Azygous Vein Dysfunction in POTS
- Graham Exelby
- Aug 20
- 2 min read
Results of supine and standing echocardiography
Dr Graham Exelby August 2025
As we start seeing clear echocardiographic evidence of preload failure—with real-time loss of stroke volume when upright—it’s important to understand where the blood is going and why it can’t return efficiently. One of the key players may be the azygous vein system, which is increasingly coming into focus in our work.
What Is the Azygous Vein?
The azygous system is a deep venous return pathway that drains blood from the chest wall, spine, and much of the thoracic and abdominal interstitial space, connecting directly into the superior vena cava. It’s a critical bypass route when upright—especially when IVC flow is compromised, lymphatics are overloaded, or cerebral venous outflow is sluggish.
In POTS and Long COVID, we suspect this system may be functionally or mechanically impaired:
Compressed by fascial tension or kyphotic thoracic posture
Obstructed post-surgically (e.g. from cardiac clips or central lines)
Choked by lymphatic congestion or impaired venous recoil
Dysregulated by brainstem autonomic failure, preventing the normal “pump” of venous tone
Why Target It?
If the azygous system can’t offload the thorax and upper abdomen, then venous return to the heart is insufficient, especially during upright stress. This fits the picture of what we’re seeing on echo: small, underfilled ventricles and collapsing stroke volume despite normal cardiac muscle function.
By identifying and addressing azygous compromise—whether through imaging, fascial release, lymphatic therapy, or in rare cases surgical correction—we may be able to:
Improve cerebral perfusion
Reduce upright head pressure and tinnitus
Restore effective preload and stroke volume
Support long-term recovery in POTS and allied syndromes
This is a developing area of interest that ties directly into our current preload investigations. As we gather more data from echocardiography and imaging, the azygous system may prove to be a missing link in explaining both mechanical and neurovascular failure in these patients.