this lecture ( psychological aspects of bronchial asthma) has been presented by Dr. Heba ashebani/ Abusetta chest center, in the event of Global asthma day 2018.
2. ETIOLOGIC HYPOTHESES
• Psychological factors may predispose to asthma and may also act as a trigger of
asthmatic attack. These observations support the etiological hypothesis of
psychosomatic origin of asthma.
3. Psychosomatic theory of bronchial asthma:
• Mechanisms by which psychological stress can induce or exacerbate asthmatic changes
include:
1- Stress and autonomic dysregulation :
Experimental studies in which asthmatic patients are exposed to stressful situations have
focused on stress induced vagal reactivity as a mediator of emotionally induced
bronchoconstriction.
Asthma patients tend to show greater bronchoconstriction than healthy controls in response
to stress, both in the laboratory, and in everyday life.
4. • Beta-sympathetic activation produces bronchodilation, whereas alpha-
sympathetic activity and parasympathetic activity produce bronchoconstriction.
• ( psychophysiological principle of individual response stereotypy )
found that in response to various laboratory tasks, defensive patients with
asthma displayed a response pattern involving bronchoconstriction, lower skin
conductance levels, and greater respiratory sinus arrhythmia amplitudes: an
autonomic response pattern suggestive of parasympathetic and
sympathetic arousal. Defensive people without asthma tend to show increased
sympathetic .
5. Acute psychological stress
Activation of sympathetic
adrenomedullary and HPA axis
Secretion of CRH
Secretion of ACTH
Secretions of corticosteroids
Anti-inflammatory action.
Chronic psychological
stress
Hyporesponsive HPA axis
Reduced cortisol level
Reduced anti-inflammatory activity
6. 2-Stress and Endocrinal Imbalance:
• Psychological stressors have been associated with the activation of
the sympathetic and adrenomedullary system and the
hypothalamicpituitary-adrenocortical (HPA) axis.
3-Stress and Immunomodulations:
NHLBI’s (1997) guidelines define asthma as an immune system process,
but do not include immunologic testing as part of asthma assessment.
7. • a small in Th2 cytokine response profile among asthma patients during
examination stress, while there is in IL-5 among healthy participants but not
asthma patients during examination stress, and this has been interpreted by
authors as:
1 - a vulnerability to stress-related airway inflammatory reactions among people
with asthma.
2- long-term exposure to stress can increase susceptibility to respiratory illnesses
,which in turn can exacerbate asthma.
8. ASTHMA AND DEPRESSION
• The relationship between asthma and depression, is bidirectional .
• A study demonstrated that film-induced sadness can produce bronchoconstriction
among children with asthma.
• the wellknown relationship between depression and an attitude of helplessness
a passive behavioral response to stress, which appears to be particularly associated
with vagal activation .
• On the other hand, some of the common effects of asthma also can contribute to
depression, particularly fatigue, disability, and self-perception as being sick.
• There also may be a genetic link between asthma and certain mood disorders.
9. PANIC DISORDER AND ASTHMA
many of the manifestations in panic attack are similar to
manifestations of acute attack of asthma.
10. Panic Disorder symptoms (American Psychiatric Association):
*Four or more of the following symptoms
1. Palpitations, accelerated heart rate
2. Sweating
3. trembling or shaking
4. Sensations of shortness of breath or smothering
5. Feeling of choking
6. Chest pain or discomfort
7. Nausea or abdominal distress
11. 8. Feeling dizzy, unsteady, lightheaded, or faint
9. Feelings of unreality (derealization) or being
detached from oneself (depersonalization)
10. Fear of losing control or going crazy
11. Fear of dying
12. Numbness or tingling sensations
(paresthesias)
13. Chills or hot flushes
13. Chills or hot flushes
12. Approximately 1 asthma patient in 10 has panic disorder whereas
asthma and other chronic respiratory diseases are 3 times more
common in patients with panic disorder than among those with
other psychiatric disorders or general population.
Causal direction between asthma and panic may be
bidirectional:
The psychophysiological stress response that accompanies panic
may elicit autonomic and inflammatory responses among people
with asthma.
13. On other hand, dyspnea and other unpleasant body sensations accompanying
asthma may trigger panic.
There is poor correlation between asthma severity and panic symptoms
Symptoms of mild asthma might more easily be confused with panic symptoms,
whereas symptoms of more severe asthma are more recognizable and lead to
a clearer path of coping behavior, thus decreasing the panicogenic effect.
panic disorder and asthma seem to be independently transmitted in families of
those with asthma.
14. Other pathophysiological events may elicit both disorders and, in
turn, be elicited by them. Chief among these is Hyperventilation,
which commonly occurs in panic disorder .
Another possible bidirectional pathway is shared respiratory
dysregulation that may contribute to the pathophysiology of both
problems. For example, the experience of dyspnea in both disorders
may be linked by CO2 sensitivity. Medullary chemoreceptors and the
locus coeruleus may be stimulated by bronchoconstriction in asthma,
inducing the expression of an underlying vulnerability to panic.
15. Repeated stimulation of chemoreceptors may lead to dysfunction of the
brain’s suffocation alarm system to underlie the development of panic
disorder. This mechanism may stimulate hyperventilation, thus
exacerbating both panic and asthma.
16. DEPRESSION, ANXIETY, AND LIFE-THREATENING ASTHMA ATTACKS
A high prevalence of denial and anxiety has been found among asthma
patients who have experienced a near-fatal attack.
Depression in asthma
Poor cognition
Poor concentration &
memory
Low energy
Low motivation
Hopelessness
helplessness
Poor treatment compliance
Poor self management to
asthma
Asthma exacerbations
“Feedback loop”
How depression affects asthma outcome negatively
17. PSYCHOLOGICAL INTERVENTIONS
Psychological therapies are effective at improving various aspects of asthma
control or quality of life.
1. Behavioral therapies :
focus on identifying the processes by which behaviour has been learned via
association, reward, or observation and modifying behaviour using methods such
as systematic desensitization, selective reinforcement, and positive modeling.
18. 2. Cognitive therapies :
act by identification and constructive management of incorrect and
damaging thoughts, such as perceptions of helplessness or
inappropriate fear of asthma attack, that can trigger episodes.
Information (eg, about the relationships between anxiety and
bronchoconstriction) also targets cognitions.
3-Cognitive behavior therapy (CBT):
CBT combines the key elements of both behavioural and cognitive
models and is currently used more frequently previouse ones alone.
19. predisposing factors and precipitating event
Automatic
thoughts
Emotions
Bodily reaction
Panic attack
Catastrophic
misinterpretation
Focus on
sensation
Amplification
of sensation
PAPحPPPANIC CYCLE: Cognitive behavioral explanation.
20. 4. Relaxation techniques :
Relaxation techniques control stress and anxiety, which, in asthma, may
improve breathing and respiratory function.
These programs include progressive relaxation, and hypnosis or deep
relaxation, which may be induced using mental imagery. This is often
accompanied by autosuggestion to create positive thoughts and
feedback of biologic indicators, which the subject must control via
relaxation. A study for dr Alexander and Weingarten measured the effect
of relaxation therapy on peak expiratory flow and found effects favoring
21. the treatment group compared with the control group. .
6. Counseling involves:
talking over problems with a health professional. In supportive counseling, the
counselor acts primarily as a good listener who provides emotional support.
Supportive therapy sometimes has a problem-solving focus and may be helpful
for patients experiencing an acute crisis.
7. Educational approaches:
do not attempt to alter core psychological processes and therefore are not
psychological therapies as such. They are already the subject of systematic
reviews and are included as necessary components of optimal asthma care.
22. 9. Breathing retraining exercises:
include a range of techniques for improving breathing control in
asthma (e.g., yoga, and transcendental meditation). These are not
regarded as standard psychotherapies, although aspects of breathing
retraining may be included in behavioural therapy or CBT.
23. BEHAVIORAL ASPECTS OF MEDICATIONS USED IN BRONCHIAL
ASTHMA
Drugs Behavioral aspects
Theophyllin
Side effects: anxiety, nausea, tremor, and restlessness, and disrupted
sleep especially at higher doses. careful timing of dose can help reduce
the sleep-related effects.
B-adrenergic
bronchodilators
Anxiety, tachycardia, and tremor, particularly in patients who overuse
their inhalers. High dose can cause cardiac dysfunctions because of
tachyarrhythmias and hypokalemia.
Inhaled
anticholinergics
like atropine and
ipratropium
Reduce sputum volume without changing viscosity, and induce desired
bronchodilatation. These drugs are absorbed less hence CNS effects are
minimal.
24. DRUGS BEHAVIORAL ASPECTS
Corticosteroids
Controversial. Only few patients who have coincident asthma may benefit
from short or long term treatment. For some such patients alternate day
oral dosing / inhaled steroids may be useful. These measures brain levels of
steroids and thereby psychiatric symptoms like mood changes, cognitive
disturbance delirium and sleep disturbance.
Benzodiazepin
es
Can significantly reduce the ventilatory response to hypoxia. this may
precipitate respiratory failure in a patient with marginal respiratory
reserve and contraindicates their use in patients with carbon dioxide
retention. Benzodiazepines are not contraindicated for use in all patients
with COPD and asthma.
Benzodiazepines may actually improve respiratory status in some
patients, especially in those with asthma or emphysema (“pink puffers”).
Severe bronchitis (“blue bloaters”), severe restrictive lung disease, and
sleep apnea are the most vulnerable to the adverse effects of
benzodiazepines.
25. Benzodiazepines
In elderly patients, shorter-acting benzodiazepines with no active
metabolites, such as lorazepam and oxazepam, are preferred.
buspirone , does not adversely affect pulmonary function, its limitations
are its potency and delayed therapeutic effect.
Benzodiazepines should be avoided in obstructive sleep apnea
antidepressa
nts
Little or no effect on respiratory function.
SSRIs other than fluvoxamine have few drug interactions that are
problematic in pulmonary patients. One exception is the antituberculosis
drug rifampin. Rifampin is a CYP 3A4 substrate and may compete with
many psychotropic drugs, including the antidepressants amitriptyline,
imipramine, fluoxetine, sertraline, bupropion, venlafaxine, and
trazodone.
Rifampin may compete through the same site with anticonvulsants (eg,
carbamazepine, tiagabine, and valproate) and with benzodiazepines,
zolpidem, and haloperidol.
26. SUMMARY AND CONCLUSIONS
• Bronchial asthma, a chronic disease of childhood and adolescence, is
characterized by airway obstruction that is, to a variable degree, reversible,
either spontaneously or with treatment, airway inflammation, and increased
airway responsiveness to a variety of stimuli. Current biopsychosocial
approach emphasizes need to consider biological, psychological and social
factors to understand and treat the disease effectively.