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Why are oxygen masks given to patients? Can't they take in the atmospheric oxygen? Also, why do they die if the oxygen mask stops providing oxygen?
Oxygen masks can provide up to near 100% oxygen, whereas the atmosphere contains only ~20%. Typically, oxygen is provided in cases where patients' blood oxygen saturation is low or is likely to be low.
Giving a patient supplemental oxygen helps them to achieve oxygen saturation even if their breathing or circulation is impaired, and allows slightly more oxygen to be dissolved in the blood, which can be helpful in cases of blood loss or other traumatic insults.
I'm not sure of any cases where patients simply die immediately if their oxygen mask fails, outside of movies/TV; it's more of an issue of trying to provide the best outcome possible in a difficult situation.
There are also some negative side effects of oxygen supplementation. Overall, Wikipedia has a reasonable overview of these, as well as the indications for oxygen supplementation.
Masks and oxygen delivery devices
Baha Al-Shaikh FCARCSI, FRCA , Simon Stacey FRCA , in Essentials of Anaesthetic Equipment (Fourth Edition) , 2013
Mechanism of action
The Venturi mask uses the Bernoulli principle, described in 1778, in delivering a predetermined and fixed concentration of oxygen to the patient. The size of the constriction determines the final concentration of oxygen for a given gas flow. This is achieved in spite of the patient's respiratory pattern by providing a higher gas flow than the peak inspiratory flow rate.
As the flow of oxygen passes through the constriction, a negative pressure is created. This causes the ambient air to be entrained and mixed with the oxygen flow ( Fig. 6.14 ). The FiO2 is dependent on the degree of air entrainment. Less entrainment ensures a higher FiO2 is delivered. This can be achieved by using smaller entrainment apertures or bigger ‘windows’ to entrain ambient air. The smaller the orifice is, the greater the negative pressure generated, so the more ambient air entrained, the lower the FiO2. The oxygen concentration can be 0.24, 0.28, 0.31, 0.35, 0.4 or 0.6.
The Bernoulli effect can be written as:
where κ is the density, v is the velocity, P is the pressure.
The total energy during a fluid (gas or liquid) flow consists of the sum of kinetic and potential energy. The kinetic energy is related to the velocity of the flow whereas the potential energy is related to the pressure. As the flow of fresh oxygen passes through the constricted orifice into the larger chamber, the velocity of the gas increases distal to the orifice causing the kinetic energy to increase. As the total energy is constant, there is a decrease in the potential energy so a negative pressure is created. This causes the ambient air to be entrained and mixed with the oxygen flow. The FiO2 is dependent on the degree of air entrainment. Less entrainment ensures higher FiO2 is delivered and smaller entrainment apertures are one method of achieving this ( Fig. 6.8 ). The devices must be driven by the correct oxygen flow rate, calibrated for the aperture size if a predictable FiO2 is to be achieved.
Because of the high fresh gas flow rate, the exhaled gases are rapidly flushed from the mask, via its holes. Therefore there is no rebreathing and no increase in dead space.
These masks are recommended when a fixed oxygen concentration is desired in patients whose ventilation is dependent on the hypoxic drive.
For example, a 24% oxygen Venturi mask has an air : oxygen entrainment ratio of 25 : 1. This means an oxygen flow of 2 L/min delivers a total flow of 50 L/min, well above the peak inspiratory flow rate.
The mask's side holes are used to vent the exhaled gases only (as above) in comparison to the side holes in the variable performance mask where the side holes are used to entrain inspired air in addition to expel exhaled gases.
The Venturi face masks are designed for both adult and paediatric use ( Fig. 6.14 ).
The Venturi attachments, with a reservoir tubing, can be attached to a tracheal tube or a supraglottic airway device as part of a T-piece breathing system ( Fig. 6.15 ). This arrangement is usually used in recovery wards to deliver oxygen-enriched air to patents.
A Randomized Trial of Long-Term Oxygen for COPD with Moderate Desaturation. Long-Term Oxygen Treatment Trial Research Group. N Engl J Med. 2016 Oct 27375(17):1617-1627. PMID: 27783918.
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Positive End-Expiratory Pressure and Prone Positioning in Mechanically Ventilated Adults With Moderate to Severe Acute Respiratory Distress Syndrome
For mechanically ventilated adults with COVID-19 and moderate-to-severe ARDS:
- The Panel recommends using a higher positive end-expiratory pressure (PEEP) strategy over a lower PEEP strategy (BIIa).
- For mechanically ventilated adults with COVID-19 and refractory hypoxemia despite optimized ventilation, the Panel recommends prone ventilation for 12 to 16 hours per day over no prone ventilation (BIIa).
PEEP is beneficial in patients with ARDS because it prevents alveolar collapse, improves oxygenation, and minimizes atelectotrauma, a source of ventilator-induced lung injury. A meta-analysis of individual patient data from the three largest trials that compared lower and higher levels of PEEP in patients without COVID-19 found lower rates of ICU mortality and in-hospital mortality with higher PEEP in those with moderate (PaO2/FiO2 100&ndash200 mm Hg) and severe ARDS (PaO2/FiO2 <100 mm Hg). 16
Although there is no clear standard as to what constitutes a high level of PEEP, one conventional threshold is >10 cm H2O. 17 Recent reports have suggested that, in contrast to patients with non-COVID-19 causes of ARDS, some patients with moderate or severe ARDS due to COVID-19 have normal static lung compliance and thus, in these patients, higher PEEP levels may cause harm by compromising hemodynamics and cardiovascular performance. 18,19 Other studies reported that patients with moderate to severe ARDS due to COVID-19 had low compliance, similar to the lung compliance seen in patients with conventional ARDS. 20-23 These seemingly contradictory observations suggest that COVID-19 patients with ARDS are a heterogeneous population and assessment for responsiveness to higher PEEP should be individualized based on oxygenation and lung compliance. Clinicians should monitor patients for known side effects of higher PEEP, such as barotrauma and hypotension.
Oxygen Delivery Systems
There is a wide variety of devices available to provide oxygen support. Delivery systems are classified as low-flow or high-flow equipment, which provide an uncontrolled or controlled amount of supplemental oxygen to the patient (British Thoracic Society, 2008). Selection should be based on preventing and treating hypoxemia and preventing complications of hyper-oxygenation. Factors such as how much oxygen is required, the presence of underlying respiratory disease, age, the environment (at home or in the hospital), the presence of an artificial airway, the need for humidity, a tolerance or a compliance problem, or a need for consistent and accurate oxygen must be considered to select the correct oxygen delivery device (British Thoracic Society, 2008). Table 5.2 lists the types of oxygen equipment.
Types of Oxygen Equipment
Advantages: Can provide 24% to 40% O2 (oxygen) concentration. Most common type of oxygen equipment. Can deliver O2 at 1 to 6 litres per minute (L/min). It is convenient as patient can talk and eat while receiving oxygen. May be drying to nares if level is above 4 L/min. Easy to use, low cost, and disposable.
Limitations: Easily dislodged, not as effective is a patient is a mouth breather or has blocked nostrils or a deviated septum or polyps.
Advantages: Can provide 40% to 60% O2 concentration. Flow meter should be set to deliver O2 at 6 to 10 L/min. Used to provide moderate oxygen concentrations. Efficiency depends on how well mask fits and the patient’s respiratory demands. Readily available on most hospital units. Provides higher oxygen for patients.
Disadvantages: Difficult to eat with mask on. Mask may be confining for some patients, who may feel claustrophobic with the mask on.
Advantages: With a good fit, the mask can deliver between 60% and 80% FiO2 (fraction of inspired oxygen). The flow meter should be set to deliver O2 at 10 to 15 L/min. Flow rate must be high enough to ensure that the reservoir bag remains partially inflated during inspiration.
Disadvantages: These masks have a risk of suffocation if the gas flow is interrupted. The bag should never totally deflate. The patient should never be left alone unless the one-way valves on the exhalation ports are removed. This equipment is used by respiratory therapists for specific short-term, high oxygen requirements such as pre-intubation and patient transport. They are not available on general wards due to: 1. the risk of suffocation, 2. the chance of hyper-oxygenation, and 3. their possible lack of humidity. The mask also requires a tight seal and may be hot and confining for the patient. The mask will interfere with talking and eating.
Advantages: Can deliver 10 to 12 L/min for an O2 concentration of 80% to 90%. Used short term for patients who require high levels of oxygen.
Disadvantages: The partial re-breather bag has no one-way valves, so the expired air mixes with the inhaled air. The mask may be hot and confining for the patient and will interfere with eating and talking.
Advantages: Can provide 28% to 100% O2 Flow meter should be set to deliver O2 at a minimum of 15 L/min. Face tents are used to provide a controlled concentration of oxygen and increase moisture for patients who have facial burn or a broken nose, or who are are claustrophobic.
Disadvantages: It is difficult to achieve high levels of oxygenation with this mask.
Advantages: The system can provide 24% to 60% O2 at 4 to 12 L/min. Delivers a more precise level of oxygen by controlling the specific amounts of oxygen delivered. The port on the corrugated tubing (base of the mask) sets the oxygen concentration. Delivers humidified oxygen for patient comfort. It does not dry mucous membranes.
Disadvantages: The mask may be hot and confining for some patients, and it interferes with talking and eating. Need a properly fitting mask. Nurses may be asked to set up a high-flow system. In other instances, respiratory therapists may be responsible for regulating and monitoring the high-flow systems.
- Review the protocol at your health authority prior to initiating any high-flow oxygen systems, and consult your respiratory therapist.
- In general, nasal prongs and a simple face mask (low-flow oxygen equipment) may be applied by a health care provider. All other oxygen equipment (high-flow systems) must be set up and applied by a respiratory therapist.
- For patients with asthma, nebulizer treatments should use oxygen at a rate greater than 6 L/min. The patient should be changed back to previous oxygen equipment when treatment is complete.
- Oxygenation is reduced in the supine position. Hypoxic patients should be placed in an upright position unless contraindicated (e.g., if they have spinal injuries or loss of consciousness).
- In general, for most patients with COPD, target saturation is 88% to 92%. It is important to recognize COPD patients are at risk for hypercapnic respiratory failure.
- Check the function of the equipment and complete a respiratory assessment at least once each shift for low-flow oxygen and more often for high-flow oxygen.
- In acutely ill patients, oxygen saturation levels may require additional ABGs to regulate and manage oxygen therapy.
- Oxygen saturation levels and delivery equipment should be documented on the patient’s chart.
In this study, oxygen-driven nebulisation increased the PtCO2 in hospital in-patients with an AECOPD compared with air-driven nebulisation. Despite the small mean increase in PtCO2 of 3.4 mmHg, the physiological relevance of this response is suggested by the increase in PtCO2 of at least 4 mmHg in 18/45 (40%) of participants receiving oxygen-driven nebulisation, whereas no patient had an increase of 4 mmHg or more following air-driven nebulisation. The clinical relevance of this physiological response is suggested by the requirement to withdraw one participant during the second oxygen-driven nebulisation due to the PtCO2 increasing by > 10 mmHg, and the increase of PtCO2 or PcapCO2 of at least 8 mmHg in 4/45 (9%) patients receiving oxygen-driven nebulisation, one of whom had a fall in pH of 0.06 into the acidotic range (7.32). These findings suggest that air-driven nebulised bronchodilator therapy represents an important component of the conservative titrated oxygen regimen which has been shown to reduce the risk of hypercapnia, acidosis and mortality in AECOPD .
There are a number of methodological issues relevant to the interpretation of the study findings. Both the randomised controlled design and double-blinding of this study allow for robust and reliable data capture. The length of the nebuliser regimen was chosen to ensure adequate time for complete nebulisation to occur, and to replicate ‘real-world’ back to back treatments in the acute setting, by using two nebulisations separated by five minutes. It is possible that the magnitude of the differences in PCO2 and pH may be even larger with continuous nebulisation which may occur in patients with severe exacerbations not responding to initial treatment or if the nebuliser is inadvertently left in place. The safety-based exclusion criteria of a baseline PtCO2 > 60 mmHg and an oxygen requirement of ≥4 L/minute (to maintain target SpO2 of 88 to 92%), effectively excluded patients with the most severe exacerbations of COPD.
Whilst respiratory rate and neurological symptoms were not formally assessed as outcome measures, no adverse events were identified during the interventions. However, we acknowledge that if changes in PCO2 and pH of this magnitude occurred in more severe patients at the time of their presentation, they would have been at risk of symptoms of hypercapnia and respiratory acidosis, and the requirement to escalate treatment.
The original primary outcome measure and time of measurement was PcapCO2 after 35 min. Following the first 14 study participants, it was evident that obtaining adequate amounts of blood to fill the capillary tubes from some participants was difficult or impossible to the extent that 4 out of 14 participants had one or more missed samples. For this reason, the primary outcome was changed to PtCO2 after 35 min. In other words, the method of capturing the change in PCO2 was revised, rather than the outcome itself. PtCO2 monitoring enabled continuous assessment to be undertaken, and is accurate in AECOPD,  and other acute settings [10,11,12]. The validity of this method was confirmed by the post hoc analysis of 80-paired samples, where each capillary blood gas sample obtained had a corresponding PtCO2 measurement at the same time-point. This showed that the difference between the PcapCO2 and PtCO2 in the mean change from baseline was − 0·03 mmHg with 95% confidence intervals of − 0.44 to 0.38 mmHg. This data suggests that the use of PtCO2 measurements did not adversely affect our ability to determine change in PcapCO2 from baseline.
We did not investigate the potential mechanisms by which oxygen driven nebulisation increases PtCO2. However as demonstrated in mechanistic studies of oxygen therapy in COPD, it is likely to be due to the combination of a reduction in respiratory drive, release of hypoxic pulmonary vasoconstriction, absorption atelectasis, and the Haldane effect [13, 14]. Furthermore, the study was not designed to assess costs related to each regimen, however it is reasonable to assume that improved clinical outcomes seen by avoiding a rise in PtCO2 and associated acidosis, would lead to a reduction in healthcare costs.
The findings from our study complement those of our previous randomised controlled trial of a similar design in stable COPD patients in the clinic setting, in which there was a mean PtCO2 difference between the oxygen- and air-driven nebulisation treatment arms of 3.1 mmHg (95% CI 1·6 to 4·5), p < 0·001, after 35 min.  In that study one of the 24 subjects was withdrawn due to an increase in PtCO2 of 10 mmHg after 15 min of the first oxygen-driven nebulisation. As with the previous study, an increase in PtCO2 occurred within 5 min, indicating the rapid time course of this physiological response. We had anticipated a greater effect in this current study as the patients had acute rather than stable COPD however the magnitude of the effect was similar, probably reflecting the similar severity of airflow obstruction, with a mean predicted FEV1 of 35% and 27% in this and the previous study respectively.
The two previous open crossover studies of inpatients with AECOPD both showed oxygen-driven nebulisation worsened hypercapnia in patients with Type 2 respiratory failure [4, 5]. Gunawardena et al.  studied 16 patients with COPD and reported that only those with carbon dioxide retention at baseline (n = 9) demonstrated a rise in PaCO2 after 15 min (mean of 7·7 mmHg), and one patient had a rise of 22 mmHg. Similarly, O’Donnell et al  reported that 6/10 patients, all with carbon dioxide retention at baseline, showed a rise in PaCO2 after 10 min (mean of 12.5 mmHg).
The current BTS guidelines recommend air-driven nebulisation and, if this is not available in the ambulance service, the maximum use of 6 min for an oxygen-driven nebuliser. This is based on the rationale that most of the nebulised medication will have been delivered, and is categorised as grade D evidence . We observed the mean time for dissipation of salbutamol solution from the nebuliser chamber of 5.2 min confirming that 6 min is adequate for salbutamol delivery. The proportion of participants with a PtCO2 increase ≥4 mmHg was lower after 6 min than 15 min, suggesting some amelioration of risk with the shorter nebulisation treatment. Alternative methods of bronchodilator delivery include air-driven nebulisers or multiple metered dose inhaler actuations via a spacer .
The potential for rebound hypoxia after abrupt cessation of oxygen therapy has been observed both in the treatment of asthma and COPD [9, 16, 17]. We identified some evidence consistent with this phenomenon which is a potentially important yet poorly recognised clinical issue.
Oxygen is a gas that is vital to human life. It is one of the gases that is found in the air we breathe. If you have a chronic lung disease, you may need additional (supplemental) oxygen for your organs to function normally.
Here are some conditions that may require supplemental oxygen, either temporarily or long-term:
Oxygen therapy is a treatment that provides you with supplemental, or extra, oxygen. Although oxygen therapy may be common in the hospital, it can also be used at home. There are several devices used to deliver oxygen at home. Your healthcare provider will help you choose the equipment that works best for you. Oxygen is usually delivered through nasal prongs (an oxygen cannula) or a face mask. Oxygen equipment can attach to other medical equipment such as CPAP machines and ventilators.
Oxygen therapy can help you feel better and stay active. Learning all you can about oxygen therapy can help you feel more comfortable and confident. Use the links below to learn more.
How it works
The machine operates on electricity and requires uninterrupted power supply with power-back ups.
The machine starts releasing oxygen at the push of a button.
The device filters nitrogen and increases the concentration of oxygen for inhalation.
It is recommended to use the concentrator only if the SPO2 (oxygen saturation) level drops below 95.
It is mandatory to have a doctor’s approval to use the device.
Use an oxygen mask or nasal cannula as recommended by the medical expert for inhalation.
Ensure the filters are cleaned and do not block the air entry. It may affect the performance of the device.
Patients with asthma, COPD and respiratory ailments can also use it if prescribed by the doctors.
Surgeon Destroys Myth: ‘If Masks Don’t Work, Why Do Surgeons Wear Them?’
A response to people who use the classic fallacious argument, “Well, if masks don’t work, then why do surgeons wear them?”
I’m a surgeon who has performed more than 10,000 surgical procedures wearing a surgical mask. However, that fact alone doesn’t really qualify me as an expert on the matter. More importantly, I am a former editor of a medical journal.
I know how to read the medical literature, distinguish good science from bad, and fact from fiction. Believe me, the medical literature is filled with bad fiction masquerading as medical science. It is very easy to be deceived by bad science.
Since the beginning of the pandemic, I’ve read hundreds of studies on the science of medical masks. Based on extensive review and analysis, there is no question in my mind that healthy people should not be wearing surgical or cloth masks. Nor should we be recommending universal masking of all members of the population. That recommendation is not supported by the highest level of scientific evidence.
First, let’s be clear. The premise that surgeons wearing masks serves as evidence that “masks must work to prevent viral transmission” is a logical fallacy that I would classify as an argument of false equivalence, or comparing “apples to oranges.”
Although surgeons do wear masks to prevent their respiratory droplets from contaminating the surgical field and the exposed internal tissues of our surgical patients, that is about as far as the analogy extends. Obviously, surgeons cannot “socially distance” from their surgical patients (unless we use robotic surgical devices, in which case, I would definitely not wear a mask).
The CoVID-19 pandemic is about viral transmission. Surgical and cloth masks do nothing to prevent viral transmission. We should all realize by now that face masks have never been shown to prevent or protect against viral transmission. Which is exactly why they have never been recommended for use during the seasonal flu outbreak, epidemics, or previous pandemics.
The failure of the scientific literature to support medical masks for influenza and all other viruses is also why Fauci, the U.S. Surgeon General, the CDC, WHO, and pretty much every infectious disease expert stated that wearing masks won’t prevent transmission of SARS CoV-2. Although the public health “authorities” flipped, flopped, and later changed their recommendations, the science did not change, nor did new science appear that supported the wearing of masks in public. In fact, the most recent systemic analysis once again confirms that masks are ineffective in preventing the transmission of viruses like CoVID-19.
If a surgeon were sick, especially with a viral infection, they would not perform surgery as they know the virus would NOT be stopped by their surgical mask.
Another area of “false equivalence” has to do with the environment in which the masks are worn. The environments in which surgeons wear masks minimize the adverse effects surgical masks have on their wearers.
Unlike the public wearing masks in the community, surgeons work in sterile surgical suites equipped with heavy duty air exchange systems that maintain positive pressures, exchange and filter the room air at a very high level, and increase the oxygen content of the room air. These conditions limit the negative effects of masks on the surgeon and operating room staff. And yet despite these extreme climate control conditions, clinical studies demonstrate the negative effects (lowering arterial oxygen and carbon dioxide re-breathing) of surgical masks on surgeon physiology and performance.
Surgeons and operating room personnel are well trained, experienced, and meticulous about maintaining sterility. We only wear fresh sterile masks. We don the mask in a sterile fashion. We wear the mask for short periods of time and change it out at the first signs of the excessive moisture build-up that we know degrades mask effectiveness and increases their negative effects. Surgeons NEVER re-use surgical masks, nor do we ever wear cloth masks.
The public is being told to wear masks for which they have not been trained in the proper techniques. As a result, they are mishandling, frequently touching, and constantly reusing masks in a way that increase contamination and are more likely than not to increase transmission of disease.
Just go watch people at the grocery story or Walmart and tell me what you think about the effectiveness of masks in the community.
If you can’t help but believe and trust the weak retrospective observational studies and confused public health “authorities” lying to you about the benefits and completely ignoring the risks of medical masks, then you should at least reject the illogical anti-science recommendation to block only 2 of the 3 ports of entry for viral diseases. Masks only cover the mouth and nose. They do not protect the eyes.
Dr. Jim Meehan, MD is a physician, entrepreneur, and accomplished leader who provides novel science and solutions that conform to honest, open, transparent, and patient-centered principles.
Editor's Note: This piece originally appeared on Principia Scientific International.
Girou E, Brun-Buisson C, Taillé S, Lemaire F, Brochard L. Secular trends in nosocomial infections and mortality associated with noninvasive ventilation in patients with exacerbation of COPD and pulmonary edema. JAMA. 2003290(22):2985–91.
Campbell EJ, Baker MD, Crites-Silver P. Subjective effects of humidification of oxygen for delivery by nasal cannula. A prospective study. Chest. 198893:289–93.
Chanques G, Contantin JM, Sauter M, Jung B, Sebbane M, Verzilli D. Discomfort associated with underhumidified high-flow oxygen therapy in critically ill patients. Intensive Care Med. 200935(6):996–1003.
Mayfield S, Jauncey-Cook J, Hough JL, Schibler A, Gibbons K, Bogossian F. High-flow nasal cannula therapy for respiratory support in children. Cochrane Database Syst Rev. 20143:CD009850. doi: 10.1002/1465858.
Dani C, Pratesi S, Migliori C, Bertini G. High flow nasal cannula therapy as respiratory support in the preterm infant. Pediatr Pulmonol. 200944(7):629–34.
Itagaki T, Okuda N, Tsunano Y, Kohata H, Nakataki E, Onodera M, et al. Effect of high-flow nasal cannula on thoraco-abdominal synchrony in adult critically ill patients. Respir Care. 201459:70–4.
Sztrymf B, Messika J, Bertrand F, Hurel D, Leon R, Dreyfuss D, et al. Beneficial effects of humidified high flow nasal oxygen in critical care patients: a prospective pilot study. Intensive Care Med. 201137:1780–6.
Sztrymf B, Messika J, Mayot T, Lenglet H, Dreyfuss D, Ricard J-D. Impact of high-flow nasal cannula oxygen therapy on intensive care unit patients with acute respiratory failure: a prospective observational study. J Crit Care. 201227:324.e9–13.
Roca O, Riera J, Torres F, Masclans JR. High-flow oxygen therapy in acute respiratory failure. Respir Care. 201055:408–13.
Corley A, Caruana LR, Barnett AG, Tronstad O, Fraser JF. Oxygen delivery through high-flow nasal cannulae increase end-expiratory lung volume and reduce respiratory rate in post-cardiac surgical patients. Br J Anaesth. 2011107(6):998–1004.
Frizzola M, Miller TL, Rodriguez ME, Zhu Y, Rojas J, Hesek A, et al. High-flow nasal cannula: impact on oxygenation and ventilation in an acute lung model. Pediatr Pulmonol. 201146:67–74.
Wettstein RB, Shelledy DC, Peters JI. Delivered oxygen concentrations using low-flow and high-flow nasal cannulas. Respir Care. 200550(5):604–9.
Lampland AL, Plumm B, Meyers PA, Worwa CT, Mammel MC. Observational study of humidified high-flow nasal cannula compared with nasal continuous positive airway pressure. J Pediatr. 2009154(2):177–82.
Parke R, McGunness S, Eccleston M. Nasal high-flow therapy delivers low level positive airway pressure. Br J Anaesth. 2009103:886–90.
Ritchie JE, Williams AB, Gerard C, Hockey H. Evaluation of a humidified nasal high-flow oxygen system, using oxygraphy, capnography and measurement of upper airway pressures. Anaesth Intensive Care. 201139:1103–10.
Groves N, Tobin A. High flow nasal oxygen generates positive airway pressure in adult volunteers. Aust Crit Care. 200720:126–31.
Parke RL, McGuinness SP. Pressures delivered by nasal high flow oxygen during all phases of the respiratory cycle. Respir Care. 201358(10):1621–4.
Riera J, Pérez P, Cortés J, Roca O, Masclans JR, Rello J. Effect of high-flow nasal cannula and body position on end-expiratory lung volume: a cohort study using electrical impedance tomography. Respir Care. 201358:589–96.
Bazuaye EA, Stone TN, Corris PA, Gibson GJ. Variability of inspired oxygen concentration with nasal cannulas. Thorax. 199247:609–11.
Markovitz GH, Colthurst J, Storer TW, Cooper CB. Effective inspired oxygen concentration measured via transtracheal and oral gas analysis. Respir Care. 201055:453–9.
Andres D, Thurston N, Brant R, Flemons W, Fofonoff D, Ruttimann A, et al. Randomized double-blind trial of the effects of humidified compared with nonhumidified low flow oxygen therapy on the symptoms of patients. Can Respir J. 19974:76–80.
Campbell EJ, Baker MD, Crites-Silver P. Subjective effects of humidification of oxygen for delivery by nasal cannula. A prospective study. Chest. 198893(2):289–93.
Berk JL, Lenner KA, McFadden Jr ER. Cold-induced bronchoconstriction: role of cutaneous reflexes vs direct airway effects. J Appl Physiol. 198763(2):659–64.
Fontanari P, Burnet H, Zattara-Hartmann MC, Jammes Y. Changes in airway resistance induced by nasal inhalation of cold dry, dry, or moist air in normal individuals. J Appl Physiol. 199681:1739–43.
Greenspan JS, Wolfson MR, Shaffer TH. Airway responsiveness to low inspired gas temperature in preterm neonates. J Pediatr. 1991118(3):443–5.
Saslow JG, Aghai ZH, Nakhla TA, Hart JJ, Lawrysh R, Stahl GE, et al. Work of breathing using high-flow nasal cannula in preterm infants. J Perinatol. 200626(8):476–80.
Salah B, Dinh Xuan AT, Fouilladieu JL, Lockhart A, Regnard J. Nasal mucociliary transport in healthy subjects is slower when breathing dry air. Eur Respir J. 19881(9):852–5.
Oto J, Nakataki E, Okuda N, Onodera M, Imanaka H, Nishimura M. Hygrometric properties of inspired gas and oral dryness in patients with acute respiratory failure during noninvasive ventilation. Respir Care. 201459(1):39–45.
Oto J, Imanaka H, Nishimura M. Clinical factors affecting inspired gas humidification and oral dryness during noninvasive ventilation. J Crit Care. 201126(5):535.e9–15.
Chikata Y, Izawa M, Okuda N, Itagaki T, Nakataki E, Onodera M, et al. Humidification performances of two high flow nasal cannula devices: a bench study. Respir Care. 201459(8):1186–90.
Dewan NA, Bell CW. Effect of low flow and high flow oxygen delivery on exercise tolerance and sensation of dyspnea. A study comparing the transtracheal catheter and a nasal prongs. Chest. 1994105(4):1061–5.
Brochard L, Mancebo J, Wysocki M, Lofaso F, Conti G, Rauss A, et al. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med. 1995333(13):817–22.
Ozyilmaz E, Ozsancak A, Nava S. Timing of noninvasive ventilation failure: causes, risk factors, and potential remedies. BMC Pulm Med. 201414:19.
Nicolini A, Ferrera L, Santo M, Ferrari-Bravo M, Del Forno M, Sclifò F. Noninvasive ventilation for hypercapnic exacerbation of chronic obstructive pulmonary disease: factors related to noninvasive ventilation failure. Pol Arch Med Wewn. 2014124(10):525–31.
Millar J, Lutton S, O’Connor P. The use of high-flow nasal oxygen therapy in the management of hypercarbic respiratory failure. Ther Adv Respir Dis. 20148(2):63–4.
Bräunlich J, Beyer D, Mai D, Hammerschmidt S, Seyfarth H-J, Wirtz H. Effects of nasal high flow on ventilation in volunteers, COPD and idiopathic pulmonary fibrosis patients. Respiration. 201385:319–25.
Nilius G, Franke K-J, Domanski U, Rühle K-H, Kirkness JP, Schneider H. Effects of nasal insufflation on arterial gas exchange and breathing pattern in patients with chronic obstructive pulmonary disease and hypercapnic respiratory failure. Adv Exp Med Biol. 2013755:27–34.
Chatila W, Nugent T, Vance G, Gaughan J, Criner GJ. The effects of high-flow vs low-flow oxygen on exercise in advanced obstructive airways disease. Chest. 2004126(4):1108–15.
Kelly GS, Simon HK, Sturm JJ. High-flow nasal cannula use in children with respiratory distress in the emergency department: predicting the need for subsequent intubation. Pediatr Emerg Care. 201329(8):888–92.
Lenglet H, Sztrymf B, Leroy C, Brun P, Deyfuss D, Ricard J-D. Humidified high flow nasal oxygen during respiratory failure in the emergency department: feasibility and efficacy. Respir Care. 201257:1873–8.
Rello J, Pérez M, Roca O, Poulakou G, Souto J, Laborda C, et al. High-flow nasal therapy in adults with severe acute respiratory infection. A cohort study in patients with 2009 influenza A/H1N1v. J Crit Care. 201227:434–9.
Messika J, Ahmed KB, Gaudry S, Miguel-Montanes R, Rafat C, Sztrymf B, et al. Use of high-flow nasal cannula oxygen therapy in subjects with ARDS: a 1-year observational study. Respir Care. 201560:162–9.
Poitiers University Hospital. Clinical effect of the association of noninvasive ventilation and high flow nasal oxygen therapy in resuscitation of patients with acute lung injury (FLORALI Study). http://clinicaltrials.gov/ct2/show/record/NCT01320384
Torres A, Gatell JM, Aznar E, El-Ebiary M, Puig de la Bellacasa J, González J, et al. Re-intubation increases the risk of nosocomial pneumonia in patients with needing mechanical ventilation. Am J Respir Crit Care Med. 1995152(1):137–41.
Esteban A, Anzueto A, Frutos F, Alía I, Brochard L, Stewart TE, et al. Characteristics and outcomes in adult patients receiving mechanical ventilation. A 28-day international study. JAMA. 2002287(3):345–55.
Maggiore SM, Idone FA, Vaschetto R, Festa R, Cataldo A, Antonicelli F, et al. Nasal high-flow versus Venturi mask oxygen therapy after extubation. Am J Respir Crit Care Med. 2014190:282–8.
Parke R, McGuinness S, Dixon R, Jull A. Open-label, phase II study of routine high-flow nasal oxygen therapy in cardiac surgical patients. Br J Anaesth. 2013111:925–31.
Tiruvoipati R, Lewis D, Haji K, Botha J. High-flow nasal oxygen vs high-flow face mask: a randomized crossover trial in extubated patients. J Crit Care. 201025(3):463–8.
Futier E, Paugam-Burtz C, Constantin J-M, Pereira B, Jaber S. The OPERA trial – comparison of early nasal high flow oxygen therapy with standard care for prevention of postoperative hypoxemia after abdominal surgery: study protocol for a multicenter randomized controlled trial. Trials. 201314:341.
Schwartz DE, Matthay MA, Cohen NH. Death and other complications of emergency airway management in critically ill adults. A prospective investigation of 297 tracheal intubations. Anesthesiology. 199582(2):367–76.
Mort TC. Emergency tracheal intubation: complications associated with repeated laryngoscopic attempts. Anesth Analg. 200499:607–13.
Baillard C, Fosse JP, Sebbane M. Noninvasive ventilation improves preoxygenation before intubation of hypoxic patients. Am J Respir Crit Care Med. 2006174:1710177.
Miguel-Montanes R, Hajage D, Messika J, Bertrand F, Gaudry S, Rafat C, et al. Use of high-flow nasal cannula oxygen therapy to prevent desaturation during tracheal intubation of intensive care patients with mild-to-moderate hypoxemia. Crit Care Med. 201543:574–83.
Cörtük M, Akyol S, Baykan AO, Kiraz K, Uçar H, Cayli M, Kandiş H. Aortic stiffness increases in proportion to the severity of apnea-hypopnea index in patients with obstructive sleep apnea syndrome. Clin Respir J. 2014. doi:10.1111/crj.12244
Sahlin C, Sandberg O, Gustafson Y, Bucht G, Carlberg B, Stenlund H, et al. Obstructive sleep apnea is a risk factor for death in patients with stroke. A 10-year follow-up. Arch Intern Med. 2008168(3):297–301.
Fonseca MI, Pereira T, Caseiro P. Death and disability in patients with sleep apnea – a meta-analysis. Arq Bras Cardiol. 2014104:58–66.
Marcus CL, Rosen G, Ward S, Halbower AC, Sterni L, Lutz J, et al. Adherence to and effectiveness of positive airway pressure therapy in children with obstructive sleep apnea. Pediatrics. 2006117:e442.
McGinley BM, Patil SP, Kirkness JP, Smith PL, Schwartz AR, Schneider H. A nasal cannula can be used to treat obstructive sleep apnea. Am J Respir Crit Care Med. 2007176:194–200.
McGinley B, Halbower A, Schwartz AR, Smith PL, Patil SP, Schneider H. Effect of a high-flow open nasal cannula system on obstructive sleep apnea in children. Pediatrics. 2009124:179–88.
Haba-Rubio J, Andries D, Rey V, Michel P, Tafti M, Heinzer R. Effect of transnasal insufflation on sleep disordered breathing in acute stroke: a preliminary study. Sleep Breath. 201216:759–64.
Masip J, Betbesé AJ, Páez J, Vecilla F, Cañizares R, Padró J, et al. Non-invasive pressure support ventilation versus conventional oxygen therapy in acute cardiogenic pulmonary oedema: a randomized trial. Lancet. 2000356:2126–32.
Carratalá Perales JM, Llorens P, Brouzet B, Albert Jiménez AR, Fernández-Cañadas JM, Carbajosa Dalmau J, et al. High-flow therapy via nasal cannula in acute heart failure. Rev Esp Cardiol. 201164:723–5.
Moriyama K, Satoh T, Motoyasu A, Kohyama T, Kotani M, Kanai R, et al. High-flow nasal cannula therapy in a patient with reperfusion pulmonary edema following percutaneous transluminal pulmonary angioplasty. Case Rep Pulmonol 2014. doi.org/1 k0.115/2014/837612.
Lucangelo U, Vassallo FG, Marras E, Ferluga M, Beziza E, Comuzzi L, et al. High-flow nasal interface improves oxygenation in patients undergoing bronchoscopy. Crit Care Res Pract. 20122012:506382. doi: 10.1155/2012/506382.
Diab S, Fraser JF. Maintaining oxygenation successfully with high flow nasal cannula during diagnostic bronchoscopy on a postoperative lung transplant patient in the intensive care. Case Rep Crit Care. 20142014:198262.
Schettino G, Altobelli N, Kacmarek RM. Noninvasive positive pressure ventilation reverses acute respiratory failure in select “do-not-intubate” patients. Crit Care Med. 200533(9):1976–82.
Levy M, Tanios MA, Nelson D, Short K, Senechia A, Vespia J, et al. Outcomes of patients with do-not-intubate orders treated with noninvasive ventilation. Crit Care Med. 200432(10):2002–7.
Peters SG, Holets SR, Gay PC. High-flow nasal cannula therapy in do-not-intubate patients with hypoxemic respiratory distress. Respir Care. 201358(4):597–600.
Díaz-Lobato S, Folgado MA, Chapa A, Alises SM. Efficacy of high-flow oxygen by nasal cannula with active humidification in a patient with acute respiratory failure of neuromuscular origin. Respir Care. 201358(12):e164–7.
Boyer A, Vargas F, Delacre M, Saint-Léger M, Clouzeau B, Hilbert G, et al. Prognostic impact of high-flow nasal cannula oxygen supply in an ICUY patient with pulmonary fibrosis complicated by acute respiratory failure. Intensive Care Med. 201137(3):558–9.
Byerly FL, Haithcock JA, Buchanan IB, Short KA, Cairns BA. Use of high flow nasal cannula on a pediatric burn patient with inhalation injury and post-extubation stridor. Burns. 200632(1):121–5.
Calvano TP, Sill JM, Kemp KR, Chung KK. Use of high-flow oxygen delivery system in a critically ill patient with dementia. Respir Care. 200853(12):1739–43.