Skillful use of BiPAP and high-flow nasal cannula (HFNC) can avoid intubation and improve outcomes. However, there isn't comprehensive evidence about the nitty-gritty details of these techniques. In this post I will use my opinions to fill some gaps in the evidence (1). Noninvasive respiratory support remains more of an art than a science, perhaps a dark art at that.
Fundamental concepts
Cautions:
- Inadequate monitoring: Techniques described here are designed for an environment with close monitoring and staff available to intubate 24 hours a day.
- Multi-organ failure: Noninvasive respiratory support works best in patients with single-organ respiratory failure.
Pathophysiology of failure: why do patients require intubation for respiratory failure?
To avoid intubation, we must first understand why patients require intubation:
- Hypercapneic encephalopathy (“CO2 narcosis”). These are patients with extremely high CO2 levels (usually pCO2 > 100 mm) causing obtundation.
- Refractory hypoxemia: Inability to oxygenate despite HFNC or BiPAP.
- Respiratory muscle exhaustion: This is the most common reason for intubation, because it represents a final common pathway of respiratory failure. Any type of respiratory failure increases the work of breathing. Eventually, respiratory muscles fatigue and fail. As the diaphragm fails, the ability to cough and clear secretions is lost. This may lead to mucus plugging, which causes acute deterioration.
Given the importance of respiratory muscle fatigue, this post will focus on:
- How can we assess respiratory muscle fatigue?
- How can BiPAP/HFNC reduce the work of breathing, to prevent muscle fatigue?
Goals of therapy
The goal of HFNC or BiPAP is to stabilize the patient, in order to buy time for the underlying disease process to improve. Therefore, my goals are as follows:
- Maintain adequate oxygenation.
- Provide enough ventilatory support so that the patient is comfortable and doesn't develop respiratory muscle fatigue.
- Ensure that the patient is protecting their airway.
- Serial examination (focused on #1-#3) shows that the patient's trajectory is either stable or improving (2).
That's all. Please note that these goals don't include an immediate improvement in the pH or pCO2. For example, consider the following scenario:
- A woman with exacerbated COPD presents with severe dyspnea (respiratory rate 40/min) and acute-on-chronic respiratory acidosis. After starting BiPAP she looks and feels much better (her respiratory rate decreases to 24/min, good mental status). Repeat ABG an hour after starting BiPAP shows no change.
Some would call this a “BiPAP failure” because the pCO2 is unchanged, leading them to intubate her. However, this is actually BiPAP success, because her dyspnea has resolved. Her pCO2 will eventually improve, after steroids and bronchodilators have had more time to work. Treat the patient, not the ABG. This concept was proven by Brochard 1995 in a RCT evaluating the use of BiPAP in COPD: BiPAP improved mortality despite having no effect on ABG parameters after one hour. This study shows that BiPAP can be successful, even without any immediate effect on the ABG.
Assessment
For most patients on noninvasive respiratory support, clinical assessment is all that’s needed. This involves three or four pieces:
- Oxygenation: If the patient has a good pulse oximetry waveform, the preferred method is simply to monitor pulse oximetry (ABG is rarely needed to measure oxygenation).
- Work of breathing: The best metric is the respiratory rate. Worsening tachypnea (e.g. respiratory rate >35 b/m) suggests that the patient may eventually tire out. Additional warning signs include retractions, diaphoresis, tripoding, shallow breathing, and an abdominal paradoxical breathing pattern. Asking the patient how they feel is generally useful, but some patients minimize their symptoms.
- Mentation: A patient who is easily arousible and mentating adequately doesn't have life-threatening hypercapnia (3).
- BiPAP monitor: Low tidal volumes and/or low minute ventilation may suggest hypoventilation (4). Alternatively, adequate tidal volumes and minute ventilation suggest a satisfactory response to BiPAP.
Look at the monitor and the patient, talk to the patient, perhaps try to wake them if they are sleeping. That's all. An experienced clinician will perform this assessment in about a minute.
The most common problem with assessment is excessive reliance on ABG values. This is problematic for many reasons:
- For most causes of respiratory failure (e.g. pneumonia), elevated pCO2 is a very late sign of deterioration (only occurring after the patient is profoundly fatigued and close to respiratory arrest). Thus, a normal pCO2 can be falsely reassuring.
- Many patients are on opioids, either acutely or chronically. Opioids may cause hypercapnia, which makes the ABG look like the patient is in frank respiratory failure.
- ABG values are often scary for practitioners who don't use these on a daily basis (e.g. 88% oxygen saturation corresponds to a PaO2 of ~55 mm, a number which may incite panic).
- There is a lot of random variation in serial ABG values (e.g. pCO2 values vary randomly by as much as +/- 5 mm)(5). Random variation is commonly misinterpreted as deterioration or improvement.
- Excessive trust in blood gas values may cause practitioners to ignore their instincts:
One situation where ABG/VBG is necessary is the somnolent patient who has received sedation (e.g. to facilitate tolerance of the BiPAP mask). Blood gas analysis is needed to sort out whether somnolence is due to hypercapnia or medication effect. Please note that VBGs are generally completely adequate to monitor a patient with respiratory failure. If the patient has a peripheral IV line with blood return, this is a humane and rapid approach to obtain VBGs.
The key to assessment is frequent assessment by multiple providers. Patients will be serially evaluated by a nurse, a respiratory therapist, and a physician. When in doubt, all providers should discuss their impressions. A team approach combines dozens of assessments by several experienced clinicians.
https://twitter.com/PulmCrit/status/960175317783543808
Device selection
Below is my general rubric for noninvasive respiratory support. Let's walk through it step by step.
Is immediate intubation needed?
The decision to intubate is beyond the scope of this post. However, it's worth mentioning a few “fake-out” situations, where patients look horrible but usually don't require intubation:
- Sympathetic crashing acute pulmonary edema (SCAPE) – these patients will often turn around within minutes in response to BiPAP and high-dose nitroglycerine infusion.
- Acute bronchospasm (COPD/Asthma) – may improve dramatically in response to BiPAP, bronchodilation, and sedation (e.g. dexmedetomidine or ketamine).
- Vocal cord dysfunction – patients have true upper airway obstruction, but improve rapidly with sedation or ketamine.
- Pneumothorax, pericardial tamponade, or massive pleural effusion – drain it.
Are there contraindications to full-face BiPAP?
Contraindications include:
- Significant secretions: Positive pressure and the BiPAP mask impair expectoration. Sometimes, it is possible to maintain a patient on BiPAP with occasional breaks on HFNC for secretion clearance (e.g. a COPD patient with mild secretions). However, for a patient with copious secretions, BiPAP is contraindicated. In such cases, BiPAP may initially have excellent results, but eventually mucus plugging occurs with abrupt deterioration.
- Facial trauma, burns, or other anatomic problem with mask seal.
- Risk of aspiration: Aspiration may occur if the patient vomits and is unable to remove the BiPAP mask. Therefore, evaluating aspiration risk requires judging the likelihood of vomiting (e.g. increased with bowel obstruction or pancreatitis) versus the mental status. Note that altered mental status due to hypercapnia isn't an absolute contraindication to BiPAP.
There are nearly no contraindications to HFNC, so any patient with a contraindication to BiPAP can be treated with HFNC (6). BiPAP with a nasal interface can also be considered here, especially if HFNC isn't available (7).
BiPAP-sensitive conditions
BiPAP has some important advantages compared to HFNC:
- Positive pressure reduces pre-load and after-load on the heart, improving heart failure (this works similar to an ACE-inhibitor – but easier to titrate and no nephrotoxicity).
- BiPAP can provide a greater amount of mechanical support for breathing. This is desirable for patients with respiratory muscle weakness or obesity-hypoventilation syndrome (both conditions involve an imbalance between diaphragmatic strength versus work of breathing).
- For patients with small airway obstruction (e.g. COPD/asthma), BiPAP can provide mechanical support. The expiratory airway pressure (PEEP) may also help stent open airways during exhalation (8).
For patients with these conditions, I will generally make a real effort to use BiPAP. If the patient can't tolerate BiPAP due to anxiety, it may be worth using sedation to facilitate BiPAP tolerance. Sedation is particularly useful for patients with COPD or asthma, who require a slow respiratory rate in order to exhale properly:
Some brief comments on various sedatives to facilitate BiPAP:
- Dexmedetomidine is very effective and safe if the patient can wait long enough to titrate this up (9). Dexmedetomidine can be up-titrated to induce light sleep, without affecting respiratory drive.
- Ketamine dissociation may be useful up-front, especially in asthma (because it provides bronchodilation). This only provides sedation for 30-60 minutes, so another agent may be needed for ongoing sedation.
- Fentanyl in tiny divided doses may be effective in patients who are very tachypneic, but requires caution and meticulous monitoring (explored further here)(10).
- IV haloperidol or olanzapine may be considered (with the advantage that they don't suppress the respiratory drive).
- Benzodiazepines have unpredictable effects. They sometimes work, but can also cause confusion or paradoxical agitation.
General BiPAP titration schemes are shown below (11):
HFNC for patients with parenchymal lung disease (e.g. pneumonia)
Parenchymal lung disease refers to any primary disease of the alveolar tissue itself. The advantages of HFNC here include the following:
- Reduction in work of breathing due to dead space washout
- Preserved ability to cough & clear secretions
- Excellent tolerance, including for extended periods of time (important for patients with interstitial lung disease who may take several days to recover)
- Improved ability to communicate with patients and assess their progress
Compared to heart failure and COPD, parenchymal lung disease is a less BiPAP-responsive physiology. Studies have found questionable benefit from BiPAP in this situation. The FLORALI trial showed that in a group of patients with hypoxemic respiratory failure (mostly from pneumonia), HFNC was more successful than BiPAP at avoiding intubation and improving mortality.
Treat pleural disease with drainage
If a pneumothorax or pleural effusion is causing acute respiratory failure, the best treatment is drainage. The concept of immediate drainage of a pneumothorax is universally understood. Unfortunately, emergent drainage of a pleural effusion remains under-utilized.
Temporize upper airway obstruction with Heliox
Heliox is a fixed-ratio mixture of helium and oxygen which has lower viscosity than air. This may be used to stabilize patients with upper airway obstruction. One limitation is that these ratios contain a fixed amount of oxygen (typically 70-30 mix or 60-40 mix with 30% or 40% FiO2), so they cannot be used for patients who require >40% inspired oxygen. Heliox isn't a cure for upper airway obstruction, but it may be useful:
- Stabilization of post-extubation laryngeal edema, giving steroid time to work.
- Stabilization of the patient with undifferentiated stridor, allowing time to gather materials and personnel for safe management (e.g. difficult airway cart, bronchoscope, colleague prepared for cricothyrotomy with double-setup).
Avoid BiPAP or HFNC in primary CNS disease
One practice which drives me crazy is the use of BiPAP for treatment of hypercapnia due to drug intoxication. If the patient is so severely intoxicated that they truly need ventilatory support, then they should be intubated (aspiration risk precludes the use of BiPAP here). A reasonable approach to these patients may be as follows:
- If the patient is protecting their airway and doesn't clearly need intubation, then monitor very carefully on room air or low-flow oxygen (12). If the pCO2 is moderately elevated, that's OK as long as the patient is clinically doing OK (e.g. protecting airway, oxygenating, not rapidly deteriorating). Please note that mild hypercapnia is an expected feature of opioid intoxication, so it shouldn't cause panic. Treat the patient, not the ABG.
- If the patient isn't protecting their airway, attempt antidotal therapy (e.g. naloxone). If this fails, then intubate.
Consider HFNC if the diagnosis is unclear
For a patient with unclear diagnosis, either BiPAP or HFNC could be used. My preference is HFNC for the following reasons:
- HFNC facilitates communication, including obtaining additional history.
- BiPAP may make some patients look much worse (due to anxiety) or others look much better (due to treatment of CHF or COPD). This can confuse matters if you don't know what is going on.
Choice of BiPAP vs. HFNC depends on the diagnosis, not the ABG
For example:
- Consider a patient with COPD or heart failure, who is in severe respiratory distress and has a normal pCO2 level. This patient will benefit from BiPAP, even though the pCO2 level is normal.
- Consider a patient with intoxication and elevated pCO2 level. BiPAP is not useful here to “blow off the CO2” – as discussed above it is actually contraindicated.
Selecting the treatment based on the diagnosis streamlines management. The diagnosis can generally be determined rapidly on the basis of history, physical exam, and bedside ultrasonography. This allows for immediate treatment, without waiting for an arterial blood gas measurement.
Parting shot: the value of empiricism
This post is intended to provide a rational framework, but not a rigid one. Due to individual factors (e.g., mask seal, anxiety), the response of individual patients isn't entirely predictable. If one device isn't working, try something else. As long as you are monitoring patients closely to ensure that they are responding adequately, any strategy is acceptable.
- The role of noninvasive respiratory support is generally to reduce the patient's work of breathing, thereby avoiding diaphragmatic exhaustion.
- The goal of noninvasive respiratory support isn't to immediately normalize the ABG.
- Serial evaluation by experienced practitioners is generally far more useful than monitoring ABG values.
- The choice of BiPAP vs. HFNC may be made on the basis of the patient's diagnosis (e.g. pneumonia vs. heart failure), not the ABG values.
- BiPAP should never be used to “blow off” CO2 in a patient with hypoventilation due to drug intoxication.
Links
- Optimizing respiratory drive to avoid failure (PulmCrit) – Probably most relevant companion post to this one.
- Avoiding gratuitous ABGs
- Sedation for the anxious COPD patient & more discussion of Flash COPD (PulmCrit)
- Sympathetic Crashing Acute Pulmonary Edema (SCAPE) – EMCrit's classic inaugural podcast from 2009.
- HFNC for pneumonia (FLORALI study; PulmCrit)
- HFNC to avoid reintubation part I (contains some basic information on HFNC; PulmCrit)
Notes
- I initially gave a grand rounds presentation about this topic two years ago, with the intention of posting a blog about it shortly thereafter. I wrote a blog but wasn't happy with it. Re-wrote the blog a year later, but still wasn't happy with it. The problem was that there isn't much evidence, so the blog ended up being more expert-opinion type stuff than I would like. This time around I committed to just clean it up as best as possible and post it. I expect that there will be some lively debate about much of this, which is a good thing.
- BiPAP cannot be continued without a break for too long (>24-48 hours) without causing nutritional problems and pressure necrosis of the nasal skin. Thus, if the patient fails to improve on BiPAP for 1-2 days, then a transition to HFNC or intubation is needed.
- Hypercapnia is generally extremely well tolerated. The way that patients die from hypercapnia is usually hypercapneic encephalopathy causing somnolence, airway loss, apnea, and hypoxemia. Therefore, a patient who is mentating well is unlikely to have life-threatening hypercapnia.
- The amount of minute ventilation per liter that patients will need depends on their size, their metabolic activity, and the amount of dead space in their lungs (pulmonary dysfunction). This is an important parameter to pay attention to in any patient on BiPAP or invasive ventilation. Over time, practitioners should gain a general sense of how much minute ventilation various patients will need. An average patient at rest might need about 6-7 liters/minute. A patient with COPD exacerbation will have poor pulmonary function and might need more (e.g. perhaps 8-10 liters/minute). Thus, if you encounter a COPD patient on BiPAP who is receiving 4 liters/minute, this should be concerning as it is likely rather low. Like ABG numbers, the minute ventilation is only one number which must be placed into proper clinical context. Trending the tidal volume may be more useful than focusing on a single number.
- References: Umenda 2008,Sasse 1994, Thorson 1983, Hess 1992.
- A patient with bilateral nasal packing couldn't receive HFNC. I suppose that if a patient just had nasal surgery then HFNC might not be a terrific idea, but I've never encountered this situation.
- The preferred mask type for BiPAP is a full-face mask, given some evidence that this has a lower failure rate compared to a nasal mask (Girault 2009). This post is written in reference to full-face BiPAP. However, it is certainly possible that nasal BiPAP could be used, which would avoid problems regarding aspiration. Some evidence does support the use of BiPAP with a nasal interface (e.g. Bott 1993). The helmet mask seems extremely promising, but this isn't currently available in the United States.
- There is outstanding evidence for the use of BiPAP in COPD, but much less evidence regarding the use of BiPAP in asthma. This likely reflects the fact that status asthmaticus is less common than exacerbated COPD and harder to study. Both disease processes have similar physiology, so the fact that BiPAP works well in COPD implies that it should also work well in asthma.
- Due to the potential for hemodynamic instability with boluses of dexmedetomidine, my usual practice is to start the infusion without a bolus at a relatively high level (e.g. 1-1.4 mcg/kg/hr) and then gradually titrate down over the next 30-90 minutes. This is safer than using a bolus, but doesn't achieve immediate sedation.
- The best opioid here is arguably a remifentanil infusion, because it is very titratable. Eventually if remifentanil becomes generic and comes down in cost, this could be an enormously valuable agent for these patients. Currently remifentanil isn't available in most emergency departments or ICUs.
- There are some very passionate arguments about how much PEEP should be used in various conditions. For example, many people argue that asthmatic patients should be placed on zero PEEP, to facilitate exhalation. However, this isn't possible using my machine (to achieve pressurization, the lowest possible PEEP is ~3 cm). Other folks argue that higher levels of PEEP are useful in COPD/asthma to stent open the airways during exhalation. The BiPAP settings recommended here are reasonable in a variety of situations, but not necessarily perfect. An inspiratory pressure >20-25 cm may cause gastric insufflation and promote vomiting.
- Ideally these patients should be monitored with end-expiratory CO2 to further trend their ventilation.
- PulmCrit Wee – A better classification of heart failure (HFxEF-RVxEF) - August 26, 2024
- PulmCrit Wee: Rational selection of infusion rate based on loading dose - June 25, 2024
- PulmCrit: PPIs are safe and effective for GI prophylaxis… the end. - June 18, 2024
Great post, addresses things I’ve inherently known but couldn’t verbalize. thanks Josh!
Thanks Christine, glad we’re on the same page.
Very enjoyable read. Thanks for the post.
Bloody damn brilliant I’d say…. Even if the new use of “rubric” annoys the hell out of me:)
yep, well, most of the synonyms of rheubric are annoying as well (paradigm, schema, algorithm). All of these words have been abused to provide decoration to lots of boring ideas.
Grate post. I really enjoyed reading it. Thanks a lot.
very excellent.
unlike for christine below, for me this addresses things i neither inherently knew, nor could verbalize.
but now is significantly clearer.
the trick for most of this, for many of the pearls taken from the “oysters”, of emcrit, and other treasure-sources like edecmo, steve smiths blogs, or the many others, is for me to actually incorporate these thoughts, considerations, practices back when i return to my shop….
that is, to when appropriate, make actual practice and mindset changes, for me personally, and sometimes a “culture” change for the shop generally.
thank you Josh. excellent as always.
tom
thanks, good luck. The blog may make this seem simple but the reality is often murky. Despite being obsessed with critical care for years, at times I still struggle with these decisions.
Thanks for a great post as alway!
About the tidal volume on NIV it seems that low is bad but….too high seems also bad because of a VILI-like mechanism.
Papers from Carteaux, CCM, 2016 and Frat, ICM, 2018 show a correlation between Vt > 9 ml/kg and intubation requirement and bad outcome.
Excessively high tidal volume correlates with failure, the question is why. It’s possible that higher tidal volumes reflect more dysfunction lungs (greater dead space), which requires patients to take bigger breaths to clear CO2. In short, the higher tidal volumes may be a *reflection* of more severe underlying lung disease, rather than a *cause* of harm. As always, correlational studies cannot define causality. That said, I do agree that excess pressure and volume could certainly be harmful. Unfortunately, I’m not aware of any good prospective data that evaluates this in non-intubated patients. Some people have occasionally advocated for intubation as… Read more »
I just wanted to add a caution to selection of NIV therapy, and that is, while BiPAP is easily accomplished should a patient require interfacility transfer to another hospital with more advanced capabilities, HFNC is generally not possible to do during transport because nobody carries the required equipment. So if a patient is started on HFNC at a tertiary hospital and will have to be transferred, they will have to go on BiPAP for the transfer to happen. I’ve had countless nurses look at me funny when I have had to tell them “that’s nice that they are on HFNC,… Read more »
Excellent point! Most ambulances won’t be able to accommodate HFNC, so if a patient is going to be transported then BiPAP is generally the best choice. This may also apply to long transports from one end of the hospital to the other. HFNC consumes oxygen at an enormous rate, which limits its portability.
The mobile ICU transport vans at the University of Vermont can actually deliver HFNC using liquid oxygen (don’t ask me exactly how this works, but it seems pretty neat). However, this is the exception that proves the rule.
A newly available super oxygenating mask system (SentriO Oxy, http://www.healomedical.com) for spontaneously breathing patients has been shown to outperform HFNC at 60 LPM but on just 10 LPM flow. SpO2 of 92% for a COVID patient on 60 LPM HFNC increased within two minutes to SpO2 of 99% on 10 LPM using SentriO. That’s an 83% reduction in O2 consumption, or 72,000 liters saved per patient per day. If O2 only cost one cent per liter, that’d be $720/day in oxygen savings. Bench data from UT-Health Sciences Center St. Antonio using artificial lung compared oxygen concentration in the trachea: HFNC… Read more »
Fantastic summary post!
Thanks for this amazing work Josh. I’m wondering, why don’t you put CPAP on better place in “O2” situation ? In France too, most ICU and ED use BIPAP in acute pulmonary oedema (with mainly PEEP use), even without hypercapneic acidosis. As far as I know, there is no evidence of BIPAP superiority (even in respiratory exhaustion with hypercapneic acidosis) when the basic etiology is acute pulmonary oedema, and no chronic respiratory desease like COPD in the background. That seems logical to give respiratory support in a respiratory exhaustion situation, but there is no study to show increase of morbidity/mortality… Read more »
“to show DECREASE (and not increase) of morbidity/mortality VS simple CPAP.”, sorry
Can you clear something up for me please. Is NIV contraindicated in a hypotensive and compromised patient due to reduced venous return or is that a bit of an old wives tale?
I don’t think there is an absolute yes/no answer here. First, patients in multi-organ failure (e.g. hemodynamic instability plus respiratory failure) are overall less likely to do well with noninvasive ventilation. That doesn’t mean that you absolutely can’t use NIV with these folks, but just be careful and use your clinical judgement. Second, positive pressure ventilation can reduce venous and blood pressure in some patients. So once again, added caution is required here. However, typically NIV is ramped up gradually so it’s unlikely that you would suddenly crash someone’s blood pressure (e.g. start 10/5, see how it goes, gradually ramp… Read more »
Critically ill patients on mechanical ventilatory support for a variety of etiologies often have moderate sized pleural effusions. Is it your practice to err on the side of tapping these effusions especially in patients with frailty and marginal respiratory reserve to facilitate weaning ?
Hi, not sure if you mentioned it but just wondering what your thoughts are about NIV in someone with haemodynamic instability? I’ve grown up learning that it’s a contraindication because it will knock out their venous return but is this accurate?
An interesting read again! Some miscellaneous thoughts: – The practice of obtaining an ABG as the first step in managing an acutely unwell patient drives me crazy. It’s rarely helpful in narrowing down the diagnosis of hypoxemia. Unfortunately we are often asked for this to be done early. – Most patients in respiratory distress who are managed with NIV or HFNC should probably be monitored with an arterial line (to pick up on septic shock setting in once the sympathetic drive of not breathing wanes, to titrate vasodilators in SCAPE, to not wake them up for NIBP when they’re finally… Read more »
I work as a Rapid Response RN full time. We are very frequently putting bipap on patients with non-opioid-related symptomatic hypercapniec respiratory failure after ruling out need for narcan, contraction alkalosis, etc. After consideration of any concurrent hypoxemia, I always minimize FiO2 as much as safely possible, especially in COPD, with the aim of increasing respiratory drive. Unfortunately, even though the MDs at bedside agree with this in theory, the RT and RN in the ICU seem to invariably increase FiO2 to 40% even on my patient who was fine on 21%. Is there any evidence of low FiO2 increasing… Read more »
Excellent post, thank you for providing us such accessible knowledge to be able to help our patients! You mentioned these things in your post, but I just wanted to clarify – I was taught in school that iPAP helps with work of breathing and ePAP helps with hypoxia. Would you say that is correct? If so, then in a situation where you see that the patient needs helps with work of breathing, you would increase the iPAP and leave the ePAP alone? Im imaging a COPD patient here who’s tachypneic. In a situation where someone is mainly hypoxic, would you… Read more »
@Scott Luchsinger. Farkas
Does the benefit of BiPAP in heart failure depend on the kind of heart failure? for example pre-load dependent HF (severe diastolic HF), can’t it be detrimental?
Best Non-invasive ventilatory support overview I have read. Doesn’t replace reading chapters, lectures, etc. But great overview, with the pearls to keep on a phone, for those of us who practice far away from intensivists, or cover for them at night. I’ll definitely ask rotating residents read it.
This is the best and easy-to-understand article about NIPPV I have ever read. This is coming from a 2nd year internal medicine resident! Thank you so much
Excellent explanations
Thanks Josh
Makes it easy to explain to the residents
I dint get why Higher Peep bipap titration works in chf
And how do I reduce the work of breathing in covid pts
Thank you
Excellent read thank you!
This information is very helpful. It’s educating because I’m an lpn. I’ve use cpap and couldn’t tolerate it. I just started a bipap which has lowered my apnea events. I have a hard time with the air escaping from face mask but I’m trying to use it.
Hi my fiancee is 40yrs old but had heart and lung surgery at 5months old and was incubated for 8months after. Now she suffers from hypercapnia has been hospitalized for intubation 3 times in 9months. She use 4lpm on home Concentra and has an Astral 150 bipap but complains of a fluttering in her left ear alot along with headaches in the morning. She also has anemia. I’ve had to adjust her bipap as her provider for the machine are just uncaring of her suffering. I currently have it set at 10 ipap 3 epap, rise time at 200, trigger… Read more »
Excellent clinically oriented article , great job
You are doing the Lord’s work here.
fantastic post, so handy and easy to understand