontaneous modes of ventilation should be a primary concern for clinicians. In this regard, several practical methods have been proposed to monitor patient respiratory effort (Van Oosten et al. 2024). This review will specifically examine pressure-based methods, both invasive and non-invasive, including oesophageal pressure (P_es), airway occlusion pressure at 100msec (P_0.1), end-expiratory occlusion pressure (ΔP_occ) and pressure muscle index (PMI).

Mechanisms of Lung and Diaphragmatic Injury During Spontaneous Ventilation

Mechanical ventilation can contribute to lung injury through several mechanisms collectively referred to as ventilator-induced lung injury (VILI) (Slutsky and Ranieri 2013). Although the preservation of spontaneous breathing can enhance the recruitment of dependent lung regions and mitigate ventilation-perfusion mismatch, the combination of the patient’s effort and ventilation may induce excessive lung stress and strain (Yoshida et al. 2017). This may be particularly relevant in damaged lungs, where the anatomical and functional heterogeneity of the lung parenchyma may result in regionally injurious ventilation due to variations in P_L swings throughout the pleural space (Gattinoni and Pesenti 2005).

Elevated P_L and high tidal volume (V_t) are well-established contributors to alveolar over-distention, a phenomenon known as volutrauma (ARDS Network 2000). This condition leads to an increase in the overall mechanical stress exerted on the lung parenchyma, with a predominant impact on non-dependent lung regions (Slutsky and Ranieri 2013). Such overdistension may arise from excessive patient-generated inspiratory effort or, conversely, from the combination of over-assisting P_supp levels and minimal respiratory effort (Docci et al. 2023).

A vigorous inspiratory effort amplifies pendelluft, the phenomenon of air movement from one lung region to another without causing a significant change in V_t, thereby increasing the risk of regional cycling opening and closing of alveoli within each breath, a detrimental mechanism predominantly involving dependent lung regions and known as atelectrauma (Yoshida et al. 2013). Furthermore, active expiration and patient-ventilator asynchrony may further exacerbate these effects, contributing to lung injury progression (Chanques et al. 2013).

From the lung perfusion perspective, P_L contributes to the pressure gradient across the pulmonary vessels. Elevated P_L values may increase the risk of pulmonary oedema by increasing total and extravascular lung water, particularly in the setting of inflammation and increased vascular permeability (Yoshida et al. 2017).

In addition, the appropriate application of assisted ventilation is essential to reduce the risk of diaphragm injury and weakness in critically ill patients. These conditions have been linked to weaning failure, prolonged mechanical ventilation and increased mortality (Dres et al. 2017; Goligher et al. 2015; Goligher et al. 2018). Mechanical ventilation induces myotrauma through various mechanisms, the most extensively described being muscle atrophy resulting from ventilatory assistance (Levine et al. 2008). This pathophysiological process is primarily observed during mandatory ventilation; however, minimal respiratory effort and excessive P_supp (over assistance) are associated with inefficient muscular contraction and development of diaphragm weakness (Goligher et al. 2015). The diaphragm is also sensitive to sustained excessive respiratory workload. Elevated patient effort, insufficient ventilatory assistance, and patient-ventilator asynchrony can lead to excessive muscular activity, secondary diaphragm inflammation, and tissue damage (Jiang et al. 1998).

Invasive Pressure-Based Method: The Oesophageal Pressure (P_es)

Oesophageal manometry is the reference method when assessing respiratory mechanics. The waveform analysis of P_es allows investigators to estimate several surrogate parameters that are considered the gold standard when evaluating respiratory muscle effort and work of breathing (Figure 1, Panel A) (Mauri et al. 2016a).

P_es variations reflect changes in P_pl, making the difference between P_aw and P_es a reliable estimate of P_L. It is important to consider that P_es represents the pressure surrounding the oesophageal balloon, while P_pl varies with a ventral-dorsal gradient across the pleural space due to gravitational forces, parenchymal heterogeneity, pendelluft, and the weight of the mediastinum (Yoshida et al. 2018). The safety limits of P_L in assisted ventilation remain debated, though a peak inspiratory value below 20 cmH₂O has been considered acceptable from studies on both spontaneous breathing in healthy lungs and passive ventilation in injured lungs (Table 1) (Mauri et al. 2016a; Baedorf Kassis et al. 2016).

Also, P_es directly quantifies respiratory muscle activity in assisted ventilation. Inspiratory muscle contraction generates negative P_es swings (ΔP_es), reflecting the magnitude of respiratory effort. The inspiratory muscle pressure (P_mus) is the global pressure exerted by the inspiratory muscles to expand the respiratory system, including the lungs and the chest wall. P_mus is derived from the difference between the pressure required to overcome the chest wall elastance and P_es (P_mus= P_cw – P_es), and its proposed safety thresholds range between 5 and 10 cmH₂O (Carteaux et al. 2013). Given that P_cw cannot be accurately measured during active breathing, it needs to be computed during passive ventilation or roughly estimated as 4% of predicted vital capacity (Mauri et al. 2016a). However, in routine clinical practice, it is generally accepted that the correction of P_mus for P_cwcan be omitted in most patients, acknowledging that chest wall elastance may be relevant in certain conditions such as obesity, chest wall disorders and increased intra-abdominal pressure (Brochard 2014).

In addition, the use of a double-balloon catheter enables the measurement of gastric pressure (P_ga). The difference between P_es and P_ga quantifies the transdiaphragmatic pressure (P_di). This measurement provides valuable insight into diaphragmatic activity and patient-ventilator synchronisation (Akoumianaki et al. 2024).

More complex measurements, such as the pressure-time product (PTP, the area under the P_mus curve over time) and the work of breathing (WOB, the area under the volume-pressure curve), are derived from P_es and P_mus. These parameters are considered the gold standard for assessing respiratory effort due to their strong correlation with inspiratory muscle energy expenditure and oxygen consumption. However, their clinical application remains mainly confined to the research setting (Mancebo et al. 1995).

Although oesophageal manometry provides a comprehensive and detailed evaluation of respiratory effort, its clinical implementation remains limited. Several barriers must be addressed to facilitate its broader adoption in clinical practice, including the need for specialised expertise in catheter placement, validation of balloon positioning and waveform interpretation, as well as challenges related to equipment availability, tolerance in awake patients and costs (Brochard 2014).

Non-Invasive Pressure-Based Methods

Airway occlusion techniques during spontaneous mechanical ventilation (Figure 1, Panel B) have been used for over three decades to estimate respiratory effort (Whitelaw et al. 1975; Foti et al. 1997). Numerous studies have described these parameters, emphasising their ease of use, straightforward interpretation, repeatability and non-invasiveness. These characteristics render them practical tools for bedside evaluation of respiratory effort. Moreover, adherence to standardised procedures and the averaging of repeated measurements are essential to achieve stable and reliable values (Kera et al. 2013; Bianchi et al. 2022). It should be emphasised that none of these measures has demonstrated predictive capability to exactly compute measures of respiratory effort or pulmonary mechanics; therefore, there is no definitive consensus on their cutoff values (Telias et al. 2020; Bertoni et al. 2019; De Vries et al. 2023). Table 1 shows the most frequently proposed safety thresholds.

Airway occlusion pressure in the first 100 milliseconds of inspiration (P_0.1)

P_0.1 is the decrease in pressure generated by the inspiratory muscles in the first 100ms of inspiration against an occluded airway (Figure 1, Panel B). P_0.1represents a physiological manifestation of the cerebral respiratory centres’ activity, making it a more precise estimation of the respiratory drive rather than a direct reflection of the effort generated by inspiratory muscles (Jonkman et al. 2020). This is attributable to its independence from respiratory mechanics and voluntary modulation of breathing.

Specifically, since inspiratory effort is initiated at the end-expiratory volume, the pressure drop does not include any component derived from the recoil pressure of the respiratory system. The absence of flow during the occlusion manoeuvre removes the impact of airway resistance, the ventilator valves closure guarantees no change in lung volume, and there is no conscious reaction in the first millisecond of an airway occlusion (Jonkman et al. 2020). Furthermore, evidence indicates that P_0.1 remains stable in the presence of non-severe muscle weakness and in patients with pulmonary hyperinflation (Holle et al. 1984; Conti et al. 1996).

In critically ill patients, Tellias et al. (2020) reported a moderate to strong correlation between P_0.1 and PTP/min, findings corroborated by Rittayamai et al. (2017). Moreover, consistently in multiple studies, P_0.1 has shown moderate to high accuracy in detecting both excessive effort (PTP/min ≥ 200 cmH₂O s/min) and low effort (PTP/min ≤ 50 cmH₂O s/min) (Telias et al. 2020; Rittayamai et al. 2017; Pletsch-Assuncao et al. 2018). It should be noted that although various ICU ventilators can automatically measure P_0.1, its value may be underestimated, primarily due to the circuit length (Beloncie et al. 2019).

Multiple factors have been linked to variations in P_0.1. Physiological and clinical data have demonstrated a linear association between P_0.1 and parameters such as bilateral lung disease, the severity of acute respiratory distress syndrome (ARDS), PEEP and P_supp levels, along with blood oxygen and carbon-dioxide content (Spinelli et al. 2023; Mancebo et al. 2000; Iotti et al. 1996; Alberti et al. 1995; Mauri et al. 2016b). Conversely, P_0.1 does not appear to correlate with clinical scores of sedation, pain and delirium, although the influence of type and dose of analgesic and sedative drugs remains relevant (Dzierba et al. 2021).

An abnormally high or low respiratory drive may represent both an indicator of disease severity and a contributor to harmful effects, as previously described. Consequently, P_0.1 may hold prognostic value in predicting clinical outcomes. A recent meta-analysis demonstrated a significant association between P_0.1 and successful weaning, although substantial overlap in P_0.1 values between patients who were successfully weaned and those who were not did not permit the establishment of an accurate cutoff (Sato et al. 2021). Observational data have suggested an association between higher values of P_0.1 and reduced likelihood of successful weaning, as well as increased mortality (Le Marec et al. 2024). Interestingly, Bellani et al. (2010) showed that patients who failed a weaning trial had higher P_0.1 values and a lower increase in oxygen consumption compared with patients who succeeded, suggesting muscle weakness.

End-expiratory occlusion pressure (ΔP_occ)

ΔP_occ is the maximum airway pressure drop from PEEP observed during an expiratory hold (Figure 1, Panel B). During an end-expiratory occlusion manoeuvre, the inspiratory effort produces a reduction in P_aw that correlates with the swing in P_es (Bertoni et al. 2019). Unlikely P_0.1, ΔP_occ reflects inspiratory muscle contraction rather than respiratory drive, allowing clinicians to estimate P_L (P_L ≈ P_aw – 0.66 x ΔP_occ) and P_mus (P_mus ≈ - 0.75 x ΔP_occ) (Bertoni et al. 2019).

In a small cohort of patients, ΔP_occ was validated as a reliable indicator of PTP/min, and it showed strong predictive performance for elevated dynamic P_Land P_mus (Bertoni et al. 2019). A study involving fifteen COVID-19 patients further supported these findings (Roesthuis et al. 2021). More recently, De Vries et al. (2023) reported wide limits of agreement between ΔP_occ and P_es and P_di, although higher ΔP_occ values robustly predicted elevated P_L, outperforming P_0.1in estimating high respiratory effort.

These findings suggest that ΔP_occ may serve as a suitable, non-invasive index of inspiratory muscle effort. Consequently, combining measurements of P_0.1 and ΔP_occ might offer a comprehensive screening tool to identify patients at risk for either elevated or diminished respiratory effort, as well as for a dissociation between respiratory drive and effort, thereby informing the need for more accurate respiratory monitoring.

End-inspiratory occlusion pressure: pressure muscle index (PMI)

PMI is the difference between the plateau pressure (P_plat) and P_peak measured during an end-inspiratory occlusion manoeuvre in assisted ventilation. Following a circuit occlusion at the end of inspiration, the contracted inspiratory muscles relax and generate an elastic recoil pressure that is reflected in the plateau waveform of P_aw, resulting in a P_plat value that exceeds P_peak (Figure 1, Panel B) (Foti et al. 1997). Depending on the degree of the patient’s contribution to ventilation, P_plat may be lower than, equal to, or higher than P_peak.

Under passive mechanical ventilation, an inspiratory hold manoeuvre is used to assess the driving pressure (ΔP), which represents the effective pressure distending the lung parenchyma. ΔP is determined by the interplay between V_tand the mechanical properties of the respiratory system, and increased driving pressure values have been strongly correlated with lung injury and higher mortality rates in patients with ARDS (Amato et al. 2015).

PMI enables the estimation of ΔP even in spontaneous breathing (Figure 1), although its readability requires a stable plateau phase, which can be difficult or even impossible to achieve in many patients. Obtaining a reliable P_plat includes the recently proposed criteria: performing more than one occlusion, short time to reach the plateau (<1sec), sustained plateau duration (>2sec), and limited P_awvariation (<0.6 cmH₂O) (Bianchi et al. 2022). Nonetheless, even an unstable plateau waveform may be informative, suggesting increased respiratory effort or activation of expiratory muscles (Soundoulounaki et al. 2020). PMI has shown a reliable association with reference measures of respiratory effort. For instance, Bianchi et al. (2022) reported a significant correlation of PMI with PTP, as well as with P_mus. These results are consistent with findings from other studies evaluating PMI in both adult and paediatric populations (Gao et al. 2024; Kyogoku et al. 2021).

From a practical standpoint, evaluating PMI, and by extension ΔP, may serve as an indicator of excessive mechanical stress on the lung parenchyma, following pathophysiological mechanisms similar to those observed in passive ventilation. In addition, PMI values equal to or lower than zero may suggest excessively high ventilator assistance, characterising a “quasi-passive” patient-ventilator interaction (Docci et al. 2023). These observations highlight the potential utility of PMI as a tool for identifying scenarios of over-assistance, reduced respiratory effort, and respiratory muscle weakness, thereby underscoring the need for further research.

Conclusion

Pressure-supported mechanical ventilation carries both benefits and risks, making the implementation of a lung- and diaphragm-protective ventilation strategy essential, albeit challenging. Targeting safe ranges of inspiratory effort is a reasonable strategy when designing bedside algorithms aimed at protective ventilation. For this purpose, P_es-based methods are considered the gold standard, but their invasiveness, costs and discomfort prevent their widespread use in clinical practice. In contrast, P_0.1, ΔP_occ and PMI are increasingly demonstrating their reliability and usability in inferring patient respiratory effort. Their implementation in routine clinical practice may facilitate a more comprehensive assessment of a patient's condition and disease progression, particularly in distinguishing between extremes of ventilatory assistance and the patient's own breathing effort. However, their application should always be contextualised within the individual clinical scenario, recognising that different aetiologies of ARF and varying clinical phenotypes necessitate tailored management strategies.

Conflict of Interest

None.

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