RV function training › Guides › Septum and overload
Septal flattening: pressure or volume overload?
In the parasternal short axis the normal LV is round throughout the cycle because LV pressure exceeds RV pressure. When the RV is overloaded the septum flattens and the LV becomes D-shaped. When in the cycle it flattens tells you why.
| Pattern | Septum | RV | Typical causes |
|---|---|---|---|
| Pressure overload | Flattest at end-systole (systolic D-shape), often still flat in diastole | Hypertrophied free wall (>5 mm), later dilated and hypokinetic | Pulmonary hypertension, chronic thromboembolic disease, pulmonary stenosis |
| Volume overload | Flat in diastole only, moves toward the RV in systole (paradoxical) | Dilated, thin-walled, often vigorous | Atrial septal defect, anomalous pulmonary venous drainage, severe tricuspid or pulmonary regurgitation |
| Both | Flat in systole and diastole (severe pressure overload alone can look the same: the volume cause, such as severe TR, decides) | Dilated, hypertrophied, hypokinetic | Pulmonary hypertension with severe tricuspid regurgitation, decompensated RV |
The eccentricity index quantifies it: the LV diameter parallel to the septum divided by the diameter perpendicular to it, measured in short axis at end-systole and end-diastole, at mid-LV level; a value above 1.1 is abnormal.
Acute pressure overload and McConnell's sign
A sudden rise in pulmonary pressure, classically acute pulmonary embolism, dilates a RV that has had no time to hypertrophy: the free wall stays thin (≤5 mm), the septum flattens in systole, and the mid (and basal) free wall becomes akinetic while the apex keeps contracting. That regional pattern is McConnell's sign. It is fairly specific for acute pulmonary embolism but insensitive, and it is also seen in RV infarction; other echo signs of acute PE are an RV/LV ratio above 1, the 60/60 sign and TAPSE below 16 mm. A thick free wall points instead to chronic pressure overload.
When the septum is normal
- RV infarction: inferior (RCA) infarction with a dilated, hypokinetic RV and reduced TAPSE. Look at the inferior LV wall. Patients are preload-dependent.
- Global RV systolic dysfunction without overload (cardiomyopathy, sepsis): the free wall barely moves in and the annulus barely descends; the LV stays round.
- After cardiac surgery: the annulus barely descends (low TAPSE) but the free wall still moves in normally, so overall function is preserved.
- RV hypertrabeculation (non-compaction): an excessive, spongy layer of trabeculae with deep recesses along the free wall and apex, beyond the normal RV trabeculation and moderator band. There are no accepted echo criteria; excessive trabeculation is a trait rather than a cardiomyopathy on its own, and it is usually seen with LV hypertrabeculation.
Simulated examples
One clear example of each pattern from the simulator, measured on the drawn geometry:
| Simulated case | Basal diameter | TAPSE | FAC | Free wall | Septum |
|---|---|---|---|---|---|
| Normal RV | 33 mm | 25 mm | 42% | 3.8 mm | Round LV |
| RV pressure overload (e.g. pulmonary hypertension) | 49 mm | 12 mm | 16% | 8.3 mm | Flat in systole |
| RV volume overload (e.g. ASD, severe TR) | 52 mm | 23 mm | 57% | 4.0 mm | Flat in diastole |
| Combined RV pressure and volume overload | 53 mm | 9 mm | 20% | 7.4 mm | Flat in systole and diastole |
| Acute pulmonary embolism (McConnell's sign) | 50 mm | 14 mm | 17% | 3.8 mm | Flat in systole |
| RV infarction (with inferior LV infarct) | 49 mm | 16 mm | 30% | 3.9 mm | Round LV |
| Global RV systolic dysfunction (e.g. cardiomyopathy, sepsis) | 39 mm | 6 mm | 16% | 3.8 mm | Round LV |
| RV after cardiac surgery (longitudinal function lost) | 33 mm | 9 mm | 47% | 4.0 mm | Round LV |
| RV hypertrabeculation (non-compaction) | 39 mm | 13 mm | 31% | 3.7 mm | Round LV |