When it comes to shock, it's the question: How do I know if my hypotensive patient is going to get better with IV fluids? Or more specifically, will he be fluid responsive, meaning a fluid bolus will cause an increase in his cardiac output?
Ultrasound has an important role in evaluating the hypotensive patient; the RUSH protocol offers a quick algorithm for classifying shock (distributive, cardiogenic, obstructive, hypovolemic), and can identify an etiology that has a straightforward fix (pericardial effusion causing tamponade). These patients don't have an immediately identifiable diagnosis in many cases, however, and even determining the class of shock can be tricky. (Critically ill patients can have a mixed picture of hypovolemic and other types of shock.)
The RUSH protocol emphasizes the role of ultrasound of the inferior vena cava (IVC) as a means of determining the fluid status of the patient. As part of the assessment of “the tank,” the overall size and percentage change of the vessel with inspiration are evaluated to estimate the central venous pressure (CVP). If the CVP is considered to be a marker of a patient's overall fluid status, in a simple world, it should also provide some idea of their fluid responsiveness.
But it's not that simple. Evaluation of the IVC and its change with respiration has been well correlated with a measurement of CVP, but its ability to judge fluid responsiveness (and even overall fluid status) has not been borne out. Several factors other than a patient's volume status play into the CVP, including valvular abnormalities, pulmonary hypertension, and obstructive pathologies such as a large pulmonary embolus. The status of the IVC and thus the CVP is a product of the entire clinical picture, rather than a reliable indication of overall volume status. In other words, sometimes the CVP is just the CVP.
An excellent review article by Mackenzie and Noble delves into the heart of the problem in predicting fluid responsiveness: There really isn't a perfect test. (Clin Exp Emerg Med 2014;1:67.) Most static methods (CVP, pulmonary wedge pressure) fail in this regard. Disappointingly, many dynamic methods (pulse pressure variation, plethysmography) are either not readily available or impractical for ED use. The passive leg raise, which simulates a small fluid bolus, shows promise, especially when combined with sonographic measurement of the stroke volume before and after. This technique has a fairly steep learning curve, however, and can seem daunting.
So is it time to throw out ultrasound of the IVC with the bathwater? Perhaps not quite yet. A quick assessment of the heart and the IVC can still yield valuable clues. A patient with a normal or hypercontractile heart with a small, fully collapsing IVC will likely at least tolerate a fluid bolus, if not improve. Patients with good cardiac function and a larger, less collapsing IVC will still likely tolerate a fluid bolus and can be watched closely and reassessed to determine their response.
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