Decide whether a patient will increase stroke volume with fluid, using dynamic tests (PPV/SVV, passive leg raise, end-expiratory occlusion, mini-fluid challenge).
At the bedside
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Ask first: does the patient need more flow?
Signs of hypoperfusion (lactate, CRT, mottling, oliguria) and no fluid intolerance (B-lines, rising CVP, worsening oxygenation).
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PPV/SVV if criteria met
Pulse pressure variation > 12-13% predicts responsiveness ONLY if: controlled ventilation with no spontaneous effort, sinus rhythm, Vt ≥ 8 mL/kg PBW, closed chest, no RV failure, heart rate/RR ratio > 3.6, normal intra-abdominal pressure. Grey zone 9-13%.
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Passive leg raise (PLR) - works in most patients
1-2 minStart semi-recumbent 45° → lower trunk flat and raise legs 45° (bed tilt, not lifting legs manually). Measure real-time cardiac output/stroke volume (echo VTI, pulse contour, EtCO2 rise) within 60-90 s. Positive = CO/VTI rise ≥ 10% (or EtCO2 rise ≥ 5%). BP alone is not reliable.
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End-expiratory occlusion test
In ventilated patients: 15 s end-expiratory hold; cardiac index rise ≥ 5% predicts responsiveness.
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Mini-fluid challenge
100 mL crystalloid over 1 min with VTI measurement: rise ≥ 10% predicts response (needs precise VTI).
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Act on the result
Responsive + needs flow → give 250-500 mL and reassess. Not responsive → stop fluids; vasopressor/inotrope according to cause. Repeat tests after each intervention.
Dynamic tests: thresholds and limits
| Test | Positive threshold | Not valid when |
|---|---|---|
| PPV / SVV | > 12-13% (grey zone 9-13%) | Spontaneous breathing, arrhythmia, Vt < 8 mL/kg, open chest, RV failure, low compliance |
| Passive leg raise | CO/VTI ↑ ≥ 10% or EtCO2 ↑ ≥ 5% | Intra-abdominal hypertension, leg amputation, raised ICP (caution) |
| End-expiratory occlusion (15 s) | CI ↑ ≥ 5% | Patient triggers during hold |
| Mini-fluid challenge (100 mL) | VTI ↑ ≥ 10% | Poor echo windows; measurement error |
| IVC variability | Distensibility > 12-18% (ventilated) | Spontaneous breathing (less reliable), raised IAP |
References
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Should I give more fluid?
Step 1 of ~3
Decision: Hypoperfusion present and no fluid intolerance?
Based on Monnet X, Marik PE, Teboul JL; Teboul JL, Monnet X, Chemla D, Michard F. Educational use; follow local protocol.
Pathophysiology
Positive-pressure inspiration reduces RV preload and increases RV afterload; if both ventricles are on the steep part of the Frank-Starling curve, LV stroke volume falls a few beats later, producing cyclic variation in pulse pressure. PLR transfers ~300 mL of venous blood from the legs and splanchnic bed to the heart: a reversible, self-administered fluid challenge.
Evidence
- Michard 2000: PPV > 13% predicted fluid responsiveness in ventilated septic patients [Michard 2000].
- Monnet 2006: PLR-induced increase in aortic blood flow ≥ 10% predicted responsiveness, including in patients with spontaneous breathing or arrhythmia [Monnet 2006].
- SSC 2026 suggests dynamic measures (PLR or fluid bolus with SV, SVV, PP or PPV) over examination or static measures alone (conditional, low certainty); insufficient evidence for or against minimally invasive or non-invasive cardiac output monitoring; invasive or cuff BP both acceptable, with an arterial line for high, rising or multiple vasopressors [SSC 2026].
Controversies
- Whether fluid-responsiveness-guided resuscitation improves patient outcomes: small trials suggest less fluid and less RRT, but mortality data are limited.
🇮🇳 India notes
- Most Indian ICUs lack calibrated cardiac output monitors; LVOT VTI on echo (≥ 10% rise with PLR) is cheap and reproducible once trained.
- Capnography (EtCO2) is now common on ventilators; an EtCO2 rise of ≥ 5% with PLR in a ventilated patient with constant ventilation suggests increased CO.
References
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Test yourself
Module quiz · score 70% to complete the module
Educational reference for trained clinicians. Check doses against your hospital protocol and the patient in front of you.