One of the most common reasons that clinicians do point of care ultrasounds or ask for formal echocardiography is to assess for "volume status". But does the answer to this question really lay within the heart? Going deeper, is this even the right question to ask?
Very little of total body volume is intravascular. The total body volume will shift to compensate for any loss of intravascular volume, and this is currently still poorly understood. Cursorily, we know that total body sodium - which is mostly extracellular - plays an important role in maintaining intravascular volume through osmotic forces. However, the total body sodium seems to be partitioned between an osmotically active form and an osmotically inactive form. Polymerization of the negatively charged glycosaminoglycans is one of, possibly many, mechanisms of sequestering sodium into the inactive form. In sepsis and other critical illnesses, glycosoaminoglycans are destroyed, presumably increasing soluble salt and thus extracellular fluid increases despite a relatively constant total body sodium.
Even if the question is refined to "assess an assumed constant intravascular volume", this is still not helpful. You can have a large volume or small volume of water on the ground; neither will flow anywhere unless the ground is uneven. Fluid moves from high to low. And in the body it moves from high pressure to low pressure. The high pressure in this analogy is the mean systemic filling pressure and the low pressure is the right atrial pressure. The determinants of mean systemic filling pressure is both intravascular volume and venule elastance (sometimes better conceptualized as the venule vasomotor tone). Decreases in venule vasomotor tone is how sepsis causes fluid-responsive hypotension in most cases without any losses in intravascular fluid.
A low RA pressure does not indicate hypovolemia. It should be low in the spontaneously breathing patient because this will only encourage venous return unless there is excessive collapse or kinking of the great veins. A high RA pressure does not indicate hypervolemia. It does indicate that a higher mean systemic filling pressure is necessary to encourage further venous return. But in the cases of high intrathoracic pressure, high intrapericardial pressure, or decreased myocardial compliance, more volume and more venule vasomotor tone may be helpful rather than evil.
Understanding physiology of blood flow is necessary to understand the epistemological limitations of cardiac ultrasounds in determining volume status. The heart is not the place to look for estimating the mean systemic filling pressure. And volume status is NOT mean systemic filling pressure. Nevertheless, ultrasound can be a useful tool when wielded by an astute clinician cautioned to its use.
Find the IVC in both the subcostal long axis and short axis views. It is best identified by visualizing its entrance into the RA. Catch the IVC through its maximal diameter at all times to avoid being tangential to the vessel. Using M-mode is only valid if the IVC trajectory is perpendicular to the M-mode beam - in this case (and most cases) it's not.
Measure 3cm from diaphragm or 1-2cm from hepatic vein. Notice how your measurement area moves down and even changes axis during inspiration and expiration making this measurement logistically a lot trickier than most people appreciate.
My interpretation of the IVC US: