Hyperventilation Syndrome Clinical Presentation
- Author: Brian Kern, MD; Chief Editor: Ryland P Byrd, Jr, MD more...
Patients with acute hyperventilation syndrome (HVS) may present with agitation and anxiety. Most commonly, the history is one of sudden onset of dyspnea, chest pain, or neurologic symptoms (eg, dizziness, weakness, paresthesias, or near-syncope) after a stressful event. Patients with chronic HVS present with similar symptoms, including recurrent chest pain, dyspnea, and neurologic deficits, and usually have had many similar presentations in the past.
Patients often present dramatically, with agitation, hyperpnea and tachypnea, chest pain, dyspnea, wheezing, dizziness, palpitations, tetanic cramps (eg, carpopedal spasm), paresthesias, generalized weakness, and syncope. The patient often complains of a sense of suffocation. An emotionally stressful precipitating event can often be identified.
The chest pain associated with HVS usually has atypical features, but on occasion, it may closely resemble typical angina. It tends to last hours rather than minutes, and is often relieved rather than provoked by exercise. It is usually unrelieved by nitroglycerin.
The diagnosis of HVS should be considered in young patients without cardiac risk factors who present with chest pain, particularly if the pain is associated with paresthesias and carpopedal spasm. However, this diagnosis should be reached cautiously, because many other potentially lethal conditions can also cause young patients to present with chest pain (eg, pulmonary embolism [PE] and spontaneous pneumothorax).
Electrocardiographic (ECG) changes are common in patients with HVS. Abnormalities may include prolonged QT interval, ST depression or elevation, and T-wave inversion.
In patients with subcritical coronary artery stenosis, the vasospasm induced by hypocarbia may be sufficient to provoke myocardial injury.
The incidence of HVS is high among patients with mitral valve prolapse (MVP), and the chest pain associated with MVP may be due to hyperventilation.
Prinzmetal angina (ie, coronary artery vasospasm) is triggered by HVS, but the chest pain associated with this syndrome normally would be expected to respond to nitrates or calcium channel blockers.
Central nervous system symptoms
Central nervous system (CNS) symptoms occur because hypocapnia causes cerebral artery vasoconstriction and reduced cerebral blood flow (CBF). CBF decreases by 2% for every 1 mm Hg decrease in the arterial partial pressure of carbon dioxide (PaCO2).
The symptoms of dizziness, weakness, confusion, and agitation are common. Patients may report feelings of depersonalization and may experience visual hallucinations. Syncope or seizure may be provoked by hyperventilation. Paresthesias occur more commonly in the upper extremity and are usually bilateral. Perioral numbness is very common.
Gastrointestinal (GI) symptoms (eg, bloating, belching, flatus, or epigastric pressure) may result from aerophagia.
Acute metabolic changes result from intracellular shifts and increased protein binding of various electrolytes during respiratory alkalosis.
Acute secondary hypocalcemia can result in carpopedal spasm, muscle twitching, a prolonged QT interval, and positive Chvostek and Trousseau signs. Hypokalemia tends to be less pronounced than hypocalcemia but can produce generalized weakness. Acute secondary hypophosphatemia is common and may contribute to paresthesias and generalized weakness.
The diagnosis of chronic HVS is much more difficult than that of acute HVS because hyperventilation is usually not clinically apparent. Often, these patients have already undergone extensive medical investigations and have been assigned several misleading diagnoses.
Two thirds of patients with chronic HVS have a persistently slightly low PaCO2 with compensatory renal excretion of bicarbonate, resulting in a near-normal pH level. These patients tend to have prominent CNS symptoms. In addition, they typically present with dyspnea and chest pain.
The respiratory alkalosis can be maintained with occasional deep sighing respirations, which are observed often in patients with chronic HVS.
When faced with an additional stress that provokes hyperventilation, the physiologic acid-base reserve is less, and these patients become symptomatic more readily than patients without HVS.
Dry mouth occurs with mouth breathing and anxiety. Many of these patients suffer from obsessive-compulsive disorders, experience sexual and marital difficulties, and have poor adaptations to stress.
Patients with chronic HVS may have symptoms that mimic those of virtually any serious organic disorder, but they usually have atypical features of these diseases.
In acute HVS, obvious tachypnea and hyperpnea are present. Although chest wall tenderness is common in patients with HVS, it is not a helpful finding, because chest wall tenderness is also found in pneumonia, pneumothorax, pulmonary embolism, coronary artery syndromes, and a wide variety of other serious and benign thoracoabdominal diseases.
Carpopedal spasm occurs when acute hypocarbia causes reduced ionized calcium and phosphate levels, resulting in involuntary contraction of the feet or (more commonly) the hands (see the image below). Chvostek or Trousseau signs may be positive because of hyperventilation-induced hypocalcemia. Wheezing may be heard because of bronchospasm from hypocarbia.
Tremor, mydriasis, pallor, tachycardia, and other manifestations of anxiety can occur. Evidence of depersonalization or hallucination may be noted.
Chronic hyperventilation syndrome
In chronic HVS, hyperventilation is usually not readily apparent. Frequent sighing respirations (2-3 breaths/min) and frequent yawning are noted. Chest wall tenderness, numbness, and tingling may be present. Characteristically, patients have multiple complaints without much supporting physical evidence of disease.
The complications encountered in patients with this syndrome are related mainly to the invasive procedures and investigations (eg, angiography) that are employed to rule out other diseases (see Workup).
However, complications may also occur as a result of symptoms produced indirectly by hyperventilation (eg, injuries sustained in a fall during a syncopal episode attributable to hyperventilation).
Shu BC, Chang YY, Lee FY, et al. Parental attachment, premorbid personality, and mental health in young males with hyperventilation syndrome. Psychiatry Res. 2007 Oct 31. 153(2):163-70. [Medline].
Martinez JM, Kent JM, Coplan JD, et al. Respiratory variability in panic disorder. Depress Anxiety. 2001. 14(4):232-7. [Medline].
Bartley J. Nasal congestion and hyperventilation syndrome. Am J Rhinol. 2005 Nov-Dec. 19(6):607-11. [Medline].
Castro PF, Larrain G, Perez O, et al. Chronic hyperventilation syndrome associated with syncope and coronary vasospasm. Am J Med. 2000 Jul. 109(1):78-80. [Medline].
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].
Malmberg LP, Tamminen K, Sovijarvi AR. Orthostatic increase of respiratory gas exchange in hyperventilation syndrome. Thorax. 2000 Apr. 55(4):295-301. [Medline].
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].
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].
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].
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].
Nardi AE, Freire RC, Zin WA. Panic disorder and control of breathing. Respir Physiol Neurobiol. 2009 May 30. 167(1):133-43. [Medline].