Stress and anxiety

CHAPTER 17 Stress and anxiety



Graeme D. Smith, Tonks N. Fawcett





Introduction 519

Physiological responses to stress 520
The stress response 520

Models of stress 523
The stimulus-based model 523

The response-based model 524

The transactional model 524

The phenomenological model or approach 524

The concept of resilience 524

Stress and disease 525

Psychosomatic problems 525
Anxiety attacks 525

Post-traumatic stress disorder (PTSD) 525

Migraine/headache 526

Chronic fatigue syndrome (myalgic encephalomyelitis [ME]) 526

Irritable bowel syndrome (IBS) 527

Depression 527

Coping 528
The concept of coping 528

Management of stress 528
Counselling in stress 529

Medication 529

Alcohol and stress 530

Other means of stress reduction 530

Summary: key nursing issues 532

Reflection and learning – what next? 532

References 532

Further reading 533

Useful websites 533


Introduction


Most people would probably describe themselves as being ‘stressed’ from time to time, but what does this really mean? Is stress something that resides within the environment, in situations that are threatening, harmful or unpleasant, or is it essentially an internal state, an effect of the individual’s perception of what is happening to them? Benner & Wrubel (1989), in their seminal text, defined stress as ‘the disruption of meanings, understanding and smooth functioning so that harm, loss or challenge is experienced and sorrow, interpretation or new skill acquisition is required’.


Stress may have physiological or psychosocial origins and research into stress is a highly complex field involving a number of sciences, including biology, physiology, psychology and sociology. When biologists and physiologists talk of sources of stress, they are referring to empirical phenomena. Their interest is in examining identifiable events and their measurable effects upon the organism or system under stress. Anything which affects the equilibrium of the organism may be described as a stressor; this would include bacterial infections, dehydration, extremes of temperature, inadequate food, and so on. Therefore stress can be viewed as a disturbed homeostasis that manifests itself via certain physiological and psychological imbalances (Watson & Fawcett 2003). The impact of stress occurs only when the cumulative effects of stressors surpass the individual’s ability easily to return to equilibrium. However, despite the popular connotations, not all stress is a bad thing. Having the optimal amount of stress to keep us performing at our best, adapting to life’s daily challenges, is called eustress, good stress. Distress means that our functional adaptability is impaired in some way; this can take many forms, such as anxiety, low mood or physical illness. Commonly associated triggers related to stress are outlined in Box 17.1.



Box 17.1 Reflection



Common triggers of stress (adapted from the Stress Management Society)



• Bereavement

• Illness, injury or trauma

• Interpersonal conflict

• Environmental factors

• Financial issues

• Uncertainty/change

• Work overload


Activity


Since starting your nursing course it is possible that you have been affected by one or more of the stress triggers listed above, for example work overload (with assignments), financial issues and uncertainty/change.


• Take some time to reflect on how you felt – were there physical effects or did it affect your mood?

• How did you cope with the stress and the trigger? If appropriate, discuss coping strategies with other students in your group.

Social scientists view stress in terms of the pressures upon the individual to conform (or not) to societal norms. The inherent values expressed in a society’s organisation and functioning may themselves be a source of stress to the individual. Modern industrial society, for example, provides food, safety and shelter for its members in return for a commitment to work, often at some sacrifice to personal interests, leisure and family life.


Psychologists view stress from the perspective of the interaction of individuals and groups with the environment, describing the effects of stress on cognition, emotional well-being and behaviour.


It is important for nurses to have a clear understanding of the concept of stress as they endeavour to provide the best possible care for their patients/clients and to appreciate why patients/clients might be feeling stressed and how this might be alleviated. In relation to the nurse’s own well-being, an understanding of stress and its effects is equally important. Nursing is physically and emotionally demanding work, and nurses need to recognise signs of stress in themselves, its meaning and management.


This chapter begins by looking at the physiological consequences of a stressor, identifying some of the more influential models that seek to explain the phenomenon of stress, before examining the relationship between stress and disease. The concept of ‘coping’ and various therapeutic strategies available to assist the individual in managing stress are then explored.



Physiological responses to stress


The physiological response to stress seeks to enable the individual to meet the challenges set by whatever is perceived as a stressor, by:


• the activation of the sympathetic nervous system (see Ch. 9)

• the increased secretion of several hormones from the endocrine system (see Ch. 5, Part 1).


The stress response


In 1935, Cannon summarised the response of an individual, or animal, to external threat as the ‘flight, fight or fright’ reaction, often referred to as the ‘acute stress response’. Real and imagined psychosocial stressors are an essential component of living and, when present to a moderate degree, have been described as ‘eustress’ since they optimise performance and improve learning. It is when a threat is perceived to be of an order which endangers either a person’s sense of self-worth or even life itself, that the full manifestations of the acute stress response are seen. After events such as a car crash, bomb explosion or unexpected physical attack, rapid physiological adaptations of the acute stress response are activated. This can, in some circumstances, be life saving. Consider, for example, the situation in which smoke suddenly appears in a room and, all too soon, the first flames begin to spread; a person will often find a sudden unexpected ability for rapid action to deal with such an emergency. Along with a surge of physical strength, there will be an increased ability to tackle the flames and a marked enhancement in the ability to run and thereby escape the danger. Such a response is enabled by a release of hormones brought about by activation of the sympathetic nervous system and the adrenal medulla (see Ch. 5, Part 1).


An alarm reaction of lesser magnitude is a common occurrence in the more ordinary trials of life. This occurs, for example, in such circumstances as running out of petrol on the motorway en route to an important engagement, losing one’s front door keys, or being with someone who unexpectedly becomes acutely ill. The severity of the alarm reaction varies considerably between different individuals and also between different occurrences of a similar situation. Thus, when a person’s car breaks down on the motorway for a second time, they may feel even more distressed than on the first occasion. Alternatively, they may be more confident in their ability to deal with the event and consequently be less ‘stressed’.


The manifestation of stress is derived not merely from external problems or dangers but from the way in which people attempt to manage these problems. Stress is described as the state of affairs that exists when the way in which people attempt to manage problems taxes or exceeds their coping resources. When the response to a stressor is severe, normal social relationships can be affected, as aspects of the ‘flight, fight or fright’ response potentially impinge upon rational behaviour.


As indicated, aversive physical stimuli that provoke stress events include excessive noise, cold or heat, and physiological imbalances such as those associated with sleep deprivation, lack of food or chronic pain. Such stressors not only act to bring about hormonal changes associated with the acute stress response, but also have their own selective effects on physiological functioning.


An example of such a selective effect can be seen in the body’s response to cold, as it strives to maintain homeostasis. In cold conditions, the blood supply is redistributed to less exposed areas in order to limit heat loss and, via the mechanical act of shivering, the body temperature can be increased (see Ch. 22). In addition, the secretion of thyrotrophin-releasing hormone from the hypothalamus is increased, thereby stimulating the anterior pituitary gland to secrete thyroid-stimulating hormone (TSH). This in turn causes enhanced release of the thyroid hormones thyroxine and triiodothyronine, which raise basal metabolic rate and hence increase heat production and core temperature.


To maintain homeostasis when threatened by a stressor, the body employs a range of physiological mechanisms. Some stressors are short lived, in which case the body may be able to react to the situation and quickly resolve the disturbance evoked by the stressor. Other stressors may last for days, months or even years. There are many examples of this chronic form of stress, for example when people must live with chronic disease or social disharmony. Where there has been repeated exposure to a particularly stressful or aversive event, there can be a further reaction, characterised by a conditioned fear response to any neutral stimulus experienced at the same time as the previous stressor. This effect is responsible for many of the anxiety reactions or acts of avoidance some people show in response to specific harmless objects.



The general adaptation syndrome (GAS)


Hans Selye, in his seminal work on the response-based model of stress, noted that the diverse noxious stimuli which challenged the ability of the body to maintain homeostasis induced a common pattern of effects (Selye 1936, 1976).


Selye deduced that, whatever the nature of the stressor, it resulted in a pattern of non-specific responses that formed part of what he described as a general adaptation syndrome (GAS). These responses, providing they were not overwhelming, enabled a physiological adaptation to take place (Selye 1976).


The syndrome is considered to have three phases:


• first phase – ‘alarm reaction’

• second phase – ‘resistance’

• third phase – ‘exhaustion’.

In the ‘alarm reaction’, the sympathetic nervous system and the adrenal glands are activated. Together they prepare the body for flight or fight. If the stressor continues, the triggering of neural and endocrine responses in the alarm reaction is followed by ‘resistance’ phase. Stimulation of the hypothalamo–pituitary–adrenal axis results in increased secretion of corticosteroids, the endocrine response. In this phase, the internal responses of the body mobilise resources and enable tissue defences to achieve the maximum adaptation possible. The final phase of the GAS is ‘exhaustion’, in which the body may succumb to the stressor.


The GAS is criticised for providing a somewhat simplistic, stereotypical model of the responses of the body and failing to take full account of the individual variations of psychological and physiological responses. Lazarus (1966) argued that there is a circularity about Selye’s model, in so far as something about the stimulus elicits a particular stress response while something about the response indicates the presence of a stressor.



The acute stress response


During the alarm reaction to stress, a series of physiological responses involving limbic and brain stem structures are triggered (Fox 2004). Neural pathways from nuclei in the limbic system mediate responses to emotional stress, and pathways from the reticular formation in the brain stem mediate responses to physiological stressors such as pain and injury. This activates the hypothalamo–pituitary–adrenal axis and results in the secretion of a range of hormones.


An immediate response to threat or stress involves the neural connections from the hypothalamus to the sympathetic outflow, activating both postganglionic and preganglionic sympathetic nerves passing to the adrenal medulla. This is the emergency reaction which was first described by Cannon (1935). In the adrenal medulla, acetylcholine released at preganglionic sympathetic nerve terminals activates the chromaffin cells to secrete the catecholamines adrenaline and noradrenaline. In humans, adrenaline is secreted in greater amounts than noradrenaline. The release of these hormones takes place in a matter of seconds or minutes.


The hormones liberated from the adrenal medulla have many effects which facilitate emergency reactions. For example, adrenaline and noradrenaline improve cardiac and respiratory function. Heart rate and force of contraction are increased. Bronchioles are dilated and the depth and rate of respiration are increased. Blood flow is redistributed to areas of need, i.e. the heart and skeletal muscles. Blood glucose and basal metabolism are raised and blood clotting facilitated. The increase of blood glucose is due mainly to the actions of adrenaline on the liver to promote glycogen breakdown and enhance gluconeogenesis (production of glucose from non-carbohydrate substances) from fatty acids and proteins. Adrenaline also acts on the pancreas to inhibit insulin secretion. Piloerection and pupillary dilatation, so characteristic of the behaviour of fighting cats, represent yet another physiological consequence of hormone release from the adrenal medulla. Sweating by the eccrine glands (the most abundant sweat glands) is increased. In the meantime, functioning of the digestive tract is reduced and urinary sphincters are closed.


The physiological effects of adrenaline and noradrenaline are explained in Chapter 5 (Part 1).


In the more long-term responses to stress described by Selye, the centre of activity passes from the adrenal medulla to the adrenal cortex, and to the hypothalamus and pituitary, which are responsible for activating the adrenal cortex. Corticotrophin-releasing hormone (CRH) is secreted by the hypothalamus as well as other sites in the brain. CRH acts on the anterior pituitary gland, stimulating the secretion of adrenocorticotrophic hormone (ACTH) and beta-endorphin.


Beta-endorphin reduces susceptibility to pain and is probably one of the means by which stress and the stimuli of conditioned fear give rise to endogenous analgesia. Opiates act in a similar way to endorphins, but are not rapidly degraded by the body, as natural endorphins are, and thus have a long-lasting effect on pain perception and mood (Pert 1997).


Other factors influence the release of ACTH, including antidiuretic hormone (ADH) and hypothalamic vasoactive intestinal peptide (VIP). The ACTH liberated by the anterior pituitary acts to stimulate cells in the adrenal cortex to secrete corticosteroids.


Glucocorticoids, mostly cortisol (hydrocortisone), secreted by the adrenal cortex play a key role in adaptation to stress. Glucocorticoids modify metabolism so as to increase blood glucose concentrations. They do this by mobilising tissue protein and amino acids and by these actions may induce a negative nitrogen balance (see Ch. 21). Glucocorticoids are needed to enable other hormones to bring about the mobilisation and metabolism of fat. These metabolic effects of glucocorticoids ensure the supply of adequate fuel to the cells when the body is under stress, and in this respect the adrenal cortex provides an important back-up system for the adrenal medulla. In addition, glucocorticoids play important roles in the proper functioning of many organ systems and tissues in the body, including the cardiovascular system, the nervous system, lymphoid tissue and skeletal muscle.


Glucocorticoids, such as cortisol, possess appreciable mineralocorticoid activity, retaining sodium chloride and indirectly increasing extracellular fluid (ECF) volume, although they are much less potent in this respect than aldosterone (see Ch. 20). The secretion of aldosterone is not regulated by ACTH, and so its release is independent of the stress response. Mineralocorticoid activity by hormones such as cortisol may in part underlie important, though poorly understood, actions on the cardiovascular system. An increase of ECF volume can be of great importance under circumstances when stressors induce shock or when there is loss of body fluids after haemorrhage or burn injury (see Chs 18, 29, 30).


Additionally, glucocorticoids can decrease the number of some types of circulating white blood cells and, at pharmacological concentrations, suppress the immune response. In addition to their direct effects, the corticosteroids exert an enabling influence on the actions of several other hormones and are necessary for the body to show a full response to the adrenaline and noradrenaline released from the adrenal medulla. It can be seen that due to its wide-ranging functions, especially in the maintenance of fluid and electrolyte balance, the adrenal gland is essential to life and the maintenance of physiological homeostasis and psychological equilibrium (Box 17.2).



Box 17.2 Information



Hormones and effects of short- and long-term stress



Short-term stress


Mediated by the release of the catecholamines adrenaline and noradrenaline from the adrenal medulla, short-term stress leads to:


• increased heart rate

• bronchodilatation

• increased blood pressure

• liver conversion of glycogen stores to glucose for release into the bloodstream

• altered blood flow patterns to increase arousal and decrease digestive and urinary activity via selective vasoconstriction

• increased platelet aggregation

• pupil dilatation and piloerection

• increased metabolic rate

• sweating from eccrine glands.


Long-term stress


Mediated by the release of glucocorticoids and mineralocorticoids from the adrenal cortex, long-term stress leads to:


• gluconeogenesis whereby proteins and fats are broken down to form glucose

• increased blood glucose levels

• retention of sodium and water by the kidneys (aldosterone effect)

• increased blood volume and blood pressure via the above plus vasoconstriction and reduced fluid shift

• increased coagulability and viscosity of the blood

• suppression of the immune system and inflammatory response

• altered blood biochemistry, e.g. in 5-hydroxytryptamine (serotonin), endorphin and dopamine levels.


The chronic stress response


Clearly, as Selye (1976) established, there are limits to the body’s ability to maintain its phase of resistance and adaptation in the face of excessive or continuing stress; environmental stressors can be toxic and physiologically overwhelming. As Selye noted as long ago as the 1950s, when an individual is physiologically challenged but not overwhelmed, as in conditions of prolonged, chronic stress, enlargement of the adrenal glands and atrophy of the thymus and lymphatic structures (thymicolymphatic atrophy) will occur. When stress persists beyond a certain period of time, disturbances occur in the homeostatic balance of the body and there is an ever-increasing danger that disease processes will be precipitated.


An important part of the body’s defence mechanism in the phase of resistance is the pituitary secretion of ACTH, which in turn stimulates the adrenal cortex to release corticosteroids. One of the early signs of the body’s inability to meet the demands of unremitting stress is a blunting of the amounts of ACTH released by the anterior pituitary in response to that stress. Under these circumstances, the adrenal cortex frequently shows hyperplasia, which persists despite the reduced secretion of ACTH. This blunting of the ACTH response to stress also occurs in long-standing timidity, which is possibly due to high arousal together with slow habituation to the stressors. This is coupled with an associated enlargement of the adrenal glands and hypersecretion of corticosteroids under comparatively non-threatening circumstances. Likewise, blunting of the ACTH responses to stressors is seen in depressive illness and in many forms of anxiety. In individuals experiencing low mood, there is frequently a high corticosteroid excretion associated with enlargement of the adrenal glands and an increase in the concentrations of CRH in cerebrospinal fluid.


Emotional as well as hormonal changes characterise chronic stress. These include emotional exhaustion, a decreased sensitivity to rewards and a withdrawal from decision making, which is characteristic of fatigue. This can progress to the condition known as ‘burnout’, a complex phenomenon involving extreme physical and emotional distress which, for the individual, is often linked to organisational factors (Hall 2004). In burnout, the physical and emotional fatigue may be manifest as a lack of involvement with, or sympathy or respect for, colleagues and clients. At its final stage, chronic stress may result in total collapse. Long-lasting stress in which there is a poor coping strategy is correlated with increased occurrence of a variety of diseases (Levi 1971, Cooper 2004, Hesselink et al 2004). These may be described as diseases of adaptation and are related to deranged secretion of adaptive hormones in the phase of resistance. These conditions include digestive disturbances, hypertension, myocardial infarction, allergies and sleep disturbances (see Chs 2, 4, 6, 25). Such chronic stress may also lead to anxiety, low mood or behavioural disturbances, such as appetite disorders or increased usage of alcohol, tobacco, caffeine or even illegal substances. Clearly, in such situations, physiological homeostasis and psychological equilibrium are under threat.



From homeostasis to allostasis


The concept of allostasis, as opposed to homeostasis, refers to the maintenance of stability through change. It is seen as a fundamental process by which organisms actively adjust to both predictable and unpredictable events. This theoretical development suggests that both homeostasis and allostasis are endogenous systems responsible for maintaining the internal stability of an organism. However, homeostasis means remaining stable by staying the same. Allostasis comes from the Greek allo, which means ‘variable’, thus remaining stable by being variable. Thus the allostatic state refers to the altered physiological and emotional activity in response to changing environments and challenges, e.g. an excessive or inadequate production of, for example, cortisol or cytokines (McEwan & Wingfield 2003). Cytokines are a group of intercellular signalling molecules, e.g. interleukins, interferons, which act on immune cells.


The allostatic load refers to excessive or prolonged alteration in allostatic state that is outwith the individual’s ability to cope and which arguably leads to detrimental health outcomes. The perception of stress is influenced by the individual’s unique makeup, their genetics, experiences and behaviour (Lazarus 1966). From the theoretical stance of allostasis, when a source is perceived as stressful, physiological and behavioural responses are initiated leading to an altered allostatic state and, ideally, adaptation. However if the source of stress does not resolve, over time the allostatic load can accumulate and the overexposure to neural, endocrine and immune stress mediators can begin to have adverse effects on organs and systems of the body, leading to disease.


There are considered to be four types of allostatic load:


• Simply too much ‘stress’ in the form of repeated, novel events that cause repeated elevations of stress mediators over a long period, e.g. economic hardship.

• A failure to habituate or adapt to the same stressor. This leads to the overexposure to stress mediators because of the failure of the body to dampen or eliminate the hormonal stress response to a repeated event.

• A failure to switch off either the hormonal stress response or to display the normal diurnal pattern of the glucocorticoid production in the body.

• Inadequate hormonal stress response which allows other systems, such as the inflammatory cytokines, to become overactive (McEwan & Wingfield 2003, Wingfield 2003).


Models of stress


The physicist Robert Hooke (1635–1703) used the word ‘stress’ in the 17th century to refer to the ratio of an external force (created by a load) to the area over which that force was exerted. The resultant strain created a deformation or distortion of the object by what became known as Hooke’s Law.


There is an interesting similarity between this use of the word stress and its modern application in the realm of human emotion and behaviour; indeed, people frequently use words such as ‘weight’ and ‘strain’ when describing their feelings of anxiety and stress.


During the 20th century, the adoption of the concept of stress by the biological and behavioural sciences resulted in the formulation of a number of models to describe stress and its effects, including the:


• stimulus-based model

• response-based model

• general adaptation syndrome

• transactional model

• phenomenological model or approach.


The stimulus-based model


In this model the person is viewed as being constantly exposed to general or specific ‘stressors’ in their daily life, e.g. the demands of work, family responsibilities, illness, accidents, bereavement or disability. These stressors have the potential, however, to cause both physical symptoms and distressing feelings that will undermine well-being.


In the stimulus-based model, stress is a state that can generally be empirically observed, measured and evaluated, and which can potentially be removed or altered to reduce the individual’s stress: it is possible, in theory, to persuade noisy neighbours to be quieter, for traumatic wounds to heal, or to make a cold working environment warmer. However, in many situations, such as a bereavement or disablement, the original stressor cannot be changed or adapted to reduce distressing feelings. Even in relatively simple situations, removing the stressor is not necessarily a straightforward matter (Box 17.3). It quickly becomes apparent that the stimulus-based model has substantial shortcomings when considered in relation to the breadth of human experience (Sutherland & Cooper 2000) and has difficulty explaining why some people experience stress in certain situations while others, in similar circumstances, do not, or explain why a given situation may be stressful at one time but not at another. The model offers no explanation as to why a person may be stressed in response to apparently neutral stimuli such as birds, spiders or aeroplanes. Lazarus (1966), in his seminal text, argued that it is not possible to evaluate the human experience of stress objectively; only a personal account of feelings and experiences can adequately convey the nature of an individual’s stress.



Box 17.3 Reflection



Janice


A health visitor could not understand initially why her client, Janice, an unsupported mother of two, appeared to be tense and unhappy when they met at the child health clinic. She asked how Janice was feeling, and Janice described how she had new neighbours in the flat above her who played loud music until early in the morning, preventing her and her two children from getting enough sleep. She had tried to talk with them but they had been hostile towards her and made her feel apprehensive. She didn’t dare complain to them again. The lack of sleep was affecting Janice and her children. Janice had difficulty concentrating at work and felt like crying frequently during the day; the children were overtired and generally irritable, making it even more difficult for her to cope. The health visitor asked Janice if she could intervene by contacting the environmental health department of the local council on her behalf, but Janice said that she was afraid that this would make matters worse.



Activities



• Reflect on Janice’s situation and consider how else the health visitor could support her.

• Read the chapter material covering other models of stress and discuss with your lecturer or mentor the relative advantages and limitations of each in Janice’s situation.


The response-based model


In this model, the word ‘stress’ is used to describe the response of a person who feels they are in a threatening or difficult situation. Stress is thus a person’s response to threat which, as in the stimulus-based model, is not necessarily inherent in the environment or situation. By using the response-based model, it is possible to make sense of an individual’s unique stress responses and even of responses that might seem, within the stimulus-based model, to be irrational, such as a fear of birds, spiders or of flying. Hans Selye’s extensive physiological research as an endocrinologist (Selye 1936, 1946a,b, 1976) was largely based upon the response-based model of stress.

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Oct 19, 2016 | Posted by in NURSING | Comments Off on Stress and anxiety

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