Swasa roga.

Swasa Roga is a typical respiratory problem mentioned in classical Ayurveda texts. This presentation has tried to include classical as well as modern perspectives of respiratory problems that has difficulty in breathing/dyspnoea as the major symptom.

1. SwasaRoga
Zjf; /f]u
Presented by:
Dr. NarendraP. Giri
Resident, Final year
Ayurveda Medical College,IOM, TU
Kathmandu

2. Introduction
•Difficulty in breathing is SwasaRoga.
•“Zjf; k|f0fg]’-cbflbwft'_ af6 Zjf; zAbsf] lg?StLh;sf] cy{ k|f0f
wf/0ffy{ k|f0f jfo'sf] Zjf; dfu{ leqk|j]z ug'{ x'g] .
•SwasatiVayuitiSwasah(Hem Chandra)
•SwasitiAnenaitiSwasah(ShabdaKalpaDruma)
•SwasitiItiSwasah
•Swasaword is used to denote respiration and exchange of
air in the body. The word Swasais used for both
Physiological and Pathological states

3. Nidan
•VataPrakopak
–Aahare.gRukshyaAnna sewan, Visahamasan,
ShitalJalapaan, Atibhojan, Adhyasanetc
–Vihare.gExposure to smoke, dust, cold air, living
in cold environment, excessive exercise,
Atimaithuna, Bathing with cold water, Vaman
atiyoga, excessive walking, Vegawarodhaetc.

4. Nidancontd…
•KaphaPrakopak
–Aahar-Beans, horsegram, til, flour, root of Kamal,
Bistambhi, Guru, Aquatic and Aanupmansha, Curd,
Unboiledmilk, Abhishyandifood etc
–Vihar-Living in cold environment, bathing with cold
water, exposure to cold air etc
•Internal causes-Malabarodha, Aaamavisha, Kapha
dushitpranavayu, Pranavahashrotobikar,
Accumulation of Vayuin Aamasayaand Udar, Pathology
of lungs etc.

5. •External causes-Injury to chest and/or throat, exposure
to cold , dust or smoke, excessive walking, atimaithuna
etc.
•Local causes-Inflamationin the upper portion of airway,
inflammation in chest, pathology in accessory muscles of
respiration, Tonsilitisetc
•SwasajanakRog-Pandu, Atisar, Jwar, Chhardi,
Kshatakshind, Raktapitta, Visha, Udawarta, Visuchika,
Alasak, Adhmaan, Medhobriddhi, Jalodhar, Hridroga,
Gulma, Shosa, Yaxhma, Plihodar, Agnimandhyaetc.

6. Samprapti
•The specific pathogenesis of SwasaRogais described
as exposure to etiological factors leads to vitiation of
Kaphaalong with Vatawhich causes obstruction of
PranavahaSrotas.
•This generates movement of vayuin all direction in
PranavahaSrotasand body, ultimately causes Swasa
roga

7. •Dosha-KaphaPradhan Vata
•Dushya-Rasa
•Shrotas-Pranavaha
•Adhisthan-Aamasaya( Aamasayasamudhbhava)
•Shrotodusthi-sangaand Bimargagaman(vata)
•Aanshukarivyadhi

8. Purvarupa
•Pain in HridhyaPradesh
•Parshwashool
•Adhmana
•Aanaha
•MukhBairashya
•Pricking pain in SankhaPradesh

9. Types of SwasaRoga
1.Mahaswasa:-
•Breathing with difficulty in a loud sound like a bull
•Loss of consciousness
•Random movements of eyes, dilated pupils
•Breaths with open mouth
•Urges of stool and urine do not come
•Interrupted speech
•Looks very poor
•Found in terminally ill and the patient who is going to die in
near future

10. 2. UrdhwoSwasa:
•Prolonged expiration but inability to inspire
•Pranabahashrotasand mouth are full of kapha
•Eyes focused upwards and there is random eye
movements
•Frequently loses consciousness due to pain
•Dryness of mouth
•Restlessness

11. 3. ChinnaSwas:
•The breathing is interrupted despite of full effort
•Pain in heart and other marmascause frequent
ceaseassionof breating
•Aanaha, Swedhadhikya, Murchha
•Burning sensation in VastiPradesh
•Eyes filled with tears, one eye becomes red
•Patient looks poor, Anxious, Loss of lustureof skin,
•Pralap
•Patient dies soon

12. 4. TamakSwas:
•Aggravated vatadue to exposure to causative
factors leads to its Pratilomagatior reverse
movement. Vitiated vataruns through channels
and reaches head –neck region. It exaggerates
the regional Kaphaby increasing epithelial
secretion and produce pinasa. These secretions
or malarupikaphaobstructs the passage of air
and produces ghurgurshabdaor wheezing sound

13. TamakSwasaSymptoms:
•Pinasa
•Griva-SirasaSangraha
•Ghurghurkamashabda-wheezing
•Pramoha-fainting and shock
•Kanthodhwansa-discomfort in throat
•Parshwasgraha-fatigue of accessory respiratory muscles
•Ushnamabhinandhate-ushnaaaharbiharcauses some relief
•MeghambushitaPragvatahShleshmachabhivardhate-Megha,
Ambu, shita, praghvata, slesmaetcincreases the symptoms

14. •Lalatasweda
•SlesmanivimokshanteMahuratumSukham-coughing
out some sputum relieves for some times
•Vishushkashyate-dryness of mouth
•MuhurShwas-rapid breathing
•Body shakes during breathing
•Distress

15. Types of TamakSwasa
1.PratamakSwasa
•When TamakaShwasais associated with symptoms like
Jwaraand Murcha, it is known as Pratamakashwasa.
•It is caused by Udavarta, raja, ajirna, klinnakaya and
suppression of natural urges.
•According to Madhukoshacommentary, association of
Pitta doshawith vataand kaphacauses pratamaka
shwasa.

16. 2. SantamakSwasa
This subtype of TamakaShwasaincreases during night time
and is relieved by cold things.
It is known as SantamakaShwasabecause the patient feels
as if he is drowning in the darkness usually the attacks
precipitate early in the morning.
Acharya Chakrapaniand Jejjatadescribed only Pratamaka
Shwasaas a subtype of Tamakashwasaand according to
Madhukoshacommentary; PratamakaShwasais synonym
of SantamakaShwasa.

17. 5. KshudraSwasa:
Brathlessnessdeveloped due to excessive intake of
Rukshyafood and excessive exercise and relieved itself
by rest.

18. Sadhyasahdyata
•Mahaswasa, UrdhoSwasa, and ChinnaSwasaare
incureable.
•NavinTamakSwasais cureablebut is uncureable
when long standing. It is incureablein weak patient.
•All the Swasarogaare cureablein its prodromal
phase.

19. Treatment
•Mahaswas, Urdhoswasand Chinnaswasare
incureable.
•Kshudraswasarelieves itself by rest.
•So, Tamakswasais the only to be treated

20. Chikitsasutra
•According to Acharya Charaka, any drug or dietary regime
etc. which alleviates Kaphaand Vata, have ushna
property and promotes downward movement of vata,
should be used in the patient of shwasaroga
•If both Vataand Kaphacannot be passifiedat once
Vataharatreatment is better than kaphaharatreatment
because vataharatreatment may aggravate kaphabut it
minimizes the complications associated with disease and
also improves the prognosis, whereas kaphahara
treatment pacifies kaphabut also causes depletion of
dhatuand produces serious side effects

21. Management of Swasahas two aspects
1.Management during vegaawastha
2.Management during Avegaawastha

22. Management during vegaawastha
•Local application of lawanmishrittailain the chest-the both lawanand
snehahaving suksmaproperty penetrates the tissue and reaches the lungs
to liquefy the mucus plugs ( kapha)
•Then NadiSweda, Prastara,sankaraswedais done. In infants and small
children, hasta swedais preferred. Swedanahelps to dissolve this Kapha.
Also heat applied by Swedais carried from skin to internal organ through
blood. Blood is the only medium in body to transfer heat from outer
environment to internal organs. In response to the above mentioned
procedures, Kapha, which has become stagnated and get dried, thickened
in the Srotas, gets softened and dissolved which is then eliminated from
body by Sodhanaprocedure.
•After profuse perspiration by doing swedana. Then snigdhaodna(Rice) or
soup of fish, pork, meat or the supernantantof the curd should be given to
increase the kaphadosha.

23. •Then vamanais done by pippalichoorna, Saindhavalavana, honey, but
the drugs used should not be antagonistic to vata. Thus the sputum (
DustaKapha) is easily expectorated to leave free flow of pranavayu
•After vamanathe residual doshaswhich are not completely eliminated are
cleared with help of dhumpana. For this haridrapatra, Erandamula, lac ,
realgar(Manashila) , devdaru, orpiment, jatamansipowder is utilized
along with ghee.
•A varthiis made and is smeared with ghee & used for dhumpana.
•However, in children less than 7 years, mriduvamanaand Virechanaare to
be performed if the Vega tivratais very high. Instead, Shamanadrugs of
ushnaveerya, which pacify the vata, vatanulomaka-as well as liquefying
kapha( kaphavilayaka) , making it flow out to its base in Amashaya,
where it can be pacified using kaphaharadrugs should be used.

24. Management during Avegaawasyha
•In Avegavasthadue consideration should be given to
avoid pathogenesis which further leads to
exacerbations. Hence, particularly Deepana-
Paachanaand Vatanulomakatreatment should be
adopted; DeepanaPaachanatreatments are useful in
maintenance of Agni as KaphaDoshaaggravation
results due to Mandagni. Vitiation of Doshadoesn‟t
occur if Agni is in proper state. By Vatanulomaka
treatment, Vayutraverses through its own path.

25. •sfl;g] R5b{g+ bWoft\:j/eUg] r a'l¢dfg\.
jftZn]id x/}o{'St+ tds]t' la/]rgd\.. r= lr= !&÷!@!
Swasaoriginates from the pitta sthana. So virechana
causes the excreationof excess pitta, relieves
malabarodh, anulomesthe vata, pacifies the rakta
dosha(blood purifying hence relieves allergic
condition), mantainsagni-all are helpful for relieving
Swasroga

26. SamanaChikitsa
•Single herbs-Pipali, Bharangi, Sunthi, Vasa, Somalata, Puskarmula,
Kantakari, Haridra, Sirish, Arka, Talish, Agaru, Kusmanda, Sobhanjanetc
•Churna-Jesthavasadi, Talishadi, Sitopaladi, Shringyadi, Satiyadi, Muktadi,
Haridradi, Karpuradietc
•Ghrita-Shringyadi, Talishsadi, Vasa, Kshatpal, Manashiladighritaetc
•Vati-Arkavati, Swasantakvati
•Asav/ Arista-Vasarista, Kanakasava, Dushmoolaristha, Pipalyasava
•Abaleha-Vasaharitaki, Vasabaleha, Agastyaharitaki, Vyagriharitaki,
Chyawanprash
•Rasa-Swaskutharras, Swaskaschintamaniras, Mahaswasarilauha,
Bhagottargutika, Nagarjunabhraras, Shringarabhraras, Mallasindoor,
Mayurpichhavasma, Muktavasma, Prabalvasma, sankhavasma, Tamra
vasma, Rasamanikyaetc.

27. Pathyapathya
•Pathya
Aahar-All dietary articles should be easily digestible and served
warm. Unpolished rice, wheat, green gram, horse gram
(Kulatha), goat milk, green leafy vegetables like Patola, Shigru,
brinjal, garlic, cardamom, cinnamon, pepper, ginger, honey, crab
soup ?, Kritaand AkritaMamsaRasa. Luke warm water for
drinking.
Vihar-Fomentation, hot water bath, moderate sun bath, warm
clothes etc. and staying in fresh and ventilated places. Doing light
exercises and maintaining daily routine.

28. Apathya
Aahar-All cold and heavy food should be avoided. Oily and fried items,
bakery items, fast foods, chocolates, wafers etc. should be strictly
avoided. All dairy products especially curd, paneerand ice creams
should be strictly avoided. Intake of sesame, black gram, jaggery
should be limited.
Vihar-Exposure to cold, dust, smokes and direct wind should be strictly
avoided. Hard exercises and peak sun exposure are not advisable.
Avoid air coolers and air conditioners. Avoid cold water bath and
application of oil on head especially on symptoms of cold. Do not
suppress natural urges especially coughing, sneezing and bowel and
bladder responses. Avoid day sleeping

29. Bronchial Asthma
History
•Asthma : derived from the Greek aazein, meaning "sharp breath.“
•The word first appears in Homer's Iliad.
•In 450 BC. Hippocrates: more likely to occur in tailors, anglers, and
metalworkers.
•Six centuries later, Galen: caused by partial or complete bronchial obstruction.
•1190 AD, Moses Maimonides: wrote a treatise on asthma, describing its
prevention, diagnosis, and treatment
•17th century, Bernardino Ramazzini: connection between asthma and organic
dust.
•1901: The use of bronchodilators started.
•1960s: inflammatory component of asthma was recognized and anti-
inflammatory medications were added to the regimens.

30. Definition
A reversiblechronic inflammatory airway disease which
is characterized by bronchial hyper-responsiveness of
the airways to various stimuli, leading to widespread
bronchoconstriction, airflow limitation and
inflammation of the bronchi causing symptoms of
cough, wheeze, chest tightness and dyspnoea.

31. Epidemiology
•Asthma is a common chronic disease that is
estimated to affect as many as 339 million people
worldwide.
•Globally, asthma is ranked 16th among the leading
causes of years lived with disability and 28th among
the leading causes of burden of disease, as measured
by disability adjusted life years (DALYs).-Global
Asthma Report 2018

32. •Exact prevalence of asthma remains uncertain because of
differing ways in which airway restriction is reported
•Diagnostic uncertainty (children under 2 yrs.) ,overlaps
with chronic obstructive pulmonary disease (COPD)
•Mortality is estimated around 1400 deaths/yr
•5-12% in children with a higher occurrence in boys than
girls or parents having an allergic disorder
•30-70% of children become symptom free by adulthood

33. Prevalence of Bronchial Asthma

34. •A survey on school children in Kathmandu showed that the
prevalence of current wheeze was 8.9% (95%CI: 8.0-9.7). The
prevalence of "severe asthma" (defined as at least one of the
following: Speech limitation to 1-2 words at a time between breaths
due to wheeze last year, sleep distrbance>1 time per week in
average due to wheeze last year or >12 wheezing episodes last
year) was 7.3% (95% CI 6.5-8.1).
•The prevalence tended to be higher in the peri-urban population.
Boys had significantly higher prevalence than girls in the urban but
not in the peri-urban population. ( O Hessen, J & Schei, M & Pandey,
Mrigendra& R Smith, K. (2003). Prevalence and risk factors for
asthma in Nepal.)

35. Aetiologyand Triggers
Complex and multiple environmental and genetic determinant
a) Genetic factors
b) Allergen exposure
–house dust mite,
–household pets,
–grass pollen
c) Atmospheric polution
–sulphurdioxide, ozone, ciggeratesmoke, perfume
d) Dietary deficiency of antioxidants
–vitE and selenium may protect asthma in children(fresh fruits
and vegetables)

36. Aetiologyand Triggers
e) Occupational sensitizers
–isocyanates(from industrial coating, spray painting)
–colophony perfumes(electronic industries)
e) Drugs
–NSAIDS
–B-blocker(B1 adrenergic blocker drug such as atenolol)
f) Cold air
g) Exercise
–exercise-induced wheeze is driven by histamine and leukotrienes
which are released from mast cells when epithelial lining fluid of the
bronchi become hyperosmolar owing to drying and cooling during
exercise
h) Emotion

38. Classification
•Extrinsic –implying a definite external cause
–more frequently in atopic inviduals
–often starts in childhood -accompanied by
eczema
•Intrinsic/cryptogenic –no causative agent can be
identified
–starts in middle age

39. Extrinsic Asthma Intrinsic Asthma
•Eosinophilic
•Causative factor is allergen
•More common in children
•Dust mite, IgEantibodies, Rhinovirus
(during first 3 yrsof life)
•Triggers activate Th2 lymphocytes
and mast cells
•Effected cells are eosinophil
•Causes airway inflammation
•Airway hyperesponsiveness,
irritation, Oedema, mucous
plugging, remodeling
•Non-eosinophilic
•Causative factor is usually a Virus
•More common in Adults
•Non allergic factors, viral infection ,
irritants like epithelial damage ,
mucosal inflammation, emotional
upset, parasympathetic input
•Triggers epithelial cell damage and
Macrophages
•Effected cells are neutrophils
•Causes airway inflammation
•Airway hyperesponsiveness,
irritation, Oedema, mucous
plugging, remodeling

40. Pathophysiology
•Complex, not fully understood
•numbers of cells, mediators, nerves, and vascular leakage -activated
by exposure to allergens or several mechanism
Inflammation
•Eosinophils, T-lymphocytes, macrophages and mast cell
Remodeling
•Deposition of repair collagens and matrix protein
•Loss of ciliated columnar cells-metaplasia –increase no of secreting
goblet cells

41. Pathologic features of Asthma
a)Inflammatory cell infiltration of the airways
b)Increased thickness of the bronchial smooth muscle
c)Partial or full loss of the respiratory epithelium
d)Sub-epithelial fibrosis
e)Hypertrophy and hyperplasia of the submucosalglands
and goblet cells
f)Partial or full occlusion of the airway lumen by mucous
plugs
g)Enlarged mucous glands and blood vessels

42. h. Smooth muscle contraction
i. Thickening of airway –cellular infiltration and
inflammation
j. Excessive secrectionof mucus
Genetic factor
•Cytokine gene complex (chromosome 5)-IL-4 gene cluster
IL-3, IL-4 , IL-5 and IL-13
Environment factor
•Childhood expose irritants or childhood infection

43. Early Phase
•Inhaled Antigen
–Sensitisedmast cells on the mucosal surface -mediator release.
–Histamine -bronchoconstriction, increased vascular
permeability.
–prostaglandin D 2 -bronchoconstriction, vasodilatation.
–LeucotrieneC4,D4, E4 -Increased vascular permeability, mucus
secretion and bronchoconstriction.
–Direct subepithelialparasympathetic stimulation-
bronchoconstriction.

44. Late phase
•starts 4 to 8 hours later
•Mast cell release additional cytokine
•Influx of leukocytes(neutrophil,eosinophil)
•Eosinophilsare particularly important-exert a variety
of effect

45. Pathophysiology

49. Clinical Features
•Recurrent episodes of Wheezing
•Chest tightness
•Breathlessness
•Cough
•Diurnal pattern-symptoms seen more in early
morning
•Cough variant asthma-no wheeze

50. Diagnosing Asthma
•Reversible and variable airflow limitation-as measured by
a peak expiratory flow (PEF) meter in any of the following
ways:
–PEF increases more than 15% and 200mls 15 to 20
minsafter inhaling a short acting beta2 agonist, or
–PEF varies more than 20% from morning
measurement upon arising to measurement 12 hours
later in patients who are taking a bronchodilator, or
–PEF decreases more than 15% after 6 minsof running
or exercise

51. Investigations
Specific
•respiratory function test:
-1. peak expiratory flow
-2. spirometry
•Exercise tests
•histamine/methacholinebronchial provocation test
•trial of corticosteroids

52. Non-specific
•full blood count and differential count: increase
number of eosinophilsnumber
•arterial blood gases
•sputum test: number of eosinophils
•chest X-ray: hyperinflated

53. Spirometrytest
•It is the single best diagnostic test for patients with airflow limitation.
•SpirometryTest
measures the volume of air blown out against time
gives more specific information about lung function.
A value is calculated for the amount of air blown out in one second -
“Forced Expiratory Volume” or FEV1).
This is divided by the total amount of air blown out until all air is
expired -Forced Vital Capacity or FVC).
FEV1/FVC expressed as a percentage value
In the general population, the FEV1/ FVC ratio is usually greater than
0.75–0.80 in adults, and 0.90 in children. Any values less than these
suggest airflow limitation and support a diagnosis of asthma

54. Differential Diagnosis
•Upper airway obstruction –
Tumor, Epiglottitis, Vocal
cord dysfunction,
Obstructive sleep apnea
•Bronchomalacia
•Endobronchiallesion
•Foreign body aspiration
•Congestive heart failure
•Gastroesophagealreflux
•Sinusitis
•Adverse drug reaction –
Aspirin –Beta-adrenergic
antagonist –ACE inhibitors
–Inhaled pentamidine
•Allergic bronchopulmonary
aspergillosis
•Hyperventilation with panic
attacks
•Acute Exacerbation of COPD

55. Management
Aims of management of Chronic Asthma
–to recognize asthma
–to abolish symptoms
–to restore normal or best possible long term
airway function
–to reduce morbidity and prevent mortality

56. Approach of chronic asthma
•Education of patient and family
•Avoidance of precipitating factors
•Use of the lowest effective dose of convenient
medications minimizing short and long term side
effects.
•Assessment of severity and response to treatment.

57. 1) Education of patient and family
a.Nature of asthma
b.Preventive
measures/avoidance of
triggers
c.Drugs used and their side
effects
d.Proper use of inhaled drugs
e.Proper use of peak flow meter
f.Knowledge of the difference
between relieving and
preventive medications
g.Recognition of features of
worsening asthma
•increase in bronchodilator
requirement
•development of nocturnal
symptoms
•reducing peak flow rates.
h.Self management plan for
selected, motivated patients
or parents.
i.The danger of non prescribed
self medication including
certain traditional medicines.

58. 2) Avoidance of precipitating factor
The following factors may
precipitate asthmatic attacks:
•Beta blockers-contraindicated
in all asthmatics
•Aspirin and nonsteroidalanti
inflammatory drugs-if known
to precipitate asthma, these
drugs should be avoided.
•Allergens e.g. house dust mites,
domestic pets, pollen should
be avoided whenever possible.
•Occupation-should be
considered as a possible
precipitating factor
•Smoking -active or passive.
•Day to day triggers-such as
exercise and cold air. It is
preferable to adjust treatment
if avoidance imposes
inappropriate restrictions on
lifestyle.
•Atmospheric pollution.
•Food-if known to trigger
asthma, should be avoided.

59. 3) Medication
Controllers Relievers
medications taken daily on a long-
term basis that achieve control
primarily through anti-
inflammatory effects
Eg-ICSs, leukotriene receptor
antagonists (LTRAs), LABAs in
combination with an ICS, long-
acting muscarinic receptor
antagonists (LAMAs), and biologic
agents including anti-IgEtherapy
and anti-IL-5 therapy
medications used on an as-needed
basis for quick relief of
bronchoconstriction and symptoms
Eg-rapid acting inhaled beta2-
agonists and inhaled
anticholinergics

60. Bronchodilators
•βSympathomimentics(β2 Agonist)-Salbutamol, Terbutaline,
Bambuterol, Salmeterol, Formeterol, Ephedrine
•Methylxanthines-Theophylline, Aminophylline, Choline
theophyllinate, Hydroxyethyltheophyllinate, Doxaphylline
•Anticholinergics( Muscaranicreceptor antagonist)-
Ipratropium bromide, Tiotropiumbromide
LeukotrineAntagonists-Montelukast, Zafirlukast
Mast cell stabilizers-Sodium Cromoglycate, Kitotifen
Coticosteriods-Systemic-Hydrocortisine, Prednisolone
Inhalational-Beclomethasonedipropionate, Budesonide,
Fluticasone etc
Anti-IgEantibody-Omalizumab

64. Approach To Drug Therapy
"Stepwise Approach" [step 1]
•Start at the step most appropriate to severity, moving up if
needed or down if control is good for > 3 months.
•Rescued courses of prednisolone may be needed
STEP 1 MILD EPISODIC ASTHMA
• Infrequent symptoms
• No nocturnal symptoms
• PEF 80-100% predicted
Treatment:
–inhaled beta2 agonist "as needed" for symptom relief.
–If needed more than once a day, advance to Step 2

65. STEP 2
MODERATE ASTHMA
• Frequent symptoms
• Nocturnal symptoms present
• PEF 60-80% predicted
Treatment
• inhaled steroids, e.g. beclomethasoneor budesonide 200-800
mcg/day
• inhaled sodium cromoglycateplus
• inhaled beta2 agonist "as needed"

66. •STEP 3
SEVERE CHRONIC ASTHMA
• Persistent symptoms
• Frequent nocturnal symptoms
• PEF 60% predicted or less
Treatment:
• inhaled beclomethasoneor budesonide 800-2000 mcg/day plus
• inhaled beta2 agonist as needed plus, if necessary
• oral beta2 agonist preferably long acting, or
• inhaled long acting beta2 agonist, or
• inhaled ipratropium bromide 40 mcg 3-4 times a day, or
• oral theophylline (sustained release), or
• nebulisedbeta2 agonist, 2-4 times a day

67. STEP 4
VERY SEVERE ASTHMA
• Persistent symptoms not controlled by step 3
medications
Treatment:
• as in step 3, plus oral steroids (the lowest dose
possible)

68. STEP DOWN THERAPY
• Patients should be reviewed regularly.
• When the patient’s condition has been stable for
3-6 months, drug therapy may be stepped down
gradually.
• The monitoring of symptoms and peak flow rate
should be continued during drug reduction.