Exercise hyperventilation: Hyperventilation: A Possible Explanation for Long-Lasting Exercise Intolerance in Mild COVID-19 Survivors?

18.08.202324.06.2023 by alexxlab

Exercise-induced hyperventilation: a pseudoasthma syndrome

. 1999 Jun;82(6):574-8.

doi: 10.1016/S1081-1206(10)63169-9.

A H Hammo¹, M M Weinberger

Affiliations

Affiliation

¹ University of Iowa Hospitals & Clinics, Iowa City, USA.

PMID:
10400486
DOI:
10.1016/S1081-1206(10)63169-9

A H Hammo et al.

Ann Allergy Asthma Immunol.

1999 Jun.

. 1999 Jun;82(6):574-8.

doi: 10.1016/S1081-1206(10)63169-9.

Authors

A H Hammo¹, M M Weinberger

Affiliation

¹ University of Iowa Hospitals & Clinics, Iowa City, USA.

PMID:
10400486
DOI:
10.1016/S1081-1206(10)63169-9

Abstract

Background:

Exercise-induced asthma is common and generally responds well to an inhaled beta2 agonist.

Objective:

We examined the physiologic changes in airflow and gas exchange that occurred during standardized treadmill exercise in patients previously diagnosed with exercise-induced asthma whose histories appeared atypical or where conventional treatment, including an inhaled beta2 agonist, was ineffective.

Methods:

During a 1-year period 32 patients, aged 8 to 18, met these criteria. All had been previously diagnosed as having exercise-induced asthma. Exercise consisted of treadmill running at a time when the patients had received no inhaled beta2 agonist, cromolyn, or nedocromil for at least 4 hours. Spirometry was done before and at 2, 5, 10, and 15 minutes after exercise; oxygen saturation was monitored by pulse oximetry; and end-tidal CO2 was monitored with nasal cannula.

Results:

Despite their previous diagnoses of exercise-induced asthma, 11 patients who described chest tightness during exercise had decreases in FEV1 less than 15% with all but one of those less than 10% (mean decrease 5.6%) but demonstrated decreases in end-tidal CO2 greater than in all of the other 21 patients (mean 23.2 versus 9.8%, P < .01). Only 4 patients had unequivocal evidence for bronchospasm with cough and wheezing accompanying chest tightness in association with decreases in FEV1 from 18 to 22%. Seventeen patients had neither their symptoms reproduced nor physiologic abnormalities.

Conclusions:

These data show that chest discomfort perceived as dyspnea during vigorous exercise may be associated with hypocapnia from hyperventilation without bronchospasm in children and adolescents previously misdiagnosed and treated as having exercise-induced asthma.

Cited by

Cardiopulmonary exercise testing for identification of patients with hyperventilation syndrome.
Brat K, Stastna N, Merta Z, Olson LJ, Johnson BD, Cundrle I Jr.
Brat K, et al.
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Confounders of severe asthma: diagnoses to consider when asthma symptoms persist despite optimal therapy.
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Dysfunctional breathing: a review of the literature and proposal for classification.
Boulding R, Stacey R, Niven R, Fowler SJ.
Boulding R, et al.
Eur Respir Rev. 2016 Sep;25(141):287-94. doi: 10.1183/16000617.0088-2015.
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PMID: 27581828
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Diagnosis of asthma in primary health care: a pilot study.
Ringsberg KC, Bjärneman P, Larsson R, Wallström E, Löwhagen O.
Ringsberg KC, et al.
J Allergy (Cairo). 2014;2014:898965. doi: 10.1155/2014/898965. Epub 2014 Apr 10.
J Allergy (Cairo). 2014.
PMID: 24817894
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Weiss P, Rundell KW.
Weiss P, et al.
Allergy Asthma Clin Immunol. 2009 Nov 17;5(1):7. doi: 10.1186/1710-1492-5-7.
Allergy Asthma Clin Immunol. 2009.
PMID: 20016690
Free PMC article.

See all “Cited by” articles

MeSH terms

Substances

Can’t Catch Your Breath? Could it be Exercise-induced Bronchospasm?

Have you ever had shortness of breath or tightness in the chest during exercise? Has anyone told you that your symptoms were because you are out of shape? Although high-performance athletes appear to be physically fit some of them struggle during or after intense workouts. Coaches and training staff need to be aware of a more serious underlying ailment that can affect performance.

What is exercise-induced bronchospasm?

Exercise-induced bronchospasm (EIB) is an asthma-like condition that causes the airway to temporarily narrow during strenuous activity. This condition is seen in school-aged athletes and older adults who participate in moderate to vigorous exercise.

Certain types of indoor and outdoor environments can be a major factor in an EIB attack. For example, EIB is more commonly seen in people who exercise during the winter months due to the colder temperatures and in those who also participate in aquatic exercise. Because of the decreased amount of moisture it holds, cold air causes the airway to become dehydrated. Breathing in colder temperatures can also cause inflammation in the lungs and trigger a spasm of the bronchial tubes. Additionally, the re-warming of the airways that occurs after exercise can reverse the bronchial reaction and exacerbate the symptoms of EIB.

One trigger for EIB attacks is the high concentration of gas particles found in indoor pool facilities. The chemicals used to maintain the pool and the limited airflow cause irritation and drying of the airways. Another EIB trigger that can occur is when an athlete develops hyperventilation (abnormal fast or deep breathing) during vigorous exercise. Heavy breathing causes the airways to dry out, which leads to a dehydration of the cells lining the airway. The cells’ internal chemical balance is disrupted, which causes a chain reaction of chemicals to be released, leading to the spasm of the bronchioles.

Is EIB different from asthma?

While the term exercised-induced asthma (EIA) is used almost interchangeably with EIB and their symptoms are similar, the 2 conditions are not the same. The main difference is that EIB occurs in people who do not have a history of asthma and the bronchospasms only occur during exercise; therefore, these patients only receive treatment before exercise. For those who do have asthma, their airways are always inflamed and with EIA specifically, exercise is a trigger that exacerbates their condition. Additionally, for EIA patients, treatment focuses toward reducing symptoms all the time, not just during exercise.

How are EIB and EIA similar?

In both EIB and EIA the airways become restricted, making breathing, and especially exhaling difficult. The symptoms are similar as well, such as wheezing, coughing, shortness of breath, tightness in the chest, fatigue, and lightheadedness. Triggers for each condition include cold dry air, environmental allergens, chlorine, and intense exercise. When an EIB or EIA attack occurs, both can be treated with inhaled steroids or immediate removal from activity with proper hydration. For prevention, people who suffer from either condition can benefit from the use of short-acting inhaled steroids that work to keep airways dilated (opened wider) or by performing a warm-up that consists of a short burst of exercises.

Signs and symptoms of EIB

An EIB attack will present with no symptoms most of the time, although signs such as wheezing, dry cough, and shortness of breath can develop after exertion. Some people with this ailment become fatigued more quickly than others or seem to be out of shape when trying to participate in strenuous activity. Symptoms of EIB usually occur 10 to 15 minutes after intense exercise, and last for a short duration after activity ends. With rest and proper treatment, symptoms often resolve and go away quickly.

Diagnosing EIB

There are 2 common types of testing used to diagnose EIB: exercise challenge tests and bronchial provocation tests. Exercise challenge tests can be completed in either the field or laboratory setting. The test begins with a lung capacity reading prior to the start of exercise, followed by 8 to 10 minutes of intense exercise and then the lung capacity reading is taken again immediately after the exercise. In a laboratory setting, the bronchial provocation test begins with a lung capacity measurement. Then the patient inhales a substance that causes bronchoconstriction (narrowing of the airways) to occur, followed by another lung capacity measurement.

How can an active person treat EIB?

Both nonpharmacological (without drugs) and medication strategies can be used to treat an EIB attack. Nonpharmacological methods include resting immediately after strenuous exercise and drinking room temperature water to avoid further bronchoconstriction. Another nondrug treatment is to inhale and exhale into a paper bag or mask to warm and moisten the airway. A bronchodilator is a common pharmacological treatment that consists of a metered-dose inhaler that contains a drug called albuterol. This bronchodilator is a drug that opens the airway of the lungs and when taken 15 minutes before exercise, it often lasts up to 2 hours. Salmeterol, cromolyn, and nedocromil are other inhaled medications people take prior to activity to help prevent EIB.

How can someone prevent EIB?

While it can be difficult to prevent an EIB attack in some situations, there are steps an active person can take to help decrease the likelihood of an episode occurring. These steps include exercising in a well- ventilated area, with warm, moist air, and avoiding air pollutants. A pre-activity warm-up that includes exercises that increase heart rate, such as short bursts of vigorous wind sprints (intervals), can help induce a symptom-free period that lasts up to 3 hours. Additionally, research has also shown that diets low in sodium and high in antioxidants and fish oils decrease the prevalence of EIB symptoms and frequency in active people.

Take a deep breath and get checked out

If you experience the symptoms—the shortness of breath, fatigue, dry cough, and wheezing—consult with your doctor to see if you are experiencing EIB or EIA. Once your physician makes the diagnosis, your treatment can begin. Keep in mind, however, prevention is key, such as warm-up before you begin exercise, stay hydrated, and exercise in well-ventilated areas. With the proper prevention and treatment plans, the physically active patient who suffers from EIB can exercise and play sports at their full potential.

Author: Ashley Wojnowski, MS, LAT, ATC | Sevierville, Tennessee
Author: Anna Francois, MS, LAT, ATC | Columbus, Georgia

Vol. 30, Number 2, Spring 2018

Last edited on October 18, 2021

Hyperventilation syndrome. What is Hyperventilation Syndrome?

IMPORTANT
The information in this section should not be used for self-diagnosis or self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.

Hyperventilation syndrome is a neuropsychiatric pathology that leads to the formation of an abnormal respiratory rhythm that increases pulmonary ventilation with the development of alkalosis. Accompanied by variable vegetative, algic, muscular-tonic, respiratory, mental disorders. Diagnosed by testing, hyperventilation test, study of CBS and blood electrolytes. Treatment consists of a combination of non-drug (psychotherapy, relaxation techniques, breathing exercises, biofeedback therapy) and medication (psychotropic drugs, magnesium, calcium) methods.

ICD-10

F45.3 Somatoform dysfunction of the autonomic nervous system

Causes
Pathogenesis
DHW symptoms
Complications
Diagnostics
DHW treatment
Prognosis and prevention
Prices for treatment

General

The term “hyperventilation syndrome” was introduced by the American physician Da Costa in 1871. Subsequently, variant synonymous names for the disease were proposed: “respiratory neurosis”, “neurorespiratory syndrome”, “respiratory dystonia”, however, the original term remained the most widespread. Hyperventilation syndrome (HVS) is observed in 6-11% of patients seeking medical help. The disease affects people of various age groups, including the elderly and children. The peak incidence occurs at 30-40 years of age. Women get sick 4-5 times more often than men. HVS has a predominantly chronic course, among the sick, acute cases account for only 2%.

Hyperventilation syndrome

Causes

The etiological triggers that provoke the formation of GVS are polymorphic and are realized against the background of habitually abnormal breathing that has arisen due to cultural characteristics, life experience, certain sports (running, swimming), playing wind musical instruments. Etiological factors are divided into:

Psychogenic. They occur in 60% of cases of HVS. The leading role belongs to mental disorders: anxiety disorder, depression, neurasthenia, phobic disorders, less often hysterical neurosis. Acute and chronic stressful situations can provoke hyperventilation syndrome. In some cases, the background for the development of the disease is the psychogenic childhood – childhood situations in which the patient witnessed an episode of asphyxia, an attack of bronchial asthma, and suffocation of a drowning person.
Organic. They include CNS lesions (hydrocephalus, arachnoiditis, dyscirculatory encephalopathy) and diseases of internal organs (hypertension, recurrent bronchitis, diabetes mellitus). The action of purely organic etiofactors is observed in 5% of patients with HVS.
Mixed. The action of a psychogenic trigger is realized against the background of organic pathology. They make up 35% of the total number of cases.

Hyperventilation syndrome can be provoked by drugs of the following groups: beta-agonists, salicylates, xanthine methyl derivatives, progesterone preparations.

Pathogenesis

The functioning of the respiratory system is not as autonomous as the work of other systems and organs. A person is able to regulate the depth of inhalation and exhalation, arbitrarily hold the breath, intensify it. This feature determines the close connection of the respiratory function with the psycho-emotional state. Psychogenic triggers, especially anxiety, provoke biochemical shifts that lead to calcium-magnesium imbalance. There are changes in the work of respiratory enzymes that potentiate the development of hyperventilation. Excessive release of carbon dioxide leads to a drop in its concentration in the blood – hypocapnia, a shift in blood pH to the alkaline side with the development of respiratory alkalosis. These changes cause clinical symptoms: impaired consciousness, vegetative, sensory, algic disorders, manifestations of tetany. The result is increased anxiety that supports hyperventilation. A vicious circle is formed that continues to exist even after the cessation of the provoking etiofactor.

DHW symptoms

Hyperventilation syndrome is characterized by the multiplicity and polymorphism of the symptoms that occur. Among the variety of symptoms, a typical triad can be traced: respiratory dysfunction, disorders of the emotional sphere, muscle-tonic phenomena. Respiratory disorders are represented by four forms. The first is a subjective feeling of lack of air (“empty breath”), forcing the patient to take deeper and / or frequent breaths. The second – difficulty breathing, is characterized by patients as “tightness when inhaling”, “lump in the throat”, “air flow into the lungs, requiring effort.” Arrhythmic increased breathing is noted with the participation of auxiliary respiratory muscles. The third option is a disorder of respiratory automatism, which is accompanied by a feeling of stopping breathing, prompting the patient to constantly monitor the respiratory process and consciously “correct” it. The fourth form includes the hyperventilation equivalent, which is yawning, deep sighs, sniffling, coughing.

Psycho-emotional disorders are in the nature of anxiety, fear. Typically generalized anxiety disorder. Patients note constant nervous tension, increased anxiety, loss of the ability to relax. The fear of open spaces (agoraphobia) and public places (social phobia) is reinforced by the aggravation of respiratory disorders in them. Muscle-tonic syndrome is caused by changes in the electrolyte composition of the blood, causing an increase in neuromuscular excitability. It includes paresthesias (sensory disorders felt as “crawling”, numbness, burning, tingling in certain parts of the body), tetanic phenomena (tonic convulsions of the distal extremities, muscle spasms). Possible carpopedal spasm.

The classic symptoms of the disease are combined with algic symptoms: headaches, cardialgia, abdominal pain. Complaints from the cardiovascular system include discomfort in the heart, palpitations, from the gastrointestinal tract – dyspepsia, unstable stools, flatulence. Disorders of consciousness are typical: ambiguity, fogging, syncope.

Complications

Hyperventilation crisis is an acute condition with a pronounced disorder of the respiratory rhythm. There is a fear of suffocation. Hyperventilation crisis refers to panic attacks, accompanied by typical symptoms for them: hyperhidrosis, chills, dizziness, nausea, palpitations, fear of death, a feeling of suffocation, hot flashes and / or cold, discomfort in the cardiac region. The condition is associated with psychological discomfort. Occurs in places where, according to the patient, he will not be able to provide proper assistance. A specific feature of the crisis is its relief when breathing into a plastic (paper) bag. The patient inhales the air that he exhaled into the bag. The air contains an increased concentration of CO2, which allows you to quickly reduce respiratory alkalosis and stop the symptoms caused by it.

Diagnostics

The polymorphism of manifestations, the dominance of respiratory disorders leads to an initial erroneous assumption about the presence of a pathology of the respiratory or cardiovascular system. Patients are examined by a therapist, pulmonologist, cardiologist without revealing a serious organic pathology. The reason for consulting a neurologist or a psychiatrist is the emotional coloring of complaints, the patient’s pronounced anxiety. Diagnosis of hyperventilation syndrome allows:

Psychogenic history. Pointing to a traumatic situation, children’s fears, neurosis, neurasthenia, depressive syndrome are important.
Neurological examination. Reveals distal hyperhidrosis, positive tests for latent tetany: symptoms of Khvostek, Weiss, Schlesinger, Trousseau’s test. Additionally, electromyography is performed to confirm neuromuscular hyperexcitability and tetany.
Psychological examination. Includes a study of personality structure, psychological testing. The Niimigen questionnaire developed in Holland is used, in 90% of cases allowing detection of DHW.
Hyperventilation test. It is carried out by voluntary hyperventilation carried out by the patient. A positive result (appearance of typical vegetative, psycho-emotional, tetanic changes) allows confirming the diagnosis of HVS.
KOS blood. The acid-base state is shifted towards alkalosis. The drop in the partial pressure of CO2 indicates the respiratory nature of the changes in the acid-base balance.
Blood electrolytes. There is a drop in the concentration of calcium, magnesium in the blood.
Examination of internal organs. It is necessary to exclude organic pathology. Characterized by tachycardia, lability of the pulse and blood pressure, possible extrasystole, fluctuation of the ST-segment on the electrocardiogram. X-ray of the lungs, the study of respiratory function remain normal. Examination of the gastrointestinal tract reveals functional abnormalities in the form of various types of dyskinesia.

Hyperventilation syndrome must be differentiated from diseases of the respiratory organs, hypoparathyroidism. The main difference between DHW is difficult inhalation, COPD is difficult exhalation. Hypoparathyroidism is accompanied by osteosclerosis, calcium deposition in the internal organs, and a decrease in the level of parathyroid hormone.

DHW treatment

Therapy is carried out in a complex way by combining pharmacotherapy and non-drug methods. An important role is played by explanatory conversations that explain the nature of the violations, showing the connection of somatic symptoms with the emotional state, convincing in the absence of an organic disease. The treatment includes:

Psychotherapy. Successfully applied cognitive-behavioral, psychoanalytic techniques. The presence of childhood psychogeny is an indication for psychoanalysis sessions.
Formation of correct breathing. It is carried out by regular breathing exercises. An auxiliary technique is teaching relaxation techniques. Hyperventilation crisis is stopped by breathing into the bag.
biofeedback therapy. With the help of the equipment, the patient receives objective information about the state of breathing, learns to regulate the respiratory function, taking into account the feedback received.
Medical correction of the mental sphere. The most effective antidepressants with a pronounced anxiolytic effect (fluvoxamine, amitriptyline). Perhaps the appointment of sedatives, neuroleptics, tranquilizers. In a crisis, benzodiazepines (diazepam) are used. A pronounced vegetative component is an indication for the use of vegetotropic drugs.
Elimination of electrolyte disorders. It is achieved by taking calcium and magnesium supplements. Calcium reduces the tendency to tetany, magnesium has a calming, anticonvulsant effect.

The duration of therapy is usually 4-6 months. Patient follow-up is necessary to prevent recurrence.

Prognosis and prevention

Hyperventilation syndrome does not pose a threat to life, but significantly reduces its quality. Lack of treatment leads to further implementation of the vicious circle, aggravation of symptoms. Correct complex therapy promotes recovery. In the future, the resumption of the action of trigger factors can cause the development of a relapse. Prevention of DHW includes the formation of a benevolent optimistic outlook on life, an adequate response to stressful situations, and timely correction of emerging psychological problems.

Sources

treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.
Hyperventilation syndrome and dysfunctional breathing | #08/07
Clinical features, diagnostic criteria for hyperventilation syndrome (HVS) and dysfunctional respiration (DD) are not well known to a wide range of physicians [1, 2, 3]. One of the historical milestones associated with the concepts of functional respiratory disorders include 1871, when Da Costa (Da Costa Jacob, 1833–1900), an American physician who took part in the US Civil War, used the term “hyperventilation syndrome” (HVS) in patients with the so-called “soldier’s heart”. Since then, various alternative definitions have been proposed to characterize respiratory disorders: “respiratory neurosis”, “neurorespiratory dystonia”, “respiratory syndrome”, “respiratory dyskinesia”, “idiopathic hyperventilation”, “neurorespiratory syndrome”, “unstable breathing”, etc. However, these terms are not widely accepted. They are quite general and do not reflect the features of respiratory disorders in a particular patient [4]. These definitions are often associated with the concept of “incomprehensible shortness of breath” (unexplained dyspnea).
HVS occurs in 6–11% of general practice patients. The ratio of men and women is 1:4, 1:5; more commonly observed in 30-40 years, but may develop in other age groups, including children and the elderly. L. Lum (1987) emphasized that “every doctor can meet at least one patient with GVS within a week.” Doctors of various specialties – neuropathologists, cardiologists, pulmonologists, psychiatrists – can observe the phenomena of hyperventilation in their patients. The acute course of HVS is much less common than the chronic one, and accounts for only 1–2% of the total number of patients [2, 6, 7].
The reasons for the development of GVS are quite numerous. These are neurological and mental disorders, autonomic disorders, respiratory diseases, some diseases of the cardiovascular system, digestive organs, exogenous and endogenous intoxications, drugs (salicylates, methylxanthines, β-agonists, progesterone), etc. It is believed that in 5% cases of HVS has only an organic nature, in 60% of cases – only psychogenic, in the rest – a combination of these causes [6].
An important feature of the development of HVS is the fact that if the causes that are triggers are eliminated, then hyperventilation, which no longer meets the requirements of a particular situation, persists, and hypocapnia also persists. There is a stabilization of hypocapnic disorders of gas exchange and a “vicious circle” of hot water is formed, which begins to circulate autonomously, and the symptoms can persist for a long time – the “flywheel” phenomenon. These changes in breathing response indicate a vulnerable respiratory control system that is unable to maintain normal partial pressure of carbon dioxide in the blood (PCO ₂ ) and acid-base homeostasis [8, 9, 10, 11].
The development of clinical manifestations of HVS is based on hypocapnic disorders of gas exchange [2, 3, 10]. Among the many clinical manifestations of HVS, shortness of breath is the leading complaint and occurs in almost 100% of cases. Shortness of breath may be the only clinical manifestation, but is more often combined with other symptoms.
Main clinical manifestations of HVS
Respiratory: shortness of breath, sighing, yawning, dry cough.
General: decreased ability to work, weakness, fatigue, subfebrile condition.
Cardiac: cardialgia, extrasystole, tachycardia.
Psychoemotional: anxiety, restlessness, insomnia.
Gastroenterological: dysphagia, epigastric pain, dry mouth, aerophagia, constipation.
Neurological: dizziness, syncope, paresthesia, tetany (rare).
Muscular: muscle pain, tremor.
Diagnosis of HVS primarily relies on the knowledge of doctors of various specialties about the features of the clinical picture of HVS. DHW should be installed only after differential diagnosis with other diseases occurring with dyspnea syndrome. The polymorphism of clinical manifestations of HVS causes diagnostic problems. Numerous examinations are prescribed, expensive, unnecessary, and sometimes dangerous for the patient. L. Lum (1987), discussing diagnostic problems, names useless abdominal surgeries, operations on the spine and other organs, invasive studies that are not without risk, and, worse, diagnoses such as epilepsy and myocardial infarction among medical errors. The relationship between hypocapnia and its associated symptoms is extremely complex. Many doctors, when registering in patients with low values of RSO ₂, automatically diagnose GVS, which is incorrect. It is known that the phenomena of hypocapnia can be in patients with restrictive pulmonary processes, in febrile conditions, cardiac pathology, however, there may not be “classic” hypocapnic complaints. Conversely, so-called hypocapnic complaints, such as anxiety, dyspnea, paresthesia, etc., occur in patients with normocapnia.
In practical medicine, a patient with HVS is a patient who complains of shortness of breath, which does not correspond to the data of an objective examination, indicators of clinical and instrumental breathing studies, with disproportionate, incomprehensible shortness of breath, the subjective perception of which is rather painful. Unfortunately, in the absence of reliable explanations for shortness of breath, patients are usually referred for consultations to various medical institutions. Ultimately, they form the main contingent of alternative medicine, various pseudo-specialists “in training proper breathing. ”
The study of the function of external respiration, which is important in the differential diagnosis of dyspnea, does not help in the verification of functional respiratory disorders. The main confirmation of DHW is the identification of hypocapnic disorders of gas exchange. A decrease in RCO ₂ is a direct evidence of alveolar hyperventilation. However, initial hypocapnia in patients with HVS is less common. Therefore, in cases where normal values of carbon dioxide are determined in a patient with presumptive GVS at rest, it is recommended to determine changes in the level of CO2 during various provocative tests. The “gold standard” for diagnosing DHW is a sample with arbitrary hyperventilation.
The Department of Pulmonology at the University of Nijmegen (Holland) developed the Nijmegen Questionnaire to identify physiological indicators of ventilation dysregulation comparable to DHW (Table). The questionnaire contains 16 items, which are evaluated on a 5-point scale (0 – never, 4 – very often). The minimum and maximum reachable numbers are 0 and 64, respectively.
This questionnaire has found its application primarily for screening diagnostics of DHW. There is a provision according to which the use of this questionnaire allows you to correctly predict the DHW at 90% of all cases [2, 12].
In recent years, the concept of “dysfunctional breathing” (DD) has been introduced into clinical practice. The priority of introducing the term belongs to J. van Dixhoorn, who introduced it in Hyperventilation and dysfunctional breathing (1997). The reason for this was the understanding that with functional respiratory disorders, various changes in the breathing pattern and PCO ₂ values are possible, and not only hypocapnic disorders characteristic of HVS. DD can also be manifested by rapid, arrhythmic, shallow breathing, frequent sighs, and the predominance of the chest type of breathing.
One of the complex and debatable problems in pulmonology is the understanding of the relationship between HVA, DD, and bronchial asthma (BA) [15–18]. S. I. Ovcharenko et al. (2002) revealed respiratory disorders in 22 out of 80 patients with BA that corresponded to the criteria for HVA. There is little information on the occurrence of dysfunctional respiratory disorders in asthma. Among individuals diagnosed with asthma and with at least one prescription of an anti-asthma drug, 29% have been found to have clinical signs of DD [19]. It is indicated that DD can exacerbate the symptoms of AD and lead to excessive prescription of drugs.
It is quite difficult to understand the mechanisms of development of dysfunctional respiratory disorders in BA; there are a number of assumptions. Quite reasonable factors in the development of hyperventilation include anxiety disorders. The use by patients of bronchodilators (β-2-agonists, theophylline), which have the effects of stimulating respiration, is also referred to as a factor in the development of hyperventilation. The role of changes in the perception of dyspnea in BA is discussed. An analysis of the existing problems of the relationship between DD and BA was carried out by M. Morgan (2002), presenting the following key provisions:
- DD (DHW, disproportionate dyspnea) is a syndrome that includes dyspnea and various other somatic symptoms that are associated (but not always) with hypocapnia.
- DD may exacerbate asthma symptoms and lead to overprescribing of medications.
- There is no “gold standard” for diagnosing DD other than clinical signs; The Niimigen questionnaire can be used to identify DD among healthy people.
- There are no reliable methods for verifying DD in patients with pulmonary diseases, including asthma.
- The actual frequency of DD in patients with AD remains unreliable until the definition of this condition is agreed and verification methods are not approved.
- There is insufficient evidence for the benefit of treating DD in patients with asthma.
Depending on the establishment of the features of DD, a program for the treatment of patients should also be carried out.