SMACC Back 2 – IVC for Decisions on Fluid Status


Justin Bowra gave a fantastic lecture on the use of IVC ultrasound at SMACC.


Here is the audio, if you want to hear the original lecture:

There was a post on Life in the Fast Lane by Justin as well.

His slides from the talk are here:

Now let’s get to the SMACCing back…

I agree with 90% of Justin’s talk, but as to the other 10%:


Mech Ventilated Patients


Diagnosis of Undifferentiated Shock

Quick look at size and collapsibility gives huge amounts of information

Fluid Responsiveness

Need a strategy for Spontaneously Breathing Patients

  1. Go bronze and give a bunch of fluid until you feel slightly uncomfortable
  2. Then go for the silver and resus until IVC starts to lose easily discernible collapse (20-30%)
  3. If you want to be really cool, at this point go for the gold-use some marker of stroke volume to see if additional fluid will be of benefit (either with empiric add. bolus or passive leg raise). If you want to be lazy, just put them on some norepi at this point.

Now if you use this strategy, you need to look at the operator receiver thingy-me-bobs [sic]

Spont. breathing IVC-CI trials fail due to the misfounded desire for dichotomy.



(Lanspa M et al. Shock 2013. 39(2). pp. 155-160)


Muller ROC

(Muller L et al. Critical Care 2012, 16:R188)

This makes sense as respiratory-dynamic CVP demonstrates the same thing (Shock 2006;26(2):140)

Splint IVC open-Tamponade, Tension PTX, Massive PE, Status Asthmaticus, Right heart disease

Don’t sniff test, don’t tell the pt to do weird abdominal yoga breathing

Fluid Tolerance

IVCCI 15% had good accuracy (92% sens/84% spec) for CHF (Blehar et al. The American Journal of Emergency Medicine 2009;27(1):71)

and (Miller at al. Am J Emerg Med 2012;30:778) showed similar text characteristics.

by all means add in the Lichtenstein Lung Ultrasound, but only if negative when you start

We need more and better Studies

  • Get a bunch of sick patients
  • Do an IVCCI with a cut off of something like 30%
  • Give fluid (500-1000 ml crystalloid)
  • See if there was a 15% increase in SVi with a REAL cardiac output monitor or skilled evaluation of LV VTI
  • AND
  • see if there was a >5 mm Hg increase in arterial line MAP

and now on to the SMACC Down…


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  1. Hi Scott,

    Fantastic podcast and SMACC back! I absolutely love your approach which is a great way to apply evidence in physiological and clinical fashion, and the bronze/silver/gold approach is fantastic.

    I can’t agree more on how sadly close minded some physicians can be, so meticulous in packing that poo box, while not offering anything substantial – or physiological – instead, opting for the passive “watchful waiting” mode until someone (likely a big name in ED/CC) comes up with “the perfect resuscitation recipe” which will fit all patients (NOT!).

    I follow a highly similar approach to undifferentiated shock, because I fundamentally believe it is biologically impossible for a single recipe to work for all. It may work for most, but we don’t treat 1000, 100 or even 10 at a time, we treat 1. Therapy without individualizing to the patient is nonsensical to me.

    With your permission, I’m inserting a portion of a chapter on shock from a book I’mworking on, on integrating bedside ultrasound to clinical practice (due end 2013) which I think you will relate to:

    the patient in shock

    The principle of assessing shock reflects simple physiology. After all, there are only a few mechanisms by which our circulatory system fails. In fact, there are ?only four:
    - hypovolemic shock
    - obstructive cardiogenic shock
    - non-obstructive cardiogenic shock – vasodilatory shock

    There are, however, a number of different etiologies which result in these pathophysiological entities, and certain may result in more that one of the above. For instance, septic shock, usually associated with vasodilatory shock, may also result in hypovolemia due to fever and poor oral intake and cardiogenic shock due to septic myocarditis.

    A rapid bedside ultrasound examination can generally assess the mechanism(s) of shock in under thirty seconds:
    View 1: The IVC (epigastric longitudinal or transhepatic). In the case of shock diagnosis, only two extremes are significant.
    - If the IVC is very small, generally less than 3mm in diameter or collapses completely – “kissing walls” – there is a high likelihood that hypovolemia is at least playing a part in the shock state.
    - If the IVC is very large (>20mm) with little or no variation, this implies very elevated right atrial pressures and cardiac or obstructive state. This is even more marked when one can actually see the column of blood in the IVC stop and start – cardiac output is very low.
    This isn’t to say that if the IVC is somewhere in the middle, that there isn’t any useful information to be gained. There will be the question as to whether this patient is volume-responsive or not. However, in terms of making a hemodynamic diagnosis, an intermediate size IVC with respiratory variation is only useful in excluding hypovolemia as the sole cause of shock.
    A major advantage of starting with the IVC is that, if a diagnosis of
    ?hypovolemia or noting the presence of a volume-responsive state, the physician can order fluid resuscitation within seconds of beginning the examination.

    View 2: The Subxiphoid 4 chamber. From the epigastric IVC view, the probe is flattened and rotated, and the 4-chamber view rapidly scanned. Tamponade can be rapidly eliminated by either the absence of a pericardial effusion or, if present, good visualization of cardiac chambers, particularly the atria. a massive PE can also be eliminated by a RV to LV ratio below 1 and normal RV contractility. The LV can be assessed for severe systolic dysfunction resulting in cardiogenic shock. It would be unusual to develop cardiogenic shock with an ejection fraction (EF%) over 30%.
    This view, in the absence of surgical dressings or other physical impediments, is usually the easiest view to obtain. Some patients, however, due to bowel loops with air, may not be well visualized.

    View 3: The Parasternal short axis view at mid-papillary level. This should be done for a proper assessment of the LV function, because in long axes, only two ventricular walls are seen at any one time, making it possible to over- or underestimate LV function. Alternatively, this view can be obtained in the epigastric area by doing a 90 degree rotation.

    Additional views: the parasternal long axis and the apical four chamber can be done if the previous views were poor and unable to provide the necessary information, or if the bedside sonographer is an assistant rather than the main treating physician and has the time to do a more thorough examination. Otherwise, the three views should have provided the diagnosis in terms of hemodynamic mechanism, which is sufficient to initiate therapy, but further examination may be required to make a full diagnosis (for example, where the fluid went to result in hypovolemia, or what the source of sepsis is).

    Special Note: The only other important pathology to rule out is tension pneumothorax. The first clue to this would have been a large IVC without respiratory variation. Keep in mind that associated severe dyspnea may – by
    motion – make this hard to assess. However one should be able to note the size of the IVC. It may be difficult to find decent views of the heart, as it may be displaced and may be entirely retrosternal (in the case of a left sided pneumothorax). This should be another echographic clue. The next step would be to scan the anterior chest bilaterally, and if there is no lung sliding found to strongly consider needle decompression. In parallel, examination for tracheal deviation and auscultation should be done as, once again, bedside ultrasound is an extension and not a replacement of physical examination.

    Happy to know your thoughts – of course this is only the ultrasound part, but I think I will bring up the grey zone concept in here!

    thanks for the post and keep up the amazing work!

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