Postural tachycardia syndrome (POTS) due to posture dependent compression of the inferior vena cava by the diaphragm
The patient, who was 25 years old at the time of the examination and showed clear signs of overstretched connective tissue (Beighton score 8/9), became ill six years ago with abdominal pain and weight loss and, over the last four years, has developed a very restrictive circulatory dysregulation with tachycardia when standing, which improved when bending forward and lying down.
Comprehensive cardiological diagnostics did not reveal any cause for the tachycardia. The patient underwent two unsuccessful invasive ablations of suspected atrial pacemaker centres under the diagnosis of fast-slow AVNRT and ectopic atrial tachycardia. The patient could not tolerate the drug therapy with beta blockers. This is understandable when considering the mechanism of her disease, as described below, and the fact that the increase in heart rate to compensate for orthostatic venous pooling is suppressed by beta-blockers. With ivabradine, there was at best only a slight alleviation of her symptoms.
Despite this treatment, the patient is severely affected and cannot continue her studies. She has lost 11 kg in weight, suffers from severe menstrual pain, neck pain , headaches, pain in the genital area, nausea and severe chronic fatigue, which she explains by her constantly accelerated heartbeat.
The cause of her symptoms was identified by means of a subtle and extensive functional colour duplex sonography of the heart, the vessels in the abdominal cavity and in the pelvis in different postures. This revealed the posture-dependent compression of the inferior vena cava by the diaphragm in addition to a respiratory compression of the vena cava by the diaphragm .
Determining the aortic flow volume and the heart rate allows a calculation of the changes in the filling of the heart depending on the posture.
The characteristic of postural tachycardia syndrome (POTS) is a rapid and uncomfortable increase in heart rate in an upright position, without current physical activity being able to explain such an increase in heart rate. Patients often feel unwell. They may experience dizziness, lose consciousness (syncope), can often only stand for a short time and have to sit or lie down, which quickly normalises the heartbeat.
Patients with POTS often suffer from a change in circulatory conditions depending on their position, to which the heart merely reacts.
In general, the upright position of humans places particular demands on the circulatory system with regard to dealing with gravity. Gravity pulls the blood into the lower half of the body and supplying the brain with an adequate amount of blood requires a counteraction to return the blood to the heart and from there pump it up to the head.
The forces that accomplish such a return transport are
the constant supply of blood from the heart via the arterial system into the capillaries and veins
the tension and contractile force of the veins, which both prevent the veins from expanding too far and thus storing too much blood
the muscle pump of the legs, which massages the veins of the legs. However, this requires active muscle work in the legs, such as that generated when walking around or when the calf muscles are contarcted.
Forces that impede the return transport are:
- gravity itself
- centrifugal force, e.g. on a merry-go-round, where the legs describe a larger circle than the head
- Obstacles in the path of blood from the periphery to the heart or brain: These are all venous vascular compression syndromes that cause blood to pool in front of the obstruction and therefore cannot return to the heart
- a reduction in the heart’s driving force due to heart failure, narrowing of the aorta or aortic valve, aortic atony, aortic valve insufficiency, arterial stenoses
- Sagging of veins in connective tissue diseases, which cause the veins to expand increasingly under the pressure of gravity and therefore collect more blood instead of transporting it back to the heart.
Women with connective tissue disorders, often summarised under the term hypermobility syndrome, such as hypermobile Ehlers-Danlos syndrome, develop several of the above-mentioned factors that cause too little blood to be returned to the heart from the venous system.
These factors are, in detail,
- the softness of the connective tissue vein walls. As a result, more blood collects in the venous system under the influence of gravity than in healthy people.
- The slack ligaments of the spine allow increased lordosis.
- At the same time, there is often a flat thorax, which means that the abdominal wall is often less than 15 mm away from the more curved spine.
- This leads to a narrowing of the abdominal cavity.
- The increased pressure of the curved spine compresses the veins, which are particularly soft in these patients. As a result, they often develop venous vascular compression syndrome, which, when the body position changes, prevents enough blood from reaching the heart.
When the body is in an upright position, the heart chambers suddenly no longer fill sufficiently. If the heart rate remained constant at the level it was at in a horizontal position, this would mean that the organs would receive correspondingly less blood. This would impair their function to such an extent that a pathological disorder of individual organs would occur. This is particularly evident in brain function. Due to its high metabolic rate, the brain depends on a sustained high blood supply. Therefore, affected patients often suffer from brain function disorders such as drowsiness, lack of concentration, headaches, the feeling of an empty head, headaches, but above all, from disturbances of consciousness that can increase to the point of loss of consciousness (so-called syncope).
Since the brain occupies the highest position in the human body when the body is in an upright position, the effect of gravity on this organ is particularly strong.
The patient presented here had the peculiarity of experiencing relief of her tachycardia not only when squatting or lying down but also when bending over while standing.
The video above shows the simultaneous recording of the patient’s ECG and body position. When the body position changes, the heart rate changes within a few seconds. When the patient is standing, the heart rate is over 160 bpm (normal would be 60-80 bpm). After the patient has squatted, the heart rate drops significantly to values below 100/min. The explanation for this change is that when the patient squats, the congested veins in the lower leg and thigh are squeezed. This causes the blood that had accumulated in the legs and pelvis when the patient was standing to be returned to the circulatory system. As the amount of circulating blood increases, the left ventricle fills up more. This means that the heart can eject a greater volume of blood per contraction (heartbeat) than it can in an upright position. The volume needed to keep the brain and other organs functioning can therefore be delivered with fewer heartbeats, i.e. at a lower heart rate.
However, what is unique about this patient is that it is not just the mobilisation of blood that has sunk into the lower half of the body that can refill the circulation, as explained in the first video. This is a common mechanism in patients with vascular compression syndromes and POTS.
In her case, there was also a significant reduction in heart rate when bending forward. The reason for this is that when you bend forward, the passage of the vena cava through the diaphragm widens due to a change in diaphragmatic tension. This significantly reduces the main obstacle to normal filling of the heart chambers. As this is another way of achieving better blood filling of the heart, similar to squatting, it also causes the heart rate to drop.
The study of circulatory conditions in different postures can be accurately determined by the volume perfusion of the aorta:
In the supine position, the flow volume in the abdominal aorta was determined to be 3975 ml/min. As soon as the patient stood up, this blood volume dropped by 35% within two minutes, even though the heart rate increased by 42% from 95 to 135 beats per minute. This increase in heart rate triggered by a change in position is the core symptom of postural tachycardia. The low filling of the ventricles, which results in a lower ejection volume per heartbeat, must be at least partially compensated for by a more frequent heartbeat. The tachycardia is therefore not an autonomic dysregulation, as is often claimed, but a useful and necessary adaptation mechanism to compensate for the reduced filling of the circulation.

When the patient bent forward while standing, the observations she had made were confirmed by the measurements. Her heart rate dropped from 135 to 117 beats per minute, which reduced the speed of her heart. Blood was flowing better in her body, as the drop in the flow rate of the aorta was smaller than when she was lying down (24% instead of 35%).

The effect of posture on the filling of the left ventricle was found to be particularly pronounced. The left ventricle is responsible for pumping blood into the circulatory system.
While the filling of the ventricle decreased by 54% in the shortest possible time when compared to lying down, this decrease was less pronounced when bending forward, reaching ‘only’ 38%.These significant changes in heart filling were immediately noticed by the patient, especially since they were accompanied by a corresponding beneficial slowing of the heartbeat.
Conventional cardiological diagnostics, encompassing clinical and instrumental evaluations (including the tilt table test and ECG), yielded no informative results.The prevailing methods of investigation are only equipped to delineate the alterations that occur in the heart (e.g. acceleration of the heartbeat, potential fluctuations in blood pressure, the manifestation of clinical symptoms such as dizziness, weakness, incapacitation to stand or even loss of consciousness). However, they are inherently incapable of elucidating the underlying cause of the condition. The underlying cause is identified as impeded recirculation due to venous vascular compression syndromes, with the heart’s reaction to this altered circulation being to ensure sufficient blood supply to vital organs, particularly the brain. Arrhythmias and tachycardia can arise from abrupt changes in the filling of the heart.
In the patient presented here, heart rate increased to 160/min when standing, and decreased to well below 100 beats/min when lying down. Of particular interest was the observation that bending forward while standing, bringing the head to approximately the level of the pelvis, resulted in a significant reduction in heart rate.
The patient had been diagnosed with May-Thurner syndrome, a condition characterised by the obstruction of blood flow in the left half of the pelvis, resulting in its re-routing over the pelvic organs to the right.

Furthermore, severe compression of the left renal vein was observed, situated between the aorta and the superior mesenteric artery, as well as on the right renal artery outlet.
This resulted in flow acceleration of 10 cm/s in the obstructed segment of the vein to the left of the aorta, reaching 387 cm/s at the site of compression.Severe renal vein compression leads to an increase in the obstruction of the pelvic veins, as the obstructed renal vein blood is diverted downwards via the ovarian vein into the pelvis.
Furthermore, compression of the vena cava was observed during its traversal of the right renal artery.

Furthermore, the presence of an arcuate ligament syndrome was identified, a condition known to be associated with an increased propensity for tachycardia. This syndrome arises due to the compression of the celiac trunk by the diaphragm, as evidenced by the acceleration in flow velocity to 3 16 cm/s at an aortic flow velocity of 182 cm/s) but also the sympathetic nerve plexus of the celiac plexus, which also extends between the diaphragmatic margin and the truncus.

The primary impediment, however, was a constriction of the inferior vena cava by the diaphragm, which exhibited variability depending on respiration, as previously detailed on my website. Given the pronounced narrowing of the vena cava, conventional Doppler techniques proved ineffective in yielding definitive results. Consequently, the CW Doppler technique (continuous wave Doppler) was employed, a method capable of accurately measuring flow velocities and pressures at extremely high levels.
Utilising this technique, a flow acceleration to 200 cm/s was detected even in the supine mid-thoracic position.

which rose to 279 cm/s in Inspiration,

however, was strongest in expiration at 455 cm/s. The flow velocity in the caudal sections of the inferior vena cava was 50 cm/s.

However, a notable distinguishing feature of the patient’s condition was the observation that body posture exerted an influence on the diaphragmatic compression of the vena cava. In an upright standing position, a more pronounced blockage of the blood return flow was observed in comparison to a standing posture with the trunk bent forward. The flow velocity in the mid-breath position was measured at 137 cm/s at the point of passage through the diaphragm.
During inspiration, the flow velocity drops further to 117 cm/s with a now very wide passage through the diaphragm

However, a strong flow acceleration to 325 cm/s can still be detected in expiration even when bending forwards:

However, all these values were found to be significantly lower than those measured in an upright position. This finding indicates that the change in diaphragmatic tension caused by bending forward alleviated the narrowing of the vena cava. Bending forward significantly reduces the pull of the diaphragm muscles (crura diaphragmatica) on the spine.


In healthy individuals, there is no disturbance to the venous return to the inferior vena cava when changing from one breathing position to another. The vena cava, diaphragm and liver are connected to each other by connective tissue.
Several factors, both dynamic and static are together responsible for maintaining the posi- tion of the liver in the upper part of the abdomen. The fixed anatomical structures are represented essentially by the suspension and tethering of the liver to its vascular pedicle. The inferior vena cava, the particular importance of which was discovered by Faure, suspends the liver by way of the suprahepatic (i.e. hepatic ( TS) veins. The ligamentum teres, stretched be- tween the inferior vena cava and the anterior ab- dominal wall, supports the left hepatic lobe. (from: Anat Clin (1982) 4:125-135 ; The Mechanisms Responsible for Stabilising the Liver by JB Flament , JF Delattre , and G Hidden)
In patients exhibiting connective tissue weakness, the liver may consequently descend when in a standing posture, exerting traction on the vena cava beneath the diaphragm. This results in the constriction of the vena cava as it passes through the diaphragm.
A significant sinking of the liver of up to 1 cm above the entrance to the pelvis could be detected in the patient when standing:

It has been demonstrated that forward flexion exerts a compressive force on the lower abdomen, thereby reducing the descent of the liver and consequently maintaining a spacious passage of the vena cava through the diaphragm.
The hemodynamic effect of compressing the vena cava, as well as the influence of different postures, can be demonstrated using the PixelFlux technique.

In order to achieve this objective, the blood flow in the kidneys in different postures was measured. In line with the measurements of aortic volumetric blood flow during various postures, the kidneys respond to bending forward from a standing position by improving blood flow compared to an upright position.This demonstrates that not only aortic blood flow but also organ blood flow is affected by changing compression of the vena cava.
This study provides the first documented evidence in the medical literature of the body position-dependent compression of the vena cava by the diaphragm (22.02.2025).
I would like to express my gratitude to the patient for providing the videos and for her permission to present her medical history.