Inferior vena cava diameter and collapse
IVC (→ right atrial pressure) · Subcostal long axis, 1–2 cm from the cavoatrial junction (proximal to the hepatic vein), end-expiration
Normal range & thresholds
| IVC diameter | Inspiratory collapse | Estimated RA pressure |
|---|---|---|
| ≤2.1 cm | >50% | 3 mmHg (range 0–5) |
| ≤2.1 cm | <50% | 8 mmHg (range 5–10) |
| >2.1 cm | >50% | 8 mmHg (range 5–10) |
| >2.1 cm | <50% | 15 mmHg (range 10–20) |
The estimated RA pressure is added to 4V2 to give systolic pulmonary artery pressure — so every error here propagates directly into the pulmonary pressure you report.
Pathophysiology
With the tricuspid valve open in diastole, the right atrium, the vena cavae and the right ventricle form one continuous pressure chamber. IVC diameter reflects the filling pressure of that chamber; inspiratory collapse reflects the transmission of negative intrathoracic pressure, which requires the vein to be on the compliant part of its pressure–volume curve. A dilated, non-collapsing IVC therefore means the vein is stiff and full — high right atrial pressure — unless something else has made it non-compliant.[3,50]
Raised by
- Right heart failure of any cause; pulmonary hypertension
- Severe tricuspid regurgitation and tricuspid stenosis
- Volume overload — renal failure, over-transfusion, hepatorenal states
- Cardiac tamponade — a plethoric non-collapsing IVC is one of its cardinal signs
- Constrictive pericarditis and restrictive cardiomyopathy
- Positive-pressure ventilation (an entirely different physiology — see below)
- Athletes and young healthy subjects can have a dilated but fully collapsing IVC — the collapse is what makes it benign
Lowered by
- Hypovolaemia, haemorrhage, dehydration, over-diuresis, sepsis with vasoplegia
- Deep or forced inspiration during the measurement
- Extrinsic compression by ascites, a mass, or an abdominal binder
- IVC thrombosis or an interrupted IVC with azygos continuation
Technique & pitfalls
- Subcostal long axis, measure 1–2 cm from the cavoatrial junction, just proximal to the entry of the hepatic veins, perpendicular to the long axis of the vessel.
- Measure at end-expiration; assess collapse during a quiet sniff, not a Valsalva and not a forced inspiration.
- M-mode is acceptable only if the cursor is perpendicular; the IVC moves craniocaudally with respiration and M-mode frequently samples a different part of the vessel at each phase — 2D is safer.
- Report the diameter, the collapse and the derived pressure separately, and state the estimate as a range, not a point value.
- In mechanically ventilated patients this table does not apply: positive pressure reverses the respiratory physiology, and IVC distensibility (not collapsibility) is used instead.
Pseudo-change & artefact
- Oblique imaging of a moving cylinder — the commonest error, and it can go either way.
- Sampling too close to the right atrium (falsely wide) or too far caudally (falsely narrow).
- Forced inspiration or Valsalva during the assessment — exaggerates collapse and falsely lowers the estimated pressure.
- Positive-pressure ventilation — the algorithm is invalid.
- Athletes: a dilated IVC with full collapse and a normal right heart is physiological.
- Immediately after dialysis or large-volume diuresis, the IVC lags behind the true filling pressure.
- In severe tricuspid regurgitation the IVC is plethoric and pulsatile, and the estimate degrades.
Treatment thresholds
- Decongestion: IVC diameter and collapse are the standard bedside targets for diuretic titration in acute heart failure, and residual congestion at discharge (a plethoric IVC) predicts readmission.[11,12]
- Pulmonary hypertension: the derived right atrial pressure is a component of the ESC/ERS risk assessment, and a rising RA pressure in a treated patient signals treatment failure and the need for escalation or transplant referral.[8]
- Tamponade: a plethoric IVC supports the diagnosis and, with clinical compromise, the decision to drain — the absence of IVC plethora argues strongly against tamponade.[24,31]
- Dialysis: IVC-based volume assessment guides dry-weight prescription.
- Fluid responsiveness in critical care: the IVC distensibility/collapsibility index is used to decide whether to give fluid — a genuinely therapeutic use of this measurement, though limited to ventilated, passive patients in sinus rhythm.
Next step
- Next: hepatic vein Doppler — systolic flow reversal for severe tricuspid regurgitation, expiratory diastolic reversal for constriction.[57]
- Then: integrate with TR velocity to give systolic pulmonary artery pressure, and with RA area and RV function to build the right heart picture.
- Then: if the IVC is plethoric with a small ventricle, exclude tamponade and constriction; if plethoric with a dilated RV, pursue pulmonary hypertension.
- Then: right heart catheterisation when the estimate matters and the echo is equivocal — echo estimates of RA pressure agree with invasive values only moderately well.[51]
Drugs
- Loop diuretics and thiazide combinations — the primary tool; effect within hours.
- SGLT2 inhibitors add sustained decongestion.[82]
- Nitrates and other venodilators reduce diameter acutely by increasing venous capacitance.
- Ultrafiltration and dialysis.
- Increased by: intravenous fluids, transfusion, sodium loading, NSAIDs, thiazolidinediones, corticosteroids, and any drug promoting fluid retention.
Reversibility
Immediately and completely reversible — the IVC is a capacitance vessel and reflects the filling pressure of the moment. Diameter and collapse change within hours of diuresis, dialysis or fluid administration. This makes it an excellent treatment monitor and a poor marker of chronic disease: a normal IVC on a well-diuresed outpatient says nothing about how congested that patient becomes when treatment stops. The exceptions are mechanical: IVC thrombosis, extrinsic compression and congenital interruption do not change with volume.[3,51]