Do you have Postural Orthostatic Tachycardia Syndrome (POTS)?

Do you have Postural Orthostatic Tachycardia Syndrome (POTS)?

Have you ever experienced feelings of dizziness and heart palpitations from standing up, which you have attributed to simply getting up too quickly? Has the frequency of these complaints been more prominent in the past few years, especially after a bout of COVID or any other infection? You may in fact be presenting with symptoms of Postural Orthostatic Tachycardia Syndrome (POTS).

Normally, when we go from a supine to standing position, gravity shifts an estimated 700 to 900 mL of blood from the core/abdominal region to lower body extremities. There are receptors embedded in the heart, arterial and venous system that respond to the changes in pressure exerted by gravity acting upon us. A normal response is multiple feedforward and feedback signalling between the brain, cardiac, arterial and venous system such that an appropriate increase in heart rate meets the metabolic needs for the brain. In patients with POTS, the response is either excessive (elevated heart rate) or defective in the ability to constrict the lower extremity venous system and thereby reducing the blood return back to the heart also leading to an excess heart rate response. 

POTS is an Autonomic disorder

The nervous system can be divided into three components, the central, peripheral and autonomic nervous systems. The autonomic nervous system is further divided into a sympathetic and parasympathetic branch. The sympathetic branch helps shunt blood away from gut to the brain and extremities, increase heart rate and breathing rate. The parasympathetic branch diverts blood to our gut and reduces heart and breathing rate. These two systems are always functioning together in conjunction with one another. They are active and constantly changing at rest and during change in bodily position, exercise, environmental/chemical stress and are also influenced by the metabolic consequences of digestion and absorption of fats, carbohydrate and protein intake. This explains why some POTS patients may have symptoms such as abdominal pain and palpitations after consuming a large meal, which may easily be mistaken for other gut conditions.

Given that POTS affects the autonomic nervous system, it is not uncommon for people to experience symptoms such as palpitations, shortness of breath, chest discomfort, lightheadedness, nausea, blurred vision, cognitive dysfunction, chronic fatigue, sleeping abnormalities, migraines, hypermobile joints, abdominal pain, irritable bowel, and bladder symptoms such as excessive urination. Only 30% of individuals have reported fainting along with the symptoms of POTS.

How does this relate to COVID-19?

It has been demonstrated that a protein component of SARS-CoV-2 virus increases the permeability of the blood–brain barrier (BBB), potentially disrupting the delicate neural networks within the brain. Altered function of the BBB can result in neuroinflammation and a multitude of neurologic symptoms, such as headache, dizziness, cognitive dysfunction, sleep disturbance and mood alterations that are now seen in patients with post-COVID syndrome— symptoms that are identical to those of POTS. The integrity of BBB needs to be explored, which may offer insights into the possible alteration of the blood–brain barrier in patients with POTS.

Thankfully, we have the opportunity through functional laboratory testing to explore infective, immune and blood brain barrier dysregulation and to determine the significance of each contributing factor to your POTS presentation.

POTS is defined by the following diagnostic criteria:

1. A sustained heart rate elevation of at least 30 beats per minute (bpm) in adults and at least 40 bpm in teens 12–19 years of age from supine to standing position during a 10 minute stand test or using the gold standard tilt-table test

2. Absence of orthostatic hypotension

3. Symptoms of orthostatic intolerance must be present for at least 6 months

4. Worsening of symptoms standing which are relieved with supine repositioning

5. Absence of other causes of orthostatic symptoms or tachycardia (bleeding, medications and dehydration)


Conditions that may mimic POTS















The table above highlights many conditions that look like POTS. It is our responsibility within the integrated health paradigm to explore the many co-morbid conditions that may be associated with POTS.

POTS Subtypes


POTS may be categorised under the following subtypes:
Neuropathic POTS

This is where there is disease or demyelination of sympathetic nerves innervating the lower extremity blood vascular network. Noradrenaline is therefore not released in the lower extremity causing blood pooling in the venous system. This creates a feedback mechanism to the heart to rapidly increase heart rate.

Hyperadrenergic POTS

This is diagnosed by a standing plasma Noradrenaline reading of >600 pg/ml with increased sympathetic tone manifesting as palpitations, tremors, hypertension, heart rate > 30bpm and anxiety. Of note, patients prescribed with serotonin and noradrenaline re-uptake inhibitors for depression and anxiety may worsen hyperadrenergic POTS. 

Hypovolemic POTS

This is where you may have a low red blood cell count, low total blood volume, plasma renin and aldosterone. This can be evaluated through blood labs. 

Autoimmune POTS

This can present from post viral syndromes, autoimmune conditions and connective tissue disorders may also complicate and contribute to the POTS pathophysiology. If you have increased ANA titres on a blood test this strongly suggests Autoimmune POTS. 

There is also the consideration of Ehlers-Danlos (EDS) and Mast Cell Degranulation (MCAS) in POTS. MCAS patients have hyperadrenergic POTS and flushing. These people typically present with “attacks” of flushing accompanied by lightheadedness, dizziness, dyspnea, nausea, headache, diarrhoea, and/or syncope. Symptoms during episodes included flushing, palpitations, postural lightheadedness, nausea, diarrhoea, abdominal cramping, and excess urine volume output. Some people exhibit excessive sleep after an episode. Triggering events included prolonged standing, exercise, menses, meals, sexual intercourse, and certain medications (e.g., aspirin and β-blockers).

Many people with POTS have unique distinct subtypes, however the reality is that one patient may be experiencing a combination of these subtypes which make diagnosis and treatment a little more tricky. 

Co-existing conditions

To further complicate the matter, these subtypes may be compounded with coexisting conditions, such as seen in the figure below:

How can your POTS be investigated and differentiated?

Your integrated GP or Chiropractor Sydney can request screening tests such as Full blood count, 24-Hour urine sodium, copeptin, 24-Hour heart rate and Blood Pressure monitoring, plasma renin and aldosterone, autoimmune markers such as antinuclear, anti-Ganglionic and voltage-gated potassium channel antibody testing, supine to standing plasma noradrenaline, a thermoregulatory sweat test, thyroid function tests, serum AM and PM cortisol testing and a 24-hour ECG Holter monitor.

In addition to these, in our clinic, we can perform a comprehensive autonomic evaluation utilising Nerve express technology as well as the NASA Lean test recommended by the Australian POTS foundation. The NASA Lean test involves the measurement of pulse rate and blood pressure supine and standing, for 10 minutes. An increase in 30 bpm from supine to standing indicates POTS. We may also look into functional medicine lab testing to address chronic infective burden on the immune system and many other metabolic pathways that regulate noradrenaline metabolism. 

Without going into complex detail, the flowchart above highlights how 3 sub-types of POTS all contribute to the same symptoms despite different mechanisms. 



To sum it up, the image above explains how the blood vessels in the legs, vascular and cardiac receptors are all sites for dysregulation due to inflammation or antibodies binding to them and thereby altering their function by increasing or decreasing their responsiveness to orthostatic stress. 

Treatment for POTS:

Pharmacological management and treatment

POTS is typically managed using a pharmacological approach, although evidence for this approach is weak, not to mention the many side effects. Firstly, it is essential to evaluate for concurrent medications that may be decreasing blood volume or increasing heart rate. Pharmacological strategies include:

1. Treatments to increase oral sodium and water intake may increase blood pressure and therefore must be monitored, as well as patients with a concurrent autoimmune disorder in which sodium may increase their auto-inflammatory response. 

2. Blood volume expanders such as Desmopressin and fludrocortisone to address low volume POTS may cause low potassium levels and headache.

3. Intravenous saline may increase thrombosis risk for people with vascular co-morbidities.

4. Beta-Blockers that decrease the workload of the heart may also lower blood pressure, cause cramping, visual disturbances, worsening of asthma symptoms and impair alveoli exchange of oxygen and carbon dioxide. Drugs that reduce sympathetic tone (sympathomimetics) in order to reduce heart rate may cause hypotension, brain fog and fatigue, further worsening POTS symptoms despite managing heart rate in and of itself.

5. Vasoconstrictors, in an effort to reduce lower extremity pooling, may also cause cramping, tingling and nausea. 

Exercise and Nutritional Rehabilitation for POTS

There are various physical interventions that can improve POTS. The use of horizontal exercise (e.g.rowing, swimming, recumbent bike, etc.) at the beginning is a critical strategy, allowing you to exercise while avoiding the upright posture that elicits your POTS symptoms. As you become increasingly fit, the duration and intensity of exercise should be progressively increased, and upright exercise can be gradually added as tolerated. Supervised training is preferable to maximise functional capacity. 

Nutritional considerations are different amongst the sub-types of POTS but in general, one should aim for replenishing adequate sodium, potassium, magnesium and chloride with specific amino acids to rebalance the body’s chemistry.

Sodium intake as a therapeutic tool

A slow, progressive increase in daily sodium intake in/on the food and eating salty snacks is recommended. However, salt tablets should be avoided because they are very concentrated and can induce an osmotic load into the stomach which may cause nausea, vomiting and dehydration, leading to reduced rather than expanded plasma and blood volume. An increased water intake, up to 3 litres per day as well as an increased salt intake throughout the day – consuming them together is recommended, as water alone is not effective in long-term volume expansion. Glucose-salt rehydration solution may be more effective in the expansion of plasma and blood volume, but this depends on the glycaemic profile of the POTS patient. As mentioned above, a broader aim of re-balancing of minerals is fundamental.

Other non-pharmacological interventions, may include:
Gradual volume expansion via sleeping in the head-up position

The recommendation in the scientific literature is to elevate the head of the bed off the ground 4 to 6 inches in order to increase circulating plasma and blood volume. Large phone books, blocks of wood, or bed risers placed under the feet at the top of the bed work best for placing the entire body at a slight angle during sleeping at night. The rationale behind this approach is that mild gravitational stress causes fluid to shift to the lower body and decreases central blood volume and the effective circulating blood volume, which promote the kidneys to retain both sodium and water volume.

Reduction in venous pooling during standing by lower body compression garments

Compression of all lower body compartments (calf, thigh and low abdomen) seems to be the most efficacious, followed by abdominal compression, whereas leg compression alone appears to be less effective, presumably reflecting the large capacity of the abdomen relative to the legs. Abdomen-high rather than knee or thigh-high compression garments is recommended.

Physical Countermeasure Manoevres

Actions such as squeezing a rubber ball, leg crossing, muscle pumping, squatting, negative-pressure breathing, etc., may also be effective in preventing orthostatic intolerance and managing acute clinical symptoms in POTS patients (see table below).













The table above highlights many physical manoeuvres that form part of a rehabilitation treatment plan in conjunction with an inversion table administered in the clinic.

Cough cardiopulmonary resuscitation

Forceful coughing can maintain circulation for a brief period of time during cardiac arrest by generating sufficient blood pressure that perfuses the brain and vital organs. Each forceful cough abruptly raises intrathoracic pressure, forcing blood out of the chest, into the aorta and its branches. Between coughs, deep inspiration draws blood into the right heart.

Inspiratory resistance

The use of an impedance threshold device increases central blood volume by forcing the thoracic muscles to develop increased negative pressure, thus drawing venous blood from extrathoracic cavities into the heart and lungs, leading to increases in cardiac output, stroke volume, and mean arterial pressure.

Skin surface cooling

Whole-body skin surface cooling increases orthostatic tolerance in the heated-stressed humans and individuals following prolonged bed rest deconditioning by reducing skin vascular conductance, decreasing blood supply to the skin, and attenuating the drop in central blood volume.

So as you can see, POTS is a disorder with various overlapping symptoms and mechanisms with some unifying characteristics. Frequently, there is an identifiable event such as illness, surgery or pregnancy that precedes the onset. We have outlined above, a comprehensive list of strategies for both evaluation and diagnosis, as well as treatment, much of which can be performed within our clinic using relevant diagnostic methods or laboratory assessments, or referred on to the appropriate health professional for further intervention where necessary.

We encourage you to make an appointment here where Dr. Yazbek can provide you with the most informed evaluation and treatment possible for your suspected POTS circumstances. Simply click on the link to find a time that suits you. Alternatively, feel free to call our clinic on (02) 9317 2288 or email us directly at



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