You might be treating the wrong panic.
Not all panic attacks come from fear. Some come from your lungs, your bloodstream, your nervous system. If you mistake one for the other, you could end up in therapy for a problem that actually lives in your body.
This piece breaks down the difference — and why it matters.
Why Not All Panic Attacks Are the Same
When it comes to panic attacks, there are essentially two distinct types. Unfortunately, many doctors and psychologists fail to bring this up. As a result, patients are often left completely unaware of whether they’re suffering from conditioned panic attacks or biochemical ones. And that’s not just unfortunate or a linguistic blunder. It’s a real problem. A big one, since the treatment and the prognosis differ dramatically depending on which type you’re dealing with.
At the heart of it, the difference between a conditioned panic attack and a biochemical one comes down to a single question: What sets the whole thing off?
Skipping the full complexity—where biology, psychology, and lived experience intertwine—a biochemical panic attack, sometimes referred to in the literature as a spontaneous panic attack, is almost always triggered by one of three processes: chronic hyperventilation, gastroesophageal reflux disease, or an elevated baseline level of stress. A conditioned panic attack, on the other hand, is by definition triggered by classical conditioning, specifically interoceptive conditioning.
The Chemistry of Fear: When Panic Starts in the Body
To make sense of this tongue-twisting lingo, let’s break it down—starting with the biochemical type.
Imagine Sara. She’s been living for some time now under what most people in the modern world would consider a ‘normal’ stress level. Not excessive. Not trivial. Just… everyday life. She’s juggling classes, seeing friends, enjoying a drink from time to time, picking up shifts on the side, and commuting. Nothing out of the ordinary, at least not on the surface.
But what neither we nor Sara, for that matter, are aware of is what’s going on inside her autonomous mind and sympathetic nervous system while she’s spinning inside the gears of modern life. Down in the trenches, among receptors, hormones, and neurons, where her consciousness lacks authority, strange things are unfolding.
Due to a common genetic variation found in the COMT gene, which influences how efficiently stress-related neurotransmitters are broken down, Sara’s autonomous mind has slowly begun to interpret her daily responsibilities as physical threats—something that calls for action. And without revealing itself, bit by bit, her breathing adjusts—subtly, persistently—as if preparing for a physical challenge that never comes.
In other words, due to subtle differences in how her stress system metabolizes stimulation, her autonomous mind is more prone than others to assume that she requires a good deal of muscular effort to get through daily life, when in fact she doesn’t. Hanging out with friends or acing an exam seldom requires physical strength. Still, her mind interprets the situation otherwise, and since hard-working muscles require a steady supply of oxygen to operate sufficiently, her brain responds by slightly increasing her breathing rate. Not in a way she’s consciously aware of, but subtly—so subtly that hardly anyone would notice. And yet, it happens. Gradually. Over weeks, sometimes months, even years. And the longer she remains immersed in the ongoing pulse of modern stress, the more her breathing begins to shift. This phenomenon, often referred to as chronic hyperventilation or overbreathing, stems from the brain’s ambition to stay one step ahead of us, as well as its deeply rooted assumption that physical effort is required to meet any kind of demanding situation—even if it’s just an exam, a party, deadlines, relocating to a new city, or even emotional relationships. In response, it simply increases our respiratory rate to prepare our bodies for action.
This shift in breathing frequency is usually not a problem. The human body is designed to adjust its breathing constantly depending on the situation. The problem arises when our subtle overbreathing continues, unchallenged, or without proper recovery, for weeks, months, or even longer. Especially if we don’t use our body much. Which, like most people in Western society, Sara doesn’t. At least not in a way that matches her breathing.
So, what does interpretation of the modern way of living, and overbreathing have to do with panic attacks?
Well, every time Sara takes an unnecessarily deep or quick breath, she’s not just breathing in more oxygen than she needs—she’s also breathing out more carbon dioxide than her body can afford to lose. Whether she likes it or not, her lungs will remove carbon dioxide from her blood every time she exhales. And while this might not seem like a big deal at first glance, it’s precisely in this very process that everything begins to unravel. With each excessive breath she takes, the balance slowly begins to tip, and over time, after thousands of excessive breaths, her body is likely to settle into a state of chronically low carbon dioxide levels. A state referred to as hypocapnia.
Unfortunately, hypocapnia isn’t merely a drop in CO₂—it marks the beginning of something deeper. A hidden shift. A biochemical disturbance few would ever imagine. Since carbon dioxide plays a pivotal role in buffering hydrogen ions in the blood, a sustained drop in CO₂ will inevitably destabilize the blood by reducing the amount of free hydrogen ions swimming around in the bloodstream. To a certain degree, hydrogen ions can be thought of as the bloodstream’s tire pressure—rarely noticed when things are working, but absolutely essential for a smooth ride. When the pressure is just right, every system rolls in balance. But when these ions start to vanish, the alignment falters. The grip weakens. And soon, the whole vehicle feels unstable, veering off course without warning.
Here is how it works, as our lungs drain the bloodstream of CO₂, due to chronic hyperventilation, our precious hydrogen ions are forced to part with their closest companion—reluctantly pulled away from carbon dioxide, they fall back into old alliances, bonding with bicarbonate, proteins, and phosphate buffers that barely safeguard their freedom—a chemical process that ultimately sends the pH level through the roof and leaves the blood overly alkaline.
Without digging deeper, the pH scale might sound abstract or overly technical—but it’s actually quite simple: it is developed to measure hydrogen concentration, or in layman’s terms, how many hydrogen ions are present in a substance—in this case, the blood. That said, the scale can feel counterintuitive at first, since it’s upside down: the more hydrogen ions, the lower the pH level is—a state referred to as acidic; and the fewer hydrogen ions, the higher the pH level—indicating alkalinity.
Consequently, as Sara continues to overbreathe day after day, her body flushes out more CO₂ than it can afford. With it, free hydrogen ions begin to vanish, setting the stage for a gradual yet relentless rise in pH—subtle at first, then sharp—triggering a cascade of chemical reactions throughout the body, including disruption to one of our most vital proteins: hemoglobin.
Under normal conditions, when oxygen and carbon dioxide levels are in balance, hemoglobin works like a delivery truck, cruising through the bloodstream and releasing oxygen molecules to organs and tissues along the way. Like an old-fashioned ice cream truck rolling through a sunny neighborhood, it slows at every corner, handing out ice cream to children who’ve been waiting for a cold popsicle or a vanilla cone. But when carbon dioxide levels drop, and hydrogen ions get tied up like prisoners, hemoglobin undergoes a subtle structural shift and turns stingy. Simply put, it holds onto the oxygen. Tight. Even though the truck is full of it, it refuses to stop at every intersection and doesn’t care if some children leave empty-handed. As a result, cells throughout the body, especially in the brain, heart, and muscles, begin to experience a kind of silent suffocation, starved of the very oxygen they depend on to function properly. This phenomenon is often referred to as respiratory alkalosis.
But that’s not all.
At the same time as hemoglobin is clinging to its oxygen cargo, tighter and tighter, depriving cells and tissues of what they need, central chemoreceptors in the brainstem begin to react to the rising pH level in the blood. And this is where things truly begin to escalate. To Sara’s nervous system, a dwindling amount of hydrogen ions in her blood isn’t just a minor glitch. It’s a full-scale breach. A chemical emergency! Her blood has become alkaline. And that’s exactly what the chemoreceptors react to. Like tiny smoke alarms, they start screaming the moment they detect that something isn’t quite right. Danger! Danger! Imbalance. The fragile equilibrium between oxygen and carbon dioxide has been disrupted. And sadly, this specific condition is more often than not misinterpreted as a real oxygen deprivation, a state referred to as hypoxia—even when oxygen levels are perfectly fine, at least in the bloodstream.
And here comes the kicker. In order to attain the alleged emergency, the brain does the only thing it knows how to do: it flips the switch on the sympathetic nervous system, forcing the lungs to breathe even faster and the heart to step it up a notch. The brain, despite all its sophistication, is surprisingly dogmatic when it comes to oxygen deprivation. Faster breathing and stronger circulation—that’s the protocol for survival. No nuance. No second guessing. Just go.
But for Sara, this reaction doesn’t solve anything. In fact, it makes the whole situation worse. She doesn’t need additional oxygen, even if the brain believes otherwise—quite the opposite. Her blood is already saturated with it. And since she is not moving her body intensely and converting large amounts of oxygen into CO₂, the faster she breathes, the more carbon dioxide she loses, and the deeper the imbalance between oxygen and carbon dioxide becomes. In turn, and somewhat ironically, the surge in her sympathetic nervous system thus exacerbates the already impaired oxygen supply to her organs and tissues, rather than improving it. Meanwhile, the alarm, reacting to rising pH levels in the blood, grows louder and louder.
And it’s exactly here, in this very spiral, the accelerating loop—a panic attack is born. A moment of biochemical ignition. Simply put, once the lungs and heart have kicked into overdrive and begin to reinforce themselves like a closed circuit—through increased exhalation, rising pH levels, a stronger alarm signal, and an even greater sympathetic surge—there is no point of return. No simple off switch. Just a body going in with a bang.
Most people, as they experience this kind of pseudo-suffocation—heart palpitations and air hunger—react like any normal person would: they panic. Of course, there is no room to react in any other way. It’s almost impossible to interpret suffocation or heart palpitations as anything but catastrophic. Still, this reaction, however human it may be, only fuels the very process we are trying to escape. Like pouring gasoline on the fire, fear amplifies everything—the alarms, the signals, the rush—until the sympathetic system spins out of control. Hence, in a cruel twist, the brain—still following its one-size-fits-all solution—orders the body to push harder, the heart to pump faster and the lungs to work overtime.
It’s sometimes useful to think of a panic attack as two loops feeding into each other. One is physical—set in motion by a hidden deficit of carbon dioxide in the blood and a rising pH level. The other is mental—fueled by catastrophic interpretations about what those bodily sensations might mean. Together, they spin faster and faster, until panic takes full control.
Once Sara is swept into this double-edged storm, spinning faster and faster, a cascade of additional symptoms and sensations often begins to emerge—beyond air hunger and a racing heart—such as tingling in the fingers, numbness, chest pain, sweating, tunnel vision, nausea, and, of course, a barrage of terrifying thoughts, such as: “This is it, I’m dying or It’s over.”
From the outside, and even from the inside, it feels like a panic attack comes out of nowhere, as if it rolls in over us—suddenly, violently, without warning. Still, the truth is that a biochemical panic attack is often months, maybe years, in the making. A slow molecular build-up, a series of imperceptible shifts taking place long before the full-blown escalation makes itself known. Which means there is hope. There is time to intervene, to prevent future biochemical panic attacks—if we know where to look.
It’s not a map, but here is some insight: in broad terms, biochemical panic attacks tend to bloom and multiply in certain environments—such as during prolonged stress, fast-paced lifestyles, emotionally overwhelming settings, or demanding periods in life. They often emerge before major job interviews, during finals week, amid breakups, extensive medical examinations, relocations, or long stretches of poor sleep and overwork. In worst-case scenarios, they may strike several times a day, especially when stress levels are high. This pattern often differs from conditioned panic attacks, which tend to occur regardless of stress levels and almost always in connection with a specific stimulus, location, or behavior.
Unfortunately, regardless of what kind of panic attack we’re talking about, repeated episodes almost always present a challenge for both patients and clinicians. In fact: patients who report frequent episodes are often misdiagnosed with panic disorder—with or without agoraphobia—even when their attacks are biochemical in nature rather than conditioned, and therefore don’t meet the diagnostic criteria.
As a result, patients who report recurring episodes are often referred to a psychologist for cognitive restructuring and exposure therapy, even if they suffer from biochemical attacks rather than conditioned episodes—a treatment modality likely to prove ineffective, failing to address the root cause and potentially even backfiring. Since your brain, more precisely, your chemoreceptors, truly believes the body is suffocating, it’s nearly impossible to stay calm during a sudden spike in the blood’s pH levels. Hence, even with repeated exposure to rapid breathing or a pounding heart, the reaction may still strike hard. Your brain is simply hardwired, through its chemoreceptors, to treat it as suffocation, thus a real threat. And that response isn’t easily reasoned with. Suffocation isn’t just unpleasant. It’s primal. It’s immediate. It bypasses logic. It’s wired into our survival. That’s why exposing oneself to a biochemical panic attack is incredibly difficult and hardly ever effective, at least not from a therapeutic perspective.
That said, elite naval units within the military often train with specialized exercises to teach the body to remain calm under extreme conditions. But this kind of training goes far beyond what modern psychological exposure therapy typically offers. Exposure within the framework of psychotherapy and panic disorder primarily targets the internal triggers—like a racing heart or a perceived shortness of breath—that set off catastrophic thoughts and fear. In contrast, elite military units often operate far beyond this threshold, deliberately confronting real and immediate physical danger in order to train the body to remain composed under extreme physiological stress.
Why the Wrong Treatment Fails
In short: using CBT and exposure therapy to treat biochemical panic attacks is like removing the batteries from a smoke alarm. The alarm may stop screaming, but the fire is still burning. And sooner or later, the system will respond again—louder, more violently, and with even less warning. Biochemical panic isn’t driven by irrational thoughts or conditioned fear. It’s driven by a real, measurable physiological imbalance—often involving carbon dioxide, pH levels, and brainstem chemoreceptors. Exposure therapy for biochemical panic attacks thus risks habituating the patient to an unhealthy state, which in a worst-case scenario may result in a dangerous feedback loop of hyperventilation and alkalosis, triggering physical symptoms such as dizziness, muscle spasms, and fainting, while reinforcing panic and anxiety.
So, unless you’re enrolled in an elite military unit and receive specialized training, I don’t recommend exposure as a way out of biochemical attacks. Moreover, it’s nearly impossible to talk your way out of suffocation, reframe insufficient CO₂ levels, or trick your brainstem into calm. What’s needed isn’t desensitization to imagined threats, but restoring balance to the system that sets the fire in motion in the first place.
Consequently, a successful treatment for biochemical panic doesn’t begin with exposure—it begins with prevention. With addressing the root cause: the subtle but chronic increase in breathing rate. The slow, creeping hyperventilation that has been unfolding for months. That’s where recovery starts. The path forward usually includes breathing exercises, progressive muscle relaxation, stress reduction, sleep management, planned recovery, physical training, and fewer demands. Many up-to-date treatment approaches now also incorporate techniques such as Capnometry-Assisted Respiratory Training or combine biofeedback with emotion regulation strategies—specifically designed to help patients overcome recurring biochemical panic.
Beyond overbreathing and chronic hyperventilation, biochemical panic attacks may also build up and ignite through several other mechanisms, such as gastroesophageal reflux disease or a chronically elevated baseline level of stress. In these cases, the underlying processes differ somewhat from chronic hyperventilation. Still, over time—without diving into the intricate mechanisms—these conditions tend to generate strange and frightening bodily sensations, such as a sudden sense of breathlessness or a racing heart, which may, in turn, trigger a downward spiral and ultimately a full-blown panic attack. However, these conditions require a completely different approach than the treatment mentioned above. Take reflux, for example. The treatment doesn’t focus on the sensation of breathlessness itself, but rather on the underlying condition causing it. As such, the intervention consists of lifestyle changes—like avoiding large meals late at night, cutting down on caffeine, alcohol, and spicy foods, or elevating the head of the bed. In some cases, acid-suppressing medications like proton pump inhibitors are prescribed.
The point is this: it’s not the chest tightness or racing heart that needs to be treated directly, but the irritation in the esophagus that caused them. Only when the root issue is addressed will those misleading emergency signals begin to fade. The same is true for chronic stress. Here, the solution isn’t to restructure individual thoughts during a panic attack. It’s to lower the baseline pressure in the system through rest, proper sleep, relationships and routines that support recovery. The goal isn’t to outthink the panic—it’s to slowly calm the storm that makes panic possible in the first place.
Think of biochemical panic attacks as headaches. The headache, or the pounding sensation itself isn’t the real issue—it’s just a signal. Sometimes it’s caused by dehydration, sometimes by too much caffeine or too little sleep. Either way, the solution isn’t to numb the pain alone but to find out why it started in the first place. Biochemical panic attacks follow the same logic. They often emerge from a behavioral pattern—like chronic overbreathing, poor sleep, or unresolved physical stress. That’s why the most effective approach isn’t aimed at the panic itself, but at the hidden habits that fuel it.
Sleeping Memories: How Panic Gets Attached
Unlike biochemical panic attacks, a conditioned panic attack is triggered by classical conditioning, a phenomenon that almost always renders a profound fear and avoidance. Conditioned panic attacks are thus sustained over time through a combination of classical and operant conditioning. In psychology, we sometimes refer to this duo as avoidance learning. In short, avoidance learning describes a process in which an individual comes to associate certain internal sensations or external situations with danger, and subsequently avoids them in order to prevent another episode. However, while avoidance—or any other strategy aimed at dampening fear—may offer immediate relief, strategies like these also reinforce the connection between the perceived threat and fear, thus laying the groundwork for long-lasting and persistent problems that may endure for years.
In other words, due to classical conditioning, an internal sensation, a physical process within the body, or an external environment—such as a train car—can suddenly become associated with danger. The body and brain simply keep the score by remembering past trauma—not through words or conscious memory, but by attaching fear to specific bodily states or environmental cues following a severe incident, such as a panic attack.
Let me illustrate what I mean.
Imagine John, picking berries in a forest. He’s walking through a quiet, leafy woodland, eyes scanning the moss and underbrush. And then, out of nowhere, it happens. Something he never could have prepared for.
Silently, a thick, grey-striped snake slithers just beneath the cloudberry plants, barely visible to the naked eye. John, still fixed on a small clump of berries farther out on the marsh, unaware of the coiling creature in front of him, walks on. And then, in the blink of an eye, everything unfolds. He brings his foot down, like any other step—but right across the snake’s body.
Startled and terrified, the snake lashes out and sinks its fangs into the man above him, right through the garment, and deep into the flesh. John, even more frightened than the snake itself, lets out a scream and instinctively bolts for help. Within moments, there’s no doubt: he’s been bitten. Possibly by a venomous species. And even though he knows you’re not supposed to run when there’s venom in your bloodstream, he sprints back to the car, jumps behind the wheel, and barrels down the narrow gravel roads toward the emergency room. His body is in overdrive. Cold sweat runs down his neck, and dizziness drapes the world around him. Meanwhile, his breathing turns shallow—and then, complete exhaustion.
Half an hour later, the emergency room rises in front of him. But everything is a mess, a whirlwind—flashing lights, quick hands, fragments of sentences. Most of it slips past him like a dream he can’t hold onto. It isn’t until several hours later, when John wakes up in a hospital bed on the twelfth floor, that he finally feels calm and collected again. Fortunately, everything has gone well. The doctors were quick. They administered adrenaline and antivenom.
As his vision slowly sharpens, he becomes aware of a young nurse with freckles and curly blonde hair standing in front of him. For a moment, she quickly jots down a few notes before stepping closer, placing a warm hand firmly on his shoulder. “You’re okay. You’re awake now. You made it through.” Her voice is soft but steady, filled with reassurance. There is no doubt in her tone.
What the nurse doesn’t mention though—and probably doesn’t know—is that something else happened that day. Something far deeper.
John wasn’t just poisoned by a snake; he also developed a classically conditioned response, tucked away inside his non-declarative memory system—those deep, silent layers of memory that live far below conscious thought. And even if he never thinks about the snake again, the imprint remains. Sometimes dormant. Sometimes buried for decades. Until one day, the system gets triggered—and everything comes flooding back.
And that’s exactly what happens the following summer.
Nearly a year after the bite, John returns to the same woods, bucket in hand, ready to pick cloudberries again. But something strange happens the moment he leaves the main road and turns onto a winding forest track. A cold discomfort begins to grow in his chest. Something feels… off. The woods feel different this time. Haunted. Hostile. Dangerous in a way it never felt before.
Despite the strange feeling in his body, he parks the car on an old timber lot and walks towards the edge of the forest. Once in position, just a few meters from the nearest birch, he cautiously examines the underbrush with his right foot, brushing against the twigs as though something might lurch out from beneath the scattered lingonberries. But no matter how he tries, he can’t bring himself to take another step. It doesn’t feel right—and within seconds, anxiety closes in from within, silent and merciless, like something that’s always been there, waiting. A cold, creeping sensation. At the same time, thoughts surge up from nowhere—thoughts of snakes, and the venom they carry, swirling through his mind.
Almost frozen, he stands there—watching the birch in front of him, the red lingonberries, while the sound of a distant woodpecker echoes through the forest. For nearly ten minutes, he weighs his options, rising and falling like a surfer waiting for a wave that never comes. And then, he gives in. He can’t do it. The empty bucket goes back in the trunk, and he drives home. Blank. Confused.
It’s not until he hits the highway and the trees give way to golden fields that the fear finally releases its grip. As if he’d just slipped past death itself, he exhales—slowly. The tension in his chest fades, and a sense of calm returns.
This is classical conditioning at work.
In John’s case, the mixed forest, the gravel road, and the underbrush became conditioned with fear and catastrophic thoughts the moment the fangs sank into his flesh. As a result of this dormant memory, the moment he returns to the place where the original trauma occurred—or any similar environment—his emotions and thoughts respond in ways they never have before. The whole place has become charged. Suddenly, it holds fear, strange physical sensations, and a flood of catastrophic thoughts. Even though John never felt anxious in these surroundings before—now he does.
Classical conditioning can be compared to an invisible layer that clings to certain parts of reality. And when we come into contact with a layer—whether it’s a place, a smell, or a bodily sensation—something stirs inside us. Fear. Anxiety. Even darkness. And that’s exactly how a conditioned panic attack works. While we’re going through our very first attack—which is always a biochemical panic attack—a classical condition is unfortunately sometimes formed. Our pounding heart, the rapid breathing, the air hunger, the tingling sensation in our fingers, the sense of losing control, the chest pain, the sweat pouring from the body, and the tunnel vision… it all becomes so terrifying, so overwhelming, that the brain has no other option, but to respond by encoding it and learn from it. And that’s where a classically conditioned response is born—like a young tiger cub taking its first steps away from its mother: fragile and full of wonder, yet destined to grow into a fierce predator—one that hunts and strikes without mercy.
In other words, parts of the experience during our very first panic attack become fused with fear. Just like in John’s case, where the gravel road, the forest and the underbrush became associated with fear following the snakebite, a panic attack tends to condition sensations like a racing heart or heavy breathing with anxiety, fear, and catastrophic thoughts. This means that the next time your heart rate rises—whether from walking uphill, drinking coffee, or running—your brain may mistakenly interpret it as a sign of danger. Hence, it responds in the only way it knows how: by flipping the switch on the sympathetic nervous system, pushing the heart even harder, speeding up the breath, and tightening the chest. And just like a self-fulfilling prophecy, you’re spiraling again—right into another panic attack.
But there’s more to this story. A conditioned panic attack often involves a growing fear of experiencing certain internal sensations, even before they’ve appeared, such as a pounding heart, strained breathing, or even completely unrelated bodily cues. And before we know it, we begin to cut out parts of our life—places to go, things to do, experiences once taken for granted. In an attempt to stay one step ahead of our fear and act before it has a chance to settle in, most people start to pull back from everyday life. They stop jogging, playing football, drinking coffee or alcohol, going to the gym, or eating spicy food. In some cases, a classically conditioned fear may spread outward and attaches itself to specific places such as buildings, restaurants, trains, buses, hair salons, and so on. Locations that never used to trigger any negative sensations, physical reactions or catastrophic thoughts, suddenly feel ominous. Threatening.
In cases like this, lifestyle changes alone, like better sleep, reduced stress, or social support, rarely resolve the problem. The treatment can’t just scratch the surface. It has to dig deep—down to the root, where the real damage lives.
Hence, a solid starting point to handle conditioned panic attacks is psychoeducation—gaining a clear understanding of what a panic attack truly is. From there, cognitive strategies come into play: developing the ability to identify, challenge, and reframe the catastrophic thoughts that keep the cycle alive. And finally, the focus shifts to exposure: deliberately and gradually facing the situations, sensations, or emotions that tend to trigger panic.
That said, lifestyle interventions, breathing techniques, and relaxation exercises can still play a supporting role. But the heart of the treatment must focus on breaking the conditioned response. Because that fear, once unhooked from its trigger, is fully reversible—for most people—through evidence-based cognitive behavioral therapy (CBT).
Safety Behaviors, Quick Fixes — and Their Hidden Costs
Unfortunately, in the face of conditioned panic, people rarely search for truth—or for what actually works according to peer-reviewed science. They search for control. A shortcut. A quick fix. Desperate and disoriented, they grasp at anything: breathing apps, tapping sequences, vagus nerve massages, cold plunges, hypnosis, essential oils, craniosacral therapy, somatic shaking, magnetic bracelets, sound bowls—anything that promises immediate relief. And the internet obliges. Unconditionally. Platforms like YouTube and TikTok are overflowing with advice, delivered by influencers, doctors, and self-proclaimed experts. Even surgeons are chiming in.
What they rarely mention, though, often lacking even the most basic psychological training and speaking instead from the operating room or a wellness podcast, is the uncomfortable truth: avoidance is never neutral. It’s fuel. It’s going to cost you. The body keeps the score. Every time we dodge conditioned fear intentionally, we teach our nervous system that our conditioned response was right all along. Sounding the alarm as a reaction to strong heartbeats or sweaty palms is thus the appropriate action.
Desperate tricks, such as tapping your chest in a special way, taking deep or slow breaths, repeating affirmations, holding ice to your wrist, plunging your face into cold water, may seem harmless and even helpful in the moment. But over time, safety behaviors like these often worsen the condition. The fear tightens its grip. The chain linking together our heart with fear grows stronger. The panic becomes more entrenched. And the road to recovery becomes longer and longer.
However, it’s worth noting that this dilemma doesn’t apply to biochemical attacks to the same extent. In these cases, specific behavioral strategies—such as controlled breathing, grounding, or movement, may, in some cases, successfully prevent the panic from spiraling further without leaving a substantial debt.
Still, if you, or someone you care about, aren’t quite sure whether you’re dealing with conditioned or biochemical attacks, it’s worth asking: What kind of panic is this? The answer could change everything.
Navigating like a pro
A skilled clinical psychologist with extensive experience diagnosing panic disorder is likely to distinguish, at least conceptually, between biochemical and conditioned panic attacks—even if those terms are not explicitly used. In practice, structured interviews and diagnostic criteria found in tools like DSM-5 and MINI implicitly support this distinction through various questions.
For example, according to the DSM-5, a diagnosis of panic disorder requires not only recurrent, unexpected panic attacks, but also at least one month of persistent worry about additional attacks or maladaptive changes in behavior aimed at avoiding them. These two follow-up criteria are essential in separating isolated or purely physiological (biochemical) panic attacks from cases where the patient has developed anticipatory anxiety and behavioral avoidance—hallmarks of conditioned panic.
Hence, when a trained clinician conducts an assessment using MINI or similar tools, two questions are pivotal:
- Are your panic attacks recurrent and unexpected (not tied to a specific trigger or situation)?
- Have you developed significant worry about additional attacks, or begun to change your behavior in order to avoid anything you were previously involved in or consumed—such as exercise, certain foods or beverages, specific locations, or social situations?
If the answer to both of these questions is yes—and especially if you don’t report major life stressors, exhaustion, or other clear contributing factors over the past six months—then the pattern most likely reflects a conditioned panic disorder rather than panic attacks stemming from acute biochemical or situational causes.
A skilled clinician, however, won’t stop there. If you report frequent but seemingly “unprovoked” panic attacks, they’ll start digging—gently but precisely. They may ask about your breathing habits, posture, speaking patterns, and daily energy levels. They’ll listen for subtle signs of chronic overbreathing: frequent sighs, breath-holding, or a tendency to gasp or yawn excessively. They might even observe how you breathe while talking or sitting still. Why? Because chronic hyperventilation is often invisible to the patient—but not to a trained eye. In fact, some specialists go even further—using capnometry to measure carbon dioxide levels in real time during rest, conversation, or controlled breathing tasks. With a nasal cannula connected to a small sensor, capnometric analysis allows the clinician to observe patterns of chronic hypocapnia (low end-tidal CO₂), which is a hallmark of dysfunctional breathing. Though capnometry is more commonly used in respiratory clinics or during capnometry-assisted therapy, its diagnostic potential is remarkable.
For patients reporting recurrent panic attacks, a persistently low CO₂ level, even at rest, can be an objective marker that the issue is primarily biochemical, driven by chronic overbreathing or respiratory dysregulation. This is especially important when the clinical picture is ambiguous. A well-calibrated capnometer provides not only CO₂ readings but also respiratory rate and waveform data, enabling the clinician to distinguish between breathlessness caused by fear, poor biomechanics, or actual metabolic instability. While capnometry is rarely used in routine psychological assessments, in the hands of a trained specialist, it can provide critical clues—offering a level of physiological precision that no questionnaire can match.
On the other hand, if you describe burning sensations in the chest, frequent throat clearing, coughing, bloating, or a sour taste in the mouth, a skilled psychologist may suspect silent reflux or GERD, another common but overlooked cause of biochemical panic. In such cases, panic isn’t “irrational” at all—it’s your body sounding the alarm in response to real physiological distress. This is why identifying the true nature of your attacks is absolutely paramount: it determines whether you need cognitive restructuring and exposure therapy, or rather physiological restoration and medical guidance.
