What is the Passive Leg Raise (PLR) test?

What is the Passive Leg Raise (PLR) Test?

The passive leg raise (PLR) test is a bedside maneuver that functions as a reversible, endogenous fluid challenge by mobilizing approximately 300 mL of blood from the lower extremities to the thorax, allowing clinicians to predict which hypotensive patients will respond to intravenous fluid administration without actually giving fluid. 1, 2

Physiological Mechanism

The PLR test works by temporarily increasing venous return and cardiac preload through gravitational redistribution of blood volume:

• The maneuver recruits approximately 300 mL of stressed blood volume from the legs and splanchnic circulation, creating a transient autotransfusion effect that mimics a fluid bolus 2, 3
• This increase in preload will augment cardiac output only in patients whose ventricles are operating on the steep portion of the Frank-Starling curve (i.e., preload-dependent or "fluid responsive") 4
• The effect occurs within seconds and is completely reversible when the patient returns to baseline position, making it an ideal diagnostic test 2, 4

Clinical Performance Characteristics

In a meta-analysis of 2,260 patients, PLR demonstrated exceptional predictive accuracy with a positive likelihood ratio of 11 (95% CI 7.6-17) and pooled specificity of 92% for identifying fluid responders 1

• An increase in cardiac output during PLR strongly predicts that the patient will respond to fluid administration (pooled sensitivity 88%, negative likelihood ratio 0.13) 1
• No increase in cardiac output during PLR reliably identifies patients who will NOT benefit from fluid and instead require vasopressor or inotropic support 1
• This diagnostic accuracy is superior to traditional static measurements like central venous pressure, which cannot reliably predict fluid responsiveness 2, 5

How to Perform the Test

The standard technique involves elevating the patient's legs to 45-60° while monitoring hemodynamic parameters:

• Start with the patient in semi-recumbent position (head elevated 30-45°) 1
• Passively raise both legs to 45-60° angle while simultaneously lowering the head of the bed to flat 1
• Monitor cardiac output or stroke volume changes during the maneuver - the hemodynamic response occurs within 30-90 seconds 1, 3
• A positive test is defined as ≥10-15% increase in stroke volume or cardiac output during leg elevation 5, 6, 4

Monitoring Methods During PLR

The test requires real-time assessment of cardiac output or stroke volume changes, which can be accomplished through several methods:

• Transthoracic echocardiography measuring left ventricular outflow tract velocity-time integral (LVOT VTI) is the gold standard and well-validated 4
• Right ventricular outflow tract VTI from a subcostal view can be used when apical windows are difficult (≥15% increase predicts fluid responsiveness with 86% sensitivity and 93% specificity) 4
• Non-invasive cardiac output monitors using thoracic bioimpedance can be used, though precision may be variable 6, 7
• In resource-limited settings without advanced monitoring, clinical parameters including blood pressure, heart rate, capillary refill time, skin perfusion, and mental status can be assessed, though this is less accurate 2

Clinical Application Algorithm

When encountering a hypotensive patient, follow this structured approach:

1. Identify hypotension and perform focused bedside assessment to characterize stability and rule out obvious causes 1

2. If volume status is uncertain and the patient is not obviously fluid overloaded, perform PLR test 1, 2

3. Interpret results:

   • Positive PLR (increased cardiac output/stroke volume): Administer intravenous fluid bolus (typically 500 mL crystalloid in adults, 10-20 mL/kg in children) 1, 2
   • Negative PLR (no increase in cardiac output): Focus management on vascular tone with vasopressors or inotropy/chronotropy with inotropes 1

4. Reassess after each intervention and consider escalation of care if hypotension persists 1

Critical Limitations and Contraindications

The PLR test has important limitations that can render it unreliable or invalid:

• Intra-abdominal hypertension or abdominal compartment syndrome - PLR cannot predict fluid responsiveness in these conditions 2, 5
• Cardiac arrhythmias, particularly atrial fibrillation - beat-to-beat variability invalidates stroke volume measurements 5
• Spontaneous breathing efforts or low-level pressure support - respiratory variation interferes with interpretation 5
• Severe right ventricular dysfunction - high PLR response may indicate RV afterload dependence rather than true fluid responsiveness 8
• Increased intracranial pressure - leg elevation may worsen cerebral perfusion pressure 1

Clinical Context and Evidence Quality

The PLR test is particularly valuable in postoperative settings where approximately 50% of hypotensive patients are NOT fluid responsive, preventing unnecessary fluid administration that could lead to complications like pulmonary edema 1

• In septic shock, PLR helps guide the decision to continue fluid beyond the initial 30 mL/kg bolus, with ≥8.1% increase in stroke volume index predicting fluid response with 92% sensitivity 5
• The test is most reliable when cardiac output is measured directly rather than relying on blood pressure changes alone, as MAP changes during PLR are often non-significant even when cardiac output increases 1
• Evidence quality for PLR in normotensive subjects is low to very-low, but in hypotensive critically ill patients the evidence is more robust 1

Common Pitfalls to Avoid

Several technical errors can lead to false results:

• Insufficient leg elevation angle (should be 45-60°, not just slight elevation) 1
• Monitoring blood pressure instead of cardiac output/stroke volume - blood pressure alone is an unreliable surrogate 1
• Waiting too long to assess response - the hemodynamic effect peaks within 30-90 seconds and may dissipate by 7 minutes 1, 3
• Performing the test in patients with obvious contraindications like severe heart failure with pulmonary edema 1
• Using the test in spontaneously breathing patients without accounting for respiratory variation 5