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Hyperventilation Syndrome Workup

  • Author: Brian Kern, MD; Chief Editor: Ryland P Byrd, Jr, MD  more...
 
Updated: Sep 03, 2014
 

Approach Considerations

Upon a first attack of acute hyperventilation syndrome (HVS), the diagnosis depends on recognizing the typical constellation of signs and symptoms and ruling out the serious conditions that can cause the presenting symptoms.

Acute coronary syndrome (ACS) and pulmonary embolism (PE) are two of the most common serious entities that may present similarly to HVS. Usually, clinical assessment is sufficient to rule out these entities. Depending on that assessment, more specific testing is sometimes warranted.

A standard workup for atypical chest pain, including pulse oximetry, chest radiography, and electrocardiography (ECG), may still be warranted depending on the clinical picture.

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Laboratory Studies

Patients with a history of HVS who have undergone an appropriate workup at some earlier time may not need any further laboratory evaluation in the setting of a recurrence. Recognition of the typical constellation of dyspnea, agitation, dizziness, atypical chest pain, tachypnea and hyperpnea, paresthesias, and carpopedal spasm in a young, otherwise healthy patient with an adequate prior evaluation is often sufficient to establish the diagnosis.

A low pulse oximetry reading in a patient who is hyperventilating should never be attributed to HVS. These patients should always be evaluated for other causes of hyperventilation. A normal pulse oximetry reading is not helpful, because a severe defect in gas exchange can be masked by hyperventilation. A fraction of patients with chronic PE will have compensated chronic hyperventilation that may mimic primary chronic hyperventilation.

Arterial blood gas (ABG) measurement is indicated if any doubt exists as to the patient’s underlying respiratory status. Arterial blood gas analyses may be helpful when HVS-induced alkalosis is suspected, or when shunting or impaired pulmonary gas exchange is being considered.

In chronic HVS, ABG sampling confirms a compensated respiratory alkalosis in a majority of cases. The pH is typically near normal, with a low PaCO2 and a low measured serum bicarbonate level. ABG sampling is also useful in ruling out toxicity from carbon monoxide poisoning, methemoglobinemia, and sulfhemoglobinemia which may present similarly to HVS.[5]

Drug toxicology screening is often indicated. If acute PE is being considered, a quantitative enzyme-linked immunosorbent assay (ELISA) D-dimer assay may be helpful in young patients who are free from comorbid illnesses.

Imaging studies

Imaging studies are not indicated when the diagnosis of HVS is clear. In less obvious cases of HVS, imaging studies are typically normal. Chest radiographs may reveal hyperinflation.

Because PE can present with findings identical to those of HVS, a first-ever episode of acute HVS may warrant ventilation/perfusion scanning or computed tomography (CT) pulmonary angiography to rule out perfusion defects. Chest radiography is indicated for patients who are at high risk for cardiac or pulmonary pathology. Chest radiography is also indicated when the diagnosis is not clear.

Electrocardiography

ECG changes are common and may include the following:

  • ST depression or elevation
  • Prolonged QT interval
  • T-wave inversion
  • Sinus tachycardia

Orthostatic respiratory rate changes

In a normal individual, the respiratory rate typically increases when the person moves from a supine to a standing position. Patients with HVS have an accentuated increase in minute ventilation. End-tidal carbon dioxide is significantly lower in patients with HVS, and ventilatory equivalents for oxygen and carbon dioxide are significantly higher. Thus, noninvasive measurements of gas exchange during orthostatic testing are useful in the diagnosis of HVS.[6]

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Contributor Information and Disclosures
Author

Brian Kern, MD Staff Physician, Department of Emergency Medicine, Detroit Medical Center; Clinical Assistant Professor, Wayne State University School of Medicine

Brian Kern, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Michigan State Medical Society, Michigan College of Emergency Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Adam J Rosh, MD Assistant Professor, Program Director, Emergency Medicine Residency, Department of Emergency Medicine, Detroit Receiving Hospital, Wayne State University School of Medicine

Adam J Rosh, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association

Disclosure: Nothing to disclose.

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Edward J Newton, MD, FACEP, FRCPC Professor of Clinical Emergency Medicine, Chairman, Department of Emergency Medicine, University of Southern California Keck School of Medicine

Edward J Newton, MD, FACEP, FRCPC is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Royal College of Physicians and Surgeons of Canada, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
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  5. Ong JR, Hou SW, Shu HT, et al. Diagnostic pitfall: carbon monoxide poisoning mimicking hyperventilation syndrome. Am J Emerg Med. 2005 Nov. 23(7):903-4. [Medline].

  6. Malmberg LP, Tamminen K, Sovijarvi AR. Orthostatic increase of respiratory gas exchange in hyperventilation syndrome. Thorax. 2000 Apr. 55(4):295-301. [Medline].

  7. Gibson D, Bruton A, Lewith GT, et al. Effects of acupuncture as a treatment for hyperventilation syndrome: a pilot, randomized crossover trial. J Altern Complement Med. 2007 Jan-Feb. 13(1):39-46. [Medline].

  8. Barker NJ, Jones M, O'Connell NE, Everard ML. Breathing exercises for dysfunctional breathing/hyperventilation syndrome in children. Cochrane Database Syst Rev. 2013 Dec 18. 12:CD010376. [Medline].

  9. Chenivesse C, Similowski T, Bautin N, et al. Severely impaired health-related quality of life in chronic hyperventilation patients: exploratory data. Respir Med. 2014 Mar. 108(3):517-23. [Medline].

  10. Jones M, Harvey A, Marston L, O'Connell NE. Breathing exercises for dysfunctional breathing/hyperventilation syndrome in adults. Cochrane Database Syst Rev. 2013 May 31. 5:CD009041. [Medline].

  11. Nardi AE, Freire RC, Zin WA. Panic disorder and control of breathing. Respir Physiol Neurobiol. 2009 May 30. 167(1):133-43. [Medline].

 
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