More Than Sick of Salt

All Posts Tagged: Neuropathic POTS

Signs and Symptoms of Dysautonomia (Autonomic Dysfunction)

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By Dr. Nicholas DePace and Dr. Michael Goldis

Symptoms of Dysautonomia include fainting. drop in blood pressure with getting up, blood pressures that occur without a known cause, flushing of the face, lack of sweating or sweating too much, vomiting, constipation, diarrhea, difficulty swallowing, swelling of the belly, disturbances of urination, difficulties with erections, episodes of stopping breathing and the declining ability to see at night. Quite a lot!

Before the person actually faints, they may experience loss of strength in the muscles that keep us upright, weakness, a generalized feeling of not being well, nausea, headache, sweating, a pale complexion, difficulty seeing and a sense that they are about to lose consciousness. 

Usually low blood pressure and slow heart beat accompany these symptoms. These signs and symptoms can be caused by emotional stress, drops in blood pressure when getting up, vigorous exercise in a hot environment, blockage of blood returning to the heart, sudden onset of pain or its anticipation, and loss of fluids.

There can be a variety of other circumstances involved with these feelings faint one gets before they faint due to dysautonomia.

When a person does faint, they usually limp. Some muscle movement may occur and they may experience fainting and sometimes lose bowel control which can appear like seizure. what is different is that recovery is rapid  once the person is lying flat. After the fainting event, headache, nausea and fatigue. usually persist.

 

Reference – Current Medical Diagnosis and Treatment, Dysautonomia  2021 page 101

 

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What is Orthostatic Hypotension

Cracking the Code of Dysautonomia: POTS, Orthostatic Hypotension, and Heart Health

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by Nicholas DePace MD, FACC and Michael Edward Goldis DO, FACOI, MS, BS in Pharm

When venous pooling occurs, the cardiovascular system attempts to maintain cardiac output with activation of the sympathetic nervous system, the so called accelerator of the body.

Adrenalin is released in above normal amounts and that causes the heart to beat faster or compensatory tachycardia. In addition, increased vascular tone occurs with alpha agonist activity.

This maintains blood pressure while there is decreased preload from venous pooling and maintains cardiac output by increasing heart rate with a reduced stroke volume.

This explains how cerebral circulation and thus consciousness is maintained in compensated states like orthostatic hypotension and POTS.

The increased heart rate increased the output of the heart (the cardiac output) while the actual volume the heart puts out each stroke (the stroke volume) falls because of venous pooling.

The heart rate may increase 30, 40 or more above baseline. Therefore, POTS is known as a compensated neuro-cardiovascular dysfunction. One could argue that this is not a well-compensation as the patient has significant symptoms still resulting in orthostatic intolerance.

In contrast, Orthostatic hypotension is thought of as an uncompensated neuro-cardiovascular dysfunction. Here, the patient can become dizzy and lightheaded because the blood pressure is not maintained when there is venous pooling.

Because the heart rate generally does not increase significantly for compensation, the patient’s blood pressure drops and may even have overt syncope.

Patients with orthostatic hypotension often do not have an adequate rise in heart rate because of sympathetic nervous system decompensation.

A person can have a 30 or 40 point rise in heart rate, meeting the criteria for POTS, and in another moment, when the neuro-cardiovascular system is not compensated, they can have a blood pressure drop resulting in orthostatic hypotension.

So, while it is rare, both POTS and orthostatic hypotension can coexist. Generally, if someone demonstrates orthostatic hypotension, they rarely have POTS and vice versa.

Vasovagal syncope is a sort of form of orthostatic hypotension which is delayed.

This is whether is an increasing vagal tone that prevents blood vessels from adequate constriction and prevents the heart rate from adequately increasing.

This is an extremely delayed form of orthostatic hypotension which sometimes can be reproduced on Tilt Testing.

POTS oftentimes is due to several mechanisms. There can be hypovolemic, hyperadrenergic, and neuropathic POTS. Mast cell activation is a potential mechanism as well as certain enzyme deficiencies.

When the sympathetic nervous system is extremely overactive the blood pressure may even elevate with a rise in heart rate, which is hyperadrenergic POTS.

Regardless of the mechanism of POTS, the treatment is basically similar. But, for hypovolemic POTS a volume expander makes clinical sense and for hyperadrenergic POTS, a beta blocker makes sense.

Neuropathic POTS occurs when there are diseased small fibers, which can happen with diabetes, rheumatoid arthritis, lupus, and Sjogren’s syndrome and usually has some degree of autoimmunity, but may not necessarily occur in small fiber neuropathy.

While small fiber biopsy is the gold standard to diagnose this form of POTS, we have used psuedomotor testing as an alternative.

The end result, whether the dysautonomia is due to sympathetic overdrive or parasympathetic dysfunction is poor perfusion to the brain, leading to dizziness, syncope, vision and hearing loss, tinnitus, and brain fog.

With Sympathetic overdrive, which is a major compensation mechanism, the patient has a racing heart, insomnia, excessive sweating, high anxiety, and exacerbation of brain fog from reduced cerebral blood flow from hyperventilation. This may also explain the palpitations a person feels with dysautonomia.

 

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