Hyperventilating syndrome

Hyperventilation syndrome

TOPIC OUTLINE

SUMMARY & RECOMMENDATIONSINTRODUCTIONPREVALENCE AND EPIDEMIOLOGYCLINICAL PRESENTATIONSomatic signs and symptomsPsychological symptomsDIFFERENTIAL DIAGNOSISPATHOPHYSIOLOGYPsychopathologyRegulatory systemsNeurological symptomsPulmonary symptomsDIAGNOSISInitial evaluationFurther evaluation- Ancillary diagnostic testingSpecialist referralTREATMENTAcute managementTreatment to prevent recurrent episodesSUMMARY AND RECOMMENDATIONSREFERENCES

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FIGURES

Venn diagram hyperventilation syndrome

RELATED TOPICS

Acute stress disorder: Epidemiology, clinical manifestations, and diagnosisBronchoprovocation testingClinical manifestations and diagnosis of chronic thromboembolic pulmonary hypertensionDiagnosis of asthma in adolescents and adultsGeneralized anxiety disorder: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosisPanic disorder: Epidemiology, clinical manifestations, and diagnosisPharmacotherapy for generalized anxiety disorderPharmacotherapy for panic disorderPharmacotherapy for posttraumatic stress disorderPsychotherapy for panic disorder

Hyperventilation syndrome

Authors 
Richard M Schwartzstein, MD 
Jeremy Richards, MD, MA 

Section Editor 
Robert H Fletcher, MD, MSc 

Deputy Editor 
Fenny H Lin, MD 

Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Oct 2013. | This topic last updated: Jun 4, 2012.

INTRODUCTION  — The hyperventilation syndrome describes a condition in which an inappropriate increase in minute ventilation beyond metabolic needs (ie, a respiratory alkalosis) is associated with a wide range of symptoms without a clear organic precipitant. As with other medical “syndromes,” there is controversy about the etiology, diagnosis, and treatment of this condition. While it is generally accepted that hyperventilation episodes (or “attacks”) are frequently related to or caused by concomitant panic disorder, other precipitants may also be important.

Many questions have been raised about the term “hyperventilation syndrome” [ 1 ]. Some authors suggest that the term should be avoided, as it implies that hyperventilation is the primary cause of and trigger for a patient’s symptoms [ 2 ]. Others cite that “hyperventilation syndrome” may at best describe multiple pathophysiologic processes rather than a unique, discrete clinical entity [ 3 ]. Nonetheless, “hyperventilation syndrome” is a term in wide use clinically and is descriptive of a common objective finding.

Hyperventilation syndrome is a disorder with no widely-accepted diagnostic criteria [ 1 ]. The challenge to the clinician is to be aware of the possibility of hyperventilation syndrome, recognize the benefits and limitations of available diagnostic tools, and be cognizant of the resources and treatments available to help patients with this complex and sometimes debilitating condition.

This topic will discuss the pathophysiology, clinical presentation, diagnosis, and treatment of patients presenting with hyperventilation syndrome. Detailed discussions of associated disorders are presented separately. (See "Panic disorder: Epidemiology, clinical manifestations, and diagnosis" and "Pharmacotherapy for panic disorder" and "Psychotherapy for panic disorder" and "Generalized anxiety disorder: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosis" and "Acute stress disorder: Epidemiology, clinical manifestations, and diagnosis" .)

PREVALENCE AND EPIDEMIOLOGY  — The prevalence of hyperventilation syndrome is difficult to assess accurately given estimates based upon small sample sizes, varying diagnostic criteria, and its association with psychological symptoms. There is substantial overlap between hyperventilation syndrome and panic disorder and panic attacks [ 4 ]. The prevalence of hyperventilation syndrome has been reported to range from 25 to 83 percent in patients with an anxiety disorder [ 1,5-7 ] and up to 11 percent in patients with nonpsychiatric medical comorbidities [ 8 ].

Limited data suggest that hyperventilation syndrome occurs more commonly in women than in men [ 3,9 ].

CLINICAL PRESENTATION  — While the presentation of hyperventilation syndrome can vary significantly among individuals, the diagnosis is predicated on intermittent episodes of spontaneously resolving hyperventilation. The cardinal feature of hyperventilation syndrome is a transient increase in minute ventilation, out of proportion to metabolic needs [ 10 ]. Patients with hyperventilation syndrome present with a variety of somatic and nonsomatic complaints related to the increased respiration.

Somatic signs and symptoms  — Somatic complaints associated with hyperventilation syndrome may include:

DyspneaLight-headednessParesthesiasChest painPalpitationsDiaphoresisCarpopedal spasm

Importantly, patients with hyperventilation syndrome are only intermittently symptomatic, and symptoms typically occur with unpredictable frequency.

Paresthesias are a common symptom. Tetany, or carpopedal spasm, was described in the original clinical reports of hyperventilation attacks and is still considered a feature of the syndrome [ 11 ]. Its presence may depend on the severity of hyperventilation, to the extent that carpopedal syndrome may be triggered by alkalosis-induced hypocalcemia or cerebral vasoconstriction associated with hypocapnia. (See 'Pathophysiology' below.)

Respiratory sensations associated with an acute episode may include dyspnea, air hunger, an inability to inhale a complete breath, and/or a feeling of unsatisfying breathing (ie, a sensation that tidal volumes are too small despite the fact that the volume of each breath is actually quite large). Patients experiencing an episode of hyperventilation syndrome typically will have a breathing pattern characterized by relatively slow, very deep breaths.

Additionally, patients with hyperventilation syndrome who develop symptoms with voluntary hyperventilation or with exercise typically experience delayed resolution of respiratory symptoms after exercise compared to normal subjects. Furthermore, the intensity of exertion may not correlate with the degree of dyspnea experienced by patients with hyperventilation syndrome; relatively minimal exertion may result in significant dyspnea [ 12 ].

Psychological symptoms  — Patients with hyperventilation may complain of:

Sense of impending doom

Anxiety and fear

Anxiety and other psychologic symptoms may occur with hyperventilation attacks. In many patients, these symptoms reflect a primary psychological pathology that is the cause of hyperventilation. In other patients, anxiety and somatoform symptoms are a result of the incipient hyperventilation and the accompanying metabolic changes that cause systemic disturbance. (See 'Psychopathology' below.)

Patients may report precipitating events such as an isolated psychological or physical stressor. However, episodes may occur randomly or without an obvious precipitant. One case series evaluated psychological and emotional events in the three years prior to presentation in 31 patients with a clinical diagnosis of hyperventilation syndrome [ 5 ]. Many of these patients described events or feelings of bereavement, uncertainty about the seriousness of their symptoms, or resentment towards the medical profession because the cause of their symptoms is unexplained and they feel that their symptoms are minimized.

DIFFERENTIAL DIAGNOSIS  — Multiple serious and potentially-emergent medical conditions may present with symptoms also common in patients with hyperventilation syndrome. These conditions need to be considered early in the evaluation of a patient who presents with dyspnea and who appears to be hyperventilating. The differential diagnosis is broad, and includes [ 1 ]:

Metabolic disorders (ketoacidosis, less frequently hypoglycemia or hypocalcemia)Acute coronary syndromeArrhythmiaHeart failurePulmonary embolismPneumothoraxAsthma exacerbationChronic obstructive pulmonary disease exacerbationSeizure disorderHyperthyroidism

It is also important to remember that tachypnea or hyperventilation from any cause in the setting of airflow obstruction may lead to dynamic hyperinflation and associated physiological changes that will cause or worsen dyspnea.

PATHOPHYSIOLOGY

Psychopathology  — An association between hyperventilation syndrome and psychological pathologies (such as panic disorder) is clear, but whether the psychological condition is primary or secondary is often unclear. Both respiratory and somatic symptoms are common in patients with psychological distress. Specifically, “disproportionate breathlessness" is associated with depression, anxiety, bereavement, resentment, and uncertainty about the seriousness of one's illness [ 5 ].

The diagnosis of panic disorder or other neuroses contributing to a patient’s respiratory symptoms may be indicated by rapid shallow breathing, irregular respiratory patterns, sighing, and paroxysms of hyperventilation. These symptoms and the concomitant anxiety may be due to hyperventilation itself.  

Regulatory systems  — Abnormalities in ventilatory control are important in symptom development in some patients with hyperventilation syndrome. The reticular activating system regulates breathing patterns. Under normal conditions, healthy individuals demonstrate regular breathing with no voluntary effort. When asked to make a voluntary breathing effort, symptoms may be triggered in patients with hyperventilation syndrome. As an example, hyperventilation symptoms can be induced in such patients when they are instructed to breathe through a mouthpiece, while normal control subjects can do this with no difficulty [ 13 ]. The inability of patients with this syndrome to breathe steadily through a mouthpiece may indicate an overactive reticular activating system. 

Increased sensitivity to carbon dioxide or a hypersensitive fear network (the hippocampus, medial prefrontal cortex, amygdala and its brainstem projections) have also been proposed as mechanisms for the hyperventilation syndrome and its association with psychological symptoms [ 14 ]. An activated hypersensitive fear network may result in an increased central respiratory drive, both as a manifestation of a “fight or flight” response and as a means to reduce PaCO2 levels and thereby decrease direct stimulation of the fear network.

Neurological symptoms  — Cerebral blood flow decreases in a linear fashion with decreasing PaCO2: a decrease of 1 mmHg of PaCO2 is associated with a 2 percent decrease in cerebral blood flow [ 15 ]. A reduction in cerebral blood flow in the setting of hyperventilation, hypocapnia, and respiratory alkalosis may explain the neurologic symptoms associated with the hyperventilation syndrome such as paresthesias, headache, and light-headedness [ 16 ].

While some have proposed a mechanism in which acute changes in ionized serum calcium levels, triggered by respiratory alkalosis and the consequent binding of calcium to albumin, could result in paresthesias and/or tetany, there is no evidence (nor would it be anticipated) that hyperventilation results in changes in total serum calcium levels [ 13,17,18 ]. Hypophosphatemia has been noted, however, and may contribute to tetany [ 3,14 ]. It has also been proposed that paresthesias or tetany in patients with an acute episode of hyperventilation may be due to local vasoconstriction leading to tissue hypoxemia and/or cerebral vasoconstriction, caused by decreased PaCO2 in the setting of acute respiratory alkalosis. Tetany associated with hyperventilation should rapidly respond to normalization of arterial carbon dioxide levels (PaCO2).

Vestibular and balance disorders may play an etiologic role for some patients with hyperventilation syndrome, accounting for symptoms of light-headedness and dizziness. Specifically, the distress associated with postural symptoms in the setting of vestibular pathology may also trigger hyperventilation. Furthermore, the vestibular system affects the activity of respiratory muscles in response to changes in body position. In patients with vestibular pathology, such responses may be exaggerated and result in inappropriate increases in ventilation [ 19,20 ].

Pulmonary symptoms  — Efferent-afferent dissociation describes an imbalance between sensory signals (from pulmonary and chest wall stretch receptors) and motor signals (from the motor cortex). An imbalance between efferent and afferent signals results in dyspnea; the greater the imbalance, the greater the severity of dyspnea [ 21,22 ]. Patients with hyperventilation syndrome may have an imbalance in these signals leading to a sensation of dyspnea that then precipitates a voluntary increase in minute ventilation.

Pulmonary symptoms in some patients diagnosed with hyperventilation syndrome may be due to unrecognized pulmonary pathology. Intermittent, mild, clinically-unrecognized airway obstruction due to asthma may account for some cases of hyperventilation syndrome [ 23,24 ]. The difficulty in accurately diagnosing asthma, especially mild cases, contributes to delayed recognition of this diagnosis. (See "Diagnosis of asthma in adolescents and adults" .)

DIAGNOSIS  — There are no gold standard diagnostic tests or criteria with which to diagnose hyperventilation syndrome. The combination of clinical suspicion based upon the patient’s presentation, and the absence of findings to support an alternative diagnosis, is sufficient to diagnosis hyperventilation syndrome in the majority of cases.

The overlap of cardiopulmonary conditions and emotional conditions that include hyperventilation as a component of their clinical picture should be kept in mind. Having excluded physiologic causes for hyperventilation, however, one is often still left with a syndrome that may be characterized by features of a number of psychological and behavioral disorders ( figure 1 ).

Initial evaluation  — Clinician awareness of hyperventilation syndrome as an etiologic possibility is essential to establish this as a diagnosis and to avoid unnecessary testing in the evaluation of less likely diagnoses [ 25 ]. Only a minority of patients requires referral to appropriate specialists for more advanced evaluation.

To make the diagnosis of hyperventilation syndrome, alternative etiologies need to be considered and excluded. The patient history and physical examination should focus on excluding these potential alternative etiologies. (See 'Differential diagnosis' above.)

The diagnostic approach to a patient with suspected hyperventilation syndrome should include the following:

History — Including the frequency and duration of episodes, manifestations, precipitants, and relievers. Patients whose symptoms are not intermittent should not be considered as having hyperventilation syndrome. The absence of reproducible exertional symptoms is often helpful in excluding chronic pulmonary disease.Physical examination — Other than findings of a breathing pattern with an inordinately large tidal volume at rest, the examination should be normal.Oxygen saturation (including saturation during ambulation) should be normalSpirometry (does not have to be performed emergently, but should be done, if possible, during an episode of hyperventilation)Chest radiographyECG in patients with chest pain and no chest wall tenderness

Patients should not be asked to breathe into a paper bag to promote rebreathing of CO2 as a diagnostic test for hyperventilation syndrome, looking for rapid symptom resolution. This maneuver is of questionable diagnostic value and has been associated with adverse outcomes, due to the potential for hypoxemia during rebreathing, in patients with underlying respiratory or cardiovascular disease [ 26 ].

Further evaluation  — Further evaluation to investigate the possibility of a cardiac, metabolic, or neurologic cause of the patient’s symptoms should be based upon the patient’s history and examination findings, and the likelihood of underlying pathology.  

Other evaluations that may be indicated for certain patients include:

Bronchoprovocation testing (with methacholine or other pharmacologic agent)Chest CT imaging

Bronchoprovocation testing (such as a methacholine challenge test) may be indicated for patients with symptoms suggestive of asthma or reactive airways diseases who demonstrate normal values on routine spirometry. Patients who describe wheezing with hyperventilation attacks, or patients whose attacks are associated with environmental (dust, allergen, smoke) or other (exercise, cold air) exposures may also warrant provocation testing. Patients without wheezing, a complaint of chest tightness, or an apparent precipitant, however, are unlikely to require such testing. (See "Bronchoprovocation testing", section on 'Pharmacologic challenge' .)

In the vast majority of cases, patients with a normal chest x-ray do not require chest CT imaging. Chest CT scanning is indicated to evaluate abnormalities on chest radiography, including possible pulmonary nodules or masses, parenchymal infiltrates, or large airway abnormalities. A CT scan may be useful to assess for subtle interstitial infiltrates when physical examination suggests possible interstitial disease; approximately 10 percent of patient with interstitial lung disease present with normal chest x-rays. For patients in whom there is a suspicion of pulmonary hypertension based upon physical exam (jugular venous distention, loud P2), CT angiography may assist in the diagnosis of chronic thromboembolic disease. (See "Clinical manifestations and diagnosis of chronic thromboembolic pulmonary hypertension" .).

Ancillary diagnostic testing  — Certain ancillary tests may be indicated in patients whose diagnosis remains uncertain after the initial evaluation. These components of an advanced diagnostic evaluation are indicated only for a minority of patients with suspected hyperventilation syndrome and should be pursued in concert with a specialist (such as a pulmonologist). Such non-routine testing may include:

Measurement of PaCO2 or end-tidal CO2 during and after attacks. However, there is no consensus regarding the threshold for the decrease in PaCO2 or end-tidal CO2 that would establish a diagnosis hyperventilation syndrome [ 27 ].The hyperventilation provocation test (HVPT). Subjects are asked to hyperventilate (typically for three to five minutes) in an effort to precipitate spontaneous symptoms. A patient’s symptoms are assessed after voluntary hyperventilation and compared to the symptoms experienced by the patient during spontaneous “attacks.” Compared to normal subjects, minute ventilation may be elevated and normalization of PaCO2 after voluntary hyperventilation may be delayed in patients with hyperventilation syndrome [ 2 ]. The HVPT has several limitations, however, and its clinical utility is uncertain [ 2,28,29 ]. One study reports that in a randomized trial the HVPT was positive in 85 of 115 subjects with suspected hyperventilation (74 percent), but that 56 of the 85 also had a positive placebo test (in which CO2 levels were maintained during overbreathing) [ 12 ].

Additional testing that could be considered in the evaluation of hyperventilation syndrome includes cardiopulmonary exercise testing [ 30 ] and dyspnea questionnaires [ 31,32 ].

Specialist referral  — Referral to a specialist (typically a pulmonologist) is appropriate for patients with multiple medical comorbidities contributing to atypical presentations of dyspnea or for those in whom there is difficulty in establishing a definitive diagnosis. Patients who are refractory to standard treatment may also warrant referral to a specialist. (See 'Treatment' below.)

Patients may present with a spectrum of symptoms that in aggregate suggest an alternative diagnosis (such as COPD) but that include intermittent, transient hyperventilation. If the patient’s hyperventilation symptoms persist despite appropriate treatment of the alternative diagnosis (such as initiating bronchodilators for COPD), further evaluation may be warranted. Additionally, abnormalities on pulmonary function testing and/or chest imaging during the initial evaluation for alternative causes for hyperventilation syndrome may require referral to a specialist for evaluation.

Patients who exhibit a predominance of psychiatric symptoms associated with the presentation of hyperventilation episodes may require further assessment by a psychiatrist or mental health professional.

TREATMENT  — There is scant evidence on the effectiveness of treatments for patients with hyperventilation syndrome, either presenting with an acute episode or seeking help for management of recurrent symptoms.  

Acute management  — Immediate management of patients who are hyperventilating should focus on patient reassurance, an explanation of the symptoms the patient is experiencing, attempts to calm the patient, removal of any stressors, and encouragement to breathe at a normal rate and tidal volume. If these are unsuccessful, the patient may be given a small dose of a rapidly-acting benzodiazepine.

Forced rebreathing of CO2 by breathing into a paper bag, while it may lead to improvement in symptoms in patients with hyperventilation syndrome by normalizing PaCO2 levels, may also cause significant hypoxemia and consequent complications [ 26 ]. Asking the patient to rebreathe into a paper bag may be tried so long as it is clear that the patient is not experiencing an acute hypoxic or cardiac event; when possible, a pulse oximeter should be applied during this maneuver. Although this technique has long been used to normalize PaCO2 levels, there are no studies of the efficacy of this traditional treatment [ 3 ].

Treatment to prevent recurrent episodes  — The cornerstone of treatment for hyperventilation syndrome is behavioral therapy and education. Patient education regarding the nature of the disease process and breathing retraining may provide significant benefit to affected patients [ 33 ]. Breathing retraining, which focuses on enhancing a patient’s awareness of breathing pattern and strategies to normalize the pattern when symptoms occur, is most commonly performed in the setting of pulmonary rehabilitation, but may also be a component of psychiatric and cognitive-behavioral therapy.  

The available literature indicates that breathing retraining can have both short- and long-term effects on improving symptoms [ 33,34 ]. Long-term effects were demonstrated in a three-year follow-up study of 10 patients who underwent rebreathing training for hyperventilation syndrome [ 34 ].

Some studies of beta blockers have demonstrated short-term improvement in the frequency of hyperventilation episodes [ 35 ]. In one randomized trial over three weeks, bisoprolol 5 mg once daily led to a 75 percent decrease in the frequency of hyperventilation episodes (from 4 to 1 per week), compared to a 12.5 percent decrease (from 4.0 to 3.5 per week) with placebo [ 35 ]. However, a retrospective study of beta blockers compared to benzodiazepines and anxiolytics demonstrated no effect of either therapy on subjective complaint, and dissociation between subjective complaints and measurements of ventilation [ 36 ]. Both beta blocker and sedatives were equivalent in raising the PaCO2; side effects were less frequent with beta blockers.

Benzodiazepines are commonly prescribed for patients with overlapping psychological and/or psychiatric symptoms and hyperventilation syndrome. There are limited efficacy data on hyperventilation syndrome with or without psychological symptoms. One small study demonstrated no efficacy of benzodiazepines compared to breathing retraining [ 37 ]. In this study, 40 consecutive patients were randomly assigned to treatment with breathing retraining, treatment with benzodiazepines, treatment with “hyperventilation provocation” (breathing into a plastic bag every day for two to four weeks), or a control group. There was a significant reduction in the frequency and severity of hyperventilation episodes in all groups, and there were no differences between groups [ 37 ].

Although beneficial in the treatment of generalized anxiety disorder and posttraumatic stress syndrome, there are no studies of the efficacy of selective serotonin reuptake inhibitors (SSRIs) in the treatment of hyperventilation syndrome. (See "Pharmacotherapy for posttraumatic stress disorder", section on 'Selective serotonin reuptake inhibitors' and "Pharmacotherapy for generalized anxiety disorder", section on 'Selective serotonin reuptake inhibitors' .)

SUMMARY AND RECOMMENDATIONS

Hyperventilation syndrome is characterized by a transient increase in minute ventilation with a wide range of associated symptoms in the absence of an alternative, contributory underlying cardiorespiratory diagnosis. (See 'Introduction' above.)Patients may present with a variety of complaints: dyspnea, light-headedness, paresthesias, chest pain, palpitations, diaphoresis, sense of impending doom, and anxiety have all been associated with hyperventilation syndrome. (See 'Clinical presentation' above.)Psychological, neurological, and cardiopulmonary pathologies may all contribute to a patient’s symptoms. There is significant overlap with psychiatric comorbidities (especially panic and anxiety disorders). (See 'Prevalence and epidemiology' above.)Physician awareness is of paramount importance in diagnosing hyperventilation syndrome. The diagnosis can usually be established by a compelling history, normal physical exam, and the absence of alternative processes. (See 'Diagnosis' above.)Referral to a pulmonologist for specialty testing is only necessary in complicated diagnostic cases, in patients with multiple comorbidities, or for patients who are refractory to standard interventions. Referral to a psychologist or psychiatrist is also appropriate for many patients with recurrent episodes. (See 'Specialist referral' above.)We suggest that patients who are diagnosed with hyperventilation syndrome, who are not felt to have an underlying anxiety or panic disorder, be treated with behavioral therapy focused upon breathing retraining ( Grade 2C ). The acute management of a hyperventilation episode should focus on patient reassurance; paper bag rebreathing should be administered with caution, particularly in patients with possible respiratory or cardiac pathology. (See 'Treatment' above.)

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