That Fallible IVC - PulmCCM
Jan 212016

collapse_100_long_IVCA 58 year old man with ethanol-related cirrhosis is admitted to the floor with anuria and a rising creatinine.  Over the day, serial ultrasounds of his interior vena cava [IVC] consistently reveal that it is diminutive and collapsing.  He receives many liters of crystalloid without much change in his urine output.  In the middle of the night, a rapid-response is called for dyspnea and desaturation with a lung ultrasound revealing bilateral and ubiquitous B-lines; he is placed on non-invasive positive pressure ventilation and given IV furosemide, but his blood pressure continues to fall.  Repeat ultrasonographic assessment of his IVC reveals, again, a small and collapsible great vein; the overnight resident reaches for another liter of normal saline.

Another recent publication has analyzed the diagnostic accuracy of using IVC assessment for detecting fluid responsiveness in the ‘spontaneously breathing’ patient.  Importantly, in this study, it is clear that no patients are receiving any form of invasive or non-invasive ventilation.  This is notable, as a patient may breathe ‘spontaneously’ while triggering invasive [e.g. pressure support] or non-invasive [e.g. BiPAP] forms of respiratory support.  What was ultimately found was that an IVC collapsing index more than 42% revealed an excellent specificity, but a fairly poor sensitivity for the prediction of fluid responsiveness.  These findings are important and somewhat similar to another, previous study which considered a similar patient population, although it is unclear if this earlier study excluded spontaneously breathing patients receiving assisted ventilation.


Specificity is a measure of false positives.  Within this context, a false positive would be a patient with a collapsing IVC [therefore deemed to be a fluid responder] who ends up being resistant to fluid.  The collapse of the IVC occurs under the influence of four, independent variables: 1. The inspiratory fall in intra-thoracic pressure 2. The inspiratory rise in intra-abdominal pressure 3. The inspiratory change in cardiac function and venous return which together determine the pressure within the IVC and 4. The method of patient breathing [e.g. diaphragmatic versus thoracic].  Therefore, understanding what would cause an IVC to collapse in a fluid non-responder requires a refresher in Guytonian physiology, upon which I have previously commented extensively.  In summary, an IVC will ‘inappropriately’ collapse in a fluid resistant patient when 1. The patient is inspiring excessively, 2. The intra-abdominal pressure is abnormally high [e.g. ascites, intra-abdominal hypertension] and 3. When the venous return curve intersects the plateau of the cardiac function curve at a relatively low intra-luminal [i.e. within the vessel] pressure.  This latter situation will occur when both venous return to the heart is low and cardiac function is relatively impaired; for example, a patient with very poor venous tone [e.g. cirrhosis, sepsis, adrenal insufficiency, venodilating medications] and poor cardiac function [e.g. from alcohol-related cardiomyopathy].  Consider the diagram below which depicts the determinants of the pressure within the IVC, prior to an inspiration.


Another exceptionally important, and often ignored, determinant is how positive intra-thoracic pressure [whether applied invasively, non-invasively, or develops pathologically – e.g. auto-PEEP], also alters venous return.  Positive pressure facilitates collapse of the IVC; this has been known for many decades!  Pressurization of the upper abdomen by the application of end-expiratory pressure will make the IVC collapse much more readily when the patient triggers a breath.  In healthy volunteers, this has been demonstrated.  Consequently, the aforementioned could result in a ‘false positive’ IVC collapse in a fluid non-responder and impair specificity.  Importantly, in the study at hand, no patients were receiving ventilation of any sort and this may account for its excellent specificity [i.e. few false positives].


Sensitivity is a measure of false negatives.  Within this context, a false negative is a patient with a relatively engorged, unwavering IVC who will still respond to an IV fluid challenge.  In the study under question, like its predecessor, sensitivity tended to be quite poor, that is, many patients with plump IVCs can still respond to fluid.  Why might this be so?  Considering the analysis above, many factors may play a roll.  For example: if the patient does not inspire greatly or if the patient uses thoracic wall muscles rather than the diaphragm; if the rise in intra-abdominal pressure is poor or if the venous return curve intersects the ascending portion of the cardiac function curve at a relatively high intra-luminal pressure.  This latter situation may occur in patients with both good venous return and preserved cardiac function.  When a patient has normal venous tone and is relatively hypervolemic, the abdominal venous beds have been described as being like ‘West Zone III’ within the lungs.  Decent of the diaphragm in this situation maintains or augments venous return through the great vein which would maintain its volume and size.  If this occurs in a patient with good cardiac function, the venous return curve may still intersect the ascending portion of the Frank-Starling curve, and the patient will be volume responsive.

Volume status versus volume responsiveness

On this final point, it should be apparent that a patient’s ‘volume status’ [i.e. the degree of plasma volume] is physiologically distinct from a patient's ‘volume responsiveness’ [i.e. whether or not an increase in plasma volume will result in an increase in cardiac output].  As in the diagram above, volume status is but one determinant of venous return to the heart; however it is how the heart handles its venous return that defines volume responsiveness.  It follows that a patient can be hypervolemic and volume responsive or hypovolemic and volume unresponsive.  For further information please watch these physiology lectures [Chapters 6D, 8A & 8F]

Bedside ultrasound is a great power; it therefore demands great responsibility,


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  7 Responses to “That Fallible IVC”

  1. […] A 58 year old man with ethanol-related cirrhosis is admitted to the floor with anuria and a rising creatinine.  Over the day, serial ultrasounds of his interior vena cava [IVC] consistently reveal that it is diminutive and collapsing.  He receives many liters of crystalloid without much change in his urine output.  In the middle of [… read more] […]

  2. The fundamental problem with the resident’s decision making is repeated in the train of thought in this post.

    No comment whatsoever about true and false positives and negatives can be made using sensitivity and specificity alone. Sensitivity and specificity and be used to form a likelihood ratio which can be used to update a PRIOR PROBABILITY to a POSTERIOR PROBABILITY. Nowhere in the post is there any mention of prior or posterior probabilities. The test is considered as if has diagnostic accuracy in isolation. It does not.

    This is likewise the resident’s mistake, and all too common of one. Lacking experience and clinical acumen, the resident wishes to believe and practice as though she can identify and order a test which in isolation will tell her the answer she wishes to know – what is this patient’s volume status. But that cannot be determined with ANY test absent the context provided by prior probability. Indeed, if her clinical skills were sufficiently developed, she could determine a clinical pretest probability of the question under consideration and that probability could in many (most?) cases entirely obviate “objective” testing with that highfaluting ultrasound gizmo.

  3. I seem to have lost my first comment, so I will try again.

    I totally agree that Bayesian analysis is often neglected in clinical medicine. The thesis of the post was more to highlight the physiological mechanisms underpinning false positives and negatives as these are common questions from house-staff e.g. “how can the IVC be enlarged, but the patient be fluid responsive?” and vice versa. But as you note in your great reply to “Lactate and Sepsis” there is frequently an over-arching desire in medicine to use a single test to explain, diagnose and manage patients with little further reflection. The merits of heuristics like this are debatable as they do save the harried clinician bundles of time, but muddy and distastefully over-simplify clinical-physiological veracity. Your response above is certainly appreciated.

  4. […] limitations of IVC collapsibility are eloquently discussed in a post on […]

  5. Why cant i poSt comment?

  6. Good post. Looking at an IVC in isolation to make clinical decisions is poor medicine and akin to making decisions about fluids from your call room phone based solely on a CVP.

    Great point about the need to develop a pre-test probability about fluid status/responsiveness/ tolerance. H and P, recent I/O, BNP, CXR, recent echo, recent response to fluid challenge can are sometimes all we need to make a decision. The probe should supplement rather than supplant these data points.

    I always emphasize to residents as well that IVC ultrasound should ALWAYS be combined with bedside echo and lung ultrasound to assess fluid tolerance (LV function, presence of b-lines, RV size). These data points are especially helpful when the IVC size and collapsible index fall in the equivocal middle range. Fluids are a medication that can cause harm. Primum non nocere.

  7. Hey, what the ultrasound is fantastic that we can take information from various systems and put together a pathophysiological scenario. The collapse of the IVC in my critierio alone is not enough to be a reliable way to make effective decisions regarding patient volume tool, as countless factors influencing it (spontaneous breathing, mechanical ventilation, intra-abdominal pressure, oncotic pressure). Take a holistic view is essential, explore the lungs, heart function, speed ortica artery, and something that is not usually expora index aterias peripheral resistance as the radial, realizar.Gracias very simple.

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