Noninvasive ventilatory support


People need about 6000 ml of air to enter their lungs to maintain normal blood oxygen (O2) and carbon dioxide (CO2) levels. When respiratory muscles are too weak to accomplish this, they need ventilatory assistance or support. This can be provided via invasive or noninvasive interfaces. Noninvasive ventilatory support (NVS) involves the application of pressures to the body or to the airways to provide breath volumes and/or to increase cough flows to expel airway debris without suctioning. It is an alternative to mechanical ventilation via invasive airway tubes, such as endotracheal tubes (Figures 1 and 2) or tracheostomy tubes (Figure 3).

The former refers to tubes placed through the nose or mouth and passed down the throat (translaryngeal) into the windpipe (trachea), with the patient said to be intubated. Suction catheters are also placed through the tubes to remove secretions and other debris out of the airways. While intubated, patients receive air under pressure while inhaling (positive pressure ventilation), increasing their breath volumes and enabling even those with no respiratory muscle function and 0 ml of vital capacity (VC, normally between 3000 and 7000 ml). When people remain too weak to breathe on their own, these tubes are typically not removed (the patient is not extubated) until another invasive airway tube, a tracheostomy tube, is placed through the neck and into the trachea for continued tracheostomy mechanical ventilatory support (TMV). With NVS, the application of positive pressure via the nose and/or mouth while inhaling accomplishes the same goals as an alternative to intubation and TMV. Likewise, body ventilators such as iron lungs (Figure 4) or chest shells (Figure 5) apply negative pressure to the body to expand the lungs, allowing air to enter the nose and mouth to ventilate them. Some people have used these ventilators for continuous NVS for over 60 years. Other body ventilators ventilate the lungs by applying pressures to the body to move the diaphragm. One such ventilator is the intermittent abdominal pressure ventilator that has been on and off the market since the early 1950s. Another such ventilator, now rarely used, is the rocking bed ventilator that rocks the patient above and below the horizontal to move the diaphragm back and forth to ventilate the lungs.
In this discussion we will consider only positive pressure support, since negative pressure ventilators are considered largely obsolete in modern medicine.[1][2] NVS can be delivered as intermittent positive airway pressure via oral,[3] nasal,[4] or oronasal interfaces. It can also be delivered via bilevel positive airway pressure (BiPAP) either at high spans, that is, with the difference between inspiratory PAP (IPAP) and expiratory PAP (EPAP) being greater than 15 cm H2O, or set to full volume targeting. This difference is also known as the "drive pressure" or "pressure support" provided to inspiratory effort. At those settings, with EPAP minimized, NVS can aid or fully replace the function of respiratory muscles as well as eliminate the need for invasive airway tubes. NVS must be distinguished from noninvasive ventilation, which has become synonymous with continuous positive airway pressure (CPAP) and low-span BiPAP, usually with supplemental oxygen (O2), used to treat sleep apneas but cannot provide full ventilatory support.[5] Supplemental O2 is an important treatment for cardiopulmonary disease (e.g., chronic obstruction pulmonary disease, cardiogenic pulmonary edema) rather than ventilatory pump failure due to weak respiratory muscles, which include the diaphragm and chest wall muscles (as in neuromuscular disease, for example); it should be avoided in the latter due to risk of respiratory depression and subsequent CO2 narcosis leading to coma and death.[6] Patients with ventilatory pump failure need breathing and coughing support to avoid pneumonia and acute-on-chronic respiratory failure (ARF), especially when treated with supplemental O2 rather than NVS. To permit definitive reliance on NVS, people with ineffective cough flows who therefore cannot clear their own airway secretions often require mechanical insufflation-exsufflation (MIE) to prevent those complications. The MIE simulates an effective cough by providing inspiratory pressure at 40 to 70 cm H2O followed by expiratory pressure at -40 to -70 cm H2O to generate over 10 L/s of expiratory flow. They often benefit from mastery of glossopharyngeal breathing and air stacking, respiratory techniques which increase lung volume recruitment, thereby facilitating effective coughs.[7][8][9][10][11]
Medical Uses
Extubation and decannulation
Intubated patients with conditions including Duchenne muscular dystrophy, spinal muscular atrophy, amyotrophic lateral sclerosis, spinal cord injury, critical care neuromyopathy, morbid obesity,:[12] severe kyphoscoliosis, and other causes of ventilatory pump failure can become continuously dependent on NVS without ever requiring hospitalization or developing ARF. If intubated for any intercurrent chest infection, they can almost always be extubated and placed on NVS—or continuous NVS (CNVS), i.e., around-the-clock intermittent positive pressure support, if needed—and MIE to clear airway secretions even without respiratory muscle function (0 ml of vital capacity), provided that they satisfy certain criteria[5][13]
| Extubation Criteria for Ventilator-Dependent Patients with Ventilatory Pump Failure |
|---|
| SpO2 normal (95-100%) without supplemental oxygen |
| Afebrile |
| Normal leukocyte count |
| PaCO2 ≤ 40 mm Hg at peak inspiratory pressures < 35 cm H2O on assist/control mode ventilatory support, up to full settings |
| All deoxyhemoglobin desaturations < 95% reversed by MAC and suctioning via translaryngeal tube |
| SpO2 ≥ 95% for 12 hours or more in ambient air |
| Fully alert and cooperative without sedation |
| Any chest radiograph abnormalities cleared or clearing |
| Air leakage via upper airway sufficient for vocalization upon cuff deflation |
Therefore, cooperative patients with ventilatory pump failure never require tracheostomy tubes unless they develop upper motor neuron disease severe enough to cause upper airway closure, which can impair the delivery of NVS and the ability of MIE to clear the airways.[14][15][16][17][18] Likewise, patients on mechanical ventilation via tracheostomy, even if continuously dependent, can be offered decannulation of their tracheostomy tubes and conversion to NVS/CNVS and MIE, including those with C2 spinal cord injury.[19][20][21][22][23][24][25] The decannulation steps include, first, disconnection from the ventilator with occlusion of the tube by finger pressure and lung ventilation with manual resuscitator via a mouth or nose piece. Then the patient air stacks to determine manually assisted cough flows with an abdominal thrust. Exceeding 160-200 L/m of unassisted or assisted cough peak flows is the primary criterion for safe decannulation.[26] It is rare for flows not to exceed 160 L/m except in patients with upper motor neuron disease. The tube can also be removed to measure assisted cough peak flows and is left out permanently when the flows are adequate. A pressure dressing, Tegaderm™, is then applied to the ostomy after the patients are back on NVS. The dressing is completed with an elastic bandage over a cane tip with the walls cut down and fixed in place by tape over the pressure dressing.
Acute management of ventilatory pump failure
A patient presenting to an emergency department with respiratory distress symptoms and abnormal arterial oxyhemoglobin saturation (<95%), after ruling out cardiogenic causes and improper placement of pulse oximeter, should have the following addressed: inadequate lung ventilation with elevated CO2 levels, and airway congestion with secretions due to inadequate cough flows, which can lead to lung disease with pneumonia, pneumothorax, or gross atelectasis. The standard of care includes supplementary O2, which may alleviate symptoms but exacerbate hypercarbia, leading to CO2 narcosis, coma, or even respiratory arrest. Therefore, anyone presenting to emergency services with respiratory symptoms should not be administered O2 if there is suspicion of respiratory muscle weakness without evidence of chronic lung disease that might be causing the O2 desaturation and distress. NVS rather than low-span BiPAP can reverse hypoventilation and MIE can relieve airway congestion by providing deep breaths followed by a 100-140 cm H2O decrease in airway pressure to generate cough flows of over 10 L/s, expelling secretions the patient would be unable to expel independently, with unassisted cough flow of less than 300 L/min measured by peak flow meter. Normalizing lung ventilation and cough flows via NVS and MIE typically normalizes arterial O2 saturation levels and resolves hypercapnia. It also prevents lung disease, especially pneumonia, in many cases, as well as the need for intubation.[27] Most emergency departments should have portable ventilators capable of delivering NVS or BiPAP devices that can be used at spans of at least 18 cm H2O for that purpose (Figure 6). If an MIE device, typically the CoughAssist™ (Philips-Respironics Inc., Murrysville, PA), is not available, then air stacking (i.e., cumulative delivery of air volumes held by the glottis) followed by abdominal thrusts can increase cough flows manually. While chest physiotherapy can be helpful to mobilize secretions from the small peripheral airways to larger central airways through oscillatory, vibratory, and percussive techniques, it is not an effective substitute for the airway clearance MIE can provide.
Complementary Interventions for Noninvasive Management
These include glossopharyngeal (“frog”) breathing, active and passive lung volume recruitment (LVR), and manually assisted coughing. If the VC is only a fraction of normal, one cannot fill the rest of the lungs with air and they close down and stiffen.[28] Active LVR, or "air stacking," is the accumulation of consecutively delivered volumes of air from a manual resuscitator or volume preset ventilator to the maximum the glottis can hold. If the glottis is too weak for stacking, passive LVR can be performed by using MIE at 60 to 70 cm H2O pressures.[29][30] Once the lungs are deeply insufflated, cough flows can become effective. Air stacking followed by abdominal thrusts to increase cough flows is termed manually assisted coughing.[29] These complementary interventions, along with MIE, prevent pneumonia, hospitalizations, and intubations; therefore, they are crucial following extubation to NVS in maintaining the success of noninvasive management.
History and Outcomes
Although both positive pressure and body ventilators had been used to resuscitate smoke inhalation, drowning victims, and others since the 16th century, iron lungs and other body ventilators were the only methods of long-term ventilatory support available until 1947 when André Cournand used intermittent positive pressure breathing (IPPB) to deliver medications deep into the lungs of people with lung diseases in New York City.[31] While there was an ample supply of J. H. Emerson iron lungs available for poliomyelitis victims and others with “ventilatory pump failure” (VPF) in the United States from 1931 through 1952, there were few elsewhere.[32] For example, Denmark had only one or two for 400 polio victims who needed support. H. C. A. Lassen, professor at the University of Copenhagen and father of neurologist Niels A. Lassen, realized that applying Cournand’s IPPB via tracheostomy tubes through the necks and into the airways of people could provide full ventilatory support. In August 1952, Lassen recruited Bjørn Ibsen, an anesthesiologist, to perform the tracheostomies and place tracheostomy tubes through the ostomies in the patients’ necks for up to continuous ventilatory support (continuous TMV [CTMV]) and airway suctioning.[33][34] Medical and dental students were recruited to press manual resuscitator bags to deliver air to patients with post-polio syndrome around-the-clock, as needed, until the first positive pressure ventilator was developed there, the Pulsula™, four months later. With lungs ventilated by TMV, these post-polio survivors left their iron lungs for wheelchairs with their ventilators rolled behind them.[35] When American physicians and surgeons learned that the patients could come out of 870-pound iron lungs by using TMV, they urged all people in iron lungs to follow suit. While body ventilators provided noninvasive negative pressure ventilatory support, the term "NVS" henceforth will relate only to noninvasive positive pressure ventilatory support via oral, nasal, and oronasal interfaces (Figures 7-9).
In 1952, rather than transferring people from iron lungs to tracheostomy tubes as in Denmark, John E. Affeldt of Rancho Los Amigos Hospital in Los Angeles observed people using Zephyr™ blowers and the exhaust of chest shell ventilators via mouthpieces on tubing to get full ventilatory support (that is, NVS) via mouthpieces. He reported this in a post-poliomyelitis respiratory equipment conference in 1953:
"There is just one point I would like to mention, which has just come along which, I think, makes [noninvasive positive pressure ventilation] even more feasible. It is so simple that why it wasn't thought of long ago I don't know. Actually, some of our physical therapists, in struggling with the patients, noticed that they could simply take the positive pressure attachment, apply a small plastic mouthpiece [...], and allow that to hang in the patient's mouth. You can take him to the Hubbard tank by such means and you can do any nursing procedure, if the patient is on the rocking bed and has a zero vital capacity, if you want to stop the bed for any reason, or if you want to change him from the tank respirator to the bed, or put the cuirass respirator on, or anything to stop the equipment, you can simply attach this, hang it by the patient, he grips it by his lips, and thus it allows for the excess to blow off which he doesn't want. It works very well. We even had one patient who has no breathing ability who has fallen asleep and been adequately ventilated by this procedure, so that it appears to work very well, and I think does away with a lot of complications of difficulty of using positive pressure [via tracheostomy]. You just hang it by the patients and they grip it with their lips, when they want it, and when they don't want it, they let go of it. It is just too simple."[36]
Affeldt understood the redundancy of iron lung domes (Figure 4) and that tracheostomy tubes were not necessary for ventilatory support even when people had little to no VC at all:
"You don't have to have an attachment made for the tank respirator.”
People began to use scuba mouth pieces, pulmonary function testing mouth pieces, Tygon tubing, and anything else they could adapt for mouthpiece NVS. Some of 257 people switched from iron lungs and other body ventilators by Augusta Alba in 1956 have now been using mouthpiece NVS around-the-clock for at least 65 years (Figure 10).[23]There were no alarms signaling disconnection, many had no use of upper limbs, and the first portable positive pressure ventilator, the Thompson Bantam™, did not have a demand valve, so people had to set a rate and wait for it to deliver air. For many, loss of the mouthpiece during sleep would have meant death, but such events were rare since no O2 was delivered and sedative medications that would also have deadened the brain’s drive to maintain normal ventilation were avoided.[37]
During daytime, the mouthpiece was usually fixed adjacent to the mouth (Figure 7) but, overnight, only the tongue kept the mouthpiece in the mouth until the Bennett Lipseal™ became available in 1964 (Figure 11).[38] Sleeping without the lip cover phalange to fix the mouthpiece in place and decrease air leakage meant that people would hold the mouthpiece under the tongue, get deep breaths, then gradually let the air leak. This could cause blood O2 levels (O2 saturation) to decrease below 95%, triggering the oral muscles to hold the mouthpiece again for more effective breaths until the next leak period. After the Lipseal™ became available, this leak was greatly diminished and the mouthpiece could be physically secured for nighttime ventilation.
While TMV became the standard of care in the late 1960s for people too weak to breathe, the original mouthpiece NVS users resisted and many never underwent tracheostomies.[5] It became clear that 50 to 80% of people with VPF died due to TMV rather than their underlying diseases. For example, Carter et al. reported 17 of 35 deaths of patients with spinal cord injury due to the tube itself,[39] and other data were comparable.[21][22] Bach et al. reported 60% of 27 deaths of mostly post-polio patients were due to the tube and possibly 24 of the 27 deaths in all.[23] Ishikawa et al. reported 10 years greater survival for 88 Duchenne muscular dystrophy patients by CNVS in comparison to 28 CTMV users.[40] Bach reported that 32 of 40 deaths of amyotrophic lateral sclerosis (ALS) patients were due to the tube.[16] Thus, 50 to 90% of TMV users with VPF die because of the tubes, suggesting that tracheostomies should be avoided whenever possible.
It is commonly thought that intubated, ventilator unweanable patients require tracheostomies to be extubated and survive. However, in 2010[13] and 2015,[41] 254 of 257 patients total were successfully extubated who could not have passed spontaneous breathing trials or ventilator weaning parameters either before or after extubation and, in some cases, were CNVS-dependent for decades before being hospitalized and intubated at all. These observations suggest that no one who is intubated for any reason needs a tracheostomy tube for only being too weak to breathe. Twenty-eight of the ventilator unweanable patients extubated in 2015 had ALS; however, all but two were successfully extubated to CNVS. The two unweanable patients that failed extubation and underwent tracheostomies had predominantly upper motor neuron disease (MND) bulbar ALS.[41]
What permits successful extubation of ventilator unweanable people to CNVS?
Intact ventilatory drive, that is, drive not medically sedated or blunted by O2 therapy, prevents excessive sustained air leakage while using open circuit systems of CNVS via mouth, nasal, or oronasal interfaces during sleep.[37] This permits effective lung ventilation even for patients with 0 ml of VC. Further, MIE is used at 50 to 70 cm H2O pressures via the translaryngeal (intubation) tubes to prepare people for extubation and used post-extubation via mouthpieces or oronasal interfaces. This effectively clears airway debris to maintain normal ambient air oxyhemoglobin saturation, that is, normal blood gases without supplemental O2. An MIE device, the Cof-flator™ (OEM company, Hartford, Ct), was on the market from late 1952 through 1967.[38] With tracheostomies done for TMV, and no one ever describing the use of MIE via the tubes, the Cof-flator™ went off the market. However, patients leaving iron lungs for CNVS in 1956 who had Cof-flators™ would not give them up, knowing that their use during intercurrent respiratory tract infections protected them from hospitalizations and invasive airway tube placement.
In 1988, Jack Emerson's In-Exsufflator™, an MIE device which entered the market in February of 1993, was used to extubate ventilator unweanable patients in critical care, as described by Bach et al.[42] After preparing them for extubation with hourly use of MIE at 60 to 70 cm H2O pressures via the tubes until O2 saturation remained normal in ambient air, and with normal PaCO2 even if requiring full ventilatory support, they were extubated to CNVS (mouthpiece and/or nasal) and MIE. In general, the involvement of family members, who learn to apply MIE via oronasal interfaces for every O2 desaturation below 95% post-extubation in the critical care unit, is crucial for maintaining successful extubation to CNVS and MIE with oximetry feedback. With hypoventilation and airway secretions managed, the success rate for extubating ventilator unweanable people is about 99% since those are the main causes of extubation failure.[13][41]
Who fails extubation to CNVS and MIE?
None of the ventilator unweanable patients with myopathic or lower MNDs in the 2010 and 2015 studies, or subsequently, failed extubation to CNVS and MIE by using oximetry to maintain normal ambient air O2 saturation post-extubation.[13][41] However, people with predominantly upper motor neuron ALS, cerebral palsy, stroke, traumatic brain injury, or others with severe upper motor neuron pathology causing upper airway closure, can have MIE expiratory flows (MIE-EF) inadequate for clearing airway secretions, thereby necessitating tracheostomy. In general, MIE-EF below 150 L/m may be inadequate and flows below 120 L/m almost always necessitate tracheostomy for survival.[15] Conventional thinking is that ALS patients may have failed noninvasive management because of their severe bulbar-innervated muscle dysfunction. However, if this were true, it would not have been possible to extubate 175 ventilator unweanable infants and subsequently older patients with spinal muscular atrophy type 1 to CNVS and MIE without resort to tracheostomies, considering that many, if not most, had no bulbar-innervated muscle function at all other than eye movements.[43] Besides having no bulbar muscle function, some also had, and continue to have 0 ml of VC. Yet, all could be extubated to CNVS and MIE without resort to tracheostomies. This is because myopathies and lower motor neuron disease patients have very effective MIE-EF whereas the flows can decrease and become ineffective for people with upper motor neuron disease.
Decannulation to NVS and MIE
People with tracheostomy tubes can have them removed (decannulation), continuous ventilator dependence (CTMV) notwithstanding, as long as the bulbar-innervated muscles function and the lungs are healthy; that is, O2 saturation should be normal without supplemental O2. The 52-year-old man in Figure 12 had been CNVS-dependent with no ventilator-free breathing ability for 15 years before he developed pneumonia that led to his intubation and subsequent tracheostomy. He woke up from medical sedation outraged, had the tube removed in an outpatient clinic a week later, and was placed back on CNVS.[25]
References
- ↑ Bach, John Robert; Tuccio, Maria Chiara (February 2011). "Respiratory Physical Medicine: Physiatry's Neglected Discipline". American Journal of Physical Medicine & Rehabilitation. 90 (2): 169–174. doi:10.1097/PHM.0b013e31820171fb. PMID 21173688.
- ↑ "This man has been locked in this obsolete machine for almost 60 years". The Independent. 11 July 2018.
- ↑ Toussaint, Michel; Chatwin, Michelle; Gonçalves, Miguel R.; Gonzalez-Bermejo, Jésus; Benditt, Joshua O.; McKim, Doug; Sancho, Jesus; Hov, Brit; Sansone, Valeria; Prigent, Hélène; Carlucci, Annalisa; Wijkstra, Peter; Garabelli, Barbara; Escarrabill, Joan; Pinto, Tiago; Audag, Nicolas; Verweij-van den Oudenrijn, Laura; Ogna, Adam; Hughes, Wendy; Devaux, Christian; Chaulet, Johann; Andersen, Tiina (April 2021). "Mouthpiece ventilation in neuromuscular disorders: Narrative review of technical issues important for clinical success" (PDF). Respiratory Medicine. 180: 106373. doi:10.1016/j.rmed.2021.106373. ISSN 0954-6111. PMID 33798870 Check
|pmid=value (help). Unknown parameter|s2cid=ignored (help) - ↑ Bach, John R.; Alba, Augusta; Mosher, Richard; Delaubier, Anne (July 1987). "Intermittent Positive Pressure Ventilation via Nasal Access in the Management of Respiratory Insufficiency". Chest. 92 (1): 168–170. doi:10.1378/chest.92.1.168. PMID 3297517.
- ↑ 5.0 5.1 5.2 Bach, John R (2017). "Noninvasive Respiratory Management of Patients With Neuromuscular Disease". Annals of Rehabilitation Medicine. 41 (4): 519–538. doi:10.5535/arm.2017.41.4.519. PMC 5608659. PMID 28971036.
- ↑ Chiou, M.; Bach, J. R.; Saporito, L. R.; Albert, O. (September 2016). "Quantitation of oxygen-induced hypercapnia in respiratory pump failure". Revista Portuguesa de Pneumologia. 22 (5): 262–265. doi:10.1016/j.rppnen.2016.03.005. ISSN 2173-5115. PMID 27118611.
- ↑ Bach, John R.; Bianchi, Carlo; Vidigal-Lopes, Mauro; Turi, Sandra; Felisari, Giorgio (April 2007). "Lung Inflation by Glossopharyngeal Breathing and "Air Stacking" in Duchenne Muscular Dystrophy". American Journal of Physical Medicine & Rehabilitation. 86 (4): 295–300. doi:10.1097/PHM.0b013e318038d1ce. PMID 17413542. Unknown parameter
|s2cid=ignored (help) - ↑ Haruyama, K; Yamaha, Y; Ito, M; Otsuka, T; Kawakami, M (2020). "Strategies for learning glossopharyngeal breathing in boys with Duchenne muscular dystrophy: A feasibility case series". Journal of Rehabilitation Medicine. 52 (9): jrm00102. doi:10.2340/16501977-2729. PMID 32870317 Check
|pmid=value (help). Unknown parameter|s2cid=ignored (help) - ↑ Montero, J. C.; Feldman, D. J.; Montero, D. (December 1967). "Effects of glossopharyngeal breathing on respiratory function after cervical cord transection". Archives of Physical Medicine and Rehabilitation. 48 (12): 650–653. ISSN 0003-9993. PMID 5235188.
- ↑ Nygren-Bonnier, M.; Wahman, K.; Lindholm, P.; Markström, A.; Westgren, N.; Klefbeck, B. (May 2009). "Glossopharyngeal pistoning for lung insufflation in patients with cervical spinal cord injury". Spinal Cord. 47 (5): 418–422. doi:10.1038/sc.2008.138. ISSN 1476-5624. PMID 19002147. Unknown parameter
|s2cid=ignored (help) - ↑ Bianchi, Carlo; Carrara, Raniero; Khirani, Sonia; Tuccio, Maria Chiara (January 2014). "Independent Cough Flow Augmentation by Glossopharyngeal Breathing Plus Table Thrust in Muscular Dystrophy". American Journal of Physical Medicine & Rehabilitation. 93 (1): 43–48. doi:10.1097/PHM.0b013e3182975bfa. PMID 23739278. Unknown parameter
|s2cid=ignored (help) - ↑ Bach, J.R.; Kazi, A.W.; Pinto, T.; Gonçalves, M.R. (January 2021). "Noninvasive ventilatory support in morbid obesity". Pulmonology. 27 (5): 386–393. doi:10.1016/j.pulmoe.2020.12.003. PMID 33446455 Check
|pmid=value (help). Unknown parameter|s2cid=ignored (help) - ↑ 13.0 13.1 13.2 13.3 Bach, John Robert; Gonçalves, Miguel R.; Hamdani, Irram; Winck, Joao Carlos (2010). "Extubation of Patients With Neuromuscular Weakness". Chest. 137 (5): 1033–1039. doi:10.1378/chest.09-2144. PMID 20040608.
- ↑ Bach, John R.; Giménez, Gloria C.; Chiou, Michael (March 2019). "Mechanical In-exsufflation-Expiratory Flows as Indication for Tracheostomy Tube Decannulation: Case Studies". American Journal of Physical Medicine & Rehabilitation. 98 (3): e18–e20. doi:10.1097/PHM.0000000000000999. PMID 29994794. Unknown parameter
|s2cid=ignored (help) - ↑ 15.0 15.1 Bach, John R.; Upadhyaya, Neelam (April 2018). "Association of Need for Tracheotomy With Decreasing Mechanical In-Exsufflation Flows in Amyotrophic Lateral Sclerosis". American Journal of Physical Medicine & Rehabilitation. 97 (4): e20–e22. doi:10.1097/PHM.0000000000000755. PMID 28410251.
- ↑ 16.0 16.1 Bach, J. R. (December 1993). "Amyotrophic lateral sclerosis. Communication status and survival with ventilatory support". American Journal of Physical Medicine & Rehabilitation. 72 (6): 343–349. doi:10.1097/00002060-199312000-00002. ISSN 0894-9115. PMID 8260126.
- ↑ Bach, John R.; Gupta, Kavita; Reyna, Michael; Hon, Alice (December 2009). "Spinal Muscular Atrophy Type 1: Prolongation of Survival by Noninvasive Respiratory Aids". Pediatric Asthma, Allergy & Immunology. 22 (4): 151–162. doi:10.1089/pai.2009.0002.
- ↑ Patel, S.; Cuenant, L.; Bach, J. R. (November 2019). "Spinal Muscular Atrophy: Noninvasive Respiratory Management" (PDF). Journal of Clinical Neurology, Neurosurgery and Spine. 2 (1): 119.
- ↑ Bach, J. R. (1996). Pulmonary rehabilitation : the obstructive and paralytic conditions. Philadelphia: Hanley & Belfus. ISBN 9781560531098. Search this book on
- ↑ Bach, John R.; Hunt, David; Horton, John A. (October 2002). "Traumatic tetraplegia: noninvasive respiratory management in the acute setting". American Journal of Physical Medicine & Rehabilitation. 81 (10): 792–797. doi:10.1097/01.PHM.0000027205.42338.72 (inactive 28 February 2022). ISSN 0894-9115. PMID 12362121.
- ↑ 21.0 21.1 Bach, J. R. (February 1991). "New approaches in the rehabilitation of the traumatic high level quadriplegic". American Journal of Physical Medicine & Rehabilitation. 70 (1): 13–19. doi:10.1097/00002060-199102000-00004. ISSN 0894-9115. PMID 1994965. Unknown parameter
|s2cid=ignored (help) - ↑ 22.0 22.1 Bach, J. R.; Alba, A. S. (September 1990). "Noninvasive options for ventilatory support of the traumatic high level quadriplegic patient". Chest. 98 (3): 613–619. doi:10.1378/chest.98.3.613. ISSN 0012-3692. PMID 2203616.
- ↑ 23.0 23.1 23.2 Bach, J. R.; Alba, A. S.; Saporito, L. R. (January 1993). "Intermittent positive pressure ventilation via the mouth as an alternative to tracheostomy for 257 ventilator users". Chest. 103 (1): 174–182. doi:10.1378/chest.103.1.174. ISSN 0012-3692. PMID 8417874.
- ↑ Bach, John R.; Pham, Hoa (4 October 2021). "ALS and Noninvasive Ventilation for Ventilatory Support: "NIV" or "NVS"?". American Journal of Physical Medicine & Rehabilitation. Publish Ahead of Print (4): 400–404. doi:10.1097/PHM.0000000000001905. PMID 34657086 Check
|pmid=value (help). Unknown parameter|s2cid=ignored (help) - ↑ 25.0 25.1 Bach, J; Saporito, L; Shah, H; Sinquee, D (2014). "Decanulation of patients with severe respiratory muscle insufficiency: Efficacy of mechanical insufflation-exsufflation". Journal of Rehabilitation Medicine. 46 (10): 1037–1041. doi:10.2340/16501977-1874. ISSN 1650-1977. PMID 25096928.
- ↑ Bach, John Robert; Goncalves, MD Miguel (2004). "Ventilator Weaning by Lung Expansion and Decannulation". American Journal of Physical Medicine & Rehabilitation. 83 (7): 560–568. doi:10.1097/01.phm.0000130027.80861.b8. ISSN 0894-9115. PMID 15213482.
- ↑ Bach, J. R.; Martinez, D. (1 June 2011). "Duchenne Muscular Dystrophy: Continuous Noninvasive Ventilatory Support Prolongs Survival". Respiratory Care. 56 (6): 744–750. doi:10.4187/respcare.00831. PMID 21333078. Unknown parameter
|s2cid=ignored (help) - ↑ Bach, John R.; Kang, Seong-Woong (2000). "Disorders of Ventilation". Chest. 117 (2): 301–303. doi:10.1378/chest.117.2.301. PMID 10669664.
- ↑ 29.0 29.1 Kang, Seong-Woong; Bach, John R. (2000). "Maximum Insufflation Capacity". American Journal of Physical Medicine & Rehabilitation. 79 (3): 222–227. doi:10.1097/00002060-200005000-00002. ISSN 0894-9115. PMID 10821306.
- ↑ Kang, Seong-Woong; Bach, John R. (2000). "Maximum Insufflation Capacity". Chest. 118 (1): 61–65. doi:10.1378/chest.118.1.61. ISSN 0012-3692. PMID 10893360.
- ↑ Cournand, Andre; Motley, Hurley L.; Werko, Lars; Richards, Dickinson W. (1947-12-31). "Physiological Studies of the Effects of Intermittent Positive Pressure Breathing on Cardiac Output in Man". American Journal of Physiology. Legacy Content. 152 (1): 162–174. doi:10.1152/ajplegacy.1947.152.1.162. ISSN 0002-9513. PMID 18903440.
- ↑ Emerson, J. H. (1978). The evolution of iron lungs. Cambridge, MA: J. H. Emerson Company. Search this book on
- ↑ Lassen, H. C. (1954). "The epidemic of poliomyelitis in Copenhagen, 1952". Proceedings of the Royal Society of Medicine. 47 (1): 67–71. doi:10.1177/003591575404700119. ISSN 0035-9157. PMC 1918826. PMID 13134175.
- ↑ Ibsen, B. (1954). "The anaesthetist's viewpoint on the treatment of respiratory complications in poliomyelitis during the epidemic in Copenhagen, 1952". Proceedings of the Royal Society of Medicine. 47 (1): 72–74. doi:10.1177/003591575404700120. ISSN 0035-9157. PMC 1918820. PMID 13134176.
- ↑ Bach, John R. (2017). "Noninvasive Positive Pressure Ventilatory Support Begins During Sleep". Sleep Medicine Clinics. 12 (4): 607–615. doi:10.1016/j.jsmc.2017.07.010. ISSN 1556-407X. PMID 29108615.
- ↑ Hodes, H. L. (1955). "Treatment of respiratory difficulty in poliomyelitis". Poliomyelitis: Papers and Discussions Presented at the Third International Poliomyelitis Conference. Philadelphia: Lippincott: 91–113.
- ↑ 37.0 37.1 Bach, John R.; Robert, Dominique; Leger, Patrick; Langevin, Bruno (1995). "Sleep Fragmentation in Kyphoscoliotic Individuals With Alveolar Hypoventilation Treated by NIPPV". Chest. 107 (6): 1552–1558. doi:10.1378/chest.107.6.1552. ISSN 0012-3692. PMID 7781345.
- ↑ 38.0 38.1 Bach, J. R. "A brief history of noninvasive mechanical ventilation". Noninvasive Management of Ventilatory Pump Failure: for Neuromuscular Diseases, Spinal Cord Injury, Morbid Obesity, and General Debility. Palatine, Illinois: Book Vine Press. Search this book on
- ↑ Carter, R E; Donovan, W H; Halstead, L; Wilkerson, M A (1987). "Comparative study of electrophrenic nerve stimulation and mechanical ventilatory support in traumatic spinal cord injury". Spinal Cord. 25 (2): 86–91. doi:10.1038/sc.1987.16. ISSN 1362-4393. PMID 3495773. Unknown parameter
|s2cid=ignored (help) - ↑ Ishikawa, Yuka; Miura, Toshihiko; Ishikawa, Yukitoshi; Aoyagi, Tomoyuki; Ogata, Hitoko; Hamada, Satoshi; Minami, Ryoji (2011). "Duchenne muscular dystrophy: Survival by cardio-respiratory interventions". Neuromuscular Disorders. 21 (1): 47–51. doi:10.1016/j.nmd.2010.09.006. ISSN 0960-8966. PMID 21144751. Unknown parameter
|s2cid=ignored (help) - ↑ 41.0 41.1 41.2 41.3 Bach, J. R.; Sinquee, D. M.; Saporito, L. R.; Botticello, A. L. (2015-04-01). "Efficacy of Mechanical Insufflation-Exsufflation in Extubating Unweanable Subjects With Restrictive Pulmonary Disorders". Respiratory Care. 60 (4): 477–483. doi:10.4187/respcare.03584. ISSN 0020-1324. PMID 25492956. Unknown parameter
|s2cid=ignored (help) - ↑ Bach, John R.; Zaneuski, Richard; Lee, Hang (1990). "Cardiac Arrhythmias from a Malpositioned Greenfield Filter in a Traumatic Quadriplegic". American Journal of Physical Medicine & Rehabilitation. 69 (5): 251–253. doi:10.1097/00002060-199010000-00005. ISSN 0894-9115. PMID 2222985. Unknown parameter
|s2cid=ignored (help) - ↑ Patel, S.; Cuenant, L.; Bach, J. R. (2019). "Respiratory management of spinal muscular atrophy" (PDF). Journal of Clinical Neurology, Neurosurgery and Spine. 2 (1): 119–127.
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