Bronchial asthma is a chronic inflammatory airway disease characterized by recurrent episodes of wheezing, coughing, chest tightness, and shortness of breath. The prevalence of asthma is increasing worldwide and rates are highest in Gulf countries like Saudi Arabia, Qatar, and Kuwait. Treatment involves bronchodilators, anti-inflammatories, leukotriene antagonists, and mast cell stabilizers to prevent bronchoconstriction, suppress inflammation, and antagonize mediators.

1. Bronchial Asthma
Dr. Nooreldin Mohamed Elkosh
PGY1 Family Medicine Residency
Program, Hamad Medical Corporation

2. DEFENITION
• Asthma is a common chronic inflammatory
disease of the airways characterized by
recurent and reversible episodes of airflow
obstruction and bronchospasm.
• Common symptoms include wheezing,
coughing, chest tightness, and shortness of
breath.

3. EPIDEMIOLOGY
• As of 2004, it was estimated that as many as
300 million people of all ages suffer from
asthma. By 2025, it is expected that this
number will rise to 400 million worldwide.
• The rate of asthma increases as communities
adopt western lifestyles .

4. • The increase in the prevalence of asthma has
been associated with an increase in atopic
sensitization and other allergic disorders such
as eczema and rhinitis
• It is estimated that asthma accounts for about
1 in every 250 deaths worldwide. Many of
these could be prevented with optimal access
to medical care

5. • Asthma in the Gulf countries:
Saudi Arabia took the lead, with a rate of 24%
of the population suffering.
 Qatar and Kuwait came next, with a rate of
19.8% and 16.8% respectively, followed by
13% in the United Arab Emirates
Oman had the lowest prevalence among the
Gulf Cooperation

6. • Prevalence of asthma among Qatari
schoolchildren aged 6-14 years according to
International Study of Asthma and Allergies in
Childhood, Qatar:
A cross-sectional study of 3,283 school children
living in both urban and rural areas was
conducted between February 2003-February
2004:

7. • The population sample had a high prevalence
of diagnosed asthma (19.8%), allergic rhinitis
(30.5%), eczema (22.5%), and chest infection
(11.9%).
• The frequency of asthma, allergic rhinitis, and
eczema among parents reflected the same
pattern as seen in their children

8. • Overall, males had more asthma, allergic
rhinitis, and chest infections than females
• In general, the prevalence rate of asthma and
allergic rhinitis decreased with age

9. • Genetic factors related to the high rates of
consanguinity may play an important role in
the high prevalence rates noted in the Qatari
population, but changes in lifestyle and
environmental factors cannot be discounted
as possible causes of the high prevalence
noted in this study.

10. The Impact of Asthma and Allergic Diseases
on Schoolchildren: Are they at Increased
Risk of Absenteeism and Poor
School Performance?
Dept. of Epidemiology and Medical Statistics, Hamad
Medical Corporation
Dept. of Public Health, Weill Cornell Medical College
State of Qatar

11. • Asthma is the most common chronic illness
among school children and an important
cause of school absenteeism and reduced
participation in sports and other activities
• Asthma is the principal cause of school
absences due to chronic disease in childhood
accounting for 20% of school days lost among
elementary and high school students

13. RISK FACTORS
• GENDER —
 There are clear-cut gender differences in the
prevalence of asthma. Childhood asthma
tends to be a predominantly male disease,
with the relative male predominance being
maximal at puberty.
After age 20, the prevalence remains
approximately equal until age 40, when the
disease becomes more common in females.

14. • Airway hyperreactivity —
Abnormal and exaggerated airway
responsiveness to noxious stimuli is a central
feature in the pathophysiology of asthma, and
all patients with asthma have airway
hyperresponsiveness

15. • FAMILIAL HISTORY OF ASTHMA —

16. • ATOPY AND ALLERGENS —
 Atopy may be defined as the state of having IgE antibodies
to specific allergens, which is a prerequisite for developing
allergic disease.
 The association between asthma and other atopic
conditions is well-documented.
 The "atopic march" is a term used to describe the pattern
of onset of different allergic diseases that is observed in
some atopic individuals.
 This pattern begins with atopic dermatitis in infancy and
childhood, followed by the onset of allergic rhinitis and
then asthma during later childhood and adolescence.

17. • Allergen exposure —
Sources of indoor allergens include:
house dust mites, animal proteins (particularly
cat and dog allergens), cockroaches, and fungi
• RHINITIS —
Adults with rhinitis are at greater risk than
those without rhinitis for developing adult-
onset asthma

18. • OCCUPATIONAL EXPOSURES —
 The European Community Respiratory Health
Surveys (ECRHS and ECRHS-II) identified several
occupations that are associated with an
increased risk of new onset asthma; nursing and
cleaning were responsible for the most cases
.Inhalational accidents (eg, fires, mixing cleaning
agents, industrial spills) were also associated with
an increased risk of new onset asthma.

19. In the Agricultural Health Study of 25,814
adult farm women, growing up on a farm was
protective against asthma, but use of certain
pesticides (eg, organophosphates) was
associated with an increased risk of adult-
onset atopic asthma

20. • Outdoor pollution — There is a known
correlation between levels of air pollution and
lung disease, but the association between air
pollution and asthma is less clear
• Indoor pollution— Gas stoves are the primary
source of indoor NO2 which is responsible for
increasing wheeze ,shortness of breath and
chest tightness

21. • RESPIRATORY INFECTIONS —
Viral and bacterial respiratory infections are
well-known triggers that can cause
exacerbations in children and adults with
asthma
There are no conclusive epidemiologic data
linking infections to causation of asthma in
previously normal adults

22. • SMOKING AND EXPOSURE TO
ENVIRONMENTAL TOBACCO SMOKE —
1- Active smoking — Several studies have
demonstrated that active smoking increases
the risk for developing asthma
Secondhand smoke — There is a growing
evidence that secondhand smoke exposure is
associated with the development of asthma in
early life

23. • Maternal smoking is the most important cause
of secondhand smoke exposure, because of
the greater exposure of the child to the
mother than the father

24. • OBESITY —
There is a linear relationship between BMI and
the risk of developing asthma
• EARLY MENARCHE —
asthma symptoms and bronchial hyperreactivity
are more common among adult women with
menarche before the age of 11 years
compared with menarche at age 13 or later
based on a large multinational study

25. • MEDICATION USE —
 Epidemiologic studies have found
associations between the development of
asthma and both the regular use of
acetaminophen and exposure to antibiotics
during infancy.
However, these studies have inadequately
accounted for confounding bias. Both of these
associations warrant further study.

26. • Asprin induced asthma (Samter's triad ):
is a medical condition consisting of asthma,
aspirin and NSAID sensitivity, and
nasal/ethmoidal polyposis.

27. • Mode of delivery —
Delivery by Cesarean section may increase the
risk of childhood asthma compared with
vaginal delivery
• Exercise, Cold exposure, Excessive laughing

29. PATHOGENESIS
• 1- Allergic Asthma (Extrensic Asthma )
• 2-Non allergic Asthma (Intrensic Astma )

30. EXTRENSIC ASTHMA

32. • Allergic (Extrinsic) Asthma :
 Bronchoconstriction
 Airway edema
Airway hyperresponsiveness
Airway remodeling

33. • Non allergic (Intrinsic) Asthma:
 triggered by factors not related to allergies
 Many of the symptoms of allergic and non-allergic
asthma are the same (coughing, wheezing, shortness of
breath or rapid breathing, and chest tightness), but non-
allergic asthma is triggered by other factors such as
anxiety, stress, exercise, cold air, dry air,
hyperventilation, smoke, viruses or other irritants
 the immune system is not involved in the reaction.

36. THANK YOU

37. Drugs used in Bronchial Asthma
Dr. Sherif Adel Saleh, PGY-1
Family Medicine Residency Program,
Hamad Medical Corporation

38. Pathophysiology
of asthma

39. Classification
• Bronchodilators
– β Sympathomimetics: Salbutamol, Terbutaline, Bambuterol,
Salmeterol, Formoterol, Ephedrine.
– Methylxanthines: Theophylline (anhydrous), Aminophylline, Choline
theophyllinate, Hydroxyethyl theophylline, Theophylline ethanolate of
piperazine, Doxophylline.
– Anticholinergics (muscarnic receptor antagonist): Ipratropium
bromide, Tiotropium bromide.

40. Classification
• Leukotriene antagonists: Montelukast, Zafirlukast.
• Mast cell stabilizers: Sodium cromoglycate, Ketotifen.
• Corticosteroids
– Systemic: Hydrocortisone, Prednisolone and others.
– Inhalational: Beclomethasone dipropionate, Budesonide, Fluticasone
propionate, Flunisolide, Ciclesonide.
• Anti-lgE antibody: Omalizumab

41. Bronchial Asthma: Treatment approaches
• Prevention of antigen antibody reaction: Avoidance of antigen,
hyposensitization
• Neutralization of IgE: Omalizumab
• Suppression of inflammation and bronchial hyper reactivity:
Cotricosteroids
• Prevention of release of mediators: Mast cell stabilizers
• Antagonism of released mediators: Leukotriene antagonists,
antihistamines, platelet aggravating factor (PAF) antagonist
• Blockade of constrictor neurotransmitter: Sympathomimetics
• Directly acting bronchodilators: Methylxanthines

42. Bronchodilators
Stimulates
β2-adrenergic
receptors of bronchi
β2-agonists
Anticholinergic
drugs
Smooth
muscle
relaxation
reduce tonus
of vagus
Methylxanthines
inhibit phosphodiesterase
β2-agonists: treatment of
acute asthmatic attacks
Muscarinic antagonist: Less
useful in asthma, may be
given in refractory cases
Methylxanthines: Long-term/
prevent bronchoconstriction
β2-agonists: treatment of
acute asthmatic attacks
Muscarinic antagonist: Less
useful in asthma, may be
given in refractory cases
Methylxanthines: Long-term/
prevent bronchoconstriction

43. Sympathomimetics
• The selective β2 agonist is the primary bronchodilators used in
acute asthmatic attacks.
• β2 adrenergic receptor agonists increase the cAMP concentration
in smooth muscles causing bronchodilatation.
• Types:
– Long-acting β2 adrenergic receptor agonists (Salmeterol; formoterol)
– Short-acting β2 adrenergic receptor agonists (salbutamol, levalbuterol,
metaproterenol, terbutaline, and pirbuterol )

44. Sympathomimetics
• Salbutamol:
– Selective β2 agonists with less cardiac side effects
– Inhaled salbutamol produce bronchodililation within 5-min and the action lasts
for 2-4 h.
– Used for acute asthmatic attack. Not suitable for prophylaxis
– Side effect: Palpitation, restlessness, nervousness, throat irritation and ankle
edema.
– Metabolism: metabolized in gut; oral bioavailability is 50%.
– Duration of action: oral salbutamol acts 4-6 h.
– Dose: 2-4 mg/ oral; 0.25- 0.5 mg/ i,.p., or s.c.,; 100-200 μg/ inhalation
• Terbutaline:
– Similar to salbutamol; regular use dose not reduce bronchial hyper-reactivity
– Dose: 5 mg/ oral; 0.25 mg/ i,.p., or s.c.,; 250 μg/ inhalation
Cont.,

45. Sympathomimetics
• Bambuterol:
– prodrug of terbutaline
– Slowly hydrolyzed in plasma and lung by pseudocholinesterase to release the
active drug over 24 h. It also reversely inhibits pseudocholinesterase in a dose
dependent manner.
– Used in chronic bronchial asthma in a singe evening dose of 10-20 mg/ oral.
• Salmeterol:
– First long acting selective β2 agonists with slow onset of action
– Twice daily for maintain the therapy/ nocturnal asthma, but not for acute asthma
– Concurrent use of inhaled glucocorticoid with salmeterol is advised for patient
with persistent asthma.
– COPD: equivalent to inhaled anticholinergics in COPD. Reduce breathlessness by
abolishing the reversible component of airway obstruction.
• Formoterol:
– Long acting selective β2 agonists which acts 12 h when inhaled.
– Compare to salmeterol it has a faster onset of action (with in 10 min)
Cont.,

46. Methylxanthines
• Caffeine (from coffee) , theophylline (from tea) and theobromine
(from cocoa) are naturally occurring xanthine alkaloids which have
qualitatively similar actions.
• Mechanism of action:
– Methylxanthines inhibits cyclic nucleotide phosphodiesterase (PDEs),
thereby lead to an accumulation of intracellular cAMP and cGMP
causing bronchodilation.

47. Methylxanthines
• Mechanism of action:
BronchodilationBronchodilation
Bronchial tone
Muscarinic antagonistMuscarinic antagonist
Acetylcholine
Adenosine
Theophylline
cAMP
ATP
AMP
Adenylyl cyclaseAdenylyl cyclase
Phosphodiesterase (PDE)Phosphodiesterase (PDE)
TheophyllineTheophylline
Beta agonistBeta agonist

48. Pharmacological actions
of Methyl xanthines
CNS
Stimulation
Increase motor activity
Improve the performance
CVS
Stimulate the heart
Increase the force of contraction
High dose: cardiac arrhythmias
BP: effect is variable
Stimulation of
Vegas stimulation: ↓ BP
Vasomotor center : ↑ BP
Smooth muscle
Relaxation
Lungs vital capacity- increased
Biliary spasm: relieved
Kidney
Mild diuretics (Inhibiting reabsorption of Na+
& H2O)
Increase the renal blood flow
Increase the g.f.r.
Mast cell
Inhibit the release of histamine
Stomach
Enhance the secretion of acid, Pepsin
Metabolism
Increase BMR
It has variable physiological actions

49. Methylxanthines- Theophylline Cont.,
• Adverse effects:
– Narrow margin safety,
– Multiple drug interactions (Erythromycin, ciprofloxacin, cimetidine, oral
contraceptives, allopurinol, phenytoin, rifampicin, phenobarbital)
– CVS and CNS stimulant; ADRs not dependent to dose; GIT distress
– Children are more liable to developed CNS toxicity
– Rapid IV injection cause- precordial pain, syncope and sudden death

50. Anticholinergics
Ipratropium (derivative of atropine)
• Parasympathetic activation causes bronchoconstriction and increases mucus
secretion.
• Blocking the action of ACh by anticholinergic drugs produce bronchodilation
and also reduce the volume of respiratory secretion.
• Less effective bronchodilator than sympathomimetic.
• ADR: Dry mouth, respiratory tract discomfort

51. Leukotriene antagonists
Montelukast, Zafirlukast
• Block the cys-leukotrienes C4, D4 and E4 (LTC4, LTD4, LTE4)
• Alternative for inhaled glucocorticoids
• Prophylactic therapy for mild, moderate asthma; not used for
terminating asthma.
• Both are very safe drugs and ADRs are few (headache, rashes);
eosinophilia and neuropathy are infrequent. Few cases Churg-Strauss
syndrome (vasculitis with eosinophilia) have been reported.
• Dose: Montelukast 10 mg OD, Zafirlukast 20 mg BD

52. Leukotriene antagonists
• Mechanism of action of leukotriene antagonist, antiinflammatory drugs
Cont.,
Bronchoconstriction,
Inflammation,
increased mucus
Bronchoconstriction,
Inflammation,
increased mucus
Bronchoconstriction,
Inflammation, Pain
Bronchoconstriction,
Inflammation, Pain
Block by steroidal
antiinflammatory
drugs
Block by steroidal
antiinflammatory
drugs
Block by nonsteroidal
antiinflammatory
drugs
Block by nonsteroidal
antiinflammatory
drugs
Block by
Leukotriene
antagonists
Block by
Leukotriene
antagonists

53. Corticosteroids
• Corticosteroids are not bronchodilators; benefit by reducing
bronchial hyperreactivity/mucosal edema and by suppressing
inflammation.
• Inhaled glucocorticoids are partially absorbed and because of their
systemic AEs systemic glucocorticoids are usually reserved for
patients with severe refractory asthma.
• Systemic steroid therapy
– Severe chronic asthma: Not contorted by bronchodilator and inhaled steroids.
– Status asthmaticus/ acute asthma exacerbation

54. Mast cell stabilizers
Sodium cromoglycate, Ketotifen
• Inhibits degranulation of mast cell by trigger stimuli by blocking
calcium channels
• Once degranulation has occurred, mast cell stabilizers are ineffective
(in the acute setting)
• Long time therapy reduce cellular inflammatory response.
• Pharmacokinetic:
– Not absorbed orally. It is administered as an aerosol through metered dose
inhaler delivering 1 mg per dose; 2 puffs 4 times a day
– Not popular- production of cough and bronchospasm because of particulate
nature of the inhalation.
– Small fraction of the inhaled drug is absorbed systemically and excreted
unchanged form in urine and bile.

55. Mast cell stabilizers
• Use:
– Bronchial asthma: Sodium. Cromoglycate is used as a long term prophylactic in
patients not adequately controlled by inhaled bronchodilators. Alternative for
inhaled steroids in mild to moderate asthma but not severe cases.
– Allergic rhinitis: Cromoglycate is not nasal decongestant, regular prophylactic
use as a nasal spray produces symptomatic improvement in many patients.
– Allergic conjunctivitis: Regular use as eye drops is benificial in some chronic
cases
Cont.,
Adverse effect (cromoglycate):
Bronchospasm
Throat irritation
Cough, headache
Arthralgia, rashes and dysuria
Rarely nasal congestion
Adverse effect (Ketotifen):
Generally well tolerated
Sedation and dry mouth
Dizziness, nausea and weight gain

56. Anti-lgE antibody: Omalizumab (Xolair)
• recombinant DNA-derived monoclonal antibody
• Selectively binds to human immunoglobulin E (IgE) and decrease binding
affinity of IgE to the high-affinity IgE receptor on the surface of mast cells
and basophils, reduce allergic response.
• Omalizumab may be particularly useful for treatment of moderate to severe
allergic asthma in patients who are poorly controlled with conventional
therapy.
• Due to the high cost of the drug, limitations on dosage, and limited clinical
trial data, it is not currently used as firstline therapy.

58. Acute Management ofAcute Management of
AsthmaAsthma
Dr. Mohamed Suliman Abdelhamid,Dr. Mohamed Suliman Abdelhamid,
PGY-1PGY-1
Family Medicine Residency Program,Family Medicine Residency Program,
Hamad Medical CorporationHamad Medical Corporation

59. Status AsthmaticusStatus Asthmaticus
TreatmentTreatment
– AlbuterolAlbuterol
– AtroventAtrovent
– SteroidSteroid
– TerbutalineTerbutaline
– EpinephrineEpinephrine
– HelioxHeliox
– BIPAPBIPAP
– IntubationIntubation
– KetamineKetamine
– Inhalational anestheticsInhalational anesthetics

60. Status AsthmaticusStatus Asthmaticus
Severe bronchospasm that does not respond toSevere bronchospasm that does not respond to
aggressive therapies within 30-60 minutesaggressive therapies within 30-60 minutes
Severe asthmatic attack with one or more of theSevere asthmatic attack with one or more of the
following:following:
– Dyspnea (precluding speech), accessory muscle use,Dyspnea (precluding speech), accessory muscle use,
RR 35/minRR 35/min
– Hr > 140/minHr > 140/min
– Peak expiratory flow < 100 l/minPeak expiratory flow < 100 l/min
– Hypercapnea ( >= 50 mmHg)Hypercapnea ( >= 50 mmHg)

61. Acute Severe AsthmaAcute Severe Asthma
Critical limitation of expiratory flowCritical limitation of expiratory flow
Increased airway resistanceIncreased airway resistance
Premature airway closurePremature airway closure
Lung and chest wall dynamicLung and chest wall dynamic
hyperinflationhyperinflation
High intrinsic PEEPHigh intrinsic PEEP
Respiratory muscle fatigueRespiratory muscle fatigue

62. Near-Fatal AsthmaNear-Fatal Asthma
Respiratory arrest or respiratory failureRespiratory arrest or respiratory failure
(PCO2 > 50 mmHg)(PCO2 > 50 mmHg)

63. Fatal AsthmaFatal Asthma
Slow-onsetSlow-onset
– Gradual deterioration of asthma symptoms overGradual deterioration of asthma symptoms over
several daysseveral days
– Usually associated with chronic poorly controlledUsually associated with chronic poorly controlled
asthmaasthma
– EosinophilicEosinophilic predominance and mucus inpredominance and mucus in
submucosasubmucosa
Rapid-onsetRapid-onset
– Symptom onset and progression to life-threateningSymptom onset and progression to life-threatening
status within 3 hoursstatus within 3 hours
– ““Greater” hypercapneaGreater” hypercapnea
– NeutrophilicNeutrophilic predominance in airway submucosapredominance in airway submucosa

64. The Four CompartmentsThe Four Compartmentso
o

65. Respiratory MechanicsRespiratory Mechanics
The lung is not homogenous during acuteThe lung is not homogenous during acute
severe asthmasevere asthma
Driving force for expiratory flow isDriving force for expiratory flow is
decreaseddecreased
Persistent activation of inspiratoryPersistent activation of inspiratory
muscles during expirationmuscles during expiration------
– Abnormal low pulmonary elastic recoilAbnormal low pulmonary elastic recoil
– High outward recoil of chest wallHigh outward recoil of chest wall
Resistance to airflow strongly increasedResistance to airflow strongly increased

66. Respiratory MechanicsRespiratory Mechanics
Markedly prolonged expirationMarkedly prolonged expiration
Inspiration starts before static equilibriumInspiration starts before static equilibrium
is reachedis reached
Positive End-Expiratory alveolarPositive End-Expiratory alveolar
PressurePressure
– Auto-PEEP (intrinsic PEEP, PEEPi)Auto-PEEP (intrinsic PEEP, PEEPi)

67. Dynamic HyperinflationDynamic Hyperinflation
Incomplete alveolar emptying atIncomplete alveolar emptying at
the end of expirationthe end of expiration
– Intrinsic PEEPIntrinsic PEEP
Measure end-expiratory flow orMeasure end-expiratory flow or
End-expiratory pressureEnd-expiratory pressure
Increased ventilatory requirementIncreased ventilatory requirement
Prolonged expiratory timeProlonged expiratory time
Increased inspiratory threshold loadIncreased inspiratory threshold load

68. Dynamic HyperinflationDynamic Hyperinflation
Shortening of:Shortening of:
– DiaphragmDiaphragm
– Inspiratory intercostalsInspiratory intercostals
– Accessory musclesAccessory muscles
Decreased mechanical efficiencyDecreased mechanical efficiency
– Increased risk of fatigueIncreased risk of fatigue
With increased obstruction:With increased obstruction:
– CO2 production > Elimination by alveolar ventilationCO2 production > Elimination by alveolar ventilation
CO2 increasesCO2 increases

69. Dynamic HyperinflationDynamic Hyperinflation
Mean pleural pressure becomes moreMean pleural pressure becomes more
negativenegative
– Interstitial pressures are also loweredInterstitial pressures are also lowered
– Vascular pressure is maintainedVascular pressure is maintained
The result:The result:
– Interstitial edema and further increase inInterstitial edema and further increase in
airway resistanceairway resistance

70. Asthmatic PatientsAsthmatic Patients
Who do we worry about?Who do we worry about?
– Previously intubatedPreviously intubated
– Noncompliant or poorly controlledNoncompliant or poorly controlled
– Psychosocial or emotional problemsPsychosocial or emotional problems
– Frequent flyersFrequent flyers
– Environmental triggersEnvironmental triggers

71. What do we look for on exam?What do we look for on exam?
Severe respiratory distressSevere respiratory distress
Accessory muscle useAccessory muscle use
May be hypoxemicMay be hypoxemic
TachypneicTachypneic
TachycardicTachycardic
DiaphoreticDiaphoretic
AnxiousAnxious
1-2 word dyspnea1-2 word dyspnea

72. What do we do?What do we do?
Rapid assessmentRapid assessment
Manage the airwayManage the airway
Aggressive treatmentAggressive treatment
Respiratory therapist at bedsideRespiratory therapist at bedside
Have all the needed equipment at the bedsideHave all the needed equipment at the bedside
– Intubation…Intubation…
Team approachTeam approach
2 IVs2 IVs

73. TreatmentTreatment
Albuterol nebAlbuterol neb
Atrovent nebAtrovent neb
Methylprednisolone 125 mg IVMethylprednisolone 125 mg IV
TerbutalineTerbutaline
– 0.25 mg SQ q20 minutes x 3 doses0.25 mg SQ q20 minutes x 3 doses
EpinephrineEpinephrine
– 1:1000, 0.3 mg SQ or IM q20 minutes x 31:1000, 0.3 mg SQ or IM q20 minutes x 3
dosesdoses
Magnesium sulfateMagnesium sulfate

74. MgSO4MgSO4
Possible inhibition of calcium influx intoPossible inhibition of calcium influx into
airway smooth muscleairway smooth muscle
Inhibits cholinergic neuromuscularInhibits cholinergic neuromuscular
transmissiontransmission
Stabilization of mast cells and TStabilization of mast cells and T
lymphocyteslymphocytes
Stimulation of nitric oxide and prostacyclinStimulation of nitric oxide and prostacyclin

75. PregnancyPregnancy
EpinephrineEpinephrine
– Concern re: alpha effect and vasoconstriction inConcern re: alpha effect and vasoconstriction in
uteroplacental circulationuteroplacental circulation
– Avoid during pregnancy except in anaphylaxisAvoid during pregnancy except in anaphylaxis
TerbutalineTerbutaline
– Preterm laborPreterm labor
High dose steroids in animal studies:High dose steroids in animal studies:
– ??? cleft palate??? cleft palate
Palatal closure usually by 12Palatal closure usually by 12thth
weekweek
Albuterol, Atrovent safeAlbuterol, Atrovent safe

76. PedsPeds
Acute severe asthmaAcute severe asthma
AlbuterolAlbuterol
– 0.15mg/kg/hr0.15mg/kg/hr
Albuterol continuous:Albuterol continuous:
– 20 mg/hr if > 20 kg20 mg/hr if > 20 kg
AtroventAtrovent
– 0.5 mg/dose if > 20 kg or > 6y.o.0.5 mg/dose if > 20 kg or > 6y.o.
MgSO4MgSO4
– 25-75 mg/kg IV25-75 mg/kg IV
TerbutalineTerbutaline
– 10 mcg/kg IV over 10 minutes10 mcg/kg IV over 10 minutes
– Infusion of 0.1-10 mcg/kg/minInfusion of 0.1-10 mcg/kg/min

77. HelioxHeliox
Usually 70% Helium: 30% oxygenUsually 70% Helium: 30% oxygen
– Inert gasInert gas
– 3X reduction in density compared to air3X reduction in density compared to air
Reduces resistance in airways with nonlaminar flowReduces resistance in airways with nonlaminar flow
– Upper and ProximalUpper and Proximal
Reduces respiratory muscle workReduces respiratory muscle work
May improve gas exchangeMay improve gas exchange
May increase the mass ofalbuterol deliveredMay increase the mass ofalbuterol delivered
– Allows smaller particles to better penetrate the lung peripheryAllows smaller particles to better penetrate the lung periphery
May use with:May use with:
– Face maskFace mask
– BIPAPBIPAP
– Mechanical ventilationMechanical ventilation

78. CPAPCPAP
Seems to increase Functional residualSeems to increase Functional residual
capacity and lung compliancecapacity and lung compliance
May decrease fatigue of respiratoryMay decrease fatigue of respiratory
musclesmuscles
Decreases the adverse hemodynamicDecreases the adverse hemodynamic
effects of large negative inspiratory swingseffects of large negative inspiratory swings
in pleural pressure which compromise RVin pleural pressure which compromise RV
and LV performanceand LV performance

79. BIPAPBIPAP
Provides CPAPProvides CPAP
Delivers higher pressure in inspirationDelivers higher pressure in inspiration
than expirationthan expiration

80. When to IntubateWhen to Intubate
When do you intubate an asthmaticWhen do you intubate an asthmatic
patient?patient?
Persistent hypercarbiaPersistent hypercarbia
Hemodynamic instabilityHemodynamic instability
Inability to tolerate the face mask, BIPAP..Inability to tolerate the face mask, BIPAP..
ExhaustionExhaustion
Altered mental status….Altered mental status….

81. SummarySummary
Look for the “sick” asthmaticsLook for the “sick” asthmatics
Be aggressive in their treatmentBe aggressive in their treatment
Do not forget aboutDo not forget about
– Terbutaline ( SQ)Terbutaline ( SQ)
– Epi ( SQ or IM)Epi ( SQ or IM)
If they are young and “fighting”, consider:If they are young and “fighting”, consider:
– BIPAPBIPAP
– HelioxHeliox
– IV EpinephrineIV Epinephrine
Intubate if the patient is:Intubate if the patient is:
– FatiguedFatigued
– Unable to cooperate with interventionsUnable to cooperate with interventions

82. Thank YouThank You

83. Dr. Mostafa Hamdy Rashed, PGY-1
Family Medicine Residency Program,
Hamad Medical Corporation

84. Levels of Asthma
Control
Characteristic
Controlled
(All of the following)
Partly controlled
(Any present in any week)
Uncontrolled
Daytime symptoms
None (2 or less /
week)
More than
twice / week
3 or more
features of
partly
controlled
asthma
present in
any week
Limitations of
activities
None Any
Nocturnal
symptoms /
awakening
None Any
Need for rescue /
“reliever” treatment
None (2 or less /
week)
More than
twice / week
Lung function
(PEF or FEV1) Normal
< 80% predicted or
personal best (if
known) on any day
Exacerbation None One or more / year 1 in any week

85. Goals of Long-term Management
 Achieve and maintain control of symptoms
 Maintain normal activity levels, including
exercise
 Maintain pulmonary function as close to
normal levels as possible
 Prevent asthma exacerbations
 Avoid adverse effects from asthma
medications
 Prevent asthma mortality

86. 1. Develop Patient/Doctor Partnership
2. Identify and Reduce Exposure to Risk Factors
3. Assess, Treat and Monitor Asthma
4. Manage Asthma Exacerbations
5. Special Considerations
Asthma Management and PreventionAsthma Management and Prevention
Program: Five ComponentsProgram: Five Components

87. Asthma Management and
Prevention Program
 Asthma can be effectively controlled in
most patients by intervening to suppress
and reverse inflammation as well as
treating bronchoconstriction and related
symptoms
 Early intervention to stop exposure to the
risk factors that sensitized the airway
may help improve the control of asthma
and reduce medication needs.
.

88. Asthma Management and
Prevention Program
 Although there is no cure for asthma,
appropriate management that includes
a partnership between the physician
and the patient/family most often
results in the achievement of control

89.  Clear communication between health care
professionals and asthma patients is key to
enhancing compliance
Component 1: Develop
Patient/Doctor Partnership

90. Component 1: Develop
Patient/Doctor Partnership
 Educate continually
 Include the family
 Provide information about asthma
 Provide training on self-management skills
 Emphasize a partnership among health
care providers, the patient, and the patient’s
family

91. Component 1: Develop
Patient/Doctor Partnership
Key factors to facilitate communication:
 Friendly demeanor
 Interactive dialogue
 Encouragement and praise
 Provide appropriate information
 Feedback and review

92. Example Of Contents Of An Action Plan To Maintain Asthma Control
Your Regular Treatment:
1. Each day take ___________________________
2. Before exercise, take _____________________
WHEN TO INCREASE TREATMENT
Assess your level of Asthma Control
In the past week have you had:
Daytime asthma symptoms more than 2 times ? No Yes
Activity or exercise limited by asthma? No Yes
Waking at night because of asthma? No Yes
The need to use your [rescue medication] more than 2 times? No Yes
If you are monitoring peak flow, peak flow less than________? No Yes
If you answered YES to three or more of these questions, your asthma is uncontrolled and
you may need to step up your treatment.
HOW TO INCREASE TREATMENT
STEP-UP your treatment as follows and assess improvement every day:
____________________________________________ [Write in next treatment step here]
Maintain this treatment for _____________ days [specify number]
WHEN TO CALL THE DOCTOR/CLINIC.
Call your doctor/clinic: _______________ [provide phone numbers]
If you don’t respond in _________ days [specify number]
______________________________ [optional lines for additional instruction]
EMERGENCY/SEVERE LOSS OF CONTROL
If you have severe shortness of breath, and can only speak in short sentences,
If you are having a severe attack of asthma and are frightened,
If you need your reliever medication more than every 4 hours and are not improving.
1. Take 2 to 4 puffs ___________ [reliever medication]
2. Take ____mg of ____________ [oral glucocorticosteroid]
3. Seek medical help: Go to _____________________; Address___________________
Phone: _______________________
4. Continue to use your _________[reliever medication] until you are able to get medical
help.

93. Factors Involved in Non-Adherence
Medication Usage
 Difficulties associated
with inhalers
 Complicated regimens
 Fears about, or actual
side effects
 Cost
 Distance to pharmacies
Non-Medication Factors
 Misunderstanding/lack of
information
 Fears about side-effects
 Inappropriate expectations
 Underestimation of severity
 Attitudes toward ill health
 Cultural factors
 Poor communication

94. Component 2: Identify and Reduce
Exposure to Risk Factors
 Measures to prevent the development of asthma,
and asthma exacerbations by avoiding or reducing
exposure to risk factors should be implemented
wherever possible.
 Asthma exacerbations may be caused by a variety
of risk factors – allergens, viral infections,
pollutants and drugs.
 Reducing exposure to some categories of risk
factors improves the control of asthma and
reduces medications needs.

95.  Reduce exposure to indoor allergens
 Avoid tobacco smoke
 Avoid vehicle emission
 Identify irritants in the workplace
 Explore role of infections on asthma
development, especially in children and
young infants
Component 2: Identify and Reduce
Exposure to Risk Factors

96. Influenza Vaccination
 Influenza vaccination should be
provided to patients with asthma when
vaccination of the general population is
advised.

97. Component 3: Assess, Treat
and Monitor Asthma
The goal of asthma treatment, to
achieve and maintain clinical
control, can be achieved in a
majority of patients with a
pharmacologic intervention strategy
developed in partnership between
the patient/family and the health
care professional

98. Component 3: Assess, Treat
and Monitor Asthma
 Depending on level of asthma control,
the patient is assigned to one of five
treatment steps
 Treatment is adjusted in a continuous
cycle driven by changes in asthma
control status. The cycle involves:
- Assessing Asthma Control
- Treating to Achieve Control
- Monitoring to Maintain Control

99.  A stepwise approach to pharmacological
therapy is recommended
 The aim is to accomplish the goals of
therapy with the least possible medication
Component 3: Assess, Treat
and Monitor Asthma

100. The choice of treatment should be guided by:
 Level of asthma control
 Current treatment
 Pharmacological properties and availability
of the various forms of asthma treatment
 Economic considerations
Component 3: Assess, Treat
and Monitor Asthma

101. Controller Medications
 Inhaled glucocorticosteroids
 Leukotriene modifiers
 Long-acting inhaled β2-agonists
 Systemic glucocorticosteroids
 Theophylline
 Cromones
 Long-acting oral β2-agonists
 Anti-IgE
 Systemic glucocorticosteroids

102. Reliever Medications
 Rapid-acting inhaled β2-agonists
 Systemic glucocorticosteroids
 Anticholinergics
 Theophylline
 Short-acting oral β2-agonists

103. controlled
partly controlled
uncontrolled
exacerbation
LEVEL OF CONTROLLEVEL OF CONTROL
maintain and find lowest
controlling step
consider stepping up to
gain control
step up until controlled
treat as exacerbation
TREATMENT OF ACTIONTREATMENT OF ACTION
TREATMENT STEPS
REDUCE INCREASE
STEP
1
STEP
2
STEP
3
STEP
4
STEP
5
REDUCEINCREASE

106. Step 1 – As-needed reliever medication
 Patients with occasional daytime symptoms of
short duration
 A rapid-acting inhaled β2-agonist is the
recommended reliever treatment (Evidence A)
 When symptoms are more frequent, and/or
worsen periodically, patients require regular
controller treatment (step 2 or higher)

108. Step 2 – Reliever medication plus a single
controller
 A low-dose inhaled glucocorticosteroid is
recommended as the initial controller
treatment for patients of all ages (Evidence
A)
 Alternative controller medications include
leukotriene modifiers (Evidence A)
appropriate for patients unable/unwilling to
use inhaled glucocorticosteroids

110. Step 3 – Reliever medication plus one or two
controllers
 For adults and adolescents, combine a low-dose
inhaled glucocorticosteroid with an inhaled long-
acting β2-agonist either in a combination inhaler
device or as separate components (Evidence A)
 Inhaled long-acting β2-agonist must not be used
as monotherapy
 For children, increase to a medium-dose inhaled
glucocorticosteroid (Evidence A)

111. Additional Step 3 Options for Adolescents and Adults
 Increase to medium-dose inhaled
glucocorticosteroid (Evidence A)
 Low-dose inhaled glucocorticosteroid
combined with leukotriene modifiers
(Evidence A)
 Low-dose sustained-release theophylline
(Evidence B)

113. Step 4 – Reliever medication plus two or more
controllers
 Selection of treatment at Step 4 depends
on prior selections at Steps 2 and 3
 Where possible, patients not controlled on
Step 3 treatments should be referred to a
health professional with expertise in the
management of asthma

114. Step 4 – Reliever medication plus two or more controllers
 Medium- or high-dose inhaled glucocorticosteroid
combined with a long-acting inhaled β2-agonist
(Evidence A)
 Medium- or high-dose inhaled glucocorticosteroid
combined with leukotriene modifiers (Evidence A)
 Low-dose sustained-release theophylline added
to medium- or high-dose inhaled
glucocorticosteroid combined with a long-acting
inhaled β2-agonist (Evidence B)

116. Step 5 – Reliever medication plus additional controller options
 Addition of oral glucocorticosteroids to other
controller medications may be effective
(Evidence D) but is associated with severe
side effects (Evidence A)
 Addition of anti-IgE treatment to other
controller medications improves control of
allergic asthma when control has not been
achieved on other medications (Evidence A)

117.  When control as been achieved,
ongoing monitoring is essential to:
- maintain control
- establish lowest step/dose treatment
 Asthma control should be monitored
by the health care professional and
by the patient

118. Levels of Asthma
Control
Characteristic
Controlled
(All of the following)
Partly controlled
(Any present in any week)
Uncontrolled
Daytime symptoms
None (2 or less /
week)
More than
twice / week
3 or more
features of
partly
controlled
asthma
present in
any week
Limitations of
activities
None Any
Nocturnal
symptoms /
awakening
None Any
Need for rescue /
“reliever” treatment
None (2 or less /
week)
More than
twice / week
Lung function
(PEF or FEV1) Normal
< 80% predicted or
personal best (if
known) on any day
Exacerbation None One or more / year 1 in any week

119. Stepping down treatment when asthma is controlled
 When controlled on medium- to high-
dose inhaled glucocorticosteroids: 50%
dose reduction at 3 month intervals
(Evidence B)
 When controlled on low-dose inhaled
glucocorticosteroids: switch to once-daily
dosing (Evidence A)

120. Stepping down treatment when asthma is controlled
 When controlled on combination inhaled
glucocorticosteroids and long-acting
inhaled β2-agonist, reduce dose of inhaled
glucocorticosteroid by 50% while
continuing the long-acting β2-agonist
(Evidence B)
 If control is maintained, reduce to low-
dose inhaled glucocorticosteroids and
stop long-acting β2-agonist (Evidence D)

121. Stepping up treatment in response to loss of control
 Rapid-onset, short-acting or long-
acting inhaled β2-agonist
bronchodilators provide temporary
relief.
 Need for repeated dosing over more
than one/two days signals need for
possible increase in controller therapy

122. Stepping up treatment in response to loss of control
 Use of a combination rapid and long-acting
inhaled β2-agonist (e.g., formoterol) and an
inhaled glucocorticosteroid (e.g., budesonide)
in a single inhaler both as a controller and
reliever is effecting in maintaining a high level
of asthma control and reduces exacerbations
(Evidence A)
 Doubling the dose of inhaled glucocortico-
steroids is not effective, and is not
recommended (Evidence A)

123. Childhood and adult asthma share the
same underlying mechanisms.
However, because of processes of
growth and development, effects of
asthma treatments in children differ
from those in adults.
Children 5 Years and Younger

124. Many asthma medications (e.g.
glucocorticosteroids, β2- agonists,
theophylline) are metabolized faster in
children than in adults, and younger
children tend to metabolize medications
faster than older children
Children 5 Years and Younger

125.  Rapid-acting inhaled β2-agonists are the
most effective reliever therapy for
children
 These medications are the most
effective bronchodilators available and
are the treatment of choice for acute
asthma symptoms
Children 5 Years and Younger

126. Special Considerations
Special considerations are required to
manage asthma in relation to:
 Pregnancy
 Surgery
 Rhinitis, sinusitis, and nasal polyps
 Occupational asthma
 Respiratory infections
 Gastroesophageal reflux
 Aspirin-induced asthma
 Anaphylaxis and Asthma

127. THANK YOU