More females than males have HVS/BPDs, ranging from a ratio of 2:1 to 7:1. The peak age of incidence is 15 to 55 years, although other ages can be affected.² Women may be more at risk because of hormonal influences, because progesterone stimulates respiratory rate, and in the luteal (postovulation/premenstrual) phase, CO₂ levels drop on average 25%. Additional stress can then “increase ventilation at a time when CO₂ levels are already low.”³ A case report linked progesterone (medroxyprogesterone) therapy as a cause of hyperventilation in a 52-year-old menopausal woman.⁴

Normal Breathing Pattern

To recognize HVS/BPDs, one must be aware of the characteristics of a normal breathing pattern.

• The breathing rate should be 10 to 14 breaths/min, moving 3 to 5 L of air per minute through the airways of the chest.

• During the active inhalation phase, air flows in through the nose where it is warmed, filtered, and humidified before being drawn into the lungs by the downward movement of the diaphragm and the outward movement of the abdominal wall and lower thoracic structures.

• The upper chest and accessory breathing muscles should remain relaxed.

• The expiratory phase is ideally effortless as the abdominal wall and lower intercostals relax downward and the diaphragm ascends back to its original domed position, aided by the elastic recoil of the lung.

• A relaxed pause at the end of exhalation releases the diaphragm briefly from the negative and positive pressures exerted across it during breathing.

• Under normal circumstances individuals are quite unaware of their breathing.

• Breathing rates and volumes increase or fluctuate in response to physical or emotional demands, but in normal subjects they return to relaxed low chest patterns after the stimuli ceases.

Patients, especially those whose symptom presentation includes chronic fatigue or anxiety, or both, and who display or report a number of the following signs or symptoms, might be considered suitable candidates for respiratory treatment (see also Diagnostic Considerations).

Benefits of Normal Respiratory Function

The exchange of gases involving acquisition of oxygen (O₂) and elimination of CO₂ leads to enhanced cellular function and facilitates the following:

• Normal performance of the brain, organs, and tissues of the body

• Normal speech and human nonverbal expression (e.g., sighing)

• Fluid movement (lymph, blood)

• Spinal mobility through regular, mobilizing, thoracic cage movement

• Digestive function via rhythmic positive and negative pressure fluctuations, via normal diaphragmatic function

Any chronic alteration in breathing function automatically modifies these functions negatively.

The impact of habitual BPDs, such as hyperventilation, on an individual’s physiology can be profound, potentially resulting in or exacerbating a wide range of health problems, sometimes severely, ranging from anxiety and panic attacks to fatigue and chronic pain.

The Carbon Dioxide–Oxygen Balancing Act

Chaitow et al ¹⁰ addressed the misconception that oxygen is “good” and carbon dioxide is “bad” by stating:

“Yet if one considers that life-giving oxygen can also be corrosive and toxic, and that a deficiency of the waste gas carbon dioxide (CO₂) can cause fainting, seizures, or death, then the “good/bad” distinction must be restated as “good within certain limits” and “bad within certain limits.” Maintaining these two gases within those limits is a complex task for the body, even more so because the supply of each gas fluctuates with each breath.”

Respiratory Homeostasis

Jennett ⁵ described the delicate homeostatic balancing act in which pH and CO₂ are key features:

When there are not other overriding drives affecting breathing, the neural control system acts to maintain a constant arterial PCO₂. This must mean that the volume of CO₂ expired continually balances the volume produced by tissue metabolism. Measurements show that alveolar and arterial concentrations of CO₂ stay constant, which means that the volume of gas breathed out from the functional (alveolar) volume of the lungs must vary precisely with the rate of metabolic CO₂ production. In rest and activity, when the system is left to itself, it is so efficient that the matching occurs virtually breath-by-breath, even when metabolic activity is continually changing.

Pathophysiology

Physiologic and Pathophysiologic Causes of Altered Patterns of Breathing

Hyperventilation can be an appropriate physiologic response to the body’s metabolic needs; for example, tachypnea (rapid breathing) or hyperpnea (increase in respiratory rate proportional to increase in metabolism) may result as the respiratory centers respond automatically and appropriately to rising CO₂ production due to exercise or organic disease that may be creating acidosis. It is therefore important to exclude organic causes that diminish PaO₂ or elevate PaCO₂ levels.⁶

Organic causes of HVS/BPDs that should be excluded and/or identified before breathing rehabilitation is initiated include the following:

• Respiratory: asthma, chronic obstructive respiratory disease, pneumonia, pulmonary embolus, pneumothorax, and pleural effusion. A case of carbon monoxide poisoning presenting as HVS has been reported.⁷

• Cardiovascular: acute and chronic left heart failure, right heart failure, tachyarrhythmias

• Hematopoietic: anemia

• Renal: nephrotic syndrome, acute and chronic kidney failure

• Endocrine: Diabetes with ketoacidosis, pregnancy

• Metabolic: liver failure

• Pharmaceutic: aspirin, caffeine, amphetamine, nicotine, progesterone therapy

BPDs may also emerge from a background of established pathology (e.g., asthma, cardiovascular disease, kidney failure, chronic pain). Even tumor infiltrates into brain respiratory centers and central chemoreceptors have caused hyperventilation.⁸ Where this is the case, the aim of this chapter is not to explore these states, since they are discussed elsewhere in this textbook.

Fluctuating blood glucose levels may trigger HVS/BPD symptoms in patients with high carbohydrate diets, which produce rapid rises followed by sharp falls to fasting levels or below.^6,⁹

Chaitow et al ¹⁰ noted that the following factors could lead to altered breathing patterns through pH shifts:

• Ketoacidosis promotes deeper, faster breathing because the breathing centers respond to the higher CO₂ content.

• Diarrhea results in the loss of alkaline plasma bicarbonate ions, which if prolonged, leads to acidosis. This stimulates corrective overbreathing to remove CO₂ (as carbonic acid [H₂CO₃]) and normalizes the pH.

• Excessive vomiting causes loss of hydrochloric acid, shifting the body toward alkalosis, slowing breathing to allow CO₂ to build up and restore pH. Hypoventilation is the result.

• Use of steroids and diuretics can lead to alkalosis.

Categorization of Causes

It is possible to place the common etiologic features of HVS/BPD into biomechanical, biochemical, psychological, environmental, pathologic, and habitual categories.

The reasons for an individual breathing inappropriately can derive directly from structural, biomechanical causes, such as a restricted thoracic spine, rib immobility, or shortness of key primary and accessory respiratory muscles.

Causes of breathing dysfunction can also have a more biochemical etiology, possibly involving allergy or infection, which triggers narrowing of breathing passages and subsequent asthmatic-type responses. Acidosis, resulting from conditions such as kidney failure, also directly alters breathing function as the body attempts to reduce acid levels via elimination of CO₂ through hyperventilation.

The link between psychological distress and breathing makes this another primary cause of many manifestations of dysfunctional respiration. Examining a person with anxiety or depression without breathing dysfunction being noted is difficult to imagine.

Other catalysts that may affect breathing function include environmental factors (e.g., altitude, humidity).¹¹

The etiology of HVS/BPD may involve combinations of the factors listed previously; however, in most instances, altered breathing patterns, whatever their origins, seem to be maintained by nothing more sinister than pure habit.^6,¹²

The Hydrogen Ion Factor

Chaitow et al ¹⁰ stated the following:

The story [of HVS/BPD] might best begin with pH, because this factor influences every organ of the body. The variable of relative acidity facilitates many metabolic exchanges and it must be kept in careful balance. Since pH describes proportion of hydrogen ions available for combination, and the pH is on a log scale, a small change in pH, such as 7.4 to 7.2, means roughly a doubling of the number of hydrogen ions present. The binding of hydrogen to negative sites helps to regulate enzymatic action, endocrine secretion, integrity of protein molecules, and cellular metabolism, including oxygen absorption and release. A pH of 7.2 would seriously compromise many physiologic functions. The physiologic normal pH in the arterial blood is around 7.4, with an acceptable range from 7.35 to 7.45. Outside these limits lie ill effects of many kinds. The body will sacrifice many other things in order to maintain proper pH.

The Carbon Dioxide–Hydrogen Ion Connection

• The acidity of the blood is determined mainly by CO₂.

• CO₂ is the end-product of aerobic metabolism, deriving mainly from the mitochondria. CO₂ is odorless, heavier than air and, if inhaled in its pure form, causes suffocation.

• CO₂ is present in the atmosphere at a concentration of around two-hundredths of 1%, and is harmless to humans but adequate to sustain plant life.

• Transportation of CO₂ occurs from the tissues into the blood and then to the lungs for exhalation. The body converts CO₂ to H₂CO₃, of which there is a perpetual surplus.

• The lungs exhale around 12,000 mEq of H₂CO₃ per day, compared with less than 100 mEq of fixed acids excreted by the kidneys. Normal range of end-tidal CO₂ pressure is 35 to 45 mm Hg.¹³

• Any increase in bodily activity produces CO₂, acidifying the blood, unless more CO₂ is excreted and/or exhaled.

• It is therefore obvious that changes in breathing volume relative to CO₂ production regulate the moment-to-moment concentration of pH of the bloodstream (longer term regulation of pH is shared with the kidneys).

• It is the concentration of CO₂ in the blood, not oxygen, that is the major regulator of breathing drive.

• Higher CO₂ levels immediately stimulate more breathing, apparently on the assumption that abundance of CO₂ means oxygen-poor air is being breathed, breathing has stopped, or something else is happening that is an antecedent to suffocation.

The Bicarbonate Buffer

Chaitow et al ¹⁰ explained the following:

There exists a further balancing mechanism, the bicarbonate buffer. The bicarbonate ion (HCO₃–) is derived from CO₂ during its ride in the bloodstream; CO₂ dissociates into hydrogen ions (H+) and (HCO₃–). This bicarbonate reserve is adjustable as needed, up to a point, and constitutes a major alkaline buffer system which opposes rises in acidity. The kidneys regulate the regulators by adjusting the amount of bicarbonate returned to the bloodstream. If the kidneys detect excess acidity (a surplus of positively-charged hydrogen ions) they will try to retain more bicarbonate to balance the acid, but this is not a fast process; adjusting their filtration characteristics takes hours to days. In the short run, meanwhile, if bicarbonate buffering of excess acid is not sufficient, or if the bicarbonate is depleted, a faster back-up buffering system is available: hyperventilation. Excessive breathing exhales more CO₂ (acid), thereby bringing pH closer to normal.

Oxygen Delivery and Smooth Muscle Constriction

The blood carries oxygen mainly in molecules of hemoglobin, which are contained in red blood cells. In an appropriate environment, hemoglobin combines readily with oxygen (to form oxyhemoglobin). This process varies according to local pH, as well as PO₂. This ability to combine is important for both absorbing oxygen through the alveoli and also for releasing oxygen through the capillary walls, where oxygen diffuses into the tissues.

These two properties are largely determined by local conditions, so that when pH is low (i.e., the blood is more acidic), hemoglobin in that area is stimulated to release additional oxygen. This is true of metabolically active tissues in general but especially of muscles. An exercising muscle needs all the oxygen it can get, and this is assisted by its chemical nature, explained by West as follows:

An exercising muscle is acid, hypercarbic, and hot, and it benefits from increased unloading of oxygen from its capillaries.¹¹

The effect of pH on oxyhemoglobin dissociation is called the Bohr effect.

In the lungs the need is to bind oxygen to hemoglobin, not release it. Not surprisingly, the lungs have a more alkaline environment.

The fact that a shift of the blood toward acidity promotes dissociation and release of oxygen from the hemoglobin is particularly important when considering hyperventilation, because the resulting alkalinity causes the hemoglobin molecule to retain more oxygen than usual. With increased alkalinity encouraging smooth muscle contraction and therefore diminished diameter of blood vessels, as well as the reluctance of hemoglobin to release its oxygen, a relative oxygen deficit is likely in tissues and the brain, leading to symptoms such as fatigue, aching, cramping, and cognitive problems.

Psychology and Hyperventilation Syndrome/Breathing Pattern Disorders

On a psychological level, Bradley ¹⁴ described a “cascade of symptoms” (see Figure 55-1) in which an original cause (emotional or physical) leads to tension and anxiety that results in hyperventilation, possibly an acute hyperventilation attack, which (with repetition) over time, results in anticipation, anxiety, and avoidance behaviors or phobias, or both.

FIGURE 55-1 Negative health influences of a dysfunctional breathing pattern such as hyperventilation.

(From Chaitow L, Bradley D, Gilbert C. Multidisciplinary approaches to breathing pattern disorders. London: Churchill Livingstone, 2002:90.)

Chaitow et al ¹⁰ described aspects of the influence of emotion on breathing¹⁵^–¹⁷:

Increased variability from breath to breath is known to correlate with anxiety states. Low PCO₂ and increased frequency of sighing are typical of those with panic disorder even when not panicking. These generalizations miss individuals who do not have a chronic BPD, but who do experience disrupted breathing under particular conditions. These “conditions” can provoke either an amygdala “alarm” discharge or some specific, learned breathing response, as well as occasional panic.

Conway et al ¹⁸ used hypnosis to investigate the sources of hyperventilation episodes and found emotional events such as loss, separation, and impotent anger were common precipitating factors that began the hyperventilation trend. They concluded that hypnosis might be helpful in discovering the underlying cause of hyperventilation.

Freeman et al ¹⁹ also showed that individuals who reported several symptoms indicating hyperventilation (including chest pain/palpitations and dizziness—not exclusively respiratory symptoms) displayed rather strong hyperventilation in response to recalling emotionally disturbing events, whereas the control subjects did not. Bereavement, loss of control, grief, and anger were common topics associated with the symptoms.

Chaitow et al ¹⁰ concluded (Figure 55-2):

“Aside from medical problems, there are still many factors in the psychological and behavioral realms competing for control of breathing. Successful regulation must take all factors into account, with special consideration for priorities of survival. The human brain adds a layer of complication with its power to imagine, project, and recall, often stimulating breathing reflexes without apparent reason.”

FIGURE 55-2 Final modulation of the breathing act includes input from many possible sources: the need for vocalization (a cry for help, a shouted warning, perhaps a growl); preparation for exertion; the need to freeze and become less noticeable; the need to maximize sensory acuity by keeping the body still; and the need to either remain calm or return to a baseline state of calmness. These inputs often conflict with each other, but if there is a hint of a threat to survival, they seem to have priority over all other considerations.

(From Chaitow L, Bradley D, Gilbert C. Multidisciplinary approaches to breathing pattern disorders. London: Churchill Livingstone, 2002:122.)

Diagnostic Considerations

Symptoms

Acute hyperventilation represents approximately 1% of all cases of hyperventilation, which is well outnumbered by chronic hyperventilation.²⁰ The symptoms and signs of HVS are extremely variable, and none are absolutely diagnostic. The following symptoms are indications of possible breathing pattern dysfunction:

Table 55-1 is not fully comprehensive, but does represent the most common symptoms and signs of HVS/BPD. For greater depth, see Timmons and Ley,⁶ Gardner,²¹ Nixon,²² and Chaitow et al.¹⁰

TABLE 55-1 Most Common Symptoms and Signs of Hyperventilation Syndrome/Breathing Pattern Disorders

SYSTEM	SYMPTOMS	SUGGESTED CAUSES
Cardiovascular	Chest pain and angina, palpitation and arrhythmias, tachycardia, lightheadedness and syncope, altered ECG features	Reduced coronary blood flow, altered excitability of SA and AV nodes of cardiac muscle, reduced cardiac output, peripheral vasodilatation
Gastrointestinal	Discomfort in lower chest and epigastric area, esophageal reflux and heartburn, bloating/distension, exacerbation of hiatal hernia symptoms, dry mouth, air swallowing and belching	Aerophagia, increased swallowing rate, mouth breathing
Neurologic	Headache; numbness and tingling (mainly involving extremities and perioral); positive Trousseau’s and Chvostek’s signs; dizziness/giddiness; ataxia and tremor; blurred and tunnel vision; anxiety and panic; phobias; irritability; depersonalization; detachment from reality; impaired concentration, cognition, performance; easy fatigue; insomnia; hallucinations	Cerebrovascular constriction (see notes on smooth muscle contraction below); vasoconstriction of vertebral or carotid arteries, or both; reduced oxygen delivery, neuronal excitability resulting from alkalosis; hypocalcemia
Respiratory	Breathlessness; restricted sensation around thorax; sighing/yawning; obvious use of upper chest, accessory breathing muscles (e.g., scalenes) on inhalation; chest tenderness	Overuse of accessory breathing muscles and fatigue of primary respiratory muscles
Muscular	Stiffness and aching, weakness in limbs, cramping, carpopedal spasm, tetany	Hyperexcitability of motor nerves, muscle fatigue, calcium/magnesium imbalance

AV, atrioventricular; ECG, electrocardiogram; SA, sinoatrial.

Metabolic Disturbances and Hyperventilation Syndrome

• Two tests of nerve hyperexcitability produced by hypocapnia-induced hypocalcemia are Trousseau’s and Chvostek’s signs.

• Chest pain associated with HVS/BPDs requires that heart disease is excluded as a diagnosis. Adrenaline-induced electrocardiographic changes can occur in hyperventilation, uncomplicated by coronary heart disease. One study suggested that up to 90% of noncardiac chest pain is thought to be induced by HVS/BPDs.²³

In older patients, established coronary artery disease can be exacerbated by vasoconstriction arising from hypocapnia, which puts them at risk of coronary occlusion and myocardial damage.

Alternatively, hyperventilation can trigger spasms of normal caliber coronary arteries.

• Rapid breathing or mouth breathing instigates aerophagia from air gulping, causing bloating, burping, and extreme epigastric discomfort. Irritable bowel syndrome is listed as a common symptom of chronic overbreathing. Fear and anxiety may induce abdominal cramps and diarrhea.¹ The median swallowing rate in healthy, nondyspeptic controls is 3 or 4 swallows per 15 minutes. In the absence of food, up to 5 mL of air accompanies saliva into the gastrointestinal tract with each swallow.²⁴

• Hyperventilation leading to hypocapnia causes cerebral arterioles to constrict, increasing vascular resistance and reducing cerebral blood flow. This is a natural response to changes in CO₂ to regulate oxygen delivery to the brain.²⁵

Acute Hyperventilation Progression

• The patient presenting with an acute hyperventilation episode appears distressed.

• The pattern of respiration is of deep, rapid breaths, using the accessory muscles visible in the neck and the upper chest.

• Wheezing may be heard as a result of bronchospasm triggered by hypocapnia.

• A stressful precipitating event is usually reported.

• Hypocapnia reduces blood flow to the brain (2% decrease in flow per 1 mm Hg reduction in arterial CO₂), causing frightening central nervous system symptoms. The reduced oxygenation of brain and tissues of the body results from contraction of smooth muscle surrounding blood vessels and a reluctance of the hemoglobin carrier molecule to release oxygen in the increasingly alkaline environment caused by excessive loss of CO₂.

• Poor concentration and memory lapses may occur as a result, with tunnel vision and onset in those susceptible to migraine-type headaches or tinnitus.

• Sympathetic dominance brings on tremors, sweating, clammy hands, palpitations, and autonomic instability of blood vessels causing labile blood pressures.²⁶

• Bilateral perioral and upper extremity paresthesia and numbness may be reported. Unilateral tingling is most often confined to the left side.

• Dizziness, weakness, visual disturbances, tremor, and confusion—sometimes fainting or even seizures—are typical symptoms.

• Spinal reflexes become exaggerated through increased neuronal activity caused by loss of CO₂ ions from the neurons.

• Tetany and cramping may occur in severe bouts.²⁷

Chronic Hyperventilation

The diagnosis of chronic and intermittent hyperventilation is more difficult than acute hyperventilation. A careful history and systemic inquiry, checking all other symptoms in the other body systems, usually highlights a suspicious pattern, particularly to the experienced clinician who can think beyond his or her own specialist area. Examination must exclude organic diseases of the brain and nervous system; the heart, particularly angina and heart failure; respiratory disease; and gastrointestinal conditions, especially if there are suspicious symptoms in these systems.

Careful inquiries as to the precipitating causes of attacks helps both with the diagnosis and focusing on choice of treatment. Nixon ²² suggested that there are often attacks where there is no preceding stressful event. For example, in chronic hyperventilators, the respiratory center may have been reset to tolerate a lower than normal partial pressure of PaCO₂ levels in the blood. In such patients, a single sigh or one deep breath may reduce the PaCO₂ enough to trigger symptoms.

Laboratory and Office Tests for Hyperventilation Syndrome/Breathing Pattern Disorders

Many possible tests for respiratory function exist. Some are difficult to perform (e.g., airway resistance), and some are invasive (e.g., blood gases).¹⁴ A selection of tests are listed as follows:

• Preliminary tests to exclude respiratory and cardiac disease including peak expiratory flow rate, chest radiograph, ECG, and an exercise ECG if chest pain is present.

• Palpation and observation can demonstrate a paradoxic breathing pattern in which the abdomen retracts and the upper chest expands on inhalation (as opposed to normal abdominal protrusion and lower thorax expansion).

• The breath-holding time test does not require additional measurements or equipment. The time a hyperventilating patient can hold his or her breath is usually greatly reduced, often not beyond 10 to 12 seconds. Thirty seconds has been used as the approximate dividing line between hyperventilators and normals by some clinicians. It is worth noting that breathless patients without hyperventilation may have equal difficulty in breath holding.²¹

• A peak expiratory flow rate measurement, compared with age, sex, and height tables, provides a simply done, quick exclusion of significant respiratory restriction in the clinic room.

• If a hyperventilation provocation test (HVPT) is performed (during which the patient is asked to voluntarily overbreathe to bring on symptoms), ECG should be monitored (see “Caution” later).

• Elevated erythrocyte carbonic anhydrase (ECA) was recently (2009) suggested as a clinical marker for hyperventilation. The values of ECA were significantly elevated (~31 U/g hemoglobin) in patients who hyperventilated compared with controls (24.7 U/g hemoglobin). However, hyperventilation sensitivity and specificity were only 52.1% and 76.7%, respectively. There are other conditions that might elevate ECA, such as glucose-6-phosphate dehydrogenase deficiency and different anemias (aplastic, iron deficiency, autoimmune hemolytic, β-thalassemia).²⁸

• Arterial blood gas determination is invasive and painful (arterial puncture) but appropriate in the emergency department, where the diagnosis of acute hyperventilation is required. For patients in whom chronic hyperventilation is suspected, the pressure of end-tidal carbon dioxide (PET CO₂) can be measured noninvasively from a continuous sampling through nasal prongs or cannula with the mouth occluded, or the tube can be sited in an oral airway for those with nasal obstruction to monitor CO₂ deficits. The PET CO₂ is the level of CO₂ released at the end of expiration.

• Capnography: PET CO₂ can be evaluated after a 4-minute quiet breathing rest period, followed by exercise and recovery, or a HVPT can be conducted in the recovery period. Most patients with chronic hyperventilation have a PET CO₂ at or below 30 mm Hg and a markedly delayed recovery from hypocapnia after overbreathing, sometimes lasting 30 minutes after testing.^29,³⁰ By measuring PET CO₂ or transcutaneous CO₂ levels while a hyperventilation provoking activity is performed, a potential link can be made between symptoms and CO₂ levels.³¹

• The think test ³² may be initiated 3 to 4 minutes into the recovery period. The patient is asked to recall a painful emotional experience during which symptoms developed. If the PET CO₂ drops 10 mm Hg, the test supports hyperventilation. Bradley¹⁴ noted: “In some patients with hyperventilation the PaCO₂ and the PET CO₂ may be in the normal range. In those who are asymptomatic at the time of testing, this finding could be accepted. However, a normal level while experiencing symptoms negates hypocapnia as the cause of symptoms. It prompts a search for an alternative explanation.”

• Buteyko performed comparative studies with a simple breath-holding technique to test CO₂ levels and found that a simple technique of breath holding after expiration could predict the percent of alveolar CO₂ and therefore the degree of hyperventilation to a high degree of accuracy. According to his calculations, optimal levels of alveolar PCO₂ correlated with postexpiratory breath-holding time of 40 to 60 seconds. Many asthmatics and hyperventilators are found to be able to hold the breath out for less than 10 seconds.³³^–³⁵

Caution

Bradley ¹⁴ cautioned the following:

“The hyperventilation provocation test is best done before explanations of symptoms, to prevent suggestion and bias. Patients need to be warned only of a dry mouth. The patient is asked to concentrate on how they feel during the 1-2 minute period when they are over breathing at the rate of 30-40 per minute. The rate is set by the examiner’s hand movements. The operator must stress the importance of the test and the need to continue for as long as they can. An arterial blood gas determination at the end of the test can be of use to establish the depth of hypocapnia. Some clinicians rely on as little as 12 deep breaths which the patient can recover from easily, and subjective symptoms produced are recorded. In both the breath holding and voluntary over-breathing tests, the skills of the clinician are important for maintaining the trust and co-operation of patients.”

The Nijmegen Questionnaire

Bradley ¹⁴ pointed out that no “gold standard” exists for chronic HVS, but the Nijmegen Questionnaire is noninvasive with a high level of sensitivity (up to 91%)³⁶ and specificity (up to 95%).³⁷ It is also a way to monitor the progress of treatment by re-evaluating symptoms. Bradley noted that the results of this simple test also helped indicate whether the initiating trigger causing the HVS/BPDs resolved, suggesting that the patient had to deal with only the “bad breathing” habit and musculoskeletal and motor pattern changes, or whether the initiating triggers were ongoing or unresolved and might need further cognitive help (Figure 55-3).

FIGURE 55-3 Nijmegen questionnaire.

(From Chaitow L, Bradley D, Gilbert C. Multidisciplinary approaches to breathing pattern disorders. London: Churchill Livingstone; 2002:176.)

Warburton and Jack ³⁰ stated the Nijmegen Questionnaire was neither sensitive nor specific for chronic idiopathic hyperventilation without physiologic testing because many of the symptoms on the questionnaire were common to an organic respiratory disease.

Biomechanical (Structural) Considerations

The Structure–Function Continuum

Nowhere in the body is the axiom of structure governing function more apparent than in its relation to respiration. Just as prolonged changes in patterns of use, such as an inappropriate (hyperventilation) breathing pattern, induce structural changes involving the muscles and joints (e.g., rib) of respiration, so do these changes ultimately prevent normal function.

Ultimately, the self-perpetuating cycle of functional change creating structural modification, leading to reinforced functional tendencies, can become complete, from whichever direction dysfunction derives. Examples follow:

• Structural adaptations can prevent normal breathing function.

• Abnormal breathing function ensures continued structural adaptational stresses.³⁸

Restoration of normal function demands restoration of adequate structural mobility, whereas maintenance of restored biomechanical flexibility requires that function (how the individual breathes) should be normalized through reeducation and training.

Individually, neither approach is as useful as a combination of restoration of structural integrity, combined with functional improvement. It should be obvious that other underlying etiologic features, whether these relate to psychosocial, biochemical, or biomechanical factors, should be addressed as far as possible as a prerequisite of rehabilitation.

The Muscles of Breathing

The muscles associated with breathing function can be grouped as either inspiratory or expiratory. They are either primary in that capacity or provide accessory support.

Because expiration is primarily an elastic response of the lungs, pleura, and “torsion rod” elements of the ribs, all muscles of expiration could be considered accessory muscles, since they are recruited only during increased demand. They include internal intercostals, abdominal muscles, transverse thoracis, and subcostales. With increased demand, iliocostalis lumborum, quadratus lumborum, serratus posterior inferior, and latissimus dorsi may support expiration, including during the high demands of speech, coughing, sneezing, singing, and other special functions associated with breathing.

Space does not permit in-depth discussion of the muscles of respiration, further details of which can be found in Chaitow et al.¹⁰

Neural Regulation of Breathing

Respiratory centers in the brainstem unconsciously influence and adjust alveolar ventilation to maintain arterial blood oxygen and CO₂ pressures at relatively constant levels, to sustain life under varying conditions and requirements.¹⁰

The three main groups are as follows:

• The dorsal respiratory group, located in the distal portion of the medulla, receives input from peripheral chemoreceptors and other types of receptors via the vagus and glossopharyngeal nerves. These impulses generate inspiratory movements and are responsible for the basic rhythm of breathing.

• The pneumotaxic center in the superior part of the pons transmits inhibitory signals to the dorsal respiratory center, controlling the filling phase of breathing.

• The ventral respiratory group, located in the medulla, causes either inspiration or expiration. It is inactive in quiet breathing but is important in stimulating abdominal expiratory muscles during levels of high respiratory demand.

The Hering-Breuer reflex prevents overinflation of the lungs and is initiated by nerve receptors in the walls of the bronchi and bronchioles, sending messages to the dorsal respiratory centre, via the vagus nerve. The reflex “switches off” excessive inflation during inspiration, as well as excessive deflation during exhalation.

The autonomic nervous system enables the automatic unconscious maintenance of the internal environment of the body in ideal efficiency and adjusts to the various demands of the external environment, be it sleep with repair and growth, quiet or extreme physical activity, or stress (Figure 55-4).

FIGURE 55-4 Schema of the autonomic innervation (motor and sensory) of the lung and the somatic (motor) nerve supply to the intercostal muscles and diaphragm.

(From Scanlan C, Wilkins R, Stoller J. Egan’s fundamentals of respiratory care, ed 7. St. Louis: Mosby; 1999.)

A “third” nervous system regulating the airways has been recognized, called the nonadrenergic noncholinergic (NANC) system. Containing inhibitory and stimulatory fibers, nitric oxide has been identified as the NANC neurotransmitter.³⁹

• NANC inhibitory nerves cause calcium ions to enter the neuron, mediating smooth muscle relaxation and bronchodilation.

• NANC stimulatory fibers—also called C-fibers—are found in the lung supporting tissue, airways, and pulmonary blood vessels, and appear to be involved in bronchoconstriction after exercise-induced asthma.⁴⁰

Chemical Control of Breathing

The central role of respiration is to maintain balanced concentrations of oxygen and CO₂ in the tissues. Increased levels of CO₂ act on the central chemosensitive areas of the respiratory centers themselves, increasing inspiratory and expiratory signals to the respiratory muscles. In contrast, oxygen acts on peripheral chemoreceptors located in the carotid body (in the bifurcation of the common carotid arteries) via the glossopharyngeal nerves and the aortic body (on the aortic arch), which sends the appropriate messages via the vagus nerves to the dorsal respiratory center.

Voluntary Control of Breathing

Automatic breathing can be overridden by higher cortical conscious input (directly via the spinal neurons, which drive the respiratory muscles) in response to, for instance, fear or sudden surprise. Speaking requires voluntary control to interrupt the normal rhythmicity of breathing, as do singing and wind instrument playing. Evidence indicates that the cerebral cortex and thalamus also supply part of the drive for normal respiratory rhythm during wakefulness. (Cerebral influences on the medullary centers are withdrawn during sleep.) Habitual BPDs and HVS probably originate from some of these higher centers.⁶

Therapeutic Considerations and Therapeutic Approach

Treatment and Rehabilitation of Hyperventilation Syndrome/Breathing Pattern Disorders

Different models of care in managing HVS/BPDs are available.

It is assumed that all organic causes of breathing pattern changes have been excluded and that coexisting problems such as asthma, chronic obstructive airway disease, chronic pain, and hormonal imbalances receive appropriate specialized attention. It is also assumed that manual therapy approaches would be incorporated as an essential element of rehabilitation.

Bradley’s ^14,⁴¹ physical therapy rehabilitation follows stages that are summarized in the acronym BETTER: Breathing retraining, Esteem/self-image, Total body relaxation, Talk/breath control, Exercise prescription, Rest/sleep.

Breathing retraining incorporates a number of elements:

• Awareness of faulty breathing patterns

• Relaxation of the upper chest, shoulders, and accessory muscles

• Abdominal/low chest breathing pattern retraining

• Awareness of normal breathing rates and rhythms both at rest and during activity

The elements of the physical therapy protocol involving relaxation, exercise, talk/breath control, and sleep are all individualized and are not described here.

An Osteopathic/Naturopathic Protocol for Care of Hyperventilation Syndrome/Breathing Pattern Disorders

• Initial (and continual or periodic) assessment of breathing function based on functional evidence and palpation determines what needs to be done to improve breathing function.

• Education and information are vital for creating motivation and awareness as to why homework is essential in normalizing BPDs.

• The patient must understand clearly that the practitioner or therapist can do no more than create an environment, a possibility, for restoration of more normal function, but the breathing work itself is up to the patient.

• Treatment of muscles and joints alone, no matter how appropriate, can never restore normal breathing patterns without cooperative effort.

• Conversely, breathing retraining without the freeing of restricted structures is far more difficult to achieve.

• Psychotherapy and counseling are also unlikely to be successful unless retraining is introduced, and structural factors are dealt with.

• Manual attention to the upper fixators and/or accessory breathing muscles (upper trapezii, levator scapulae, scalenes, sternocleidomastoid, pectorals, and latissimus dorsi) is usually required.

• The diaphragm area also requires direct attention as a rule (lower anterior intercostals, sternum, costal margin, beneath costal margin, abdominal attachments, quadratus lumborum, and psoas).

• Active trigger points in these muscles may need deactivating manually or via acupuncture.

• Acupuncture being administered for 30 minutes, twice weekly, for 4 weeks showed reduction in Nijmegen score from 31 to 24. The focus was on reducing anxiety, thereby reducing hyperventilation. The points used were colon 4, liver 3, and stomach 36 bilaterally.⁴²

• The thoracic spine and ribs may require mobilization (osteopathic or chiropractic adjustments).

• Osteopathic lymphatic pump methods may be required if there is evidence of stasis.

• Retraining: various breathing exercises should be introduced, individualized to the specific needs of the patient, commonly on the basis of pursed lip breathing and pranayama yoga methods (see Box 55-1).⁴³^–⁴⁷

• Relaxation methods, including autogenic training or progressive muscular relaxation, or both, might usefully be introduced.

• Sleep pattern disturbances might require attention.

• Exercise of aerobic nature should be carefully introduced.

• Dietary advice and counseling should be introduced as appropriate.

BOX 55-1 Breathing Rehabilitation Exercises

1. Pursed lip breathing ⁴⁴^–⁴⁵

Pursed lip breathing, combined with diaphragmatic breathing, enhances pulmonary efficiency.

• The patient is seated or supine with the dominant hand on the abdomen and the other hand on the chest.

• The patient is asked to breathe in through the nose and out through the mouth, with pursed lips, ensuring diaphragmatic involvement by means of movement of the abdomen against the hand on inhalation.

• Exhalation through the pursed lips is performed slowly and has been shown to relieve dyspnea, slow the respiratory rate, increase tidal volume, and help restore diaphragmatic function.

Author’s Note: Essentially blowing firmly and slowly, through a narrow aperture such as pursed lips, effectively tones the diaphragm via eccentric isotonic activity.

2. Antiarousal breathing ^43,⁴⁶

The patient is asked to sit or recline comfortably and exhale slowly and fully through pursed lips, and the following guidance is given:

• Imagine a candle flame about 6 inches from your mouth, and blow a thin stream of air at it (pursed lip breathing).

• As you exhale, count silently to establish the length of the “out breath.”

• When you have exhaled fully, without strain, pause for a count of “1,” then inhale through the nose.

• Full exhalation creates a “coiled spring,” making inhalation easier.

• Count to yourself to establish how long your “in breath” lasts.

• Without pausing to hold the breath, exhale slowly and fully, through pursed lips, blowing the air in a thin stream, and then pause for a count of 1.

• Repeat the inhalation and exhalation for at least 30 cycles twice daily.

• After some weeks of daily practice you should achieve an inhalation phase that lasts 2 to 3 seconds and an exhalation phase of 6 to 7 seconds, without strain.

• Exhalation should always be slow and continuous; there is little value in breathing the air out in 2 seconds and then simply waiting until the count reaches 8 before inhaling again!

• Feelings of anxiety should reduce with this exercise.

• Practice twice daily, and repeat the exercise for a few minutes (6 cycles takes about 1 minute) every hour if anxious or when stress increases.

• Practice on waking; before bedtime; and, if possible, before meals.

3. Recitation of mantra or prayer

• The respiratory (and cardiovascular) effects of rosary prayer (“Ave Maria” in Latin) and recitation of a yoga mantra were assessed.⁴⁷

• Results were similar, showing a slowing of respiration to approximately 6 counts per minute and synchronization of all cardiovascular rhythms (Traube-Hering-Mayer oscillations), representing blood pressure, heart rate, cardiac contractility, pulmonary blood flow, cerebral blood flow, and movement of cerebrospinal fluid.

• This influence on autonomic activity, represented by the Traube-Hering-Mayer oscillations, is clearly health enhancing, because it slows respiratory rate to the level considered optimal in breathing rehabilitation.^1,^6,¹²

Breathing Rehabilitation Exercises

Box 55-1 describes three breathing rehabilitation exercises.

Chronic HVS/BPDs are commonly successfully treated; however, a time frame of 12 to 26 weeks may be required, with active patient participation throughout to break well-established habits.

Lum ¹ reported that more than 1000 anxious and phobic patients were treated using breathing retraining, physical therapy, and relaxation. Results indicated the following:

• Symptoms were usually abolished in 1 to 6 months, with some younger patients requiring only a few weeks.

• At 12 months, 75% were free of all symptoms, 20% had only mild symptoms, and about 1 in 20 patients had intractable symptoms.

Breathing rehabilitation therapy was evaluated in patients with HVS; the diagnosis was based on the presence of several stress-related complaints and reproduced by voluntary hyperventilation.⁴⁸ Patients with organic diseases were excluded, and most patients met the criteria for an anxiety disorder.

Therapy was conducted in the following sequence:

• Brief, voluntary hyperventilation to reproduce the reported complaints

• Reattribution of the cause of the symptoms to hyperventilation

• Explaining the rationale of therapy involving reduction of hyperventilation by acquiring an abdominal breathing pattern, with slowing down of expiration

• Breathing retraining for 2 to 3 months working with a physiotherapist

After breathing therapy, the sum scores of the Nijmegen Questionnaire were markedly reduced. A canonical correlation analysis relating the changes of the various complaints to the modifications of breathing variables showed that the improvement of the complaints was correlated mainly with the slowing down of breathing frequency.