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Review Article
Anesthesiology Rehabilitating the diaphragm: an integrated approach to intensive care unit-acquired dysfunction in critical illness: a narrative review

DOI: https://doi.org/10.4266/acc.004375
Published online: March 4, 2026

1Unidad de Paciente Crítico, Hospital Las Higueras de Talcahuano, Talcahuano, Chile

2Escuela de Kinesiología, Universidad San Sebastián, Sede Tres Pascualas, Concepción, Chile

3Department of Surgical Sciences and Integrated Diagnostics, University of Genova, Genoa, Italy

4Anesthesia and Intensive Care, IRCCS Azienda Ospedaliera Metropolitana, Genoa, Italy

5Intensive Care Respiratory Physiotherapy, Rehabilitation and Functional Education, San Martino Policlinico Hospital, IRCCS for Oncology and Neurosciences, Genoa, Italy

6Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

Corresponding author: Denise Battaglini Department of Surgical Sciences and Integrated Diagnostics, University of Genova, Viale Benedetto XV, Genoa 16132, Italy Tel: +39-10-555-4970 E-mail: denise.battaglini@unige.it
• Received: September 18, 2025   • Revised: November 5, 2025   • Accepted: November 12, 2025

© 2026 The Korean Society of Critical Care Medicine

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Improved survival in critical illness has increased recognition of intensive care unit (ICU) complications, particularly ICU-acquired weakness, which affects up to 25% of patients. Diaphragm involvement is common and contributes to prolonged ventilation, difficult weaning, and worse outcomes. Dysfunction arises from ventilator-induced injury, sepsis-related myopathy, or both. Although early mobilization and physiotherapy improve recovery, their effectiveness is often limited by respiratory muscle fatigue and dyspnea. Non-invasive ventilation (NIV) reduces the work of breathing, sustains spontaneous effort, and enhances exercise tolerance, thereby facilitating earlier and safer rehabilitation. This review summarizes the current understanding of the pathophysiology of ICU-acquired diaphragm dysfunction. It explores the role of NIV and other respiratory supports as an adjunct to physiotherapy aimed at optimizing recovery in critically ill patients.
  • Key Words: intensive care unit-acquired dysfunction; intensive care unit-acquired weakness; non-invasive ventilation; physical therapy modalities; ventilator-induced diaphragmatic dysfunction
Advances in critical care have substantially improved survival in critically ill patients; however, prolonged intensive care unit (ICU) stays are frequently accompanied by complications that impair recovery and long-term outcome [1]. Neuromuscular dysfunction develops in up to 80% of ICU patients [2], arising from neurogenic, myogenic, or mixed mechanisms [3]. ICU-acquired weakness (ICUAW), characterized by diffuse and symmetrical weakness of limb and respiratory muscles, typically sparing ocular and facial muscles, affects nearly 40% of ICU patients and is associated with prolonged mechanical ventilation (MV), delayed weaning, extended hospital stays, and impaired quality of life [3,4]. Notably, reduced lower limb strength is independently associated with extubation failure [5]. The injury associated with critical illness involves not only the lungs and peripheral musculature but also the diaphragm [6]. Diaphragmatic weakness (DW) and consequent dysfunction (DD) may result from excessive sedation, inappropriate levels of mechanical ventilatory assistance—either over- or under-assistance—and from the systemic inflammatory processes associated with critical illness and sepsis [7]; such injury has been linked to poorer weaning outcomes, increased in-hospital morbidity, and higher mortality [8].
Early mobilization and physical therapy improve functional status, muscle strength, and quality of life while reducing complications from immobility [9]. Despite concerns about safety and ventilatory stability during mechanical MV [10]; several studies confirm its feasibility, with adverse event rates below 3%, mostly related to transient instability within the first 72 hours after ICU admission [11,12]. Consequently, fewer than 10% of MV patients achieve out-of-bed mobilization, and physical therapy is often postponed until after weaning [13,14]. Persistent post-extubation dyspnea further limits participation in rehabilitation [15]. In this context, non-invasive ventilation (NIV) can play a key role by enhancing oxygenation, reducing respiratory muscle load, and alleviating dyspnea, thereby enabling earlier and more effective rehabilitation in critically ill patients [15].
The aim of this review is to summarize current evidence on the pathophysiology, assessment, and management of ICU-acquired DD, with a particular focus on the role of NIV as an adjunct to physiotherapy and early rehabilitation.
This narrative review was conducted following standards for evidence synthesis in non-systematic reviews. A structured search was performed in PubMed and Medline covering studies published between 2000 and 2025, using combinations of the following keywords: “ICU-acquired diaphragm dysfunction,” “intensive care unit-acquired weakness,” “physical therapy, mobilization, or rehabilitation modalities,” “non-invasive ventilation,” and “ventilator-induced diaphragmatic dysfunction.” Only original clinical or experimental studies and systematic reviews involving adult ICU populations were considered. Each article was examined for methodological design, population characteristics, and contribution to understanding the role of NIV as an adjunct to rehabilitation. The evidence was critically appraised and synthesized to integrate physiological mechanisms, therapeutic rationale, and clinical applicability.
ICUAW and DD
ICUAW—characterized by weakness of limb and respiratory muscles—is clinically defined by a Medical Research Council sum score below 48 in the absence of alternative explanations beyond critical illness [16,17]. Risk factors include prolonged MV, use of neuromuscular blocking agents or corticosteroids, sepsis, malnutrition, and immobility [1]. These factors promote skeletal muscle catabolism, disuse atrophy, and respiratory muscle dysfunction, which collectively contribute to adverse clinical outcomes [17-19].
From Controlled to Assisted MV: Pathways to Diaphragm Injury
The diaphragm is the principal inspiratory muscle, and its function is typically assessed by its force-generating capacity, measured through inspiratory pressures, or by structural and functional changes, such as thickening, variations in lung volume, or chest wall displacement [20,21]. Effective diaphragm shortening occurs when respiratory workload is appropriate, respiratory drive is sufficient, and the diaphragm is strong, all of which are associated with successful weaning from MV [22]. DW is defined as the inability to generate normal maximal force [7,23]; it is often underdiagnosed but affects 60%–80% of critically ill patients [24]. DW is a marker of disease severity, associated with prolonged weaning, increased ICU mortality, and poor long-term outcomes [24-26]. In patients with acute respiratory distress syndrome, diaphragmatic impairment can persist for years, contributing to long-term respiratory disability [27]. DW may preexist ICU admission or develop during critical illness. Two ICU-acquired conditions contribute to DW: ventilator-induced diaphragmatic dysfunction (VIDD), caused by MV, and sepsis-induced diaphragm dysfunction (SIDD), triggered by systemic inflammation [28,29]. If, during the first 48 hours of MV, more than 25% of the total breaths are fully controlled by the ventilator (i.e., patient not contributing spontaneous effort), this level of controlled MV is associated with rapid diaphragm atrophy—loss of diaphragmatic muscle thickness and contractile capacity [30]. VIDD and SIDD involve overlapping molecular mechanisms, including oxidative stress, mitochondrial dysfunction, enhanced proteolysis, and impaired protein synthesis [31-33]. These processes contribute to myotrauma, prolonged MV, and global muscle dysfunction, with DW after several days of MV strongly predicting weaning failure [24-26]. In relation to VIDD [34], respiratory overexertion represents another pathway of injury, typically emerging during sedation discontinuation and the shift from controlled to pressure-support spontaneous ventilation [35]. Overstimulation of the respiratory centers may occur because of mechanical, metabolic, or gasometric disturbances. This can generate excessive efferent activity to the diaphragm, leading, on one hand, to potentially injurious diaphragmatic contractions and, on the other, to possible lung tissue damage due to the generation of large tidal volumes (VTs) in shunt regions [36], which are not associated with effective lung recruitment [36]. This phenomenon, known as pendelluft [36], could be responsible for the patient self-inflicted lung injury (P-SILI). P-SILI results from spontaneous breathing efforts in critically ill patients [37], and may contribute to weaning failure [38]. In summary, excessive respiratory effort can cause both pulmonary and DD, leading to dyspnea and potentially contributing to post-traumatic stress in affected patients [39]. Higher negative pleural pressure can lead to the development of microvascular injury and negative pressure pulmonary edema [40]. This condition increases the transvascular pressure gradient, promoting venous congestion within the lung parenchyma and resulting in shunt-type areas of perfusion without effective ventilation [40].
DD associated with critical illness may develop within 18 hours of MV. Histological studies have shown a marked reduction in both type I and type II muscle fibers, with a predominant loss of type II fibers [41]. From a pathophysiological perspective, the reduction in diaphragmatic contractile strength that characterizes DD is associated with a loss of myofibrillar protein content, structural disorganization of the diaphragm, and alterations in excitation–contraction coupling as well as in the super-relaxed state of myosin [41]. DD may result from eccentric diaphragmatic contractions occurring when the ventilator initiates expiration before the neural inspiratory phase has ended, as seen in patient–ventilator asynchronies such as reverse triggering or premature cycling [42].
Clinical indicators of DW and DD include abdominal paradox breathing, elevated rapid shallow breathing index, radiographic signs of hemidiaphragm elevation, and possibly the Hoover’s sign, which may be detectable during deep inhalation. Diagnosis is one of exclusion, requiring consideration of endocrine or electrolyte disturbances (e.g., hypophosphatemia, hypomagnesemia, hypocalcemia, hypothyroidism) [43,44]. The gold standard for assessing diaphragm strength is transdiaphragmatic twitch pressure elicited via bilateral anterior magnetic phrenic nerve stimulation. Surrogates, such as twitch pressure measured at the endotracheal tube, diaphragm electromyography, and neurally adjusted ventilatory assist, allow bedside monitoring of diaphragmatic activity [45]. However, these strategies require specific equipment, limiting their applicability in daily clinical practice. Simpler bedside approaches focus on monitoring the patient during spontaneous inspiratory efforts by applying an expiratory pause and assessing effort-related pressure changes [46]. A negative inspiratory force (also referred to as maximum inspiratory pressure) below 30 cm H2O—reflecting impaired inspiratory muscle strength—is associated with extubation failure, prolonged ICU stay, and higher 1-year mortality. This measurement requires the patient to perform an active maximal inspiratory effort against an occluded airway and is therefore applicable only in cooperative patients with spontaneous breathing activity [7]. Other simple bedside techniques, like P0.1, occlusion pressure (POCC), and inspiratory muscle pressure can be assessed in patients exhibiting spontaneous breathing activity, even if they are not fully cooperative [39]. P0.1 represents the airway pressure drop during the first 100 ms of an occluded inspiration, with cutoff values between 1 and 4 cm H2O. POCC is the pressure drop during a fully occluded inspiratory effort, typically ranging from −4 to −20 cm H2O. Predicted muscle pressure (PMUS,pred) can be estimated as POCC ×0.75, with expected values between 3 and 15 cm H2O [47]. Values below the lower limit indicate over-assistance, whereas values above the upper limit reflect excessive diaphragmatic load—both conditions potentially contributing to DD [47]. Another bedside tool is ultrasonography, which provides a non-invasive, real-time assessment of diaphragmatic structure and function. Key parameters include the diaphragmatic thickening fraction (TFdi) and diaphragmatic excursion measured in M-mode [48]. Diagnostic criteria for DW via ultrasound include diaphragmatic atrophy (thickness <1.5 mm at end-expiration), reduced contractility (TFdi <30%–34%, with <20% indicating severe weakness), and abnormal excursion (<10 mm or paradoxical movement). Through this monitoring, the aim will be to achieve a balance that is gentle on both the lung and the diaphragm (Figure 1) [44]. Diaphragmatic atrophy impairs respiratory function, complicating weaning from MV [44]. Ultrasound enables early detection of diaphragm changes, underscoring the importance of targeted interventions to preserve strength [49].
From Assisted Ventilation to Active Stimulation: Novel Tools to Preserve Diaphragm Function
Regarding therapeutic tools, adjusting ventilatory support to maintain diaphragm activity—such as reducing pressure support or using proportional assist ventilation—can prevent atrophy and reduce oxygen consumption during physical therapy [50]. Recent evidence suggests using transvenous phrenic nerve stimulation. This technique delivers electrical stimulation to the phrenic nerve during controlled MV, reducing diaphragmatic inactivity and potentially preventing disuse-induced DD [51]. In addition, inspiratory muscle training (IMT) has emerged as a promising adjunctive strategy: an exploratory study in patients with weaning difficulties showed increased inspiratory effort and respiratory muscle activation during IMT [52]; furthermore, a 2024 systematic review and meta-analysis demonstrated that both low-medium and high-intensity threshold IMT prevented DD and shortened weaning duration [53], while a 2025 systematic review found that IMT significantly increased maximum inspiratory pressure and reduced rapid shallow breathing index, although without a conclusive effect on weaning success [54]. Collectively, these approaches may shorten MV duration and enhance overall recovery in critically ill patients [55].
Rehabilitation Strategies to Counteract ICU-Acquired DD
Rehabilitation, including early mobilization, is a cornerstone intervention for mitigating ICU-acquired DD and is strongly recommended for critically ill patients, particularly those experiencing difficult or prolonged weaning from MV. Strategies such as patient positioning and mobilization improve ventilation-perfusion (V’/Q’) matching by exploiting gravitational forces to facilitate alveolar recruitment and enhance regional perfusion [56]. Early mobilization has been associated with shorter hospital stays and improved functional outcomes post-discharge. Mobilization protocols should ideally initiate within 24–72 hours of ICU admission to prevent complications associated with prolonged immobility [57]. Candidates for early mobilization should be cooperative, minimally sedated, and either spontaneously breathing or supported by NIV for at least 48 hours [58,59]. In uncooperative patients, prolonged passive range of motion (PROM) exercises or cycle ergometry can help preserve joint mobility and muscle integrity. Brief passive movements alone may not be effective; a systematic review already highlighted more than a decade ago the potential role of prolonged PROM in critically ill patients [60], and recent evidence confirms that standard passive movements may not prevent stiffness, while structured and continued PROM within early mobilization protocols is associated with better preservation of muscle and joint function [61].
Respiratory exhaustion remains a primary barrier to initiating rehabilitation in the ICU [62], with dyspnea frequently reflecting fatigue secondary to VIDD [63,64]. Exercise-induced diaphragmatic fatigue, defined as a decline in diaphragmatic function due to increased respiratory load [64], triggers activation of group III/IV metaboreceptors in the respiratory muscles. This respiratory muscle metaboreflex increases sympathetic vasoconstriction, reduces limb perfusion, limits exercise performance, and intensifies perceived exertion (Figure 2) [65].
For those ICU patients who can stand and walk, 6-minute walk test (6MWT) can be considered, as its performance correlates with the severity of dyspnea and fatigue [66]. In patients recovering from coronavirus disease 2019 (COVID-19) pneumonia, abnormal lung ultrasound scores were associated with oxygen desaturation during the 6MWT, an impairment that persisted for up to 15 months after discharge [66]. In critically ill patients with limited ability to move, simpler bedside functional assessments such as the 30-second sit-to-stand test have demonstrated favorable clinometric properties—including validity and responsiveness at ICU and hospital discharge—making it a practical surrogate for functional capacity when the 6MWT is not feasible in that setting. In both settings, NIV may support mobilization by reducing dyspnea and increasing patient tolerance to exercise [67].
NIV as a Bridge between Ventilatory Support and Early Rehabilitation
Within the framework of early rehabilitation aimed at minimizing the deleterious effects of bed rest, the use of NIV during rehabilitation sessions represents a physiologically grounded approach to facilitate mobilization by unloading the respiratory muscles, improving gas exchange, and attenuating exercise-induced diaphragmatic fatigue. By reducing respiratory effort and dyspnea, NIV enables patients with limited ventilatory reserve to engage in active rehabilitation earlier and more effectively, thereby potentially accelerating recovery and shortening the duration of MV and ICU stay. NIV reduces the work of breathing (WOB), improves dynamic lung compliance [68], promotes alveolar recruitment by increasing functional residual capacity, and alleviates respiratory muscle fatigue and exertional dyspnea, thereby enhancing exercise tolerance [69]. By unloading the respiratory muscles, NIV preserves oxygen delivery to peripheral musculature and reduces the sensation of breathlessness [70]. Assessment of WOB, the energy expenditure per respiratory cycle, can identify excessive respiratory effort or underlying muscle weakness; low WOB may reflect over-assistance or oversedation, whereas high WOB indicates under-assistance or excessive effort, potentially leading to P-SILI [71]. Muscle unloading occurs via two primary mechanisms: (1) reduction in inspiratory effort and (2) decreased muscular workload to achieve a given VT during assisted ventilation [72]. These effects may counteract respiratory muscle fatigue, attenuate excessive neural respiratory drive, and improve inspiratory muscle function and global pulmonary performance (Figure 3) [73]. In this context, strict attention should be paid to preventing P-SILI, especially in patients with non-chronic obstructive pulmonary disease (COPD) etiologies such as acute pulmonary edema or severe pneumonia, where uncontrolled inspiratory effort during NIV may aggravate lung injury. These patients should undergo early rehabilitation only when hemodynamically and respiratory stable, with close monitoring of drive and effort. In this sense, there is a clear link between the physiological mechanisms described and the use of NIV. Adjusting the level of assistance during physical exercise may help maintain both lung- and diaphragm-protective targets, enabling patients to safely achieve higher exercise intensity within post-extubation rehabilitation programs.
Clinical Evidence Supporting NIV during Rehabilitation
The literature on NIV as an adjunct to rehabilitation has expanded considerably over the past two decades. A key advantage of NIV is the preservation of spontaneous ventilation and diaphragm activity [74]. Studies consistently show that NIV can improve exercise tolerance, reduce dyspnea, and preserve diaphragm activity [75]. A Cochrane review and a randomized trial conducted in patients with chronic respiratory failure demonstrated that combining NIV with exercise training enhanced endurance and reduced perceived exertion compared with training alone [75,76]. More recent work confirmed these findings in hypercapnic COPD using high-intensity NIV during exercise, improving ventilatory efficiency and tolerance [77]. NIV during physical therapy enhances exercise performance and quality of life in patients with COPD [78].
NIV can also be integrated into respiratory physiotherapy for patients with reduced inspiratory effort secondary to VIDD, thereby enhancing airway clearance and improving lung capacity [79]. When applied continuously during exercise training, NIV has been shown to reduce dyspnea, increase endurance, and enhance walking distance and exercise intensity [69,72,73]. In a recent systematic review and network meta-analysis, NIV significantly improved 6MWT distance, peak work rate, VO2 peak, VT, minute ventilation, and lactate clearance in patients with stable COPD [80]. Recent evidence regarding the titration of ventilatory support pressure, based on the dynamic respiratory effort of the critically ill patient, has been shown to provide a protective strategy for both the lung and the diaphragm [81]. If close monitoring of ventilatory effort is added to this, there could be results that generate this double gain in mitigating damage to the diaphragm and lung [82].
Bilevel positive airway pressure is commonly employed in acute exacerbations of COPD, as post-extubation support, and during the weaning process in patients with hypercapnic respiratory failure [83]. In patients treated with NIV for an average of three days, significant improvements in gas exchange and respiratory mechanics have been reported, including correction of respiratory acidosis and increases in forced vital capacity. Ultrasonographic monitoring has further demonstrated preservation of diaphragm structure and function through maintenance of the diaphragm shortening fraction [84].
Beyond COPD, the role of NIV extends to both acute and chronic cardio-respiratory failure [85]. In the acute setting, studies in ICU and post-extubation patients highlight that NIV helps maintain spontaneous breathing, unloads respiratory muscles, and supports early mobilization while reducing reintubation risk [86]. Specific guidelines recommend its use to prevent post-extubation respiratory failure in patients with ICUAW [87]. In this context, the physiological mechanisms of NIV—muscle unloading, improved oxygenation, and preserved diaphragmatic excursion—are directly relevant to mitigating ICU-acquired diaphragm dysfunction and facilitating safe early mobilization. Across different modalities, NIV has consistently improved exercise tolerance and reduced exertional dyspnea during rehabilitation [83].
However, in critically ill patients, the use of NIV must be individualized, as ICU-acquired DD most frequently develops in patients who have undergone invasive MV and for whom NIV is not universally indicated [88]. In this context, NIV may be considered in selected post-extubation patients presenting with persistent DW, borderline pulmonary function, or early-onset dyspnea that limits participation in rehabilitation [89]. These patients may benefit from NIV as an adjunct to physical therapy to unload the respiratory muscles, reduce the perception of effort, and enable safer exercise performance [90]. To clarify this clinical scenario, Figure 4 illustrates patient selection criteria for the use of NIV during physical rehabilitation, with emphasis on factors related to post-extubation DW and safety thresholds to prevent P-SILI [91]. P-SILI has gained increasing attention as a mechanism of lung damage in spontaneously breathing or NIV-supported patients. During NIV, excessive inspiratory effort and high negative pleural pressure may generate elevated transpulmonary pressures and pendelluft phenomena, resulting in volutrauma, barotrauma, and microvascular injury, as observed in severe pneumonia and COVID-19. Therefore, early rehabilitation under NIV should be limited to carefully selected patients with stable gas exchange and controlled respiratory drive, while those with acute pulmonary edema or severe parenchymal injury require cautious monitoring or may not be suitable candidates [91,92].
Monitoring and Safety Considerations during NIV-Assisted Rehabilitation
At the bedside, NIV monitoring requires continuous assessment of respiratory rate, patient-generated VT, and respiratory effort. The HACOR score, which incorporates heart rate, acidosis (arterial pH), consciousness level, oxygenation (PaO2/FiO2), and respiratory rate, has been validated as a predictor of NIV failure and the need for escalation to invasive MV [93,94]. A score >5 after one hour of NIV is strongly associated with treatment failure, particularly in acute respiratory failure due to COPD exacerbations, acute pulmonary edema, or pneumonia [94].
Quantifying WOB during NIV is challenging because the system is open to leaks and lacks a sealed circuit for direct airway pressure measurement, indexed either per volume (J/L) or per minute:
WOBvolume=WOBbreath/VT
WOBminute=WOBbreath×respiratory rate
However, these indices have important limitations. If an inspiratory effort fails to generate a VT (e.g., ineffective efforts or patient–ventilator asynchrony), WOB may appear falsely as zero despite substantial energy expenditure. Similarly, inspiratory work performed to overcome auto-PEEP during the isometric phase of inspiration (before flow generation) is not captured by WOB calculations. For this reason, the esophageal pressure-time product (PT-Pes), obtained via esophageal balloon catheter, is considered a more accurate surrogate of total respiratory muscle effort. PT-Pes integrates esophageal pressure over the entire inspiratory contraction and reflects the combined activity of all inspiratory muscles, including the diaphragm and intercostals [95]. Excessive inspiratory effort may increase transpulmonary and transvascular pressures, predisposing to P-SILI [40]. To minimize this risk, strict monitoring is recommended, targeting VT <8 ml/kg predicted body weight, esophageal pressure swings <10 cm H2O, and a respiratory rate <30 breaths/min [96,97].
Other techniques include ultrasound assessment of TFdi during NIV, which provides a non-invasive indicator of respiratory effort. A TFdi between 15%–30% typically corresponds to adequate diaphragm activation, while values 15%-20% suggest over-assistance and >40% excessive load [98,99]. Further, in research or specialized centers, diaphragmatic electromyography—via surface or nasogastric electrodes—offers a dynamic estimate of neural respiratory drive during NIV, though not yet standard in routine practice [100-102].
NIV Delivery Systems and Practical Considerations in the ICU
During early mobilization or exercise, effective ventilatory assistance requires maintaining synchrony and minimizing air leaks to ensure consistent unloading of the respiratory muscles. Oro-nasal or full-face masks are generally preferred for this purpose, as they limit leaks and optimize pressure delivery when ventilatory demand rises [85]. Notably, a substantial proportion of ICU patients undergo tracheostomy as a consequence of difficult or prolonged weaning, typically defined as the inability to sustain spontaneous breathing after multiple failed attempts or more than seven days of weaning trials. In these patients, tracheostomy facilitates gradual liberation from MV by reducing dead space, airway resistance, and the WOB, while improving secretion management and comfort [103]. As respiratory function recovers, many tracheostomized patients reach a transitional stage: they can breathe spontaneously for part of the day but still experience limited ventilatory reserve or residual DW, predisposing them to fatigue during exercise or early mobilization.
At this stage, complete discontinuation of ventilatory support may expose the diaphragm to excessive load and promote reintubation or weaning failure. Conversely, non-invasive ventilatory assistance—delivered via face mask or through the tracheostomy—can provide physiological unloading of the respiratory muscles while allowing the patient to engage in progressive physical therapy [104]. In this way, tracheostomy NIV serves as an intermediate step between invasive ventilation and full spontaneous breathing, ensuring adequate gas exchange and respiratory muscle protection during active rehabilitation [105]. From a technical standpoint, NIV can be administered either directly through the tracheostomy cannula, using a single-limb circuit with the leak port positioned close to the cannula to ensure adequate exhalation [106]; or via a face mask, with the tracheostomy capped and cuff deflated. The use of an early speaking valve (e.g., Passy Muir or one-way valve), may reduce airway obstruction and alleviate symptoms of vocal cord dysfunction by restoring upper airway patency, facilitating subglottic pressure, improving swallowing and airway protection, and ultimately aiding mobilization and decannulation [107]. Dual-limb ventilators generally provide superior leak compensation and are therefore preferred for tracheostomized patients [108]. When face-mask NIV is well tolerated under these conditions, and clinical stability is achieved, decannulation may be considered [108]. In this context, alternative interfaces such as helmet continuous positive airway pressure have also been evaluated, with recent evidence comparing turbine-driven ventilators and Venturi devices demonstrating their feasibility and performance [109]. Modern NIV devices also allow adjustment of rise time, enabling clinicians to tailor the pressure support ramp-up and improve patient comfort. Their compact and portable design facilitates early mobilization, including ambulation out of bed [64]. In this sense, tracheostomy NIV should not be viewed as a separate technique, but rather as a continuum within the broader NIV-assisted rehabilitation strategy. Both share the same physiological rationale—respiratory muscle unloading, preservation of diaphragmatic function, and facilitation of active mobilization—while differing only in the interface and timing along the patient’s recovery trajectory.
Beyond NIV: Complementary Non-invasive Strategies Post-Extubation
Although NIV offers well-documented physiological advantages, its use requires substantial resources, clinician expertise, and patient cooperation. Nocturnal NIV, combining ventilatory support during sleep with daytime exercise training, has been proposed as a practical approach to enhance exercise tolerance without the logistical challenges of delivering NIV during active rehabilitation sessions [17]. High-flow nasal cannula is generally easier to administer and better tolerated than NIV; however, current evidence does not support its superiority over NIV in terms of clinical outcomes. Notably, alternating NIV with high-flow nasal cannula immediately after extubation has been associated with lower reintubation rates [110] and reduced ICU length of stay [110].
ICU-acquired diaphragm dysfunction significantly impairs respiratory function, complicates weaning from MV, and contributes to prolonged ICU stays and adverse patient outcomes. Early recognition and systematic assessment of diaphragm dysfunction, combined with tailored interventions such as early mobilization and physical therapy, are essential to mitigate muscle atrophy and improve recovery. NIV represents an important adjunct to rehabilitation by unloading respiratory muscles, reducing dyspnea, and improving exercise tolerance. Although its application during physiotherapy requires technical expertise and additional resources, evidence supports its role in preserving diaphragmatic function and facilitating earlier mobilization in critically ill patients. Future studies should aim to define standardized protocols for NIV integration into rehabilitation programs to optimize functional outcomes and reduce ICU-related disability.
▪ Intensive care unit (ICU)-acquired diaphragm dysfunction is prevalent and contributes to prolonged mechanical ventilation, weaning failure, and poor outcomes in critically ill patients.
▪ Non-invasive ventilation reduces respiratory muscle workload and dyspnea, improving patient participation in early mobilization and physical therapy.
▪ Incorporating non-invasive ventilation into rehabilitation protocols may preserve diaphragm function and enhance functional recovery, supporting its use as an adjunctive strategy in ICU care.

CONFLICT OF INTEREST

No potential conflict of interest relevant to this article was reported.

FUNDING

None.

ACKNOWLEDGMENTS

None.

AUTHOR CONTRIBUTIONS

Conceptualization: RA, AP, NAP, DB. Methodology: NAP, PRMR, DB. Writing – original draft: RA, AP, DB. Writing – review & editing: DN, FG, VF, PRMR, DB. All authors read and agreed to the published version of the manuscript.

Figure 1.
Protective mechanical ventilation (MV) for lung and diaphragm. In this figure, cutoff values are proposed in relation to measurements that can be carried out both in any MV device and through ultrasonography, which together will allow the clinician to safeguard a protective MV not only avoiding pulmonary injury induced by MV, but also avoiding diaphragmatic injury, especially during the transition to ventilatory spontaneity. VT: tidal volume; PBW: predicted body weight; ARDS: acute respiratory distress syndrome; iPEEP: intrinsic positive end-expiratory pressure; PaCO2: arterial partial pressure of carbon dioxide; TFdi: diaphragmatic thickening fraction; ΔPes: esophageal pressure swing; ΔPdi: transdiaphragmatic pressure swing; PMUS,pred: predicted inspiratory muscle pressure; POCC: occlusion pressure; P0.1: airway occlusion pressure at 100 ms.
acc-004375f1.jpg
Figure 2.
Respiratory muscle metaboreflex. Early respiratory muscle fatigue activates afferent signaling through the phrenic nerve, eliciting sympathetic vasoconstriction in the limbs. This response reduces oxygen delivery to locomotor muscles, exacerbates peripheral fatigue, and ultimately limits tolerance and progression during physical therapy. VO2: oxygen consumption.
acc-004375f2.jpg
Figure 3.
Effect of non-invasive ventilation (NIV) during physical therapy: by unloading the respiratory muscles, NIV decreases oxygen consumption (VO2) and delays activation of the metaboreflex, thereby improving exercise tolerance and facilitating participation in physical therapy among critically ill patients.
acc-004375f3.jpg
Figure 4.
Selection of non-invasive ventilation (NIV) candidate patients during rehabilitation in the intensive care unit (ICU). This figure emphasizes the need to select the appropriate patient to use NIV as an adjuvant to physical therapy during the rehabilitation process in the ICU. Special mention is made of factors related to diaphragmatic weakness after extubation, a factor that could lead to the early onset of the metabolic reflex. In addition, safety values are proposed to be observed during physical therapy, to prevent the appearance of eventual patient self-inflicted lung injury (P-SILI) during this therapeutic act. TFdi: diaphragmatic thickening fraction; MIP: maximum inspiratory pressure; NIF: negative inspiratory force; IPAP: inspiratory positive airway pressure; EPAP: expiratory positive airway pressure; CPAP: continuous positive airway pressure; FiO2: fraction of inspired oxygen; ARDS: acute respiratory distress syndrome; VT: tidal volume; ΔPes: esophageal pressure swing; SpO2: peripheral oxygen saturation.
acc-004375f4.jpg
  • 1. Ji HM, Won YH. Early mobilization and rehabilitation of critically-ill patients. Tuberc Respir Dis (Seoul) 2024;87:115-22.ArticlePubMedPMCPDF
  • 2. Jolley SE, Bunnell AE, Hough CL. ICU-acquired weakness. Chest 2016;150:1129-40.ArticlePubMedPMC
  • 3. Vanhorebeek I, Latronico N, Van den Berghe G. ICU-acquired weakness. Intensive Care Med 2020;46:637-53.ArticlePubMedPMCPDF
  • 4. Fan E, Cheek F, Chlan L, Gosselink R, Hart N, Herridge MS, et al. An official American Thoracic Society clinical practice guideline: the diagnosis of intensive care unit-acquired weakness in adults. Am J Respir Crit Care Med 2014;190:1437-46.ArticlePubMed
  • 5. Thille AW, Boissier F, Muller M, Levrat A, Bourdin G, Rosselli S, et al. Role of ICU-acquired weakness on extubation outcome among patients at high risk of reintubation. Crit Care 2020;24:86.ArticlePubMedPMCPDF
  • 6. Goligher EC, Dres M, Patel BK, Sahetya SK, Beitler JR, Telias I, et al. Lung- and diaphragm-protective ventilation. Am J Respir Crit Care Med 2020;202:950-61.ArticlePubMedPMC
  • 7. Dres M, Goligher EC, Heunks LM, Brochard LJ. Critical illness-associated diaphragm weakness. Intensive Care Med 2017;43:1441-52.ArticlePubMedPDF
  • 8. Laffey CM, Sheerin R, Khazaei O, McNicholas BA, Pham T, Heunks L, et al. Impact of frailty and older age on weaning from invasive ventilation: a secondary analysis of the WEAN SAFE study. Ann Intensive Care 2025;15:13.ArticlePubMedPMCPDF
  • 9. Schaller SJ, Scheffenbichler FT, Bein T, Blobner M, Grunow JJ, Hamsen U, et al. Guideline on positioning and early mobilisation in the critically ill by an expert panel. Intensive Care Med 2024;50:1211-27.ArticlePubMedPDF
  • 10. González-Seguel F, Camus-Molina A, Jasmén A, Molina J, Pérez-Araos R, Graf J, et al. Respiratory support adjustments and monitoring of mechanically ventilated patients performing early mobilization: a scoping review. Crit Care Explor 2021;3:e0407. ArticlePubMedPMC
  • 11. Parada-Gereda HM, Merchán-Chaverra R, Medina-Parra J, Benavides-Cruz J, Gaitán-Duarte H. Safety of early mobilisation in the intensive care unit: a prospective and multicentre cohort study protocol. BMJ Open 2025;15:e101772. ArticlePubMedPMC
  • 12. Paton M, Chan S, Serpa Neto A, Tipping CJ, Stratton A, Lane R, et al. Association of active mobilisation variables with adverse events and mortality in patients requiring mechanical ventilation in the intensive care unit: a systematic review and meta-analysis. Lancet Respir Med 2024;12:386-98.ArticlePubMed
  • 13. Nydahl P, Ewers A, Brodda D. Complications related to early mobilization of mechanically ventilated patients on intensive care units. Nurs Crit Care 2016;21:323-33.Article
  • 14. Marra A, Ely EW, Pandharipande PP, Patel MB. The ABCDEF bundle in critical care. Crit Care Clin 2017;33:225-43.ArticlePubMedPMC
  • 15. Waters A, Hill K, Jenkins S, Johnston C, Mackney J. Discordance between distance ambulated as part of usual care and functional exercise capacity in survivors of critical illness upon intensive care discharge: observational study. Phys Ther 2015;95:1254-63.ArticlePubMedPDF
  • 16. Hiser SL, Casey K, Nydahl P, Hodgson CL, Needham DM. Intensive care unit acquired weakness and physical rehabilitation in the ICU. BMJ 2025;388:e077292. ArticlePubMed
  • 17. Chen J, Huang M. Intensive care unit-acquired weakness: recent insights. J Intensive Med 2024;4:73-80.ArticlePubMed
  • 18. Dennis CJ, Menadue C, Schneeberger T, Leitl D, Schoenheit-Kenn U, Harmer AR, et al. Perceptions of noninvasive ventilation during exercise in noninvasive ventilation-naïve patients with COPD. Respir Care 2022;67:543-52.ArticlePubMed
  • 19. Latronico N, Rasulo FA, Eikermann M, Piva S. Illness weakness, polyneuropathy and myopathy: diagnosis, treatment, and long-term outcomes. Crit Care 2023;27:439.ArticlePubMedPMC
  • 20. Goligher EC, Dres M, Fan E, Rubenfeld GD, Scales DC, Herridge MS, et al. Mechanical ventilation-induced diaphragm atrophy strongly impacts clinical outcomes. Am J Respir Crit Care Med 2018;197:204-13.ArticlePubMed
  • 21. Marques MR, Pereira JM, Paiva JA, de Casasola-Sánchez GG, Tung-Chen Y. Ultrasonography to access diaphragm dysfunction and predict the success of mechanical ventilation weaning in critical care: a narrative review. J Ultrasound Med 2024;43:223-36.ArticlePubMed
  • 22. Blumhof S, Wheeler D, Thomas K, McCool FD, Mora J. Change in diaphragmatic thickness during the respiratory cycle predicts extubation success at various levels of pressure support ventilation. Lung 2016;194:519-25.ArticlePubMedPDF
  • 23. Le Stang V, Latronico N, Dres M, Bertoni M. Critical illness-associated limb and diaphragmatic weakness. Curr Opin Crit Care 2024;30:121-30.ArticlePubMedPMC
  • 24. Panahi A, Malekmohammad M, Soleymani F, Hashemian SM. The prevalence and outcome of intensive care unit acquired weakness (ICUAW). Tanaffos 2020;19:250-5.PubMedPMC
  • 25. Jung B, Moury PH, Mahul M, de Jong A, Galia F, Prades A, et al. Diaphragmatic dysfunction in patients with ICU-acquired weakness and its impact on extubation failure. Intensive Care Med 2016;42:853-61.ArticlePubMedPDF
  • 26. Supinski GS, Callahan LA. Diaphragm weakness in mechanically ventilated critically ill patients. Crit Care 2013;17:R120.ArticlePubMedPMCPDF
  • 27. Fazzini B, Battaglini D, Carenzo L, Pelosi P, Cecconi M, Puthucheary Z, et al. Physical and psychological impairment in survivors of acute respiratory distress syndrome: a systematic review and meta-analysis. Br J Anaesth 2022;129:801-14.ArticlePubMed
  • 28. Petrof BJ, Hussain SN. Ventilator-induced diaphragmatic dysfunction: what have we learned? Curr Opin Crit Care 2016;22:67-72.ArticlePubMed
  • 29. Petrof BJ. Diaphragm weakness in the critically ill: basic mechanisms reveal therapeutic opportunities. Chest 2018;154:1395-403.ArticlePubMed
  • 30. Grosu HB, Lee YI, Lee J, Eden E, Eikermann M, Rose KM, et al. Diaphragm muscle thinning in patients who are mechanically ventilated. Chest 2012;142:1455-60.ArticlePubMed
  • 31. Itagaki T, Nakanishi N, Takashima T, Ueno Y, Tane N, Tsunano Y, et al. Effect of controlled ventilation during assist-control ventilation on diaphragm thickness: a post hoc analysis of an observational study. J Med Invest 2020;67:332-7.ArticlePubMed
  • 32. Jaber S, Petrof BJ, Jung B, Chanques G, Berthet JP, Rabuel C, et al. Rapidly progressive diaphragmatic weakness and injury during mechanical ventilation in humans. Am J Respir Crit Care Med 2011;183:364-71.ArticlePubMed
  • 33. Levine S, Nguyen T, Taylor N, Friscia ME, Budak MT, Rothenberg P, et al. Rapid disuse atrophy of diaphragm fibers in mechanically ventilated humans. N Engl J Med 2008;358:1327-35.ArticlePubMed
  • 34. Goligher EC, Brochard LJ, Reid WD, Fan E, Saarela O, Slutsky AS, et al. Diaphragmatic myotrauma: a mediator of prolonged ventilation and poor patient outcomes in acute respiratory failure. Lancet Respir Med 2019;7:90-8.ArticlePubMed
  • 35. Battaglini D, Rocco PR. Challenges in transitioning from controlled to assisted ventilation in acute respiratory distress syndrome (ARDS) management. J Clin Med 2024;13:7333.ArticlePubMedPMC
  • 36. Yoshida T, Torsani V, Gomes S, De Santis RR, Beraldo MA, Costa EL, et al. Spontaneous effort causes occult pendelluft during mechanical ventilation. Am J Respir Crit Care Med 2013;188:1420-7.ArticlePubMed
  • 37. Brochard L. Ventilation-induced lung injury exists in spontaneously breathing patients with acute respiratory failure: yes. Intensive Care Med 2017;43:250-2.ArticlePubMedPDF
  • 38. Dres M, Rozenberg E, Morawiec E, Mayaux J, Delemazure J, Similowski T, et al. Diaphragm dysfunction, lung aeration loss and weaning-induced pulmonary oedema in difficult-to-wean patients. Ann Intensive Care 2021;11:99.ArticlePubMedPMCPDF
  • 39. Battaglini D, Rocco PR. Beyond the ventilator: rethinking daily evaluation of respiratory drive and effort. Lancet Respir Med 2025;13:1045-6.ArticlePubMed
  • 40. Deshwal H, Elkhapery A, Ramanathan R, Nair D, Singh I, Sinha A, et al. Patient-self inflicted lung injury (P-SILI): an insight into the pathophysiology of lung injury and management. J Clin Med 2025;14:1632.ArticlePubMedPMC
  • 41. Fu W, Guan L, Liu Q, Xie Z, You J, Chen R, et al. Ventilator-induced diaphragmatic dysfunction: pathophysiology, monitoring and advances in potential treatment and prevention. Eur Respir Rev 2025;34:250069.ArticlePubMedPMC
  • 42. Gallardo A, Castro-Sayat M, Alcaraz M, Colaianni-Alfonso N, Vetrugno L. Debate on the role of eccentric contraction of the diaphragm: is it always harmful? Healthcare (Basel) 2025;13:565.ArticlePubMedPMC
  • 43. Bordoni B, Kotha R, Escher AR. Symptoms arising from the diaphragm muscle: function and dysfunction. Cureus 2024;16:e53143. ArticlePubMedPMC
  • 44. Supinski GS, Morris PE, Dhar S, Callahan LA. Diaphragm dysfunction in critical illness. Chest 2018;153:1040-51.ArticlePubMed
  • 45. Dres M, Demoule A. Diaphragm dysfunction during weaning from mechanical ventilation: an underestimated phenomenon with clinical implications. Crit Care 2018;22:73.ArticlePubMedPMCPDF
  • 46. Castellví-Font A, Goligher EC, Dianti J. Lung and diaphragm protection during mechanical ventilation in patients with acute respiratory distress syndrome. Clin Chest Med 2024;45:863-75.ArticlePubMed
  • 47. van den Berg MJ, Heunks L, Doorduin J. Advances in achieving lung and diaphragm-protective ventilation. Curr Opin Crit Care 2025;31:38-46.ArticlePubMed
  • 48. Kim WY, Suh HJ, Hong SB, Koh Y, Lim CM. Diaphragm dysfunction assessed by ultrasonography: influence on weaning from mechanical ventilation. Crit Care Med 2011;39:2627-30.ArticlePubMed
  • 49. Haaksma ME, Smit JM, Boussuges A, Demoule A, Dres M, Ferrari G, et al. Expert consensus on diaphragm ultrasonography in the critically ill (EXODUS): a Delphi consensus statement on the measurement of diaphragm ultrasound-derived parameters in a critical care setting. Crit Care 2022;26:99.ArticlePubMedPMCPDF
  • 50. Akoumianaki E, Dousse N, Lyazidi A, Lefebvre JC, Graf S, Cordioli RL, et al. Can proportional ventilation modes facilitate exercise in critically ill patients? A physiological cross-over study: pressure support versus proportional ventilation during lower limb exercise in ventilated critically ill patients. Ann Intensive Care 2017;7:64.ArticlePubMedPMC
  • 51. Morris IS, Bassi T, Bellissimo CA, de Perrot M, Donahoe L, Brochard L, et al. Proof of concept for continuous on-demand phrenic nerve stimulation to prevent diaphragm disuse during mechanical ventilation (STIMULUS): a phase 1 clinical trial. Am J Respir Crit Care Med 2023;208:992-5.ArticlePubMedPDF
  • 52. Poddighe D, Van Hollebeke M, Clerckx B, Janssens L, Molenberghs G, Van Dyck L, et al. Inspiratory effort and respiratory muscle activation during different breathing conditions in patients with weaning difficulties: an exploratory study. Aust Crit Care 2025;38:101152.ArticlePubMed
  • 53. Patsaki I, Kouvarakos A, Vasileiadis I, Koumantakis GA, Ischaki E, Grammatopoulou E, et al. Low-medium and high-intensity inspiratory muscle training in critically ill patients: a systematic review and meta-analysis. Medicina (Kaunas) 2024;60:869.ArticlePubMedPMC
  • 54. Alonso-Pérez JL, Riquelme-Aguado V, Rodríguez-Prieto D, López-Mejías A, Romero-Morales C, Rossettini G, et al. Inspiratory muscle training and its impact on weaning success in mechanically ventilated ICU patients: a systematic review. J Funct Morphol Kinesiol 2025;10:111.ArticlePubMedPMC
  • 55. Wang SJ, Fang TP, Rowley DD, Liu NW, Chen JO, Liu JF, et al. Inspiratory muscle training facilitates liberation from mechanical ventilation in subacute critically ill patients-a randomized controlled trial. Front Med (Lausanne) 2024;11:1503678.ArticlePubMed
  • 56. Pathmanathan N, Beaumont N, Gratrix A. Respiratory physiotherapy in the critical care unit. Contin Educ Anaesth Crit Care Pain 2015;15:20-5.Article
  • 57. Ruo Yu L, Jia Jia W, Meng Tian W, Tian Cha H, Ji Yong J. Optimal timing for early mobilization initiatives in intensive care unit patients: a systematic review and network meta-analysis. Intensive Crit Care Nurs 2024;82:103607.ArticlePubMed
  • 58. Vitacca M, Ambrosino N. Non-invasive ventilation as an adjunct to exercise training in chronic ventilatory failure: a narrative review. Respiration 2019;97:3-11.ArticlePubMedPDF
  • 59. Sepúlveda P, Gallardo A, Arriagada R, González E, Rocco PRM, Battaglini D, et al. Protocolized strategies to encourage early mobilization of critical care patients: challenges and success. Crit Care Sci 2025;37:e20250128. ArticlePubMedPMC
  • 60. Kayambu G, Boots R, Paratz J. Physical therapy for the critically ill in the ICU: a systematic review and meta-analysis. Crit Care Med 2013;41:1543-54.ArticlePubMed
  • 61. Stiller KR, Dafoe S, Jesudason CS, McDonald TM, Callisto RJ. Passive movements do not appear to prevent or reduce joint stiffness in medium to long-stay ICU patients: a randomized, controlled, within-participant trial. Crit Care Explor 2023;5:e1006. ArticlePubMedPMC
  • 62. Eggmann S, Timenetsky KT, Hodgson C. Promoting optimal physical rehabilitation in ICU. Intensive Care Med 2024;50:755-7.ArticlePubMedPDF
  • 63. Bissett B. Dyspnoea in COVID-19 recovery beyond the intensive care unit: the potential impact of inspiratory muscle weakness. ERJ Open Res 2023;9:00521-2022.ArticlePubMedPMC
  • 64. Kabitz HJ, Walker D, Prettin S, Walterspacher S, Sonntag F, Dreher M, et al. Non-invasive ventilation applied for recovery from exercise-induced diaphragmatic fatigue. Open Respir Med J 2008;2:16-21.ArticlePubMedPMCPDF
  • 65. Romer LM, Polkey MI. Exercise-induced respiratory muscle fatigue: implications for performance. J Appl Physiol (1985) 2008;104:879-88.ArticlePubMed
  • 66. Regmi B, Friedrich J, Jörn B, Senol M, Giannoni A, Boentert M, et al. Diaphragm muscle weakness might explain exertional dyspnea 15 months after hospitalization for COVID-19. Am J Respir Crit Care Med 2023;207:1012-21.ArticlePubMedPMCPDF
  • 67. O'Grady HK, Edbrooke L, Farley C, Berney S, Denehy L, Puthucheary Z, et al. The sit-to-stand test as a patient-centered functional outcome for critical care research: a pooled analysis of five international rehabilitation studies. Crit Care 2022;26:175.ArticlePubMedPMC
  • 68. Ambrosino N, Xie L. The use of non-invasive ventilation during exercise training in COPD patients. COPD 2017;14:396-400.ArticlePubMed
  • 69. de Medeiros Nogueira MG, Silva GA, Marinho MH, de Fátima Costa Brito O, de Brito Vieira WH, Ururahy MA, et al. Acute effects of NIV on peripheral muscle function and aerobic performance in patients with chronic obstructive pulmonary disease: a pilot study. BMC Pulm Med 2022;22:399.ArticlePubMedPMC
  • 70. Dennis CJ, Menadue C, Schneeberger T, Leitl D, Schoenheit-Kenn U, Hoyos CM, et al. Bilevel noninvasive ventilation during exercise reduces dynamic hyperinflation and improves cycle endurance time in severe to very severe COPD. Chest 2021;160:2066-79.ArticlePubMed
  • 71. Cabello B, Mancebo J. Work of breathing. Intensive Care Med 2006;32:1311-4.ArticlePubMedPDF
  • 72. Deniz S, Tuncel Ş, Gürgün A, Elmas F. Adding non-invasive positive pressure ventilation to supplemental oxygen during exercise training in severe chronic obstructive pulmonary disease: a randomized controlled study. Thorac Res Pract 2023;24:262-9.ArticlePubMedPMC
  • 73. De Backer LA, Ides K, Daems D, Dieriks B, De Backer WA, Germonpre P, et al. Pulmonary rehabilitation and non-invasive ventilation in COPD. Acta Clin Belg 2010;65:330-5.ArticlePubMed
  • 74. Halbert J, McGraw P, Gray C, O'Brien G, Maheshwari V, Caplan R, et al. Noninvasive ventilation for early mobilization of acutely hypoxic patients. Chest 2016;150:215A.Article
  • 75. Menadue C, Piper AJ, van 't Hul AJ, Wong KK. Non-invasive ventilation during exercise training for people with chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2014;2014:CD007714.ArticlePubMedPMC
  • 76. Márquez-Martín E, Ruiz FO, Ramos PC, López-Campos JL, Azcona BV, Cortés EB, et al. Randomized trial of non-invasive ventilation combined with exercise training in patients with chronic hypercapnic failure due to chronic obstructive pulmonary disease. Respir Med 2014;108:1741-51.ArticlePubMed
  • 77. Schneeberger T, Dennis CJ, Jarosch I, Leitl D, Stegemann A, Gloeckl R, et al. High-intensity non-invasive ventilation during exercise-training versus without in people with very severe COPD and chronic hypercapnic respiratory failure: a randomised controlled trial. BMJ Open Respir Res 2023;10:e001913. ArticlePubMedPMC
  • 78. Bruce RM, Turner A, White MJ. Ventilatory responses to muscle metaboreflex activation in chronic obstructive pulmonary disease. J Physiol 2016;594:6025-35.ArticlePubMedPMCPDF
  • 79. Piper AJ, Moran FM. Non-invasive ventilation and the physiotherapist: current state and future trends. Phys Ther Rev 2006;11:37-43.Article
  • 80. Chen X, Xu L, Li S, Yang C, Wu X, Feng M, et al. Efficacy of respiratory support therapies during pulmonary rehabilitation exercise training in chronic obstructive pulmonary disease patients: a systematic review and network meta-analysis. BMC Med 2024;22:389.ArticlePubMedPMCPDF
  • 81. de Vries HJ, Jonkman AH, de Grooth HJ, Duitman JW, Girbes AR, Ottenheijm CA, et al. Lung- and diaphragm-protective ventilation by titrating inspiratory support to diaphragm effort: a randomized clinical trial. Crit Care Med 2022;50:192-203.ArticlePubMedPMC
  • 82. de Vries HJ, Tuinman PR, Jonkman AH, Liu L, Qiu H, Girbes AR, et al. Performance of noninvasive airway occlusion maneuvers to assess lung stress and diaphragm effort in mechanically ventilated critically ill patients. Anesthesiology 2023;138:274-88.ArticlePubMedPDF
  • 83. Xiang G, Wu Q, Wu X, Hao S, Xie L, Li S, et al. Non-invasive ventilation intervention during exercise training in individuals with chronic obstructive pulmonary disease: a systematic review and meta-analysis. Ann Phys Rehabil Med 2021;64:101460.ArticlePubMed
  • 84. Hernandez-Voth A, Sayas Catalan J, Corral Blanco M, Alonso Moralejo R, Perez Gonzalez V, De Pablo Gafas A, et al. Long-term effect of noninvasive ventilation on diaphragm in chronic respiratory failure. Int J Chron Obstruct Pulmon Dis 2022;17:205-12.ArticlePubMedPMC
  • 85. Rochwerg B, Brochard L, Elliott MW, Hess D, Hill NS, Nava S, et al. Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir J 2017;50:1602426.ArticlePubMed
  • 86. Mauri T, Grasselli G, Jaber S. Respiratory support after extubation: noninvasive ventilation or high-flow nasal cannula, as appropriate. Ann Intensive Care 2017;7:52.ArticlePubMedPMCPDF
  • 87. Thille AW, Muller G, Gacouin A, Coudroy R, Decavèle M, Sonneville R, et al. Effect of postextubation high-flow nasal oxygen with noninvasive ventilation vs high-flow nasal oxygen alone on reintubation among patients at high risk of extubation failure: a randomized clinical trial. JAMA 2019;322:1465-75.ArticlePubMedPMC
  • 88. Battaglini D, Lassola S, Schultz MJ, Rocco PR. Innovations in protective mechanical ventilation for acute respiratory distress syndrome management. Expert Rev Med Devices 2024;21:789-92.ArticlePubMed
  • 89. Béduneau G, Pham T, Schortgen F, Piquilloud L, Zogheib E, Jonas M, et al. Epidemiology of weaning outcome according to a new definition. The WIND study. Am J Respir Crit Care Med 2017;195:772-83.ArticlePubMed
  • 90. Sepúlveda P, Gallardo A, Arriagada R, Souza B, Patroniti N, Battaglini D, et al. Weaning failure from mechanical ventilation: a scoping review of the utility of ultrasonography in the weaning process. Br J Anaesth 2025;135:1441-55.ArticlePubMedPMC
  • 91. Battaglini D, Robba C, Ball L, Silva PL, Cruz FF, Pelosi P, et al. Noninvasive respiratory support and patient self-inflicted lung injury in COVID-19: a narrative review. Br J Anaesth 2021;127:353-64.ArticlePubMed
  • 92. Cruces P, Retamal J, Hurtado DE, Erranz B, Iturrieta P, González C, et al. A physiological approach to understand the role of respiratory effort in the progression of lung injury in SARS-CoV-2 infection. Crit Care 2020;24:494.ArticlePubMedPMCPDF
  • 93. Carteaux G, Millán-Guilarte T, De Prost N, Razazi K, Abid S, Thille AW, et al. Failure of noninvasive ventilation for de novo acute hypoxemic respiratory failure: role of tidal volume. Crit Care Med 2016;44:282-90.ArticlePubMed
  • 94. Duan J, Chen L, Liu X, Bozbay S, Liu Y, Wang K, et al. An updated HACOR score for predicting the failure of noninvasive ventilation: a multicenter prospective observational study. Crit Care 2022;26:196.ArticlePubMedPMCPDF
  • 95. Ball L, Talmor D, Pelosi P. Transpulmonary pressure monitoring in critically ill patients: pros and cons. Crit Care 2024;28:177.ArticlePubMedPMCPDF
  • 96. Boscolo A, Pettenuzzo T, Sella N, Zatta M, Salvagno M, Tassone M, et al. Noninvasive respiratory support after extubation: a systematic review and network meta-analysis. Eur Respir Rev 2023;32:220196.ArticlePubMedPMC
  • 97. Pelosi P, Tonelli R, Torregiani C, Baratella E, Confalonieri M, Battaglini D, et al. Different methods to improve the monitoring of noninvasive respiratory support of patients with severe pneumonia/ARDS due to COVID-19: an update. J Clin Med 2022;11:1704.ArticlePubMedPMC
  • 98. Tuinman PR, Jonkman AH, Dres M, Shi ZH, Goligher EC, Goffi A, et al. Respiratory muscle ultrasonography: methodology, basic and advanced principles and clinical applications in ICU and ED patients-a narrative review. Intensive Care Med 2020;46:594-605.ArticlePubMedPMCPDF
  • 99. Santana PV, Cardenas LZ, Albuquerque AL. Diaphragm ultrasound in critically ill patients on mechanical ventilation-evolving concepts. Diagnostics (Basel) 2023;13:1116.ArticlePubMedPMC
  • 100. Barwing J, Pedroni C, Olgemöller U, Quintel M, Moerer O. Electrical activity of the diaphragm (EAdi) as a monitoring parameter in difficult weaning from respirator: a pilot study. Crit Care 2013;17:R182.ArticlePubMedPMCPDF
  • 101. Tonelli R, Protti A, Spinelli E, Grieco DL, Yoshida T, Jonkman AH, et al. Assessing inspiratory drive and effort in critically ill patients at the bedside. Crit Care 2025;29:339.ArticlePubMedPMCPDF
  • 102. Warnaar RS, Cornet AD, Beishuizen A, Donker DW, Oppersma E. Advanced serial analysis of the diaphragm surface EMG: insights into the effect of pressure support on the neuro-ventilatory response during the ICU stay. Crit Care 2025;29:258.ArticlePubMedPMCPDF
  • 103. Diehl JL, El Atrous S, Touchard D, Lemaire F, Brochard L. Changes in the work of breathing induced by tracheotomy in ventilator-dependent patients. Am J Respir Crit Care Med 1999;159:383-8.ArticlePubMed
  • 104. Jaeger JM, Littlewood KA, Durbin CG. The role of tracheostomy in weaning from mechanical ventilation. Respir Care 2002;47:469-80.ArticlePubMedPDF
  • 105. Ghiani A, Paderewska J, Sainis A, Crispin A, Walcher S, Neurohr C, et al. Variables predicting weaning outcome in prolonged mechanically ventilated tracheotomized patients: a retrospective study. J Intensive Care 2020;8:19.ArticlePubMedPMCPDF
  • 106. Liu Y, Li T, Shi L. Long-term home mechanical ventilation using a noninvasive ventilator via tracheotomy in patients with myasthenia gravis: a case report and literature review. Ther Adv Respir Dis 2023;17:17534666231165914.ArticlePubMedPMCPDF
  • 107. Wang H, Jiang H, Zhao Z, Liu J, Zhang C. Application and safety of speaking valves in tracheostomy patients. Crit Care 2024;28:424.ArticlePubMedPMCPDF
  • 108. Ibrahim SG, Silva JM, Borges LG, Savi A, Forgiarini Junior LA, Teixeira C, et al. Use of a noninvasive ventilation device following tracheotomy: an alternative to facilitate ICU discharge? Rev Bras Ter Intensiva 2012;24:167-72.PubMed
  • 109. Coppadoro A, Zago E, Pavan F, Foti G, Bellani G. The use of head helmets to deliver noninvasive ventilatory support: a comprehensive review of technical aspects and clinical findings. Crit Care 2021;25:327.ArticlePubMedPMCPDF
  • 110. Vaschetto R, Longhini F, Persona P, Ori C, Stefani G, Liu S, et al. Early extubation followed by immediate noninvasive ventilation vs. standard extubation in hypoxemic patients: a randomized clinical trial. Intensive Care Med 2019;45:62-71.ArticlePubMedPDF

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      Rehabilitating the diaphragm: an integrated approach to intensive care unit-acquired dysfunction in critical illness: a narrative review
      Image Image Image Image
      Figure 1. Protective mechanical ventilation (MV) for lung and diaphragm. In this figure, cutoff values are proposed in relation to measurements that can be carried out both in any MV device and through ultrasonography, which together will allow the clinician to safeguard a protective MV not only avoiding pulmonary injury induced by MV, but also avoiding diaphragmatic injury, especially during the transition to ventilatory spontaneity. VT: tidal volume; PBW: predicted body weight; ARDS: acute respiratory distress syndrome; iPEEP: intrinsic positive end-expiratory pressure; PaCO2: arterial partial pressure of carbon dioxide; TFdi: diaphragmatic thickening fraction; ΔPes: esophageal pressure swing; ΔPdi: transdiaphragmatic pressure swing; PMUS,pred: predicted inspiratory muscle pressure; POCC: occlusion pressure; P0.1: airway occlusion pressure at 100 ms.
      Figure 2. Respiratory muscle metaboreflex. Early respiratory muscle fatigue activates afferent signaling through the phrenic nerve, eliciting sympathetic vasoconstriction in the limbs. This response reduces oxygen delivery to locomotor muscles, exacerbates peripheral fatigue, and ultimately limits tolerance and progression during physical therapy. VO2: oxygen consumption.
      Figure 3. Effect of non-invasive ventilation (NIV) during physical therapy: by unloading the respiratory muscles, NIV decreases oxygen consumption (VO2) and delays activation of the metaboreflex, thereby improving exercise tolerance and facilitating participation in physical therapy among critically ill patients.
      Figure 4. Selection of non-invasive ventilation (NIV) candidate patients during rehabilitation in the intensive care unit (ICU). This figure emphasizes the need to select the appropriate patient to use NIV as an adjuvant to physical therapy during the rehabilitation process in the ICU. Special mention is made of factors related to diaphragmatic weakness after extubation, a factor that could lead to the early onset of the metabolic reflex. In addition, safety values are proposed to be observed during physical therapy, to prevent the appearance of eventual patient self-inflicted lung injury (P-SILI) during this therapeutic act. TFdi: diaphragmatic thickening fraction; MIP: maximum inspiratory pressure; NIF: negative inspiratory force; IPAP: inspiratory positive airway pressure; EPAP: expiratory positive airway pressure; CPAP: continuous positive airway pressure; FiO2: fraction of inspired oxygen; ARDS: acute respiratory distress syndrome; VT: tidal volume; ΔPes: esophageal pressure swing; SpO2: peripheral oxygen saturation.

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      Rehabilitating the diaphragm: an integrated approach to intensive care unit-acquired dysfunction in critical illness: a narrative review
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