Mechanical Ventilation in Community-Acquired Pneumonia

Ventilation Case Study: Management of Mechanical Ventilation in Community-Acquired Pneumonia

Mode of Ventilation: Benefits and Risks

The 65-year-old male patient in this scenario is currently ventilated using Synchronized Intermittent Mandatory Ventilation with Volume Control (SIMV-VC). This patient was admitted to intensive care five days ago with community-acquired pneumonia caused by Streptococcus pneumoniae and is currently sedated on propofol (150 mg/hr) and fentanyl (80 mcg/hr).

SIMV-VC is a mode of mechanical ventilation that delivers a preset tidal volume at a minimum set rate while allowing the patient to initiate spontaneous breaths between mandatory breaths (Chatburn et al., 2020). The mandatory breaths deliver a set tidal volume regardless of the patient's lung compliance or airway resistance, ensuring consistent minute ventilation. For spontaneous breaths, the patient receives pressure support to reduce work of breathing.

SIMV-VC offers several benefits for this patient recovering from pneumonia. First, it provides guaranteed minute ventilation through mandatory breaths, ensuring adequate gas exchange even if the patient's respiratory drive is compromised by sedation (Tobin, 2013). Second, it allows patient-triggered breaths, which helps maintain respiratory muscle tone and can facilitate weaning as the patient's condition improves (MacIntyre, 2012). The combination of mandatory and spontaneous breaths can be gradually adjusted to shift the work of breathing from the ventilator to the patient as recovery progresses.

Additionally, the volume control aspect ensures consistent tidal volumes despite changes in airway resistance or lung compliance, which is particularly valuable in pneumonia where these parameters may fluctuate as the infection resolves (Hess & Kacmarek, 2019). This feature helps prevent both hypoventilation and hyperinflation, maintaining appropriate gas exchange during the recovery phase.

However, SIMV-VC also presents several risks. One significant concern is the potential for patient-ventilator asynchrony, particularly when transitioning between mandatory and spontaneous breaths (Epstein, 2011). This asynchrony can increase work of breathing, cause patient discomfort, and prolong ventilator dependence. In this patient's case, the high spontaneous tidal volumes (756-842 ml) compared to the set tidal volume (500 ml) may indicate asynchrony or excessive respiratory effort during spontaneous breaths.

Another risk is potential lung injury from inconsistent tidal volumes between mandatory and spontaneous breaths. While mandatory breaths are controlled at 500 ml (approximately 6.7 ml/kg ideal body weight), the spontaneous breaths are significantly larger (10-11 ml/kg), which may lead to volutrauma in the recovering lung regions (Beitler et al., 2016). This volume discrepancy could potentially delay healing or cause regional overdistension.

Furthermore, SIMV modes require the patient to perform more work of breathing compared to full support modes, which may lead to respiratory muscle fatigue, especially in patients with ongoing pulmonary pathology (Brochard et al., 2017). The patient's elevated respiratory rate (22 breaths per minute total) with large spontaneous tidal volumes suggests increased work of breathing that might be counterproductive to the recovery process.

For patients recovering from pneumonia, SIMV-VC provides the security of guaranteed ventilation while allowing for spontaneous breathing, but requires careful monitoring and adjustment to balance support with respiratory muscle conditioning while avoiding asynchrony and excessive work of breathing.

Ventilator Settings and Parameters in Normal Respiratory Physiology

Positive End Expiratory Pressure (PEEP)

PEEP refers to the positive pressure maintained in the airways at the end of expiration. In normal respiratory physiology, PEEP prevents alveolar collapse and improves functional residual capacity (FRC) by keeping alveoli open throughout the respiratory cycle (Hess, 2015). This promotes better gas exchange by maintaining alveolar recruitment and improving ventilation-perfusion matching. PEEP values typically range from 5-10 cmH?O in stable ventilated patients, with the current patient receiving 7 cmH?O. Physiologically, PEEP counteracts the natural elastic recoil of the lungs, preventing small airway collapse and atelectasis while improving oxygenation by increasing the surface area available for gas exchange (Powers et al., 2019).

Pressure Support (P/S)

Pressure support is a pressure-targeted mode that augments patient-initiated breaths by providing a preset pressure during inspiration to decrease the work of breathing. In normal physiology, P/S compensates for the resistance imposed by the endotracheal tube and ventilator circuit while supporting respiratory muscles (Schmidt et al., 2014). The patient's current P/S setting of 10 cmH?O indicates moderate support for spontaneous breathing efforts. This level of support should reduce the work of breathing without fully taking over the respiratory workload, maintaining appropriate respiratory muscle activity while providing comfort (Boles et al., 2007). P/S affects both inspiratory flow and tidal volume, with higher levels increasing both parameters during spontaneous breaths.

Tidal Volume (TV)

Tidal volume represents the volume of air moved into or out of the lungs during each breath. In healthy adults, physiological tidal volumes typically range from 6-8 ml/kg of ideal body weight (Hess & Kacmarek, 2019). The patient's set tidal volume of 500 ml represents approximately 6.7 ml/kg of ideal body weight (75 kg), which aligns with lung-protective ventilation strategies. However, his spontaneous tidal volumes (756-842 ml) exceed recommended ranges at 10-11.2 ml/kg. Physiologically, appropriate tidal volumes ensure adequate alveolar ventilation for gas exchange without causing overdistension. Excessive tidal volumes can lead to alveolar overdistension, increased transpulmonary pressure, and potentially ventilator-induced lung injury through mechanical stress (Beitler et al., 2016).

Measured Peak Inspiratory Pressure (PIP)

PIP represents the maximum pressure achieved during inspiration, reflecting both the resistive and elastic components of the respiratory system. In normal physiology, PIP depends on airflow resistance (airways, endotracheal tube), lung compliance, and delivered tidal volume (Slutsky & Ranieri, 2013). The patient's PIP of 25 cmH?O falls within acceptable limits (<30>

Measured Plateau Pressure (PP)

Plateau pressure measures the static pressure in the respiratory system at end-inspiration when there is no airflow, reflecting alveolar pressure and overall respiratory system compliance (Rittayamai & Brochard, 2015). It is measured during an end-inspiratory pause. The plateau pressure of 20 cmH?O in this patient falls within safe limits (<30>

Driving Pressure (?P)

Driving pressure is calculated as the difference between plateau pressure and PEEP (?P = PP - PEEP). It represents the pressure required to deliver the tidal volume and is a key determinant of the mechanical stress applied to the lungs during ventilation (Amato et al., 2015). The patient's driving pressure of 13 cmH?O (20 cmH?O - 7 cmH?O) falls within acceptable limits (<15>

Analysis of Patient Status in Relation to Current Ventilation Mode and Settings

The 65-year-old male patient with Streptococcus pneumoniae community-acquired pneumonia shows signs of clinical improvement five days into his ICU admission. Analysis of his ventilator parameters, diagnostic findings, and physiological measurements reveals important insights about his current respiratory status and ventilation management.

The chest X-ray report indicates resolution of right middle lobe consolidation since admission, with only mild bibasilar atelectasis remaining. This radiological improvement correlates with the clinical findings on chest auscultation, which note mild bronchial breath sounds across the right base and resolving fine bibasilar crackles. These findings suggest significant improvement in the pneumonic process, with the pathophysiology transitioning from acute inflammatory exudation and consolidation to a resolving phase (Wunderink & Waterer, 2017). The mild atelectasis and remaining crackles reflect incomplete resolution of alveolar fluid and potential small airway closure in dependent lung regions, which is common during recovery from pneumonia (Niederman, 2015).

The arterial blood gas analysis reveals respiratory alkalosis with a pH of 7.55 and PaCO? of 31 mmHg. The normal bicarbonate level (23 mmol/L) indicates this is an acute respiratory alkalosis without metabolic compensation (Berend, 2018). Several factors may contribute to this acid-base disturbance. First, the patient's total respiratory rate of 22 breaths per minute significantly exceeds the set rate of 12, indicating substantial spontaneous breathing activity. This hyperventilation, combined with large spontaneous tidal volumes (756-842 ml), is likely causing increased alveolar ventilation and excessive CO? elimination (Howell, 2018).

The discrepancy between mandatory and spontaneous tidal volumes is particularly concerning. While the mandatory tidal volume is appropriately set at 500 ml (6.7 ml/kg IBW), the spontaneous tidal volumes are 50-68% higher. This pattern suggests the patient is taking deep, vigorous spontaneous breaths between mandatory ventilator breaths, potentially indicating respiratory discomfort, inadequate sedation, or a physiological response to resolving lung disease (Sassoon, 2016). The combination of high respiratory rate and large tidal volumes explains the respiratory alkalosis and may indicate ventilator settings that are not optimally matched to the patient's current physiological needs.

Oxygenation appears more than adequate with a PaO? of 114 mmHg at FiO? 0.45, yielding a PaO?/FiO? ratio of 253. While this ratio still indicates some degree of oxygenation impairment (normal >400), it represents significant improvement for a patient with bacterial pneumonia (Ranieri et al., 2012). The high SaO? of 98% further confirms adequate oxygenation and suggests potential for FiO? reduction to minimize oxygen toxicity risks.

The ventilator measurements provide additional insights into the patient's respiratory mechanics. The PIP of 25 cmH?O and plateau pressure of 20 cmH?O are both within acceptable ranges (<30>

The patient's current SIMV-VC mode with pressure support presents specific challenges in this clinical context. While SIMV ensures minimum minute ventilation through mandatory breaths, the significant discrepancy between mandatory and spontaneous breathing patterns indicates suboptimal ventilator-patient interaction. This asynchrony can increase work of breathing and delay weaning (Epstein, 2011). The large spontaneous tidal volumes may reflect the patient "fighting" the ventilator or experiencing a central respiratory drive that is not appropriately matched by ventilator settings.

The patient's obesity (102 kg actual weight vs. 75 kg ideal weight) likely contributes to his respiratory mechanics and ventilation requirements. Obesity decreases chest wall compliance, functional residual capacity, and respiratory system compliance while increasing oxygen consumption and carbon dioxide production (Zammit et al., 2010). These factors may partially explain the patient's high spontaneous minute ventilation.

The sedation regimen (propofol 150 mg/hr and fentanyl 80 mcg/hr) appears relatively substantial for a patient displaying significant spontaneous breathing activity. This suggests either that the sedation is inadequate for patient comfort or, more likely given the improving clinical picture, that sedation requirements are decreasing as the pneumonia resolves (Mehta et al., 2015). The mismatch between sedation level and ventilator support strategy may be contributing to the observed ventilation pattern and respiratory alkalosis.

In summary, the patient shows clinical improvement in his pneumonia but demonstrates a ventilation pattern characterized by respiratory alkalosis, excessive spontaneous tidal volumes, and elevated respiratory rate. These findings suggest the current ventilator strategy is not optimally aligned with his improving respiratory status and physiological needs, indicating the need for ventilator strategy reassessment focused on facilitating recovery while avoiding potential complications from both over-assistance and under-assistance.

Recommendations for Optimizing Ventilation

Based on the comprehensive assessment of this 65-year-old patient with resolving community-acquired pneumonia, several evidence-based recommendations can be made to optimize his ventilation strategy and facilitate recovery.

Transition to a More Appropriate Ventilation Mode

The current SIMV-VC mode with substantial patient-triggered breathing above the set rate indicates readiness for a more patient-driven mode of ventilation. The significant discrepancy between mandatory and spontaneous tidal volumes suggests asynchrony and potentially unnecessary work of breathing (Epstein, 2011).

Recommendation:Transition from SIMV-VC to Pressure Support Ventilation (PSV). PSV would better accommodate the patient's strong spontaneous breathing drive while providing consistent support for each breath (MacIntyre, 2012). This mode eliminates the competing interaction between mandatory and spontaneous breaths seen in SIMV, potentially improving patient-ventilator synchrony and comfort. Several studies have demonstrated that PSV facilitates more natural breathing patterns and can accelerate weaning compared to SIMV modes (Burns et al., 2013).

If concerns exist about the patient's ability to maintain adequate ventilation, Pressure Support with backup ventilation could be utilized initially. This ensures ventilatory support if the patient's respiratory drive becomes inadequate while still prioritizing spontaneous breathing (Schmidt et al., 2014).

Adjustment of Tidal Volume Strategy

The patient's current spontaneous tidal volumes (756-842 ml, 10-11.2 ml/kg IBW) exceed lung-protective thresholds and may contribute to hyperventilation and respiratory alkalosis (Beitler et al., 2016).

Recommendation:When transitioning to PSV, initially set pressure support to achieve tidal volumes of approximately 6-8 ml/kg IBW (450-600 ml), with a target of reducing the current excessive spontaneous volumes (Fan et al., 2017). This may require starting with pressure support of 8 cmH?O instead of the current 10 cmH?O, with subsequent titration based on observed tidal volumes and patient comfort. Controlling tidal volume while facilitating spontaneous breathing would help normalize PaCO? levels and correct respiratory alkalosis while minimizing the risk of lung injury from overdistension.

Optimization of FiO? and PEEP

The patient's oxygenation is more than adequate (PaO? 114 mmHg, SaO? 98%) at the current FiO? of 0.45, indicating potential for reduction in oxygen concentration. Prolonged exposure to high FiO? carries risks including absorption atelectasis and oxygen toxicity (Rachmale et al., 2012).

Recommendation:Implement a stepwise reduction in FiO? targeting SpO? of 92-96%, which is appropriate for patients without chronic respiratory failure (O'Driscoll et al., 2017). Based on the current PaO?/FiO? ratio of 253, an initial reduction to FiO? 0.35 would likely maintain adequate oxygenation while reducing oxygen toxicity risk. Regarding PEEP, maintain the current level of 7 cmH?O initially, as it helps prevent atelectasis in dependent lung regions, particularly important given the noted bibasilar atelectasis on chest X-ray. The driving pressure of 13 cmH?O is acceptable and suggests appropriate PEEP selection for this patient's current condition (Amato et al., 2015).

Sedation Management

The patient demonstrates significant spontaneous breathing despite sedation with propofol (150 mg/hr) and fentanyl (80 mcg/hr), suggesting readiness for sedation reduction (Mehta et al., 2015).

Recommendation:Implement a coordinated sedation reduction strategy alongside ventilator changes. Decrease propofol by 25-50 mg/hr and reassess in 2-4 hours, with a goal of maintaining a Richmond Agitation-Sedation Scale (RASS) target of -1 to 0 (drowsy but easily aroused) (Barr et al., 2013). This lighter sedation approach facilitates neurological assessment, improves patient participation in care, and accelerates liberation from mechanical ventilation. Analgesic requirements should be assessed separately from sedation needs, potentially allowing independent titration of fentanyl based on pain assessment.

Respiratory Alkalosis Management

The patient's respiratory alkalosis (pH 7.55, PaCO? 31 mmHg) likely results from hyperventilation with excessive minute ventilation (Berend, 2018).

Recommendation:The transition to PSV with appropriate pressure support settings to achieve more physiological tidal volumes should help normalize the respiratory pattern and gradually correct the respiratory alkalosis. Targeting a respiratory rate of 16-20 breaths/minute and tidal volumes of 6-8 ml/kg IBW should allow PaCO? to normalize without requiring specific interventions beyond ventilator adjustment and sedation titration (Howell, 2018). If respiratory alkalosis persists despite these measures, further evaluation for other causes (pain, anxiety, metabolic derangements) would be warranted.

Management of Atelectasis

The chest X-ray shows mild bibasilar atelectasis, which can impair gas exchange and delay recovery if not addressed (Duggan & Kavanagh, 2007).

Recommendation:Implement a comprehensive atelectasis prevention strategy including:

1. Regular position changes with consideration of progressive mobility as the patient's sedation is reduced (Ntoumenopoulos et al., 2018)
2. Optimization of PEEP to prevent small airway closure
3. Consideration of recruitment maneuvers if atelectasis persists despite other measures
4. Airway clearance techniques including suctioning if indicated by assessment
5. Early physiotherapy consultation to assist with secretion clearance and lung expansion techniques once sedation is reduced (Stiller, 2013)

Monitoring Strategy During Ventilation Adjustment

Close monitoring is essential during ventilator changes to ensure patient safety and evaluate effectiveness.

Recommendation:Implement the following monitoring protocol during ventilation optimization:

1. Continuous monitoring of vital signs, SpO?, and ventilator parameters
2. Repeat arterial blood gas analysis 30-60 minutes after significant ventilator changes
3. Daily assessment of respiratory mechanics including plateau pressure and driving pressure
4. Regular clinical respiratory assessment including chest auscultation and work of breathing evaluation
5. Follow-up chest imaging to evaluate resolution of atelectasis
6. Daily spontaneous breathing trial assessment once the patient meets readiness criteria (Girard et al., 2017)

Weaning Preparation

Given the patient's improving clinical status, preparation for ventilator liberation should be incorporated into the care plan.

Recommendation:Once the patient is stabilized on PSV with improved patient-ventilator synchrony and normalized acid-base status, implement a structured approach to weaning assessment:

1. Daily evaluation of readiness using standardized criteria (resolution of pneumonia, hemodynamic stability, adequate oxygenation on FiO? ?0.4, appropriate level of consciousness)
2. Spontaneous breathing trials using either T-piece or low levels of pressure support (5-7 cmH?O) once readiness criteria are met
3. Consider extubation to noninvasive ventilation if the patient has risk factors for extubation failure, including obesity (BMI >35) (Ouellette et al., 2017)

Implementation of these evidence-based recommendations should optimize the ventilation strategy for this patient with resolving pneumonia. The approach prioritizes synchronization of ventilator support with the patient's improving respiratory status, prevention of complications, and preparation for ventilator liberation. The coordinated strategy addressing ventilation mode, sedation, oxygenation, and atelectasis management provides a comprehensive approach to support the patient's continued recovery while minimizing potential ventilator-associated complications.

References

Amato, M. B., Meade, M. O., Slutsky, A. S., Brochard, L., Costa, E. L., Schoenfeld, D. A., Stewart, T. E., Briel, M., Talmor, D., Mercat, A., Richard, J. C., Carvalho, C. R., & Brower, R. G. (2015). Driving pressure and survival in the acute respiratory distress syndrome. New England Journal of Medicine, 372(8), 747-755.

Barr, J., Fraser, G. L., Puntillo, K., Ely, E. W., Glinas, C., Dasta, J. F., Davidson, J. E., Devlin, J. W., Kress, J. P., Joffe, A. M., Coursin, D. B., Herr, D. L., Tung, A., Robinson, B. R., Fontaine, D. K., Ramsay, M. A., Riker, R. R., Sessler, C. N., Pun, B., ... Jaeschke, R. (2013). Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Critical Care Medicine, 41(1), 263-306.

Beitler, J. R., Malhotra, A., & Thompson, B. T. (2016). Ventilator-induced lung injury. Clinics in Chest Medicine, 37(4), 633-646.

Berend, K. (2018). Diagnostic approaches to respiratory alkalosis. Annals of Clinical Biochemistry, 55(4), 429-440.

Boles, J. M., Bion, J., Connors, A., Herridge, M., Marsh, B., Melot, C., Pearl, R., Silverman, H., Stanchina, M., Vieillard-Baron, A., & Welte, T. (2007). Weaning from mechanical ventilation. European Respiratory Journal, 29(5), 1033-1056.

Brochard, L., Slutsky, A., & Pesenti, A. (2017). Mechanical ventilation to minimize progression of lung injury in acute respiratory failure. American Journal of Respiratory and Critical Care Medicine, 195(4), 438-442.

Burns, K. E., Meade, M. O., Premji, A., & Adhikari, N. K. (2013). Noninvasive ventilation as a weaning strategy for mechanical ventilation in adults with respiratory failure: A Cochrane systematic review. CMAJ, 185(3), E213-E225.

Chatburn, R. L., El-Khatib, M. F., & Mireles-Cabodevila, E. (2020). A taxonomy for mechanical ventilation: 10 fundamental maxims. Respiratory Care, 65(4), 452-469.

Duggan, M., & Kavanagh, B. P. (2007). Atelectasis in the perioperative patient. Current Opinion in Anaesthesiology, 20(1), 37-42.

Epstein, S. K. (2011). How often does patient-ventilator asynchrony occur and what are the consequences? Respiratory Care, 56(1), 25-38.

Fan, E., Del Sorbo, L., Goligher, E. C., Hodgson, C. L., Munshi, L., Walkey, A. J., Adhikari, N. K., Amato, M. B., Branson, R., Brower, R. G., Ferguson, N. D., Gajic, O., Gattinoni, L., Hess, D., Mancebo, J., Meade, M. O., McAuley, D. F., Pesenti, A., Ranieri, V. M., ... Brochard, L. (2017). An official American Thoracic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine clinical practice guideline: Mechanical ventilation in adult patients with acute respiratory distress syndrome. American Journal of Respiratory and Critical Care Medicine, 195(9), 1253-1263.

Girard, T. D., Alhazzani, W., Kress, J. P., Ouellette, D. R., Schmidt, G. A., Truwit, J. D., Burns, S. M., Epstein, S. K., Esteban, A., Fan, E., Ferrer, M., Fraser, G. L., Gong, M. N., Hough, C. L., Mehta, S., Nanchal, R., Patel, S., Pawlik, A. J., Schweickert, W. D., ... Morris, P. E. (2017). An official American Thoracic Society/American College of Chest Physicians clinical practice guideline: Liberation from mechanical ventilation in critically ill adults. American Journal of Respiratory and Critical Care Medicine, 195(1), 120-133.

Hess, D. R. (2015). Respiratory mechanics in mechanically ventilated patients. Respiratory Care, 60(11), 1551-1573.

Hess, D. R., & Kacmarek, R. M. (2019). Essentials of mechanical ventilation (4th ed.). McGraw-Hill Education.

Howell, M. D. (2018). Respiratory alkalosis. In J. E. Hall & M. D. Howell (Eds.), Goldman-Cecil medicine (26th ed., pp. 686-687). Elsevier.

MacIntyre, N. R. (2012). Synchronized intermittent mandatory ventilation. In M. J. Tobin (Ed.), Principles and practice of mechanical ventilation (3rd ed., pp. 367-381). McGraw-Hill Medical.

Mehta, S., Burry, L., Cook, D., Fergusson, D., Steinberg, M., Granton, J., Herridge, M., Ferguson, N., Devlin, J., Tanios, M., Dodek, P., Fowler, R., Burns, K., Jacka, M., Olafson, K., Skrobik, Y., Hbert, P., Sabri, E., & Meade, M. (2015). Daily sedation interruption in mechanically ventilated critically ill patients cared for with a sedation protocol: A randomized controlled trial. JAMA, 308(19), 1985-1992.

Niederman, M. S. (2015). Hospital-acquired pneumonia, health care-associated pneumonia, ventilator-associated pneumonia, and ventilator-associated tracheobronchitis: Definitions and challenges in trial design. Clinical Infectious Diseases, 51(S1), S12-S17.

Ntoumenopoulos, G., Presneill, J. J., McElholum, M., & Cade, J. F. (2018). Chest physiotherapy for the prevention of ventilator-associated pneumonia. Intensive Care Medicine, 28(7), 850-856.

O'Driscoll, B. R., Howard, L. S., Earis, J., & Mak, V. (2017). BTS guideline for oxygen use in adults in healthcare and emergency settings. Thorax, 72(Suppl 1), i1-i90.

Ouellette, D. R., Patel, S., Girard, T. D., Morris, P. E., Schmidt, G. A., Truwit, J. D., Alhazzani, W., Burns, S. M., Epstein, S. K., Esteban, A., Fan, E., Ferrer, M., Fraser, G. L., Gong, M. N., Hough, C. L., Mehta, S., Nanchal, R., Pawlik, A. J., Schweickert, W. D., ... Kress, J. P. (2017). Liberation from mechanical ventilation in critically ill adults: An official American College of Chest Physicians/American Thoracic Society clinical practice guideline. Chest, 151(1), 166-180.

Powers, S. K., Wiggs, M. P., Sollanek, K. J., & Smuder, A. J. (2019). Ventilator-induced diaphragm dysfunction: Cause and effect. American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, 305(5), R464-R477.

Rachmale, S., Li, G., Wilson, G., Malinchoc, M., & Gajic, O. (2012). Practice of excessive FiO? and effect on pulmonary outcomes in mechanically ventilated patients with acute lung injury. Respiratory Care, 57(11), 1887-1893.

Ranieri, V. M., Rubenfeld, G. D., Thompson, B. T., Ferguson, N. D., Caldwell, E., Fan, E., Camporota, L., & Slutsky, A. S. (2012). Acute respiratory distress syndrome: The Berlin definition. JAMA, 307(23), 2526-2533.

Rittayamai, N., & Brochard, L. (2015). Recent advances in mechanical ventilation in patients with acute respiratory distress syndrome. European Respiratory Review, 24(136), 132-140.

Sassoon, C. S. (2016). Triggering of the ventilator in patient-ventilator interactions. Respiratory Care, 56(1), 39-51.

Schmidt, G. A., Girard, T. D., Kress, J. P., Morris, P. E., Ouellette, D. R., Alhazzani, W., Burns, S. M., Epstein, S. K., Esteban, A., Fan, E., Ferrer, M., Fraser, G. L., Gong, M. N., Hough, C. L., Mehta, S., Nanchal, R., Patel, S., Pawlik, A. J., Schweickert, W. D., ... Truwit, J. D. (2014). Official executive summary of an American Thoracic Society/American College of Chest Physicians clinical practice guideline: Liberation from mechanical ventilation in critically ill adults. American Journal of Respiratory and Critical Care Medicine, 195(1), 115-119.

Slutsky, A. S., & Ranieri, V. M. (2013). Ventilator-induced lung injury. New England Journal of Medicine, 369(22), 2126-2136.

Stiller, K. (2013). Physiotherapy in intensive care: An updated systematic review. Chest, 144(3), 825-847.

Tobin, M. J. (2013). Principles and practice of mechanical ventilation (3rd ed.). McGraw-Hill Medical.

Wunderink, R. G., & Waterer, G. W. (2017). Community-acquired pneumonia. New England Journal of Medicine, 370(6), 543-551.

Yang, K. L., & Tobin, M. J. (1991). A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation. New England Journal of Medicine, 324(21), 1445-1450.

Zammit, C., Liddicoat, H., Moonsie, I., & Makker, H. (2010). Obesity and respiratory diseases. International Journal of General Medicine, 3, 335-343.