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Timișoara 2019


Authors (in alphabetical order):

Bălă Gabriel, MD, PhD student, pneumology resident doctor

Bertici Nicoleta, MD, PhD, Senior Lecturer

Ciucă Ioana, MD, PhD, Senior Lecturer

Crișan Alexandru, MD, PhD, Associate Professor

Fira-Mlădinescu Ovidiu, MD, PhD, Associate Professor

Frenț Ștefan, MD, PhD, Assistant Professor

Hogea Patricia, MD, PhD student, pneumology resident doctor

Manolescu Diana, MD, PhD, Associate Assistant Professor

Marc Monica, MD, PhD, Associate Assistant Professor

Mihăicuță Ștefan, MD, PhD, Senior Lecturer

Mihuța Camil, pneumology resident doctor

Oancea Cristian, MD, PhD, Professor

Pescaru Camelia, MD, PhD, Assistant Professor

Pop Liviu-Laurențiu, MD, PhD, Professor

Porojan-Suppini Noemi, MD, PhD student, Associate Assistant Professor

Socaci Adriana, MD, Phd, Tuberculosis Department Coordiantor

Țiplea Cosmin, MD, specialist pneumology doctor

Trăilă Daniel, MD, PhD, Assistant Professor

Tudorache Emanuela, MD, PhD, Associate Assistant Professor

Tudorache Voicu, MD, PhD, Professor


Editura „Victor Babeș‟

Piața Eftimie Murgu 2, cam 316, 300041 Timișoara Tel./Fax: 0256495210

e-mail:[email protected] www.umft.ro/editura

Director general: Prof. univ. emerit dr. Dan V. Poenaru Director: Prof. univ. dr. Andrei Motoc

Colecția: MANUALE

Coordonator colecție: Prof.univ.dr. Sorin Eugen Boia

© 2019 Toate drepturile asupra acestei ediții sunt rezervate.

Reproducerea parțială sau integrală a textului pe orice suport, fără acordul scris al autoarelor este interzisă și se va sancționa conform legilor în vigoare.

ISBN 978-606-786-157-0




(Emanuela Tudorache, Noemi Porojan-Suppini) ... 5

2. FUNCTIONAL PULMONARY EXPLORATION IN CLINICAL PRACTICE (Ovidiu Fira-Mladinescu, Emanuela Tudorache, Noemi Porojan-Suppini) ... 18


4. RESPIRATORY FAILURE (Ovidiu Fira-Mlădinescu, Noemi Porojan-Suppini) ... 40

5. BRONCHIAL ASTHMA OF ADULT (Voicu Tudorache, Camil Mihuța) ... 50



8. PULMONARY ABCESS (Patricia Hogea, Cristian Oancea) ... 96

9. CYSTIC ECHINOCOCCOSIS (Patricia Hogea, Oancea Cristian) ... 102

10. BRONCHIECTASIS (Voicu Tudorache, Cosmin Țiplea) ... 106

11. CYSTIC FIBROSIS (Ioana Ciucă, Liviu-Laurentiu Pop, Cosmin Țiplea) ... 113

12. PLEURAL EFFUSIONS (Ștefan Frenț, Ștefan Mihaicuță) ... 120

13. LUNG CANCER (Emanuela Tudorache, Bălă Gabriel) ... 133

14. SLEEP DISORDERED BREATHING (Ștefan Mihaicuță) ... 133

15. IDIOPATHIC PULMONARY FIBROSIS (Daniel Trailă, Manolescu Diana) ... 149


17. SARCOIDOSIS (Camelia Pescaru) ... 165

18. TUBERCULOSIS (Adriana Socaci) ... 173

19. PULMONARY EMBOLISM (Noemi Porojan-Suppini, Voicu Tudorache) ... 214


21. PULMONARY REHABILITATION (Cristian Oancea, Patricia Hogea) ... 241





… Like all other men,

… Like some other men,

… Like no other man”

(Kluckhohn C, Murray HA., Personality in Nature, Society and Culture., 1948)

I. Anamnesis and physical examination of the patient with respiratory pathology

A careful and complete medical history completed with a thorough clinical examination, are the strengths of a good clinician. For a correct diagnosis, it is important to continue collecting anamnestic information as they become available.

1. Major pulmonary symptoms:

Dyspnea is described by the patient as "shortness of breath", "choking sensation", "inability to draw air in the chest", "fatigue"; According to ATS (American Thoracic Society) dyspnea is a subjective perception of respiratory distress, variable in intensity, consisting of qualitatively distinct sensations.

- The Borg Scale, and questionnaires, such as the mMRC (Modified Medical Research Council) Dyspnea Scale (Table 1) and Pulmonary Functional Status and Dyspnea Questionnaire can be evaluated.

Table 1. mMRC (Modified Medical Research Council) Dyspnea Scale 0 Dyspnea from intense physical effort

1 Dyspnea from sustained walking or on easy slope

2 Dyspnea prevents walking at the same pace with an individual of the same age or requires stops on a flat ground

3 Important dyspnea that requires stops after 100m or a few minutes of walking on flat ground

4 Severe dyspnea in daily activities (getting dressed)

It can be determined by cardiac, pulmonary, neuromuscular, metabolic, hematological pathologies. Figure 1 shows the dyspnea diagnosis algorithm


Figure 1. The diagnostic algorithm for dyspnea

Cough is an essential reflex mechanism (abrupt expiration with closed glottis), with the protective role of the airways from harmful substances, and the protective role of the lungs by draining excess secretions.

Figure 2. Cough diagnosis algorithm


In the evaluation of a coughing patient, special attention is paid to the following aspects: whether the onset is acute or chronic, whether it is productive or not, the type and quantity of sputum, associated symptoms.

Hemoptysis - the elimination by cough of an amount of blood. When it appears de novo, it requires a thorough examination, including tomographic examination, bronchoscopy.

The quantity can be: small (under 50 ml), medium (50-100 ml), large (100-300 ml), massive (over 300 ml).

Differential diagnosis: haematemesis (digestive pathology, preceded by nausea, colored black- in coffee grounds, accompanied by alimentary content), posterior epistaxis (preceded by salty taste, eliminated by mouth without effort of vomit, highlighted by the objective examination on the posterior pharyngeal wall).

Figure 3. Algorithm for diagnosis of patients with hemoptysis

Chest pain

Figure 4. Diagnostic algorithm of the patient with chest pain


2 Family history: provides information on genetic diseases, such as cystic fibrosis, alpha 1- antitrypsin deficiency, Rendu-Osler's disease, imotile cilia syndrome, etc. Family exposure to contagious diseases such as tuberculosis can be identified.

3. History of smoking, other pollutants: the patient should be asked about the smoking habit, if he has ever smoked. If the answer is positive, you should ask when he started smoking, when he stopped smoking, how much he smoked, respectively about different forms of tobacco and exposure in the workplace or at home. In developing countries, steaming, smoke from cooking inside, wood burning stove can be a major risk factor for lung diseases, especially among women.

4. Medication and Allergies: To be noted the complete medication of the patient, possible allergic or toxic reactions that occurred to these drugs. Consumption of alcoholic beverages (their type and quantity) should also be asked and noted.

5. Occupational history: Identifying the relevant occupational exposure can lead to job change, thus preventing progressive and irreversible pulmonary destruction.

6 Travel history: Previous homes in endemic areas for fungal infections such as histoplasmosis or coccidioidomycosis may be helpful in diagnosis. A recent travel history may bring the disscussion of the possibility of contacting diseases specific to certain geographical areas.

II. Objective examination of the chest

Inspection: of the skin and soft tissue: scars, color changes, edema, tumor formation can be identified

Table 2. Chest deformities

Barrel chest - globular appearance (antero- posterior diameter = 1), obtuse xiphoid angle, raised shoulders, short neck, full subclavicular pits, horizontal ribs, wide intercostal spaces; met in COPD, BA.

Chest with sunken sternum (pectus excavatum) - sunken sternum in cone shape, the heart is rotated and pushed laterally.

Chicken chest (pectus carinatum) – sternum is shifted anteriorly, antero-posterior diameter isenlarged.

Thoracic kyphoscoliosis - abnormal curvature of the spine, rotation of the vertebrae.


Palpation: it is necessary for the examination of the breasts, lymph nodes, bone deformities (such as cervical rib, subcutaneous calcinosis, multiple sclerosis)

- palpation of respiratory enlargement

The patient positioned in orthostatism, the doctor is behind the patient, with the palms located on his chest wall, forming two skin folds between the patient's spine and the two police officers. At the time of inhale, the doctor's hands are drifted apart, the skin folds disappear, and in exhale they return to their original position

Figure 5. Palpation of respiratory enlargements:

A. Exhale; B. Inhale (According to Illustrated Guide for Respiratory System Examination, Dr. Farid Ghalli, 2016) When respiratory enlargements are diminished, the folds remain present even in inhale (apical:

tuberculosis, neoplasm, pahipleuritis; basal: pleurisy, pneumothorax, pahipleuritis, pneumonia, neuralgia).

- Palpation of the quiver of the chest: the patient positioned in orthostatic or sitting position, the doctor is behind the patient, with palms symmetrically palpating his chest wall while the patient will repeatedly say 33 (thirtythree). The quiver can be altered in bronchial obstructions, pulmonary emphysema, thick chest wall, pleurisy, pneumothorax.


This technique evaluates the loudness of the pulmonary parenchyma, by creating vibrations in the tissues. Maneuver: the doctor's left hand is applied to the patient's chest, with his fingers separated, the medius is placed in the intercostal space, parallel to the ribs, and with the medius of the right hand bent, the middle phalange of the left medius is percutted.

Figure 6. The sites of percussion and pulmonary auscultation (According to Illustrated Guide for Respiratory System Examination, Dr. Farid Ghalli, 2016)

Table 3. Percussion of the chest

Hipersonority Diffuse

Thin chest wall, Pulmonary emphysema Pneumothorax


Caverns, Evacuated cysts, Evacuated abscesses

dullness Fluid Pahipleuritis, Plural effusions

Lung condensation with free bronchitis

Pneumonia, Lung Infarction, Stasis Atelectasis

Auscultation: appreciation of the passage of air flow through the tracheobronchial tree and the parenchyma pulmonary; Maneuver : The patient breathes deeply, mouth open.


Breathing types Characteristics Causes

Apnea Prolonged breathing pauses Cardiac arrest Biot breathing Irregular breathing with long

apnea periods

Intracranial hypertension

Cheyne-Stokes breathing

Irregular type of breathing;

breath grows and decreases in depth and frequency

alternating with apnea periods

Central nervous system diseases; Congestive heart failure

Kussmaul breathing Deep and rapid breathing Metabolic acidosis Staccato breathing Prolonged inhale Cerebral injury Paradoxal breathing Partial or global movement

towards interior of the ribcage in inhale, and towards exterior in exhale

Chest trauma; Dyphragm paralysis; Muscular fatigue

Asthmatic breathing Prolonged exhale Airway obstruction

Physiological respiratory noises: physiological tubular blowing, broncho-vesicular respiration, vesicular murmur (MV).

A. Modification of vesicular murmur:

- Tight breathing: bronchiolitis, tachypnea

- Decreased MV: obstructive causes (high: foreign bodies, glotic edema associated with stridor, low: COPD, asthma crisis, endobronchial tumors associated with wheezing); restrictive causes:

pneumonia, diffuse interstitial pneumopathy, changes in the chest wall (kyphoscoliosis), small pleurisy, pneumothorax

- MV abolition: severe asthma attack with bronchoplegia, atelectasis, massive pleurisy, massive pneumothorax, massive pahipleuritis

B. Adventitious Breath sounds

Table 4. Pathological respiratory noises

Rales Friction rub

Bronchial rales

-in both times of the breath - modified by cough

Bronchovascular rales

- by bubbling the fluid from the alveoli / bronchioles / cavities

- by rubbing the two thickened pleural sheets on which fibrin was deposited

- does not change after coughing

In: pahipleuritis, after evacuation of pleural fluid, carcinomatous infiltration

Wheeze -high-pitched

Rhonchus - snoring character

Crackles - at the end of the inspiration

Subcrackles - at the beginning of the inspiration, in exhale

Bronchial asthma COPD

Bronchitis Bronchiectasis Pulmonary neoplasm Foreign bodies

Pneumonia Pulmonary infarction Diffuse interstitial pneumopathies

Bronchopneumonia Pulmonary stasis Bronchitis Bonchiectasis


Depending on the time of appearance, inspirational rales can be characterized as follows:

Inhale Exhale

Inhale Exhale

Inhale Exhale

A. Onset of inspiration:

COPD, chronic bronchitis , emphysema, asthma

B. End of inspiration: atelectasis, pneumonia, pulmonary edema, PID

C. Throughout the inspiration: severe pneumonia, severe bronchitis

Figure 7. Inhale rales

(adapted after Egan’s fundamentals of respiratory care, 8th ed.)

2. Elements of functional anatomy of the patient with respiratory pathology

The respiratory system consists of all the organs that contribute to the exchange of gases between the body and the external environment, ensuring their homeostasis. Table 1 shows the main functions of the respiratory system.

Table 5. Functions of the respiratory system

Function Effector

Breathing control Respiratory centers, peripheral chemoreceptors, afferent and efferent nerves

Ventilation pump Chest wall, pleura, respiratory musculature Distribution of ventilation Upper and inner airways, bronchioles Blood distribution Pulmonary arteries and veins, capillaries The gas exchange Terminal respiratory unit

Clearance and defense mechanisms

Mucociliary escalator, alveolar clearance, pulmonary lymphatics

1. Breathing control

The innervation of the lung is provided by the vegetative nervous system (the medullary center) through the anterior pulmonary nerve plexus and the posterior pulmonary nerve plexus.

The motor innervation represented by the sympathetic nervous system, more precisely by the postganglionic fibers, which provides the bronchodilating, vasodilating action, the relaxation of the bronchial muscles. Regarding the parasymaptic activity (performed by the Vagus nerve), it causes bronchoconstriction, vasoconstriction, mucus hypersecretion.

In certain situations, voluntary respiratory control may exceed the respiratory centers at the brain stem level, the orders start at the cortical level. Such examples are apneea, hyperventilation,


cases in which blood gas alterations may occur. Other examples are: voluntary coughing, singing, talking, measuring maneuvers of vital capacity.

Thoracic wall mechanoreceptors: compounds from receptors in the muscle fibers and tendons, measure and modulate the forces generated by the inspiratory effort.

Pulmonary mechanoreceptors: there are 3 types: irritation (located in the epithelium, producing bronchoconstriction, tachypnea in contact with pollutants), stretching (at the level of smooth muscles, respond to changes in lung volume), juxtacapillary (at the level of the alveolar wall, stimulation edema, fibrosis).

Chemoreceptors : detects changes in the level of PaO2, PaCO2, pH, sends signals to the respiratory centers to correct ventilation in case of changes in the metabolic needs of the body.

Table 6. PaO2, PaCO2 pressures

PaCO2 (mmHg) PaO2 (mmHg)

Hypoventilation 80 40

Normal 40 90

Hyperventilation 20 115

The effects of PaCO2 modification - carbon dioxide is the most important chemical stimulus in the regulation of respiration (the ventilation per minute increases with CO2 level). The chemoreceptors from the peripheral circulation and the CNS detect the differences and send signals to the associated respiratory centers, to correct the ventilation. The body's ability to store CO2 exceeds its oxygen storage capacity, so changes in the dynamics of ventilation will occur faster and will be more significant in the case of changing the PaO2 level.

The complete stop of the ventilation for 1 minute of a person (breathing in the air in the room), will cause the increase of 6-10 mmHg of PaC02 and the decrease of PaO2 by 40-50 mmHg.

The effects of PaO2 modification - hypoxia determine the increase of the ventilatory effort by stimulating the peripheral chemoreceptors at the carotid and aortic level, and at the central respiratory depression level.

Changing pH - both hydrogen ions (stimulates peripheral and central chemoreceptors) as well as changes in PaCO2 level change ventilation. Increased ventilation per minute can also be determined by decreasing the pH to constant PaCO2 values.

2. Ventilation pump

It is composed of the thoracic wall (spine, ribs, sternum, connected by ligaments and cartilages), respiratory musculature and pleural space.

The respiratory musculature is composed of the inspiratory muscles (diaphragm, inspiratory intercostal muscles, scalenes, sternocleidomastoids).

- Under normal conditions the expiration does not require active work of the musculature (internal intercostal muscles, abdominal wall musculature), but this may be necessary in pathological conditions such as obstructive diseases.

- The fatigue of the respiratory muscles is translated by the increase of the respiratory frequency, superficial breaths, tachypnea, the growth of PaCO2, later respiratory acidosis. In this situation, the accessory function of the accessory muscles creates negative pressure in the chest, with the diaphragm ascending, making the paradoxal breathing.


Figure 8. Respiratory muscles

Pleurae: is a serous membrane that forms the coating of the lung, it is composed of 2 parts:

parietal pleurae (6 layers) - it contains numerous pain receptors, derived from the nerves of the intercostal musculature, their irritation produces the pleuritic chest pain; respectively visceral pleurae (5 layers). The pleural cavity is a virtual space, contains 1-15 ml of fluid, which plays a role in the mechanics of breathing.

3. Air distribution

The upper airways have a role in purifying, heating, and humidifying the air:

Nasal cavity - is composed of nasal pits, separated by the nasal septum.

Pharynx - has digestive and respiratory function

Larynx - contains vocal cords, which play a role in coughing (by closing vocal cords and contracting the respiratory and abdominal muscles. It is a major clearance mechanism for material collected in large airways, initiated by nerve endings from the tracheae and large airways).

This segment of the airways is colonized with saprophytic germs, sometimes pathogenic germs, which, passing through the glottic barrier, are responsible for infections at this level.

Lower airways include trachea, main bronchi, terminal bronchioles, respiratory bronchioles.

Trachea - starts from the base of the neck, extending to the level of the fork of the main bronchi, called carina (length = 10-12cm). It is located anterior to the esophagus, and posterior to the aorta. It consists of 15-20 incomplete cartilaginous rings, posteriorly connected by fibrous bands.

The main bronchi - at the T4 level (the pulmonary spine) the trachea branches into the 2 main bronchi, which subsequently branch off, forming the bronchial tree. This structure is similar to the trachea, fibro-cartilaginous. The right bronchus is shorter (2.5 cm), thicker, with a more vertical path, favoring the appearance of suction pneumonias on this side. The left main bronchus is thinner and longer (5 cm), with a more horizontal path. Irritating receptors at this level may initiate cough reflex, and motor stimuli of the vagus nerve cause bronchoconstriction and mucus hypersecretion. The main bronchus wall is composed of 4 tunics (see table 7).


Cells Mucous Cilia-cylindrical, caliciform

(mucus secretion),

Dendritic, undifferentiated, neuroectodermal (secretion mediators and hormones)

May be affected by inhalation pollutants, infections, lowering the body's defense capacity Tumors, foreign bodies may occur

Lamina propia

Elastin, collagen, blood vessels, lymphatics, nerve fibers

Submucosal Glandular tissue Fibro-


Elastic fibers, collagen, cartilaginous ring

The absence of cartilaginous ring, structural alterations determines at this level traheobronhomalacy, changing the caliber and the trajectory of bronchi = bronchiectasis.

The bronchial tree is formed through the division of the main bronchi as follows: lobe- segmentation- supralobular- intralobular- terminal. The terminal bronchioles are less than 1 mm in diameter, consisting predominantly of smooth muscle tissue

Up to this level their main function is air management. They are then divided into respiratory bronchioles (acinar, lined by flat, paved epithelial cells, the ciliated cells disappear at this level), which are part of the intermediate zone, followed by the alveolar channels, alveolar sacs, respectively alveoli (300 mil. Alveoli). These form the respiratory surface, approx. 70sqm (the size of a tennis court).

Figure 9. Pulmonary arborization

Pulmonary segment: it is the morphological and functional unit, it is composed of several lobules. It is anatomical territory with precise boundaries, the own bronchovascular pedicle.



Upper lobes (1) apical, (2) posterior, (3) anterior, (4) superior lingular, (5) inferior lingular; Middle lobe: (4) lateral, (5) medial; Lower lobes (6) apical (superior), (7) medial, basal, (8) anterior basal, (10) posterior basal. The medial basal segment (7) is absent from the left lung.

Figure 10. Pulmonary segmentation

4. Blood distribution

Pulmonary vascularization is double:

- Functional 100% of the cardiac output, realizes the gas exchanges (small circulation)

At a heart rate of 80 beats / minute, the gas exchange in 100ml of liquid from the pulmonary capillaries takes 0.75sec. In the case of physical effort, the blood flow increases, reducing the time required for gas exchange.

- Nutritious 2% of cardiac output, through arteries (derived from aorta) and bronchial veins (large circulation). These follow the path of the bronchial tree.

5. Gas exchange

Terminal respiratory unit (acini) = pulmonary portion distal to non-respiratory bronchiole

3-5 acini form the pulmonary lobe; they are separated from each other by septa visualized through the Kerley B lines in the case of fluid or fibrosis accumulations.

The terminal bronchiole enters the terminal respiratory unit, accompanied by the branching of the pulmonary artery, supplying non-oxygenated (venous) blood from the right ventricle. It is divided into a rich capillary network that covers the alveolar wall, and drains into the pulmonary venules located at the periphery of the alveolus.

Alveolar cells - 5 types:

Cellular type %

Type 1 pneumocytes 8.3 Pneumocytes type 2 15.9 Endothelial cells 30.2 Interstitial cells 36.1

Macrophages 9.4


The number of endothelial cells is higher than the pneumocytes, which is why the effect of pollutants is more harmful to the cardiovascular system than to the respiratory system.

The alveolar epithelium and the capillary epithelium form the alveolo-capillary membrane, allowing the gas exchange through diffusion. The thickening of this membrane determines the decrease of the capacity of gas diffusion (interstitial pneumopathy, fibrosis). The surface of the alveolar epithelium is covered by a thin surfactant film. Alteration of it causes alveolar collapse (alveolar prosthesis, SDRA).

Interstitial cells - provide structure to the alveolar walls. Alveolar macrophage plays an important role in alveolar clearance. Type 1 pneumocytes cover the surface of one or more alveoli through cytoplasmic extensions. The destruction of type 1 pneumocytes causes the proliferation of type 2 pneumocytes. They have the ability to carry electrolytes, which plays a role in the resolution of edema.

6. Alveolar clearance and defense mechanisms

Passage of particles in the airways : particles with a diameter greater than 10 microns are deposited in the upper airways passage, those between 2-10 microns at the level of the bronchial tree, and those between 0.5-3 microns can penetrate the level of the terminal respiratory unit.

Pulmonary transport system : it has a role in the removal of the particles reached at the alveolar level, it is composed of:

Mucociliary escalator: it is made up of ciliated epithelial cells, mucus producing cells. The mucus is the transport medium of the particles and is made up of 2 layers: gelatinous upper, which captures the particle, and a lower, more liquid layer, through which the microvilli of the cells can move easily. It transports the particles from the terminal bronchioles to the large airways, from where they can be eliminated by coughing, expectoration, or swallowing. The transport speed is 3mm / minute, and increases at the proximal level. 90%

of the mucosal particles are removed in 2 hours.

Cigarette smoke or other harmful inhalers can "paralyze" the movement of the cilia, causing the mucus to stagnate, favoring the multiplication of microorganisms. A particular situation is the immobile cell syndrome.

Alveolar macrophage - phagocytic cell of the alveolar wall; is a monocyte from the bone marrow, which can adapt to the oxygenated environment at the alveolar level. It plays a role in detoxification, destruction and transport of particles that have reached the alveoli. If the macrophage cannot phagocytose the particles (bacterial toxins, large quantities), it produces humoral factors that cause the migration of neutrophils and other phagocytic cells to the lung, as the second line of defense.

Lymph-hematogenous drainage - the environment of migration of macrophages from the alveoli under inflammatory conditions. Migration through lymphatic vessels can take months, years. Collections of macrophages with foreign particles can be observed in the pulmonary lymph nodes, where they can remain throughout life.



1. Pneumology course for resident doctors, edited by Voicu Tudorache, Mirton Publishing House 2013, pages 7-15 2. Murray & Nadel's Textbook of Respiratory Medicine, 6th ed., 2016 Saunders, Elsevier, pp. 263- 277

3. Medical Semiology vol. 1, edited by Mirela Cleopatra tomescu, Victor Babes Publishing House 2010, pages 139- 162

4. An Illustrated Guide to Respiratory System Examination, Dr. Farid Ghalli, 2016 5. OSCE And Clinical skills handbook: Hurley KF, second edition.Elsevier Canada 2011 6. OSCEs at a glance, first edition 2013

7. Macleod`s Clinical Examination, thirteenth ed. 2013

8. Step by Step Clinical examination Skills: Iqbal F, first edition 2009

9. ERS Handbook of Respiratory Medicine 2nd Edition, publisher European Respiratory Society, 2013 10. Harrison's Pulmonary and Critical Care medicine, 2nd edition, Joseph Loscalzo, 2013, pages 2-45

11. Chest medicine, Essentials of pulmonary and critical care medicine, second edition, Ronald B. George, Richard W. Light, Michael A. Matthay, Richard A. Matthay, 1990, pp. 3- 73

12. A guide to phisical examination and history taking, fifth edition, Barbara Bates, 1991, pp. 3-26

13. Egan's Fundamentals of Respiratory Care, Eighth Edition, Robert L. Wilkins, James K. Stoller, Craig L.

Scanlan, 2003, ISBN 0-323-01813-0, pag 1-37

14. http://www.bimjonline.com/Imageoftheweek/Imagewk31%2805-09-2011%29.htm




Functional pulmonary testing allows accurate, reproducible evaluation of the functional status of the respiratory apparatus. Through the detected changes, these tests help quantify the seriousness, they facilitate early diagnosis and the evaluation of response to treatment for chronical pulmonary diseases.

The results one gets through functional testing are to be interpreted only in a clinical environment, as they have no specificity when it comes to the causes of the disease, but only affect the mechanisms that regulate lung function.

Some simple test can be carried aut with no difficulty even in a GP’s office:

- pulsoximetry;

- spirometry.

Others, on the contrary, require costly equipment and qualified staff:

- body-plethysmography;

- measuring the gas transfer rate Dlco (gas diffusion test);

- analyzing blood gas (arterial blood gases);

- bronchial challenge tests;

- cardio-pulmonary effort testing (exercise stress test).

Figure 1. The main tests according to the analyzed mechanism ans symptoms

(Adapted after Pneumology Course for resident doctors under the editorial Voicu Tudorache, Mirton 2013 edition)


I. Tests of pulmonary ventilation

Before testing pulmonary ventilation, it is important for the patient not to smoke for at least 1 hour previously, not to have any alcohol for at least 4 hours before, not to have stressful physical effort/heavy exercise for at least 30 minutes before and not to have had a heavy meal for at least 2 hours before. Patients should also avoid wearing tight clothing that might hinder chest and abdomen expansion.

A. Spirometry

This is a simple test, useful in the diagnosis and evaluation of chronical lung diseases.

The test measures the amount of air inhaled and exhaled in a time unit (ventilation flow).

Table 1. Indications, contraindications and complications of spirometry

Indications Contraindications Complications

 Detecting presence/absence of ventilatory disfunctions

 Assessing change of lung function over a period of time, disease preogression or response to treatment

 Evaluating response to

professional or environmental emissions

 preoperatory, in order to asses the risk rate of surgical procedures that might affect lung function

 hemoptysis

 pneumothorax

 unstable cardiovascular disease

 cerebral aneurysm

 recent eye surgery

 recent abdominal, otorhinolaryngologic or chest surgery

 dementia

 pneumothorax,

 intracranial hipertension

 syncope, dizziness

 chest pain

 paroxysmal cough

 worsening

respiratory failure

 bronchospasm

 contamination with nosocomial germs

In order to get quality data, both the expirogramm and the flow-volume curve have to be recorded, and the criteria of acceptability and repeatability of respiratory maneuvers have to be met.

Table 2. Criteria of acceptability and repeatability of respiratory maneuvers in spirometry.

(Adapted from Course of Pneumology for resident doctors, red. Voicu Tudorache, publ.

Mirton 2013)

Criteria of acceptability:

1. Corresponding beginning of expiration, without hesitancy or false extrapolation (extrapolated volume smaller than 150ml or smaller than 5% of the forced vital capacity, depending on which value is bigger).

2. Full expiration (longer than 6 seconds and obtaining a plateau on the forced expirogramm).

3. No occurency of artefacts like:

 cough in the first second of forced expiration or other episodes of cough that, according to the technicians judgement, interfere with the accuracy of the results;

 effort that is not maximal during the whole period of expiration;

 premature closure of the glottis;

 early termination of the expiration;

 obstruction or loss of air in the mouth.

Criteria of repeatability:

The first two maximum values of FVC (forced vital capacity), respectively of ale MEVS (maximum expiratory volume per second), do not differ more than 150ml (if FVC < 1l, the difference should not be more than 100ml).


The data on lung volume and forced flows obtained by spirometric measurement are compared to the predicted data, corresponding to the age, height, sex and race of the patient.

When interpreting spirometry, we considerthe highest values of the forced vital capacity (FVC) and of the maximum expiratory volume per second (MEVS) obtained in at least 3 acceptable measurings, and for the rest of the ventilatory parameters we consider the values from the maneuver with the highest sum of FCV and MEVS. Though the most correct approach is the one comparing each parameter to the lower limit of its normal, we consider normale the percentual variations between 80-120% of the predicted value. For expiration flows compared to FVC, too, we can use default values setting the boundaries of normality:

- MEVS/FVC (indicator for bronchic permeability IBP) ≥ 0,7;

- FEF50%/CVF (indicator for distal permeability IDP) ≥ 0,8.

Table number 3 presents respiratory disfunctions and the main spirometric parameters analysed. When speaking about obstructive disfunctione (for example bronchial asthma, chronic obstructive bronchopneumopathy, cystic fibrosis, bronchiectasis, foreign bodies, endobronchial tumors, post-tuberculous syndromes) in early stages, we can find modifications only for parameters of distal obstruction that is: MEV25-75%, respectively FEF50%/FVC are low.

Table 3. Ventilometric parameters in ventilatory disfunctions

(Adapted from Course of Pneumology for resident doctors, red. Voicu Tudorache, publ. Mirton 2013)

Parameter Distal obstructive syndrome

DV obstructive DV restrictive DV mixed**

CVF N N (possible )  

MEVS N   (possible N) 

MEVS/CVF N  N (possible *) 

MEV25-75%    (possible N or *) 

FEF50% /CVF   N (possible *) 

Severity of respiratory disfunction (in order to appreciate this severity, the consent about interpreting strategies for functional testing recommends the use of MEV, percentually expressed from the predicted value) can be:

- light MEVS > 70% prez.

- moderate MEVS = 60 - 70% prez.

- moderate-severe MEVS = 50 - 59% prez.

- severe MEVS = 35 - 49% prez.

- very severe MEVS < 35%

The aspect of the flow-volume curve can furnish data on the type of ventilatory disfunction (see table 4).


Table 4. The aspect of the flow-volume curve (Adapted from Course of Pneumology for resident doctors, red. Voicu Tudorache, publ. Mirton 2013)

Restrictive syndrome Tipical obstructive syndrome

(asthma, BPOC)

Obstructive syndrome of the upper respiratory tract (CRS fixed stenosis)

Narrow curve:

Instant ventilatory flow maintained, lung volume diminuished

Hollow expiratory slope: all instant ventilatory flows dropped


appearance: the tip and the base of the loop are flattened

Bronchomotorical tests can be useful in diagnosing bronchial hiperreactivity in bronchial asthma. The bronchomotorical response is analyzed, based on modifications of MEVS, after administering aerosol.

Figure 2. Algorithm in order to use bronchomotorical tests for emphasizing HRB.

(as in Course of Pneumology for resident doctors, red. Voicu Tudorache, publ. Mirton 2013)) A.


Tests of broncho-dilating (BD)

- Are carried aut for diagnostic purposes (emphasizing bronchial spasm and its reversability) or for therapeutical purposes (evaluating the efficiency of treatment by inhaling bronchodilators);

- Administering by inhalation beta-andrenergic medication (400 µg Salbutamol) or parasimpaticolitic short-acting medication (40 µg ipratropiu);

- positive test: a significant rise of MEVS ≥ 12% and 200 ml compared to the initial value,

- in bronchial asthma, in the situation of a partial reversibility (8-11%), because of bronchial inflammation, the corticosteroid test is performed → oral corticotherapy is recommended for 7-10 days, or inhalatory for 3-4 weeks, then reevaluation through spirometry with bronchodilating test, where the significant rise of MEVS indicates a positive test.

Tests of bronchial challenge

- These tests are used to identify, characterize and quantify the severity of the hyperreactivity of the airways (HRB);

- They are performed for patients showing symptoms of bronchospasm, with normal spirometric parameters or unclear results after administering the bronchodilating test;

- The agents used in tests of bronchial challenge can be classified according to their action mechanism:

 direct stimuli: methacholine, histamine, prostaglandins, leukotrienes;

 indirect stimuli: mannitol, adenosine, physical exercise, voluntary eucapnic hyperventilation, hypertonic saline solution;

- prior to testing the following substances are to be administered:


Short-acting Beta-agonists (inhaler) 8 hours Long-acting Beta-agonists (inhaler) 48 hours

Anticholinergics 24 hours

Preparations with theophylline 12-24 hours

Antihistamines 72-96 hours

Anti-leukotrienes 24 hours

Products based on caffeine (cola, coffee) 6 hours Corticosteroids

Testing for metacholine:

Table 5. Contraindications to testing for metacholine

Absolute Relative

Myocardical infarction in the last 3 months Aortic aneurysm*

Uncontrolled hypertension (high blood pressure) *

FEV1< 50% out of the predicted (or < 1 l)

Pregnancy, confinement after birth Treatment with cholinesterase inhibitors VEMS < 60% aut of the predicted (or < 1,5 l)

Mintal or physical disability

Notă: * these contraindications have been eliminated from the ATS-ERS criteria for per forming spirometry


- patients are administered inhaler doses with ever growing concentrations of metacholine (for patients with HRB, one can notice obstruction of the airways in low doses of metacholine);

- administration can be made by breathing aerosol at current volume for 2 minutes or by using the technique of dosimetry with 5 breaths;

- in dosimetry with 5 breaths, the following concentrations of metacholine are to be used: 0 mg/ml  0,065 mg/ml  0,25mg/ml  1mg/ml  4mg/ml  16mg/ml;

- positive test: decrease of MEVS by 20% of the initial value;

- the effect of metacholine on the airways is determined on the response-dosis curve, the severity of HRB is evaluated according to the concentration of metacholine determinig the lowering of MEVS by 20% (PC20%):

 0,02 – 1 mg/ml severe hyperreactivity,

 1 – 4 mg/ml moderate hyperreactivity,

 4 – 8 mg/ml slight hyperreactivity,

 8 – 16 mg/ml „border-line” hyperreactivity.

Figure 3. Dosis-response curve in administering cumulative doses of metacholine by the technique of dosymeria with five breaths.

(Adapted from Course of Pneumology for resident doctors, red. Voicu Tudorache, publ. Mirton 2013)

B. Peak-flowmetria

This is a method that cannot replace spirometry, but it is simple and useful in self- monitoring of asthma patients at home, both from the point of view of disease control, as from the point of view of response to treatment. The device called peakflowmeter measures the maximum instantaneous peak expiratory flow (|PEF). The PEF value i sone of the criteria for the functional defining of control zones for asthma patients, that is:

Controlled (green zone): normal values, PEF > 80% from predicted or personal „best” with a circadian variation < 20%;

Partially controlled (yellow zone): alert values, PEF of 50 – 80 % from predicted or personal „best” and circadian variations of 20-30%;

Uncontrolled (red zone): emergency zone, values of PEF

< 50% from predicted or personal „best” and a circadian variation > 30%.


C. Body-pletismography

This is a method of investigation that offers further information, more than spirometry, through which the forced inspiration and expiration flow is measured and thus the measurement of absolute lung volume (static) is made possible:

Residual functional capacity = the air volume in the lungs after a normal expiration,

Total lung capacity = the air volume in the lungs after a maximum inspiration,

Residual volume = the air volume that cannot be exhaled from the lungs, not even after a maximum exhaling effort.

The technique is based on the Boyle-Mariotte law according to which the volume of air in a precinct varies in inverted proportion to the pressure it is exposed to, in isothermia (constant temperature). This is the most precise method of measuring the entire air volume in the lungs, estimating those spaces too, that are excluded from ventilation by the total obstruction of the bronchioles (emphysema bubbles), and also estimating the air in the hypoventilated territories.

Interpretation: the rise of CPT and VR

- normal values the 80 - 120% from predicted;

- slightly increased values 120 - 150% from predicted;

- moderately increased values150 - 180% from predicted;

- severely increased values > 180% from predicted.

Parenchymal restrictive ventilatory dysfunctions (pulmonary resections; increase of elastic recoil from: diffusive interstitial pneumopathy, pneumoconioses, colagenoses, sarcoidoses, tuberculosis, etc.) or extraparenchymal (pleural or thoracic wall pathology, neuromuscular diseases, limitation of diaphragm movement) is characterized by reduced lung volume, mainly CV and CPT ( table 6).

Table 6. Changes in lung volumes in ventilatory dysfunctions

(Adapted from Course of Pneumology for resident doctors, red. Voicu Tudorache, publ. Mirton 2013)

Parameter Obstructive dysfunction Restrictive dysfunction with



"trapped air *"


parenchymal disorder

By extra- parenchymal limitation of inspire

By extra-

parenchymal limitation of inspire and expire

CV N→    

VR    N→ 

CPT  N   

VR/CPT   N  

Notes: N – normal; – increased; lowered; → – to; *trapped air – keeping supplementary air in the lungs at the end of forced expire by early collaboration of bronchioles.

Another parameter determined by this method is the resistance to flow of the airways (Raw), the indicator that evaluates the mechanical properties of the lungs. Approzimate normal values are about 0,05-0,22 KPa/L/s with an interindividual variability of 25%. This parameter, respectively the relations MEVS/CVF and FEF50%/CVF, helps define more functional images characteristic to obstructive syndromes in earlz stages of lung diseases (table 7).


Table 7. Functional images characteristic in early obstructive syndromes

(Adapted from Course of Pneumology for resident doctors, red. Voicu Tudorache, publ. Mirton 2013) Parameters Patent obstructive


Discrete distal

obstructive syndrome

Discrete central obstructive syndrome




Raw N

Notes: N – normal; – increased; low; → – towards.

II. Evaluation of lung gas exchange

This can be made by measuring the gas transfer factor of carbon dioxide through the capillary alveo membrane (DLco), and by determining the respiratory gases in the arterial blood (ASTRUP).

DLco furnishes data on the integrity of the capillary alveo membrane and the respiratory gases offer data on the ventilation/infusion rate in all pulmonary functional units. Some patients may display hypoxemia with a normal DLco (severe bronchial asthma), others may present normal values of arterial blood oxygen associated with a low DLco (pulmonary emphysema).

A. Determining gas transfer through the pulmonary capillary alveo membrane (pulmonary diffusion) for carbon monoxide (DLco)

This is the only investigation usually performed that can detect anomalies in pulmonary microcirculation. Tha gas transfer through the capillary alveo membrane depends on:

- Characteristics of the membrane: surface, thickness, functional efficiency;

- Circulatory characteristics: blood volume in capillaries, hemoglobin value (the Dlco value is corrected by the actual heoglobin concentration of the patient).

The transfer constant (Kco) = Dlco divided to the value obtained for alveo ventilation (VA), because Dlco is the product of the transfer rate by the capillary alveo membrane and VA.

Normal DLco values: 80-120% from predicted values based on age, height, sex and race.

Decrease of Dlco is considered:

 light when > 60% prez.

 moderate when it is 40 - 60% prez.

 severe when < 40% prez.

Decrease of DLco can be seen in three major types of diseases:

- Interstitial lung disease: shrinking of the surface of the diffusion membrane, respectively decrease of the blood volume in pulmonary circulation, because of fibrosis of functional units;

- Emphysema: shrinking of surface of the alveo membrane because of the destruction of the alveolar walls;

- Pulmonary vascular disease: (pulmonary hypertension, pulmonary embolism, etc.) by reducing the volume of the vascular bed.

In table 8 the main disease are presented, where gas transfer through capillary alveo membrane is affected, respectively the pathophysiological mechanisms that can lead to these changes.


Table 8.Mechanisms of changhe of DLco and derived parameters (Adapted from Course of Pneumology for resident doctors, red. Voicu Tudorache, publ. Mirton 2013)

Diagnosis DLco

(%from pred)


(%from pred)


(%from pred)


Bronchial asthma ↑ ↑ N Even distribution of infusion

Neuro-muscular disease

↓ ↑ ↓ Reduction of alveolar


Pneumectomy ↓ N ↓ Loss of functional units

Pulmonary fibrosis

↓ N/↓ ↓ Growth of elastic recoil

± alteration of capillary alveo membrane

Emphysema ↓ ↓ N/↑ Alteration of capillary alveo

membrane HTP or

pulmonary arteriopathies

↓ ↓ N Alteration of vascular bed

Figure 4 presents the current interpreting strategy for the results of pulmonary functional tests according to the guides.

Figure 4. Interpreting algorithm for the results of pulmonary functional tests

(Adapted from Course of Pneumology for resident doctors, red. Voicu Tudorache, publ. Mirton 2013)


B. Blood gas analysis in arterial blood (ASTRUP)

It is performed by measuring the partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) in the arterial blood. It is not an ideal method of monitoring, as it requires arterial puncture and provides intermittent data on the oxygenation level of the patient's blood,

Normal values: PaO2 = 80-100 mmHg PaCO2 = 35-45 mmHg

For the calculation of the alveolo-arterial oxygen gradient (PA-aO2) a simplified form of the alveolar gas equation is used:

Normal values: PA-aO2 <15 mmHg (under 30 years), increasing by 3 mm Hg for every decade of life over 30 years.

Hypoxemia can be induced by the following pathophysiological mechanisms:

• decrease of inspired PO2 level (high altitude);

• global alveolar hypoventilation (neuromuscular diseases, central regulation disorders);

• arterio-venous shunt (pulmonary atelectasis, pneumonia, pulmonary edema, congenital heart disease with shunt);

• ventilation / perfusion ratio disorder (diseases

respiratory tract, interstitial lung disease, alveolar disease, pulmonary vascular disease);

• due to diffusion alteration (special clinical situations).

Determining the cause of hypoxemia also depends on the value of PaCO2, the calculation of the alveolo-arterial oxygen gradient (PA-aO2) and the response to oxygen supplementation (see the chapter Respiratory Insufficiency). Table 9 shows the changes of the respiratory gases according to the mechanism responsible for hypoxemia,

Table 9.

Modification of arterial respiratory gases and alveolo-arterial oxygen gradient depending on the mechanism responsible for respiratory failure (hypoxemia)

(Adapted from the Pneumology Course for resident doctors under the editorial Voicu Tudorache, Publishing House Mirton 2013)

Mechanism PaO2 PaCO2 PA-aO2

Global alveolar hypoventilation

  ↔

Mismatch of reports infusion - ventilation

 ↔  

Diffusion disorders  ↔  

Arteriovenous shunt  ↔  

Note: ↔ – unchanged; – - low.

C. Pulse oximetry

It measures the saturation of blood hemoglobin with O2 (SaO2). Normal values: 95-97%.


- is a non-invasive method, alternative to gasometry, which allows continuous monitoring of the patient.


2 150 1,25 PCO


PA    a



- there are discrepancies between PaO2 and SaO2, the pulse oximeter having a relatively low sensitivity to changes in partial pressure above 60 mmHg, a value that corresponds to a 90%

saturation, due to the sigmoid type of the oxyhemoglobin dissociation curve;

- in the case of cutaneous peripheral vasoconstriction (low cardiac output or the use of vasoconstrictors), the pulse oximeter signal may be less accurate or not taken;

- the existence of other forms of hemoglobin (carboxyhemoglobin and methemoglobin) determines measured values of unreacted SaO2;

- does not provide data on PaCO2 level, which can be modified even in the case of peripheral saturation SaO2 ≥ 90%.

III. Effort tests

A. Cardiopulmonary testing during exertion

Testing requires complex equipment, laboratory with strict test quality control, as well as experienced and trained medical personnel. The test is also addressed to other devices and systems (cardio-vascular, muscular, metabolic), it has a synthetic character, but in evaluating the capacity to adapt to the effort of patients with pulmonary pathology it represents the "gold standard".


- useful in differentiating dyspnea from pulmonary etiology, cardiac etiology or other causes;

- some incipient functional disorders can only be detected under conditions of physical request;

- the capacity to adapt to the effort of patients with clinically-functional pulmonary disorders is evaluated, as well as the limits of the physical training within the lung recovery program;

- it allows the deciphering of the main pathophysiological mechanism limiting the stress tolerance;

- provides data on the evolution and prognosis of chronic lung diseases, as well as on the results of pulmonary rehabilitation programs;


- the test is carried out on an ergometric bicycle or a rolling mat, with a loading on the ramp;

- from the analysis of the parameters measured directly or indirectly during the test, conclusions are drawn about the capacity to adapt to the effort of the cardiovascular and pulmonary apparatus, respectively the cardiovascular and / or pulmonary functional deficit is determined (a simplified algorithm for interpreting the results of the cardiopulmonary testing at effort is shown in Figure 5).

B. The 6-minute walk test

It is a simple test, easy to perform, which does not require complex equipment. It may be indicated to patients with chronic pulmonary pathology in view of the assessment of functional capacity, but it has proved useful in determining the hypoxia during the effort, being such a help in the decision on the administration of oxygen therapy at home


- before testing the following are noted: SaO2, heart rate, blood pressure, respectively level of dyspnea and fatigue validated on the Borg scale;


- on a 30 m long corridor, without obstacles, the patient is asked to go in a hurry step, while being timed;

- the most important parameter being followed is the distance traveled which is compared with the predicted value depending on a number of anthropometric parameters (age, height and weight) and sex, respectively the post-test values of the listed parameters.

Figure 5. Diagnostic algorithm of the main factor for limiting stress tolerance.

(Adapted from the Pneumology Course for resident doctors under the editorial Voicu Tudorache, Publishing House Mirton 2013)

IV. Special tests

A. Evaluation of the respiratory muscles strength

The strength of the respiratory muscles is essential for maintaining adequate respiratory tract’s ventilation and protection.

Muscle function is assessed by measuring the maximum inspiratory pressure (PImax = the lowest pressure during a forced obstacle sustained by adequate respiratory tract obstruction) and the maximum expiratory pressure (PEmax = the highest pressure developed during a forced expiration sustained by obstacle on the adequate respiratory tract).

Normal values: Pimax = - 50 cmH2O women, - 75 cmH2O men

The decrease of PImax causes restrictive dysfunctions of an extra-parenchymal nature, with only limitation of inspiration: neuromuscular diseases, diseases of the diaphragm, intercostal muscles, accessories, pulmonary emphysema by flattening the diaphragm, kyphoscoliosis, obesity. In this situation CPT is low and the VR modified is insignificant.

Normal values: Pemax = 80 cmH2O women, 100 cm H2O men

PEmax decrease: neuromuscular diseases, especially those with generalized muscular weakness, high cervical spine fractures, abdominal musculature innervation dysfunctions. In this situation VR is increased and associated with the inability to cough effectively.

In the case of a restrictive ventilatory dysfunction of neuromuscular nature, in the early stages of the disease, it is useful to determine the maximum direct ventilation (Vmax.dir).


Table 9. Evaluation of the respiratory muscles strength

(Adapted from the Pneumology Course for resident doctors under the editorial Voicu Tudorache, Publishing House Mirton 2013)

Clinical symptoms and signs that require the evaluation of the respiratory muscles strength

Clinical situations that require repeated measurements of the respiratory muscles strength

• Unexplained reduction of vital capacity

• CO2 retention during waking or during sleep, specifically in the absence of severe obstruction of the respiratory tract

• Orthopnoea

• Dyspnea during bathing or swimming

• Lack of air during the speech

• tachypnea

• Paradoxical movements of the abdomen or chest wall

• Cough problems (with recurrent infections)

• Generalized muscle weakness

• Known diseases that affect the respiratory muscles

• Dyspnea installed after thoracic surgery (phrenic nerve paresis)

• Progressive lung disease with possible impact on respiratory muscle function

• Patients treated with high doses of corticosteroids

• Patients undergoing specific programs of training of the respiratory musculature

• Patients removed from mechanical ventilation

B. Measurement of bronchial inflammation

The measurement of bronchial inflammation is possible by 2 noninvasive techniques: by analyzing the sputum induced with hypertonic saline (only in specialized centers) or by determining the concentration of nitric oxide in the exhaled air (FENO).

Eosinophils raised in induced sputum (> 2%) or increased FENO in exhaled air (> 25 ppb at 50 mL / sec) are found in 75% of asthmatic patients, as well as 33% of patients with COPD or chronic cough. Studies show that eosinophilic bronchial inflammation is more associated with corticosteroid response than with asthmatic phenotype.


- useful in diagnosing eosinophilic bronchial inflammation, response to corticosteroid treatment and monitoring of selected cases of severe refractory asthma;

- there is a minimal correlation in these patients between the FENO level and the lung functional tests;

- responds faster than spirometry to inflammatory changes due to exposure to allergens = marker more sensitive to disease;

- can also be measured at the level of the nasal cavities or sinuses, as a marker of nasal inflammation (rhinitis).


- FENO <5 ppb: primary ciliary dyskinesia, cystic fibrosis, bronchopulmonary dysplasia;

- FENO = 25 - 50 ppb in adults: possible inflammation (from 20 to 35 ppb in children);

- FENO > 50 ppb: permanent eosinophilic inflammation (35 ppb in children).

In the case of smokers, the amount of NO in the exhaled air is reduced and the above interpretations cannot be taken into account.


Table 10. Interpretation of FENO values

(Adapted from the Pneumology Course for resident doctors under the editorial Voicu Tudorache, Publishing House Mirton 2013)



Absence Absence Present but easy significant ADULTS

FENO (ppb)* < 5 5-25 25-50 > 50

(or an increase of> 60%

from a previous determination)

Children < 12 ani

FENO (ppb)* < 5 5-20 20-35 > 35

* At a flow of 50 ml / sec Important:

• Smoking?


• Primary ciliary dyskinesia (check NO nasal)

• Cystic fibrosis

• Chronic lung disease at the premature

If symptoms occur

• Review of the diagnosis

(To be considered:

neutrophilic asthma, anxiety /

hyperventilation, vocal cord dysfunction, gastro- oesophageal reflux, rhinosinusitis and heart disease. In addition to children:

bronchitis, ENT and immunodeficiencies)

If no symptoms appear under treatment

• Patient compliant

• Consider reducing the dose or giving up anti-inflammatory medication

Interpretation based on the clinical aspect

If symptoms appear under anti-

inflammatory treatment:

• infection

• Exposure to increased levels of allergens

• Increased dose

• Add LABA

In addition to children:

• Verification:

- compliance - inhalation technique

(For children, consider using MDI and spacer if the patient is using a dry powder device)

If no symptoms appear under treatment

• Do not change the dose of anti-inflammatory medication if the patient is stable

Consider allergic asthma if there is a history of the disease A positive response to inhalation or oral administration of steroids is likely

In addition to children:

• If there is objective evidence of respiratory tract obstruction reversibility, asthma is very likely

If symptoms appear under anti-

inflammatory treatment:

• Verification:

- compliance - inhalation technique -dose of medicines

• To be considered - Exposure to levels - High in allergens - Imminent exacerbation

or relapses - Steroid resistance


If no symptoms appear under treatment

• Do not change the dose of anti- inflammatory

medication if the patient is stable



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