When Your Body’s Autopilot Goes Rogue: Understanding Dysautonomia

Oct 24

October is Dysautonomia Awareness Month, which makes this the perfect time to admit something: I was diagnosed with dysautonomia in the last year, and prior to that had no idea what that even meant.

Before my diagnosis, the term autonomic nervous system sounded like something I vaguely remembered from a systems biology class in undergrad, filed somewhere between “vagus nerve” and “stuff that runs itself so you don’t have to think about it.” I could barely have told you what it did, let alone why mine had decided to go rogue.

Looking back, the clues were there long before the acronym POTS (Postural Orthostatic Tachycardia Syndrome) ever entered my vocabulary. I just didn’t know what they meant. Once the word “dysautonomia” landed, my brain did what it always does when it doesn’t understand something, full research mode! Call it autistic hyperfocus, call it a PhD problem, or maybe its just self-preservation, but I wasn’t stopping until I could map every pathway from baroreceptor to brainstem. Somewhere between PubMed tabs and neuroanatomy diagrams, the chaos started making sense. When you finally understand the logic underneath it, talking to your doctor gets more productive, and you start recognizing your body’s cues for what they are: information you can actually use to help stabilize it.

Last month was Pain awareness month and I did a 2 part series on the biology of pain. If you missed those you can read them Here and Here!

When the Autopilot First Faltered

I’ve always had temperature regulation issues. I was the fat chick who was always freezing, especially my fingers, toes, nose, and ears. Moving from California to New England winters was a rude awakening. Now my cold fingers and toes literally turn white and blue just walking around the house!

After losing weight, the freezing got worse and now came with new tricks. If I jumped up too fast, say, to stop my kids from destroying each other (or the furniture), I’d get so lightheaded I had to lie down to prevent falling down. Hardly the image of the scary mom keeping chaos in check.

Then came the night sweats... so intense I’d wake up feeling like I just rolled out of the shower. I’m too young for menopause, right? That’s when my EDS specialist suggested a tilt-table test. I went into it not really knowing what to expect...other than I might pass out. What followed was ten minutes of my nervous system having a complete meltdown in front of witnesses: nausea, dizziness, head spinning, heart racing, blood pooling, the works. I didn’t pass out, but it confirmed what was going on. Clearly my autonomic nervous system did not have its shit together.

The Autonomic Nervous System: Your Body’s Hidden Regulator

Your autonomic nervous system (ANS) is the body’s built-in autopilot, or the behind-the-scenes operator keeping your heart beating, lungs breathing, digestion flowing, and temperature regulated. It manages all the automatic bodily functions that happen without you thinking about them.

It has two main branches:

Sympathetic Nervous System (SNS): The “fight-or-flight” accelerator. Raises your heart rate, increases blood flow to muscles, and keeps you alert and ready to react.
Parasympathetic Nervous System (PNS): The “rest-and-digest” brake. Slows the heart, supports digestion, and restores balance once the perceived threat has passed.

When they’re balanced, your body hums along smoothly. When they’re not? You get dizziness, palpitations, GI chaos, temperature swings, and fatigue. It’s kinda like trying to drive with one foot on the gas and the other one on the brake.

Why It Goes Haywire

So, what actually goes wrong?

Tiny pressure sensors in your arteries, called baroreceptors, constantly monitor blood pressure and send feedback to the brainstem. The brainstem then tells your blood vessels when to tighten or relax and adjusts your heart rate to keep everything stable.

In dysautonomia, those messages get scrambled. The baroreceptors misfire, the brainstem over- or under-reacts, and your circulatory system behaves like a confused intern on their first day. Blood pools in your legs, your heart overcompensates by racing, and your brain doesn’t get enough oxygen. Cue dizziness, nausea, and the sudden need to sit (or sprawl dramatically on the floor).

For people with Ehlers-Danlos syndrome, the connective tissue that supports blood vessels is weaker and more elastic than normal. That extra stretch changes the tension on vessel walls and confuses the baroreceptors that rely on that tension to sense blood pressure. The result is inconsistent feedback to the brain, which can trigger the racing heart, dizziness, and fatigue many of us recognize.

The Sensors and Signals Behind the Chaos

If you really want to know why dysautonomia feels like your body can’t pick a lane, we’ve got to zoom in past the nerves and into the sensors, or the receptors and chemical messengers that control the autopilot. This is where it gets nerdy, but also where it starts to make sense.

Baroreceptors: The Pressure Managers

These stretch-sensitive nerve endings live in your carotid arteries (the major blood vessels in your neck that carry oxygen-rich blood to your brain) and your aortic arch (the curved portion of your heart’s main artery where blood leaves the heart to circulate through your body). They measure blood pressure in real time and instantly report those readings to the brainstem (the control hub at the base of your brain that manages vital functions like heart rate, breathing, and blood pressure).

When baroreceptors sense a drop in pressure (like when you stand up), they tell the brainstem to raise your heart rate and tighten blood vessels to keep blood flowing upward.

In dysautonomia, these sensors lose calibration. They might under-report pressure, tricking your body into overcompensating with tachycardia (racing heart).

Chemoreceptors: The Oxygen Monitors

Chemoreceptors are specialized sensors found in the carotid bodies and aortic bodies, small clusters of cells near those same arteries. They monitor oxygen, carbon dioxide, and pH levels in your blood. When oxygen drops or carbon dioxide rises, they alert the medulla oblongata (a region of the brainstem that controls breathing) to increase your respiratory rate and heart rate.

In dysautonomia, these receptors can become hypersensitive or sluggish, triggering shortness of breath, anxiety, or sudden heart-rate changes even when oxygen levels are normal.

Mechanoreceptors: The Stretch Sensors

These sensors are embedded in the walls of your heart’s atria (the upper chambers that collect blood) and in your pulmonary vessels (the arteries that carry blood from the heart to the lungs). They detect how full the heart is, essentially monitoring your blood volume status. When blood pools in the legs and less returns to the heart, mechanoreceptors release hormones like atrial natriuretic peptide (ANP), which signal your kidneys to adjust salt and water retention.

When this system is unstable, like in chronic low blood volume (a common feature of POTS), the signals misfire. The brain gets confused about how much fluid you have, and your cardiovascular system starts chasing its tail.

Osmoreceptors: The Fluid Regulators

Osmoreceptors live in the hypothalamus, (the small but mighty brain region that acts as your body’s thermostat and hormonal command center). These receptors track how concentrated your blood is (how much salt versus water). When your blood gets too salty or you’re dehydrated, the hypothalamus tells the pituitary gland to release antidiuretic hormone (ADH), also known as vasopressin. ADH then signals the kidneys to conserve water.

In dysautonomia, that timing can go haywire, releasing ADH too late, too little, or not at all. You end up drinking plenty of fluids, but your body doesn’t retain them efficiently, leaving you lightheaded, thirsty, and constantly running to the bathroom.

Catecholamines: The Fight-or-Flight Chemicals

Your adrenal medulla (the inner part of your adrenal glands, which sit on top of your kidneys) produces catecholamines, a class of fast-acting stress hormones and neurotransmitters that control heart rate, blood pressure, and alertness. The main ones are adrenaline (epinephrine) and norepinephrine. These chemicals activate your sympathetic nervous system, preparing your body to respond to stress by raising heart rate, tightening blood vessels, and keeping you on high alert.

In hyperadrenergic POTS, your body releases too much norepinephrine when standing, leading to tremors, rapid heartbeat, sweating, and anxiety-like surges. Over time, this constant adrenaline flood desensitizes receptors, creating bigger and more erratic swings.

Acetylcholine: The Rest-and-Digest Messenger

The vagus nerve, the longest cranial nerve, running from your brainstem to your chest and gut, uses the neurotransmitter acetylcholine to signal the parasympathetic nervous system. Its job is to slows the heart, promote digestion, and help maintain calm equilibrium.

In some autoimmune forms of dysautonomia, antibodies attack the ganglionic acetylcholine receptors, blocking the signal that normally slows the heart and supports digestion. The vagus nerve is still sending messages, but the organs on the receiving end can’t hear them clearly, and regulation breaks down. The result is an erratic heart rate, poor digestion, and difficulty regulating temperature.

Nitric Oxide: The Body’s Vascular Chill Pill

Nitric oxide (NO) is a gas produced by the endothelial cells that line your blood vessels. It relaxes smooth muscle, dilates vessels, and improves blood flow. For this reason, nitric oxide is sometimes referred to as the “vascular chill pill.”

In inflammatory conditions or mast-cell activation, excess nitric oxide leads to too much vasodilation (widening), causing blood pooling and fatigue. Too little nitric oxide, on the other hand, constricts vessels and leaves extremities icy cold.

Putting It All Together

When you combine these misfires, baroreceptors giving poor pressure data, chemoreceptors misreading oxygen, stretch sensors confused by volume, and chemical messengers overcompensating, you get left with a massive feedback loop of miscommunication.

Your brainstem interprets the noise as emergency after emergency, flooding you with adrenaline one moment and slowing you down the next. For those of us with connective-tissue disorders like EDS, this chaos is amplified by vascular walls that stretch too easily and send distorted signals to begin with.

It’s not a random malfunction, it’s a system-wide communication breakdown. Once you understand that, the symptoms start making sense.

The Dysautonomia Spectrum

Clinically, this breakdown in communication doesn’t look the same for everyone. Depending on which sensors or pathways are disrupted, dysautonomia can present as a few distinct but overlapping syndromes, each reflecting where the signal first fails.

Postural Orthostatic Tachycardia Syndrome (POTS)

When you stand up, gravity naturally pulls blood toward your legs. Normally, your blood vessels tighten to push that blood back toward your heart and brain, a reflex mediated by your sympathetic nervous system and baroreceptors.

In POTS, that tightening response is weak or delayed, so blood pools in the lower body. To keep blood flowing to the brain, the heart rate spikes by 30 or more beats per minute (sometimes well over 120).

There are three main POTS subtypes:

Hyperadrenergic POTS: driven by excessive norepinephrine release, or too much “fight-or-flight” chemistry.
Neuropathic POTS: caused by small-fiber nerve damage that impairs blood vessel constriction.
Hypovolemic POTS: related to low overall blood volume, so the body’s working with less fluid to start with.

Symptoms include lightheadedness, fatigue, “brain fog,” tremors, and heart palpitations, especially when upright for too long.

Neurocardiogenic (Vasovagal) Syncope

This is the most common cause of fainting, a sudden overreaction by the vagus nerve, which slows the heart rate and dilates blood vessels all at once. When that happens, blood pressure and heart rate both plummet, briefly cutting off blood flow to the brain.

Triggers include heat, stress, standing for long periods, or pain. Although the fainting episode looks dramatic, recovery is usually quick once the body resets.

Orthostatic Hypotension (OH)

Here, the baroreflex (the rapid feedback loop between baroreceptors and the brainstem) doesn’t kick in fast enough when you stand. Blood pressure drops by at least 20 points systolic or 10 points diastolic within three minutes of standing, causing dizziness or vision dimming.

Unlike in POTS, the heart rate doesn’t rise enough to compensate, so blood flow to the brain remains low and lightheadedness persists longer.

Small Fiber Neuropathy (SFN)

The small fibers are thin, unmyelinated nerves responsible for controlling tiny blood vessels, sweat glands, and temperature regulation. When these nerves are damaged, whether by autoimmune inflammation, diabetes, infection, or genetic causes, the fine-tuned control of circulation fails.

SFN can cause burning pain, numbness, abnormal sweating, and temperature dysregulation, and often overlaps with both POTS and orthostatic hypotension.

Autoimmune Autonomic Ganglionopathy (AAG)

A rare but severe form of dysautonomia, AAG occurs when antibodies attack the nicotinic acetylcholine receptors in the autonomic ganglia (the relay stations where autonomic nerves connect). This disrupts both sympathetic and parasympathetic signaling.

Symptoms include severe blood pressure drops, gut paralysis, inability to sweat, and unpredictable heart-rate swings. It’s rare but shows just how vulnerable this network is to immune system interference.

Secondary Dysautonomia

Dysautonomia can also appear secondary to other conditions that damage nerves or connective tissue, such as Ehlers-Danlos syndrome (EDS), Mast Cell Activation Syndrome (MCAS), Long COVID, autoimmune disorders, mitochondrial disease, and diabetes.
Each affects the same feedback loops from a different angle, through inflammation, nerve injury, or structural instability.

Note: these categories aren’t distinct, they’re coordinates on the same map. They describe which part of the feedback circuit failed first, not separate diseases.

The Connective-Tissue Connection

This part fascinated me most because understanding the science helped me make sense of what I was living. Connecting the dots between structure, signaling, and symptoms, helped me realize they were all part of the same interconnected story.

Connective tissue, that intricate web of collagen, elastin, and extracellular matrix holding everything together, isn’t just structure. It’s also a communication layer: every stretch or shift sends mechanical and biochemical cues that help nerves, vessels, and nearby cells coordinate. It anchors the endothelium (the single-cell-thick lining of every blood vessel), which senses stretch, flow, and shear stress. Through mechanotransduction, those physical forces become electrical and chemical messages that tell the nervous system what’s happening.

In Ehlers-Danlos syndrome, that connective scaffolding is too compliant. Vessels stretch excessively, endothelial cells misread the strain, and baroreceptors embedded in those walls send distorted pressure data to the brainstem. Meanwhile, mast cells (immune cells that release histamine and other inflammatory mediators) dump histamine, prostaglandins, and nitric oxide into the system, causing additional dilation and permeability.

The result? A perfect storm of mixed messages: blood pooling, fatigue, temperature swings, and that “adrenergic rollercoaster” of trying to compensate for a problem the body can’t quite measure accurately.

It’s not just bad veins, but a systems-level issue where weak scaffolding creates bad communication between sensors, signals, and structure.

Diagnosis, Management, and Living With It

Diagnosis

Because the autonomic nervous system touches nearly every organ system, dysautonomia hides behind a thousand different symptoms. Traditional medicine tends to chase each one separately, dizziness, fatigue, tachycardia, and digestive issues, instead of recognizing the common thread.

Because dysautonomia overlaps with so many systems, there isn’t a single “right” specialty for diagnosis. In most cases, neurologists (especially those focused on autonomic or peripheral nerve disorders) and cardiologists (often electrophysiologists familiar with POTS and orthostatic intolerance) are the main specialists who handle evaluation and management.

Some patients also work with rheumatologists or geneticists when connective-tissue conditions like Ehlers-Danlos syndrome are involved, or with immunologists if autoimmune or mast-cell activation is suspected.

Primary-care clinicians can start the process by ordering basic labs and referrals, but finding a provider experienced in autonomic testing is key. Many large hospitals and academic centers have dedicated autonomic or dysautonomia clinics (which tend to provide the most comprehensive, coordinated care).

Diagnosis often comes through a combination of:

Tilt-table testing: to observe heart-rate and blood-pressure response to upright posture.
Heart-rate variability (HRV) analysis: to measure balance between sympathetic and parasympathetic tone.
QSART (Quantitative Sudomotor Axon Reflex Test): to test nerve control of sweating.
Skin biopsy: to count small-fiber nerve density.

For many patients, the true relief comes not from the numbers but from validation: finally having a framework that explains why the body keeps glitching.

Management

Once you understand the feedback loops, the treatment strategies stop feeling random and start to make sense.

Fluids and Salt: Expanding plasma volume helps baroreceptors read pressure accurately. Electrolyte supplements (like LMNT, Ultima, or Liquid I.V.) help to replace what’s lost through high output or poor retention. Note: If you can't tolerate the liquid versions, or want something a little more conveninet, I've been liking SaltStick tablets.
Compression garments: External pressure supports blood return to the heart, effectively “stabilizing” the mechanical signal for the baroreceptors. There are tons of options for compression garments, but just starting with a good pair of compression socks will go a long way.
Targeted exercise: Recumbent biking, rowing, or swimming retrains the baroreflex and strengthens vascular tone without the orthostatic stress of upright exercise.
Medications: (REMINDER: always consult with your Dr. when considering new meds)
- Fludrocortisone increases fluid retention.
- Midodrine tightens blood vessels.
- Beta-blockers reduce tachycardia.
- Pyridostigmine enhances parasympathetic signaling.

Each of these acts on a specific node in the feedback circuit, mechanical, chemical, or neurological.

Emerging Therapies

A 2025 PubMed clinical trial reported that transcutaneous vagus nerve stimulation (tVNS), a noninvasive form of electrical stimulation applied to the outer ear, improved cardiovagal tone and reduced symptoms in people with hyperadrenergic POTS after two weeks of daily sessions. While still early, these findings suggest that modulating the vagus nerve directly may help restore balance between the sympathetic and parasympathetic systems.

Living With It

Living with dysautonomia means becoming your own systems analyst. You start noticing how hydration, hormones, temperature, and stress shift your symptoms. You learn pacing, not as a weakness, but as a method of preventing sensory overload on an already strained network.

For me, mobility and weight training, hydration discipline, and a healthy respect for compression socks keep me functional most days. But just as important, is knowing why these things help! Every salt packet, slow exhale, or recovery day is part of stabilizing a feedback loop that my body struggles to maintain on its own.

Understanding the mechanics unfortunately doesn’t cure it, but it gives me a way to work with my body instead of constantly fighting it.

Reflection

A 2025 NIH-backed quality-of-life study confirmed what patients have been yelling from the rooftops: EDS and POTS symptoms don’t stop at the physical. They affect every layer of daily life, from psychological, to social, and emotional, demanding multidisciplinary care that reflects that complexity.

I’m slowly making peace with the fact that my body runs on a glitchy operating system. The signals get crossed, the wiring misfires, and sometimes gravity wins. But learning the physiology behind it is giving me leverage by turning guesswork into strategy. I'm starting to understand when to push and when to rest, and ultimately learning to stop blaming myself for what’s built into the code.

The science helped strip away the mystery. I know what my baroreceptors are doing, why my heart races, why the floor tilts when I stand too fast. And that knowledge, that ability to name what’s happening instead of fearing it, gives its own kind of control.

If your body’s running its own unpredictable experiment, I get it. It’s not fair, it’s not simple, and it’s not going to magically fix itself, but knowledge gives you a fighting chance. You can read the signals, make the adjustments, and survive the chaos on your own terms.

TL;DR Summary

The autonomic nervous system (ANS) is the body’s command network for everything that happens automatically, heart rate, blood pressure, temperature, digestion, and more. It’s the autopilot that keeps your body running...until it doesn’t. When its sensors or signaling pathways misfire, the result is dysautonomia, a family of disorders (like POTS, orthostatic hypotension, and neurocardiogenic syncope) that all stem from faulty communication between the brain, nerves, and blood vessels.

The causes vary: some forms are autoimmune, some stem from nerve damage or infections, and others, like those tied to Ehlers-Danlos syndrome, come from weak connective tissue that throws off the body’s pressure and feedback systems. Diagnosis relies on connecting patterns across tests like the tilt-table, heart-rate variability, or sweat-gland function, not just isolated symptoms.

Management means supporting what’s failing: fluids and salt to expand blood volume, compression to improve circulation, pacing and gentle exercise to retrain the system, and medications to stabilize signals when needed.

Dysautonomia isn’t rare, mysterious, or random. It’s the body’s control center glitching under faulty wiring. Learn its signals, understand its rules, and you can start working with your physiology instead of against it. That’s not surrender. That’s strategy.

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Jaime Prout