Hyperventilation

Hyperventilation is ventilation of the lungs, more than is required to achieve normal arterial blood gases. Hence it does not really apply to the normal increased breathing with exercise. Hyperventilation has little effect on arterial pO₂ and almost no effect on oxygen saturation that is nearly 100% under normal circumstances. The main effect is that it does lower pCO₂ and in doing so it produces a respiratory alkalosis. This shifts the dissociation of calcium towards a less ionic form so that it produces, in effect, hypocalcaemia.

Hyperventilation may be the result of events that have upset blood chemistry and so the homeostatic mechanisms have stimulated the respiratory centre to increase the rate and depth of breathing. It can be a voluntary act in that we can all choose to over-breathe if we wish. It may also be a psychological response to anxiety or stress.

There are many factors that influence the respiratory drive including the elasticity of the lungs and the resistance in the airways but the most important factors are arterial pH, pCO₂ and pO₂. Of these pCO₂ is most important although some people with COPD, especially blue bloaters can be dependent upon the hypoxic drive.

It is quite common but precise prevalence is unknown. It can occur at any age after infancy but the onset is usually between the ages of 15 and 55 years with a female preponderance of around 7:1.

In patients treated for asthma, dysfunctional breathing may account for as many as 1 in 3 women and 1 in 5 men.¹

• The commonest reason for increasing respiratory rate and depth is exercise, the extent depending upon the level of exercise. However, as this is a physiological response to a normal situation, it is inappropriate to call it hyperventilation.
• Metabolic acidosis will cause compensatory hyperventilation. This may occur with diabetic ketoacidosis or with renal failure. Carbon dioxide is a very weak acid but the volume exchanged in a day makes it the most important contributor to acid base balance.
• There may be problems of respiratory exchange including V/Q imbalance as a result of pulmonary embolism or perhaps poor gas exchange with pulmonary oedema.
• Hypoxia can be the result of climbing to altitude, especially when ascent has been too rapid and acclimatization has not occurred. Hyperventilation can cause mountain sickness with cerebral oedema. Rapid descent is imperative as the condition can be fatal.
• Fever, toxins and drugs can all increase the respiratory rate, possibly by a central action on the brain. Aspirin overdose leads first to a primary hyperventilation and respiratory alkalosis by central stimulation and then a secondary hyperventilation for the metabolic acidosis caused by the acidic nature of the drug.
• Iatrogenic hyperventilation by over-ventilating patients with head injuries was once a common technique but it has fallen from favour as it has been shown to produce a worse outcome.²
• Hyperventilation in response to anxiety is common. It is more likely in women and may be associated with panic attacks.
• Hyperventilation may also occur as part of dysfunctional breathing is in asthma sufferers.¹

The remainder of this article will concentrate on the hyperventilation syndrome as it may present in Primary Care.

Symptoms

• The complaint is usually of a paroxysmal rather than a continuous nature although chronic hyperventilation can occur.
• The patient may complain of shortness of breath when an attack occurs.
• Pain or discomfort in the chest is common.
• Paraesthesiae usually affects both arms. The complaint is often of numbness or tingling in the fingers and perhaps toes too.
• Dizziness.
• Tingling around the mouth.
• Weakness.
• Tinnitus.
• Palpitations.
• Feeling of choking or suffocation. There may be complaint of wheezing.
• Sweating.
• Loss of consciousness is uncommon but can occur.³

It may be worth enquiring specifically about some of the above if they are not volunteered but they are not all essential for the diagnosis. Ask about precipitating of relieving factors and what does the patient do when she gets an attack.

Signs

There are unlikely to be any signs unless the patient is seen in an acute attack although she may appear rather agitated or anxious. During an attack:

• The patient will look very anxious and will be struggling to breath.
• Speech is difficult and the accessory muscles of ventilation are employed.
• Note the ratio of the inspiratory duration to the expiratory duration. In quiet breathing this is about 1:2. In asthma the expiratory phase is prolonged, especially if severe and the patient may expire through pursed lips. In hyperventilation, the inspiratory phase may be more energetic and the expiratory phase is not prolonged.
• Trousseau's sign is also called "main d'acoucher" or carpo-pedal spasm. Muscle spasm produces hands with the tips of the fingers and thumb apposed and the fingers straight. Muscle spasm results from hypocalcaemia.
• Chvostek's sign is also due to hypocalcaemia. Flick behind the ear, just in front of the mastoid bone where the facial nerve emerges. The hypersensitive facial nerve makes the muscles of the face twitch.
• Another sign (really an investigation) is that hypocalcaemia may produce a prolonged QT interval on the ECG.

Chronic Hyperventilation

Chronic hyperventilation may be rather more difficult to diagnose. The patient is not so obviously hyperventilating and may have experienced numerous investigations already.

• The hyperventilation usually is not clinically apparent and so diagnosis is rather more difficult.
• There may be a persistently low arterial pCO₂ with a high renal excretion of bicarbonate so that pH is normal.
• Occasional deep, sighing breathes may be noted. These keep the pCO₂ depressed.
• They may hyperventilate more obviously when stressed and readily produce symptoms.

• The diagnosis may be obvious from the history.
• There may also be panic attack or agoraphobia.
• It may present as asthma and there may be asthma but the patient hyperventilates when the asthma is mild. Mild asymptomatic asthma is not associated with clinically significant hyperventilation but is associated with a significant reduction in both arterial and end tidal pCO₂ which relates to airway hyperresponsiveness rather than to the degree of airway obstruction or mucosal inflammation. Anxiety and depression appear not to be implicated.⁴
• It may present as chest pain and hyperventilation can precipitate angina.
• Beware of recurrent pulmonary emboli or pneumothorax.
• Patients with exercise-induced hyperventilation are more likely to have a psychiatric than a cardiac disorder. Early detection and treatment of these patients may reduce the potential morbidity associated with unnecessary invasive investigations.⁵
• If pins and needles down the arms and into the hands are unilateral, consider a problem in the neck instead.
• In adolescents with dizziness and headache, consider migrainous vertigo.⁶

Essentially, the diagnosis is clinical but it may be necessary to perform various tests to exclude other conditions. Arterial blood gases in an attack may be helpful but pCO₂ can also be measured in end expiratory air. The latter test is more often used as it is less invasive, less painful and so less likely to induce hyperventilation. ECG may exclude ischaemic heart disease or arrhythmia and D-dimers and chest x-ray may be required in case of pulmonary embolism or pneumothorax.

Simply getting the patient to hyperventilate to produce the symptoms is called the hyperventilation provocation test but its specificity is poor and its value dubious.⁷

The patient needs explanation as to the nature of the condition. It may not be easy to get her to accept the aetiology. Reproduction of the symptoms by voluntary hyperventilation may be useful.

One problem can be that the patient gets anxious and so hyperventilates. This produces symptoms that are interpreted as indicative of physical and serious illness. This causes more hyperventilation, worse symptoms and a vicious circle.

After reassurance and explanation, rebreathing into a paper bag can be used to help build up the pCO₂ again. However, this should only be used if the diagnosis is sure. If there is physical disease, it could be dangerous.⁸

Relaxation techniques and breathing exercises may be taught.⁹ Patients who hyperventilate are often thoracic rather than diaphragmatic breathers and teaching diaphragmatic breathing may be helpful, especially with chronic hyperventilation.

Drugs

The basis of treatment should be cognitive and behavioural therapy rather than medication but there may be a place for drugs. Benzodiazepines can be used in the acute situation if severe but care must be exercised if they are used more than occasionally as there are problems with sedation and dependence. Propanolol may be of value after asthma and heart failure have been excluded. Tricyclic antidepressants and SSRIs may be of value. Treatment may also be needed for associated conditions.

Approximately 50% of patients with panic disorder and 60% of patients with agoraphobia hyperventilate as part of their disorder but only 25% of patients with hyperventilation syndrome also have panic disorder.

They may suffer from obsessive-compulsive disorders, experience sexual and marital difficulties, and have poor adaptations to stress. Not all patients have demonstrable psychological pathology.¹⁰

Chronic hyperventilation may mimic many serious organic disorders, but features are often atypical.

It tends to be a long term and recurrent condition, especially if it started at an early age.