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.