"If You Can See It, You Can Believe It" – Part II of Fluid Resus

Dear readers,

After a much needed break we are finally back to conclude our discussion of fluid resuscitation in the septic patient. The official EGDT Bar-Mitzvah after party!

By this point I hope you've come to fully internalize the concepts presented in part I. To briefly review:

  • In all sick, septic patients expect a certain level of volume depletion requiring resuscitation

  • Rivers produced an elegant (now slightly outmoded) algorithm for resuscitating septic patients. It begins by filling the tank (initial 20 cc/kg of fluid) and then, if still hypotensive, dropping a central line and titrating fluid boluses to a CVP of 8-12 mmHg. At that point pressors become an option for elevating MAP and improving peripheral perfusion.

  • CVP, unless extremely low (0-2 mmHg), is no longer considered a valid marker of fluid status--it only indicates RA pressure.

  • Ultrasound measurement of IVC diameter fluctuance with respirations is a better correlate to a patient's volume status

And so here we are. You checked the IVC, you bolused your patient. The IVC now shows minimal fluctuation. Hurray! Hold the celebration Shlomo; the patient is still hypotensive and poorly perfusing.

Is this full septic shock? Are pressors be the right call? Maybe we still need to give more fluid first? More importantly, if we do give more fluid, will it help to improve cardiac output (and in turn increase perfusion and MAP) or will it just back up and lead to ARDS and pulmonary edema?

Before addressing these conundrums, we must first revisit a simple concept that Guyton outlined decades ago. I'm talking of course about the Frank-Starling curve of cardiac function.

"Learn it, no pressure. ZING! See what I did there?"
Patients who have a PMH of CHF or ESRD may be on the low end of the curve, but would that preclude them receiving fluid? This is a common pitfall for many resuscitationists who fear iatrogenic pulmonary edema and fall short of adequately repleting these patients.

On the other end, sepsis and acidotic states can induce cardiac dysfunction in patients without previous cardiac insufficiency.

Measuring CVP or looking at IVC diameter is a reflection of preload to the right heart in static and dynamic terms, respectively. It says nothing of the left heart or its ability to pump more volume forward if given the opportunity with more fluid. The patient, therefore, may lie at any point along the graph. But which slope they occupy would otherwise remain a mystery.
Left heart is the dark side of the moon.
The topic surfacing here is the concept of fluid responsiveness: that increasing volume leads to an increase in cardiac output. Patients on a low slope of the F-S curve have minimal if any room to increase contractility with added volume, whereas healthier hearts maintain an ability to increase contractility to greater extents when more and more volume is added.

In his talks, Mike Stone advocates empiric fluid loading in septic patients with 4+ liters of IV fluid (the "Bronze medal" approach).

Scott Weingart would have you check the IVC dynamics until diameter fluctuations cease (the "silver medal" approach)

Mike and Matt go one step further and assess the actual cardiac response to a small fluid bolus that is fully reversible (passive leg raising)--visualizing the F-S response. To assess whether your patient is a responder--that is, with added bolus the cardiac output increases by 5-10%, you would have to perform a complex set of measurements to arrive at the CO. Even though this is the most validated and thorough approach (the "gold medal") it comes at the cost of more calculations, operator skills, time consumption, and holding a pair of legs in the air for 2 minutes.

Consolidating the above I propose a simple, rapid, etiology-driven approach to resuscitating your sick and septic patients with the aid of an ultrasound - a way to decide which patients need more fluid and which will no longer benefit (no positive response)

By crudely scanning just 3 parameters--heart, lung, IVC--you will uncover your patients' fluid status and plot their Frank-Starling slope.

It all starts with the IVC: if it collapses > 50% with each breath (or distends > 18% with each mechanical breath), your patient--with very high certainty--needs volume.
-When the IVC no longer shows dramatic fluctuation, a benefit from additional fluid is dubious. In some it may cause harm, overwhelming the myocardium leading to back flow (the patient on a lower F-S slope).

Near 100% collapse. Better give fluid.
Fully distended. Need to check left heart.
At this point we scan the heart. A detailed echo is not necessary; just one view qualitatively checking for LV systolic function (is the LV hyper dynamic with kissing walls or is it severely dilated with poor contractility?) can provide you with the information needed in less than 15 seconds.

Dilated LV, poor systolic function.
If the left heart appears to be contracting well, an additional bolus may very well increase cardiac output--the patient is fluid responsive (or at least tolerant).

If the heart appears overloaded, with poor systolic function proceed to a quick scan of the lungs. Numerous B lines, as in pulmonary edema, indicate that this patient occupies a lower slope along the Frank-Starling graph (poor cardiac function) and would likely not respond well (cannot tolerate) to additional volume. In this scenario, initiation of vasopressors to increase output and MAP would be more appropriate.

Thanks Medscape!
If the lungs defy expectations and appear rather clear (no greater than 3-4 B lines per intercostal field) than this patient may still be fluid tolerant and accommodate an additional small fluid bolus.

check IVC (large diameter variability?) ---YES--->give fluid
                                                               ----NO----> proceed to...
check the HEART (hyperdynamic/normal systolic function?) ---YES-->give fluid
                                                                                                  ---NO----> proceed to...
check the LUNGS (clear? No more than 2-3 B-lines?) ---YES--->give fluid
                                                                                       ---NO--->consider pressors


If Early Goal Directed Therapy Had a Bar Mitzvah…

Manage Sepsis like a Baawwss! "Wwughh!"

It's been nearly 13 years since the publication of the landmark Rivers early goal directed therapy study in the NEJM. As with a Bar Mitzvah, the Jewish rite of passage from youth to manhood, it's now time for EGDT's transformation and to face post-pubescent changes that go hand-in-hand with maturity, development, and the right to start drinking Maneschwitz. The developments I allude to here are reflections of the various (improved, more accurate) modalities many of us now use to detect the different goal posts set out in Rivers' algorithmic approach to severe sepsis. Let's explore this growth together.

First, consider a case scenario:

A 66 year old female (history of diabetes, hypertension, CHF) from home presents with fever and productive cough with the vitals: BP 88/50, HR 120, RR 20, T 39 C. She is confused and has dark urine.

You place her on a monitor, insert a foley catheter, add supplemental oxygen via nasal cannula, and place an IV to send labs and administer an initial bolus of 20-30 cc/kg of crystalloid fluid. Antibiotics are running in the IV. 15 -20 minutes later, she is still hypotensive. Do you give more fluid? Or do you now place a central line and add pressors (like norepinephrine)? 

In the original Rivers model, once the presence of severe sepsis/septic shock is recognized and the decision is made to  proceed with EGDT to guide us in reaching the ultimate point in a severely septic patient--normalize tissue perfusion--we will first and foremost satisfy the most important goal of "filling up the tank" completely and adequately with IV fluid. Only then can we begin moving further to subsequent potential deficiencies/goals that demand addressing: "tightening the pipes" (MAP > 65 with pressors), "optimizing the pump" (optimize cardiac output with inotropy), and "adding passengers" (transfusion of blood product to increase oxygen carrying capacity). With each subsequent step, you keep going back to check and see if you've met your ultimate goal of improved tissue perfusion/oxygenation by looking to surrogate marker of perfusion: ScvO2 (Rivers) or, in the 2008 Jones non-invasive model, serum lactate clearance.  

Here's the algorithm:

For a more detailed explanation of the above analogy on tank/pipes/pump/and passengers, see the previous blog post on water slide physiology

We kosher so far? Good. Let's move along.

The meat of this discussion and important question to ask yourself next is "have I really given enough fluid? Was the initial crystalloid bolus adequate for volume repletion or does the patient still require more to meet the primary goal of filling up the tank?" Rivers' answered this dilemma by dropping a central line in all his patients and measuring the CVP: if it was less than 8-12 mmHg, he gave more fluid until the goal pressure (8-12) was achieved. If CVP was eventually optimized to 8-12 mmHg ('an adequate preload') and the patient was still hypotensive, he'd move down the chain and begin pressors to address the MAP ('optimize afterload'). (See above figure). The assumption here of course is that CVP is a good marker of a patient's fluid status--a fuel tank gauge on the physiologic dashboard, if you will. 

Today we know that isn't true. There are two huge shortcomings to this approach:
1. CVP does NOT in fact correlate well with volume status, if at all! Reference article by Paul Marik
2. Measuring CVP requires insertion of a central venous catheter, which is invasive, carrying risks and complications

With the risk of giving too little or too much fluid and increasing the morbidity/mortality, we welcome a better, more accurate evolutionary approach to detecting a patient's volume status at the bedside...

Ultrasound! What else??
There is now sufficient data to support the use of ultrasound-based measurement of IVC diameter fluctuation during the respiratory cycle  in order to gauge volume status. (EMCrit reviews them here). The background concept is quite simple:

-In a volume depleted spontaneously breathing patient: each breath lowers intrathoracic pressure, which in turn increases cardiac return (like a suction pump). As the already low reserve of intravascular volume is shifted up into the chest with each inspiration, the highly-compliant IVC will collapse. 
(ignore the bit about a sniff test)
Balloon is the IVC, collapsed with sucked-out volume
-In a volume depleted mechanically ventilated patient: each administered breath from the vent increases intrathoracic pressure, which in turn lowers cardiac return and pushes blood back down into the abdomen (like a piston). The depleted IVC, now receiving an inspiratory surge of volume, will noticeably distend. 
Man is the ventilator; balloon is IVC
Most of the papers validating the use of IVC ultrasound are based on mechanically ventilated patients, since tidal volume is set and each breath is controlled, The literature is not as clear for spontaneously breathing patients due to an inherent variability with each breath taken. These are the patients we care for more frequently though and for obvious reasons we prefer to use a less invasive approach to fluid monitoring when possible.

That's ok. 

There is good news however; research does agree with good consistency and relatively high specificity that on the lowest extreme of the fluid status spectrum--volume depletion--grossly (easily) visible IVC collapse (of greater than 40%) on B-mode sonography is suggestive of a fluid depleted state where patients will benefit from further volume resuscitation. As Weingart puts it: "if you see it collapse give more fluid, if you see it collapse give more fluid, if you see it collapse give more fluid!" 

So true is the above notion regarding IVC that its diameter measurement is now tantamount to assessing a patient's volume status in the 2012 Surviving Sepsis Campaign Guidelines

So move over CVP! Make way please. 

At this point we're beginning to run long, so I'm going to take a much-needed pause here. We will resume our discussion in part II, where I'll be addressing the pressing concern of how to determine if your patient requires more fluid therapy if or when the IVC does NOT show obvious fluctuation with respirations  (>40% collapse in spontaneously breathing and <18% dissension in mechanically ventilated patients). This is the scenario, unfortunately, that we are more likely to encounter--"the gray zone" as it were--while working up septic patients--especially if checking the IVC after an initial bolus. In other words, just because it's not collapsing (distending in MV patients) does it imply they no longer need IVF, that the tank is completely full? Be sure to check back in soon for the explanations and illustrations. 


Water Slide Physiology

I was recently playing and swimming with my 2 year old nephew at the local pool. This particular pool had a water slide. As we splashed around blissfully and took our turns shooting out from the green tubing I realized something: basic physiology and critical care pathophysiology can be simplified into a water slide model. To understand the basic mechanics of the water slide is to understand the basic principles of treatment of the septic patient, as in Rivers' early goal directed therapy.

The components of a typical water slide are:

  • pump
  • water
  • slide/tube
  • people!

Vessels in the body, like the tube of the water slide, transport blood and plasma (people and the water) to the systemic circulation of the body (the swimming pool). Then a long stem pipe (IVC) carries fluid back up to the top of the tower via a pressure gradient generated by a large water pump (the heart). The people, like red blood cells, carry excitement (oxygen) as they begin at the top and prepare for descent. On the way down, they let out a gleeful cry until reaching the bottom and, like the water in the system, emerge from its depths and make their way back up to the top--but using stairs instead of the water pipe of course. 

Make sense? Good. Now let's see what can go wrong with the system and how we repair it. 
  1. Drained pool, no water -- the volume depleted patient
Without water the tube has no lubrication to facilitate the passage of people (cells, contents) from the tower down the tube (vessels) and into the pool (body). Septic patients are generally fluid depleted and lack proper perfusion to tissues, unable to bring oxygen-rich RBCs to the body. They therefore require initial fluid repletion as an initial modality of their resuscitation [how much fluid and how to gauge their response to fluid therapy will be covered in a future post]. The above concept has been summarized in various podcasts and described as "filling the tank."

    2.  Broken tube, cracks in the slide -- vasodilation/distributive shock

If the water slide has a broken tube or large cracks and gaps in the tube, water would leak through its pores or, worse yet, people may get stuck in the misshaped apparatus. To be fully functional, the actual tube would require tightening and readjustment in order to once again allow safe and efficient passage of people down the slide. In the same vein (pun intended), septic patients who are persistently hypotensive often require vasopressor therapy to facilitate organ tissue perfusion once initial volume (fluid) repletion is assured. In the past, this has been referred to as "fixing or tightening the pipes."

    3. Pump failure -- poor cardiac output/cardiac dysfunction
Without a properly functional pump generating enough force and pressure to bring water from the bottom of the pool back up to the top of the slide, the system will fail and people can no longer be properly shuttled. Analogous to the above scenario poor cardiac output secondary to cardiac dysfunction and poor cardiac contractility demonstrates the same type of deficiency. We often observe this in septic patients who require require inotropic agents to optimize their cardiac output, whether determined by direct observation of the heart using an ultrasound (preferable) or once volume and and vessels are corrected (steps 1 and 2 above) and a shock state remains. This is commonly referred to as "fix the pump."

    4. No people or a lack of excitement -- anemia, hypoxemia

It's simple: if there's a water slide, but no one there to go ride it, does it even exist? Similarly, if people are present but apathetic about the slide, will anyone ride? To make the analogy, people--previously described as red blood cells--are essential to a successful water slide system. They carry excitement and glee (oxygen). If they are missing--as in a state of anemia--or are apathetic and cannot be excited (hypoxemia) the system is again broken. We must either replace missing people (transfusion of packed RBCs) or rile them up (provide oxygen whether by face mask, nasal cannula, or mechanical ventilation). 

Following these steps along the analogy's path essentially covers the basic tenants of severe sepsis, shock, and the concept behind correcting the broken physiology of such patients, as described in 2001 by Manny Rivers and all those who followed.  

Now go have fun!


I get no respect!
In keeping with our most recent theme of EKGs, this post will be a case series scenario.

If you haven't already, I highly recommend watching Amal Mattu's EKG video on the importance of the (forgotten) 12th lead, aVR. You can also read about it here from Wellens et al and here from our Aussie masters of LITFL.

Consider this case I had the other week:

A 75 year old female with a history of hypertension presented via EMS complaining of 1 day of unrelenting bilateral upper chest pain, described vaguely, and was a first occurrence without any associated symptoms. She received 1 sublingual nitroglycerin tab en route to the hospital and, upon arrival, had syncope. She was resuscitated with IV crystalloid fluid and placed on a cardiac monitor.

Initial 12-lead ECG obtained is shown below:

Our initial concern was for aortic rupture or dissection. After blood draw, she was sent for a immediate CT chest/abd/pelvis (vitals holding stable without marked hypotension or tachycardia).

When she returned, we repeated the 12-lead, shown below:

Notice the evolving elevation of ST segment in lead aVR with reciprocal depression in the anterior and lateral leads--surely an ominous sign.

We called the cardiologist and activated the cath lab for what we considered a STEMI but cardiology refused to acknowledge as anything more than NSTEMI. Politics aside, the patient was found to have severe 90% stenosis of her mid LAD! She was stented and did well.

This is just another case shedding light on the improtance of the Rodney Dangerfield ("I get no respect!") lead: aVR.

Just remember, in the setting of suspected ACS, ST elevation in lead aVR could mean:
-Left main occlusion
-LAD occlusion
-triple vessel occlusion

Be forewarned!


"Doctor, should we call the cath lab?" -said the ED RN, med student, resident, and tech everywhere.

When the difference between life and death, in-patient or out-patient, and a decision to activate massive resources in your hospital comes down to one piece of pink-and-white paper, you better know your EKGs.

The guru of emergency cardiology Amal Mattu said that EKG is the cheapest and perhaps most important test we order as emergency physicians. For that reason, our job demands an ability to read 'em and screen 'em better than anyone else...and quickly!

An array of systems and texts are devoted to decoding the squiggles on the page. If you have one you love, great. If not, or you're just looking for an alternative (or better) approach, here I present mine.

I give you the "X^2 test" of ECG's. Well, not quite. Make that: R-R-A, CHI^2.

As in all systems, start with your Rate, Rhythm, Axis.

Then, check the following:

  • Conduction
  • Hypertrophy
  • Ischemia/Infarct (I^2)
Conduction - there are 4 main points to consider in terms of cardiac conduction. The SA node, the AV node, and the ventricular (Bundle of His/Purkinje), and finally the QTc 
  • You've already addressed the SA conduction by analyzing the rhythm (sinus etc)
  • AV node conduction exists along the PR interval
  • Ventricular conduction is assessed by QRS width
  • For a quick QT, make sure the T wave ends before the half-way point between any two R waves
Hypertrophy - atrial and ventricular hypertrophy
  • For atria, look at lead II. If p wave's Longer than 2.5 mm boxes consider Left atrial hypertrophy. 
    • If it's more upRight than 2.5 mm, consider Right atrial hypertrophy
  • For ventricles, use the classic methods for LVH, RVH. 
    • R wave in aVL > 11mm
    • S in V3 + R in aVL > 28 mm (men) or > 20 mm (women) -- "Cornell method"
    • RVH = tall R wave in aVR or rightward axis, etc
Ischemia - nothing new here: ST depression, T wave inversions, hyperacute T waves, etc etc...
Infarct - again, ST elevation, q waves, Wellen's sign, de Winter's sign, and so on...

So try it out and lemme know what you think!

For more in depth discussion on EKG basics go here. The guys at LITFL do a great job. 

Check Please!

Greetings EMBS readers, welcome back! It's been a minute since my last post, due mostly to recent orphanage from residency (St Vincent's, I now feel your pain) and travels abroad. Speaking of which, I've just returned from amazing Australia, a land where Fosters pours from drinking fountains and blooming onions sprout from cracks in sidewalks. Not really. But Australia is truly beautiful.

My time was spent working with Air Ambulance Victoria, a team of the most advanced, capable, brave, and friendly paramedics I've ever encountered. I learned so much from them and had the opportunity to accompany the Air MICA's on helicopter and fixed wing missions (think: intubate in a swaying aircraft or sunny beach).
Arriving on scene for a job. (Photo: yours truly)
To top it all off my trip culminated at a 3-day gathering of the world's most impressive names in EMCC--Scott Weingart, Minh Le Cong, and all the blokes of LITFL to name just a few. That's right--I'm talking SMACC!
Best conference ever
Perhaps one of the most important take-away points from presenters at SMACC and ride-alongs with Air MICAs is the utilization of airway (RSI) checklists. It's a discipline ubiquitous to most EDs and paramedics in Australia and--from what I gather--some spots in the US. In this author's opinion it should be used everywhere. In fact, if you've read Atul Gawande's latest book on checklists you might agree. Checklists are in!

I've sifted through several featured airway/RSI checklists and picked out my two favorites, which are attached below. In a nutshell, a uniting theme among the lists can be precipitated out:

"PET Fail", or Patient, Equipment/meds, Team and a Failed airway algorithm or back-up plan.

Putting this into a mnemonic will help with recall in a pinch but I strongly suggest reviewing it thoroughly and then posting one up in your ED in case a checklist/algorithm is not already available. And if you're not convinced just ask yourself "What Would Weingart Do?"
Ruben Strayer Checklist It's incredibly thorough, including medications/doses and algorithms all into one 2-page set.

George Durous Checklist (as featured in LITFL) It's simpler to read and is broken down into 2 separate pdf's--one for an initial checklist, the second as a failed airway algorithm.

Enjoy and stay tuned for lots more to come very very soon!!