High-flow nasal cannula oxygen therapy in patients undergoing thoracic surgery: current evidence and practice Always give credit when credit is due and cite your sources. The article below isn't free, but if you can get your hands on it, it has some really nice tables. In particular, there is one table where they compare non-invasive ventilation to high-flow nasal cannula with regards to comfort, airway pressure and PEEP (see more on my post about that yesterday), anatomical dead space, CO2 washout, mucociliary function, pulmonary effects, extra pulmonary effects, skin breakdown and sores. It's worth checking out if you have access to this journal.
Wittenstein, J., Ball, L., Pelosi, P.; Gama de Abreu, M. (2018). High-flow nasal cannula oxygen therapy in patients undergoing thoracic surgery. Current Opinion in Anaesthesiology, 1. Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
Please note that I have sorted out this issue and the following rant is a rant on my thought process leading up to my eventual resolution. I was trained, or maybe even made it up in my head, that for every 10L of flow increase on the high flow nasal cannula, HFNC, you get 1cmH2O of "PEEP". Is this accurate? The short answer in my opinion is no. At least not the way you're thinking about it. I've been digging pretty deep into the topic because although much data is suggestive of it, but I can't find something that I can clearly understand. Maybe it's just my lack of intelligence or lack of direct pulmonary training. Positive end-expiratory pressure (PEEP) is defined by UpToDate as the alveolar pressure above atmospheric pressure that exists at the end of expiration. Therefore, we need to look at alveolar pressure directly. In particular, we need to look at extrinsic PEEP. Without a closed system, we cannot obtain that data. I have run into several papers cited below that discuss methodologies used to estimate what PEEP should be in the HFNC system. The 2009 Parke study looked at the mean nasopharyngeal airway pressure and deemed it to be 2.7cmH2O with a flow of 35L and the mouth closed. That's not the alveolar pressure. The Corley study utilized electrical impedance tomography along with a transducer placed nasally that ran down into the esophagus that measured the airway pressure. With the flow in the study between 35-50L on the HFNC system, the authors found that there was an increase in the airway pressure by 3cmH2O. Is this what's being considered as PEEP? Lastly, Parke performed another study in CVICU patients where she and her team measured nasopharyngeal pressures at 30L, 40L, and 50L, and concluded that the HFNC system provided 3-5cmH2O of PEEP. I guess that's where the numbers I was taught came from. But in reality does that translate to PEEP? Do we just need to accept that we are comparing apples and oranges? Do we just need to change our language since we are just so comfortable of saying "PEEP" because we're used to it on our ventilators? Am I just going to have to delete this post after I am exposed as being a moron when a number of people just comment about how silly am I that I do not know this stuff? Why are we even trying to compare the two? We know that pharyngeal pressure is increased by the HFNC system. That's fine and dandy. Patients do well on HFNC when used in the correct setting. Plenty of data to support that. But this system uses flow rather than pressure and we are comparing apples to oranges. The three articles are all FREE! Links below. Addendum: tonight is 9/24/19 and it's 4:34 in the am. I am currently working a night shift. I have run into additional data that has provided me with some perspective as to the whole PEEP/Paw discussion. Parke performed a study that was published in 2015 using Electrical Impedance Tomography where there was a marked improvement in the end-expiratory lung volumes. Then Frat, the main author of the FLORALI trial, commented on the mechanism of how this happens by stating that the large nasal prongs create a resistance to the exhaled air by continuously pushing high flow air and in turn this causes positive pressure. The issue lies when the patient opens their mouth. This could be highly variable. Anyway, I still take issue with the numerical measurement of it.
Corley A, Caruana L, Barnett A, Tronstad O, Fraser J. Oxygen delivery through high-flow nasal cannulae increase end- expiratory lung volume and reduce respiratory rate in post-cardiac surgical patients. Br J Anaesth. 2011;107(6):998- 1004.
Parke RL, McGuinness SP: Pressures delivered by nasal high flow oxygen during all phases of the respiratory cycle. Respir Care 2013; 58:1621–1624. Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
Nasal high flow oxygen therapy in do-not-intubate patients with hypoxemic respiratory distress This topic is very dear to me because I am a huuuuuuuge proponent for appropriate end of life care. I'm an Intensivist after all and people unfortunately die on my service. We all are going to have our day. My goal with the patients I take care of is to make their passing to the next life as comfortable as possible with as much love surrounding the individual as humanly possible. It irks me at times when clinicians write patients off just because they have a DNR/DNI order written. For the non-medical people around here that means do not resuscitate/do not intubate. Also, what are you doing around here? Those patients also need our best efforts as they are already cognizant of their impending mortality. That usually means their friends and family members are also aware and would rather be around when the inevitable to all of us occurs and they pass. In this article, the authors attempted to avoid utilizing non-invasive ventilation, or as most of us just call it, BiPAP, by placing patients on high flow nasal cannula. Small study, 50 patients. Can you imagine the difficulty in enrolling patients into a study like this? It must have been quite challenging. In short, although mortality in hospital was appropriately high, they found that they were able to avoid placing patients on BiPAP in 82% of patients. To me, this is particularly important because that means these patients were able to comfort eat, speak to their families, say their goodbyes, give them unobstructed hugs (due to the BiPAP mask), kisses, and smiles without a NIV mask in the way. The decreased RR as a clinician to me is significant because if there's one thing that makes me uncomfortable, it's a patient who is in frank respiratory distress sucking wind to survive. A respiratory rate decrease from 30.6 to 24.7 is something I'd take any day. This is something I do in my practice. I was very happy to run into their article and find some data to support what I anecdotally believed.
A hat tip to the authors.
-EJ
Peters S, Holets S, Gay P. Nasal high flow oxygen therapy in do-not-intubate patients with hypoxemic respiratory distress. Respir Care. 2013 ; 58(4): 597-600.
Link to full FREE article Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
Association between soft drink consumption and mortality in 10 European countries This study is trying to tell me that soft drinks, whether they are diet or sweetened by sugar are associated with higher mortality? I honestly can't say I'm surprised. Glad I'm not investing in the Coca Cola company. I personally do not drink sodas but I do indulge on a Diet Dr Pepper every now and then. Guess I'll be cutting that out soon. But you're here for the data. I am omitting some of the data because I can't analyze and cover it all. Let's take a good look at this study.
They started off by stating that sugar sweetened drinks could cause approximately 184000 deaths due to cardiovascular issues, cancer, and diabetes. To look at the numbers in Europe, where this study took place, they used the European Prospective Investigation into Cancer and Nutrition cohort that has followed up patients from the general population of 10 European countries which include Denmark, France, Germany, Greece, Italy, the Netherlands, Spain, Sweden, and the UK. In America we tend to think that these countries are healthier than ours. This "EPIC" cohort, pun intended, had 521330 patients in it. They ruled out a number of patients for reasons specified in the paper and ended up with 451743 patients. The famously large Framingham heart study has been going on for 70 years now and doesn't have anything remotely close to that many patients involved. 451743 to be exact. WOW!
They figured out if and how many soft drinks these people consumed by different methods including interviews and questionnaires. People lie. That's a limitation of the study in my opinion but with almost half a million patients, the liars could be mitigated. They also asked many other questions, like smoking and exercise habits, in the questionnaires, etc, so this data isn't only for soft drink consumption. They used ICD-10 codes to figure out for what reasons the 41693 patients died. The researchers did a bunch of statistical jumping jacks that I am not going to go through. I'm am honestly going to lump together the patients who were drinking both soft drinks with sugar and soft drinks without sugar for the sake of simplicity. Again, read the article for yourself.
Here are the results that I find interesting about the groups: 1. Amongst all the patients, 43.2% of patients died from cancer. 2. Women made up 76.5% of the group that drinks less than 1 glass per months vs 60.9% of the group that drinks greater than or equal to 2 glasses per day. 3. The BMI is 1 point higher in those who drink greater than or equal to 2 glasses per day (median) 4. People who drink greater than or equal to 2 glasses per day claimed to be more physically active than with 27.8% of them saying they are physically active versus 15.5% in the 5. The greater than or equal to 2 glasses per day group also ate more red meat, fewer fruits and vegetables, more coffee, and more fruit and vegetable juices. No notable difference in alcohol consumption in my humble opinion.
Let's talk mortality Higher all cause mortality with greater than or equal to glasses per day of soft drinks. That includes sugar sweetened and artificially sweetened. That also includes if you're male or female.
Regarding circulatory diseases Same thing here. Higher circulatory mortality risks for those consuming greater than or equal to 2 glasses of soft drinks per day. If you break it down between the sugar vs artificial sweetener groups, however, the sugar group was not statistically significant. I guess that can be interpreted as don't drink the diet stuff.
Regarding Cancer This was interesting because they only found an association in colorectal cancer deaths. I expected them to find a risk with overall cancer.
There was an association with soft drinks, both types, and risk of Parkinson disease mortality.
All in all, the researchers found that higher risks were observed when people would consume more than 125ml (that's just half a glass!!) of diet stuff and 250ml (just one glass!!) of the not diet stuff. I wonder what they considered high fructose corn syrup to be? They were also perplexed as to why artificial sweeteners caused the increase in mortality despite being "zero calorie". They don't have an answer to that and are seeking more data.
As with every other study, this one has some notable limitations such as the fact that it is an observational study. There's no other way, honestly, to be able to perform a study of this scale. They also cannot identify causality. They also only asked the people in the study only once (upon enrollment) if they consumed soft drinks. That means that patients could have changed their habits, either started consuming soft drinks or stopped. Or switched to diet or switched to regular. No way of knowing.
Overall I know the media is on a frenzy right now with this study and I thought it was pretty cool so I hope that you all gained something from it.
As always, a big hat tip to the authors!
-EJ
Mullee A, Romaguera D, Pearson-Stuttard J, et al. Association between soft drink consumption and mortality in 10 European countries [published online September 3, 2019]. JAMA Intern Med.
Link to Abstract Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
Understanding lactatemia in human sepsis: potential impact for early management
Having an elevated lactate in septic acid on admission is bad. Trending it, as studies that I have shown on this page does not change mortality. Seeing the numbers downtrend do give us that warm and fuzzy feeling inside, though. We give off a sigh of relief when that number becomes "euboxic". This article was published in April 2019 and authors explained the different mechanisms by which lactic acid is elevated in septic patients. 1. a deficit in oxygen delivery or extraction 2. shunting 3. stress 4. increased adrenergic stimulation
Notice that none of these mean that we have to drown the lactates with a bunch of fluids thereby diluting the value. We need to go after the etiology of it in a more specific manner. The authors of this study looked at the patients enrolled in the ALBIOS study (you know, the 2014 study where they sorted out that giving patients in septic shock albumin was good for depleting hospital resources but not a survival benefit? I guess I need to cover that trial on here) and used more than 1700 patients in whom lactate and central venous oxygen saturation were measured. They did a bunch of calculations and statistics that I am not going to cover here but you can click on the link for the article and go to town on it if you so wish.
Something really interesting was found in this study. The authors found that 1017 patients had a lactic acidosis but 57% of those patients had a normal serum pH. I would've thought that the number would have been lower. And it's not because these patients were on bicarbonate drip band-aids either.
The Early Goal Directed Therapy trial made us infatuated with checking central venous oxygen sats and our target was to get that to be over 70%. This study showed us that only 35% of that patients they looked at had a value less than 70%. 65% of patients with an elevated lactic acid had a normal or high ScVO2. Strange. We do know that the extremes of ScVO2 are bad and that ultimately ScVO2 has a number of limitations within itself. Anyway, I'm not going to dive too deep into all that, I'll leave it for the authors to explain.
All in all their main conclusion in this study, and the important takeaway is that lactate is not primarily created in sepsis by of the cells not receiving enough oxygen, but rather by impaired tissue oxygen utilization. This is a game changer. In my opinion, it doesn't mean that fluids are the answer, but rather, to find a way to help the tissues use said oxygen. Now let's all change our practice.
Don't take my word as gospel on all this, I could be wrong. Read the article for yourself. A hat tip to the authors.
Gattinoni, L., Vasques, F., Camporota, L., Meessen, J., Romitti, F., Pasticci, I., … Marini, J. J. (2019). Understanding Lactatemia in Human Sepsis: Potential Impact for Early Management. American Journal of Respiratory and Critical Care Medicine.
Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work!
Balanced Crystalloids Versus Saline in Sepsis: A Secondary Analysis of the SMART Trial
Sometimes we need to make minor adjustments in what we do in the ICU to see a difference. I have been going off for several years now on my instagram account as well as YouTube channel regarding the importance of utilizing balanced crystalloids such as lactated ringers or plasma-lyte and I keep on hearing "there's no mortality benefit". Well, now there's data showing that there is. I knew it was just a matter of time. It just makes sense. This analysis is a piggyback on the SMART trial performed by the good people over at Vanderbilt published last year in the NEJM. In that study and therefore this study, they looked at using saline solution versus either lactated ringers or plasma-lyte. You may be asking yourself "but I thought that study didn't show any mortality benefit". You are correct, it didn't, but that finding was regarding all critically ill patients.
This study looked at 30 day mortality in patients in the MICU who were septic. All in all, they looked at 1641 patients with the diagnosis of sepsis. Note: not necessarily septic shock. 34.1% of patients were on vasopressors and 40% were on the vent.
Here are the outcomes: 30 day mortality: 26.3% in the balanced crystalloids group vs. 31.2% in the saline group (p=0.01) Patients who received balanced crystalloids had more days free of vasopressors, free of dialysis days, lower plasma lactate concentrations after ICU admission. Debate settled? Well, no. But check out the article for yourself before taking my opinion as gospel.
Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure. Want to know which patients to use BiPAP on? This guideline published in the American Thoracic Society journal in conjunction with the European Respiratory Society in 2017 provides some good answers for the most common questions we all encounter in our daily practice. Should NIV be used in COPD exacerbation? Should NIV be used in ARF due to a COPD exacerbation to prevent the development of respiratory acidosis? Should NIV be used in established acute hypercapnic respiratory failure due to a COPD exacerbation? Should NIV be used in ARF due to cardiogenic pulmonary oedema? Should NIV be used in ARF due to acute asthma? Should NIV be used for ARF in immunocompromised patients? Should NIV be used in de novo ARF? Should NIV be used in ARF in the post-operative setting? Should NIV be used in patients with ARF receiving palliative care? Should NIV be used in ARF due to chest trauma? Should NIV be used to prevent respiratory failure post-extubation? Should NIV be used in the treatment of respiratory failure that develops post-extubation? Should NIV be used to facilitate weaning patients from invasive mechanical ventilation? Fortunately, this article is free for you to download. The link is below.
Rochwerg B, Brochard L, Elliott MW, et al. Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir J 2017; 50: 1602426
Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.
Clinical Practice Guidelines for the Prevention and Management of Pain, Agitation/Sedation, Delirium, Immobility, and Sleep Disruption in Adult Patients in the ICU
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Siegler, J., M. Kroll, S. Wojcik, and H.P. Moy, Can EMS Providers Provide Appropriate Tidal Volumes in a Sim- ulated Adult-sized Patient with a Pediatric-sized Bag- Valve-Mask? Prehosp Emerg Care, 2017. 21(1): p. 74-78.
