The Gasping Syndrome

By Dr. Bastian M.D.

A few times a year, distressed patients present from their internists or pulmonologists to see if I can explain their shortness of breath. The patient has already undergone numerous tests: e.g. chest x-ray, pulmonary function tests, EKG, stress test, echocardiogram, CT, blood tests, and even bronchoscopy. Everything has come back normal, or anything even slightly abnormal (the reader can fill in the blank) has been treated maximally without any reduction of the patient’s symptoms.

In short, the patient has complied with every test and treatment recommendation; yet there is still no apparent explanation for this difficulty breathing, and no relief provided by numerous treatment trials.

The patient seems weary of the problem. My “antennae” do not pick up any signals of la belle indifference (a peculiar lack of concern about symptoms that when present suggests that the problem may be non-organic). She tells me that her breathing is never noisy, and that her shortness of breath may or may not be associated with exercise. I apply my subjective but extremely useful “flow-volume loop” by asking her to exhale to “empty” and then rapidly breathe in until completely full, and there is no unusual noise, and no prolongation of the time required to fill.

My initial thought in this scenario? The gasping syndromeWhat is that? A recognizable but to my knowledge previously undescribed disorderHere is my composite description, meaning that individual patients may not fit every element of what follows:

  1. Either with exertion or at rest, the patient has an abrupt* sense of “smothering,” or air hunger. It happens almost from one second to the next. Like the abrupt shooting pain of neuralgia, the abrupt tickle of sensory neuropathic cough / throat clearing, or the abrupt laryngeal closure of laryngospasm. The patient says she can be engrossed in a movie or a book strolling with the dog when suddenly her consciousness is invaded by a need to “get more air.”
  2. She responds by taking a deep breath, but there is no relief and the sensation remains. So, she takes a series of deep breaths, all of them to no avail. The feeling is oppressive, anxiety-provoking, gaspingThis sensation may last for a few seconds, to several hours.* Unfortunately, it can happen again some time later, or maybe just a time or two per day or even per week.

Having seen many people who fit the gasping syndrome across the decades, though not usually more than a handful per year, I have speculated that this is a sensory disturbance. After all, I ponder, if it represents more than a primary neuropathic sensation, why is oxygen saturation measured by oximetry, including during exercise, always normal? Why are all the tests of heart and lung function normal? Why no mitral valve prolapse, or something to explain this? Why nothing on imaging? Why no noisy breathing?

My mind goes to patients who describe a similar sensation at the moment IV contrast is injected for a CT scan. In addition to “warmth,” “a sensation of needing to urinate,” etc., they can have a sensation of abrupt, quite compelling, and thankfully transient smothering.  Or to someone I know who in the middle of an IV infusion of a biologic modifier for cancer, (with prior warning) experienced profound air hunger that started abruptly and was completely gone 20 seconds later. In each of these cases, it seems like a primary sensory phenomenon more than an alerting and protective sensation in response to low oxygen or high carbon dioxide levels.

How would one conceptualize a mechanism? Here is one thought experiment: consider that we are all supplied with pulmonary stretch receptors. They send messages “in the background” several times across the day and night to the respiratory center: Excuse me… Take a deep breath; expand those alveoli; your surfactant is giving you some atelectasis. And so, without being aware of it, we sigh now and then. We roll over in our sleep, mutter, grind our teeth, and take a deep breath. While reading a book we subconsciously shift in our seat and inspire deeply as we turn a page. Again, we are unaware of this, but an observer watching us read or, equipped with night vision goggles and watching us sleep, will see it.

What if the pulmonary stretch receptors send a signal Hey! Time to take a deep breath! and despite our taking a deeper breath outside of conscious awareness, the respiratory center does not receive the return communication, Action completed. Even with normal O2 and CO2 levels, if the brain thinks that deep breath did not happen, would it not intrude on conscious thought to re-command more urgently: Hey! Deep breath please!

Where does one go to help the patient with this thought experiment diagnosis? Just give her this explanation and leave it there? Or, maybe punt back to the primary care or pulmonary or cardiology physician…? But what if the person has already seen 3 of each specialty—one who is local, another at a nearby university center, and a third at a national referral center? What if “every conceivable test” has already been done 3 times?

A follow-on thought experiment: to the patient, and via a summary letter to her doctors, explain the concept of dysesthesia or sensory disturbance. Give her analogies: at the dentist, after anesthesia is in place to allow that root canal or filling, your tongue/lip can feel swollen, but a look in the mirror shows them to be normal. When a leg goes to sleep, it can feel fatter and heavier than the other one, but it is not. When you suffer nerve damage from diabetes, it can feel like bees are stinging your feet, but none are present in the room.

And then explain scenarios where persons have to accommodate to or neglect the feeling of contact lenses. The sound of new tinnitus. The tickling of an indwelling tracheotomy tube. The dramatic sensation a sword swallower must ignore during the show. Or the sensation of air hunger the pearl diver must overcome to stay submerged for 2 minutes while swimming vigorously.

Perhaps point out that it appears there is no danger from this ominous-feeling sensation.  Remind her of the multiplicity of prior “normal” tests. Maybe suggest that she experiment with assuming “control” of her response to the sensation by saying to herself: It is just a feeling! Or, Stupid pulmonary stretch receptors! Maybe gently alter behavior to see if it has any impact. Introduce inspiratory resistance via “straw-breathing.” Or a gentle Valsalva maneuver. Or, exhale slowly through pursed lips whose opening is the size of a coffee-stirrer.

And if nothing else works, suggest trying to mentally shrug and “throw the sensation over the shoulder.” And then keep going. The very worried individual can purchase an oximeter. Or even a stethoscope as a “crutch” to allay anxiety.

All of this can be offered with a physician’s apologies that he or she has nothing better to offer. And also with encouragement that these ideas have “liberated” other patients struggling with the same problem.

A final thought: just as neuromodulators can help persons suffering from neuralgia or sensory neuropathic cough/throat clearing, and laryngospasm, consider a “sensory neuropathic cough” strategy of working one-by-one, from medication to medication such as amitriptyline, gabapentin, etc., hoping to find one that helps.

*Some describe a more continuous, lower-grade background sensation of difficulty breathing with abrupt “peaks”

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Idiopathic Subglottic Stenosis

A subtype of subglottic stenosis that is inflammatory. One view is that this entity is actually a limited expression of Wegener’s Granulomatosis (aka Granulomatosis with polyangiitis).



Idiopathic subglottic stenosis has different levels: Series of 4 photos

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dilation of idiopathic subglottic stenosis

Post dilation (1 of 4)

Six months after dilation of idiopathic (inflammatory) subglottic stenosis, the patient has noted only slight deterioration, and breathing ability remains acceptable to her.
closer view of idiopathic subglottic stenosis

Closer view (2 of 4)

At closer range, the inflammatory component appears more evident.
vascular pattern

Rich vascular pattern (3 of 4)

The rich vascular pattern accompanying the lesion is seen better and is a visual finding of inflammation.
congested capillaries

"Sharing" the airway (4 of 4)

Here, the scope has been passed through the area of maximal narrowing and the patient becomes acutely aware of greater difficulty breathing. "Sharing the airway" is a way of 'measuring' it functionally. Note again the congested capillaries.

Another way to inject idiopathic subglottic stenosis: Series of 3 photos

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idiopathic inflammatory subglottic stenosis

Idiopathic inflammatory subglottic stenosis (1 of 3)

This patient is about to receive a triamcinolone (steroid) injection into her idiopathic inflammatory subglottic stenosis, while sitting in a chair under topical anesthesia. Dotted circle is for reference with Photo 2.
infused medication into cricoid

Priot to injection (2 of 3)

A needle has been passed through anterior neck skin and its tip rests out of sight, submucosally just inferior to the anterior cricoid ring. Note that the milky white medication has been infused submucosally within the dotted ring.
needle in tracheal wall

Injection (3 of 3)

Here, the 27-gauge needle traverses the trachea in order to inject the posterior tracheal wall. The submucosal white medication appears at the *.

Subglottic stenosis

Subglottic stenosis is narrowing just below the vocal cords, in the lowest part of the larynx and immediately above the first tracheal ring. Examples of causes include scarring from a breathing tube used during a long ICU stay, Wegener’s Granulomatosis (aka Granulomatosis with polyangiitis), and idiopathic subglottic stenosis (aka limited Wegener’s Granulomatosis).

Photos of subglottic stenosis:

Subglottic stenosis, after treatment

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Subglottic stenosis

Subglottic stenosis, before treatment (1 of 2)

Subglottic and high tracheal stenosis, inflammatory, idiopathic (Lab).
Subglottic stenosis

Subglottic stenosis, after treatment (2 of 2)

Same patient, a few days after dilation and steroid injection (Lab).

Vocal Cord Synechia

Vocal cord synechia is a strand of scar tissue that tethers the vocal cords to each other. It can prevent the vocal cords from opening fully for breathing.

A synechia can also form in other parts of the body. (Note the subglottic synechia shown below.)


Vocal Cord Synechia: before, during, and after surgery

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Post-intubation synechia

Vocal Cord Synechia (1 of 9)

Post-intubation synechia tethers the arytenoid cartilages together. This patient is tracheotomy-dependent.
Vocal cord synechia during surgery

Vocal cord synechia, during surgery (2 of 9)

Operative view of synechia ("v" of the vocal cords is inverted). Notice that the vocal cords are completely approximated because the synechia has bound them together.
Tiny forceps are separating the cords

Vocal cord synechia, during surgery (3 of 9)

Tiny forceps is separating the cords (arrows) and more clearly shows the extent of the synechia.
Micro-scissors in position to divide the synechia cleanly

Vocal cord synechia, during surgery (4 of 9)

Micro-scissors in position to divide the synechia cleanly. For perspective, the blade of the scissors is only a few millimeters long.
Vocal cord synechia

Vocal cord synechia, during surgery (5 of 9)

After division of the synechia and topical application of an anti-scarring agent.
Vocal cord synechia after surgery

Vocal cord synechia, after surgery (6 of 9)

Five days after surgery. Vocal cords are able to separate for breathing, and the tracheotomy tube can be removed. Compare with photo 1.
healed larynx after release of synechia

Vocal Cord Synechia, after surgery (7 of 9)

Completely healed larynx after release of synechia. Abduction completely restored.
vocal cords are coming together for phonation

Vocal cord synechia, after surgery (8 of 9)

As the vocal cords are coming together for phonation (not yet completely adducted).
Vocal cord synechia

Vocal cord synechia, after surgery (9 of 9)

Closer view. Can hardly see where the synechia was. Compare again with photo 1.

Ossified synechia resists thulium laser

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Ossified synechia

Ossified synechia (1 of 8)

This 75-year-old woman suffered complications after open heart surgery, and was intubated for three weeks. Nearly two years later, she remains short of breath and bothered by difficulty mobilizing secretions. On initial examination, a synechia was identified; at patient request, microlaryngoscopy was scheduled both to divide the synechia and to inject voice gel into the deficient posterior commissure. At surgery, a view sufficient to divide the synechia was not possible. The patient was rescheduled for office-based thulium laser division of the synechia.
Tip of glass fiber near the Ossified Synechia

Ossified Synechia, during first laser treatment (2 of 8)

Close-range view of the synechia. The tip of the glass fiber through which laser energy will be delivered is seen just inferior to the synechia.
Laser energy reveals bone underneath

Ossified synechia, during first laser treatment (3 of 8)

As the synechia is divided, a core of bone formation is exposed. More than half of the laser energy has been delivered to this spar of bone, yet it will not yield. The tip of the scope has also been flexed against the synechia to no avail. A second attempt with higher energy laser has been scheduled.
Ossified synechia 4 months later

Ossified synechia, 4 months later (4 of 8)

Four months later. The synechia remains, and there is residual granulation tissue on its undersurface. It's not yet known whether the spar of bone is still present. Compare with photo 2.
Second surgery attempt of thulium laser

Ossified synechia, 4 months later (5 of 8)

Now, with the thulium laser, beginning a second attempt at dividing the synechia.
Thulim laser reveals no bone remaining in ossified synechia

Ossified synechia, 4 months later (6 of 8)

The spar of bone is not found within the synechia (apparently turned to ash during the original procedure four months earlier), and now the scar band is divided. The patient could feel the difference in her breathing immediately.
synechia is now gone 6 months later

Synechia gone, 6 months later (7 of 8)

Six months after the initial laser treatment for this patient's bone-containing synechia. The synechia is now gone, with only a small residual projection remaining, left of photo. The vocal cords also separate more widely, to a wider "V".
divots from pressure necrosis of the endotracheal tube remain evident

Synechia gone, 6 months later (8 of 8)

During phonation. The divots from pressure necrosis of the endotracheal tube remain evident. In spite of them, the patient's voice is excellent.

Vocal cord synechia

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Vocal cord synechia

Vocal cord synechia (1 of 4)

Note that the vocal cords cannot fully abduct, due to the presence of a synechia, which tethers them to each other posteriorly.
Vocal cord synechia

Vocal cord synechia (2 of 4)

Same patient during phonation.
Vocal cord synechia

Vocal cord synechia (3 of 4)

Same patient at closer range.
Vocal cord synechia

Vocal cord synechia (4 of 4)

Same patient. Synechia in full view.

Intubation injury, including a subglottic synechia

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Intubation injury, including a subglottic synechia (1 of 2)

View of the vocal cords, in abducted position, in a patient with voice change after long-term intubation due to brain injury. Injury of the left posterior vocal cord (right of image) can be seen, where pressure from the breathing tube caused an erosion or divot (arrow). The synechia is not yet visible from this viewing perspective.

Intubation injury, including a subglottic synechia (2 of 2)

Same patient, just below the level of the cords. This synechia, located posteriorly, is additional evidence of breathing tube injury.

Synechia hidden by overhanging arytenoid superstructure

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Maximum possible abduction of the vocal cords

Synechia hidden by overhanging arytenoid superstructure (1 of 4)

Maximum possible abduction of the vocal cords, as seen a few months after an illness that required endotracheal intubation for 3 weeks. This person experienced noisy breathing with any significant exertion.
involuntary inspiratory phonation

Synechia hidden by overhanging arytenoid superstructure (2 of 4)

With elicited sudden inhalation the inspiratory air draws the vocal cords together, and the result is involuntary inspiratory phonation.
overhanging arytenoid superstructure

Synechia hidden by overhanging arytenoid superstructure (3 of 4)

Close-up view of the posterior vocal cords reveal a synechia or scar band tethering the vocal cords to each other and preventing their abduction. This kind of injury can exist in isolation; it can also occur together with cricoarytenoid joint ankylosis.
Synechia hidden by overhanging arytenoid superstructure

Synechia hidden by overhanging arytenoid superstructure (4 of 4)

An even closer view of the synechia.

Nasal and inter-arytenoid synechiae, with subglottic stenosis in forme fruste Wegener’s

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inflammatory adhesion in left nasal cavity

Nasal cavity (1 of 4)

View in left nasal cavity, showing inflammatory adhesion between septum and turbinate/ lateral wall of nose. Note intense erythema at “e.” Dotted line shows where normal separation would be seen.
adhesion of septum and turbinates

Closer view (2 of 4)

Closer, brighter view, again with dotted line where there should be no tissue bridge, but instead separation between septum and turbinates. This adhesion is asymptomatic, and therefore does not need to be treated.
Panoramic view of larynx

Panoramic view (3 of 4)

Panoramic view of larynx, showing adhesion between arytenoid cartilages indicated by vertical hashed lines. Horizontal dashed line is for reference with the next photo.
interarytenoid synechia is no longer seen after dilation

Post dilation (4 of 4)

After dilation, the interarytenoid synechia is no longer seen. Subglottic stenosis is present but not shown in this series.

Ulcerative laryngitis and resulting synechia – fixed!

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a synechia attaching the cords together

Synechia (1 of 3)

This woman developed a sore throat and lost her voice a week after a chemotherapy treatment for her metastatic breast cancer. Here, 6 weeks later, note the hazy area representing resolving “ulcerative” laryngitis (surrounded by tiny dotted line). There is a synechia attaching the cords together.
slight separation of attached vocal cords

Attempted to detach (2 of 3)

The flexible scope has been used once to “twang upwards” from below in order to detach the cords from each other. At the arrow, slight separation can be seen.
adhesion has been released

Successfully detached (3 of 3)

Just after the second attempt. That is, for the second time, the scope was passed below the cords, angulated sharply underneath the synechia, and then pulled upwards. The adhesion has been released. Voice is instantly and dramatically restored (though still hoarse, of course).

Posterior Commissure Synechiae

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tissue band tethers the vocal cords closer together

Tethered vocal cords (1 of 5)

This man has right vocal cord paralysis and a history decades ago of Teflon injection into the right vocal cord, resulting in posterior commissure synechiae. He is short of breath, partly due to the tissue band and partly because it tethers the vocal cords closer together than they would otherwise need to be as seen in photo 4 after the band is removed. See also photo 5.
Tethered vocal cords

Tethered vocal cords (2 of 5)

At closer range.
thulium laser fiber is touching the synechiae

Before laser removal (3 of 5)

The thulium laser fiber (F) is touching the synechiae, with laser energy about to be delivered.
thulium laser division of the band

Immediately after laser (4 of 5)

This is just after the thulium laser division of the band using topical anesthesia only, with patient sitting in a chair.
Vocal cords free of synechiae

One month post-op (5 of 5)

A month later, no residue of the synechiae is seen, and the vocal cords can spring farther apart than in photo 1.

Difficulty Breathing After A 3-day Intubation

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granulation tissue at the posterior commissure

Noisy, restricted breathing following intubation (1 of 5)

This teenager was intubated for 3 days due to tongue swelling. Breathing became noisy and restricted approximately 6 weeks later. Note that the vocal cords do not abduct fully and there is what appears to be granulation tissue at the posterior commissure (anterior asterisk).
vocal cords come into contact

Normal voice (2 of 5)

The vocal cords can come into contact as shown here, consistent with her normal-sounding voice.
small tract is seen posterior to the granulation

At close range (3 of 5)

At very close range within the posterior commissure, a small tract is seen posterior to the "granulation" which is now seen more clearly to be a broad-based synechiae with asterisks marking anterior and posterior limits.
posterior tract

At even closer range (4 of 5)

An even closer view verifies a posterior tract, and this makes it less likely that the cricoarytenoid joints are also injured.
small superficial-looking scar

Mucosa-only scar (5 of 5)

This view is taken with the scope passed just between the vocal cords and just anterior to the synechiae and angled directly posteriorly. A small superficial-looking "mucosa-only" scar is seen bilaterally, surrounded by dotted line. It can be confidently predicted that when the synechiae is released, the arytenoid cartilages will likely be able to abduct fully.

Vocal Cord Synechia
Vocal cord synechia is a condition wherein a scar band tethers the vocal cords to each other. Therefore, the vocal cords cannot fully open for breathing. This video provides a clear example — using laryngeal videostroboscopy — of a vocal cord synechia.


Abnormal narrowing of a passageway in the body. At our practice, stenosis typically refers to narrowing in the breathing passage, such as for narrowing in the glottic, subglottic, or tracheal areas.

Stenosis in the airway can be the result of prolonged endotracheal intubation, external trauma such as gunshot wound, crush injury, or tracheotomy, an inflammatory or auto-immune process, surgical resection of part of the airway for tumor, or other causes. Persons with airway stenosis will note a reduced capacity for exercise. Often the clinician hears noisy breathing on inhalation, especially when the patient is asked to fill the lungs quickly. Esophageal stenosis gives symptoms of difficulty swallowing solids more so than liquids.

Photos of Stenosis:


Nuances of Endotracheal Tube Injury

This woman with high-risk comorbidities of diabetes and obesity, was in ventilated in ICU more than a month for pulmonary complications of Covid-19 infection. She had an orotracheal tube in place for 3.5 weeks, and then a tracheotomy tube was placed. Now at her first visit a year later, she remains tracheotomy-dependent, and is told she has bilateral vocal cord paralysis (disproven in the following photo series).

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Maximum glottic opening (1 of 8)

Is it paralysis, as diagnosed elsewhere? At a fairly distant view, the maximum opening between the vocal cords at any phase of breathing appears to be approximately a 4mm glottic opening.

Undersurface mucosa indraws (2 of 8)

When the patient inspires rapidly with tracheotomy tube plugged, the vocal cord undersurface mucosa indraws (grey bands at dotted lines), further narrowing the glottic chink. One sees a faint suggestion of breathing tube injury (divot) at the arrow. Notably, there is a very low pitched rumbling sound heard that does not come from the glottis.

Phonation (3 of 8)

During phonation, the cords approximate fully, and in fact the voice is remarkably normal-sounding and she even has an excellent upper range.

Posterior commissure divot (4 of 8)

At close range while breathing with trach plugged, the posterior commissure divot subtly visible in Photo 2 is confirmed. A divot in the right posterior cord “always” indicates that the tube was taped to the left corner of the mouth. The patient’s mother confirmed that this was so.

Further evidence of scarring (5 of 8)

Angling farther posteriorly, additional evidence of inter-arytenoid and possible joint capsule injury is seen. Faint dotted lines outline this area. The problem is not bilateral vocal cord paralysis but posterior commissure scarring, tethering the arytenoids together.

View into trachea (6 of 8)

Looking now into the subglottis and trachea, there is narrowing only at trach entry site, accentuated functionally because the membranous trachea (MT) moves in and out with respiratory phase.

Vibration of trachea (7 of 8)

When the patient plugs the trach tube and inspires rapidly, the deep rumbling sound is again heard, and comes from vibration of the membranous trachea indrawing (arrows) and vibrating (zigzag line).

Open trachea beyond the tube (8 of 8)

A view past the tip of the trach tube shows no secondary area of tracheal stenosis.

The plan here is posterior commissuroplasty, followed by placement of a smaller trach tube and a trial of plugging. If plugging is tolerated during the day, she will need a sleep study with it plugged at night, given the tracheomalacia and her obesity.

Videos of Stenosis:

Tracheal Stenosis: Before and After
In this video, trachea (windpipe) blockage causes shortness of breath until the narrowed segment is removed. You will see views of the trachea before and after surgical repair.
Post-Radiation Hypopharyngeal Stenosis
People with larynx or pharynx (voice box or throat) cancer often undergo radiation therapy as part of their treatment regimen. An uncommon complication is stenosis (narrowing, scarring) of the entrance to the upper esophagus at the junction of the throat and esophagus. This video provides an example of this disorder.


A dilated outpouching from the normal contour of the pharynx.


Redundant supraglottic mucosa

An excess of mucosa overlying one or more structures in the larynx above the vocal cords. Mucosa in this area should “fit” snugly, like leggings, but in the case of redundant supraglottic mucosa, the fit becomes more like baggy pants.

Symptoms and treatment:

This redundant supraglottic mucosa most commonly develops on the apex and posterior surface of the arytenoid cartilage. Such mucosa sometimes draws inward during breathing and fills the laryngeal vestibule. In a severe case, inspiration can become noisy (stridor) or even effortful. When symptoms like these become troublesome, the excess mucosal tissue can be removed with endoscopic laser surgery.

Redundant supraglottic mucosa vs. laryngomalacia:

Redundant supraglottic mucosa is similar to the disorder laryngomalacia. In both disorders, supraglottic tissue is pulled into the laryngeal vestibule during breathing and can cause stridor. However, the causes of these symptoms are different. In the case of redundant supraglottic mucosa, the main problem is an excess of overlying mucosa, but in the case of laryngomalacia, the main problem is that the underlying structural tissue, such as that which comprises the aryepiglottic cord and epiglottic cartilage, is abnormally weak or soft.


Nonorganic breathing disorder, laryngeal

A nonorganic disorder in which a person’s vocal cords partially or fully close during breathing, which causes noisy breathing. Also called vocal cord dysfunction (VFD) or vocal cord dysfunction (VCD).

The fundamental disorder is not in the mechanism itself, but rather in the patient’s “use” of the mechanism. Consciously or sub-consciously, the patient inappropriately narrows the space between the vocal cords, usually for secondary gain. Unlike with asthma or nonorganic breathing disorder of the trachea, the noisy breathing is mostly heard when the person breathes in (inspiration). Still, on occasion, individuals with this disorder are treated for years as having asthma before this diagnosis is finally made.



Nonorganic Breathing
This video portrays a breathing abnormality that is non-organic / functional.

Nonorganic breathing disorder, tracheal

A breathing disorder, often mistaken for asthma, in which a person induces his or her trachea to narrow, causing wheezing or apparent shortness of breath. The person’s oxygen saturation remains normal, but his or her description of the problem and apparent breathing distress may be quite dramatic; in severe instances, the person may have been intubated and placed in intensive care, based purely upon the “drama”—that is, the person’s distressed appearance and audible noises. The extent of medical intervention prompted by this pseudo-asthma can be remarkable.

How it happens:

The person’s trachea momentarily narrows or collapses, but unlike with tracheomalacia, this narrowing or collapse is not due to any anatomical or physiological disorder of the person’s trachea. Instead, it can be seen as an added capability of the trachea: an unusual, heightened capability of the membranous tracheal wall to flex inward and decrease the caliber of the “pipe.” A person whose trachea has this added capability may figure out how, with inconspicuous excessive expiratory effort—a sort of semi-Valsalva maneuver that isn’t evident to observers—to induce this tracheal or tracheobronchial collapse that creates the wheezing heard by family, friends, or co-workers.

The nonorganic element:

Often, this upper airway wheezing ability can be just a personal quirk (like double-jointedness) that has no particular significance to the person’s life; think of a “wheezy laugh.” Such a case would not be a nonorganic breathing disorder case. In extreme cases, however, a person may begin to use this wheezing ability to masquerade (perhaps sub-consciously) as having asthma, in order to achieve some kind of “secondary gain”; this added element puts a case into the category of a nonorganic breathing disorder. Sometimes, the person does have asthma, but is able to markedly amplify the asthma’s apparent severity by overlaying on it this dramatic nonorganic upper airway wheezing ability.

How it is diagnosed:

If a clinician listens to this person’s breathing with a stethoscope placed over the lung fields, the wheezing can indeed sound exactly like asthma. However, there are some key diagnostic criteria that help the discerning clinician to recognize a case of nonorganic breathing:

  • The wheezing is louder over the manubrium (uppermost part of the sternum) than over the peripheral lung fields.
  • There is a surprising incongruity between, on the one hand, the person’s apparent distress and, on the other hand, his or her objective findings, such as oxygen saturation, pulmonary function tests, blood gas measurement, and so forth.
  • Potent treatments for asthma do not seem to diminish or abolish the wheezing.
  • There appears to be some kind of “secondary gain” (mentioned above). Examples of secondary gain might be simple increased attention from family, healthcare workers, and so forth, or else avoidance of school or work, or an enhancement of the chance of winning a lawsuit, or release from responsibility for losing a competitive race, or the ability to manipulate others who have high levels of empathy combined with low levels of discernment of others’ motivations.