Élodie R. is thirty-five. A literature teacher, she describes herself as rational, not particularly anxious about her health, and generally inclined to look for an explanation before drawing a conclusion.
For several months, however, her body has been producing a series of symptoms she can no longer connect: intermittent palpitations, hot flushes, diffuse dizziness, episodes of numbness, and at times a disturbing sensation of not getting enough air despite the fact that she is breathing.
She seeks medical advice.
Then she seeks it again.
Cardiology, ENT, neurology, endocrinology: each specialty appropriately investigates the area within its field. The examinations performed reveal no structural or biological abnormality capable, on its own, of explaining the entire clinical picture.
The reports become progressively more reassuring.
Élodie does not.
“I’ve had everything checked. So why do I still feel unwell?”
That question contains the real clinical problem.
The investigations are not wrong. And the symptoms do not become imaginary simply because those investigations are reassuring.
There is a discrepancy that has not yet been explained.
A normal result is medical information.
It should neither be dismissed nor turned into a universal answer.
A reassuring electrocardiogram answers specific cardiovascular questions. Normal neurological imaging can make certain structural abnormalities less likely or exclude them, depending on the investigation performed. Thyroid results within the expected range provide information about thyroid function under the conditions in which they were measured.
None of these investigations, however, is designed to summarise the functioning of an entire organism.
This is where Élodie’s situation becomes clinically interesting.
Not because her investigations somehow “missed” something.
But because several investigations can be correctly interpreted and still fail to explain a clinical trajectory when each one is answering a different question.
A normal result and an explanation for a symptom are not the same clinical conclusion.
After several reassuring investigations, continued monitoring or consideration of a functional component is entirely coherent.
The reasoning becomes incomplete when new information appears but is not reintegrated into the case as a whole.
In Élodie’s case, that information concerns breathing.
When the chronology is reconstructed, one pattern gradually becomes more visible: some episodes combine dizziness, paraesthesia, an unusual respiratory sensation and a measurable change in carbon dioxide.
At this stage, the purpose is still not to manufacture another diagnosis.
It is to recognise that a physiological variable previously peripheral to the reasoning may now warrant closer examination.
The chronology reveals another element: the symptoms began after a minor procedure performed under general anaesthesia.
That temporal proximity deserves to be recorded.
It does not establish causality.
The fact that one phenomenon occurs after another does not demonstrate that the first caused the second. Anaesthesia, the procedure itself, the postoperative period, changes in physical activity, altered sleep or other coinciding events may all represent variables worth examining.
Chronology is therefore not proof.
It is a tool for determining where to look.
And when the available respiratory data are placed on that same timeline, a more precise question emerges: has Élodie’s breathing pattern changed over time, and is that change present when certain symptoms occur?
Carbon dioxide plays an important physiological role in ventilatory regulation and cerebral circulation.
When ventilation exceeds what is required to eliminate metabolically produced CO₂, arterial carbon dioxide pressure can fall. This is hypocapnia.
That reduction alters acid-base balance and produces measurable vascular effects.
Cerebral circulation is particularly sensitive to changes in PaCO₂. A reduction in arterial CO₂ produces cerebral vasoconstriction and decreases cerebral blood flow.
This physiological mechanism is well established.
What is considerably less certain in an individual patient is the precise contribution it makes to each symptom experienced.
Physiology can therefore establish that a mechanism is possible.
Without additional evidence, it cannot establish that the same mechanism explains Élodie’s entire clinical history.
The question is no longer:
“Which specialist has she not yet seen?”
It becomes:
“Is there a reproducible relationship between Élodie’s symptoms, her breathing pattern and the changes in CO₂ that have been observed?”
In April 2026, Élodie becomes unwell while teaching.
She undergoes medical assessment.
Among the measurements recorded during the episode are a pCO₂ of 27 mmHg and a pH of 7.50.
This time, the information is no longer purely symptomatic.
Depending on the sampling conditions and the clinical context, a reduced carbon dioxide pressure associated with alkalemia is compatible with respiratory alkalosis related to excessive ventilation.
This does not mean that every possible cause has now been excluded.
It means that during this particular episode, the symptoms were accompanied by an objectively measurable physiological change.
That distinction matters.
Before this episode, a ventilatory hypothesis was plausible.
After it, there is an additional objective finding that justifies investigating that hypothesis more systematically.
A reduction in PaCO₂ rapidly alters cerebral vascular tone.
Physiological research has consistently shown that hypocapnia causes cerebral vasoconstriction and reduces cerebral blood flow.
Depending on its severity, speed of onset, duration and clinical context, hypocapnia may be associated with dizziness, light-headedness, weakness and other transient neurological manifestations.
Changes in pH associated with hyperventilation may also contribute to certain neuromuscular or sensory symptoms.
But caution remains essential.
The coexistence of dizziness and hypocapnia does not automatically mean that every episode of dizziness is caused by hypocapnia.
Likewise, a low pCO₂ measured during one episode does not necessarily demonstrate chronic hypocapnia between episodes.
The clinically relevant information is therefore not an isolated number.
It is whether the relationship between breathing, CO₂, context and symptoms can be reproduced.
The respiratory literature describes a group of conditions commonly discussed under terms such as dysfunctional breathing or breathing pattern disorders.
These conditions do not necessarily correspond to structural lung disease.
They describe abnormalities in breathing patterns that may contribute to symptoms, sometimes in the presence of otherwise reassuring standard cardiopulmonary investigations.
Their assessment remains complex.
There is no single biological marker capable of automatically converting a cluster of symptoms into a diagnosis of functional breathing disorder.
Clinical history, observation of the breathing pattern, CO₂ measurements when appropriate, exclusion of relevant organic causes and, in some cases, specialist assessment need to be considered together.
This is precisely why the word “functional” should never be understood to mean “imaginary”.
Here, it describes a question of function.
In Élodie’s case, three levels of reasoning must remain separate.
What is established: she experiences recurrent symptoms; several investigations have not identified a structural cause capable of explaining the entire picture; and during one documented episode, a low pCO₂ and alkalemia were measured.
What is physiologically plausible: excessive ventilation can reduce PaCO₂; hypocapnia causes cerebral vasoconstriction and reduces cerebral blood flow; these changes may contribute to certain transient neurological or sensory manifestations.
What remains to be demonstrated: whether Élodie’s breathing pattern is persistently altered, whether this change systematically precedes her symptoms, and whether it represents their principal mechanism rather than an associated phenomenon.
Making these distinctions does not weaken the case.
It gives the reasoning scientific structure.
A robust clinical hypothesis does not attempt to explain immediately everything that remains unexplained.
It produces a proposition precise enough to be tested — and potentially disproved.
Once an immediate serious cause has been reasonably excluded, an episode may be described as benign in prognostic terms.
That word answers an important question: has an immediate danger been identified?
It does not necessarily answer another: why do the symptoms keep returning, and why are they affecting the patient’s life to this extent?
Confusing these two questions accounts for much of the misunderstanding experienced by some patients.
A phenomenon may not be life-threatening and still be sufficiently reproducible, physiologically coherent and disabling to deserve investigation.
When a breathing pattern disorder is reasonably suspected and causes requiring specific medical management have been appropriately considered, specialist respiratory management may be discussed with the professionals involved.
Its purpose is not to force breathing towards an arbitrary theoretical value.
The objective is to assess the breathing pattern and, where indicated, work on its relationship to metabolic demand, its coordination with activity and the ability to avoid ventilation that is unnecessarily excessive.
One point is important: no universal breathing technique can be derived from this case alone.
A rate of “six breaths per minute”, for example, is used in some contexts involving slow breathing and autonomic modulation, but it does not in itself constitute a proven treatment for every form of hypocapnia or hyperventilation syndrome.
The strategy must depend on the mechanism actually identified.
And if symptoms improve following respiratory intervention, that response provides additional clinical information.
It does not retrospectively prove, by itself, that the original hypothesis was the only possible explanation.
It would be inaccurate to say that “conventional medicine stops when no abnormality is found”.
Respiratory physiology, sleep medicine, pulmonology, neurology, cardiology and psychosomatic medicine all have tools capable of investigating aspects of these phenomena.
The difficulty lies elsewhere.
It emerges when information is dispersed across several consultations, obtained at different moments and interpreted within separate specialist frameworks.
The cardiologist may have correctly answered the cardiovascular question.
The neurologist may have correctly answered the neurological question.
The endocrine assessment may quite appropriately be reassuring.
And yet no one may have been responsible for reconstructing the temporal relationship between the symptoms, breathing, circumstances of onset and biological data obtained during the episodes.
The problem, then, is not an absence of medicine.
It is the absence of a transversal reading of the case.
The first question was:
“What disease have we missed?”
The next becomes:
“What measurable phenomenon accompanies the symptoms, in what sequence does it occur, and can that relationship be reproduced?”
First, it changes the way the investigations already performed are interpreted.
They are no longer simply a succession of “normal” results. They become a map of what has already been investigated and what remains unresolved.
It also changes the way the symptoms themselves are used.
Rather than simply adding them together — dizziness, palpitations, numbness, unusual respiratory sensations — the sequence is reconstructed: which appears first, under what circumstances, for how long, alongside what respiratory change, and followed by what pattern of recovery?
Finally, it changes the investigative strategy.
The objective is no longer to multiply tests indiscriminately.
It becomes possible to investigate a specific relationship between a clinical manifestation and a physiologically plausible mechanism.
Élodie’s case does not demonstrate the existence of some mysterious territory between “normal” and “ill” that medicine is incapable of recognising.
It demonstrates something more precise.
One investigation may be normal because the abnormality it was designed to detect is not present.
Another investigation, performed at a different time and addressing a different question, may nevertheless identify a clinically relevant physiological phenomenon.
Those two findings are not contradictory.
They describe different dimensions of the same case.
The difficulty begins when those dimensions are never brought together.
This is why a trajectory can sometimes provide information that no isolated value contains.
Not because trajectory replaces thresholds.
But because it shows when a value changes, what changes with it, and what happens next.
Élodie did not have “nothing”.
She had undergone several investigations that did not identify the conditions they were designed to detect.
Those are not the same thing.
Once the chronology is reconstructed, new information emerges: some episodes are accompanied by an objectively measurable change in CO₂ and acid-base balance, making a ventilatory hypothesis sufficiently plausible to justify specific assessment.
That hypothesis should neither be dismissed because previous investigations were normal nor prematurely converted into a universal explanation.
It needs to be tested.
The most informative distinction here is therefore not simply the boundary between normal and pathological.
It is the relationship between a symptom, a moment in time, a measurement, and what came before it.
This is precisely the relationship that can disappear when a medical record is interpreted one test at a time.
When investigations have already been performed but symptoms persist, the next question is not necessarily which new abnormality should be sought.
It may instead become necessary to reconstruct what the different investigations have actually established, what they have reasonably excluded, and which relationships between the available findings have never been examined.
Clinical Biological Decoding® reconstructs the chronology, compares the available data, examines the interactions between symptoms, biological findings, treatments and clinical evolution, and searches the international scientific literature for evidence that may help clarify the remaining inconsistencies.
The objective is not to produce an additional diagnosis.
It is to reconstruct a clinical situation that has become difficult to read.
This analysis does not replace medical diagnosis, medical prescription or ongoing care by the treating physician.
Ainslie PN, Duffin J. Integration of cerebrovascular CO₂ reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology. 2009;296:R1473–R1495.
Immink RV, Pott FC, Secher NH, van Lieshout JJ. Hyperventilation, cerebral perfusion, and syncope. Journal of Applied Physiology. 2014;116(7):844–851.
Hoiland RL, Fisher JA, Ainslie PN. Regulation of the cerebral circulation by arterial carbon dioxide. Comprehensive Physiology. 2019.
Gardner WN. The pathophysiology of hyperventilation disorders. Chest. 1996;109(2):516–534.
Boulding R, Stacey R, Niven R, Fowler SJ. Dysfunctional breathing: a review of the literature and proposal for classification. European Respiratory Review. 2016;25:287–294.
Vidotto LS, Carvalho CRF, Harvey A, Jones M. Dysfunctional breathing: what do we know? Jornal Brasileiro de Pneumologia. 2019;45(1).
Clinical Analysis · Complex Medical Situations
