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Contributors Randolph W Evans MD, contributing editor. Dr. Evans of Baylor College of Medicine received honorariums from GlaxoSmithKline, Merck, Pfizer, Lilly, and Accera for speaking engagements
Publication dates Originally released December 6, 1996; last updated January 27, 2010; expires January 27, 2013
Synonyms Hyperventilation; Neurocirculatory asthenia; Soldier's heart; Soldier heart
Historical note and nomenclature
According to 1 consensus definition, "hyperventilation syndrome is a syndrome characterized by a variety of somatic symptoms induced by physiologically inappropriate hyperventilation and usually reproduced in whole or in part by voluntary hyperventilation" (Lewis and Howell 1986). Acute hyperventilation with obvious tachypnea accounts for about 1% of all cases of hyperventilation (Lum 1975). The other 99% of cases are due to chronic hyperventilation where there may be a modest increase in respiratory rate or tidal volume, which may not even be apparent to the patient or a medical observer. The symptoms of hyperventilation syndrome have been recognized for at least 125 years. In 1871, Da Costa published a paper, On Irritable Heart; a Clinical Study of a Form of Functional Cardiac Disorder and its Consequences , describing 300 Union soldiers in the American Civil War with a mysterious illness (Da Costa 1871). He felt the condition could be seen in private practice as well. Symptoms included palpitations, chest pain, shortness of breath or oppression on exertion, indigestion, abdominal distention, and diarrhea. Headache, giddiness, disturbed sleep, and dizziness were "all indicative of disturbed circulation in the cerebro-spinal centres." Da Costa reasoned that "the heart has become irritable, from its over-action and frequent excitement...." During World War I, similar symptoms often associated with fatigue were also attributed to cardiovascular dysfunction and described as "soldier's heart" (Lewis 1919) or "neurocirculatory asthenia" (Levine 1965). In contrast, Gowers used the terms "vagal" and "vaso-vagal" for these symptoms, which could include numbness and tingling of the extremities (Gowers 1907). In 1922, Goldman was the first to make the connection between "forced ventilation" and tetany and postulated that the tetany was due to alkalosis (Goldman 1922). Kerr and colleagues introduced the term "hyperventilation syndrome," and they described the variety of symptom complexes caused by physical phenomena associated with anxiety states, which could often be reproduced in the examining room with the "hyperventilation test" (Kerr et al 1937; 1938). Lewis contended that acute and chronic hyperventilation syndrome occurred frequently and described the common and atypical presentations, pathophysiology, and therapy (Lewis 1953). He reported that paresthesias were occasionally asymmetrical and could even be unilateral. Tavel described patients with hyperventilation syndrome presenting with unilateral paresthesias at times associated with subjective unilateral weakness that involved the left side of the face and body more commonly than the right (Tavel 1964).
Clinical manifestations
The manifestations of hyperventilation syndrome are listed in Table 1. Patients with different symptoms may see different specialists. Cardiologists may see those with complaints of chest pain, palpitations, and shortness of breath. Neurologists frequently see patients describing dizziness and paresthesias (Pincus 1978; Perkin and Joseph 1986).
Table 1. Symptoms and Signs of Hyperventilation Syndrome
General
- Fatigability, exhaustion, weakness, sleep disturbance, nausea, sweating
Cardiovascular
- Chest pain, palpitations, tachycardia, Raynaud phenomenon
Gastrointestinal
- Aerophagia, dry mouth, pressure in throat, dysphagia, globus hystericus,
- Epigastric fullness or pain, belching, flatulence
Neurologic
- Headache, pressure in the head, fullness in the head, head warmth
- Blurred vision, tunnel vision, momentary flashing lights, diplopia
- Dizziness, faintness, vertigo, giddiness, unsteadiness
- Tinnitus
- Numbness, tingling, coldness of face, extremities, trunk
- Muscle spasms, muscle stiffness, carpopedal spasm, generalized tetany, tremor
- Ataxia, weakness
- Syncope, seizures
Psychological
- Impairment of concentration and memory
- Feelings of unreality, disorientation, confused or dream-like feeling, déjà vu
- Hallucinations
- Anxiety, apprehension, nervousness, tension, fits of crying, agoraphobia
- Neuroses, phobias, panic attacks
Respiratory
- Shortness of breath, suffocating feeling, smothering spell, inability to get a good breath or breathe deeply enough, frequent sighing, yawning
The most common cause of distal symmetrical paresthesias is hyperventilation syndrome (Macefield and Burke 1991). Although physicians generally recognize bilateral paresthesias of the face, hands, and feet as due to hyperventilation syndrome, many neurologists are not aware that hyperventilation can cause unilateral paresthesias. In 2 studies of volunteer groups, hyperventilation produced predominantly unilateral paresthesias in 16%, and these involved the left side in over 60% (Tavel 1964; Evans 1995; 2005). Of those with hand numbness, often only the fourth and fifth fingers are involved. Unusual patterns of numbness reported include 1 side of the forehead, the shoulders, and 1 side of the abdomen. Unilateral paresthesias more often involving the left side have also been reported (Tavel 1964; Blau et al 1983; Perkin and Joseph 1986; Brodtkorb et al 1990; O'Sullivan et al 1992). Patients may report a variety of psychological complaints, commonly including anxiety, nervousness, unreality, disorientation, or feeling "spacy." Impairment of concentration and memory may be described as part of episodes or alternatively as symptoms of an
finding that there is no relationship between the rate of fall of pCO2 and the onset of dizziness and paresthesias suggests that symptoms may be due to hypophosphatemia (Rafferty et al 1992). Hypophosphatemia can result in symptoms such as tiredness, dizziness, poor concentration, disorientation, and paresthesias. A hyperadrenergic state may result in tremor, tachycardia, anxiety, and sweating. Hypokalemia can cause muscle weakness and lethargy. The cause of bilateral and unilateral paresthesias is not certain; evidence exists for both a central and peripheral mechanism. A reduction in the concentration of extracellular Ca2+ may increase peripheral nerve axonal excitability, resulting in spontaneous bursting activity of cutaneous axons, perceived as paresthesias (Macefield and Burke 1991). Lateralization of symptoms might be explained by anatomic differences in the peripheral nerves and their nutrient vessels (Galin et al 1977). Alternatively, symmetrically decreased cerebral perfusion could account for bilateral paresthesias and asymmetrically decreased perfusion for unilateral paresthesias. O'Sullivan and colleagues reported nonspecific, asymmetric slowing of brain waves in the hemisphere opposite to the side of unilateral paresthesias in hyperventilators and normal bilateral somatosensory evoked potentials (O'Sullivan et al 1992). Although anatomic differences in the cerebral vasculature might explain the unilateral paresthesias, normal magnetic resonance angiographic findings in 2 cases argue against this (Evans 1995). Additionally, there is a single report of asymmetrically decreased cerebral blood flow with decreased flow in the right parietal area with left-sided symptoms (Evans 1995). It is not known why unilateral paresthesias occur more often on the left side of the face and body. One hypothesis is that psychosomatic symptoms are associated with right hemisphere psychic processes. During stress and emotional arousal, the right hemisphere is activated more than the left (Tucker et al 1977). Symptoms of conversion or hyperventilation are more likely to occur on the left side of the face and body (Galin et al 1977; O'Sullivan et al 1992). However, this hypothesis does not explain the increased frequency of left-sided paresthesias in normal subjects who are asked to hyperventilate.
Epidemiology
Hyperventilation syndrome occurs in about 6% to 11% of the general patient population (Brashear 1983). In a clinic that evaluated patients with dizziness, hyperventilation syndrome accounted for 24% of the cases (Drachman and Hart 1972). Most studies have reported hyperventilation syndrome occurring 2 to 7 times more frequently in women than in men, with most patients ranging in age between 15 and 55 years (Garssen and Rijken 1990). One large study reported that patients with acute hyperventilation syndrome ranged in age from 5 to 85 years and was particularly prevalent in women in their late teens (Hirokawa et al 1995). The prevalence of chronic hyperventilation is highest in middle-aged women (Hirokawa et al 1995). In studies of patients with neurologic symptoms of hyperventilation syndrome, the percentage of females ranges from 50% (Blau et al 1983) to 67% (Perkin and Joseph 1986; Brodtkorb et al 1990; O'Sullivan et al 1992) to 87% (Pincus 1978).
Prevention
For psychogenic cases of hyperventilation syndrome, avoidance of triggers is a preventative measure.
Differential diagnosis
Hyperventilation syndrome has organic and physiological as well as emotional and habitual causes. Less than 5% of hyperventilation has a solely organic cause, 60% has a psychogenic (emotional and habitual) basis, and the remainder has varying combinations (Brashear 1984). The variety of organic disorders that can result in hyperventilation
include: (1) effects of salicylate, caffeine, topiramate (Laskey et al 2000), and other drugs; (2) cirrhosis and hepatic coma; (3) acute pain such as that accompanying a myocardial infarction; (4) splenic flexure syndrome, cholecystitis, fever, and sepsis; and (5) dissecting aortic aneurysm, respiratory dyskinesia, pulmonary embolism, pneumothorax, interstitial lung disease, asthma, and heat and altitude acclimatization (Brashear 1983; Block and Szidon 1994). Neurologic disorders that may cause hyperventilation include Rett syndrome, Joubert syndrome, Reye syndrome, pyruvate dehydrogenase deficiency, biotin-dependent multiple carboxylase deficiency, malignant hyperthermia, brainstem tumor, primary cerebral lymphoma, encephalitis, brainstem strokes, thalamic hemorrhage, syringobulbia, and neurogenic pulmonary edema due to intracranial hypertension (Beumer and Bruyn 1993). Severe hyperventilation can occur in the absence of psychiatric, respiratory, neurologic, or other organic abnormalities (Bass and Gardner 1985). In patients diagnosed with hyperventilation syndrome by neurologists, the misdiagnoses of referring physicians have included epilepsy, migraine, multiple sclerosis, arteriovenous malformation, cerebrovascular disease, vertebrobasilar insufficiency, brachial neuritis, angina, malingering, vasovagal attacks, functional illness, hypoglycemia, and cerebral tumor (Blau et al 1983; Perkin and Joseph 1986). Hyperventilation might also contribute to some of the manifestations of migraine such as syncope. Cardiac abnormalities should certainly be considered in those patients with chest pain. The distinction between angina and hyperventilation syndrome at times is difficult because hyperventilation can produce electrocardiogram changes including T-wave inversions, systolic time-segment depression, and systolic time-segment elevation in patients without coronary artery disease (Heckerling and Hanashiro 1985). Some patients with angina may hyperventilate in response to their pain and anxiety. The symptoms of mitral valve prolapse and hyperventilation syndrome overlap. In some patients, symptoms may be due to hyperventilation (Tavel 1990). The symptoms of panic attacks greatly overlap with hyperventilation syndrome, and the differential diagnosis is quite similar (Tesar and Rosenbaum 1993; Stahl and Soefje 1995). The pathophysiology of panic attacks is controversial; hyperventilation syndrome has been suggested as a cause (Ley 1985; Nutt and Lawson 1992; Folgering 1999). Patients diagnosed with panic attacks that report brief episodic unilateral paresthesias or weakness may have the neurologic symptoms reproduced with the hyperventilation test (Coyle and Sterman 1986). Tonic spasms (paroxysmal dystonia) of multiple sclerosis can be somewhat similar to the muscle spasms, tetany, and paresthesias of hyperventilation syndrome. The episodes consist of brief, recurrent, often painful abnormal posturing of 1 or more extremities without alteration of consciousness, loss of sphincter control, or clonic movements. They last for 10 seconds to 3 minutes and recur as often as 30 times daily. Some patients may experience brief sensory disturbances in the involved extremity before or during the attack. Because the episodes can be the initial presentation of multiple sclerosis (Heath and Nightingale 1982) and can be triggered by hyperventilation (Shibasaki and Kuroiwa 1974), diagnostic confusion might result.
Diagnostic workup
The acute form of hyperventilation syndrome is easily recognized. However, the chronic form is less easily recognized because the breathing rate is not reported as rapid or does not appear rapid and because the symptoms may appear to be atypical. For example, a respiration rate of 18 per minute combined with an increased tidal volume of 750 mL per minute may lead to overbreathing that is not easily detectable. Because the chronic disorder is intermittent, spot arterial pCO2 or end tidal volume pCO2 results can be normal. The diagnosis depends on reproducing some or all of the symptoms with the
test, despite its recognized shortcomings (Gardner 2000), is useful. In the individual case, if the hyperventilation provocation test fails to reproduce the symptoms but clinical suspicion persists, treatment such as breath holding, slow breathing, or breathing into a paper bag can certainly be suggested on a trial basis.
Prognosis and complications
In a followup study of children and adolescents, 40% were still hyperventilating as adults and many suffered from chronic anxiety (Herman et al 1981). One half of patients with acute hyperventilation recover without treatment (Hirokawa et al 1995). In 10% of those with chronic hyperventilation, symptoms may persist for more than 3 years (Hirokawa et al 1995). With proper management, about 70% to 90% of adults become symptom-free (Lum 1976; Campernolle et al 1979).
Management
The various treatments for hyperventilation that have been proposed include patient reassurance and education, instructions to hold the breath, breathe more slowly, or breathe into a paper bag, along with breathing exercises and diaphragmatic retraining, biofeedback, hypnosis, psychological and psychiatric treatment, and medications such as beta blockers, benzodiazepines, and antidepressants (Beumer and Bruyn 1993). A study of nonpharmacologic treatments found efficacy for educational sessions, breathing techniques and retraining, and progressive relaxation; the greatest improvement occurred in the group given an explanation and 8 sessions of breathing retraining (Monday et al 1995). A small pilot study found benefit from acupuncture (Gibson et al 2007). There is a lack of well-controlled treatment trials comparing these approaches (Herxheimer 1991). In my experience, most patients respond to reassurance, education, and instructions to hold the breath, breathe more slowly, or breathe into a paper bag. Providing the patient with written materials such as those used by Lance may be worthwhile (Lance and Goadsby 2005). If significant symptoms of stress, anxiety, or depression are present, use of appropriate medication and psychological or psychiatric referral may be helpful.
Pregnancy
Although hyperventilation syndrome has often been seen during pregnancy, studies on the incidence are not available.
Anesthesia
Not applicable.
ICD codes
ICD-9:
Hyperventilation: 306.
ICD-10:
Hyperventilation: R06.
Associated disorders
Acute hyperventilation Anxiety Chronic hyperventilation Distal symmetrical paresthesias Panic attacks
Raynaud phenomenon
Related summaries
Dizziness Psychophysiological vertigo (psychogenic vertigo) Syncope Tension-type headache
Differential diagnosis
epilepsy migraine arteriovenous malformation cerebrovascular disease vertebrobasilar insufficiency brachial neuritis angina malingering vasovagal attacks functional illness hypoglycemia cerebral tumor cardiac abnormalities mitral valve prolapse panic attacks multiple sclerosis
Demographics
For more specific demographic information, see the Epidemiology, Etiology, and Pathogenesis and pathophysiology sections of this clinical summary.
Age 06-12 years 13-18 years 19-44 years 45-64 years 65+ years
Population None selectively affected.
Occupation None selectively affected.
Sex female>male, >2: female>male, >1:
Family history None
Heredity None
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