Volume Status
Physiology
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.
Respirophasic IVC Diameter
Measurement
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:
- Anyone trying to dichotomize the IVC diameter (i.e. > 2.1cm is hypervolemic and < 2.1cm is hypovolemic) is just plain wrong. The IVC exists over a wide range of normal (1-2.5cm) probably because it is heavily affected by body habitus, size of posterior lobe of liver, and intra-abdominal pressure. And who knows how to interpret this in the context of positive pressure ventilation!
- It is erroneous to conclude that a generous sized IVC reflects a generous pool of venous volume. Blood is stored in the venules, not the great veins.
- Collapsibility is not as miraculous a variable as is touted because it is hard to isolate this variable from ultrasound technique (see above). And it is significantly affected by venous return . The faster the flow of blood, the greater the venturi effect, and greater the collapse. IVC ultrasounds during passive leg raise can demonstrate smaller dimensions and increased collapse!
- The concept of "volume tolerance" has developed with the argument that a collapsing IVC indicates that additional fluid boluses will not lead to organ venous congestion. This makes little physiologic sense. Retrograde flow can occur in the IVC with preserved respirophasic IVC variation (i.e. severe TR). And pulmonary venous congestion causing pulmonary edema can occur independent of IVC blood flow or dimensions.
- IVC measurements, when severely abnormal (>2.5cm and no variation) probably does predict high RA-pressures. But what this means depends on the clinical context: Pericardial fluid? Mediastinal shifts from pleural fluid/air? RV infarct? Positive pressure ventilation? Air trapping from obstructive lung disease? All of the above suggests that fluid loading to a higher mean systemic filling pressure is necessary rather than diuresis to a lower RA-pressure.
- Need to use IVC and hepatic vein flows which is validated in positive pressure ventilation (see below).