KGD P6 Emergency Medicine: Tambahan

KGD P6 (TAMBAHAN)
EMERGENCY MEDICINE
Cindy Claudia
405140139
ASTHMA
 Asthma is a chronic inflammatory disorder of the airways
characterized by marked variability in airflow obstruction that
is often reversible, either spontaneously or with treatment.
 presents clinically in susceptible patients with :

 recurrent symptoms of wheezing, chest tightness, cough, and,
occasionally, dyspnea and contributes to the heightened airway
hyperresponsiveness to specific and nonspecific stimuli
 Acute allergic bronchoconstriction results from
immunoglobulin E–dependent release of mediators from mast
cells.
 These mediators include histamine, leukotrienes, tryptase, and

prostaglandins that directly contract airway smooth muscle.
 Bronchospasm induced by aspirin and other nonsteroidal anti-

inflammatory drugs also involves mediator release from
airway cell
 Inhaled antigens activate immunoglobulin E, mast cells, and T

helper cells in the airway and induce the production of
inflammatory mediators and cytokines.
PATHOPHYSIOLOGY
 Characterized by an abnormal accumulation of
eosinophil,lymphocytes ,mast cells ,macrophages ,dendritic
cell & myofibroblast in airwa
 Pathophysiologic hallmark of asthma  a reduction in airway

diameter caused by smooth muscle contraction,vascular
congestion ,bronchial wall edema & thick secretion these
changes are reflected in pulmonary function changes
,increased work of breathing & abnormal distribution of
pulmonary blood flow.
 Airways are infiltrated with eosinophils & mononuclear cells

 The airway smooth muscle is hypertrophied & characterized by new
vessel formation ,an increased number of epithelial goblet cell &
deposition of interstisial collagen
RISK FACTOR OF ASTHMA
PHYSICAL EXAMINATION
 The most typical physical finding in asthma is wheezing on auscultation
which is usually caused by turbulent airflow through narrowed airways.
 Wheezing may be heard throughout the chest & is classically polyphonic
 present to a greater extent during expiration, although it may also be heard during
inspiration.
 Examination of the upper respiratory tract may reveal clinical signs of rhinitis,
sinusitis, or nasal polyps.
 During an acute exacerbation of disease

 physical signs of increased ventilation may be observed with the use of accessory
muscles of respiration
 chest signs of hyperinflation.
 sign of severe airway obstruction is pulsus paradoxus
 which is the exaggerated decrease in systolic blood pressure during inspiration by >10 mm Hg
 As ventilatory effort can be diminished with respiratory muscle fatigue, pulsus
paradoxus may be absent
 Stridor is a high-pitched inspiratory sound & indicates airflow turbulence in the
upper airways.
LABORATORY INVESTIGATION
 Arterial blood gas measurements may be normal during a
mild asthma exacerbation.
 During severe exacerbations, hypoxemia develops and
the Paco2 returns to normal.
 The combination of increased Paco2 +respiratory
acidosis  indicate impending respiratory failure and the
need for mechanical ventilation.
 The evaluation for asthma should therefore include:
 Spirometry
 forced expiratory volume in 1 second [FEV 1 ]
 forced vital capacity [FVC] , FEV/FVC) before and after the
administration of a short-acting bronchodilator.
 Airflow obstruction is indicated  by a reduced
FEV/FVC ratio.
 Significant reversibility of airflow obstruction is defined
by  an increase of 12% or more & 200 mL in FEV1 or
FVC after inhaling a short-acting bronchodilator
PULMONARY FUNCTION TEST
 Spirometry measures the expiratory volume and flow of
air using forced maneuvers from full lung inflation, as a
function of time.
 Simple spirometry  important for objectively

demonstrating airflow obstruction, confirming the
diagnosis of asthma, establishing the severity of the
disease, and monitoring the response to therapy
 Patients with asthma typically show 
 a reduced forced expiratory flow in 1 second (FEV1), reduced PEF,
preserved forced vital capacity(FVC),FEV1/FVC ratio of 0.7 / greater
 with worsening disease, FEV1 < than 60% predicted the FEV1/FVC
ratio is more usually <0.7
 Home PEF monitoring may be of diagnostic use,

 confirming the diurnal variations in airflow obstruction, especially in
patients who demonstrate normal spirometry during clinic visits.
 Bronchodilator reversibility is a measure of the magnitude of

airway smooth muscle relaxation.
 postbronchodilator increase in FEV of >12% and 200 mL is often
1
considered evidence of reversible airway obstruction, where measures

are taken 15 minutes after an inhaled short-acting β -agonist (SABA).
2
PEAK EXPIRATORY FLOW ( PEF)
 Handheld devices designed as personal monitoring tools
 PEF monitoring can establish peak flow
variability,quantify asthma severity & provide both
patient & clinicial with objective
 It is generally lowest on first awakening and highest

several hours before the midpoint of the waking day.
 PEF should be measured in the morning before the
administration of a bronchodilator and in the afternoon
after taking a bronchodilator
BRONCHIAL CHALLENGE TEST
 Bronchial challenge tests  assess the abnormally increased
airway hyperresponsiveness observed in patients with asthma,
by detecting the exaggerated response to inhaled
bronchoprovocative agents
 The provocation agents can be classified into two categories:

direct and indirect
 Direct stimuli such as histamine and methacholine, which are normally

used in the clinic, act on airway smooth muscle receptors
 Indirect stimuli act through intermediate pathways that include the

release of mast cell mediators, and/or through local and central
neurologic reflexes
 Increased BHR is typically defined as the inhaled concentration
of the bronchoprovocative agent that reduces FEV1 by 20%
(PC20)
 Exercise testing of patients using cycle, treadmill / free
running challenges is occasionally undertaken to show
postexercise bronchoconstriction if there is a suggestive
history of exercise-induced asthma
 Bronchial provocation testing with inhaled
histamine/methacoline ( may be useful when asthma is
suspected but spirometry is nondiagnostic)
 Bronchial provocation is not recommended if the FEV1 is <
65% of predicted
 + methacoline test : defined as a fall in the FEV1 of 20% or
more at exposure to a concentration of 16 mg/mL /less
 Exercise challenge testing may be useful in patient with
symptoms of exercise induced bronchospasm
BLOOD TEST
 Blood Test
 The eosinophil count in the peripheral blood film may be raised
in atopic conditions and eosinophilia may support a diagnosis of
asthma
 Total serum immunoglobulin E (IgE) may be measured in
patients
 Acute exacerbations of disease
 Arterial blood gases may reveal  hypoxemia & the arterial
PaCO2 may be reduced due to hyperventilation
 With a severe exacerbation  the arterial PaCO2 may
rise due to respiratory muscle fatigue and an inability to
maintain the required alveolar ventilation.
ADDITIONAL TESTING
 Routine chest radiographs in patients with asthma
 usually normal /show only hyperinflation
 Other findings include : bronchial wall thickening & diminished
peripheral lung vascular shadows
 Chest imaging is indicated
 when pneumonia, another disorder mimicking asthma, or a
complication of asthma such as pneumothorax is suspected.
 Skin testing / in vitro testing to assess sensitivity to

environmental allergens can identify atopy in patients with
persistent asthma.
Complications
Complications of asthma include exhaustion, dehydration,
airway infection, and tussive syncope.
Pneumothorax occurs but is rare. Acute hypercapnic and
hypoxemic respiratory
failure occurs in severe disease.
HOW TO ASSES ASTHMA CONTROL
TREATMENT OF ASTHMA
 The goals of asthma therapy are to :
 minimize chronic symptoms that interfere with normal
activity (including exercise)
 to prevent recurrent exacerbations
 to reduce or eliminate the need for emergency department
visits or hospitalizations
 to maintain normal or near-normal pulmonary function.
THERAPEUTIC DRUG
 Bronchodilators
 reverse the bronchoconstriction of asthma, principally by acting to relax airway
smooth muscle & this results in the rapid relief of symptoms.
 The classes of bronchodilators in current clinical use include
 β2-adrenergic agonists, anticholinergics, and theophylline, where β2-agonists
are the most efficacious.
 β2-Adrenergic AgonistsInhaled β2-adrenergic agonists are the drugs of

choice for relief of respiratory symptoms due to acute airway obstruction.
 Mode of action : β -Agonists activate β -adrenergic receptors resulting  in an
2 2
increase in intracellular cyclic AMP  leads to relaxation of airway smooth muscle

cells
 Clinical use : SABA ( albuterol & terbutaline ) rapid onset of action ( rapid onset
of bronchodilation allows these drugs to be used as quick relief medication/” reliever”
 Long-acting β -agonists (LABAs) include formoterol and salmeterol
2
 LABA should not be used as monotherapy for the control of asthma of any severity
and should not be given in the absence of ICS therapy as they do not control the
underlying inflammation
Adverse effect The commonest adverse effects of β2-agonists are palpitations and
muscle tremor
β-blockers are contraindicated during acute asthma
exacerbations and the risk–benefit ratio should be considered before
they are used in stable patients with asthma
Anticholinergic Muscarinic receptor antagonists, such as ipratropium
Bromide  induce airway smooth-muscle relaxation by blocking
muscarinic receptors on airway smooth muscle
inhibiting vagally mediated cholinergic tone and preventing mucus

secretion
Clinical use anticholinergics tend only to be used as add-on bronchodilator treatment
in asthmatics who remain uncontrolled on other inhaled therapy
Adverse effect most commonly experienced side effect is dry mouth,
and in elderly patients, glaucoma and urinary retention can occur
Theophylinne Oral theophylline was primarily used as an adjunct bronchodilator
treatment
Clinical severe asthmatic patients theophylline may be used as an add-on bronchodilator
use treatment, although plasma concentrations
of 10 to 20 mg/L are typically needed, and these levels are usually associated with
adverse effects
Adverse Headaches, nausea, and vomiting are the commonest
Effect adverse effects, which arise from the inhibition of phosphodiesterase.
Palpitations and diuresis
Corticoster Corticosteroids (CSs) are potent anti-inflammatory agents and when
oid administered by the inhaled route are the most effective therapy
available for treating and controlling asthma
The reduction in eosinophils, activated T lymphocytes,
and surface mast cells in the airways contribute to the lessening in
the airway hyperresponsiveness that is seen with CS therapy
Clinical Usually administered by the inhaled route for mainenance controller therapy
use— in patient with asthma
Inhaled ICS have been shown to prevent the symptom of asthma ,reduce severe
Corticoster exacerbation rates ,improve lung function & reduce airway
oids hyperesponsiveness
1st line therapy for patient with persistent asthma & usually administered 2x
shari
If low – to medium doses of ICS do not control persistent asthma symptom ( it
usual practice now to add a LABA )preferably as combination
Clinical use – Oral CSs are reserved to treat acute exacerbation of asthma.
systemic -Typically prednisolone/prednisone 30-45 mg is given 1x daily (for
corticosteroid 5-10 days) & on finishing the course of treatment
-Css may also be administered intravenously (

metylprednisolone/hydrocortisone) for the treatment of acute
severe asthma
Adverse effect -ICS may give rise to local oropharyngeal adverse effect such as oral
candidiasis ,dysphonia & hoarseness
Oral CS gives rise to greater systemic adverse effects than ICS, with a
greater potential in those on chronic maintenance therapy.
Adverse effects include bruising, diabetes, truncal obesity,
osteoporosis, duodenal and gastric ulceration, hypertension, mood and
behavioral changes, proximal myopathy, and cataracts
Antileukotrien Leukotriene pathway inhibitors are a group of compounds that
alter the pathophysiologic effects of leukotrienes derived from
the 5-lipoxygenation of arachidonic acid.
Clinical use Antileukotrienes have less effect on airway inflammation and provide
modest clinical benefit compared to ICS
ICSs are more effective anti-inflammatory agents and clinically

superior in controlling asthma than antileukotrienes
Antileukotrienes are usually well tolerated, but can sometimes
give rise to gastrointestinal upset, hepatotoxicity, and
hypersensitivity reactions including anaphylaxis and
angioedema.
 Most effective in achieving prompt control of asthma
during exacerbations / when initiating long-term asthma
therapy in patients with severe symptoms.
 Concurrent treatment with calcium supplements and

vitamin D should be initiated to prevent corticosteroid-
induced bone mineral loss in long-term administration
QUICK RELIEF MEDICATION OF ASTHMA
COPD Definition
► Chronic Obstructive Pulmonary Disease (COPD) is a
common, preventable and treatable disease that is
characterized by persistent respiratory symptoms and
airflow limitation that is due to airway and/or alveolar
abnormalities usually caused by significant exposure to
noxious particles or gases.
The chronic airflow limitation that is

characteristic of COPD is caused
 by a mixture of small airways disease
(e.g., obstructive bronchiolitis) and
parenchymal destruction (emphysema), the
relative contributions of which vary from
person to person
© 2017 Global Initiative for Chronic Obstructive Lung Disease

COPD Etiology, Pathobiology &
Pathology

COPD
Definition and Overview
OVERALL KEY POINTS (1 of 2):
► Chronic Obstructive Pulmonary Disease (COPD) is a common,

preventable and treatable disease that is characterized by
► persistent respiratory symptoms & airflow limitation that is
due to airway and/or alveolar abnormalities usually caused
by significant exposure to noxious particles or gases.
► The most common respiratory symptoms include :

► dyspnea, cough and/or sputum production.
► The main risk factor for COPD :

► tobacco smoking
► other environmental exposures such as biomass fuel
exposure and air pollution may contribute.

Definition and Overview
OVERALL KEY POINTS (2 of 2):
► Besides exposures, host factors predispose individuals to

develop COPD. These include genetic abnormalities,
abnormal lung development and accelerated aging.
► COPD may be punctuated by periods of acute worsening

of respiratory symptoms, called exacerbations.
► In most patients, COPD is associated with significant

concomitant chronic diseases, which increase its morbidity
and mortality.

Factors that influence disease progression
► Genetic factors
► Age and gender
► Lung growth and development
► Exposure to particles
► Socioeconomic status
► Asthma & airway hyper-reactivity
► Chronic bronchitis
► Infections

THE RISK OF DEVELOPING COPD IS RELATED
TO THE FOLLOWING FACTORS
 Tobacco smoke
 Indoor air pollution - from biomass fuel used for
cooking and heating in poorly vented dwellings
 Occupational exposures - including organic and
inorganic dusts, chemical agents and fumes
 Outdoor air pollution - also contributes to the lungs’
total burden of inhaled particles, although it appears to
have a relatively small effect in causing COPD.
 Genetic factors - such as severe hereditary deficiency
of alpha-1 antitrypsin (AATD)
 Age and gender - aging and female gender increase
COPD risk.
Pathology, pathogenesis & pathophysiology
► Pathology
 Chronic inflammation
 Structural changes
► Pathogenesis
 Oxidative stress
 Protease-antiprotease imbalance
 Inflammatory cells
 Inflammatory mediators
 Peribronchiolar and interstitial fibrosis
► Pathophysiology
 Airflow limitation and gas trapping
 Gas exchange abnormalities
 Mucus hypersecretion
 Pulmonary hypertension

CLINICAL FEATURE
SIGN AND SYMPTOM
 complaining of excessive cough, sputum production, and shortness of breath

(Symptoms have often been present for 10 years or more.)
 Dyspnea
 In severe disease, dyspnea occurs at rest.
 As the disease progresses, two symptom patterns tend to emerge, historically
referred to as "pink puffers" and "blue bloaters
 Most COPD ps have pathologic evidence ( central control of ventilation &
concomitant sleep disordered breathing)
 Late stage of COPD : pneumonia,pulmonary hypertension,cor pulmonal &
chronic respiratory failure
 Hallmark of COPD  periodic exacerbation of symptoms beyond normal
day –to –day variation ( often including increased dyspnea ,an increased
frequency /severity of cough & increased sputum volume/change in sputum
character)
 These exacerbation commonly precipitated by infection ( more often viral
)/enviromental factor
LABORATORY FINDINGS
 Spirometryprovides objective information about pulmonary function &
assess the response to therapy
 Pulmonary function test early in the course of COPD  reveal only evidence
of abnormal closing volume & reduced midexpiratory flow rate
 Reductions in FEV1 and in the ratio of forced expiratory volume to vital

capacity (FEV1% or FEV/FVC ratio)later occur
 Arterial blood gas measurements characteristically show no abnormalities early

in COPD measurement is unnecessary unless
( 1 ) hypoxemia (occurs in advanced disease ( when chronic bronchitis
predominates) or hypercapnia is suspected
(2) the FEV1 is less than 40% of predicted
(3) there are clinical signs of right heart failure
+SVT arrhytmia & ventricular irritability also occur

IMAGING
 Patient with chronic bronchitistypically show only
nonspecific peribronchial & perivascular marking
 In emphysema show hyperinfaltion with flattening of
diaphragm/peripheral arterial deficiency
 CT of chest ( using high resolution CT)more sensitive
& specific
 Pulmonary hypertension may be suggested by

enlargement of central pulmonary arteries on radiographs
COMPLICATION
 Acute bronchitis, pneumonia, pulmonary
thromboembolism, atrial dysrhythmias (such as atrial
fibrillation, atrial flutter, and multifocal atrial
tachycardia)
 concomitant left ventricular failure may worsen
otherwise stable COPD
 Pulmonary hypertension, cor pulmonale, and chronic
respiratory failure are common in advanced COPD
 Spontaneous pneumothorax ( in small fraction of patient
with emphysema)
 Hemoptysis may result from chronic bronchitis
DIAGNOSIS AND ASSESMENT OF COPD
DIAGNOSIS
 COPD should be:
 considered in any patient who has  dyspnea, chronic cough /
sputum production, and/or history of exposure to risk factors for the
disease
 Spirometry is required to make the diagnosis
 the presence of a post-bronchodilator FEV /FVC < 0.70 confirms
1
the presence of persistent airflow limitation

Diagnosis and Initial Assessment

► Symptoms of COPD
 Chronic and progressive dyspnea

 Cough
 Sputum production
 Wheezing and chest tightness
 Others – including fatigue, weight loss,
anorexia, syncope, rib fractures, ankle
swelling, depression, anxiety.


Medical History
► Patient’s exposure to risk factors

► Past medical history
► Family history of COPD or other chronic respiratory disease.
► Pattern of symptom development
► History of exacerbations or previous hospitalizations for respiratory
disorder
► Presence of comorbidities
► Impact of disease on patient’s life
► Social and family support available to the patient.
► Possibilities for reducing risk factors, especially smoking cessation.


ASSESMENT
Choice of thresholds
► COPD Assessment Test (CAT TM )
► Chronic Respiratory Questionnaire (CCQ® )
► St George’s Respiratory Questionnaire (SGRQ)
► Chronic Respiratory Questionnaire (CRQ)
► Modified Medical Research Council (mMRC) questionnaire

ABCD Assessment Tool
Example
► Consider two patients:

 Both patients with FEV1 < 30% of predicted
 Both with CAT scores of 18
 But, one with 0 exacerbations in the past year and the other with
3 exacerbations in the past year.
► Both would have been labelled GOLD D in the prior classification

scheme.
► With the new proposed scheme, the subject with 3 exacerbations in
the past year would be labelled GOLD grade 4, group D.
► The other patient, who has had no exacerbations, would be classified
as GOLD grade 4, group B.

Assessment of Exacerbation Risk
► COPD exacerbations are defined as an acute worsening of respiratory

symptoms that result in additional therapy.
► Classified as:
 Mild (treated with SABDs only)
 Moderate (treated with SABDs plus antibiotics and/or oral
corticosteroids) or
 Severe (patient requires hospitalization or visits the emergency
room). Severe exacerbations may also be associated with acute
respiratory failure.
► Blood eosinophil count may also predict exacerbation rates (in
patients treated with LABA without ICS).

Summary

Alpha-1 antitrypsin deficiency (AATD)
AATD screening
► The World Health Organization recommends that all patients with a

diagnosis of COPD should be screened once especially in areas with
high AATD prevalence.
► AATD patients are typically < 45 years with panlobular basal

emphysema
► Delay in diagnosis in older AATD patients presents as more typical

distribution of emphysema (centrilobular apical).
► A low concentration (< 20% normal) is highly suggestive of

homozygous deficiency.

EVIDENCE SUPPORTING PREVENTION AND MAINTENANCE
THERAPY
SMOKING CESSATION
VACCINATION
Influenza vaccine
 Influenza vaccination can reduce serious illness (such as lower respiratory tract infections
requiring hospitalization)and death in COPD patients
Pneumococcal vaccine
 Pneumococcal vaccinations, PCV13 and PPSV23, are recommended for all patients ≥ 65 years of
age
 The PPSV23 is also recommended for younger COPD patients with significant comorbid
conditions including chronic heart or lung disease.
 PPSV23 has been shown  to reduce the incidence of community-acquired pneumonia in COPD
patients < 65 years, with an FEV1 < 40% predicted, or comorbidities (especially cardiac
comorbidities)
Pharmacologic therapy for Stable COPD used to reduce symptoms, reduce the frequency
and severity of exacerbations, and improve exercise tolerance and health status.
Bronchodilators Bronchodilator medications in COPD are most often given on a regular
Bronchodilators basis to prevent or reduce symptoms.
are medications that
increase FEV1 Toxicity is also dose-related
and/or change other  Use of short acting bronchodilator on a regular basis not generally
spirometric recommended
variables.
1) Beta2-agonists Function : relax airway smooth muscle by stimulating beta2-
adrenergic receptors  increases cyclic AMP  produces functional
antagonism to bronchoconstriction
There are short-acting (SABA) and long-acting (LABA) beta2-agonists
Formoterol & salmeterol are 2xdaily
 LABAs that significantly improve FEV1 and lung volumes, dyspnea,
health status, exacerbation rate and number of hospitalizations
Indacaterol 1x daily LABA: improves breathlessness,health status &
exacerbation rate
Oladaterol & vilanterol additional ( 1x daily LABA )improve lung
function & symptom
Adverse effect Can produce resting sinus tachycardia & potential to precipitate cardiac
rhytm disturbances ,somatic tremor ( some patient treated with higher
doses )
2) Antimuscarinic ` block the bronchoconstrictor effects of acetylcholine on M3
muscarinic receptors expressed in airway smooth muscle
-Short-acting antimuscarinics (SAMAs), namely ipratropium and
oxitropium
- long-acting antimuscarinic antagonists (LAMAs), such as tiotropium,
aclidinium, glycopyrronium bromide and umeclidinium
Clinical trials have shown a greater effect on exacerbation rates for
LAMA treatment
Adverse effect Extensive use of this class of agents in a wide range of doses and clinical
settings has shown them to be very safe.
The main side effect is dryness of mouth
3) Methylxanthines Theophylline the most commonly used methylxanthine, is

metabolized by cytochrome P450 mixed function oxidases
Addition of theophylline to salmeterol produces a greater improvement
in FEV1 and breathlessness
Adverse effect Toxicity is dose-related, which is a particular problem with xanthine
derivatives because their therapeutic ratio is small
COMBINATION BRONCHODILATOR THERAPY
 Combining bronchodilator with different mechanism &
duration of actionmay increase the degree of
bronchodilation
 SABAs + Sama s superior compared to either medication

alone ( improving FEV1 & Symptoms)
 Treatment with formoterol & tiotropium in separate

inhalerbigger impact on FEV1
 A lower dose ( 2x daily ) regimen for LABA/LAMA

improve symptom & health status in COPD patient
Pharmacologic Therapy

Pharmacologic Therapy

Bronchodilators in Stable COPD

Anti-inflammatory agents
 exacerbations (e.g., exacerbation rate, patients with at least one
exacerbation, time-to-first exacerbation)
Inhaled CS ICS + LABA patients with moderate - very severe COPD and
exacerbations
More effective improving lung function, health status and
reducing exacerbations
Adverse higher prevalence of oral candidiasis, hoarse voice, skin bruising
effects and pneumonia
Triple inhaled therapy
inhaled treatment to LABA + LAMA + ICS (triple therapy) can
occur by various approach improve lung function and patient
Adding a LAMA to existing LABA/ICS improves lung function and patient

reported outcomes, in particular exacerbation risk
Oral glucocorticoids
Various s.e myopathy (which can contribute to muscle weakness, decreased
functionality, and respiratory failure in subjects with very severe COPD)
oral glucocorticoids play a role in the acute management of exacerbations (but
no role in chronic daily treatment )
Anti-inflammatory Therapy in Stable COPD

The Inhaled Route

Palliative, End of Life & Hospice Care
► In many patients, the disease trajectory in COPD is marked by a

gradual decline in health status and increasing symptoms, punctuated
by acute exacerbations that are associated with an increased risk of
dying.
► Although mortality rates following hospitalization for an acute

exacerbation of COPD are declining, reported rates still vary from
23% to 80%.

Oxygen Therapy & Ventilatory Support in
Stable COPD
► During exacerbations of COPD.

► Noninvasive ventilation (NIV) in the form of noninvasive positive
pressure ventilation (NPPV) is the standard of care for decreasing
morbidity and mortality in patients hospitalized with an exacerbation
of COPD and acute respiratory failure

Interventional Therapy in Stable COPD
► Lung volume reduction surgery (LVRS) is a surgical procedure in

which parts of the lungs are resected to reduce hyperinflation making
respiratory muscles more effective pressure generators by improving
their mechanical efficiency.
► Due to the morbidity and mortality associated with LVRS, less
invasive bronchoscopic approaches to lung reduction have been
examined.

Management of Stable COPD
Identify and reduce exposure to known risk factors
► Identification and reduction of exposure to risk factors is important in the

treatment and prevention of COPD.
► Cigarette smoking is the most commonly & easily identifiable risk factor for
COPD
► smoking cessation should be continually encouraged for all individuals
who smoke.
► Reduction of total personal exposure to occupational dusts, fumes, and gases,

and to indoor and outdoor air pollutants, should also be addressed.

Management of Stable COPD

Treatment of Stable COPD
Pharmacologic treatment
► Pharmacologic therapies can reduce symptoms, and the risk and severity of
exacerbations, as well as improve health status and exercise tolerance.
► Most of the drugs are inhaled so proper inhaler technique is of high

relevance.




Pharmacologic treatment algorithms
Group A
► All Group A patients
► should be offered bronchodilator
treatment based on its effect on
breathlessness.
► This can be either a short- or a

long-acting bronchodilator.
► This should be continued if

symptomatic benefit is documented.

Group B
► Initial therapy should consist of a long acting
bronchodilator.
► Long-acting inhaled bronchodilators are

superior to short-acting bronchodilators taken
as needed
► In the individual patient

► the choice should depend on the patient’s
perception of symptom relief.
► For patients with persistent breathlessness on

monotherapy the use of two bronchodilators is
recommended.

Group B (continued)
► For patients with severe breathlessness 
initial therapy with 2 bronchodilators may
be considered.
► If the addition of a second bronchodilator does

not improve symptoms
► we suggest the treatment could be
stepped down again to a single
bronchodilator.

Group C
► Initial therapy should consist of a single long
acting bronchodilator.
► Comparison the tested LAMA was superior to

the LABA regarding exacerbation prevention
(theraphy starting with LAMA)
► Patients with persistent exacerbations may benefit

from 
► adding a second long acting bronchodilator
(LABA/LAMA) OR
► using a combination of a long acting beta2-

agonist & an inhaled corticosteroid
(LABA/ICS).
► As ICS increases the risk for developing

pneumonia in some patients, our primary
choice is LABA/LAMA.
Group D
► We recommend starting therapy with a
LABA + LAMA combination because:
 If a single bronchodilator is chosen as initial

treatment  LAMA is preferred for
exacerbation prevention
 LABA/LAMA combination was superior to a

LABA/ICS combination in preventing
exacerbations and other patient reported
outcomes in Group D patients
 Group D patients are at higher risk of

developing pneumonia when receiving
treatment with ICS.

Group D (continued)
► Some patients initial therapy with  Switch to LABA/ICS.
LABA/ICS may be the 1st choice.
► These patients may have :  but there is no evidence
► a history and/or findings that switching from
suggestive of asthma-COPD LABA/LAMA to
overlap. LABA/ICS results in better
► High blood eosinophil counts exacerbation prevention.
may also be considered as a
parameter to support the use of  If LABA/ICS therapy does
ICS, although this is still under not positively impact
debate exacerbations/symptoms, a
LAMA can be added.
► In patients who develop further
exacerbations on LABA/LAMA
therapy we suggest two alternative
pathways:
 Escalation to
LABA/LAMA/ICS.
Group D (continued)
If patients treated with LABA/LAMA/ICS still have
exacerbations the following options may be considered:
► Add roflumilast.
► This may be considered in patients with an
FEV1 < 50% predicted and chronic
bronchitis,particularly if they have experienced
at least one hospitalization for an exacerbation
in the previous year.
► Add a macrolide best available evidence exists for

the use of azithromycin.
► Stopping ICS.
► an elevated risk of adverse effects (including
pneumonia)

Non-Pharmacologic Treatment
Education and self-management
► Self-management education and coaching by healthcare professionals should

be a major component of the “Chronic Care Model” within the context of the
healthcare delivery system.
► The aim of self-management education is to motivate, engage and coach the

patients to positively adapt their health behavior(s) and develop skills to
better manage their disease.

Oxygen therapy
Long-term oxygen therapy is indicated for stable patients who

have:
► PaO2 at or < 7.3 kPa (55 mmHg) / SaO2 at or < 88%, with or
without hypercapnia confirmed twice over a three week period;
or
► PaO2 : 7.3 kPa (55 mmHg) - 8.0 kPa (60 mmHg)

► SaO2 of 88%
► if there is evidence of pulmonary hypertension, peripheral
edema suggesting congestive cardiac failure, or
polycythemia (hematocrit > 55%).

Management of Exacerbations
COPD exacerbations are defined as an acute worsening of

respiratory symptoms that result in additional therapy.
► They are classified as:
 Mild (treated with short acting bronchodilators only, SABDs)

 Moderate (treated with SABDs plus antibiotics and/or oral
corticosteroids) or
 Severe (patient requires hospitalization or visits the emergency room).
Severe exacerbations may also be associated with acute respiratory
failure.

Classification of hospitalized patients
No respiratory failure:
Respiratory rate: 20-30 breaths per minute
no use of accessory respiratory muscles; no changes in mental
status; hypoxemia improved with supplemental oxygen given via
Venturi mask 28-35% inspired oxygen (FiO2); no increase in
PaCO2.

Acute respiratory failure — non-life-threatening: Respiratory

rate: > 30 breaths per minute; using accessory respiratory muscles;
no change in mental status; hypoxemia improved with
supplemental oxygen via Venturi mask 25-30% FiO2; hypercarbia
i.e., PaCO2 increased compared with baseline or elevated 50-60
mmHg.

Acute respiratory failure — life-threatening:

Respiratory rate: > 30 breaths per minute; using accessory
respiratory muscles; acute changes in mental status; hypoxemia not
improved with supplemental oxygen via Venturi mask or requiring
FiO2 > 40%; hypercarbia i.e., PaCO2 increased compared with
baseline or elevated > 60 mmHg or the presence of acidosis (pH <
7.25).



- Summary

The three classes of medications most commonly used for COPD

exacerbations are:
► Bronchodilators
 Although there is no high-quality evidence from RCTs, it is recommended that
short-acting inhaled beta2-agonists, with or without short-acting anticholinergics,
are the initial bronchodilators for acute treatment of a COPD exacerbation.
► Corticosteroids
 Data from studies indicate that systemic glucocorticoids in COPD exacerbations
shorten recovery time and improve lung function (FEV1). They also improve
oxygenation, the risk of early relapse, treatment failure, and the length of
hospitalization.
► Antibiotics

Respiratory support

Respiratory support



KGD P6 Emergency Medicine: Tambahan

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KGD P6 Emergency Medicine: Tambahan

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KGD P6 (TAMBAHAN)

 presents clinically in susceptible patients with :

 These mediators include histamine, leukotrienes, tryptase, and

 Bronchospasm induced by aspirin and other nonsteroidal anti-

 Inhaled antigens activate immunoglobulin E, mast cells, and T

 Pathophysiologic hallmark of asthma  a reduction in airway

 Airways are infiltrated with eosinophils & mononuclear cells

 During an acute exacerbation of disease

 Simple spirometry  important for objectively

 Home PEF monitoring may be of diagnostic use,

 Bronchodilator reversibility is a measure of the magnitude of

considered evidence of reversible airway obstruction, where measures

 It is generally lowest on first awakening and highest

 The provocation agents can be classified into two categories:

 Direct stimuli such as histamine and methacholine, which are normally

 Indirect stimuli act through intermediate pathways that include the

 Skin testing / in vitro testing to assess sensitivity to

 β2-Adrenergic AgonistsInhaled β2-adrenergic agonists are the drugs of

increase in intracellular cyclic AMP  leads to relaxation of airway smooth muscle

inhibiting vagally mediated cholinergic tone and preventing mucus

-Css may also be administered intravenously (

ICSs are more effective anti-inflammatory agents and clinically

 Concurrent treatment with calcium supplements and

The chronic airflow limitation that is

© 2017 Global Initiative for Chronic Obstructive Lung Disease

© 2017 Global Initiative for Chronic Obstructive Lung Disease

► Chronic Obstructive Pulmonary Disease (COPD) is a common,

► The most common respiratory symptoms include :

► The main risk factor for COPD :

© 2017 Global Initiative for Chronic Obstructive Lung Disease

► Besides exposures, host factors predispose individuals to

► COPD may be punctuated by periods of acute worsening

► In most patients, COPD is associated with significant

© 2017 Global Initiative for Chronic Obstructive Lung Disease

► Age and gender

► Lung growth and development

► Asthma & airway hyper-reactivity

© 2017 Global Initiative for Chronic Obstructive Lung Disease

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 complaining of excessive cough, sputum production, and shortness of breath

 Reductions in FEV1 and in the ratio of forced expiratory volume to vital

 Arterial blood gas measurements characteristically show no abnormalities early

+SVT arrhytmia & ventricular irritability also occur

 Pulmonary hypertension may be suggested by

the presence of persistent airflow limitation

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Chronic and progressive dyspnea

© 2017 Global Initiative for Chronic Obstructive Lung Disease

© 2017 Global Initiative for Chronic Obstructive Lung Disease

► Patient’s exposure to risk factors

© 2017 Global Initiative for Chronic Obstructive Lung Disease

© 2017 Global Initiative for Chronic Obstructive Lung Disease

© 2017 Global Initiative for Chronic Obstructive Lung Disease

► Consider two patients:

► Both would have been labelled GOLD D in the prior classification

© 2017 Global Initiative for Chronic Obstructive Lung Disease

► COPD exacerbations are defined as an acute worsening of respiratory

© 2017 Global Initiative for Chronic Obstructive Lung Disease

© 2017 Global Initiative for Chronic Obstructive Lung Disease

► The World Health Organization recommends that all patients with a

► AATD patients are typically < 45 years with panlobular basal

► Delay in diagnosis in older AATD patients presents as more typical

► A low concentration (< 20% normal) is highly suggestive of