What No COVID? Then at Least Lets Talk Steroids- in ARDS that is…

Reference: Villar. Dexamethasone treatment for the acute respiratory distress syndrome: a multicentre, randomised controlled trial. Lancet Respir Med 2020; 8: 267–76.

I know what you are thinking, “What gives? No COVID!” Well the two of you who read this are probably inundated with COVID info. So to give our brains a change I thought I would do a study that would DEFINITELY BE A HEADLINE if we weren’t COVID CRA. But just as DC gets overshadowed by Marvel so to this good (but slightly methodologically flawed) study may go unnoticed.

This study look at the utility of dexamethasone (dex) to treat MODERATE to SEVERE ARDS. I say this in bold because other trials didn’t have an entry criteria of a PaO2/FiO2 (“P/F” Ratio) of <200 (usually its worse like <150)…but this one did. Boy did they find a difference. The primary outcome was ventilator free days and they found that dex ALMOST halved this (7.5 vs 12.3)! Secondary outcomes (sloooowwww down those are hypothesis generating…quiet you, I want to be happy about something): All-cause mortality…halved!: (29 vs 50); ICU Mortality halved! (26 vs 43). Well not quite but pretty close. Now before we celebrate like its the end of social distancing* there are a TWO MAJOR FLAWS in the armor of this trial.


Flaw #1. Not only was it open label (the docs knew they were giving a steroid) but there WASN’T a placebo…what the what!!!! They state as follows:

“According to the ethical principles for medical research of the Declaration of Helsinki,19 the use of no placebo (no intervention) is acceptable when no proven intervention exists and when the patients who receive a placebo could be subjected to additional risks (eg, intravenous catheter-associated infections and interaction with other medications). The Spanish Agency of Drugs and Medical Devices and the referral Ethics Committee did not mandate a blinded design nor the administration of a placebo.”

“Although dexamethasone was not administered in a masked manner, the risk of assessment bias is very low because one of the outcomes of interest (mortality) is objective.”

Any who has ever been a patient or spent time as learner (and we are all learners) knows NOTHING is OBJECTIVE. The decision to take someone off the vent earlier COULD absolutely have been influenced.

Flaw #2: The trial was stopped short. The trial was calculated to have 317 parties with 157 in each arm but only ended up with 139 (+1) in each.
The trial was stopped at 88% enrollment due to low enrollment. Stopping a trial short can OVERESTIMATE the effect size.

A minor flaw in this study is that they also took less sick patients than other trials. As is the mantra with research “If it didn’t work, you didn’t give it early enough”…once again this was “right”.

Two good things they did correctly is look at new infections and hyperglycemia in both groups and found no difference.

That being said there looks like a signal here. Im sure when it comes down to it the GIANT changes seen here, they won’t pan out to be as big in real life but I bet there is something to giving dex to ARDS…at least I can hope. As an ER/ICU doc its another reason for me to give steroids… and you can’t spell stERoids without ER!

*I REALLY don’t like the term social distancing/isolation…we should call it “physical distancing/isolation”. We can stay in touch, without the touching!

ESETT: A Randomized Trial of 3 AEDs for Status Epilepticus

Kapur, J et al. Randomized Trial of Three Anticonvulsants Medications for Status Epilepticus. NEJM 2019;381;2103-13

This was a randomized, double-blinded, national multicenter pragmatic study to determine comparative effectiveness of traditional anti-epileptic medications in status epilepticus. The purpose of this study is to see if there is a difference between levetiracetem (Keppra), fosphenytoin (Cerebyx), and valproate (Depakote) in treatment of status epilepticus. By definition, these are second line treatments as first line treatment remains benzodiazepines (BZD). This is a well designed trial that was developed by the NIH and FDA then conducted by Neurological Emergencies Treatment Trials (NETT) and Pediatric Emergency Care Applied Research Network (PECARN). It utilized a response adaptive design to attempt to find the “best” AED (see below). Clear primary endpoint was established of seizure resolution and improving mental status one hour after starting trial medication. The protocol was guideline based as patients received cumulative BZD doses of 10 mg diazepam, 4 mg of lorazepam, or 10 mg of midazolam or weight based for children. Leaving the discussion of adequacy of those doses for another time, patients then went on to receive a weight based, unmarked vial of medication no more than 30 minutes after last dose of BZD. Dosing for these trial drugs were based off the Established Status Epilepticus Treatment Trial (ESETT) using 60 mg/kg of Levetiracetam (big doses of >4g !), 20mg/kg fosphenytoinand 40mg/kg of valproate. Protocol deviation was marked as unmasking trial drug in less than 60 minutes. 348 adults and children were enrolled into the study with interval analysis reaching a 1:1:1 trial drug administration. The primary endpoint was reached in less than half of all patients (46%) with absolutely no difference in efficacy. No difference in secondary end points such as ICU admission, median ICU stay, median ICU stay or median time to seizure termination after drug infusion. This study was not powered for to detect the rare adverse side effects but more patients that received fosphenytoin developed hypotension.


Safety Outcome*LevitiracetumfosphenytoinValproic Acid
Composite of
and arrhythmia
Adverse Outcomes among the 3 AEDs
*Not powered to detect significance

Interestingly, pseudoseizure patients (~10%) were included which is clinically practical as there are times you simply do not know. 

JC Learning point: 

This trial did not have any statistical juijitsu as the primary endpoint was clear and there was no difference in efficacy. I speculate this will lead to use of levetiracetam as the go to second line agent as there is no difference to the other traditional agents which have their own respective drawbacks such as drug level monitoring, hypotension and arrhythmias as seen in rapid administration of fosphenytoin (which can easily happen in stressful situations like status epilepticus). The bigger take away for me here is 1 hour of status epilepticus is way too long for less than half the patients to improve from status epilepticus. The drawbacks of neurological damage, rhabdo and aspiration while waiting for these medications to take effect over an hour (which occurred in less than half of these patients) would be hard to stomach. As a newer emergency medicine physician, I have a tough time being patient for 15 minutes let alone 1 hour! Not to mention the longer these interventions take to have effect the more likely patients can develop super-refractory status which does not sound like fun. Bottom line, whichever second line anti-epileptic you go with, it likely does not make much of a difference in the short term as you continue to push BZD and move onto giving more BZD, intubation and propofol vs barbitutes.

Response Adaptive design

Adaptive designs allow for the review during the trial and then “adapting” the trial to allow to change the study for such changes as:

  • Abandoning treatments or doses
  • changing the allocation ratio of patients to trial arms
  • identifying patients most likely to benefit and focusing recruitment efforts on them
  • stopping the whole trial at an early stage for success or lack of efficacy.
  • Refining the sample size

In the ESETT trial the adaptive part was that at interim analysis points the drugs were evaluated and probabilities to determine if one was better (via Bayesian methods) were reviewed. If one drug was found to be worse then that arm could be dropped and the two remaining ones would stay. Thus you would get a larger sample size for the better treatment arms. Surprisingly in all the interim analyses THIS DID NOT HAPPEN. The three drugs were all found to be equally probably by the end of the trial. 

By Sagar Dave and Jesse Shriki

We’re Back Baby!! The Quick hit article: For ESBL, Just Say NO to PIP/TAZO

Effect of Piperacillin-Tazobactam vs Meropenem on 30-Day Mortality for Patients With E coli or Klebsiella pneumoniae Bloodstream Infection and Ceftriaxone Resistance
A Randomized Clinical Trial

This was a randomized, double-blinded, international multicenter pragmatic (phew! That’s a mouthful!) study to determine if piperacillin/tazobactam (pip-taz) is non-inferior to meropenem. The reason for this study is to see if there is a way to reduce carbapenems use and prevent further Carbapenem resistance acinetobacter (CRAB, not the Maryland kind). ESBL drugs are those that are by definition resistant to ceftriaxone or ceftazidime. This is a really well done trial with the trial being registered at clinicaltrials.gov and meeting all the important qualities of an RCT. The only missing item (which is probably a small one given how rigorous this trial was) is the fact that of all the 9 countries the US wasn’t one of them (Isn’t Canada close enough? Probably, still too close if you aren’t a fan of Trump). The study used a non-inferiority protocol with 30 day all cause mortality as the end point. Also a home run here with a very good patient oriented outcome. They randomized 378 patients and found an impressive 12.3% vs 3.7% mortality rate for pip-taz vs meropenem. Yikes! That is an 8.6% absolute risk reduction!!! In classic statistical phrasing using double negative: This trial found pip-tazo not non-inferior. They powered the study to find 454 patients but stopped at a predefined interim-analysis of 340 patients. Its bad form to stop a trial for “benefit” when you are looking for non-inferiority but not for harm. As such the trial enrolled 391 pts. In this cohort the patients had about 86% E. Coli and 14% Klebsiella. Most of the patients came from Singapore and Australia with only 1 patient coming from Canada (C’mon Canada!). Most of the infections were either urinary (~60%) or intra-abdominal infections (~15%). Interestingly, 60% of patients were deemed to have been treated with “appropriate” empiric therapy and EVEN MORE INTERESTING is the fact that almost 45% of patients had community associated acquisition. This is probably true world wide but maybe less so in the US? But we are likely heading that way. So to sum up in patients that have ESBL need meropenem not pip-tazo! For a number needed to treat version: If you will have one death for every 12 patients you treat if you use pip-tazo and not meropenem!!

The JC learning point
This trial was performed as a “non-inferiority” trial. These trials should be looked at with a scrutinizing eye! Drug companies love to use this because they don’t have to prove the drug is better, they just have to prove its not worse. The critical point here is to make sure that the correct significance (α level) is set. Non-inferiority is established at the α significance level if a confidence interval for the difference in efficacies (new – current) is contained within a safety margin interval. In this study they used a margin of +5%; so if the studies showed a mortality within 5% of each other then we would have said that pip-tazo is non-inferior to meropenem (but it didn’t). Normally when we compare to things we can use a α of 0.05. However, in non-inferiority testing we have to use an α of 0.025 because we are really performing TWO ONE-sided tests (think of it as needing a p-value for the +margin and the -margin so you cut the p-value in half ). Lastly, interpreting a non-inferiority trial as a superiority trial is OK and doesn’t require a multiple testing correction IF the 95% confidence interval for the treatment benefit excludes the non-inferiority margin AND zero is not in the confidence interval. However, the opposite approach is not true. If a superiority trial fails to reject the null hypothesis but the trial data appear to suggest treatment non-inferiority, you cannot default to non-inferiority


  1. Effect of Piperacillin-Tazobactam vs Meropenem on 30-Day Mortality for Patients With E coli or Klebsiella pneumoniae Bloodstream Infection and Ceftriaxone Resistance A Randomized Clinical Trial. JAMA. 2018;320(10):984-994. doi:10.1001/jama.2018.12163
  2. Understanding noninferiority trials. Korean J Pediatr 2012;55(11):403-407. http://dx.doi.org/10.3345/kjp.2012.55.11.403

Quick Hit Article: Difficult vascular access: You know the drill… but do you really know the drill?

Kawano et al. Intraosseous Vascular Access Is Associated With Lower Survival and Neurologic Recovery Among Patients With Out-of-Hospital Cardiac Arrest. Ann Emerg Med. 2018;71:588-596.

This study was a secondary analysis of a large EMS trial conducted in 7 sites in the US and Canada. This is a really interesting study that looks at the association between outcome and IO access. They looked at 12,500 pts with IV access and 660 pts with IO access. The primary outcome measure was favorable neurologic outcome at hospital discharge with a mRS of 0 to 3. In the IO group 24% had rosc, 4% survived to hospital discharge, and 1.5% had a favorable neurological outcome. In the IV group 38% had ROSC, 10% survived, 8% had a favorable neurological outcomes. In the UNADJUSTED propensity matched model IO vs IV access was associated decreased probability of ROSC (25% vs 34%,OR=0.66), survival to discharge (4.5% vs 8.6%, OR=0.5), and favorable neurologic outcome (1.8% vs 5.9%, OR=0.29). The two groups differed in interventions very noticeabley in that the IO group were an almost 15% LESS therapeutic hypothermia and 9% less interventional catheterization. This is JUST AN ASSOCIATION and maybe IO is just a marker of sicker patients, HOWEVER, I think this is enough to allow for an RCT looking directly at this topic.

Difficult IV access in cardiac arrest? Just drill it! Utilize intraosseous vascular access that is. The IO has become the go to for rapid IV access in cardiac arrest patients. We can deliver drugs quickly and not muck around looking for a vein either peripherally or centrally. But are there down stream consequences? Is it REALLY better? This study takes a look at outcomes of non-traumatic cardiac arrest patients who had an IO placed.

This study was a secondary analysis of a publicly available registry conducted in 7 sites in the US and Canada. The original trial looked at the timing of the first analysis for defibrillation and application of an impedance threshold device. The original data was prospectively collected. Exclusion criteria were the typical ones including trauma, prisoners, pregnant, dnr, and hypovolemia. To the study’s benefit the obtained a cohort whose access route was the INTENDED PRIMARY CHOICE and excluded failed attempts at either route of access. The importance of this is that it MIGHT equal out the bias of a sicker patient or delays in care where a failed access attempt delays the care. The primary outcome measure was favorable neurologic outcome at hospital discharge with a mRS of 0 to 3. This is an interesting outcome change point because normally mRS is 0 to 2 is the cutoff in stroke studies. Because out-of-hospital vascular access was not randomly assigned across this cohort, they applied propensity matching to decrease selection bias and unmeasured confounder.
They found after exclusions 13,155 patients with 660 pts (5%) and 12,495 (95%) pts. Note that patients with IO access had a higher proportion of nonshockable initial rhythms, fewer public location and shorter times from call to first provider. In the IO group 24% had rosc, 3.8% survived to hospital discharge, and 1.5% had a favorable neurological outcome. In the IV group 38.3% had ROSC, 10% survived, 7.6% had a favorable neurological outcomes. They found after multiple regression with multivariate analysis that IO access was ASSOCIATED with a DECREASED probability of ROSC [OR 0.6 (CI: 0.49 to 0.74)] and DECREASED favorable neurological outcome [OR 0.24 (CI: 0.13to 0.46)].
They found 1116 patients in the propensity match. In the UNADJUSTED model IO vs IV access was associated decreased probability of ROSC (25% vs 34%,OR=0.66), survival to discharge (4.5% vs 8.6%, OR=0.5), and favorable neurologic outcome (1.8% vs 5.9%, OR=0.29). Looking at the propensity matching these groups for the
Baseline characteristics are quite well matched and markers of their propensity matching were well correlated. They did differ in some ways in the interventions. The very noticeable differences in the IO group were an almost 15% LESS therapeutic hypothermia, 5% less fibrinolytics, and 9% less interventional catheterization.

Although the propensity scoring appears quite well and there were multiple calculations to correct for confounders there are still significant biases. I think foremost the discrepancy between the number of of IO vs IV’s performed is hard to overcome (660 vs 12500). Also there were some big differences in the patients receiving hypothermia and cardiac catheterizations. I still think the data is not definitive for those two interventions but certainly this may be a marker of quality of care and attention to care. Still the OR for survival with favorable neurological outcome is impressively in favor of IV access. It is interesting that some EMS systems used IO as their first line and it would be interesting to know why IO was first line. I also wonder WHY the IO patients got less interventions. Was the IV access the reason or were they initially deemed to be sicker? Also it would be nice to know how long the IO was in and what was the time frame to when it was swapped out for IV access. Lastly, I can’t get away from the thought that sicker patients are going to get IO’s and are going to do worse.

So what’s the bottom line? IO access is critical to establishing vascular access to care for patients (depending on what you think the validity of ACLS drugs are, oh HEY OPALS TRIAL). Maybe IO access is a marker for sicker patients or maybe worse IO access biases providers against the same level of care as those with an IV…We all know the drill… but does it make our patients better? I think this is enough to allow for an RCT looking directly at this topic.

QUICK HIT ARTICLE: News Flash Breathing is good for you…next up Water, Wet! “How breathing can help you make better decisions…”

De Couck et al. International Journal of Psychophysiology 139 (2019) 1–9. doi: 10.1016/j.ijpsycho.2019.02.011

In this experimental study of 56 undergrad and grad students in France, utilizing specialized breathing patterns (see image below), the researchers sought to determine the effect of breathing on stressful decision making. They found that using breath patterns for 5 minutes prior to stressful written multiple-choice tests allowed the experimental group to answer an additional question correctly. Additionally, they found that the breathing group felt significantly less perceived stress via a visual analog scale difference of >4 than the sham control group.  Does this pertain to clincal scenarios where we think out loud or just to multiple choice questions? Do we really need to breath for 5 min to get an affect? Can we trust the French? Other than the last question, only time will tell…

Ok well we all know physiologically breathing is good for you but turns out it might be psychologically better for you also. This quick hit article was published in the aptly titled: Journal of pschyophysiology (no, not the physiology of psycho’s). This article looks at how breathing can impact the stress of decision making. Interestingly stress can negatively impact decision making. They cite a meta-analysis of 1829 pts that revealed stressful conditions lead participants to take a decision that was more risk taking than in non-stress conditions. In medicine we make stressful decision all the time so can breathing exercises help? This article tries to shed some light on the subject

In this study they postulate that deep slow breathing can increase vagal nerve activity, measured by heart rate variability (HRV) which they state is associated with better decision making. HRV is the physiological phenomenon of variation in the time interval between heartbeats. It is measured by the variation in the beat-to-beat interval.

There are anecdotes of tachycardia and stress in the military about soldiers running into battle without helmets. The thought here is stress leads to an aberrant decision and tachycardia (especially HR over 120) have been a marker of this (see “On Combat: The Psychology and Physiology of Deadly Conflict in War and in Peace by Grossman and Christensen). Therefore, we have to assume that HRV and vagal nerve stimulation are positively correlated with improved decision making.

Interestingly, and unlike most journals, this study reports two different studies under one article heading. I find this strange but we will look at them as two separate studies

The first study examines the effects of two breathing patterns on HRV, differing in their inspiratory to expiratory (I:E) ratios, in healthy men and women. In study 2, they examined whether one of the breathing patterns could result in better decision-making in stressful conditions. The research was conducted in a business school in France on 56 management students at the bachelors and masters level. 

Study 1 found that both types of breathing pattern, a symmetric and a skewed pattern (with a longer exhalation period), increased several parameters of HRV.

Study 2 examined 56 patients in two groups of 28 who were directed not to smoke, consume alcohol or caffeine 3 h before participation and were rewarded for participation. They define HRV-B as a method where people learn to use deep breathing methods to enhance their HRV with electronic biofeedback. Beat to beat intervals are termed NN (much like an R-R interval on an ECGl with N signifying Normal beat to beat intervals). SDNN or the standard deviation of NN intervals, reflects all the cyclic components responsible for variability in the period of recording, therefore it represents total variability. The standard deviation of the average NN intervals calculated over short periods (5 minutes in this study) they use is 50 ms and an SD of 16 ms. They make this very confusing to figure out and there might be some typos in the methods as well. HRV was derived from an ECG with a biofeedback system. They utilized TWO different breathing patterns termed symmetric and skewed. As you can imagine the symmetric pattern  was 5 minutes of inhalation on a 5 second count followed by breath holding for 2 count then 5 second count for exhalation. They skewed pattern was 5 minutes of inhalation on a 5 second count followed by breath holding for 2 count then 7 second count for exhalation.

The control group watched a 5 min “emotionally neutral” movie without music or sound. They utilized within subject experimental design (meaning these were repeated measures and paired statistical testing would be needed). A decision making scenario and questions were created as a business simulation consisting of two parts a reading part and a multiple choice decision part. They were asked to assume the role of someone in charge of a retail company and a writing test after with a strict time constraint. They state that “recently, Brugnera et al. (2018) found that verbal activity masked the vagal withdrawal through altered respiration patterns imposed by speaking. That is why, in this study, we opted for a task in which participants do not need to talk”. I find this interesting and we will get back to this later. Additionally, subjects were asked to evaluate their actual stress level using the VAS stress (for Pre-Stress levels). 

 They note in this first study that the deep breathing group had a significantly (that should be stated STATISTICALLY) higher percentage of correct choices (47% vs 32%; p=0.005) which translated to on average one more question right than the control (2.25 ± 1.35 vs 3.32 ± 1.36 correct answers). I think the more interesting part was the perceived stress by the two groups. 

 The control group had a VAS for pre- stress of 3.57 vs post stress of 8.16. The breathing group had a VAS for pre- stress of 4.40 vs post stress of 5.7. Assuming a clinically significant difference is 3 for a VAS on a 10-point scale (extrapolating from 30 on a 100 pt scale) then this would be significant. 

So put together what does this all mean? It would seem that breathing might be associated with less perceived stress but the effect here seems small with such a small and specialized sample size. Does this apply to medicine where we can sometimes think out loud? The study cited here would suggest that there is masking of the difference when one can verbalize decision. Also does this study mean we have to breath from 2-5 min to reap a benefit of this breathing pattern? What is the optimal length of time for breathing? Does it have to be isolated or can I multitask and do it while I prepare for a stressful situation? Lastly, can we really trust the French?  Certainly, my apple watch tells me that breathing will make me feel better! While all of this makes sense I’m not sure this really is conclusive evidence or always practical. I guess for my clinical practice I’ll try it out and see for myself. It certainly is interesting given the concern over bias in decision making these days.

Case Report: IV access in a dialysis patient: An Evidence free zone!

So the below is only my opinion! We are definitely in an evidence free zone and this is not meant to guide management! However this is my nightmare. 

A 53 yo ESRD is BIB EMS to a small community hospital. Her chief complaint: missed dialysis. She reports staying at her NH and not having been picked up for dialysis for the past week. She is on HD, Tues, thurs, and Saturday. Her last IHD was a week ago and her most recent one was unable to be continued because her graft had clotted off. She does not feel short of breath but does note her body is more swollen. SHe has no other symptoms. Past medical history includes (but not limited to): DM, HTN, ESRD on HD, and a right sided CVA with deficit on the right side. On exam her BP is 224/112, HR is 78, RR 20 (as usual), and afebrile. On exam she is in no acute distress and non-toxic appearing, she is morbidly obese, she speaks in full sentences, she has keloid formation on both sides of her neck and anterior chest wall. She has a moderate contracture on the right arm from her prior CVA, she has a Arteriorvenous graft (AVG) on the left arm with no palpable thrill or bruit. She further has bilateral above the knee amputations. Bilateral radial vessels are palpable no other findings. The nurses are unable to find a vein on the arm with the CVA and tell you they cannot do an IV on her arm with the graft. The lab tech is unable to obtain a blood draw given her skin changes and lack of venous access.  You are asked to obtain blood and you do so by radial arterial draw. Her ECG shows no peaked T waves and her Potassium (K) is 6.8.

So, to sum up this is a 53 yo female on dialysis with a clotted graft, no accessible veins peripherally by 2 different nursing attempts and the charge RN, no accessible EJ on the neck (visually or by US) due to keloid, no accessible mammary veins on the chest due to b/l keloid, no legs, an AV graft on the left arm and the right arm is fixed ADducted and held in flexion and cannot be straightened due to the stroke.

What do you do? Where and How do you get IV access? Do you put in a central line? If so where?


Where do we start?

As far as IV access goes, we are all aware that we “shouldn’t” use the arm with the AV graft (AVG) or fistula (AVF). But when we NEED blood and IV access as in the above case where do we start? Let’s look at this.

There are slim to none guidelines in this area. The only semblance of guidelines is from the 2006 KDOQI (Kidney Disease Outcomes Quality Initiative, http://www.KDOQI.org). In the section on “Clinical Practice Guidelines for vascular access”, pg 340 states “1.1 The veins of the dorsum of the hand should be the preferred site for IV cannulation.” And  under patient preparation for permanent access states “ In patients with CKD stage 4 or 5 forearm and upper-arm veins suitable for placement of vascular access should not be used for venipuncture or placement of IV catheters, subclavian catheters, or PICCs)

Does this mean both hands? Does this mean after or before placement of the AV access. No one will ever know…

The rationale for these recommendations are for PRESERVATION of the veins to create an AV fistula or graft, and maximize chances or successful fistula placement and maturation. Furthermore it is for prevention of thrombosis. These are the reasons for the PIV cautions. They report the incidence of central vein stenosis and occlusion after upper extremity placement of PICC and venous ports is 7% in 1 retrospective series of patients. PICCs are also associated with an incidence of upper extremity  varies between 11% and 85%. Thus PICCs should not be used in CKD.

And that sums up all the recommendations!

At kidney.org, the housing site for the KDOQI guidelines, there is a post that states:

“Post date: February 10, 2014

I have permitted peripheral IV access in the back of the hand on the same side as the AV fistula. I do not permit IV access above the wrist on the same side as the fistula. I do not permit Peripherally Inserted Central venous Catheters (PICC) access to be placed in any dialysis patient with a fistula. I only permit centrally lines in the Right Internal Jugular position. The KDOQI guidelines recommend right sided central venous catheters, avoiding subclavian catheters and avoiding peripheral IV access in any dialysis patient or pre-dialysis patient. They also mention using the back of the hand veins for peripheral access but avoiding the arm veins for peripheral IV access.”

Obviously not high quality data…

The nurses were unable to obtain IV access or blood from either hand or veins on the chest wall.

Next step for me was to look for an EJ… sadly, no luck too much keloid formation over both sides of the neck nor could I find distended EJ’s visually  or by ultrasound.  Because of the left arm contracture and her soft tissue edema I had a very difficult time finding a deep brachial vein. In my own personal experience I feel the basilic vein is more likely to infiltrate whether you happen to “back wall” the vessel or not. However, after getting more help positioning the patient and have a few people hold her I was able to get a peripherally inserted 20 ga 1.88” (48mm) Angio catheter in the most anterior deep brachial at the level of the mid bicep. Now to find a new pair of underwear!

If that failed, I guess I would have done a right IJ since her graft is on her left arm and guidelines say to avoid Subclavian vessels. Also theoretically, an IO of the right humerus could be done emergently but being a renal patient I’m sure her bone strength is minimal.

So in summary, obtaining IV access in an HD patient would be in the following order:

  1. Dorsal veins in the hand
  2. Peripheral on the contralateral AVF/AVG side
  3. External Jugular (either
  4. IJ contralateral to the AVF/AVG; if CKD 3-5 then Right IJ preferred but either is Ok
  5. If PICC is needed substitute in a tunneled EJ/IJ catheter by IR


  1. Above the wrist on the AVF/AVG side
  2. Subclavian central line
  3. PICC

In case you were wondering what the steps are for accessing a fistula I found this wonderful article, by Manning, on how to do that:

Any gauge and type of needle may be used, although a large-bore (14, 16, or 18 gauge) needle is recommended in emergency circumstances. A needle is preferable to an angiocatheter because it is easier to secure with tape under the high pressure of the fistula. A tourniquet should be used when cannulating an AV fistula and removed immediately after cannulation. The tourniquet should be placed in the axilla area and applied lightly. These precautions will help prevent thrombosis, the most common cause of AV fistula and AV graft failure. One should scrub the skin at the puncture site with povidone-iodine, allow the skin to dry, and follow with a scrub using isopropyl alcohol.  The needle should be inserted into the AV fistula at an angle of 20 to 35 degrees until a flashback of blood is noted (The angle should be increased to 45 degrees if the nurse is cannulating an AV graft.) After the flashback, insert the needle up to 0.32 cm (1/8 inch) further and decrease the angle until the needle is flat with the skin. The needle or catheter should be advanced to the hub to prevent bleeding around the insertion site. If using an intravenous catheter, one should be prepared to attach intravenous or saline lock tubing quickly to avoid unnecessary blood loss. Blood flowing through the AV fistula travels at a high velocity, so fluids need to be infused under pressure. One must take care to tape the needle or catheter to the skin securely in a chevron fashion to prevent dislodging.

If the fistula has been accessed in the previous 24 hours and the needle puncture sites are visible, the nurse should take care to access the fistula at least 2.5 cm (1 inch), either proximal or distal, from the previous site to allow healing time and to avoid the formation of an aneurysm. Prior to and after cannulation, the emergency nurse should assess the AV fistula for a thrill and document its presence. The AV fistula can be de-accessed in the same manner as a peripheral intravenous line, with pressure applied after the needle or catheter has been removed. The nurse should take care to hold gentle, nonocclusive pressure for a full 10 minutes at the insertion site.


  1. Manning, M. Use of dialysis access in emergent situations.J Emerg Nurs 2008;34:37-40. Available online 18 October 2007. doi: 10.1016/j.jen.2007.03.018. PMID: 18237665
  2. https://www.kidney.org/blog/ask-doctor/what-recommendation-peripheral-iv-placement-dialysis-patients-avf-and-avg-i-am
  3. February 2012 ASN kidney news. The PICC conundrum: Vein preservation and Venous Access. https://www.kidneynews.org/kidney-news/special-sections/interventional-nephrology/the-picc-conundrum-vein-preservation-and-venous-access

LVAD Complications: A review

This is a nice little review by Dr. Long in Dallas entitled:

B. Long, J. Robertson, A. Koyfman, et al., Left ventricular assist devices and their complications: A review for emergency clinicians, American Journal of Emergency Medicine, https://doi.org/10.1016/j.ajem.2019.04.050


A ventricular assist device (VAD) can be placed into the right, left, or both ventricles thus the patient can have a right ventricular assist device, left ventricular assist device, or biventricular assist device. The goals of these devices include three different strategies: bridge to recovery, bridge to transplantation, or destination therapy (i.e., the patient is unlikely to recover and not a candidate for cardiac transplant). Contraindications to placement include metastatic cancer, irreversible renal/hepatic failure, and CVA with severe neurologic deficits. The LVAD has two basic designs which produce different patterns of perfusion, including the pulsatile and continuous-flow devices. More commonly these days are the non-pulsatile continuous flow devices.

Device Components

The continuous-flow LVAD has several basic parts including: the internal pump an external power source, and a control unit.The specific components of the LVAD include the inflow cannula, pumping chamber, outflow cannula, percutaneous driveline, controller, and power source. The inflow cannula, usually placed in the apex of the left ventricle (LV), provides the route for blood flow from the native LV cavity to the LVAD pumping chamber.

The pumping chamber, the component of the circuit which provides perfusion, is located in different positions depending upon the LVAD model type: the LV apex for the (HeartMate) HMIII and HVAD devices and the subdiaphragmatic space adjacent to the heart for the HMII device. The pumping chamber contains the impeller, a near-friction-less rotor with rotation speeds ranging from 2500 to 9800 rpm; these types of impeller designs can generate blood flow up to 10 L per minute. The outflow cannula provides the conduit back to the patient’s native cardiovascular system and connects the pumping chamber to the ascending aorta,

The percutaneous driveline provides a conduit for the electrical wiring, connecting the pump to the system controller. These wires not only connect the power source to the pump, but they also provide controlling and sensing functions for the LVAD. The driveline is tunneled

subcutaneously from the pump and exits the skin in the anterior abdominal area to connect to the controller. Thus, it is a frequent source of infection in the LVAD patient. The controller performs multiple functions and contains several important components. It controls LVAD functioning, including power source monitoring and regulation, overall system monitoring, data collection, and alarm system function. subcutaneously from the pump and exits the skin in the anterior abdominal area to connect to the controller. Thus, it is a frequent source of infection in the LVAD patient. 


A continuous flow LVAD will not typically produce a palpable pulse on its own, but patients may have enough native ventricular function to produce pulsatile flow and a pulse. A palpable pressure may also be due to pump thrombosis, and thus, it is important to determine if the patient has a palpable pulse at baseline. If a pulse is palpable, a standard sphygmomanometer may detect a blood pressure, which reflects a systolic blood pressure, rather than mean arterial pressure (MAP). If the pulse is not palpable, a pencil Doppler probe should be placed over the radial or brachial artery. The point at which Doppler signal returns corresponds to the MAP for continuous flow devices. If this is unobtainable, an arterial line may be required, which is the most accurate device for monitoring MAP. Invasive arterial monitoring will demonstrate minimal pulse pressure or flat arterial waveform. Caution is recommended in using pulse oximetry, as a low reading commonly reflects a lack of pulsatile flow. However, a normal value may be accurate. 

LVADs, especially those with continuous-flow, are sensitive to afterload and preload. Guidelines recommend maintaining a MAP of 70–90 mm Hg. Acute hypertensive adverse event is associated with MAP N110 mm Hg in patients with continuous flow pumps. The mechanical hum indicates device power and function. Signs of volume overload (extremity edema, ascites, elevated jugular venous pressure) can be due to subacute or chronic right ventricular failure. However, acute dyspnea, pulmonary edema, or hypotension are more commonly due to acute malfunction of the device, such as cannula obstruction or pump thrombosis. The device exit site, which is normally covered with a sterile dressing, and line should be examined with sterile gloves and mask for warmth, erythema, and discharge, which suggest infection. Finally, the patient should be asked if he/she brought the back-up battery and back-up controller. Sustained ventricular dysrhythmias may be due to underlying cardiomyopathy or decompressed left ventricle due to elevated pump speed or right ventricular failure. Patients with an LVAD will typically demonstrate normal sinus rhythm.


Chest radiograph provides important diagnostic information including position and the type of LVAD, as well as the presence or absence of an ICD or pacemaker. Deep space infection of the LVAD components requires assessment with computed tomography (CT). Sustained ventricular dysrhythmias may be due to underlying cardiomyopathy or decompressed left ventricle due to elevated pump speed or right ventricular failure. Patients with an LVAD will typically demonstrate normal sinus rhythm.

Echocardiogram can evaluate cardiac function and assess for complications such as regurgitation, right ventricular failure, and thrombus formation, though thrombi can be difficult to detect on ultrasound alone.  Key components of the assessment include valvular function, inflow/outflow abnormalities, ventricular size and function, and septal position.

Laboratory assessment includes hemoglobin/hematocrit, lactate dehydrogenase (LDH), haptoglobin, free hemoglobin, and coagulation panel. Hemoglobin and hematocrit with type and screen/cross are needed if concern of bleeding is present. Patients with LVADs are anticoagulated with a vitamin K antagonist, with a goal INR of 2–3 well as aspirin. Free hemoglobin and haptoglobin can assess for hemolysis. Elevated LDH >2.5 times the upper limit of normal suggests hemolysis, which is most commonly due to pump thrombosis in an LVAD patient.  Troponin is recommended in patients with new ECG findings, chest pain, or dyspnea. BNP is a sensitive indicator of volume overload in patients with an LVAD and may be elevated in those with new right heart failure or pump thrombosis or malfunction.

Patients should have a controller tag around their waist indicating the type of device, the institution that placed it, and a phone number. Alarms and functional parameters are shown on the external system controller. Pump speed controls flow. Pump power, flow, and speed should be noted, with assessment of alarms and battery. RPMs and pulsatility index must also be evaluated. 

LVAD specific complications:


A suction event is a common LVAD complication and is associated with low flow events, including dysrhythmia, hemorrhage, and other hypovolemic states such as diarrhea or vomiting.  Reduced LV preload results in collapse of the LV and decreased inflow into the LVAD. Low flow, speed, and power will be present on the controller. While bedside US can demonstrate decreased LV volume, this is often difficult in LVAD patients due to poor acoustic windows, and assessment of the LV diameter may assist in evaluating volume status. Treatment requires fluid resuscitation and managing the underlying etiology. With improved preload and intravascular volume, pump speed and flow will improve. 


Continuous-flow LVADs place patients at high risk of thrombosis, which may originate in the pump or the components such as the inflow or outflow cannula. Types of pump thrombi include acute catastrophic red thrombi entrapped within a fibrin mesh and white thrombi rich in platelets. Red thrombi form at the inlet and outlet areas due to blood stasis, while white thrombi typically form on the pump surface and are associated with turbulent flow. Thrombosis can result in pump dysfunction, hemolysis, emboli, stroke, and death, but patients with thrombosis present with a variety of symptoms due to these potential complications, ranging from no symptoms to cardiac arrest and death. On examination, evidence of hemolysis may be present with scleral icterus, dark urine, and fatigue. Serum LDH is typically >2.5 times normal. Urinalysis may demonstrate hematuria. Other important laboratory assessments include hemoglobin, free hemoglobin, haptoglobin, and coagulation panel. Thrombolysis may be required if patients are hemodynamically unstable. Emergent surgical pump exchange may be needed if the pump stops, the patient is unstable, or if alarms are present. 


Mechanical failure is the second most common cause of death in LVAD patients and may result from several different issues. Pump failure is the most important life-threatening complication requiring immediate care. The controller may demonstrate low flow, low voltage, and power loss. A low flow alarm should always be evaluated by first checking the power. Physicians should auscultate over the LVAD and evaluate for disconnected leads and cannula issues such as kinking or obstruction. A disconnected lead should be reconnected. However, if auscultation reveals no pump activity but all leads are in place, the clinician must assess power and power leads. If all leads are connected, the pump can be reset. If a power lead is not connected to the batteries or unit cable, the cable disconnect advisory will alarm and demonstrate a flashing symbol.  However, if the device has been off for over an hour and the patient is stable, consultation with the LVAD specialist is required, as the device should not be immediately restarted due to high risk of thromboembolic events. In the setting of hemodynamic instability, the device should be restarted immediately no matter the duration of stoppage, with continuous anticoagulation. If the clinician and/or LVAD specialist cannot restart the LVAD, pump exchange is needed, which requires discussion with the LVAD specialist and surgeon. For patients with inadequate perfusion and hemodynamic instability without an alarm activated, resuscitation with IV fluids and standard ACLS protocol is needed.

LVAD-associated complications 


Patients with LVAD are at elevated bleeding risk. Bleeding can occur from several sources: pump connections, grafts in the conduits, and most commonly, mucosal surfaces such as the gastrointestinal (GI) tract. GI bleeding affects 15–30% of patients with an LVAD. Bleeding in the immediate postoperative period is often due to hepatic congestion associated with severe heart failure and the effects of extracorporeal circulation of the bypass machine. Patients may also develop an acquired form of von Willebrand factor (vWF) disease due to the high shear stress associated with LVAD circulation resulting in cleavage and deficiency of vWF. Bleeding in elderly patients with acquired vWF is more severe. Resuscitation of patients with significant hemorrhage with LVAD includes product replacement and reversal agent administration. However, reversing anticoagulation should be weighed with the risk of thrombotic complications, and consultation with the LVAD. Lesions are typically treated with coagulation or clips. Due to the risk of sensitization and reducing the success of heart transplant, blood product transfusion should not be reflexive in patients who are hemodynamically hemodynamically stable. Leukoreduced and irradiated blood products are recommended if available. Octreotide has demonstrated efficacy in LVAD-related GI bleeding in several studies. Desmopressin can be provided, which is a synthetic analogue of vasopressin, or infusion of vWF concentrates. Discussion of platelet transfusion is needed with the LVAD specialist if the patient is thrombocytopenic and bleeding, as well as those with severe hemorrhage.


Ischemic and hemorrhagic stroke can result in poor outcomes and demonstrate a prevalence of 6.8% and 8.4%, respectively. There is an increased risk with every 5 mm Hg increase in systolic blood pressure. The ENDURANCE trial found a lower stroke rate with MAP 90 mm Hg, with patients receiving close blood pressure control demonstrating a 24.7% reduction in total neurologic events and 50% decrease in hemorrhagic stroke rate. Acute ischemic stroke more commonly affects the right cerebral hemisphere in patients with an LVAD. 


Patients with an LVAD are at high risk of sepsis, with rates of infection approaching over 42% in the first year post-implant, usually 2 weeks to 2 months. The driveline and VAD pump pocket are the most common infectious sites, with 80% of driveline infections occurring in the first 30 days of transplant. The system controller may demonstrate a high-flow alarm with distributive shock due to loss of vascular tone. LVAD-related infections include those that may occur in patients without an LVAD, but occur with greater frequency in LVAD patients such as mediastinitis, endocarditis, and bacteremia.  Non-LVAD infections include pneumonia, Clostridium difficile infection, and urinary tract infection (UTI). Within the first 3 months post implantation, the most common sources of infection typically include catheters, pneumonia, and C. difficile, while later sources of infection are more commonly related to the device.  Only half of patients will demonstrate fever, leukocytosis, or meet criteria for systemic inflammatory response syndrome. Discussion with the LVAD specialist and cardiothoracic surgery is recommended.  Deep infections typically require surgical debridement, while persistent bacteremia may require removal and implantation of a new device. 

RV Failure

RV failure is a major cause of morbidity and mortality, occurring in 15–40% of patients. Late onset right heart failure is increasingly being reported with RV dysfunction, ventricular dysrhythmias, pulmonary hypertension, tricuspid regurgitation, and device thrombosis or malfunction. This can result in reduced preload to the LV, decreasing LVAD flows and triggering a low-flow alarm. RV failure may result in elevated liver function tests, creatinine, and lactic acid. RV failure requires inotropes and/or vasopressors, pulmonary vasodilators, and LVAD specialist consultation. Patients may require careful fluid resuscitation, with 250 mL boluses. 

Ventricular Dysrhythmias

Patients may tolerate severe ventricular dysrhythmias with minimal symptoms due to the LVAD producing adequate cardiac output to meet end organ perfusion despite poor venous return. Patients often have an ICD prior to LVAD placement. Dysrhythmias may eventually result in compromised blood flow and can also contribute to RV dysfunction, suction events, thrombus formation, and poor perfusion. The controller will demonstrate low flow in patients with hypotension due to the dysrhythmia.

Aortic Regurgitation

Aortic regurgitation (AR) may develop de novo in up to 25% of patients after LVAD placement. AR more commonly occurs in patients with a closed aortic valve compared to patients in whom the valve frequently opens. AR results in decreased LVAD efficacy and may require modifications in pump speed, managed by the LVAD specialist. Patients may require aortic valve replacement.


Standard procedures for resuscitation are recommended as needed. Hypotension in LVAD patients is defined by MAP <60 mm Hg. Patients who are conscious should be assessed with history and examination, with close assessment of volume and perfusion status. ECG and bedside echocardiogram are vital components of the assessment, with analysis of LVAD components. Patients who are unresponsive and hypotensive require external chest compressions. Literature suggests no cases of dislodgement during cardiopulmonary resuscitation (CPR). If the patient has a MAP N<50 mm Hg or end tidal CO2 <20 mm Hg with a device possessing an audible hum, perfusion is likely adequate, and compressions are not necessary MAP <50 mm Hg without an audible hum in the unresponsive patient is associated with compromised perfusion and requires chest compressions at the same depth and frequency as in those without an LVAD. Defibrillation should be performed for unstable ventricular dysrhythmia. The pads should be placed distant from the pump, and if an ICD is present, the pads should not be placed directly over the ICD. In patients with adequate perfusion and respiration but who remain unconscious, evaluate for hypoglycemia, stroke, hypoxia, sedation, and coma.


Chest thoracostomy with chest tube placement in the setting of trauma with pneumothorax and/or hemothorax is recommended, but clinicians must avoid the driveline. Arterial line placement can be beneficial, and US guidance is recommended. Pericardiocentesis should be avoided due to risk of serious device complications, but it is recommended in the case of pericardial tamponade with hemodynamic compromise.





ST segment elevation in aVR is probably NOT a STEMI…BUT, damn, are they sick!

There I said it. Well Ok I’ve been saying it for a while. But say this to a room full of doctors and you might be ostracized! Well there has been mounting evidence that would argue aVR ST elevation is not an acute STEMI/ STEMI equivalent for a while now. I think this article clinches it for me. However, just because its not a STEMI equivalent doesn’t mean they are ok, nor does it mean we should forget about aVR…


In this blinded retrospective review of 99 patients with ST elevation in aVR (STE-aVR) and multi-lead ST depression, only 10% had a definite culprit lesion,  none had left main or LAD occlusions, and 40% had no disease or mild to moderate disease on PCI. However, this group had an overall in-hospital mortality of 31% compared with 6% in a matched conventional STEMI group. Patients with aVR ST elevation represent a very sick cohort of patients who need critical care and a workup for why they are having poor diffuse coronary perfusion.


This was a retrospective study with actually quite good blinding and decent methods that looked at 854 consecutive STEMI activations in a 35 month period. They identified 99 patients with ST elevation in aVR (STE-aVR) and multi-lead ST depression in the final analysis. Cardiologists reading the ECGs and catheterizations were blinded to the study outcome. The primary outcome was the number of patients presenting with STE-aVR and multilead ST depression who had an acutely occluded culprit coronary artery on PCI. Secondary outcomes were number of patients who presented with cardiac arrest, and survival-to-hospital discharge compared to the non-aVR ST elevation STEMI population. None of these 99 patients had ST elevation in 2 contiguous leads (STEMI definition). Of the original 99, 79 underwent PCI. Interestingly the 20 that did not undergo PCI were a very sick population including known severe coronary artery disease on recent coronary angiogram, neurological emergency, obvious extra-cardiac etiology for arrest, and very long down time with poor prognosis. Of the 79 patients that had PCI, 8 (10%) had evidence of a definite, acute, thrombotic, culprit coronary occlusion but none had an acutely occluded left main or left anterior descending coronary artery. 19 of these 79 had angiographically normal vessels and 40% of them had either no disease or only mild to moderate disease on PCI. However, these were a pretty sick group though: 47 developed respiratory failure, 15 developed cardiogenic shock , 48 developed acute kidney injury( 9 of them requiring hemodialysis), and 36 patients underwent in-hospital coronary revascularization (29 PCI and 7 CABG). Wow are these a sick cohort! Those with STE-aVR had a 31% in- hospital mortality, whereas those with a non-aVR STEMI had a 6.2% in-hospital mortality (p <0.00001)! The presence of a critical medical condition or severe multivessel subocclusive disease with intact distal flow was the most common etiology for this ECG finding. This emphasizes working up these patients for the underlying issue. These patients don’t likely need immediate PCI of a culprit lesion they likely need resuscitation and eventually treatment by a multi-specialty heart team for their multi-vessel disease.


Harhash, A et al. aVR ST Segment Elevation: Acute STEMI or Not? Incidence of an Acute Coronary Occlusion. The American Journal of Medicine (2019) 000:1−9. PMID: 30639554. DOI: 10.1016/j.amjmed.2018.12.021

How much FIO2 do you get from that non-rebreather (NRB) mask? (aka There’s a hole in breather, dear Liza, a hole)


A non-rebreather (NRB) mask ONLY delivers high FIO2 when the flow meter valve is opened fully and even then only gets to about 90%.


I find great joy in reading old literature. I’m pretty sure I would be camped out in a medical library if it weren’t for the interwebs, thank goodness I can do all this from home…For this installment of the basics we look at how much oxygen that non-rebreather (NRB) mask actually delivering.

First, we need to talk about what a non-rebreather does. It’s mostly in the name but it isn’t always intuitive as I see it often used incorrectly. A non-rebreather should not allow you to re-breathe; yes I know how silly that sounds. However, when the NRB is working correctly the reservoir should not deflate with inhalation otherwise you are rebreathing. The NRB has two one-way valves. One is between the reservoir and the mask to allow oxygen to flow into the mask when you breathe in but not when you breath out. The other is at the side of the mask and allows the exhaled air to escape to the world. Ideally, the 100% FIO2 (Fraction of Inspired oxygen) in the bag is inhaled and thus the patient gets 100% oxygen delivery. Unfortunately in the real world this does not happen. One important reason is most NRB’s only have the one one-way valve so the patient doesn’t suffocate if the wall oxygen were to fail. Also the mask may not fit as tightly so oxygen will escape from the mask further decreasing the FIO2. Finally, we use oxygen on sick patients who may have increased respiratory rates and abnormal tidal volumes. Thus the normal minute volume will be abnormal in a sick patient. The goal of preoxygenation is to get the nitrogen part of normal air washed out and replace it with oxygen so our blood will be “super-saturated” and we will have longer times of apnea without the oxygen saturation dropping while a patient is being intubated. Thus we would like as high as possible FIO2 going into the patient. Also we really cant tell what the PaO2 is from the pulse ox monitor because no correlation can be made once SaO2 is >98%.

Thus we NEED to know the FIO2 of the non-rebreather going in. To figure this out we go back in time to 1991 while this might sound scary to go to a time period without iphones; we only have to be there long enough to see the article by Farias, Delivery of High Inspired Oxygen by Face Mask in the Journal of Critical Care. The recruited 5 healthy male volunteers and changed respiratory rates, tidal volumes and oxygen flow rates to see the effect on the FIO2 of a non-rebreather. Now here is the impressive part of the study “FIO, was measured from a catheter positioned through the nose so that its tip was in the pharynx”. The “catheter” was a 6Fr Foley that was inflated once in the oropharynx! These people volunteered for this? You sure they didn’t get paid something???? Yikes! This is why the old literature is entertaining! Anyway…. All wall oxygen comes through a flow valve with a little metal ball that measures the flow out. Normally, with a NRB the flow is set to 15L on the meter and sadly this is the highest the meter reads. So to test various flow rates they had to use their own flow meter and tested rates of 15, 20,30,40 and 60 L/min. They note, “by opening the valve fully on the flow meter, it was possible to attain an 02 flow of 60 L/min. “. At each flow rate the volunteers produced respiratory rates (RR) of 20, 30, and 40 breaths/min (brpm) and also varying tidal volumes (VT) of 500, 750, and 1000 mL. Normal tidal volume is around 500 ml or 7 ml/kg. For a normal RR of 20 and a “normal” VT of 500ml, when the flow was set to 15L the best FIO2 obtained was just shy of 60%. When the RR was 40 brpm and the VT was 1000 ml, this fell to 40% . The study notes, “When the O2 flow rate was increased to 60 L/min, the FIO2, remained at approximately [90%] despite increasing respiratory frequency and tidal volume.”

Hence, this is the reason I say crank that little knobby thing on the oxygen until it stops. Because only then are you getting 60 L/min of oxygen and only then, regardless of RR and VT, does one approximate FIO2 of 100%…well ok 90% but I’ll take it! The study also looks at ways to improve the masks by doing stuff to them but since I’m just using the NRB before I intubate I’ll be sufficiently happy with a 90% FIO2 to preoxygenate my patients besides I don’t need to look any crazier to the staff by making an art project out of the masks before I intubate someone…


Farias, E. et al. Delivery of high inspired oxygen by face mask Journal of Critical Care. Volume 6, Issue 3, September 1991, Pages 119-124.


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