Bedside Ultrasound Clip Quiz #8. #FOAMed, #FOAMcc

So a patient presents with worsening peripheral edema and right upper quadrant discomfort. Biochemical data only reveals some mild elevation of the transaminases.

Here is what you see:

These are the right sided chambers.

And this is a hepatic vein.

 

What do you think is going on?  Scroll below for the answer!

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

This patient has severe tricuspid regurgitation. The second clip shows significant retrograde flow in the hepatic vein (red doppler signal). Hepatic congestion was the cause of pain.

Analysis of hepatic vein flow can be useful to establish the presence of right heart dysfunction when cardiac views are difficult.

 

cheers!

 

Philippe

The IVC Assessment by bedside ultrasound: Let’s apply some common sense! #FOAMed, #FOAMcc

So I have a huge issue the IVC and its ultrasound assessment. For the most part, neither the yay-sayers or the nay-sayers are applying much sound physical principles, as far as I’m concerned.

To assess a patient’s volume status, it may be practical to begin with the sub-xiphoid view of the IVC, since the decision to give fluids or not – especially in emergency situations – can then be taken within the first few seconds of examining the patient. The physiological rationale behind assessing the IVC as a marker for volume responsiveness is simple and solid. As the venous compartment fills, the size of the IVC will gradually increase until it reaches a maximal size of about 20-25mm or even 30mm, depending on physical size and chronicity.

Concomitantly, the phasic respiratory variation will decrease as the venous pressure increases and the effect of varying intrathoracic pressure is no longer felt. At this point, the flat part of the Starling curve of the right ventricle is approaching, and there is little response to volume, and little physiological rationale to support giving more.

Currently, many use a variation of about 20% or more to suggest a volume responsive state in ventilated patients or an inspiratory collapse “sniff test” of 50% or more in spontaneously breathing patients.

There remains controversy around using IVC assessment for volume responsiveness, and with good reason! There are a few important reasons why:

a. technique – First of all, there is the manner in which IVC measurement has been taught: the M-mode measurement of the antero-posterior (AP) diameter during breathing (usually of ventilated patients) about 3 cm below the diaphragm. Although highly practical and reproducible, it has many shortcomings. If we look at the physiology, what changes with cycles of respiration is the volume of blood entering the chest/right atrium. Hence the key variable we are trying to assess is the transient variation in IVC size – which is a volume, not a linear dimension (I’m getting painful flashbacks of using pressure  to determine volume!)Hence the use of a single linear measure on one point along the length of the IVC to assess this is inherently flawed. For instance, the figure to the left shows how, if this IVC were to be measured in its AP diameter, the variability may not be that great. In the short axis, however, one can clearly see the significant change in surface area, and hence volume between phases of mechanical ventilation. Also, the IVC is rarely perfectly circular, but often ovoid, and occasionally with the greatest diameter in an anteroposterior axis, making that single AP measurement even less relevant.

b. intrathoracic pressure – Secondly, the variation in intrathoracic or intrapleural pressure (Pip) must be measured, as, for instance, a young and fit patient can generate large changes, which would result in more significant IVC variation, as compared to a frail elderly patient, even if they are on the same point of their Starling curve, invalidating the IVC measurement. All “sniffs” are not created equal.

c. intra-abdominal pressure – Finally, the intra-abdominal pressure (IAP) must also be assessed, since an elevated pressure would decrease the size of the IVC and make that measure no less accurate, but less relevant in terms of representing venous filling.

So what should we do?

Instead, a more global assessment of the IVC volume, measuring short axis area measurements and variation at several points along the IVC would give a much more accurate estimate of IVC volume variation. This is currently being studied by our group.

“Eyeballing the IVC” Attempting to link evidence and physiology, some bedside sonographers’ approach is to take a global look at the IVC in both long and short axis during respiration, while clinically assessing the respiratory effort and the abdominal pressure. This approach is analogous to the “eyeballing” of LV function – versus more formal measurements such as Simpson’s disk method, etc – which has been proven just as accurate with sufficient clinical experience.

The figure below shows an IVC that is about 10-12mm along most of its intrahepatic segment on expiration, and collapses almost completely on inspiration. If this belongs to a patient breathing with little effort and with a soft abdomen to palpation, it is physiologically quite clear that this patient would be fluid responsive. It also shows how impressive the collapse is in the short axis.

IVC insp dual

For instance, let’s say Patient A is in respiratory distress and using accessory muscles and presents to the ER with a respiratory rate of 35 and a systolic BP of 80. His IVC measures approximately 21 mm in diameter at several points along its axis, and has a brief collapse to about 10 mm with strong inspiratory efforts. His abdomen is soft during inspiration but firm during a prolonged expiratory phase.

Patient B is brought to the ER somnolent with a respiratory rate of 10 and a systolic BP of 80. His IVC measures 15 mm with minimal respiratory variation. His respirations are shallow and his abdomen soft. These two patients show how the IVC assessment needs to be taken in clinical context.

Patient A has some 50% inspiratory collapse of a large IVC in the context of large variations in Pip, whereas Patient B has little variation of a mid-sized IVC in the context of very small variations in Pip. In all likelihood, Patient A is not very volume responsive, while Patient B probably is.

Volume Responsiveness vs. Volume Tolerance – it is critically important to distinguish the difference between these two concepts as they are often misused interchangeably: Volume responsiveness refers to an increase in cardiac output (CO) to a fluid challenge. This is a purely hemodynamic concept. Volume Tolerance refers to whether or not a patient can tolerate volume without clinically significant side effects. This is a complex clinical assessment that should include: -the patient’s plasma oncotic pressure (serum albumin) and level of capillary leak, if present, -the patient’s pathology – is there risk of capillary leak in critical tissues such as lung, brain, abdomen? -the type of fluid being considered (isotonic crystalloid vs hypertonics or colloids/blood products). It is important to distinguish that not all patients who are volume responsive are necessarily volume tolerant.

Volume assessment summary – this issue remains a difficult one, even with the use of bedside ultrasound, because the optimal point for any one patient to be on his or her Starling curve at any one time in different clinical conditions remains elusive. Despite considerable study and several proposed management algorithms, there is no means by which to determine exactly how much of any given fluid is enough, without being too much.

In my opinion… – no direct evidence – keeping an IVC below 20mm and probably below 15mm with significant respiratory variation, if hemodynamics allow, is probably ideal. However, bedside ultrasound allows to clearly identify the cases where fluid is clearly needed and those where fluid is unlikely to benefit. Both of these scenarios are easily and routinely missed by traditional examination. Additionally, when the IVC assessment is done in conjunction with lung ultrasound, it becomes possible to detect early development of pulmonary edema and halt aggressive fluid resuscitation (FALLS Protocol, Daniel Lichtenstein).

 

Technical Pearl: the part of the IVC we generally assess being the intrahepatic segment, it is possible to find it almost by scanning through any part of the liver, which happens to provide a great acoustic window. This may be particularly useful when the epigastric area is difficult to access (incision/bandage, drains, in the OR, etc…) or when there is bowel gas in the epigastrium. The figures below show the same IVC, first in a “traditional” epigastric view, then in a view approximately along the plane of the red arrow on the CT scan.

2 views IVC std:liver

CT liver IVC views

 

Bottom line?

When assessing volume status, it is absolutely essential to keep the clinical question in mind. It is a great minority of patients who are volume responsive who actually need volume. Normal, healthy humans are very much fluid responsive and fluid tolerant but certainly not in need of any. Much of the current studies and literature focus on assessing volume responsiveness in the setting of shock, which, although arguably the most important, is not the only type of information that can be obtained from the IVC. For instance, as will be discussed in the chapter on congestive heart failure, knowing that your patient is very “full” should prompt further diuresis. If you are dealing with managing severe anasarca, knowing that a patient’s intravascular volume is low may prompt the use of albumin or hypertonics prior to further diuresis to help resorb some of the interstitial fluid. Another critical question to which there is currently no answer is just how much fluid to give to patients in shock. There are many opinions but no certainty. It is common practice to fill a patient in shock until they are no longer fluid responsive, in an effort to avoid or minimize the use or dose of vasopressor medications. There is no study to date that compares a “moderate fluid/early vasopressors” vs “aggressive fluid/avoid-vasopressors-if-possible” approach.

Hopefully this will be answered soon. In light of the clear evidence linking positive fluid balance and mortality, it would seem wise to fill to a “moderate fullness” where some respiratory variation remains, rather than to the point of no longer being fluid responsive. After all, physiologically, the only time humans are really full (>20mm IVC with little or no variation) is in pathological states of congestive heart failure or obstructive shock. So again, when assessing an IVC, keep in mind what your clinical question is and interpret the sonographic data accordingly.

 

cheers!

 

Comments:

Marco says:

Thanks Philippe, very interesting post.
Using your great categorization, I think that the worst scenario is represented by a patient who is volume responsive but poorly volume tolerant. In that case, it is important to have clear in mind which is our target: cerebral perfusion, oxygenation and lung extravascular fluid, ventilatory weaning, renal function, avoiding vasopressors or mechanical ventilation, etc…
Very often, maintaining a brain dead heart beating donor, every organ would require a different volemic status, and if all of them are suitable for transplantation you have to compromise.
Just a last thought: as well as “all sniffs are not created equal”, also tidal volumes are very variable. Assessing respiratory variations during protective (low TV) ventilation requires a thoughtful interpretation of the results.

 

Absolutely. Interpretation of the findings in each individual case is key. 

Philippe

CCUS Annual Symposium 2014 – only a few spots left! Take your ultrasound game to a whole new level!

May 10th and 11th (pre-congress courses on may 9th), Montreal.

Great speakers, great topics, great city, great weather (well…hopefully no snow!).

Do you know how to use ultrasound to help you diagnose or manage coma, bowel obstruction, CHF, dyspnea, swollen joints and renal failure, among other things?  No matter how good you are at the bedside, you’re not as good as you + ultrasound. None of us are. And if you take care of patients where time is of the essence, then you need to make sure your game is as good as it gets.

Mike Stone, Vicki Noble, Haney Mallemat, JF Lanctot, Michael Woo, Catherine Nix, Max Valois, Rob Chen, Edgar Hockmann, Massimiliano Meineiri, Sarah Sebbag, Alessandra Bruns, Alberto Goffi, Ashraf Fayad and Andre Denault have put together some great talks about how to add ultrasound to your approach of common clinical scenarios.

We’ve got the #FOAMed spirit, too. If you really can’t make it, all the lectures will be freely available on our website in the weeks following the symposium.

The workshops will be awesome, faculty-led and will also feature the use of simulators.

The best part is the atmosphere. It’s a great exchange among like-minded people, eager to learn form each other. I know I always come out of that weekend with my head buzzing and brimming with ideas and things I need to learn and others to put into practice.

…and if you’re an educator, then there is a pre-course you will find extremely interesting, as Catherine Nix has put together an educator’s half-day to help overcome the common hurdles faced by budding ultrasound programs at the undergraduate or post-graduate level:

CCUS US Educator May 9th program

We’re not in a huge venue, so if you’re thinking of coming, register now, there are only a handful of spots left.

http://ccusinstitute.org/Symposium6.html

looking forward to meeting you!

Philippe

NEJM: The Septic Shock Issue…groundbreaking or same old same old? #FOAMed, #FOAMcc

Ok, so it was pretty cool to see an NEJM issue basically dedicated to septic shock management, I must admit. But let’s dig a little deeper, shall we?

So here is where they are: http://www.nejm.org, and fully available for now.

I won’t go through all the details and numbers, after all they are in the papers, so let’s just analyze them from two principles:

a. the N=1 principle – how was therapy individualized?

and

b. was there any integrated monitoring of the therapeutic goals?

…and we’ll conclude by looking at the potential practice-changing potential of each of these studies.

So first of all,

High vs Low BP Target in Septic Shock, by Asfar et al.

So basically a negative study except for two findings, the increased incidence of afib in the high target group and the decreased need for renal replacement therapy among chronic hypertensives in the high target group.

so N=1 is not really revealed:

“Refractoriness to fluid resuscitation was defined as a lack of response to the administration of 30 ml of normal saline per kilogram of body weight or of colloids or was determined according to a clinician’s assessment of inadequate hemodynamic results on the basis of values obtained during right-heart catheterization, pulse-pressure measurement, stroke-volume measurement, or echocardiography (although study investigators did not record the values for these variables).”

So lets just hope that the variability evens itself out between the groups, since we don’t really know. The numbers don’t really tell the tale, because the average fluids received (10 liters over 5 days) could mean one patient got 15 and one got 5 – although let’s trust they followed the French Fluid Resus protocol…

So the atrial fibrillation makes total sense – more B agonism should result in that, and the decreased renal failure also does.

As the authors note, the actual BP averages were higher than planned. For those of us practicing critical care, we know most nurses titrating prefer having a little bit of extra BP – even when I prescribe MAP 65, I usually see the 70 or so unless I make a point to tell them. Understandable. They also note the underpowered-ness of their own study, but I think it is still worth looking at their results.

So…bottom line?  I think it’s a great study for a couple of reasons.

The first is to remind us to pay a little more N=1 attention to the chronic hypertensives, and that it is probably worth aiming for slightly higher MAPs.

The second, debunking the myth of “levophed, leave’em dead” (which I heard throughout residency at McGill), and the concept of doing everything (ie juicing patient into a michelin man) in order to avoid the “dreaded and dangerous” vasopressors. So really I think an alternative way to conclude this study is that it isn’t harmful to have higher doses of vasopressors. I think this is actually a really good study on which to base assessment of more aggressive vasopressor support vs fluid resuscitation, in the right patients.

It would have been interesting to have echo data on those who developed a fib – were they patients who had normal to hyperdynamic LVs who in truth did not need B agonism at all and would have been fine with phenylephrine?  Perhaps…

Cool. I like it.

Next:

Albumin Replacement in Patients with Severe Sepsis or Septic Shock, by Caironi et al. The ALBIOS study (a Gattinoni crew)

So basically showed no difference, so pretty much a solid italian remake of the SAFE study in a sense, confirming that albumin is indeed safe overall, and may be better in those with shock.  As the authors note, mortality was low, organ failure was low, so study power a little low as well. Note the mean lactates in the 2’s at baseline. The albumin levels of the crytalloid only gorup were also not that low, low to mid 20’s, whereas I often see 15-20 range in my patients, especially if I inherit them after a few days, as I do use albumin myself a fair bit. They also used a target albumin level, not albumin as a resuscitation fluid purely.

In my mind the benefit of albumin would be greatest in those with significant capillary leak, particularly those with intra-abdominal and pulmonary pathology. It would have been nice to see a subgroup analysis where extravascular lung water was looked at (especially coming from a Gattinoni crew!).

Another interesting thing would have been to know the infusion time of the albumin, since animal data tells us that a 3hr infusion decreases extravasation and improves vascular filling vs shorter infusion times. I routinely insist on 3hr infusion per unit, which sometimes results in 9-12hr infusions, almost albumin drips!

Bottom line?

I like it. Reinforces that albumin is safe, so makes me even more comfortable in using it in the patients where my N=1 analysis tells me to be wary of third-spacing. Also the fact that they used 20% – in Canada we have 100cc bottles of 25% for the most part – is nice, since the SAFE data used 4%.

Next!

A Randomized Trial of Protocol-Based Care for Early Septic Shock – The ProCESS Trial.

So right off that bat my allergy to protocols flares up, so I’ll try to remain impartial. It just goes against the N=1 principle. The absolutely awesome thing about protocols is that it primes the team/system to react – so clearly protocols are better than no-protocol-at-all, but strict adherence would clearly not fit everyone, so that some built-in flexibility should be present.

This being said, the ProCESS study is really interesting, for a number of reasons. They have three groups, and compare basically (1) Rivers’ EGDT to (2) their own protocol (see the S2 appendix online) which gives a little more flexibility and (3) “usual care”.  Net result is that all are pretty equal, no change in mortality. As the authors note, their mortality was low, so again may not have been able to detect a difference.

So, what does this mean. To me it’s a little worrisome because I doubt that the “usual care” represents the true usual care found in EDs/ICUs all over the world, so I am concerned that many docs will use this as a reason to justify not changing their practice, similarly to many I’ve heard say they don’t need to cool anymore after the TTM trial. Human nature for some I guess.

Bottom line? You don’t have to follow EGDT if you’re conscientious and reassessing your patient frequently and have done all the other good things (abx, source control, etc). I think that’s really important because giving blood (see my post about S1P) to those with hb > 70 and giving dobutamine to patients with potentially normal or hyper dynamic LVs never made physiological sense to me, and the problem with a multi intervention study such as EGDT is that you can’t tease out the good from the bad or the neutral. Again, studies such as EGDT are pivotal in changing practice and raising awareness, so this is not a knock against a necessary study, just to highlight the point that each study is a step along the way of refining our resuscitation, and the important thing is to move on. In fact, the reason that this is a negative study is probably due to the improvement in “usual care” that EGDT brought along.

Conclusion: No new ground broken, but these studies do make me feel more confident and validated in continuing to not do certain things (strict EGDT) and  doing others (albumin and earlier use of vasopressors).

Kudos to all investigators.

 

let me know what you think!

 

P

 

Bedside Ultrasound and PEA: CPR or no CPR…? #FOAMed, #FOAMcc

The usefulness of bedside ultrasound in cardiac arrest is clear, giving the clinician instant information on the hemodynamic process resulting in arrest. My arrest sequence is generally done as follows:

Step 1: IVC assessment

Step 2: Subxiphoid cardiac views

Step 3: Lung views if pneumothorax suspected.

Step 4: remaining views if possible (eg abdominal views to find source of bleeding, etc…)

The important part (as per current recommendations) is to have minimal interference on chest compressions. The IVC view, albeit jumpy, can generally be obtained during CPR.  The subxiphoid view should be “prepared” during CPR, meaning that the sonographer warns the team member doing CPR not to stop compressions until he is told to do so (unless the team are already used to ultrasound in cardiac arrest), the probe positioned optimally, then instruction given to stop for five seconds while a look +/- loop is acquired. This should be enough to look for pericardial effusion, RV/LV ratio and LV contractility. In fact, experienced sonographers can usually get this while CPR is going on in many cases. Then CPR should be restarted. Hence for now, minimal interruptions in CPR (until the concept of “stutter CPR” really emerges!!!).

Here are a couple of views with active CPR:

In this case there is  a clear RV overload with a dynamic but underfilled LV.

From the information obtained in those 5 seconds, one should be able to consider the need for volume (hypovolemia), thrombolytics  (pulmonary embolism suspected) or drainage of fluid (tamponade) or air (pneumothorax). The possibility of an acute myocardial infarction must be considered as it is one of the most common causes but is difficult to confirm by ultrasound.

Pulseless Electrical Activity

This may be the most exciting area in which ultrasound will change management.  In the absence of ultrasound, all PEA is more or less alike: there is organized electrical activity, but no pulse. Physiologically however, the range of diagnoses is very wide, with on one end, a perfectly good heart that is empty (hypovolemic shock in extremis), and on the other, cardiac standstill despite electrical activity. An astute physician does not need a randomized clinical trial to know that the management and prognoses of those two extremes are very different. Without bedside ultrasound, however, these would appear identical: “PEA.”

 The heart rate cannot be relied on since it will largely depend on the phase (both would begin as tachycardic, then eventually bradycardic until asystole occurs).

Notwithstanding guidelines,  the information obtained should be considered strongly. If we start by looking at the first end of the spectrum, there would be no physiological rationale for performing chest compressions or an empty and hyperdynamic ventricle: rapid infusers and vasopressors (to recruit venous unstressed volume) should be used instead. At the other end, the heart in standstill definitely needs compressions. Of course, there is then the whole range of varying RV and LV pathologies, tamponade, etc, all of which need to be dealt with individually. It is really a huge grey zone…

CPR or no CPR?

A very important question is whether CPR should or should not be performed in certain cases of PEA.  Certainly ACLS protocol dictates so. However, ACLS has not yet truly integrated bedside ultrasound into management, only suggests in a very loose way – understandably since the protocols must be applied by all, and still only few use it regularly.

I have to credit Dr. Sue, an ER doc from Atlanta, who asked me the question about CPR in extreme hypotension, and I had to rewind in my mind the cases in which I had used physiological information to overrule the ACLS protocol in one direction or another and try to formulate an answer.

It is an excellent question and made me realize that there is no clear answer for two reasons:

One: PEA is not a diagnosis but a clinical syndrome. It relies on manual pulse check (unless the arrest occurs in a patient with an arterial line), hence the line between severe hypotension and true PEA is difficult to determine. Technically and physiologically speaking, if the LV contraction is sufficient to open the aortic valve, there is a “pulse.” Now how far along the arterial circuit this pulse travels is not known…unless it is monitored.

Two: The key question then becomes the following: at what level of endogenous blood pressure is the perfusion better than with “good” CPR?  We do not yet have that answer. The coronary perfusion pressure (diastolic pressure – wedge pressure) data often quotes a minimal range of 15-25 mmhg, which – if we arbitrarily choose a high-ish wedge – would suggest we need a diastolic pressure in the 40’s (also note that that data is imperfect). Hence the arterial line. Perhaps there could be a role for tissue saturation/near-infrared spectroscopy or other microvascular flow indices in the future…

Now what about the huge spectrum of cases in between?  Let us exclude the cases with immediately reversible causes such as tamponade and pneumothorax, where the initial management is clear, and instead focus on differing levels of RV and LV dysfunction resulting in the absence of a palpable pulse.

Predominant RV failure – although PE should be strongly suspected and thrombolysis considered, the question remains about management if you see a hyperdynamic but underfilled LV.  CPR would appear reasonable in an effort to try to get some RV to LA flow. Endotracheal milrinone, sometimes used in cardiac anasthesia, can be an option as it provides inotropy and pulmonary vasodilation.

Predominant LV or biventricular failure – if cardiac activity is present, it seems imperative to start an infusion of vasopressors, and traditionally, do CPR until there is a measurable blood pressure. I have used CPR with progressing bradycardic rhythms for a few seconds to circulate the epinephrine, with at least short-term success.

Here is a typical LV “PEA” from the subxiphoid view:

Ideally, an arterial line would be very useful in these patients, and may help to decide on an individual basis when CPR should be used. Remember that CPR on a beating heart will likely worsen cardiac output as asynchronicity and increased mean intrathoracic pressure will impair filling.

Additionally, the arterial line also allows us to notice small trends during resuscitation, such as seeing that a few seconds of CPR may help circulate a bolus of vasopressor and enable it to take effect – progressive BP increase, or that the BP may be trending downwards despite vasopressor infusion – CPR may be useful until enough vasopressor/inotropes have infused.

Bottom Line:

1. if possible, put in an arterial line

2. bedside ultrasound is mandatory if you don’t want to miss anything reversible

3. if you don’t have a palpable pulse and your diastolic pressure (arterial line) is less than 40, consider some CPR until vasopressors/inotropes have had effect.

4. if you are lucky enough to have ECMO (shout out to Joe and Zack at http://www.edecmo.org)  or other mechanical support, it would be the time to consider!

I think this is actually a really interesting area to develop, and I’d really, really like to hear what other sonographer-resuscitationists are doing, or what anyone else might think!

 

Philippe

 

Joe Bellezzo – yes, THE Joe, says:

Phil, I agree with all your points here. Great post! As you know, Shinar, Weingart and I recently published a rant on PEA (over at http://www.edecmo.org/13) and Weingart threw out two possible new monikers: PRE-M (Pulseless Rythm with Echocardiographic – Motion) and PRE-S (Pulseless Rythm with Echocardiographic – Standstill). I don’t disagree with any of those concepts but I think its simpler than that.

PRE-S (standstill) = asystole and you start compressions.
PRE-M (organized cardiac activity) = profound shock. In this setting I like the recent Littmann paper that gives a simplified approach (http://edecmo.org/wp-content/uploads/2014/08/A-Simplified-and-Structured-Teaching-Tool-for-the-Evaluation-and-Management-of-Pulseless-Electrical-Activity.pdf).

As you pointed out above, the real big question is at what point do you start compressions when you have cardiac motion? Your points above are spot on. The problem with compressions on a beating heart is that you don’t know what your end-point is. You lose the ability to do minute-minute diagnostics and doing any procedures with ongoing compressions is tough. And it seems to be a knee-jerk reaction for the RN or pharmacist to have an amp of epi ready to blast away at this point. NO!

I wait. I do stuff first. Step 1 is ECHO. If PRE-M (aka profound shock): EKG and arterial line NOW. Step 2: Stop, think and decide what you think is your top probable etiology of this profound shock and fix that. Step 3: reassess = repeat echo, EKG, and see what your art line pressures are doing. I try to do all that before I start compressions.

Example: “PEA” hits your door. Echo shows a wall motion abnormality and hypokinesis. EKG suggests ischemia but is not obvious STEMI. art line goes in simultaneously. I think this is MI. This heart does NOT NEED epi 1 mg! This is cardiogenic shock and I need to fix some stuff before I start pushing on the chest and blasting superhuman doses of epi! I usually start with a push dose epi (10-20 mics or so) while a pressor drip is prepped. Calcium bolus is given. I likely start dobutamine here (or milrenone if beta blocked). If that fixes your problem, then the pt goes to the cath lab. If it doesn’t, I cannulate and put the pt on VA-ECMO.

And what if I were wrong? what if this were a big PE? massive beta blocker OD? the protocol above is works in those cases too.

An aside, since you already placed a femoral venous line….and you popped in the Art line immediately, you have nice conduits to upsize to ECMO cannulas.

Great post Phil!

 

Thanks for sharing your approach!  As you know and clearly show, a sensical physiological approach is absolutely needed in a day and age when we can (bedside ultrasound) see what’s really going on, and we can (ECMO) give these patients a fighting chance!  See you at BMBTL in a couple of weeks!

Philippe

 

PS Joe (and Zack and Scott) will be talking about all this and more at CCUS 2015! http://www.ccusinstitute.org to register soon!

CCUS 2014 – The Ultrasound-Assisted Clinical Assessment!

If you’re thinking of coming to Montreal to beef up your clinical skills and decision making, hurry up and register, we have to cap the participants to 100 (physical restrictions of the venue) and there aren’t too many spots left!

Myself, am looking forward to learning a bunch of things: how to diagnose bowel obstruction (Vicki Noble), how Andre Denault likes to integrate hemodynamic modalities in shock, how Mike (Stone) uses ultrasound to manage CHF patients, how Haney (Mallemat) uses it to manage abdominal pain, and many more…

Screen Shot 2014-02-26 at 9.26.21 AMScreen Shot 2014-02-26 at 9.26.33 AM

 

Montreal, May 9-11, 2014, Santa Cabrini Hospital.

More info and registration at:   http://ccusinstitute.org/Symposium6.html

 

See you there!

 

Philippe

 

 

“Doc, I can breathe!” – Thrombolysis in PE…a case discussion. #FOAMed, #FOAMcc

So I was on call last weekend and got a call from one of the internists on the ward about a potential admission who may need dialysis.   She was a woman in her 60’s, diabetic, hypertensive with minimal baseline renal dysfunction, who had been admitted with a hepatic abscess due to biliary obstruction. This had been stented and a pigtail catheter had been inserted to drain the abscess.  However, over the last few days, her creatinine had risen to about 500 and she was becoming oliguric.  Her O2 requirements had also increased and she was now on 15 liters by nasal prongs. This had been ascribed to pleural effusion and possible pneumonia.

When I saw this lady, she was visibly dyspneic at 30 with a heart rate 115-120 and a systolic BP of about 105-110, saturating 90% on 50% face mask.

So on physical examination, she had a soft abdomen (the first thing I feel just before I put probe to skin), her skin was cool, and the CUSE revealed a large (>20mm) IVC with no respiratory variation (despite the effort).  I unfortunately forgot to hit the record clip button…and the parasternal long axis and apical 4 chamber are here:

Lung views showed “A” profiles except for the right base which had a small effusion and some consolidation/atelectasis and some B lines, but not very extensive.

So further assessment revealed she was not a smoker, previously quite active and easily able to go up and down several flights of stairs.  She had noted dyspnea about 3 days ago, without chest pain. There were no leg symptoms, and she had been on LMWH for dot prophylaxis.  The CXR was not very impressive – in a sense that there was not enough parenchymal disease to explain pulmonary hypertension.

This is PE until proven otherwise, and I would have been comfortable without further confirmation, but with the presence of some lung disease and an intrahepatic catheter, I preferred to have 100% confirmation before initiating thrombolysis.

After CT angiogram confirming bilateral and extensive embolism, I had a thorough discussion with her and her family and they all agreed to go ahead with TPA.  She was quite concerned with cardiorespiratory limitation, given that she was quite active. She was comfortable with a quoted risk of intracerebral bleeding below 2%. I used the MOPETT half-dose of 50mg.

Overnight, her HR slowed to about 100, and sats increased to 93-94%.

When I rounded on her in the morning, she said “Doc, I can breathe!” with a big grin. Her HR was 95-100, she was not on 3 litters by NPs, BP 115-120 systolic, and CUSE showed:

So we can see that even though the RV is still quite impaired, it has decreased in size and the LV is now filling better. This was about 12-13h post thrombolysis. She was able to sit up without dyspnea and mobilize to the chair. Her IVC, although it remained around 18-19 mm, had clear respiratory variation.

So…success? Who really knows. It is concievable that, with heparin alone, she might have improved similarly. It is possible. I’m not putting this up to formally support the concept of thrombolysis in “submassive” PE but more to contribute to the #FOAMed discussion regarding the “grey zone” of thrombolysis, since she was technically not in shock (eg SBP>90, lactate normal), but the degree of impairment of the RV to me and the clinical picture, 3 days post, was concerning enough to warrant thrombolysis, but importantly to stress the following:

Point 1: the importance of bedside ultrasound, especially in acute cases.  Without it, over a weekend, and with a patient in renal failure, how quickly would I have ordered a CT angio?  Not without some hesitation…

I won’t review the MOPETT trial, these guys did a much better job than I could hope to, so definitely listen to this if this topic is of any interest to you (and it should!!!):

http://emcrit.org/wee/mopett-trial/

http://ragepodcast.com/rage-session-two/

Great case debates in the RAGE podcast.

Keep in mind that morbidity, not mortality, is the main thing to focus on in sub-massive embolism and the MOPETT – even though I don’t really like the term, its quite vague – benefit in embolism with shock is quite clear.

Point 2: Equally interesting to me was the fact that the renal failure improved. In fact, overnight following thrombolysis, she had a urine output (without diuretic) over a litre, and over the next few days her creatinine normalized and renal replacement therapy was not needed.  Interesting, since she even got a good blast of toxic dye with the CT.  Some will feel that it is the improvement in CO that improved renal function, and this may be partly true, but in view of the lack of “systemic shock,” I think that venous decompression resolved the congestive renal failure, which I think was the main cause of her ARF. I posted about this topic a few months ago, so for more on this see:

http://thinkingcriticalcare.com/2013/09/25/chf-associated-renal-failure-low-flow-or-not/

so thanks for reading and love to hear anyone’s opinion!

PR

COMMENTS:

QUESTION. IF SOMEONE DOES NOT HAVE A PALPABLE PULSE BUT HAS CARDIAC ACTIVITY ON THE ECHO AND RATE IS 90 AND BP IS 50.  DO YOU CONSIDER THIS PEA AND INITIATE CPR?

SEAN

Great question!  There is a whole grey area in “PEA” and management is unclear. I don’t think there is a single answer to that, but physiologically and without further information about RV/LV, I would say your patient needs vasopressor/inotrope support, so I would probably give a small bolus of epi (maybe 100ug) and start an infusion. If I see little reaction (eg HR/BP doesn’t pick up in 30 seconds, I would probably give a short cycle of CPR to get the epi back to the heart.   Of course, hopefully there is a reversible cause (MI/PE), that can be addressed.

Thanks!

 

Philippe

Central line insertion: US-spotted “Blind” technique Video (HERE IT IS!) #FOAMed, #FOAMcc

My apologies, had technical issues with the video uploading so here it is in two formats:

 

 

 

…please let me know if there is a problem!

 

thanks

 

Philippe

Central line insertion: US-spotted “Blind” technique video. #FOAMed, #FOAMcc

So a few months ago I posted about central line insertion and my concerns about the current standardization of care of ultrasound guidance:

http://thinkingcriticalcare.com/2013/10/21/ultrasound-guided-central-venous-catheter-insertion-standard-of-care-or-preventing-procedural-skills-foamed-foamcc

I promised a video so finally got around to remembering to do it.  This one actually happens to be a dialysis catheter so a bit bigger, but otherwise the technique is the same. In this case I am using my standard ultrasound-spotted procedure with “blind” insertion.

So here, I spot the vein, confirm it is just lateral to the carotid, and that it collapses nicely, without thrombosis:

Now, I insert the line. A few important points to note that are not seen in the frame:

Line Insertion video:

a. my introducer needle/syringe and loaded guide wire (pulled pack and “loaded”)  are ready  and within my vision, and also nearby are the dilator and catheter.

b. note that the off hand (right hand in this line) protects the carotid and stays in place until there is venous flashback, then secures the needle position.

 

Note that in this particular case, I didn’t quite make a large enough incision so the dilator insertion was a little difficult – unnecessary delay, and also unfortunately lost the last few seconds as my iPhone memory was full. 

Next, I confirm position in the internal jugular vein, and verify for lung sliding to rule out and anterior/apical pneumothorax.

In me experience, the key mistake I see inexperienced operators (and sadly, some experienced ones also) make is not to have a proper setup, such that once they do find the vein with the introducer needle, their subsequent steps are not immediately ready, and in the process, the relationship between needle tip and vein is lost, resulting in an inability to thread the guidewire (often blamed on mysterious anatomical abnormalities). It is key to find the vein with the freezing/searcher needle, fix the depth/angle relationship in your mind, withdraw and reach for the introducer needle/syringe using peripheral vision so as not to break the visual fix, and reproduce this while introducing it.

This is what I try to install in students/residents rounding with me, and in fact this approach is useful for any procedure.  Not having to turn your head, reach and fiddle with things that are not ready prevents mistakes.

If you haven’t read my previous post on central line insertion, I’m not advocating agains the use of ultrasound guidance, but for the maintenance of the ability to insert blind lines if necessary.

cheers!

Philippe

Pleural Effusion Podcast – physiology and clinical approach! #FOAMed, #FOAMcc

…just for those who prefer to listen rather than stare at a screen…

…and also because I had my sick toddler napping on me for two hours and typing was not an option.

Part 3 with the vid coming in the next couple days, though, apologize for the delay!

 

Philippe