Chapter 6 Asthma

INTRODUCTION

Asthma is a common disorder of the respiratory system affecting more than 5 million people in the UK (NAC 2001). Although deaths have been declining steadily, asthma still causes much unnecessary suffering for patients. Overall however, asthma care is greatly improved due to significant improvements in treatment.

In asthma, the airways are narrowed after exposure to a trigger or an allergen causing difficulty in breathing. In many people, treatment with an inhaler and/or systemic drugs will keep this condition under control allowing them a normal, active life span. Stress is one of the factors that can aggravate asthma, and pregnancy and childbirth, causing both physiological and psychological stress, may result in a worsening of the condition. It is essential therefore that the midwife has a good understanding of this common condition to prevent asthma complicating the childbearing process.

RELEVANT ANATOMY AND PHYSIOLOGY

The respiratory system is responsible for providing oxygen to body cells to enable metabolism to take place. It is also responsible for removing carbon dioxide, which is the main waste product of this process. The cardiovascular system is closely associated with this function, as blood is the means by which oxygen and carbon dioxide are transported to and from the cells. Any dysfunction of respiration (or circulation) will result in a disturbance of the homeostatic environment (Box 6.1), which is essential for cellular function. The relevant organs of the respiratory system are shown in Figure 6.1

Box 6.1 Homeostasis

Homeostasis is a condition in which the body’s internal environment remains within certain physiological limits. For body organs and tissues to function efficiently, the composition of surrounding fluids must be precisely maintained at all times. Three factors are involved in maintaining homeostasis:

1. The optimum concentration of gases, nutrients, ions and water

2. An optimum body temperature

3. The correct volume of fluids within each fluid compartment.

Disturbance in homeostasis must be corrected quickly or illness may result. The body is constantly making adjustments to the internal environment to ensure homeostasis.

In asthma, carbon dioxide is retained in the body. Normally a rise in carbon dioxide levels within the body results in an increase in respiratory rate to remove the excess. In asthma, movement of air into and out of the alveoli is inhibited and carbon dioxide cannot be removed by this route. An increase in carbon dioxide results in a build up of H⁺ (hydrogen ions) in the blood and a decrease in pH – respiratory acidosis. This causes an imbalance in homeostasis and other mechanisms will attempt to correct the acid-base imbalance. Substances in the blood (buffers) will bind with the hydrogen ions but these will quickly be used up. The renal system will excrete H⁺ but again this can only partially compensate for the respiratory problems. Normal blood pH should be between 7.35–7.45. A pH < 7.35 will depress the nervous system and prevent normal body function. A pH < 7 will seriously depress the nervous system; the individual will becomecomatose and die if the respiratory acidosis is not quickly corrected.

Figure 6.1 Organs and structures of the respiratory system.

Ventilation

Respiration occurs by the inflation and deflation – ventilation – of the lungs. Air is thus takeninto the alveoli of the lungs where gases are exchanged with the blood circulating in a capillary network surrounding these alveoli (Fig. 6.2). This occurs by simple diffusion across the membranes that separate the lumens of the alveolus and capillary (Fig. 6.3).

Figure 6.2 Capillary network surrounding the alveoli.

Figure 6.3 Diffusion of oxygen and carbon dioxide between capillary and alveoli.

Inflation of the lungs – inspiration – is an active process; the muscles of the rib cage and diaphragm contract in response to nerve stimuli from the respiratory centre in the medulla of the brain. This causes the rib cage to enlarge and expand the lungs to which they are attached by membranes. Lung volume increases with a resultant decrease in pressure (Boyle’s’ Law). Air is drawn into the lungs down the pressure gradient, through the bronchi and bronchioles, to the alveoli where gases are exchanged as required.

Deflation of the lungs – expiration – is however a passive process. The muscles of the rib cage and diaphragm relax causing recoil of the elastic fibres of the lungs. Lung volume decreases and air is expelled. If there is excessive demand on the respiratory system, such as during exercise or breathing difficulties, the accessory muscles of respiration – those of the neck, shoulders and abdomen, become involved.

The amount of air moving into and out of the lungs in one ventilation is termed the tidal volume. With changing demand for oxygen and the removal of carbon dioxide, tidal volume is altered by an increase or decrease in ventilation rate and depth.

Control of ventilation

Control of ventilation is normally involuntary. Voluntary control occurs to enable speaking or singing or, for example when swimming underwater or entering a smoke filled room. However, voluntary control is limited if homeostasis is severely threatened.

Ventilation is controlled by nerve cells in the respiratory centre in the brain stem. These receive input from chemoreceptors in the brain stem (bathed in cerebrospinal fluid) and in the aorta and carotid arteries. The composition of both cerebrospinal fluid (CSF) and blood reflect the levels of carbon dioxide (pCO₂) in the body. Chemoreceptors respond very quickly to any rise in pCO₂ by increasing the rate and depth of respiration. Thus, the respiratory system is able to rapidly respond to the needs of cells and ultimately of the body as a whole.

Factors that influence ventilation:

• Elasticity: Lung tissue consists of elastic connective tissue which allows expansion and contraction of lung size and volume. Damage to this tissue may cause a loss in elasticity and will necessitate forced expiration and increased effort on inspiration

• Compliance: Alveoli collapse when deflated. Some effort is required to reinflate them and this is aided by the presence of surfactant and the elasticity of alveolar walls. Compliance is a measure of the effort required to inflate the lungs, i.e. the alveoli

• Airway resistance: The diameters of the bronchi and bronchioles affect the volume of air that can move into and out of the lungs. If the airways are constricted by, for example bronchoconstriction (as in asthma), more effort is required to inflate the lungs.

ASTHMA

Asthma is a chronic inflammatory disease of the airways of the lungs. It is a common condition which is increasing in prevalence around the world (Rees & Kanabar 2000). The term ‘asthma’ comes from an ancient Greek word meaning ‘panting’. The airways become narrowed and inflamed as a result of an inhaled allergen or trigger resulting in cough, wheeze and dyspnoea. An acute asthmatic attack can range in severity from mild shortness of breath to respiratory failure and death (Gutierrez & Peterson 2002). The alveoli themselves are not involved.

Asthma is thought to occur in 15% of children and 6% of adults in the UK (NAC 2001). Asthma that develops in childhood is usually provoked by an identifiable trigger, such as an allergen or by exercise. This is known as extrinsic asthma (Rees & Kanabar 2000). When asthma first develops in adult life, there is often no obvious stimulus other than respiratory tract infection – intrinsic asthma (Box 6.2). Many asthma sufferers however do not fit into either category.

Box 6.2 Occupational asthma

At least 1 in 10 cases of new or recurrent asthma in adults are caused by exposure to substances at work (McDonald 2005). There are many known substances that cause occupational asthma, including isocyanates that are found in many paints, flour and grain dust, animals and latex. Latex is a common product in use in the health services and latex allergies are becoming more common among midwives, as they have regular and prolonged exposure to the substance, mostly in examination gloves. Between 4% and 15% of healthcare workers have a reaction to latex, although this is usually contact dermatitis.

The risk of developing occupational asthma is connected to the level of exposure to the trigger and therefore, where possible, removing or reducing exposure will reduce the likelihood of developing a severe form of the disease.

Asthma is commonly considered to go through two primary stages: hyperreactivity and inflammation.

• In the hyperreactivity response, smooth muscles in the airways constrict and narrow inappropriately in response to an inhaled allergen. This is a normal protective reaction of therespiratory system but the healthy person is able to breathe deeply and relax the airways to get rid of the allergen or irritant. In the asthmatic, the muscles of the airway do not relax and thus prevent deep breathing

• Subsequently, in the asthmatic, the immune system responds to the allergen by triggering the inflammatory response. White blood cells and other immune factors are delivered to the airways. These factors cause the airways to swell, fill with fluid and produce thick sticky mucus. This results in wheeze, breathlessness, inability to exhale adequately and a productive cough. The alveoli of the lungs stay partially inflated preventing sufficient fresh air, and therefore oxygen, from filling them. Effective diffusion of oxygen and carbon dioxide is thus prevented stimulating the asthmatic to increase ventilation depth and speed.

Causes of asthma

The incidence of asthma has risen dramatically worldwide over the past few decades and the reason for this is unclear. Many asthma sufferers also have allergies, but not all people with allergies have asthma. Some forms of asthma do not have an allergic trigger. Evidence to date suggests that asthma is due to a genetic susceptibility along with a variety of environmental triggers such as infection, diet, pollution and allergens (Siddall 2001). There is some evidence to implicate the overuse of antibiotics in early life with the increase in childhood asthma (Shirakawa et al 1997).

Pathophysiology of asthma

Asthma is caused by overactivity of the inflammatory response as a result of exposure to an allergen or trigger. Helper T cells overproduce a group of immune factors called interleukins which stimulate the production and release of antibodies known as immunoglobulin E (IgE). These IgE antibodies bind to mast cells found predominately in the lungs, skin and mucous membranes. In the lungs, mast cells release chemicals such as histamine, prostaglandins and thromboxane A₂. These result in spasm of the airways and theproduction of mucus. The presence of interleukins attracts leucocytes, specifically eosinophils, T lymphocytes and platelets, which accumulate in the airways. These remain in the airways for some weeks causing a late phase inflammatory response.

Repeated exposure to an allergen and the initiation of the above process causes permanent pathological changes to the structure and function of the airways resulting in chronic asthma (Fig. 6.4). The epithelial lining of the airways become thinned or destroyed causing increased sensitivity to the allergen on subsequent exposure. The damaged basement membrane of the epithelial layer is replaced with collagen and thus becomes less elastic preventing the airways from responding to the body’s respiratory demands.