Severe Sepsis and Septic Shock: Using SvO2 and ScvO2 to Guide Resuscitation

You've heard all these fancy terms, mixed venous blood gas, ScvO2, SvO2, thrown around the ICU all the time. Regardless of whether you're a nurse, respiratory therapist, medical student, resident, or even a fellow, these terms may sometimes be quite confusing as everyone talks about them like, "duh, you're supposed to know this".

You're here because you don't know this. Or perhaps you don't know that you don't know this. Or perhaps you need a refresher course. I am not going to get into the deep dive complexities of venous oxygen levels as that could be a complete chapter in a textbook but feel free to ask questions below and either I or our community will try to answer the questions. 

SvO2: 
- venous oxygen saturation 
- taken from a Swan Ganz catheter. without a PA catheter, you can't measure this 
- also called a mixed venous oxygen saturation. 
- this is a combination of venous oxygen from both the SVC and IVC

ScvO2
- stands for central venous oxygen saturation
- taken from a central line that terminates in the SVC or right atrium. Could be an internal jugular, subclavian, or axillary line.
- it's easy to confuse the two because the PA is more "central" but think about it as getting this value from the "central line"

Correlation
ScvO2 is generally 5-6% higher (sometimes more) as this blood comes from the brain and upper extremities which generally consume less O2 than the organs and lower extremities. This is more pronounced in shock states. 

I'll dig deeper into this in the near future. The article where these images were taken from is FREE! A hat tip to the authors. 

-EJ

Rivers EP, McIntyre L, Morro DC, Rivers KK. Early and innovative interventions for severe sepsis and septic shock: taking advantage of a window of opportunity. CMAJ. 2005;173(9):1054‐1065. doi:10.1503/cmaj.050632

Link to Website with Article

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Link to Reinhart Paper

ABIM Board Certification Exam: How I passed my critical care medicine boards

Back in December 2017, I found out that I had passed my ABIM board certification exam for critical care medicine. I created this video on youtube for those who are interested in learning about the methodologies I pursued to be able to pass this challenging exam. Needless to say, it was the most challenging board exam I have taken. Below is the link to the YouTube video. Thanks for following along.

-EJ

Link to Video on YouTube

ABIM Board Certification Exam: How I Passed my Internal Medicine Boards

Several years ago, I took and passed my ABIM Board Certification exam for internal medicine. I made this video for YouTube when I was a younger whipper snapper and it has proven to have been quite helpful for some. In this video, I go over the different methods which I used to study for and ultimately, pass the exam. 

You can watch the video here or click the link at the bottom to watch it directly on youtube where you can have greater control of the video regarding speed and other parameters. Thanks for following along! 

Link to video on youtube

-EJ

Resuscitation and Fluid Responsiveness and Mean Arterial Pressure

We take care of sick patients. In doing so, we have various tools in our disposal including the physical exam, history, and hemodynamic parameters. We check the blood pressure on our patients and depending on that number, we do things for them (hopefully not to them). 
We place the blood pressure cuff on their extremity, hopefully the right size, and cycle it. We have learned about the limitations of the oscillometric devices as I have covered that extensively and we have learned to trust the mean arterial pressure (MAP). 

We all learned that the equation for MAP is:
MAP= [(2 x diastolic)+systolic]/3
We also learned that we should target a MAP of 65 based on the surviving sepsis guidelines and I generally agree with this. Sometimes I target a higher MAP, sometimes a lower MAP. Every patient is needs personalized care in my book. 

Here's the other equation that we should know but don't. 
MAP= (CO x SVR) + CVP
- CO= cardiac output, also HR x SV (and don't forget that the stroke volume is affected by preload, contractility, and afterload)  
- SVR= systemic vascular resistance
- CVP= central venous pressure (tends to be zero in a spontaneously breathing patient). This value tends to be ignored for the sake of simplicity. 

We all give IV fluids to increase the MAP, because that is what we see on the monitor, but that's the missing the point. 
Fluid responsiveness is defined as an increase in stroke volume or cardiac output/cardiac index after being provided with a bolus. 

Studies have shown us that only 50% of patients who are septic actually respond to fluid resuscitation. The other 50% who we blast with fluids, well, they just get overloaded and have complications secondary to that. 

The point of this post is for us to think a bit more outside the box when we have a patient who is hypotensive. We can't just look at the blood pressure after being given a liter of fluid and call the patient fluid responsive. 

The FENICE study looked at 2213 patients and 42.7% of the time, the clinicians gave IVF without looking at any hemodynamic parameters. Even when the patient had a "negative response" to the fluid bolus, 49.4% of the time, the clinician gave an additional bolus after that! I think you can call that insanity per the Einstein definition of it. 

The clinicians were looking at primarily an increase of BP followed by urine output, decrease in HR, decrease in lactate rather than changes in CO or SV. Let's just say that we have all been guilty of this in the past but need to get better on the matter. 

Here are some examples on where that thinking can lead us astray:
If the MAP is low but their CO or SV is looking great but their SVR is on the floor, they may need earlier vasopressors and nuanced fluid challenges. In the case of cardiogenic shock, you may find that the CO is on the floor and their SVR is in the clouds, those patients may benefit from some careful peripheral vasodilators with some inotropes. That undefined patient who is hypotensive and we give a liter of fluids to indiscriminately is quite dangerous at the end of the day. People come to the hospital to be helped, in those cases, we may actually be causing harm. 

If we are going to call ourselves the best, we need to practice that way. Understanding hemodynamics are crucially important to saving lives. 

-EJ

Cecconi M, Hofer C, Teboul JL, et al. Fluid challenges in intensive care: the FENICE study: A global inception cohort study [published correction appears in Intensive Care Med. 2015 Sep;41(9):1737-8. multiple investigator names added]. Intensive Care Med. 2015;41(9):1529‐1537. doi:10.1007/s00134-015-3850-x

FENICE Link

Ivermectin in COVID-19: Taking another look

Ivermectin in COVID, this is the second time I cover this medication during this pandemic. 

This paper has NOT been peer reviewed. I will try to peer review it myself. Ultimately, I recommend you not trust me and read the paper for yourself. A healthy dose of skepticism is needed for peer-reviewed papers these days, much more for these non-peer reviewed. 

Observational trial with all the limitation that come with it. This is not a randomized controlled trial. At least the authors went through the trouble of propensity matching some controls to help out with the outcomes. This was also international and multicenter. I'm a fan of ivermectin as it is widely available and inexpensive (ahem, tocilizumab, remdesivir).

n=1408, 704 got the study drug
Drug: 150mcg/kg x 1 dose

Primary outcome: mortality
If on mechanical ventilation: Mortality 7.3% vs 21.3% (NNT=7.1)
Overall death rates: 1.4% vs. 8.5% (NNT=14.1)<0 .0001="" font="">

Issues: no comment on PF ratio of these patients, their underlying organ dysfunction, adverse effects of the study drug. We also don't know where in the course of the illness did they get the study drug. We also don't know if they were getting other therapies outside of them being matched in the two groups. 

The patients in the Ivermectin group seems sicker at baseline: more CAD (p=0.03), more COPD/asthma, black race (which seems to be harder hit), more immunocompromised (these are not statistically significant, but there is a trend). 

Ivermectin was associated with a higher likelihood of survival. The authors claim a shorter length of stay but this is not reported anywhere in the paper. The authors recommend an RCT, I agree. 

Credit to Dr Tim Connelly who was one of my mentors during training for sharing this paper with me. 

Link to Article

Remdesivir: NOT a Game Changer

How I wish that this was a positive study. We’re in need of a helpful tool. I’ve thrown every possible treatment including tPA at patients to try to save them and nothing is 100% at this point. I took apart the first Remdesivir study several weeks ago and was not impressed. History is repeating itself.

This study was published to much fanfare and media attention yesterday. It was so good that the Lancet hid it behind the paywall when they had made all their COVID coverage free until this point. Shady shady (EDIT: it is now free to download). I have to credit my partner Kelly for getting me this paper. My NP Cody texted me about it 45 seconds before Kelly. I love my team.

There’s much to go over here. Too much to fit in the limited character count on IG but I’ll try my best. I could be wrong, don’t trust me, read the data for yourself. There are many details I just can’t cover because I’m trying to live my life. Let’s go!

Investigator initiated: they weren’t randomized from the get-go based on certain criteria, someone chose these patients. If your patients have renal failure or are on CRRT, these data do not apply as they were excluded from the study. The placebo group had more males which it’s the sex harder hit by COVID but the Remdesivir group had more HTN, DM, and CAD. These patients were less ill than the prior study. Interpret that as you may.

Remdesivir, 200mg on day 1, 100mg days 2-10 vs. placebo (2:1); n=158 vs. 78

Primary endpoint: time to clinical improvement within 28 days after randomization. What type of vague endpoint is that? Correct me if I’m wrong but that's a very uncommon endpoint. Either way, there was no statistically significant difference. Now, they admit that it’s not statistically significant, but they said there’s a trend that if they started the study drug within 10 days there’s possibly a benefit for faster clinical improvement. That’s a lot of ifs but this is where I figure there should be a benefit if there was to be one. Even with this caveat in mind, there was no difference in mortality if started early or late.

Secondary endpoints that you and I care about: all-cause mortality at day 28; frequency of invasive mechanical ventilation; duration of oxygen therapy; duration of hospital admission. No difference in any of these. There wasn’t even a difference in viral loads. This is an antiviral drug, by the way.

To be honest with you I’m not even going to go over the adverse effect stuff because I’m not convinced this works and I don’t think I can get my hands on it for my patients even if I wanted it. Well, maybe now since others may feel the same way I do and many aren’t going to want it.

The study was stopped early because they didn’t have enough patients to continue. Why not phone some friends and make the study multicentered? I disagree. I’m not a research conducting guy. I don’t want to further expose my ignorance.

I’m tired. This COVID stuff has exhausted me and I’m not even in an epicenter. I sympathize for all my colleagues in busier places than me. I have a strange survivorship guilt thing going on. I’m here for you all.

-EJ

Wang Y Zhang D Du G et al. Remdesivir in adults with severe COVID-19: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet. 2020; (published online April 29.)

Addendum: the Lancet now made the paper open access. I can't take the credit for them doing that! 

Link to Article

Link to PDF

Resuscitation and Fluid responsiveness, what is it?

You have a patient who is hypotensive. You want to make them not hypotensive. The first thing the vast majority of clinicians reach for is some sort of IV fluid. We give it and cross our fingers that they won't be hypotensive after the fluids were provided. This is what is done in every single hospital throughout the world.

I've already posted before that even in a healthy person, if they get a liter of fluid, 68% of it will be extravasated within 1 hour. Much more and far quicker will that volume be lost in someone who is critically ill; approximately 80% in 30 minutes. No wonder the "response" to that liter of fluid was so short lived.

Fluid overload has many complications which many of you know of already. Perhaps I'll do a post solely on that. This is just one post of many, so feel free to ask questions below and I will address all of them in full posts in the near future.

The whole purpose of providing a fluid challenge is to increase either the cardiac output or stroke volume, not increase MAP. This excellent paper was written by some resuscitation geniuses who I often fanboy over their work. It's completely free and I suggest you download it and read it for yourself. 

Monnet X, Marik PE, Teboul JL. Prediction of fluid responsiveness: an update. Ann Intensive Care. 2016;6(1):111. doi:10.1186/s13613-016-0216-7

Link to Article

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Resuscitation and Fluid Responsiveness: Passive Leg Raising + Stroke Volume

Don't think that I'm anywhere close to being finished on discussing fluid resuscitation and when to stop, I think I could spend a whole career just talking about this once concept. Drowning our patients with fluids is bad, we all know that.

Check out my YouTube video on the matter where I break down this study.

Douglas IS, Alapat PM, Corl KA, Exline MC, Forni LG, Holder AL, Kaufman DA, Khan A, Levy MM, Martin GS, Sahatjian JA, Seeley E, Self WH, Weingarten JA, Williams M, Hansell DM, Fluid Response Evaluation in Sepsis Hypotension and Shock: A Randomized Clinical Trial, CHEST (2020), doi: https://doi.org/10.1016/j.chest.2020.04.025.

Link to Article

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Resuscitation and Passive Leg Raise: Don't use the arterial blood pressure to determine fluid responsiveness

Passive leg raising (PLR) is a technique I am going to cover extensively as I am writing a lecture where this will be a hot subtopic. I've covered it before on my blog and instagram. It's all in the effort to NOT drown our patients in IV fluids when they're hypotensive. 

When I was a younger whipper snapper in training, I thought I could perform the passive leg raise assessments by picking up some legs, looking at the BP increase and call it a day. Boy, was I wrong. I learned some further principles behind why I was wrong but today I found the data as to how wrong I was. Needless to say, I was very wrong. Did I mention I was wrong? Glad we're clear. I wasn't born knowing everything and still have a ton to learn.

In this paper they placed a swan in their patients and did some other stuff that I will cover at a later date. As some background and to define certain principles, a person who is fluid responsive is one who receives an amount of fluid, in this case PLR is approximately 300cc, is one who has an increase in their stroke volume or cardiac index/output. It is NOT someone who's blood pressure goes up just because they got fluids. Looking at the sensitivity and specificity of looking at the arterial blood pressure versus the measures generated via thermodilution, you can see how looking at the BP is absolute poop and should not be used. 

I altered a copyrighted photo to help illustrate the area under the curve. I'll take it down if I upset anyone. At the end of the day I'm just trying to save lives. Haney Mallemat @criticalcarenow has done some great coverage on End-tidal CO2 so check out his work on the matter. 

Monnet X, Bataille A, Magalhaes E, et al. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test. Intensive Care Med. 2013;39(1):93–100. doi:10.1007/s00134-012-2693-y



Link to Abstract

Standard BP Measurements in the Critically Ill

Taking a quick COVID break and let's get back to some simple critical care basics: measuring blood pressure. We do this on all of our patients at least hourly for the stable patients and continuously on our unstable patients. Ultimately, though, we need to do this right. After all, this is critical care and the details matter.

I have already detailed my concerns with oscillometric BP cuffs in the past and have even created a youtube video about it meaning I'll skip that here. Ultimately, the values generated by the oscillometric devices leave much to be desired. When someone is sick (everyones definition of what sick is varies) they need an arterial line. Plain and simple. No healthcare professional has ever complained about having an arterial line. Win-win for all involved.

This paper touches on a 5 step approach to using an arterial line.
Step 1. Catheter insertion sites. I am a fan of brachial artery catheterization, ultrasound (US) guided. I tend to look at the radial artery first via US and eyeball the caliber of the vessel. I weigh on complexity of the procedure if they're on jet fuel to keep them alive and quickly scurry up the arm. I don't want to spend 2 hours sticking an artery like we have all done at one point or another. Someone who gloats about how good they are at a-lines hasn't been humbled enough. I asked my nurse colleagues to grab me a dart as well as the femoral line kit. Before anyone gives me a hard time about my preference for brachial artery preference, please note the complication rate is 0.2%. I have placed a number of axillary lines but this is an option of last resort for me. I choose the femoral route in code situations where I knock out a "dirty double" and place both the central line and arterial line depending on what blood return I get from the stick. 

Step 2. Catheter length: I use the 4.45cm catheter for radial arteries and the 16cm catheter for all others. When you place the US probe over the brachial artery you'll quickly see why the 4.45cm catheter won't cut it, especially in an extremity with significant adipose tissue. 

Step 3 is being skipped.

Step 4 and 5 are primarily for my critical care nursing colleagues as they describe the leveling and zeroing of the transducer, as well as checking the quality of the waveforms. They go further into dampening and a number of key concepts that are much better explained by the authors than I can ever do. 

You should definitely check out this article for yourself as it is worth your time. Did I mention that it's free?

Saugel, B., Kouz, K., Meidert, A. et al. How to measure blood pressure using an arterial catheter: a systematic 5-step approach. Crit Care 24, 172 (2020). https://doi.org/10.1186/s13054-020-02859-w

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