In this Five Minute Sono, we demonstrate how to use ultrasound to evaluate the inferior vena cava (IVC). The primary goal is to estimate central venous pressure (CVP), which can help determine a patient’s fluid tolerance.
Here are Dr. Spiegel’s Notes:
1. The discussion of what an IVC tells you is a fairly nuanced discussion but essentially it is telling you the difference in the RA pressure compared to the intra-abdominal pressure. It is our job as clinicians to interpret what that means. I find if you teach IVC US from that perspective than all the variability in techniques make a whole lot of sense.
So let’s assume the patients intra-abdominal pressure is around 5-8 cm H20, then any time the RA pressure drops below this level the IVC will collapse. In a spontaneously breathing patient the RA pressure decreases with inspiration. The amount it decreases depends on the pressure change that occurs with breathing. More forceful breathing will lead to greater changes in intrathoracic pressure, and RA pressure, leading to a greater likelihood of collapse. So a patient that has a collapsing IVC with comfortable breathing has a lower RA pressure than one who requires a forceful sniff to see their IVC collapse. Asking the patient to sniff is an attempt to standardize that pressure change. In my opinion, it is a futile attempt, but an attempt nonetheless. Pts with severe respiratory distress can generate such large swings in their intrathoracic pressure that they can cause their IVC to collapse despite having fairly high RA pressures.
In contrast a pt who is intubated and synchronous with the ventilator spend the majority of the respiratory cycle with a positive intrathoracic pressure this will lead to much smaller changes in the IVC as the RA pressure is usually higher than the intra-abdominal pressure throughout the respiratory cycle. This is why the changes in IVC diameter are much smaller in intubated pts than their spontaneously breathing counterparts. Because of this it’s much harder to use IVC alone as a marker of fluid status.
2. Examining the IVC in the longitudinal plain alone assumes that the IVC collapses in a sagittal fashion on all pts, which is not necessarily true (https://pubmed.ncbi.nlm.nih.gov/29032036/). If one is going to access the collapsibility of the IVC one should probably look at it in the transverse plane as well.
3. The IVC is unable to reliably tell you anything about fluid responsiveness but fluid responsiveness is a flawed outcome and we have to start taking a more holistic view on the administration of fluid. There is no one dichotomous test that will tell you whether to give fluid or not. That is a holy grail that we have to stop chasing. Rather we have to make a clinical judgement on whether fluid is more likely to harm or help a pt. For this we use clinical judgement, US findings, PE findings. For example a pt in the ED with sepsis, and a collapsible IVC, dry lungs and no peripheral edema is more likely to benefit from fluid than be harmed.
Take that same pt, with the same US and physical exam findings and make it 72-hrs later in the ICU after 6-10 L. Additional fluid is unlikely to be beneficial independent of the US findings simply because there is diminishing benefits and increasing harms to the administration of fluid over a patient’s course.
