How is it used?

Blood gas measurements are used to evaluate a person's lung function and acid/base balance.
They are typically ordered if someone is having worsening symptoms of a respiratory problem, such as difficulty
breathing or shortness of breath, and a condition such as asthma or chronic obstructive pulmonary disease
(COPD) is suspected. Blood gases may also be used to monitor treatment for lung diseases and to evaluate the
effectiveness of supplemental oxygen therapy.
Blood gases are used to detect an acid-base imbalance, such as can occur with kidney failure, heart failure,
uncontrolleddiabetes, severe infections, and drug overdose. They may be ordered along with other tests, such
as electrolytes to determine if an electrolyte imbalance is present, glucose to evaluate blood sugar
concentrations, and BUN and creatininetests to evaluate kidney function.
^ Back to top

When is it ordered?
A blood gas analysis is ordered when someone has symptoms of an oxygen/carbon dioxide or pH imbalance,
such as difficulty breathing, shortness of breath, nausea, or vomiting. It may also be ordered when someone is
known to have a respiratory, metabolic, or kidney disease and is experiencing respiratory distress.
When someone is "on oxygen" (ventilation), blood gases may be measured at intervals to monitor the
effectiveness of treatment. Other treatments for lung diseases may also be monitored with blood gases.
Blood gases may also be ordered when someone has head or neck trauma, which may affect breathing, and
when someone is undergoing prolonged anesthesia particularly for cardiac bypass surgery or brain surgery to
monitor blood gases during, and for a period after, the procedure.
Checking blood gases from the umbilical cord of a newborn may uncover respiratory problems as well as
determine acid/base status. Testing is usually only done if a newborn is having difficulty breathing.
^ Back to top

What does the test result mean?

Normal values will vary from lab to lab. They are also dependent on elevation above sea level as a person's
blood oxygen level will be lower if they live higher than sea level.
Results from an arterial blood gas analysis are not diagnostic; they should be used in combination with the
results of other tests and exams to evaluate someone for a respiratory, metabolic, or kidney problem.
Abnormal results of any of the blood gas components may indicate one or more of the following issues:

A person is not getting enough oxygen

A person is not getting rid of enough carbon dioxide

There is a problem with a person's kidney function

A low partial pressure of oxygen (PaO2) suggests that a person is not getting enough oxygen, while results that
are within normal range usually mean that oxygen intake is sufficient.

All other components of the blood gas analysis (pH, PaCO2, HCO3-) are interrelated and the results must be
considered together. Certain combinations of results, if abnormal, may indicate a condition that is
causing acidosis or alkalosis. These may include the following:

Respiratory acidosis is characterized by a lower pH and an increased PaCO2 and is due to respiratory
depression (not enough oxygen taken in and carbon dioxide removed). This can be caused by many things,
including pneumonia,chronic obstructive pulmonary disease (COPD), and over-sedation from narcotics.

Respiratory alkalosis, characterized by a raised pH and a decreased PaCO2, is due to over-ventilation

caused by hyperventilating, pain, emotional distress, or certain lung diseases that interfere with oxygen
exchange.

Metabolic acidosis is characterized by a lower pH and decreased HCO3-, causing the blood to be too
acidic for proper metabolic/kidney function. Causes include diabetes, shock, and renal failure.

Metabolic alkalosis is characterized by an elevated pH and increased HCO3- and is seen

in hypokalemia, chronic vomiting (losing acid from the stomach), and sodium bicarbonate overdose.

Examples of test results associated with the above conditions are summarized below:
pH result

Less than

Bicarbonate
result

PaCO2result

Low

Low

7.35
Greater

High

High

than 7.45
Less than

High

High

7.35
Greater
than 7.45

Low

Low

Condition

Common causes

Metabolic

Kidney failure, shock, diabetic ketoacidosis,

acidosis

intoxication with methanol, salicyate, ethanol

Metabolic

Chronic vomiting, low blood potassium, heart

alkalosis

failure, cirrhosis

Respiratory

Narcotics, lung diseases such as asthma, COPD,

acidosis

airway obstruction

Respiratory

Hyperventilation, pain, anxiety, brain trauma,

alkalosis

pneumonia, certain drugs (salicylate,

catecholamines)

If left untreated, these conditions can create an imbalance that can eventually become life-threatening. A health
practitioner can provide the necessary medical intervention to regain normal acid/base balance, but the
underlying cause of the imbalance must also be addressed.
^ Back to top

Is there anything else I should know?

Arterial blood sample collection is usually a bit more painful than regular venipuncture. You may experience
moderate discomfort, and a compress is required for some time to prevent any bleeding from the site.
Sometimes mixed venous blood taken from a central line is used in particular situations, such as in cardiac
catheterization labs and by transplant services. Careful interpretation of the results is required. Peripheral venous
blood, such as that taken from a vein in the arm, is of no use for oxygen status because it has decreased oxygen
content due to the fact that it is composed of blood returning to the heart.

https://labtestsonline.org/understanding/analytes/blood-gases/tab/test/#top

Wheezing may result from localized or diffuse airway narrowing or obstruction from the
level of the larynx to the small bronchi. The airway narrowing may be caused by
bronchoconstriction, mucosal edema, external compression, or partial obstruction by a tumor,
foreign body, or tenacious secretions. Wheezes are believed to be generated by oscillations or
vibrations of nearly closed airway walls. Air passing through a narrowed portion of an airway
at high velocity produces decreased gas pressure and flow in the constricted region
(according to Bernoulli's principle). The internal airway pressure ultimately begins to
increase and barely reopens the airway lumen. The alternation of the airway(s) between
nearly closed and nearly open produces a "fluttering" of the airway walls and a musical,
"continuous" sound. The flow rate and mechanical properties of the adjacent tissues that are
set into oscillation determine the intensity, pitch, composition (monophonic or polyphonic
notes), duration (long or short), and timing (inspiratory or expiratory, early or late) of this
dynamic symptom and sign. Wheezes are heard more commonly during expiration because
the airways normally narrow during this phase of respiration. Wheezing during expiration
alone is generally indicative of milder obstruction than if present during both inspiration and
expiration, which suggests more severe airway narrowing. However, most asthmatic patients
are unable accurately to correlate their wheezing (or other respiratory symptoms) to the
severity of airway obstruction as measured objectively by pulmonary function tests.
In contrast, the absence of wheezing in an asthmatic may indicate either improvement of the
bronchoconstriction or severe, widespread airflow obstruction. The latter suggests that the
airflow rates are too low to generate wheezes or the viscous mucus is obstructing large
regions of the peripheral airways. Increasing exhaustion and a "silent chest" are ominous
signs of respiratory muscle fatigue and failure, leading to status asthmaticus.
In asthma, the markedly increased airway resistance (airflow obstruction) contributes to the
characteristic physiologic and clinical changes observed during active or symptomatic
periods. The airway obstruction is diffuse and nonuniform in distribution, resulting in
ventilationperfusion inequalities and hypoxemia. Airways tend to close early during
expiration, and hyperinflation results. Although breathing at high lung volumes tends to
maintain open airways, this response demands increased muscular work of breathing to
provide adequate ventilation, which is increased secondary to stimulation of airway receptors
and hypoxia. Most asthmatics complain of greater difficulty during inspiration than
expiration, due to the uncomfortable work of breathing necessary to ventilate hyperinflated,
abnormally stiff, or noncompliant lungs.
Several hypotheses have been proposed to explain the pathogenesis of bronchoconstriction
and other airway abnormalities in asthma. None completely accounts for all the clinical forms
of asthma. The proposed mechanisms probably overlap and interrelate even in the same
individual.
The immediate, type I immunologic reaction occurs primarily in "allergic" asthma and
involves biochemical reactions between an antigen and a specific antibody (immunoglobulin
E, IgE) bound to sensitized airway mast cells and basophils. This immunologic reaction

results in the release of potent biochemical mediators that contract bronchial smooth muscle,
increase vascular permeability and mucus secretion, and attract inflammatory cells.
Preformed histamine, neutrophil and eosinophil chemotactic factors, and platelet-activating
factors are released. In addition, membrane-associated oxidative metabolism of arachidonic
acid generates prostaglandins (PGF2 and PGD2) and leukotrienes (LTC4, D4, E4), which are
potent bronchoconstrictors. Type III (arthus) immunologic reactions have also been
implicated in some cases of asthma and in the related allergic bronchopulmonary
aspergillosis.
A neurogenic or reflex mechanism is observed in "nonallergic" asthma provoked by
nonspecific stimuli (e.g., exercise, infection, air pollution) that apparently do not initiate type
I immunologic responses. This nonimmunologic hypothesis stresses the importance of the
parasympathetic nervous system (vagus nerve) in regulating airway caliber. Chemical or
mechanical inflammation stimulates cholinergic irritant receptors in the airway mucosa to
hyperreact, leading to vagally mediated reflex bronchoconstriction. This reflex is produced by
either direct mediator release or secondary stimulation of irritant receptors by smooth muscle
constriction.
A partial beta-adrenergic blockade or deficiency has also been proposed to explain some
types of "nonallergic" asthma (e.g., propranolol-induced asthma) because bronchial smooth
muscle tone appears to be modulated by beta-adrenergic receptors and alterations in the
metabolism of intracellular cyclic nucleotides. Beta-adrenergic stimulation increases cyclic
3,5-adenosine monophosphate (AMP) and decreases cyclic 3,5-guanosine monophosphate
(GMP), resulting in smooth muscle relaxation (bronchodilation). Beta-adrenergic inhibition
produces opposite effects, resulting in bronchoconstriction. Therefore, asthmatics may have
relative beta-adrenergic hyporesponsiveness and an imbalance between adrenergic and
cholinergic regulation that favor the latter, resulting in greater than normal mediator
generation and unopposed bronchoconstriction.
Go to:
Clinical Significance
Although most patients presenting with acute asthma can be readily recognized and
diagnosed, the clinician must always be cognizant that "all that wheezes is not asthma."
Almost any respiratory disorder that leads to airway narrowing or obstruction can be
associated with wheezing. The differential diagnosis of wheezing is long (Table 37.2) and, at
times, complicated, particularly if asthma coexists with another pulmonary disease.

Table 37.2
Differential Diagnosis of Wheezing.
Wheezing may be acute or chronic (recurrent) in children with nonasthmatic disorders. Acute
wheezing in small children suggests bronchiolitis, particularly if the child was well prior to an
upper respiratory tract infection (frequently respiratory syncytial virus) and has relatively
irreversible airway obstruction without evidence of atopy. Many children with acute
bronchiolitis may develop asthma; the long-term course of the illness may be the best
diagnostic determinant because bronchiolitis does not usually recur. In a child, wheezing that
is most prominent during inspiration suggests laryngotracheobronchitis (croup), epiglottitis,
aspiration of a foreign body, or congenital laryngeal or tracheal narrowing. Wheezing occurs
during both inspiration and expiration as the airway caliber becomes increasingly smaller.
Wheezing may become confused with stridor, which is a high-pitched musical or "crowing"
sound localized in the larynx or trachea. Chronic wheezing and respiratory infections in a
child should raise the possibility of cystic fibrosis, with or without gastrointestinal
complaints.
Adults with a new onset of wheezing generally have different nonasthmatic disorders from
those in children. In adults, stridor or localized wheezing may be caused by mechanical
obstruction of a central airway, such as by a tumor, foreign body (especially food), goiter, or
stenosis. In addition to laryngeal edema (resulting from angioedema or anaphylaxis) and
vocal cord paralysis, some individuals may have spastic adduction of the vocal cords due to
functional or psychological factors. Wheezing in combination with productive cough and/or
exertional dyspnea is not infrequent in chronic bronchitis or emphysema. Some patients may
have increased wheezing during the early morning hours ("nocturnal asthma") as a result of
congestive heart failure with pulmonary edema ("cardiac asthma"), gastric aspiration, or
sinusitis in which the recumbent position during sleep promotes pulmonary sequelae.
Transient wheezing occurs in some patients with pulmonary embolism, the carcinoid
syndrome, and systemic mastocytosis as a result of the release of bronchoactive amines or
mediators. Parenchymal lung disorders such as sarcoidosis, extrinsic allergic alveolitis, and
the adult respiratory distress syndrome (non-cardiogenic pulmonary edema) can occasionally
produce wheezing due to airway compromise by granulomas or edema fluid, release of
mediators, or underlying asthma. A large group of diseases characterized by pulmonary
infiltrates and peripheral blood eosinophilia may produce asthma-like wheezing: Loeffler's
syndrome, chronic eosinophilic pneumonia, tropical eosinophilia, hypereosinophilic
syndrome, various vasculitides, and allergic bronchopulmonary aspergillosis.

Macam-macam asthma
Extrinsic (allergic) asthma commonly occurs in young patients who have other allergic or
atopic disorders, as well as a family history of asthma and/or atopy. A specific, often seasonal
antigen characteristically produces a type I hypersensitivity reaction, resulting in paroxysmal
bronchoconstriction. Eosinophils in the sputum, eosinophilia, increased IgE, and positive skin
tests for immediate hypersensitivity are common findings.
Intrinsic (nonallergic or infective) asthma occurs primarily in adulthood (more than 30 years
of age) and is not usually associated with atopy, seasons, eosinophilia, increased IgE, or
positive skin tests. These patients are hyperreactive to a wide variety of stimuli and have
some intrinsic abnormality of bronchomotor tone. In many patients the onset of asthma is
preceded by an upper respiratory infection, and asthmatic symptoms tend to persist for years
with variations in severity rather than asymptomatic remissions.
Asthmatic bronchitis occurs in elderly, nonatopic patients who have a long or heavy smoking
history and active chronic cough and sputum production with superimposed hyperreactive
airways. The latter is supported by partial reversal of airway obstruction by
bronchoconstriction during inhalation challenge with methacholine or histamine. Sinusitus
and sputum rich in polymorphonuclear leukocytes (rather than eosinophils) are frequently
present. Allergy evaluation is negative.
Exercise-induced asthma occurs in the majority of asthmatic patients who exercise (e.g.,
running, cycling). Wheezing and dyspnea characteristically develop shortly after completion
of a sustained physical activity and may be the only symptoms of asthma. The severity of the
symptoms depends on the duration and type of exercise and how recently the individual
previously exercised. This phenomenon is caused by respiratory heat or water loss, which
then releases mast cell mediators.
Drug-induced asthma occurs in patients shortly after exposure to certain medications (e.g.,
propranolol, timolol, aspirin, nonsteroidal anti-inflammatory agents, cholinergic drugs),
additives (e.g., tartrazine, metabisulfite, alcohol), or certain medical procedures (e.g., studies
using iodinated radiographic contrast dyes, hemodialysis). A patient with wheezing
temporally related to aspirin ingestion, rhinitis, and nasal polyps suggests aspirin
hypersensitivity. Foods may also contain potentially asthmagenic chemicals, such as
monosodium glutamate and bisulfite preservative. In general, asthma related to these agents
does not appear to have an immunologic mechanism and is more frequent in adult, nonatopic
asthmatic patients.
Occupational asthma may be provoked in susceptible individuals following exposure to
irritants present in a work setting or at home. The list of occupations and related asthmagenic
substances used or generated is long and continually expanding. A further discussion is
presented in Chapter 41, Environmental Inhalation.

Variant or atypical asthma occurs in some patients who present without wheezing but with
acute or chronic cough or dyspnea as the sole symptom of asthma. Paroxysms of cough or
dyspnea may or may not be related to a specific stimulus, season, time of day, activity,
postnasal drip, or respiratory infection. Asthmatic patients with cough as the major or only
symptom develop bronchoconstriction localized primarily in the central or large airways
where subepithelial cough receptors abound and reflex bronchoconstriction occurs following
exposure to various stimuli. Patients complaining of episodic dyspnea have involvement
predominantly in the peripheral airways where bronchoconstriction, mucosal edema, and
secretion contribute to the airway obstruction. Although most patients with atypical asthma
are adults, the physical examination and routine pulmonary functions tests are not helpful
(usually normal), making the diagnosis difficult and confusing. The diagnosis must begin
with a high index of suspicion. It is supported by the patient's response during an inhalation
challenge with methacholine or histamine and/or an empirical trial of bronchodilators. This
subgroup of asthmatics emphasizes the fact that wheezing is not always a cardinal
manifestation of asthma.
http://www.ncbi.nlm.nih.gov/books/NBK358/

Pulmonary function tests

Pulmonary function tests are a group of tests that measure how well the lungs take
in and release air and how well they move gases such as oxygen from the
atmosphere into the body's circulation.

How the Test is Performed

Spirometry measures airflow. By measuring how much air you exhale, and how
quickly, spirometry can evaluate a broad range of lung diseases. In a spirometry test,
while you are sitting, you breathe into a mouthpiece that is connected to an
instrument called a spirometer. The spirometer records the amount and the rate of
air that you breathe in and out over a period of time. When standing, some numbers
might be slightly different. The most important issue is to perform the test always
while at the same position.
For some of the test measurements, you can breathe normally and quietly. Other
tests require forced inhalation or exhalation after a deep breath. Sometimes you will
be asked to inhale the substance or a medicine to see how it changes your test
results.
Lung volume measurement can be done in two ways:

The most accurate way is to sit in a sealed, clear box that looks like a
telephone booth (body plethysmograph) while breathing in and out into a
mouthpiece. Changes in pressure inside the box help determine the lung volume.

Lung volume can also be measured when you breathe nitrogen or helium gas
through a tube for a certain period of time. The concentration of the gas in a
chamber attached to the tube is measured to estimate the lung volume.
To measure diffusion capacity, you breathe a harmless gas, called a tracer gas, for a
very short time, often for only one breath. The concentration of the gas in the air you
breathe out is measured. The difference in the amount of gas inhaled and exhaled
measures how effectively gas travels from the lungs into the blood. This test allows
the doctor to estimate how well the lungs move oxygen from the air into the
bloodstream.

How to Prepare for the Test

Do not eat a heavy meal before the test. Do not smoke for 4 to 6 hours before the
test. You will get specific instructions if you need to stop using bronchodilators or
inhaler medications. You may have to breathe in medication before or during the
test.

How the Test will Feel

Since the test involves some forced breathing and rapid breathing, you may have
some temporary shortness of breath or light-headedness. You breathe through a
tight-fitting mouthpiece and you will have nose clips. If you are claustrophobic, the
clear box part of the test may feel uncomfortable.

Why the Test is Performed

Pulmonary function tests are done to:

Diagnose certain types of lung disease (such as asthma, bronchitis, and

emphysema)
Find the cause of shortness of breath
Measure whether exposure to chemicals at work affects lung function
Check lung function before someone has surgery
It also can be done to:

Assess the effect of medication

Measure progress in disease treatment

Normal Results

Normal values are based upon your age, height, ethnicity, and gender. Normal
results are expressed as a percentage. A value is usually considered abnormal if it is
less than 80% of your predicted value.
Normal value ranges may vary slightly among different laboratories. Talk to your
doctor about the meaning of your specific test results.
Different measurements that may be found on your report after pulmonary function
tests include:

Diffusion capacity to carbon monoxide (DLCO)

Expiratory reserve volume (ERV)

Forced vital capacity (FVC)

Forced expiratory volume (FEV)

Forced expiratory flow 25% to 75%

Functional residual capacity (FRC)

Maximum voluntary ventilation (MVV)

Residual volume (RV)

Peak expiratory flow (PEF).

Slow vital capacity (SVC)

Total lung capacity (TLC)

What Abnormal Results Mean

Abnormal results usually mean that you may have chest or lung disease.
Some lung diseases (such as emphysema, asthma, chronic bronchitis, and infections)
can make the lungs contain too much air and take longer to empty. These lung
diseases are called obstructive lung disorders.
Other lung diseases make the lungs scarred and smaller so that they contain too
little air and are poor at transferring oxygen into the blood. Examples of these types
of illnesses include:

Extreme overweight

Fibrosis of the lungs

Lung cancer

Sarcoidosis and scleroderma

Muscular weakness can also cause abnormal test results, even if the lungs are
normal, similar to the diseases that cause smaller lungs

Risks
The risk is minimal for most people. There is a small risk of collapsed
lung (pneumothorax) in people with a certain type of lung disease. The test should
not be given to a person who has experienced a recent heart attack, has certain
other types of heart disease, or has had a recent collapsed lung.

https://www.nlm.nih.gov/medlineplus/ency/article/003853.htm
FAAL PARU
Umumnya penderita asma sulit menilai beratnya gejala dan persepsi mengenai
asmanya , demikian pula dokter tidak selalu akurat dalam menilai dispnea dan mengi;
sehingga dibutuhkan pemeriksaan objektif yaitu faal paru antara lain untuk menyamakan
persepsi dokter dan penderita, dan parameter objektif menilai berat asma. Pengukuran faal
paru digunakan untuk menilai:

obstruksi jalan napas

reversibiliti kelainan faal paru

variabiliti faal paru, sebagai penilaian tidak langsung hiperes-ponsif jalan napas
Banyak parameter dan metode untuk menilai faal paru, tetapi yang telah diterima secara luas
(standar) dan mungkin dilakukan adalah pemeriksaan spirometri dan arus puncak ekspirasi
(APE).
Spirometri
Pengukuran volume ekspirasi paksa detik pertama (VEP 1) dan kapasiti vital paksa
(KVP) dilakukan dengan manuver ekspirasi paksa melalui prosedur yang
standar. Pemeriksaan itu sangat bergantung kepada kemampuan penderita sehingga
dibutuhkan instruksi operator yang jelas dan kooperasi penderita. Untuk mendapatkan
nilai yang
akurat,
diambil
nilai
tertinggi
dari 2-3
nilai
yang reproducible danacceptable. Obstruksi jalan napas diketahui dari nilai rasio VEP1/ KVP
< 75% atau VEP1 < 80% nilai prediksi.
Manfaat pemeriksaan spirometri dalam diagnosis asma :

Obstruksi jalan napas diketahui dari nilai rasio VEP 1/ KVP < 75% atau VEP1 < 80%
nilai prediksi.

Reversibiliti, yaitu perbaikan VEP1 15% secara spontan, atau setelah inhalasi
bronkodilator (uji bronkodilator), atau setelah pemberian bronkodilator oral 10-14 hari,
atau setelah pemberian kortikosteroid (inhalasi/ oral) 2 minggu. Reversibiliti ini dapat
membantu diagnosis asma

Menilai derajat berat asma

Arus Puncak Ekspirasi (APE)

Nilai APE dapat diperoleh melalui pemeriksaan spirometri atau pemeriksaan yang lebih
sederhana yaitu dengan alat peak expiratory flow meter (PEF meter) yang relatif sangat
murah, mudah dibawa, terbuat dari plastik dan mungkin tersedia di berbagai tingkat layanan
kesehatan termasuk puskesmas ataupun instalasi gawat darurat. Alat PEF meter relatif mudah
digunakan/ dipahami baik oleh dokter maupun penderita, sebaiknya digunakan penderita di
rumah sehari-hari untuk memantau kondisi asmanya. Manuver pemeriksaan APE dengan
ekspirasi paksa membutuhkan koperasi penderita dan instruksi yang jelas.
Manfaat APE dalam diagnosis asma

Reversibiliti, yaitu perbaikan nilai APE 15% setelah inhalasi bronkodilator (uji
bronkodilator), atau bronkodilator oral 10-14 hari, atau respons terapi kortikosteroid
(inhalasi/ oral , 2 minggu)

Variabiliti, menilai variasi diurnal APE yang dikenal dengan variabiliti APE harian
selama 1-2 minggu. Variabiliti juga dapat digunakan menilai derajat berat penyakit
(lihat klasifikasi)
Nilai APE tidak selalu berkorelasi dengan parameter pengukuran faal paru lain, di samping
itu APE juga tidak selalu berkorelasi dengan derajat berat obstruksi. Oleh karenanya
pengukuran nilai APE sebaiknya dibandingkan dengan nilai terbaik sebelumnya, bukan nilai
prediksi normal; kecuali tidak diketahui nilai terbaik penderita yang bersangkutan..
Cara pemeriksaan variabiliti APE harian
Diukur pagi hari untuk mendapatkan nilai terendah, dan malam hari untuk
mendapatkan nilai tertinggi. Rata-rata APE harian dapat diperoleh melalui 2 cara :

Bila sedang menggunakan bronkodilator, diambil variasi/ perbedaan nilai APE pagi
hari sebelum bronkodilator dan nilai APE malam hari sebelumnya sesudah
bronkodilator. Perbedaan nilai pagi sebelum bronkodilator dan malam sebelumnya
sesudah bronkodilator menunjukkan persentase rata-rata nilai APE harian. Nilai > 20%
dipertimbangkan sebagai asma.
APE malam - APE pagi
Variabiliti harian = -------------------------------------------- x 100 %
(APE malam + APE pagi)

Metode lain untuk menetapkan variabiliti APE adalah nilai terendah APE pagi sebelum
bronkodilator selama pengamatan 2 minggu, dinyatakan dengan persentase dari nilai
terbaik (nilai tertinggi APE malam hari).
Contoh :
Selama 1 minggu setiap hari diukur APE pagi dan malam , misalkan didapatkan APE
pagi terendah 300, dan APE malam tertinggi 400; maka persentase dari nilai terbaik (%
of the recent best) adalah 300/ 400 = 75%. Metode tersebut paling mudah dan mungkin
dilakukan untuk menilai variabiliti.

PERAN PEMERIKSAAN LAIN UNTUK DIAGNOSIS

Uji Provokasi Bronkus

Uji provokasi bronkus membantu menegakkan diagnosis asma. Pada

penderita dengan gejala asma dan faal paru normal sebaiknya dilakukan uji
provokasi bronkus . Pemeriksaan uji provokasi bronkus mempunyai
sensitiviti yang tinggi tetapi spesifisiti rendah, artinya hasil negatif dapat
menyingkirkan diagnosis asma persisten, tetapi hasil positif tidak selalu
berarti bahwa penderita tersebut asma. Hasil positif dapat terjadi pada
penyakit lain seperti rinitis alergik, berbagai gangguan dengan penyempitan
jalan napas seperti PPOK, bronkiektasis dan fibrosis kistik.

Pengukuran Status Alergi

Komponen alergi pada asma dapat diindentifikasi melalui pemeriksaan
uji kulit atau pengukuran IgE spesifik serum. Uji tersebut mempunyai nilai
kecil untuk mendiagnosis asma, tetapi membantu mengidentifikasi faktor
risiko/ pencetus sehingga dapat dilaksanakan kontrol lingkungan dalam
penatalaksanaan.
Uji kulit adalah cara utama untuk mendiagnosis status
alergi/atopi, umumnya dilakukan dengan prick test. Walaupun uji kulit
merupakan cara yang tepat untuk diagnosis atopi, tetapi juga dapat
menghasilkan positif maupun negatif palsu. Sehingga konfirmasi terhadap
pajanan alergen yang relevan dan hubungannya dengan gejala harus selalu
dilakukan. Pengukuran IgE spesifik dilakukan pada keadaan uji kulit tidak
dapat dilakukan (antara lain dermatophagoism, dermatitis/ kelainan kulit pada
lengan tempat uji kulit, dan lain-lain). Pemeriksaan kadar IgE total tidak
mempunyai nilai dalam diagnosis alergi/ atopi.

DIAGNOSIS BANDING
Diagnosis banding asma antara lain sbb :

Dewasa

Penyakit Paru Obstruksi Kronik

Bronkitis kronik
Gagal Jantung Kongestif
Batuk kronik akibat lain-lain
Disfungsi larings
Obstruksi mekanis (misal tumor)
Emboli Paru

Anak

Benda asing di saluran napas

Laringotrakeomalasia
Pembesaran kelenjar limfe
Tumor
Stenosis trakea
Bronkiolitis

Pemeriksaan faal paru

Pemeriksaan faal paru yang umumnya dapat dilakukan pada penderita usia di atas 5
tahun adalah untuk diagnosis, menilai berat asma, dan selain itu penting untuk memonitor
keadaan asma dan menilai respons pengobatan. Penilaian yang buruk mengenai berat asma
adalah salah satu penyebab keterlambatan pengobatan yang berakibat meningkatnya
morbiditi dan mortaliti. Pemeriksaan faal paru pada asma dapat dianalogkan dengan
pemeriksaan tekanan darah pada hipertensi , atau pemeriksaan kadar gula darah pada diabetes
melitus. Dengan kata lain pemeriksaan faal paru adalah parameter objektif dan pemeriksaan
berkala secara teratur mutlak dilakukan.
Spirometri
Sebaiknya spirometri dilakukan pada :
1.
awal penilaian / kunjungan pertama
2.
setelah pengobatan awal diberikan, bila gejala dan APE telah stabil
3.
pemeriksaan berkala 1 - 2 tahun untuk menilai perubahan fungsi jalan
atau lebih sering bergantung berat penyakit dan respons pengobatan.

napas,

Manfaat lain pemeriksaan spirometri berkala :

1.
Bila dilakukan berkala, setahun sekali, untuk menilai akurasi peak flow meter
2.
Bila diinginkan ketepatan pengukuran faal paru, misalnya evaluasi respons
bronkodilator pada uji provokasi bronkus, menilai respons tindakan step down
therapy pada pengobatan (lihat tahapan penanganan asma)
3.
Bila hasil pemeriksaan APE dengan peak flow meter tidak dapat dipercaya, misalnya
pada penderita anak, orangtua, terdapat masalah neuromuskular atau ortopedik,
sehingga dibutuhkan konfirmasi dengan pemeriksaan spirometri.
Pemantauan Arus Puncak Ekspirasi (APE) dengan Peak Flow Meter
Monitoring APE penting untuk menilai berat asma, derajat variasi diurnal, respons
pengobatan saat serangan akut, deteksi perburukan asimptomatik sebelum menjadi serius,
respons pengobatan jangka panjang, justifikasi objektif dalam memberikan pengobatan dan
identifikasi pencetus misalnya pajanan lingkungan kerja.
Pemeriksaan APE mudah, sederhana, kuantitatif dan reproducible untuk menilai ada
dan berat obstruksi jalan napas. Peak flow meter relatif murah dan dapat dibawa kemanamana, sehingga pemeriksaan itu tidak hanya dapat dilakukan di klinik, rumah sakit tetapi
dapat dilakukan di fasiliti layanan medik sederhana (puskesmas), praktek dokter bahkan di
rumah penderita. Pengukuran APE membutuhkan instruksi yang jelas bila perlu dengan
demonstrasi yang berulang (lihat teknik pemeriksaan APE dengan peak flow meter, lampiran
1).
Pengukuran APE dianjurkan pada:
1.
Penanganan serangan akut di darurat gawat, klinik, praktek dokter, dan oleh
penderita di rumah
2.
Pemantauan berkala di rawat jalan, klinik, praktek dokter
3.
Pemantauan sehari-hari di rumah, idealnya dilakukan pada asma persisten usia di
atas > 5 tahun, terutama bagi penderita setelah perawatan di rumah sakit, penderita
yang sulit/ tidak mengenal perburukan melalui gejala padahal berisiko tinggi untuk
mendapat serangan yang mengancam jiwa.
Interpretasi pengukuran APE

Nilai prediksi APE didapat berdasarkan usia, tinggi badan, jenis kelamin dan ras, serta
batasan normal variabiliti diurnal berdasarkan literatur. Tetapi pada umumnya penderita asma
mempunyai nilai APE di atas atau di bawah rata-rata nilai-nilai prediksi tersebut. Sehingga
direkomendasikan, objektif APE terhadap pengobatan adalah berdasarkan nilai terbaik
masing-masing penderita, demikian pula variabiliti harian penderita, daripada berdasarkan
nilai normal/prediksi. Setiap penderita mempunyai nilai terbaik yang berbeda walaupun sama
berat badan, tinggi badan, dan jenis kelamin. Penting untuk mendapat nilai terbaik tersebut,
karena rencana pengobatan sebaiknya berdasarkan nilai terbaik, bukan nilai prediksi. Kecuali
pada keadaan sulit mendapatkan nilai terbaik, misalnya penderita tidak dapat melakukan
sendiri di rumah, asma sulit terkontrol dan sebagainya ; maka dapat digunakan nilai prediksi,
lihat nilai prediksi orang Indonesia (lampiran 2).
Nilai terbaik APE dengan peak flow meter
Mendapatkan nilai APE terbaik dan variabiliti harian yang minimum adalah saat
penderita dalam pengobatan efektif dan kondisi asma terkontrol, dilakukan pengukuran APE
pagi dan malam setiap hari selama 2 minggu. Pada masing-masing pengukuran dilakukan
manuver 3 kali dan diambil nilai tertinggi, jika dalam pengobatan bronkodilator maka
pengukuran APE dilakukan sebelum dan sesudah bronkodilator. Nilai APE terbaik adalah
nilai APE tertinggi yang dapat dicapai selama periode penilaian (2 minggu) tersebut, saat
dalam pengobatan efektif dan asma terkontrol. Bila nilai APE terbaik yang didapat <80%
prediksi walau setelah bronkodilator, atau variabiliti harian > 20% (setelah bronkodilator);
maka pengobatan agresif diberikan untuk mendapatkan nilai terbaik dan monitor harian
dilanjutkan. Pengobatan agresif adalah steroid oral 30 mg /hari selama 5-10 hari selain
pengobatan rutin lainnya sesuai berat asma. Dalam pengobatan agresif tersebut, monitor APE
dilanjutkan dan diambil nilai APE tertinggi sebagai nilai APE terbaik (personal best).
Variabiliti harian
Variabiliti APE merupakan petunjuk stabiliti dan berat asma. Salah satu metode yang
digunakan adalah nilai APE harian yaitu perbedaan nilai APE pagi dan nilai APE malam
sebelumnya. Metode lain adalah APE minimum pagi selama 2 minggu menunjukkan % the
recent best (lihat diagnosis), adalah petunjuk terbaik menilai labiliti jalan napas karena
dilakukan setiap hari, berkorelasi dengan hiperesponsif jalan napas dan perhitungannya
mudah.
Penggunaan APE untuk pengelolaan asma mandiri
Untuk membantu pengelolaan asma dengan peran aktif penderita (asma mandiri) dapat
digunakan sistem zona (pelangi asma). Sistem ini berkorelasi dengan pengukuran APE dan
variabiliti harian dengan pengobatan yang sesuai untuk mendapatkan asma terkontrol. Setiap
zona (daerah warna) ditetapkan sebagai fungsi dari nilai terbaik atau nilai
prediksi, berdasarkan nilai APE tertinggi atau variabilitinya. Penekanan bukan semata-mata
kepada membacanya, tetapi lebih kepada variabilitinya dari nilai terbaik atau dari waktu satu
ke waktu lainnya.
Pada asma mandiri pengukuran APE dapat digunakan untuk membantu kesepakatan dokter
dan penderita dalam pengobatan /self medication seperti:

Mengetahui apa yang membuat asma memburuk

Memutuskan apa yang akan dilakukan bila rencana pengobatan berjalan baik

Memutuskan apa yang akan dilakukan jika dibutuhkan penambahan atau penghentian
obat

Memutuskan kapan penderita meminta bantuan medis/ dokter/ IGD

PENCEGAHAN
Pencegahan meliputi pencegahan primer yaitu mencegah tersensitisasi dengan
bahan yang menyebabkan asma, pencegahan sekunder adalah mencegah yang sudah
tersensitisasi untuk tidak berkembang menjadi asma; dan pencegahan tersier adalah
mencegah agar tidak terjadi serangan / bermanifestasi klinis asma pada penderita yang sudah
menderita asma.
Pencegahan Primer
Perkembangan respons imun jelas menunjukkan bahwa periode prenatal dan perinatal
merupakan periode untuk diintervensi dalam melakukan pencegahan primer penyakit asma.
Banyak faktor terlibat dalam meningkatkan atau menurunkan sensitisasi alergen pada fetus,
tetapi pengaruh faktor-faktor tersebut sangat kompleks dan bervariasi dengan usia gestasi,
sehingga pencegahan primer waktu ini adalah belum mungkin. Walau penelitian ke arah itu
terus berlangsung dan menjanjikan.
Periode prenatal
Kehamilan trimester ke dua yang sudah terbentuk cukup sel penyaji antigen (antigen
presenting cells) dan sel T yang matang, merupakan saat fetus tersensisitasi alergen dengan
rute yang paling mungkin adalah melalui usus, walau konsentrasi alergen yang dapat
penetrasi ke amnion adalah penting. Konsentrasi alergen yang rendah lebih mungkin
menimbulkan sensitisasi daripada konsentrasi tinggi. Faktor konsentrasi alergen dan waktu
pajanan sangat mungkin berhubungan dengan terjadinya sensitisasi atau toleransi imunologis.
Penelitian menunjukkan menghindari makanan yang bersifat alergen pada ibu hamil
dengan risiko tinggi, tidak mengurangi risiko melahirkan bayi atopi, bahkan makanan
tersebut menimbulkan efek yang tidak diharapkan pada nutrisi ibu dan fetus. Saat ini, belum
ada pencegahan primer yang dapat direkomendasikan untuk dilakukan.
Periode postnatal
Berbagai upaya menghindari alergen sedini mungkin dilakukan terutama difokuskan
pada makanan bayi seperti menghindari protein susu sapi, telur, ikan, kacang-kacangan.
Sebagian besar studi menunjukkan mengenai hal tersebut, menunjukkan hasil yang
inkonklusif (tidak dapat ditarik kesimpulan). Dua studi dengan tindak lanjut yang paling lama
menunjukkan efek transien dari menghindari makanan berpotensi alergen dengan dermatitis
atopik. Dan tindak lanjut lanjutan menunjukkan berkurangnya bahkan hampir tidak ada efek
pada manifestasi alergik saluran napas, sehingga disimpulkan bahwa upaya menghindari
alergen makanan sedini mungkin pada bayi tidak didukung oleh hasil. Bahkan perlu
dipikirkan memanipulasi dini makanan berisiko menimbulkan gangguan tumbuh kembang.
Diet menghindari antigen pada ibu menyusui risiko tinggi, menurunkan risiko
dermatitis atopik pada anak, tetapi dibutuhkan studi lanjutan (bukti C).
Menghindari aeroelergen pada bayi dianjurkan dalam upaya menghindari sensitisasi.
Akan tetapi beberapa studi terakhir menunjukkan bahwa menghindari pajanan dengan kucing
sedini mungkin, tidak mencegah alergi; dan sebaliknya kontak sedini mungkin dengan kucing
dan anjing kenyataannya mencegah alergi lebih baik daripada menghindari binatang tersebut.
Penjelasannya sama dengan hipotesis hygiene, yang menyatakan hubungan dengan mikrobial
sedini mungkin menurunkan penyakit alergik di kemudian hari. Kontroversi tersebut

mendatangkan pikiran bahwa strategi pencegahan primer sebaiknya didesain dapat menilai
keseimbangan sel Th1dan Th2, sitokin dan protein-protein yang berfusi dengan alergen.
Pencegahan primer di masa datang akan berhubungan imunomodulasi menggunakan sel
Th1 ajuvan, vaksin DNA, antigen yang berkaitan dengan IL-12 atau IFN-, pemberian
mikroorganisme usus yang relevan melalui oral (berhubungan dengan kolonisasi flora
mikrobial usus). Semua strategi tersebut masih sebagai hipotesis dan membutuhkan
penelitian yang tepat.
Asap rokok lingkungan (Enviromental tobacco smoke/ ETS)
Berbagai studi dan data menunjukkan bahwa ibu perokok berdampak pada kesakitan
saluran napas bawah pada anaknya sampai dengan usia 3 tahun, walau sulit untuk
membedakan kontribusi tersebut pada periode prenatal atau postnatal. Berbagai studi
menunjukkan bahwa ibu merokok selama kehamilan akan mempengaruhi perkembangan
paru anak, dan bayi dari ibu perokok, 4 kali lebih sering mendapatkan gangguan mengi dalam
tahun pertama kehidupannya.Sedangkan hanya sedikit bukti yang mendapatkan bahwa ibu
yang merokok selama kehamilan berefek pada sensitisasi alergen. Sehingga disimpulkan
merokok dalam kehamilan berdampak pada perkembangan paru, meningkatkan frekuensi
gangguan mengi nonalergi pada bayi, tetapi mempunyai peran kecil pada terjadinya asma
alergi di kemudian hari. Sehingga jelas bahwa pajanan asap rokok lingkungan baik periode
prenatal maupun postnatal (perokok pasif) mempengaruhi timbulnya gangguan/ penyakit
dengan mengi (bukti A).
Pencegahan sekunder
Sebagaimana di jelaskan di atas bahwa pencegahan sekunder mencegah yang sudah
tersensitisasi untuk tidak berkembang menjadi asma. Studi terbaru mengenai pemberian
antihitamin H-1 dalam menurunkan onset mengi pada penderita anak dermatitis atopik. Studi
lain yang sedang berlangsung, mengenai peran imunoterapi dengan alergen spesifik untuk
menurunkan onset asma.
Pengamatan pada asma kerja menunjukkan bahwa menghentikan pajanan alergen sedini
mungkin pada penderita yang sudah terlanjur tersensitisasi dan sudah dengan gejala asma,
adalah lebih menghasilkan pengurangan /resolusi total dari gejala daripada jika pajanan terus
berlangsung.
Pencegahan Tersier
Sudah asma tetapi mencegah terjadinya serangan yang dapat ditimbulkan oleh
berbagai jenis pencetus. Sehingga menghindari pajanan pencetus akan memperbaiki kondisi
asma dan menurunkan kebutuhan medikasi/ obat.