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Patients who arrive at the hospital with hypotension will almost all receive intravenous fluid resuscitation (one hopes). When signs of hypoperfusion occur later in a patient's hospital course, it can be much harder to decide if additional fluid will be helpful. Physical exam is unreliable, and no available technology can accurately identify how much water is in a patient's body, or in which vascular or extra-vascular compartments.
In response, clinical researchers have embarked on dozens of quests to identify predictive methods of so-called fluid responsiveness: whether a patient's blood pressure (or cardiac output) will improve with an IV fluid bolus. A JAMA review of 50 of these boutique (average n~45) studies provides the rest of us with a scorecard of their efforts.
Central venous pressure: Not Useful
The worst-performing test is the most widely used: patients with central venous pressure <8 mm Hg were 3 times as likely to respond to IV fluids, but there was little consistency between studies' results and poor predictive value overall. CVP is too poor a discriminator to be endorsed for predicting fluid responsiveness, or possibly for any purpose. (See also "Why do we bother to check CVP?" ).
Inferior Vena Cava Respiratory Variation: Not Useful, Either
Generally speaking, volume-depleted patients have greater respiratory variation in the diameter of their inferior vena cavae. In the pooled analyses, patients on positive pressure ventilation with more than 15% IVC respiratory variation on ultrasound were ~5x more likely to respond to IV fluids, but with large variability between studies. Besides its poor performance, proper conditions for this test require the absence of spontaneous respiratory efforts by the patient. (See also "Inspiratory collapse of the IVC: What is it telling us?")
Passive Leg Raise Test to Predict Fluid Responsiveness
A passive leg raise test (positioning a patient at zero degrees, then raising both legs to about 45") returns a reservoir of venous blood into the central circulation relatively quickly (30-90 seconds). It's the original, all-natural fluid bolus. Patients with a positive test have a 10% increase in cardiac output or stroke volume. A 10% increase in pulse pressure on an arterial line tracing is a commonly used surrogate measure for stroke volume. (There are also various gadgets for sale that purport to measure and display stroke volume variation in real time.)
Passive leg raise testing (with cardiac output measured invasively or by echocardiography during the PLR) performed the best by far in the pooled analyses: patients with positive PLR were about 11 times more likely to respond to IV fluids. Only about 1 in 8 patients with a negative PLR responded to fluids. The findings were relatively consistent in patients without or with spontaneous breathing efforts (but less robust in the latter).
Pulse pressure variation was a poor discriminator, with an unacceptably high 31% false negative rate.
Is Predicting Fluid Responsiveness Worthwhile?
Like Scott Aberegg on his excellent blog, intensivists may question whether testing prior to giving an IV fluid bolus for suspected hypovolemia mid-hospitalization is necessary, helpful or practical. The risks of untreated hypovolemia are real and immediate. The risks of an ordinary fluid bolus appear to be low in all but the most volume-sensitive patients with severe cardiac or renal failure. (See also "The Revised Starling Principle: Implications for Rational Fluid Therapy")
Any test (including passive leg raising) has a false negative rate, meaning fluids will consistently be withheld from hypovolemic patients who should receive them. Do benefits accrue to the volume-replete patients spared from excess IV fluids by a PLR, and do they outweigh any deleterious effects in the inevitable false-negative patients left dry? No one knows, because no meaningful clinical outcomes were captured in this analysis -- just the immediate physiologic response to IV fluids.
The studies enrolled patients not only for hypotension, but oliguria, skin mottling, tachycardia, or even a physician's sense that hypovolemia was present--problems experienced by half the average ICU census on a daily basis. The JAMA analysis suggests a reliable PLR test result would require realtime echocardiography or invasive cardiac monitoring in each of these patients. Is this really necessary or feasible for every ICU patient who might need a little extra volume? (Maybe when the ultrasound-in-every-white-coat-pocket epoch finally arrives.)
Patients' enemy during their ICU ordeal is not a liter of NS or LR thoughtfully given during a discrete clinical event. Rather, it's the oft-unnoticed normal saline running at 150 mL/hr for days after a patient is volume replete. The downstream cardiorespiratory decompensation or prolonged ventilator dependence isn't obviously caused by the excess fluid, limiting accountability or teachable moments.
One of the few things we really "know" in critical care is that diligently removing fluid from ventilated patients with ARDS helps free them from the ventilator sooner. Often this requires daily or b.i.d. intravenous furosemide. This "drier is better" principle may well apply to most ventilated patients. We also know that in certain highly selected patients (e.g., acute pulmonary embolism, advanced CHF, pulmonary hypertension with cor pulmonale), removing volume can improve cardiac output (and vice versa).
Whatever you decide to do with your patients' legs, if you give a liter of IV fluid, don't forget to consider taking it back later.
Will This Hemodynamically Unstable Patient Respond to a Bolus of Intravenous Fluids? JAMA. 2016 Sep 27;316(12):1298-309.
Does my patient need a fluid bolus? Predicting fluid responsiveness in the critically ill patient. A concise clinical review. PulmCCM Journal, September 27, 2014.
What do you think?