Impella Medical Device Stuff

This is my first of many posts on the Impella system by Abiomed. It is going to be part of my "Cardiogenic Shock: Rise of the Machines" lecture for Portland in August 2020.

I am planning on covering LVADs, RVADs, ECMO, TandemHeart, etc. in the upcoming months but one does not need to work at an ECMO or transplant hospital to see an Impella. This post is targeted for the clinician or nurse who is caring for the patient and is curious as to what’s the next step. Not intended for repositioning the device or criteria for installing it. I’ll get there. Give me time. Besides, I took a break from the Ketamine for this today.

When managing a patient on the Impella, whichever of their devices, a question always comes up when the patient becomes hypotensive. Do they need vasopressors or ionotropes? This algorithm from the Detroit Cardiogenic Shock Initiative is a helpful guide, definitely not an end-all-be-all but it’s better than flying without any instruments. Every patient with an Impella NEEDS a swan. You need to be able to measure the right heart pressures appropriately. You also need to be able to have an idea of what your SVR is. Without these parameters handy, you’re in the blind and clueless. Honestly, you should consider transferring the patient out to another shop before they get too sick to salvage.

Calculating the CPO and PAPI is something that nurses do and let the physicians know when things are going south. My favorite is to get the call followed by a suggestion to start a new med. that shows they’re vested and I love that.

Even though I do not run ECMO or have an LVAD program at my shop, I’m fortunate that I have colleagues at nearby hospitals who respond to my texts promptly and are around to help. It’s a blessing. My fellowship training provided me with a great amount of experience to where I do what I know how to do and when I need to make that call, I make it. No shame. Patients come over ego.

-EJ

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.

Be careful with Ketamine and Catecholamine-dependent Heart Failure

The Ketamine kick continues! I am not going to pretend I knew everything about everything as I've created this page over the last several months. People who walk around saying things like they were born with that knowledge sometimes need to be checked. We all had that one eye-opening day where it was like, "(explicative) I should have known that!"

I had some basic knowledge on ketamine but fortunately I have expanded that substantially over the course of working on my lectures. The whole "negative ionotrope" concept was something I was familiar with, but I never actually looked up in depth until colleagues such as the great Seiha Kim, David Convissar, and other great anesthesia colleagues who have more experience on the matter than I do. Not to mention that Seiha is both a pharmacist and an anesthesiologist.

A healthy heart should not have any issues with ketamine for sedation nor rapid sequence intubation, but, as mentioned in the Christ article linked, you can find a 21% decrease in cardiac index. This also brings me to the point where many clinicians focus on the blood pressure while ignoring the patients cardiac index/cardiac output. It makes us feel all warm and fuzzy inside to see the MAP > 65 as we keep on increasing our pressors but at the same time we have NO IDEA what this afterload increase is doing to the LV. We feel self-reassured but really our patients are going on a downward spiral. That's a discussion for another day. We really need more than a BP cuff or an a-line to get a true grasp of what's going on with our critically ill patient who is otherwise hemodynamically unstable.

-EJ

Link to Abstract

Christ G, Mundigler G, Merhaut C, Zehetgruber M, Kratochwill C, Heinz G, et al. Adverse cardiovascular effects of ketamine infusion in patients with catecholamine-dependent heart failure. Anaesth Intensive Care. 1997;25:255–259.

Link to Abstract

Bovill JG (2006). Intravenous anesthesia for the patient with left ventricular dysfunction. Semin Cardiothorac Vasc Anesth 10: 43–48.

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.

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

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Link to Abstract

Link to Full 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.

Bolus intermittent vs. continuous infusion of furosemide in heart failure

Link to Abstract

As a critical care doc, a good chunk of the consults I receive for acute hypoxemic respiratory failure are from pulmonary edema. So I do my thing, intubate when necessary, and place these patients on a BiPAP setting that’s comfortable for them. Airway, check! Now it’s time to diurese them to a potato chip. I know there are suggested dosing that you may find in the literature, and the fact the IV vs. PO dosing of #furosemide is different. Clinical practice is always an art, though, as using an exact flow every time can get your patient into trouble. Prior studies as to whether to give #lasix as a bolus or a drop were negative studies, but this one favored providing drip. The bolus arm used q12 dosing which raises my eyebrows, though, as I usually use q8 dosing in my practice. @codyperrigo and I used a drip on a pt the day after this study came out with some phenomenal results! That’s empiric data and is worthless, though 😉. Anyway, a big 🎩 tip to the authors.

-EJ

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.