Allowing spontaneous breathing with optimal inspiratory effort should be a priority in patients with acute respiratory failure under mechanical ventilation. Low and absent effort promote diaphragmatic dysfunction, creating difficulties in weaning, but also atelectasis and hypoxemia, while intense inspiratory efforts generate negative alveolar pressures and can induce lung (i.e., patient self-inflicted lung injury—P-SILI) and diaphragmatic injury (myotrauma) [1]. Low effort even occurs despite apparently spontaneous “triggered” breaths, because assisted ventilation deliver minimal minute ventilation once triggered. The transition from controlled to assisted ventilation can be associated with vigorous efforts in patients with hypoxemic failure, difficult to control [2]. In addition, lung injury and systemic inflammation are primers for P-SILI and myotrauma with excessive concentric or eccentric loading [1, 3]. Mechanisms of P-SILI include excessive global and regional lung stress (due to pendelluft) and increased transvascular pressure, and are directly associated with the magnitude and timing of inspiratory effort [3, 4]. There is also evidence of interaction between lung and other organs such as brain and kidneys. Therefore, monitoring respiratory drive and effort to adjust ventilatory settings and sedation seems necessary to achieve lung- and diaphragm-protective targets that should result in better clinical outcomes. This review describes the tools and the different parameters for monitoring respiratory effort, and suggests targets for respiratory drive and effort (Fig. 1).

Fig. 1
figure 1

Invasive and non-invasive monitoring of inspiratory effort and respiratory drive. Figure 1 shows representative traces from a mechanically ventilated ARDS patient resuming spontaneous breathing under pressure support ventilation (pressure support, 10 cmH2O; PEEP, 12 cmH2O; Flow-trigger sensitivity, 2 LPM). From top to bottom: flow, airway pressure [Paw], esophageal pressure [Pes] and transdiaphragmatic pressure [Pdi]). Two types of effort-related measurements are depicted: esophageal-pressure-derived measurements and non-invasive measurements. For invasive monitoring, esophageal pressure signal is needed. In panel A, the esophageal pressure swing (ΔPes), which represents the magnitude of inspiratory effort, is -13.8 cmH2O in the representative cycle. Muscular pressure (Pmus) generated by all the respiratory muscles is 19.7 cmH2O, calculated as the difference between chest wall elastic recoil pressure (Pcw = 5.9 cmH2O) and ΔPes during inspiration. Pcw is the product of tidal volume (VT = 578 ml in this cycle) and chest wall elastance (Ecw = 10.2 cmH2O/L). The integral of Pmus during inspiration corresponds to the esophageal pressure–time product or PTP which is 10 cmH2O*s in the same cycle. When gastric pressure (Pga) signal is also available (not shown in the Figure), the difference between Pga and Pes represents the transdiaphragmatic pressure (Pdi is 15.1 cmH2O in the same cycle). For non-invasive effort monitoring, inspiratory hold (Panel A) and end-expiratory occlusion (B) maneuvers are needed. During an inspiratory hold, (i.e., zero flow), a plateau Paw greater than the peak inspiratory pressure is observed, which accounts for the inspiratory effort. The difference between the plateau pressure and the peak inspiratory pressure is called pressure muscle index (PMI) and correlates with effort magnitude (in this example, PMI = 5.2 cmH2O). One should be aware that the activation of expiratory muscles during the inspiratory hold does not allow a reliable measurement of plateau Paw. On the other hand, during an end-expiratory occlusion, two variables may be obtained from the airway pressure signal: P0.1, which is the negative pressure measured during the first 100 ms of occlusion (in this cycle, – 3 cmH2O); and the occlusion pressure (Pocc), defined as the swing in airway pressure generated by respiratory muscle effort when the airway is briefly occluded (in the representative cycle, – 24.8 cmH2O). Pocc allows to estimate muscular pressure (with the formula Pmus =  – 0.75 × Pocc). Thus, estimated Pmus is 18.6 cmH2O. This Pmus value is concordant with the average (18.6 cmH2O) between the Pmus values directly measured using ΔPes and Pcw in panel A and B (19.7 and 17.5 cmH2O, respectively). Please note that the values of ΔPes and ΔPaw are similar during the end-expiratory occlusion test

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Monitoring inspiratory effort using esophageal pressure

Respiratory muscle contraction decreases pleural pressure and usually increases abdominal pressure (i.e., when the diaphragm works normally), generating a pressure gradient that drives gas into the lungs during spontaneous or assisted ventilation. Pleural and abdominal pressures, estimated from esophageal (Pes) and gastric (Pga) pressures, can measure respiratory muscles function and activity [5]. Transdiaphragmatic pressure (Pdi), i.e., difference between Pes and Pga, represents the pressure across the diaphragm. Changes in transdiaphragmatic (ΔPdi) and esophageal pressure (ΔPes), calculated as the positive (for Pdi) and negative (for Pes) change from the end-expiratory level, provide a simple estimate of the pressure generated by the diaphragm or all respiratory muscles (including so called “accessory” muscles often activated permanently or only with high drive), respectively [6]. ΔPes of –3 to –8 cmH2O [2], ΔPdi of > 3 to < 12 cmH2O have been proposed as safe targets [7]. A naso- or oro-gastric catheter with esophageal balloon needs to be inserted and connected to a commercially available monitor or to an additional ventilator port [5]. Proper positioning is confirmed with an occlusion test: a ratio of ΔPes to the change in airway pressure during a respiratory effort against a closed airway close to unity (0.8–1.2) indicates that the measured Pes provides a valid estimate of pleural pressure changes [5].

The gold standard to estimate global respiratory muscle effort is the calculation of the esophageal pressure–time product per minute (PTP/min) [8] correlating with energy expenditure of the respiratory muscles (see Fig. 1A). PTP is the integral of muscular pressure (Pmus) during inspiration and Pmus is the pressure generated by all the respiratory muscles, calculated as the difference between Pes and the chest wall elastic recoil pressure (Pcw) during inspiration. Pcw is the product of tidal volume and chest wall elastance (Ecw) (around 8 cmH2O/L in acute respiratory distress syndrome (ARDS)) [9]. Pcw should be ideally measured in passive conditions, but it can be estimated based on age, height, and gender when passive ventilation is not feasible. One should remember that PTP may be affected by expiratory muscles, which assist inspiration and reduce Pes when relaxing; measuring PTP is complex during asynchronies because one cannot rely on the flow signal anymore (indicating the ventilator activity, not the patient) [8]. Suggested safe values of PTP/min rely between 50 and 200 cmH2O*s/min. Possible target range for safe peak Pmus is between ≥ 5 and  < 15 cmH2O [8].

Monitoring respiratory drive and effort without esophageal pressure

Respiratory drive is the neural output of the respiratory centers in the brainstem that control the magnitude of inspiratory effort [6]. Airway occlusion pressure (P0.1) is a classical measure of respiratory drive that can be used to estimate the magnitude of breathing effort. When the airway is occluded, any change in pleural pressure is transmitted to the airways with equal magnitude and timing. P0.1 is the drop-in airway pressure (Paw) during the first 100 ms of an occluded breath. Modern ventilators can automatically and reliably measure or estimate P0.1 using different techniques and values lower than 1.0 cmH2O and higher 4.0 cmH2O have excellent diagnostic accuracy to detect low and excessively high magnitude of effort in critically ill patients (PTP/min < 50 and > 200 cmH2O*sec/min, respectively) despite frequent respiratory muscle dysfunction [10]. A P0.1 higher than 4.0 cmH2O correlated with failure to transition from a controlled to spontaneous mode of ventilation [11]. An average of 3 P0.1 values should be performed to consider breath-to-breath variability.

Absolute drop in Paw during a whole breath occlusion (Pocc) correlates with pleural pressures changes during the un-occluded tidal breaths and can be easily measured on ventilators by activating an end-expiratory occlusion maneuver (see Fig. 1B) [12]. When Pocc is multiplied by –0.75 and –0.66, Pmus and ΔPes from un-occluded tidal breaths can be estimated, respectively. Importantly, estimated ΔPes can be used to estimate dynamic driving transpulmonary pressure when added to the positive pressure delivered by the ventilator [12, 13]. Then, the clinician can determine the effect of adjusting the ventilator on effort but also on the risk of lung distension.

An end-inspiratory occlusion during assisted ventilation allows to measure a reliable plateau pressure (Pplat) if the respiratory muscles relax sufficiently during the maneuver (i.e., Pplat is flat, occurring in at least 75% of the occlusions (see Fig. 1A) [14]. Pplat represents the recoil pressure of the respiratory system at the insufflated volume and is higher than the tidal peak pressure. Indeed, it adds to the pressure from the ventilator, the contribution of the respiratory muscles to the overall driving pressure. The pressure muscle index (PMI) is the difference between Pplat and peak pressure and represents the contribution of respiratory muscles to the static overall distending pressure. If the Pplat is deemed reliable it can also be used to measure the overall static driving pressure which has been independently associated with increased risk of death in patients with ARDS during assisted mechanical ventilation [15].

Take-home message

Despite the clinical relevance of breathing effort during mechanical ventilation, for many years bedside monitoring has not been routinely performed because of a lack of simple, accurate tools for detection and quantification. Now several non-invasive tools have been developed and validated, allowing bedside implementation. It is time to start using them.