Cordis vs MAC Introducer: What is the difference between the two?

This is a topic better handled by Surgeons than myself but I haven't seen anyone do it. Here I go! @buckparker, you're invited to chime in at this party, bud. @physiciandoodles inspired me to create this post.

Quick! This patient needs to be resuscitated with blood STAT! Call for the massive transfusion protocol and grab me a Cordis STAT! Do you know what this means? Do you know what it means if they asked for an introducer? For many years I was confused myself. I mean, aren't they both just large bore central lines for the purpose of infusion blood quickly or floating a central line? Well yes, they are. But depending on what institution you work at, you may get a funny look on your face if you ask for it by the non-standard name. Non-standard for that institution, of course. I will make this clear, though, as I posted this earlier in the life of my instagram page. You can get A LOT done in a massive bleed with two solid 16 gauge peripheral IVs. Many times you do not need to puny central line. But there are times when patients mean business and they needs all and a catheter of this type is necessary. Okay, let's get started.

First of all, the MAC introducer. This is a proprietary product from Arrow/Teleflex. MAC is a trademarked name that stands for multi-lumen catheter. You may say to yourself, well Eddy, a triple lumen catheter should be a MAC line too! You're not wrong, but we can't make this already challenging job easier on ourselves, right? MAC introducers can come with anywhere from one to three lumens. You could float a swan through many of them, but not all. It is essentially like a "Cordis" but it could have another line. The MAC also has the dilator in the catheter as my colleague Zahid, @zvhvd, pointed out.




A "Cordis" is also an introducer, but the word Cordis is the brand name of the product. A Cordis is the same introducer, but only has one side port. You can also float a swan through this puppy. 

There are other manufacturers who make similar products that I am not going to cover here for the sake of time. Your friendly neighborhood ICU should have one of these introducers in stock. Familiarize yourself with where it is because the day you need it, the patient NEEDS it.

- EJ

Photo credits for Arrow/Teleflex Products

Photo credits for Cordis Products

Copyright gods: If the photos posted upset you, let me know and I will take them off. Just trying to teach here.

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Vasopressin: Titratable Doses? Monotherapy in Septic shock?

This is what I love about the community in social media. We all just push each other to be better. Rishi posted today about titratable Vasopressin and, me being the data junky that I am wanting to know every study I could possibly know under the sun, had two studies in my back pocket ready to share with everyone. I was planning on sharing this study with you all further down the road but, Rishi indirectly pushed me so here I am sharing this article with you all rather than going out for a run. No, there's no one study where they just looked at titrating vasopressin. What this study does show us, though, is that the authors used vasopressin as a titratable medication as well as a mono therapy medication (that means not just adding it to norephinephrine when it reaches X dose. Studies like this indirectly guide us to what can and can't be done moving forward in medicine. If you get into trouble with a patient, one can justify it by saying "the VANISH study showed that it's safe to use it in this manner". I'm always worried about the lawyers, I'm not going to lie.

The goodies in this article and what I want you to focus on today is not necessarily the conclusions of the article nor all the subgroup analysis, but rather I want you to look at the methods on how they performed the study.

Patients were able to receive titratable doses of vasopressin up to 0.06U/min. That means that they were able to exceed the 0.04U/min you and I use every day.

They also titrated to a MAP of 65 or 75. Note that they did not use a systolic blood pressure. I have covered why you shouldn't do that unless you have an arterial line on youtube and here in the past.

The MAP of 75 is also important because there's data that higher MAP's in patients with chronic hypertension is better for them. I see shops where the MAP goal is 60 and that's just plain stupid and only acceptable on a case by case scenario.

Patients in this study received vasopressin as monotherapy for septic shock and it did not cause issues.

There is much to be said about the methodology of this trial which I am not going to get into today. I'll be here forever. Instead, you can hear me take it apart live in Hawaii in May 2020.

A hat tip to the authors.

- EJ





Link to Abstract

Link to FREE PDF

Gordon AC, Mason AJ, Thirunavukkarasu N, et al. Effect of early vasopressin vs norepinephrine on kidney failure in patients with septic shock. JAMA 2016; 316: 509.

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Diabetic Ketoacidosis: PlasmaLyte vs. 0.9% Sodium Chloride for Resuscitation

Can we start looking at our diabetic ketoacidosis protocols and changing them? This study from 2012 is admittedly small, retrospective, and leaves a lot to be desired. But their findings are significant in my opinion. Usually studies need large sample sizes to prove their endpoints. Here, the endpoints were proved (within their methodology) with this small sample size. The article is not free and I bet that more people would benefit from the knowledge one could gain from it if it wasn't hidden behind the paywall. Grrrrrrr. Here are the benefits of using plasmalyte over saline.
1. the mean arterial pressure was improved in the PL group p less than 0.05
2. there was improved urine output in the PL group in the first 4-6 hours p less than 0.05
3. the patients who received NS had higher potassium levels than the PL group between the 6-12 hour mark. Remember, PL has 5meq/L of K while NS has ZERO. Can we drop this hyperkalemia with LR and PL nonsense already?
They disclose the COST of plasma-lyte in Australia to be $1.94/L vs. $1.17/L of NS. It's not $30 a liter like I've heard in the past. This was in 2012.
Okay, this is a short one. I need to go. My wife wants us to enjoy our Saturday and for me to not be such a nerd reading articles.
BYE!
- EJ



Link to Abstract

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HFNC: Does it Ventilate COPD Patients?

I've reviewed numerous mechanisms of action and functions of High Flow Nasal Cannula (HFNC) but I haven't touch on whether or not it works to help ventilate patients. I have discussed in the mechanisms of action that it does wash out the CO2 from the dead space in the nasopharynx, oropharynx, etc, but does that show a numerical decrease in the PCO2? The studies I had reviewed prior to this one weren't promising. 

One of the indirect ways that HFNC can bring down CO2 is by bringing down the patients respiratory rate. There's plenty of data to support the decrease in the respiratory rate. Since the person isn't breathing as hard nor as fast, less CO2 is produced. Less CO2 is produced means the patients needs to be ventilated less. Things get better. Prior to this study, though, the data just wasn't there to show that this actually happened in a statistically significant way. I've said this before and I'll say this again, I will not recommend HFNC to a patient with a COPD patient sucking wind in the ED with an exacerbation that has a gas that looks like 7.06/96/66. That patient either needs some non-invasive ventilation with a very close eye or the endotracheal tube.

In this study they placed COPD patients, not in exacerbation, on HFNC and measured a number of parameters but you and I are here for the CO2. Patients had their PCO2 measured at baseline, on 20L HFNC, and at 30L HFNC. At 20L the PCO2 was at approximately 91 (plus or minus 6.7)% of their baseline and at 30L their PCO2 was at approximately 87.4 (plus or minus 6.2) % of their baseline. That data was statistically significant.

This may be completely out of bounds but if we can (although I probably shouldn't) extrapolate that to a patient with a PCO2 of 60, 20L should bring them down to approximately 54.6 and 30L down to 52.4. Something is better than nothing and if you can hold the patient over while they get their steroids and nebulizations, it may be worth a try in the real world.

- EJ



Bräunlich J, Köhler M, Wirtz H. Nasal highflow improves ventilation in patients with COPD. International Journal of Chronic Obstructive Pulmonary Disease. 2016;1077-1085.

Link to Abstract

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Hyperchloremia: We've known it is harmful to the kidneys since 2012

It has been 7 years since this study came out, and many since. Here we are still using saline like it's benign. Part of the problem is that clinicians get set in their ways and just don't read. Sorry if that offends anyone, but it's true. Some say, "this has always worked and I haven't seen a problem with it" so they keep doing what they're doing. Our job is to cause no harm. I'm trying my best to minimize that but after all, we are all human. Being lazy is no excuse, though.

This article from 2012 shows a study that was performed on 12 healthy volunteers. It was a randomized, double blind, cross over study. I bet they were either college students or medical students; the mean age was 22. This was not disclosed in the article, of course. The participants received either 2L of 0.9% NaCl or plasma-lyte over an hour on separate occasions 7 to 10 days apart. If you still don't know what Plasma-lyte is, you must be new here. They did some bloodwork as well as MRI's. They must have had some good funding here.

Amongst the results, they found a significant difference in the serum chloride, as expected (p < 0.0001) and a much lower strong ion difference (p = 0.025) in the saline group. All the other electrolytes were unremarkable. From the MRI results, they found lower mean renal artery flow velocity (p = 0.045) and lower renal cortical tissue perfusion (p = 0.008) in the saline group. This proves that hyperchloremic metabolic acidosis is not benign.

A hat tip to the authors.

-EJ




Link to the article: 

Chowdhury AH, Cox EF, Francis ST, et al. A Randomized, controlled, double-blind crossover study on the effects of 2-L infusions of 0.9% saline and plasma-lyte 148 on renal blood flow velocity and renal cortical tissue perfusion in healthy volunteers. Ann Surg 2012; 256: 18–24.

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Diabetic Ketoacidosis: Using Balanced Salt Solutions instead of 0.9% Sodium Chloride

We all know the order sets for DKA, a bunch of 0.9% NaCl first boluses then drip, insulin drip, replace electrolytes, glucose gets to a certain number, change the fluids to 0.9% NaCl that contains dextrose, wait for the anion gap to close, give long acting insulin, wait a bit, turn off the drip, discharge planning. It's simple stuff, really. I may have oversimplified it but you know exactly what the protocol is at your facility. Truth is, though, is that the best for these sick patients? Would they do better with lactated ringers or plasma-lyte?

This study from 2011 states that there are 100,000 hospitalizations for DKA annually in the US. They knew from prior literature that using a bunch of saline solution causes a hyperchloremic metabolic acidosis. They wanted to see if it would happen in this patient population. They conducted a randomized double blind study providing these patients with either 0.9% NaCl solution or Plasma-lyte. For those of you who do not know what plasma-lyte is, go check out my YouTube videos (/shameless plug). They used their typical DKA protocol for their institution which is described in the article.

The study took 24 months and they ended up with 23 patients in the "normal saline" group and 22 patients in the plasma-lyte group. It was entertaining to see that at baseline, before a drop of fluid was even given, the serum chloride of the saline group was less than the PL group: 94 vs 98 (p=0.027). When the study was said and done, however, the chloride level was 111 in the NS group and 105 in the PL group (p < 0.001). I don't know if you've had time to look at the older things I've written/posted but there's a particular study that comes to mind where the authors found that an increase in serum chloride by 5 increases your chances of developing acute kidney injury. There was also a significant difference in the serum bicarb level where the NS group has a bicarb increase of 7 whereas the PL group had an increase of 9 (p=0.023). The authors did not follow renal function in these patients from what I am able to see. The authors admitted that they didn't know what the clinical significance of all this is. I believe we have data now with more recent studies to show us what the clinical significance actually is.

- EJ



Link to Abstract

Mahler SA, Conrad SA, Wang H, et al. Resuscitation with balanced electrolyte solution prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis. Am J Emerg Med 2011; 29: 670–674.

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High Flow Nasal Cannula in Acute Decompensated Heart Failure data leaves much to be desired.

Fortunately in the critical ill population, we do not necessarily have to abide by the saying that "if all you have is a hammer, everything looks like a nail". What I'm referring to is regarding utilizing high-flow nasal cannula in acute heart failure exacerbations. I already dissected how HFNC generated a "PEEP" equivalent airway pressure and the data behind that statement. The amount of PEEP varies and it drops by a statistically significant difference if the patient has their mouth open. If a patient presents to the emergency department, or someone gets overzealous with maintenance fluids, with an acute heart failure exacerbation, there is data that I will be reviewing here where HFNC is an option. But let's be honest with ourselves, though, non-invasive ventilation (colloquially known as BiPAP, although CPAP has data for working as well) is the better option because it provides positive airway pressure more reliably that HFNC. Sometimes these patients just need the ventilator as well. All three studies are FREE that I am going to be reviewing here and I recommend you read them for yourself rather than trusting my takedown of them. That's your disclaimer.

The first study published in 2011 out of Spain was a look at just 5 patients. I know, don't fall off of your seat. I can't criticize because I don't do any research outside of read other peoples research. One needs to remember that in 2011 the HFNC systems were not readily available for historical context. These 5 patients were treated in the emergency department with NIV and then I guess they were diuresed aggressively there. Why do I guess? Well the study does not report the BNP nor the achieved diuresis in these 5 patients. Big weakness in the study. They looked at a multitude of parameters that would be standard for a study of this nature, i.e. to see if HFNC is better than the other oxygen devices, but there are big problems. You see, the authors looked at the parameters before HFNC and then 24 hours AFTER HFNC. What they don't say is how much the patients were diuresed in the interim. Of course the PaO2 is going to improve. Of course the dyspnea is going to improve. Of course the respiratory rate is going to improve! Anyway, this is a study worth sticking in our back pockets to know it happened and move forward.

The second study by Roca also out of Spain in 2013 wanted to assess if HFNC helped with the hemodynamic parameters. They hypothesized that HFNC in patients with heart failure could be associated with a decrease in preload without changing the cardiac output. To look at this, patients got sequential echo's to assess cardiac function. Pretty good setup if you ask me. The 10 patients enrolled in this study were all stable. Therefore the data needs to be extrapolated to the sick patients. They did a baseline TTE on these patients, then hooked them up to the HFNC system at 20L, checked an echo, then at 40L of flow, and checked an echo. They did all sort of echocardiographic wizardry to obtain their results. They found that HFNC may be associated with a decrease in preload justified by the lack of IVC collapse on inspiration without any changes to cardiac function. IVC measurements are their own can of worms when used for resuscitation but this is very standardized and methodical. The most interesting finding that I enjoyed was the decrease in respiratory rate noted by these patients. At baseline, their RR was 23 breaths per minute. At 20L this fell to 17 bpm. At 40L this fell to 13 bpm. Cool stuff! Note that the patients were receiving just flow in this study as the FiO2 was set to 21% (room air). The authors chose to not use patients in acute decompensated heart failure for this study as there would have been too much variability in the subjects themselves along with their responses to the treatments interfering with to the measures. Obviously if they dump out a liter due to furosemide their hemodynamic parameters are going to change and it'll mask out the effect of the HFNC or provide confounders.

The third and last study I'm going to share with you all today comes from our colleagues in South Korea who performed a retrospective cohort analysis where patients were divided into a HFNC group or an intubation group after oxygenation with a facemask at a flow rate of 10L/min or more. These authors jumped on the opportunity to look at this data as they hadn't seen any published data about using HFNC in patients with acute heart failure exacerbations. They looked at approximately 5 years of data to place 73 patients in the intubation group and 76 patients in the HFNC group. Since this was a retrospective study, the decision as to what arm the patients fell in was at the discretion of the physician at bedside. The authors are just looking back in time at why they decided to do it and how the patients did. It seems as if they ignored the NIV data. I could be wrong. The baseline characteristics of the two arms were similar with nothing too eye catching. These patients were looked at for 6 hours. There were no statistically significant changes in the physiologic responses between the two groups. There was also no difference in the clinical outcomes between the two groups. This oddly, in my opinion, includes vasopressor/ionotrope use. I mention this because patients who are intubated typically have sedation. Also, the medications utilized for intubation could have an effect on hemodynamic parameters that are not noted here. It's just something that, from a personal experience standpoint, has me a bit curious. The p-value for that is 0.051. If the sample size would've been larger, I'm sure that would've been a notable difference. The authors noted all these limitations to their study and agree that what we really need is a prospective, multicentered, randomized, controlled trial. I agree

To conclude, I think the best we have right now in the absence of concrete data is clinical judgment, my favorite. One could try to place the patient on HFNC to either keep them away from the ventilator or even keep them from being annoyed by the CPAP/BiPAP mask which is typically uncomfortable, limits the ability to eat, speak, and other fun activities. If it fails, it fails. Your RT may be a little annoyed at you and may say "I told you so", but ultimately we have to do what's best for the patient. Thoughts? Please read these articles for yourself. A hat tip to all the authors. 

- EJ





Link to Abstract

Link to Full FREE PDF



Link to Abstract

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Link to Abstract

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Ketamine for Rapid and Delayed Sequence Intubation

Alternatives to Rapid Sequence Intubation: Contemporary Airway Management with Ketamine

What are your experiences with ketamine for intubations?

I am really glad that I stumbled onto this article that was shared by @the_resuscitationist and @medicotactico.

When you're dealing with airways and medications that have can concerning adverse effects, you really shouldn't trust me on anything and should read the article yourself. Link in bio. This one is also completely free! Also, everything I typed for this post didn't fit in the space allowed by IG, so if you want to finish reading all my thoughts, you have no choice but to head over to my website. It is what it is and this article got me fired up!

For my physicians/NP/CRNA/PA colleagues who manage airways: How do you utilize ketamine for these situations?

For my ICU and ED nurses who push this medication: what have been your experiences with it?

The first thing the authors state is something those of us in the ICU or ED’s already know, establishing an airway is the riskiest commonly performed procedure in acute care. I do not proceed with pushing meds unless I have all my ducks in a row and I have plan A, B, and C easily accessible.

Here’s what happens with ketamine versus other agents that are commonly used: the patient becomes dissociated, they get that glassy look in their eyes, basically disconnected, but the brain stem reflexes stay intact... well... most of the time. You need to be prepared for it to hit the fan at any time. The patient should continue to breath spontaneously. The patients hemodynamics should also be augmented. Again, the key word is “should”. I’ve seen patients become apneic as well as hypotensive but more on that later. I’m just glad I’m not the only one who has seen these effects which are described in the literature. Nurses, don’t push ketamine like a bolus. Push it over 30-60 seconds. I know there’s a ton of adrenaline rushing in those rooms and you're used to pushing meds.

Here’s a strategy I learned from this article. Go ahead and push the ketamine when the patient is agitated and thrashing to allow for preoxygenation. The patient should chill out and when they cease thrashing, one can move forward with a preoxygenation strategy. They even explained certain cases where patients were provided with ketamine for this reason and then didn’t even need intubation.

What’s the dose? 1-2mg/kg of IDEAL body weight.

One of the things that I have noticed clinically when administering ketamine to establish and airway is the clenched jaw. Here, the authors recommend using midazolam, propofol, or even a sub-induction dose of etomidate. Just be aware that these agents bring their own baggage to the party.

Here's what the authors say about the hypotension related to ketamine. First, you need to know whether you think the patient is catecholamine depleted. In other words, they are in shock and they are running out of steam. Those patients should be resuscitated to the best of your ability and you may have to cut the dose in half. Again, read the article for yourself.

Lastly, the authors discuss using ketamine for sedation but it should be kept at dissociative doses or else your patient is going to have some no-so-good experiences. You may need to add some propofol at that point.

For respect of the authors, I will stop there. Read it for yourself. Again, it's free! Thank youuuuu!

- EJ





Link to Article

Link to FREE PDF

Merelman, A., Perlmutter, M., & Strayer, R. (2019). Alternatives to Rapid Sequence Intubation: Contemporary Airway Management with Ketamine. Western Journal of Emergency Medicine, 20(3), 466–471.

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High-flow Nasal Cannula: What is it?

High-flow nasal cannula oxygen therapy in adults

Some of you have asked what I mean every time I post something regarding high flow nasal cannula. Let's start by defining the flow in the different oxygen devices. Regular nasal cannula provides between 1-6 liters of flow. A simple face mask can get you flows between 6-10L/min. Venti masks, aka Venturi masks can get you flow rates between 4-8L/min. The best you can potentially do with a non-high flow device is the non-rebreather which can generate a flow rate of 10-15L/min. Just so we are all clear, every time I see a patient on a non-rebreather my senses step up to the next level. To me, that thing strapped on a patients face means that a decision needs to be made stat as the person who placed it on their face needs a second opinion. It's time to either place the patient on HFNC, BiPAP, intubate, or my favorite, they just panicked and didn't know what to do. It happens.

I like the image in particular because it is not signaling any machine in particular. There are a number of different companies who make these devices and I do not know the nitty gritty as to what differentiates them. I just know I love the technology. Would you all like for me to make a YouTube video where I break down the mechanisms of action of the device?

This article is a good review for the time, published in 2015, with the data that existed at the moment. The author reviews the physiologic effects, discusses the dead space washout, the PEEP effect, the benefits of heat and humidification. In addition, they discuss clinical uses such as both hypoxemic and hypercapnic respiratory failure, pre-intubation, post-extubation, sleep apnea, heart failure, and others.

It's definitely worth a quick read.

-EJ








Nishimura, M. (2015). High-flow nasal cannula oxygen therapy in adults. Journal of Intensive Care, 3(1).

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Ringers Lactate does NOT increase Potassium more than 0.9% Sodium Chloride in this study

A comparative study of impact of infusion of Ringer's Lactate solution versus normal saline on acid-base balance and serum electrolytes during live related renal transplantation

Here's yet another article discussing Ringer's Lactate versus 0.9% saline solution in renal transplant patients. They also acknowledged the consensus to provide NS rather than LR to avoid hyperkalemia in patients but they weren't happy with that, especially understanding and running into the data suggesting that NS creates the non-anion gap metabolic acidosis from hyperchloremia which can result in hyperkalemia due to the extra-cellular shift of potassium. That's the reason why they decided to proceed with a prospective double blind clinical trial on patients undergoing kidney transplants. They had 37 patients in each group. Each group of patients, the LR and the NS groups, received a little more than 5L each. Patients who received NS had a pH drop from 7.43 to 7.33. The LR group had no change in pH. The table in the article breaks down the serum electrolytes during the study as they checked it four times throughout the course of the surgery. The authors concluded that RL may not only be safe, but also superior to NS in these patients. The article cites another study where that team had to to treat more patients for hyperkalemia in the NS arm compared to the LR arm. Cool stuff, right? A 🎩 tip to the authors!

-EJ











Modi, MP. A comparative study of impact of infusion of Ringer's Lactate solution versus normal saline on acid-base balance and serum electrolytes during live related renal transplantation.Saudi J Kidney Dis Transpl. 2012 Jan;23(1):135-7.

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0.9% Saline vs. Ringer's Lactate: Which one causes an increase in potassium?

Effects of Normal Saline vs. Lactated Ringer's during Renal Transplantation

0.9% saline is 154mmol/L of sodium and 154mmol/L of chloride. That's it. There's no potassium, calcium, magnesium, nor buffering agent in there. Ringer's lactate, however, has 130mmol/L of sodium, 109mmol/L of chloride, 4mmol/L of potassium, 28mmol/L of lactate, and 3mmol/L of calcium. One would expect that the solution containing potassium would cause a greater increase in potassium than the one without potassium, right? Well, not so fast. Large volumes of sodium chloride, produce a hyperchloremic metabolic acidosis. What happens during acidosis? Well, there's a shift of potassium from the intracellular space to the extra cellular space. Much of this has to do with the strong ion difference which I will be breaking down in the near future. In this study, 52 patients patients received either LR or NS during their renal transplants.

Here are the findings: This has been copied and pasted from the article. Please download it and read it for yourself.

"Patients in the NS group had a lower mean PH level during the transplantation compared with those who received LR (p < 0. 001).

Mean serum potassium levels in the NS and LR groups were 4.88 ± 0.7 and 4.03 ± 0.8 meq/L, respectively (p < 0.001).

Mean changes of the serum potassium were +0.5 ± 0.6 meq/L in the NS group and –0.5 ± 0.9 meq/L in the LR group (p < 0.001).

Mean changes of PH were −0.06 ± 0.05 in the NS group and –0.005 ± 0.07 in the LR group (p < 0.001)"

If next time someone tells you that LR causes hyperkalemia, you can be armed with data. I have other articles with similar results that I plan on sharing in the upcoming days.

I don't know what to make of that thrombosis phenomenon they found. Must keep an eye out for more data regarding that.





Mohammad Reza Khajavi, Farhad Etezadi, Reza Shariat Moharari, Farsad Imani, Ali Pasha Meysamie, Patricia Khashayar & Atabak Najafi (2008) Effects of Normal Saline vs. Lactated Ringer's during Renal Transplantation, Renal Failure, 30:5, 535-539

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IV Fluids Types: Do you know your -ish?

Problems with solutions: drowning in the brine of an inadequate knowledge base

More than 50% of residents do not know how much sodium is in 0.9% NaCl. I know you do, though... it's 154mmol/L. Far more than our "normal" of 140mmol/L.
Why do I nag so much with intravenous fluids and what's in them? Truth be told, I did not know my fluid composition as well as I should have even as an intern. I had an ICU attending, a mentor, now someone I'm fortunate to call a colleague, who would pimp the house staff on IV fluids and make us feel ashamed if we didn't know the answer. He was right. My embarrassment was deserved. After all, these are substances that we are mindlessly pouring into our patients. The vast majority of clinicians, I'm not even talking about nurses, I AM REFERRING TO US DOCTORS, do not know what's in these bags that are so easy to click in the EMR and order. We mindlessly just do it. I was embarrassed. I do not want you to feel the same way. I have been teaching fluids now for 4 years. It's one of my passions. I have a talk that is complete and can present at any time of the day. I know it well. But I am always reading and adding to it. The talk is going to be one of the lectures I will be presenting in Hawaii in May of 2020. It will also be presented to the Department of Anesthesia at my hospital on October 20th of this year. I am currently brushing up that talk, adding and subtracting some things, and I ran into this study from 2001 which asked preregistration house officers and senior house officers (I guess that means interns and residents) about the composition of fluids amongst other things. I won't go over the methodology but the training needs to start in medical school. Overall, 11.5% said their training in the matter was poor, 22% stated it was unsatisfactory. I have to agree with this 100%. I received ZERO training in med school regarding IVF. Since it's something so ubiquitous in our daily practice of medicine, it's something we need to do better. A lot better. If you are in medical school or residency, have you been trained in the composition of IV Fluids?

-EJ



Link to the Abstract

Lobo, D.N., Dube, M.G., Neal, K.R., et al., 2001. Problems with solutions: drowning in the brine of an inadequate knowledge base. Clin. Nutr., 20(2):125-130.
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.

HFNC/High Flow Nasal Cannula: A beautiful image of the mechanisms of action

Not Just Oxygen? Mechanisms of Benefit from High-Flow Nasal Cannula in Hypoxemic Respiratory Failure.




Link to Abstract

Link to Image

Goligher, E. C., Slutsky, A. S. (2017). Not Just Oxygen? Mechanisms of Benefit from High-Flow Nasal Cannula in Hypoxemic Respiratory Failure. American Journal of Respiratory and Critical Care Medicine, 195(9), 1128–1131.
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.

HFNC/ High Flow Nasal Cannula in the Emergency Department: Can it avoid intubations?

Randomized Controlled Trial of Humidified High-Flow Nasal Oxygen for Acute Respiratory Distress in the Emergency Department: The HOT-ER Study

This study was the first randomized control trial looking at whether high-flow nasal cannula (HFNC) decreases the need for mechanical ventilation in the emergency department. In addition they looked at emergency department and hospital lengths of stays, 90 day mortality, adverse effects in the hospital, and patient experience. I sympathize for the authors of this study because their abstract shows results that my not in fact be true. I state this because, although the study took over two years to complete, they did not collect sufficient patients to demonstrate an effect on their primary outcome which was a need for mechanical ventilation. Unfortunately, they needed 900 based on post-hoc analysis and obtained 322 patients. It would have taken them approximately 6 years to get this trial done. Sigh. The other caveat to this trial is that the sickest patients were plucked out by the physicians after recruitment because they wanted to proceed with NIV/BiPAP before even trying HFNC. I can't say I blame them. I treat patients and trials be damned if my clinical judgement is telling me to do something. That's another reason why I am not in academics nor do I do research. Patients also just weren't that sick. If you're an ER doctor, could you imagine the acuity if you just intubate 7.2% of patients in respiratory failure on standard oxygen therapy? That means these patients weren't that sick. I mean, the intubation rates for all comers in patients who are on HFNC in subsequent studies flirts with 30%. Please don't quote me on that number but I believe it to be accurate based on my prior research. I can just imagine how many clinicians would irresponsibly read through the abstract and say, HFNC is not good and just throw away the technology ignoring the benefits. Then you have to fight against their cognitive dissonance to make them change their practice. That's enough for today on this study. Thanks for checking it out.
A 🎩 tip to the authors

-EJ




Jones PG, Kamona S, Doran O, Sawtell F, Wilsher M. Randomized controlled trial of humidified high-flow nasal oxygen for acute respiratory distress in the emergency department: the HOT-ER Study. Respir Care 2016;61:291–299.

Link to Abstract

Link to FREE PDF

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.

HFNC: The Physiologic Effects

Physiologic Effects of High-Flow Nasal Cannula in Acute Hypoxemic Respiratory Failure

I have extensively covered high flow nasal cannula, HFNC on this page due to a talk I'm creating on the matter. We've witnessed it first hand keep patients off of the ventilator. This article published in the American Journal of Respiratory and Critical Care Medicine, which as an aside is the highest impact factor publication in the Critical Care world, looked at 15 patients to determine the physiologic effects of the HFNC system. The reason why they performed the study was because those physiologic effects that we all know are beneficial were just not defined at the time of the publication. The ambitious authors wanted to go ahead and define them. Although this study was published in May 2017, one can grasp more or less the time it takes to get one of these important studies published by noting that it was initially submitted in May 2016. Imagine having this data and not being able to get it out. I would lose my mind.
The authors used patients with a P/F ratio of less than or equal to 300. They performed a number of measurements which I will not cover here for the sake of it being Sunday morning and you do not want to be put into another nap.
In a quick and dirty recap, here are their findings:
1. less inspiratory effort
2. lighter metabolic work of breathing
3. less minute ventilation (due to decreased respiratory rate)
4. improved oxygenation
5. no change in PCO2 nor pH
6. increased lung volume in dependent and non-dependent lung regions
- this may be a huge key towards understanding the possible PEEP that the HFNC system may provide. The authors state that increasing the EELI with an improvement in oxygenation while not having a change in tidal volume may explain the PEEP effect
There are other findings which I will defer to the authors to describe in the article. Check it out in the link below.

- EJ






Link to Abstract

Mauri, T., Turrini, C., Eronia, N., Grasselli, G., Volta, C. A., Bellani, G., & Pesenti, A. (2017). Physiologic Effects of High-Flow Nasal Cannula in Acute Hypoxemic Respiratory Failure. American Journal of Respiratory and Critical Care Medicine, 195(9), 1207–1215.

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.

Normal Saline: A History Lesson for the Inappropriate Name

A little history lesson, my friends, regarding the origins of us calling 0.9% saline solution, aka 0.9% sodium chloride, "normal saline".

We are all disappointed in ourselves. You've been calling it normal saline, I've been calling it normal saline, we just can't stop ourselves! Of course you know I am referring to 0.9% sodium chloride solution used so commonly, and many times inappropriately, in our everyday practice. Why is it not normal? Well, I have covered this many times on my Instagram page and YouTube videos. First of all, the sodium concentration in serum is 140meq/L. The reference range in the labs are usually 135-145meq/L. What's the sodium concentration in "Normal Saline"? 154meq/L. How much chloride is in serum? 98-109meq/L. What about in "normal saline"? 154meq/L because it's equal parts sodium and chloride. We can continue talking about strong ion difference and all the adverse effects of the 0.9% saline but that will take me forever. It's Saturday and I have a birthday party to go to. Where in the world did the associate with "normal" come from? The inspiration for this post came from @anursingnote and her discussion with @med.life.crisis, two RN's who are trying to kick butt and get smarter every day. You go girl(s)!
This article is not free, unfortunately, but they do make a couple key points, all of which show that even though they used the word "normal", it's not in the appropriate way. You're never going to think about a Hamburger now without thinking about 0.9% saline solution. Sorry I ruined that for you.
Here's how all this went down in chronological order:
I credit the authors of this paper for doing much of this heavy lifting, by the way. I can't actually get my hands on many of these papers. I'm going to do my best to briefly summarize.
1888: Hamburger. This Dutch physiologic chemist performed in vitro studies (not in vivo, take a second to let that process) where he found that there was less hemolysis with 0.92% saline than other concentrations.
1888: Dr Churton. "he was ordered transfusion of ‘normal saline’ solution in order to replace the fluid thus lost". That fluid was nothing like the saline we know and are still trying to understand to this day. That particular fluid had 150meq/L of Na and 128meq/L of chloride. It also had some bicarb in it.
1892: Dr Spencer used the term "normal salt solution" but the composition of the fluid was not defined.
There are plenty more goodies in the article which I recommend you try to get your hands on. The article is going to definitely be included in my lecture regarding intravenous fluids that I will be giving to the anesthesia department in my shop next month and on various lectures I have scheduled nationally next year. It's that important. A great job by the authors!
All in all, can we really stop saying "normal saline"? I think it's too embedded in our vernacular and it'll be too challenging to fix. I am always trying to make a conscious effort to stop but it's challenging because I have been hearing it for over a decade now. I'm getting old.

-EJ





Link to Abstract


Citation:
Awad S, Allison SP, Lobo DN. The history of 0.9% saline. Clin Nutr Edinb Scotl. 2008;27:179–188.
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.

10,000 Followers on Instagram: THANK YOU!

THANK YOUUUUUU!

It finally happened; my instagram account reached 10,000 followers. I could not have done it without your support. Yeah, you. You're one of those 10,000. Thank YOU for following along in my craziness.

First of all, I know there are plenty of Instagram accounts with many more followers than mine, but I have created a niche type account which is mostly specific to Critical Care. There aren't many dedicated Intensivists in this world, unfortunately. To me, this means that 10,0000 people have the potential to learn what I am learning and be able to either utilize this information directly, or share it with the medical community they work with. There's nothing that makes me happier than a nurse or respiratory therapist who makes a great suggestion on how to help me better manage the patient. That shows interest and passion in what they are doing. In addition, when those suggestions are made, it also means that I have created an environment where the staff is not fearful of what I am going to say or think about them. After all, I say plenty of silly things just to keep the mood light and lively in an environment which is filled with critically ill patients. If I teach one medical student about fluids, and they go on to take care of thousands of patients throughout their career and potentially train other students and residents along the way. Exposing 10,000+ people to the same article at once is far more powerful. It would be an exponential effect and you bet that that keeps me incredibly motivated. I am not in academics although I obviously love to teach. At this juncture of my career, I struggle with giving up control, it's the Intensivist in me where I want to be in charge and managing as much as humanly possible. This medium of teaching on social media provides me with a release. I get immediate feedback from you all. In addition, I provide the citations for everything I post so that you don't, as you shouldn't, trust me. Sorry if the articles aren't always free. After all, I frequently say that I'm not someone who actually does clinical research and do not take credit for being the one who discovers anything I post. I have one publication and, for the moment, that's all I am going to have.

Ulterior motives

As some of you already know, I am going to be speaking at several conferences this year. I have not disclosed that publicly just yet, though. No, it's not Chest, ATS, nor SCCM, but I will be sharing the stage with certain notable clinicians who regularly present at those conferences. I have pursued this opportunity to speak because it is something I have never done before and I really wanted to push myself to be very uncomfortable. A new challenge. Do I need to do this? Absolutely not. But presenting at these conferences has lit a fire underneath my behind because I don't need to bring my A game, rather, I need to bring my A++ game. My reputation is on the line, I will be standing in front of hundreds of clinicians influencing their practice. It will be in front of a live audience of several hundred individuals who paid some good, hard earned, money for some CME credits. I do not get to hide behind my Instagram account. My information will be crucial to the care of their patients and their communities. That's a big challenge! Bring it! This ends up benefitting my IG and YouTube audience because I have shared many articles of some of talks that I am preparing. My research is getting directly to you after being masticated a bit. As always, I leave some of the lifting to you all as I cannot bear the responsibility of digesting all the data for you. If the article I share stimulates your interest, I will also provide the links to where I got the data or explain how I came to that conclusion.

Financial Compensation/Multiple Streams of Income

I am writing the following for the sake of transparency. I hope you appreciate it as such. I am disclosing that I am earning some money off of all this. No one wants to work for free. This may motivate some of you to do the same, potentially use the same or similar model, or just wonder why I am investing so much time into it all. Achieving 10,000 followers is a big part of monetizing this whole ordeal. By no means am I going to quit my job and live off of this, but it does provide incentive. The good thing is that none of this will cost you one cent. For the sake of full disclosure, here's how all this works. First of all, the swipe up feature is going to allow me to send you to a couple different locations.

My Website: eddyjoemd.com

I have this website that runs ads. Google Adsense sends me a check every month for the website. At the time of this writing, I earned $0.63 yesterday and $0.72 the day before. Let's say $20 a month. How's that for transparency? I don't have any expectations for the website to blow up but I enjoy doing it. I enjoy typing out with my improper grammar and run-on sentences what I'm thinking as I go through the articles. I have learned a lot about the google algorithms, SEO, keywords and the like. Many cool people on YouTube such as Income School and Miles Beckler for those who are interested in going down that rabbit hole. I really like to learn and expand my knowledge. This was something cool and it's rewarding.

The YouTube channel: www.youtube.com/eddyjoemd

This has been my longest running side gig. My channel is over four years old now. I had to stop and think about it. It feels newer than that. Oh well. This was a very successful and much more profitable venue to discuss medicine things with you all but recently YouTube changed their algorithm because of the vaccination and misinformation which destroyed my audience and leads. I was no longer being recommended. This is why I ask for some thumbs up during my videos because it helps YouTube see that I'm legit and not someone pretending to be a physician. I plan on making many more videos as time allows in the near future. I just need more feedback as to whether the videos are any good or if I can do better. At the moment spending 15 minutes shooting a video and 5 minutes editing it for 400 views isn't worth my time. I may have to change strategies. I just may not be that good or I may be too niche. I'll figure this out. It's also challenging to record myself. Do I really have to stress that hearing the sound of my own voice when I'm editing irks me?

Amazon Affiliates

I may start plugging in a book that I am enjoying and think it's a good value which will be helpful for you all. I may do this on a story, a blog post, or a link to my Amazon store. The fun part for me is that you don't even need to buy that particular book or item for me to earn a commission. I'm always reading something that's not medicine related. At this time I am reading this book by Dale Carnegie Titled: Public Speaking for Success. If you click on that link, it will open up the book on Amazon. In the next 24 hours, if you purchase that book OR anything else whatsoever on amazon, I will get a commission. It doesn't make your price higher. I earn something like 1-5% of the price of the item. Definitely won't make me wealthy but it pays for Netflix. I also have an Amazon Store. For those interested, creating an Amazon Affiliate account is really easy.

Tips for those who are trying to find any type of success around here.

Provide value. The results I have experienced speak for themselves. I even created a graph about it. People who know me aren't the least bit surprised that I've kept peripheral track of my follower count and more recently have kept track almost daily. At first I was naive enough to think that I could get there on just posting random things. That my life would be sufficiently interesting to carry some weight. Harsh reality struck. Truth is, as an individual, I am not that interesting. I had to come up with a way to get there without butt pics. The day I decided to start sharing what I was already doing on my free time, i.e. reading a bunch of articles, is the day my account starting making a drastic upswing.




I need to shout out to everyone who has ever shared my page. Without these kind people who did this for me and my page out of the goodness of their own heart, I would potentially never be writing this post. Apologies if you shared my page and you're not on this list. Call me out on it like Sean Dent did! I will go in alphabetical order:

@afibflutter
@amandasximd
@ambcarerx
@anishathemd
@ashleyadkinsrn
@austinchiangmd
@bedsideroundz
@breatheeasy_rrt
@brendalee_figurepro
@combatmidwife
@corporatenutritionist
@doctor.charlesclinton
@doctorwarsgame
@drbuckparker
@drcindylou
@drhakman
@drkmitchell
@drkoriashner
@drmanuelroman
@drmcsaucy84
@dr.tommymartin
@elisewitz
@grepmed
@hayleykrayburn
@herbsandfood
@icuphysiotherapist
@ingriddborges
@jacquicormier_rn
@kettyelena
@kristinyatesdo
@leahem09
@me.girlincognito
@michaelgalvezmd
@nicolekupchik
@nikiz11
@npstudentmagazine
@nurseannrn
@oneinamelon.co
@pagethepa
@paramedicpractitioner
@physiciandoodles
@plan.film.medical.memes
@poojalakshminmimd
@pre_stethoscope_life
@rn_ratched
@seanpdent
@the_resuscitationist
@thedoughnutdiary
@theencouragingdoc
@thefacetiousmurse
@themedicnurse
@xray.doctor
@yournursingeducator

That's enough for today! Hope this helps. Again, thank you all for your support!
-EJ

Check out some resources I have personally found value in and recommend over at my My Amazon Store. This is an affiliate link which means that I may make a small commission if you make any purchase on Amazon after clicking on a product, you do not even have to purchase something I recommended. Thank you for supporting my work.

Ionized Calcium in the Critically Ill

Ionized Calcium in the ICU

I have to credit Dr. Rishi Kumar for inspiring me on this ionized calcium post this today. His post on instagram regarding total versus ionized calcium made me recall this article that was transformative for me when it was published in CHEST in December of 2015. I know that the official article was published in March 2016 but cool people like me get their hands on the manuscripts from time to time. Okay, fine, I'm not cool. CHEST sends pre-release articles out all the time. As mentioned, this article was formative for me and I hope it has the same effect for you all.

ICU practitioners, nurses, doctors, respiratory therapists are all obsessed with perfection. We want the MAP to be 65, the ABG to be perfect, and for there not to be any red numbers on the labs. What happens very often in our labs is that the calcium comes back low. Then we check an albumin and correct the calcium. Then it's still low so we check an ionized calcium. We get that number and do whatever we choose with it. I rarely check ionized calcium in my practice after reading this article. This is unfortunately not a free article but when there's a will there's a way.

I'll update this blog post later when I have a little more time.

- EJ



Link to Abstract

Link to PDF

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.

BiPAP (NIV) vs. High Flow Nasal Cannula

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.

- EJ

Link to Abstract

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.

HFNC/High Flow Nasal Cannula: Does it generate "PEEP"?

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.

-EJ

Link to Abstract

Link to FREE Article

Parke R, McGunness S, Eccleston M. Nasal high-flow therapy delivers low level positive airway pressure. Br J Anaesth 2009;103:886–90.

Link to Abstract

Link to FREE Article

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.

Link to Abstract

Link to FREE Article

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.