RESPIRATORY

FAILURE
RESPIRATORY FAILURE

 • Definition
 Respiratory insufficiency is the clinical-
biological syndrome arising from the inability of
the respiratory system to provide adequate
hematosis, both at rest and during effort .
 Respiratory insufficiency is not a disease but a
functional disorder caused by diseases of the
airways, lungs, pleura, chest wall or
neuromuscular system.
RESPIRATORY FAILURE

 The definition of this syndrome includes

two components:
 - Humoral, decrease of PaO2 below 80
mmHg and PaCO2 increase over 46
mmHg,
 -clinical, represented by clinical signs
reflecting tissue suffering secondary to
hypoxemia and / or hypercapnia.
RESPIRATORY FAILURE

 Classification
 Classification of respiratory insufficiency
is performed after:
 A. The time required for the occurrence
of hypoxemia and hypercapnia:
 a. Acute respiratory failure,
 b. Chronic respiratory insufficiency
RESPIRATORY FAILURE

 B. the presence or absence of the main

humorous signs:
 a. respiratory insufficiency without
hypercapnia (partial RI);
 b. Respiratory insufficiency with
hypercapnia (global RI)
RESPIRATORY FAILURE

 C. degree of humoral changes:

 a. mild hypoxemia (PaO2 = 80-60 mmHg),
 b. moderate hypoxemia (PaO2 = 60-45
mmHg),
 c. severe hypoxemia (below 45 mmHg);
 d. mild hypercapnia (PaCO2 = 46-50 mmHg),
 e. moderate hypercapnia (PaCO2 = 50-70
mmHg),
 f. severe hypercapnia (PaCO2 over 70 mmHg);
RESPIRATORY FAILURE

 D. the presence or absence of clinical or

humoral signs at rest:
 a. manifest respiratory failure: clinical and
humoral signs are present under resting
muscles;
 b. latent respiratory failure: clinical and humoral
signs are only present during effort.
 E. presence or absence of respiratory acidosis:
RESPIRATORY FAILURE
 Causes of respiratory insufficiency
 1. Diseases of the airways
 a. Acute Obstruction:
 i. Upper respiratory tract (aspiration of foreign bodies,
glottis edema),
 ii. of the lower respiratory tract (acute broncho-
bronchiolitis, bronchial asthma, inhalation of bronchial
irritants)
 b. Chronic Obstruction: lower respiratory tract (chronic
obstructive bronchitis, obstructive pulmonary
emphysema, persistent bronchial asthma).
RESPIRATORY FAILURE

 2. Diseases of the parenchymal lung

 a. Acute: massive pneumonia,
bronchopneumonia;
 b. Chronic: diffuse pulmonary fibrosis.
 3. Pulmonary vascular diseases
 a. Acute: pulmonary thromboembolism
 b. Chronic: recurrent pulmonary
thromboembolism, collagenosis,
systemic vasculitis (Wegener's
granulomatosis).
RESPIRATORY FAILURE
 4. diseases of the pleura and of the chest wall
 a. acute: sufocant pneumothorax , massive
pleurisy, thoracic trauma;
 b. Chronic: extensive pahipleuritis,
cifoscoliosis.
 5. Diseases of the neuromuscular system
 a. Acute: poisoning with: sleeping pills,
sedatives, alcohol; acute polyradiculoneuritis;
craniocerebral trauma, brain tumors, vascular
disorders, viral encephalitis;
 b. Chronic: muscular dystrophy, myasthenia
gravis.
RESPIRATORY FAILURE
 6. Diseases that cause acute pulmonary edema
 a. acute cardiac pulmonary edema: Cardiac disease
evolving with acute left ventricular failure, acute mitral
failure and acute aortic insufficiency.
 b. Acute non-cardiogenic pulmonary edema (lesional):
systemic disorders (septicemia, toxico-septic abortion,
acute necrotic hemorrhagic pancreatitis, disseminated
intravascular coagulation, anaphylactic shock,
eclampsia) or toxic (inhalation of smoke or corrosive
products, gastric fluid, , barbiturics) that cause altered
permeability of lung capillaries, resulting in adult
respiratory distress syndrome.
RESPIRATORY FAILURE
 • Clinical presentation
 The clinical presentation of respiratory insufficiency
includes:
 Dyspnea, without a correlation between the degree of
dyspnea and the level of hypoxemia;
 Peripheral cyanosis, which occurs when SaO2 falls
below 80%;
 Neuropsychiatric manifestations: somnolence,
flapping-tremor, decreased attention, altered state of
consciousness to coma;
 Cardiovascular manifestations: tachycardia,
hypertension or hypotension and cardiogenic shock.
RESPIRATORY FAILURE
 A. The clinical presentation of acute respiratory failure
is the tissular effects of hypoxemia and acute
hypercapnia. a. Acute hypoxia is responsible for:
 i. Dyspnea, tachypnea, increased respiratory effort;
 ii. The cyanosis of the lips, superficial mucous
membranes and nails are the most important indicator
of acute hypoxemia and becomes evident when
reduced Hb exceeds 5% in capillary blood.
 iii. Neuropsychiatric manifestations are equilibrium
disturbances, altered thinking, confusion, and death by
depression of the respiratory center
RESPIRATORY FAILURE

 iv. Cardiovascular manifestations:

tachypnea, hypertension (moderate
hypoxemia: PaO2 = 60-45 mmHg),
hypotension (severe hypoxemia: PaO2
below 45 mmHg), cardiogenic shock.
RESPIRATORY FAILURE

 b. Acute hypercapnia produces

manifestations:
 i. Neuropsychics (hypercapnic
encephalopathy): somnolence, temporal
disorientation, flapping tremor, confusion,
coma.
 ii. Cardiovascular: tachycardia, sweating,
arrhythmias, headache through intracranial
hypertension, elevated, normal or low blood
pressure.
RESPIRATORY FAILURE

 iii. Respiratory, depending on the

degree of hypercapnia:
 1. tahypnnea and increased total
ventilation in case of low increase of
PaCO2;
 2. hypoventilation and worsening of the
neuropsychic condition, in case of
marked increase of PaCO2.
RESPIRATORY FAILURE
 c. Acute metabolic acidosis occurs in acute
respiratory failure with severe hypoxemia (PaO2 below
50 mmHg) and significant hypercapnia (PaCO2 above
60 mmHg) and is manifested by :
 i. Neuropsychics: altered state of consciousness;
 ii. Respiratory: dyspnea, increased pulmonary
pressure;
 iii. Cardiovascular: depression of myocardial
contractility, rhythm disorders, arterial hypotension,
cardiogenic shock.
RESPIRATORY FAILURE
 B. The clinical presentation of chronic respiratory
insufficiency includes the manifestations of:
 a. Chronic hypoxemia
 i. Neuropsychiatric: somnolence, marked physical
asthenia, decreased attention
 ii. Respiratory: polypneea, cyanosis, secondary
polyglobulia and digital clubbing are the hallmarks of
chronic hypoxemia;
 iii. Cardiovascular: Pulmonary arterial hypertension
secondary to pulmonary arterial vasoconstriction,
following hypoxemia and respiratory acidosis, leads to
the occurrence of signs of chronic pulmonary heart
RESPIRATORY FAILURE

 b. Chronic hypercapnia that produces

symptoms
 i. Neuropsychiatric: headache,
dizziness, drowsiness, convulsions,
muscle contractions and coma;
 ii. Ocular: papillary swelling in eye exam.
RESPIRATORY FAILURE

 c. Chronic respiratory acidosis that is

responsible for the occurrence of:
 i. Peripheral edema: due to increased
renal tubular resorbtion of sodium ;
 ii. Cardiovascular: depression of
inotropism and arrhythmias;
 iii. Respiratory: dyspnnea and increased
respiratory effort.
 Clinical forms of acute
respiratory failure
 Acute respiratory distress syndrome
of the adult is an acute lesional
pulmonary edema in which there is an
increase in pulmonary capillary
permeability and of the alveolar
epithelium. Thus, a severe hypoxemia
occurs with a right-left sanguine shunt
and decreased pulmonary compliance.
Pulmonary damage can occur via the
respiratory tract or via the blood stream
through circulating substances.
Acute respiratory distress
syndrome
 Appears in the following situations:
septicemia; trauma; extended burns;
inhalation of smoke or chemicals (NO2,
NH3, chlorine); disseminated
intravascular coagulation; acute
pancreatitis; gastric aspirations, drug
poisoning ( barbiturics, salicylates);
eclampsia; anaphylactic shock;
Acute respiratory distress
syndrome
 Subjective: Initially, patients present the
symptoms of the underlying disease. The first
alarm signal is progressive polypneal dyspnea.
Cyanosis is installed in parallel. Cough is
present only in patients where the lung injury
has occurred directly by respiratory tract.
 Objective: Pulmonary sonority gradually
diminishes, and at auscultation, disseminated
rallies are heard
Acute respiratory distress
syndrome
 Paraclinic:
 Pulmonary X-ray shows diffuse,
extensive, bilateral, interstitial and
alveolar infiltrates; gasometry:
 hypoxemia with initial hypocapnia, later
severe hypoxemia at the front with
hypercapnia, the major mechanism being
the right-left sanguine shunt.
Acute respiratory distress
syndrome
 Evolution: Oxygen administration can no
longer correct hypoxemia, the patient
becomes tachycardic, with hypotension,
oliguria and acidosis. The state of
consciousness is altered, showing signs
of failure from other organs, with a very
high mortality. The saved cases remain
with significant pulmonary fibrosis, with
all its pathophysiological consequences.
Acute respiratory distress
syndrome
 • Paraclinical exploration
 1. Gasometry and pulsoximetry will
highlight: decrease in PaO2, (below 70 -
80 mmHg), decrease in SaO2 (below
92%) and PaCO2 increase (over 46
mmHg).
 2. Blood pH measurement and alkaline
reserve allow assessment of acid-base
equilibrium disturbances:
Acute respiratory distress
syndrome
 3. Spirometry determines the type of ventilator
dysfunction:
 a. Obstructive ventilator dysfunction:
FEVS1 decrease and bronchial permeability
index less than 80%;
 b. Restrictive ventilator dysfunction:
decrease (vital capacity) VC;
 c. Mixed ventilator dysfunction: decrease in
VC, decrease in FEVS1, bronchial permeability
index below 80%;
Acute respiratory distress
syndrome
 4. Radiological examinations allow:
 a. Determination of the cause of respiratory
insufficiency: acute broncho-bronchiolitis,
bronchopneumonia, aspiration pneumonia,
pulmonary thrombosis, pneumothorax, adult
acute respiratory distress syndrome, COPD;
 b. Monitoring the evolution of
bronchopulmonary disease associated with
respiratory insufficiency.
Acute respiratory distress
syndrome
 5. Bronchoscopy is indicated in:
 a. Diagnosis and treatment of atelectasis;
 b. Etiological diagnosis of hemoptysis;
 c. Aspiration of foreign bodies;
 d. Collection of secretions for
bacteriological and cytological
examinations;
 e. Orotracheal intubation (PaO2 below 40
mmHg, SaO2 below 60% and PaCO2 above
80 mmHg)
Acute respiratory distress
syndrome
 6. The electrocardiogram may show:
 a. Sinus acute tachycardia (acute
hypoxemia);
 b. Atrial or ventricular arrhythmias (severe
hypoxemia with respiratory acidosis);
 c. Sinus bradycardia (severe hypoxemia);
 d. Multifocal atrial tachycardia
(decompensated respiratory insufficiency);
 e. Electrical signs of acute pulmonary heart
(qR1, rS3, T negative in V1-V3 ).
BRONCHIAL SYNDROMES
 Bronchial syndromes have common elements:
 Subjective: cough, mucosal or purulent expectoration,
and sometimes dyspnea.
 Objective: ronflant, sibilant and subcrepitant rallies
(depending on the type of affected bronchus).
 Radiological: no pathognomonic changes, the
pulmonary changes usually appear late and are the
consequences of bronchial obstruction (pulmonary
hypertransparency).
 The main bronchial syndromes are bronchial
syndrome, pulmonary hyperinflation syndrome and
bronchial asthma syndrome.
I. BRONCHITIC SYNDROME
A. ACUTE BRONCHITIC
SYNDROMES
1. ACUTE TRAHEOBRONCHITIS
 • Definition:
 Acute tracheobronchitis defines acute
inflammation of the tracheobronchial wall,
which can sometimes extend to the terminal
bronchiole, making the picture of acute
broncho-bronchiolitis.The disorder occurs after
exposure to agents:
 - viral;
 - bacterial;
 - chemical and
 - physical.
a. Viral acute
tracheobronchitis
 • Onset:
 Fever, associated with symptoms of acute
upper respiratory tract infection (AURTI):
 acute rhinitis (sneezing, nasal obstruction,
rhinorrhea);
 acute pharyngoamigdalitis (dysphagia,
odinophagia);
 acute laryngitis (dysphonia, irritable cough);
 acute sinusitis (headache, frontal pain or jaw
pain, rhinorrhea, irritable cough).
a. Viral acute
tracheobronchitis
 Status period:- the "raw" phase is manifested by:
 - an irritative cough, in the form of episodic accesses,
accompanied by a retrosternal, burn-like pain;
 - nothing objectively, or sometimes an accentuated
vesicular murmur, and some sibilant rales
 - the "productive" phase is manifested by
 - Cough becomes productive, with mucous
expectoration, reduced in quantity, then mucopurulent,
and pain is accentuated;
 - there may be some rallies in the clinical exam which
disappear in a few days;
B. CHRONIC BRONCHITIC
SYNDROMES
 1. CHRONIC BRONCHITIS
 Definition: is the chronic inflammatory disease
of the tracheobronchial wall associated with:
 - an exaggerated secretion of mucus in the
bronchial tree,
 - sufficient to produce coughing and
expectoration, at least 3 months per year, 2
consecutive years
CHRONIC BRONCHITIC
SYNDROMES
 The etiological factors involved in the
production of this disease are:
 - active and passive smoking;
 - urban air pollution;
 - professional environments with dust,
powders, gas and smoke;
 - viral and bacterial infections, which are lead
to acutization, but also in the progression of the
disease;
CHRONIC BRONCHITIC
SYNDROMES
 Clinical presentation
 Subjective: The clinical presentation is
dominated by chronic coughing, whether or not
associated with mucous or mucopurulent
expectoration and sometimes with expiratory
dyspnea.
 Objective: In auscultation, we have an
accentuated vesicular murmur, accompanied
by bronchial rallies (ronflant and sibilant).
CHRONIC BRONCHITIC
SYNDROMES
 1. The simple chronic bronchitis manifested
by:
 - persistent, morning cough, with mucous
expectoration, reduced in quantity, rarely
accompanied by effort dyspnea;
 - the chest is normally conformed with normal
pectoral murmur, normal pulmonary sound,
rare ronflant and / or sibilant and / or basal
subcrepitant rales;
 - functional ventilation tests (FVT) are normal
CHRONIC BRONCHITIC
SYNDROMES
 2. The chronic mucopurulent bronchitis is
manifested by:
 - morning cough accompanied by purulent,
recurrent or persistent expectoration (in the
absence of bronchiectasis) and sometimes
effort dyspnea;
 - the chest is normally conformed, and
sometimes ronflant bronchic rales can be
heard;
 - FVT indicates normal values ​of pulmonary
volumes and flows.
CHRONIC BRONCHITIC
SYNDROMES
 3. Chronic Obstructive Bronchitis (COB) associates- persistent
morning cough, with / without expectoration, associated with
expiratory dyspnea and bilateral wheezing;
 - thorax is hyperinflated, with low amplitude respiratory
movements, diminished pectoral murmur, pulmonary
hypersonority, diminished vesicular murmur, prolonged expiration,
diffuse sibilant rales and basal subcrepitant rales;
 - FVT indicates decreased FEVS1 (maximum expiratory volume
per second) and decreased TI ( Tiffneau index) and normal / low
VC
 . Differential diagnosis is done with infectious, chronic bronchial
asthma.
II. ALVEOLAR DISTENCY SYNDROME
(PULMONARY HIPERINFLATION)

 This clinical syndrome defines abnormal,

permanent or transient distension of air spaces
distal to terminal bronchiole, whether or not
accompanied by alveolar septal destruction at
this level, whether or not accompanied by
diffuse bronchial obstruction.
 The main diseases that are manifested by this
clinical syndrome are: pulmonary emphysema,
bronchial asthma and chronic obstructive
pulmonary disease (COPD).
II. ALVEOLAR DISTENCY SYNDROME
(PULMONARY HIPERINFLATION)

 Clinically, patients complain of: dyspnea,

intermittent (bronchial asthma) or
progressive (pulmonary emphysema),
initially with high physical effort, then with
less and less effort, until resting dyspnea,
irritating or productive coughing and
wheezing.
II. ALVEOLAR DISTENCY SYNDROME
(PULMONARY HIPERINFLATION)

 The clinical examination shows the

emphysematous chest, polypnea, inferior
costal airflow, reduction of the amplitude of the
respiratory movements and vocal vibrations,
pulmonary hypersonority, lowering of the
pulmonary bases, reduction of the pulmonary
base mobility, reduction of the vesicular
murmur, prolongation of the expiration and
presence of bronchial and subcrepit rales.
Pulmonary radiography can show various
radiological aspects, from the normal chest
aspect, to pulmonary hyperinflation.
1. PULMONARY
EMPHYSEMA
 • Definition:
 PE is the permanent, abnormal
distension of the air spaces distal to the
terminal bronchiole, accompanied by the
destruction of the alveolar septum and
the absence of pulmonary fibrosis.
1. PULMONARY
EMPHYSEMA
 Clinical presentation
 Subjective: Patients with emphysema
accuse:
 the progressive effort dispnea, which in
time becomes permanent;
 irritable cough, which can become
productive in acute respiratory infections.
1. PULMONARY
EMPHYSEMA
 Objective
 In the early stages of the disease, the physical examination of the
chest may not provide special features, except for prolonged
expiration and diminished vesicular murmur (especially at bases).
As the disease progresses, the specific objective elements are:
 emphysematous chest (increased anteroposterior diameter,
horizontal ribbs, proeminence of supraclavicular fossa, inferior
costal draft) and excessive use of accessory respiratory muscles;
 reducing the amplitude of bilateral movements and bilateral vocal
vibration,
 pulmonary hypersonority, with lower bases and reduced mobility,
 diminished vesicular murmur, with rare subcrepitant rales.
1. PULMONARY
EMPHYSEMA
 Paraclinic
 a. Pulmonary radiography highlights pulmonary
hypertransparency. The presence of air bubbles in the
pulmonary or subpleural parenchyma is the
pathognomonic sign of pulmonary emphysema.
 b. Spirometry records the decrease of FEVS1 and
Tiffneau index, and in advanced stages the decrease of
VC. Measuring pulmonary volumes shows an increase
in TPC, accompanied by marked increase in RV, so the
RV / TPC ratio is increased.
 c. The DLco diffusion coefficient is low.
 d. Pulmonary compliance is increased.
2. BRONCHIAL ASTHMA

 Definition.
 BA is an inflammatory airway disease
characterized by:
 1. hyperactivity of the tracheo-bronchial
tree at different triggers;
 2. generalized airway obstruction, which
can spontaneously (reversibly) or under
treatment subcede;
2. BRONCHIAL ASTHMA

 Clinically it is manifested by paroxysmal

episodes of:
 a. expiratory dyspnea,
 b. Coughing
 c. wheezing.
2. BRONCHIAL ASTHMA
 Essential features
 I. Existence of clinical manifestations specific to episodic or
chronic bronchial obstruction
 a. with expairatory bradipnea, irritative coughing (predominantly
nocturnal), wheezing, chest blocked in inspiration;
 b. Symptoms worsen at night and early in the morning;
 c. prolonged expiration and sibilant rales.
 II. Bronchial hyperactivity defined by obstructive ventilatory
dysfunction occurring after bronchial challenge tests
(bronchomotricity tests).
 III. Obstruction of the airway is reversible (partially or totally)
spontaneously or after bronchodilators.
2. BRONCHIAL ASTHMA
 Etiology
 The etiological factors responsible for the onset
of asthma crises are:
 1. Allergies: pneumoallergens (house dust,
pollen, molds).
 2. Professional factors in the industry:
metallurgy, pharmaceuticals, plastics,
detergents or livestock and poultry breeders.
 3. Infectious factors of viral nature are involved
in the onset of bronchial asthma attacks.
2. BRONCHIAL ASTHMA
 4. Physical effort- bronchoconstriction
correlates with the intensity of physical effort
and can trigger a bronchospasm crisis in a cold
and dry atmosphere.
 5. Pharmacological agents, aspirin and beta-
blockers may induce bronchial asthma attacks,
accompanied by ocular and nasal congestion.
 6. Atmospheric pollution can aggravate any
form of asthma.
 7. Psycho-emotional factors can accentuate or
aggravate asthma attacks.
2. BRONCHIAL ASTHMA

 Pathophysiology
 Diffuse and reversible bronchial
obstruction of the airway is due to:
 - spasm of bronchial smooth muscle
(bronchospasm);
 - wall edema,
 - vascular congestion
 - very viscous bronchial secretions.
2. BRONCHIAL ASTHMA

 Clinical forms
 Bronchial asthma presents under 3
major forms:
 A. Episodic asthma (with intermittent
episodes).
 B. Asthma status.
 C. Chronic bronchial asthma.
2. BRONCHIAL ASTHMA
 • Clinical presentation:
 The crisis suddenly starts with: expiratory dyspnea,
dry coughing and wheezing. Crises occur frequently at
night, in cold seasons or under polluted atmosphere
(dust, smoke).
 The trigger agent is usually identified by the
anamnesis. Initially the patient is bradypneic so that he
later becomes polypneic, orthopneic.
 - The thorax is stretched, blocked in the inspiratory
position, with the amplitude of low respiratory
movements, lower intercostal circulation and prolonged
expiration;
2. BRONCHIAL ASTHMA
 - Percussion highlights: pulmonary hypersonority, low lung bases
and negative Hirtz maneuver;
 - Auscultation detects: diminished vesicular murmur, prolonged
expiration, fine sibilant rales in both breathing times, sometimes
with basal subcrepitant rales;
 - Cardiac examination shows: normal or increased heart rate and
normal or high blood pressure; Spontaneously or under treatment
(inhaled bronchodilator), the patient emerges from the crisis.
 Classic, each episode ends with exacerbation of cough, which
becomes productive, expectorating being mucous, adherent,
reduced quantitatively .
 The intercritical patient is asymptomatic and does not require
treatment.
B. Asthmatic status (acute
asthma)
 Defines the asthma crisis:
 - persistent,
 - prolonged (> 24 hours),
 - refractory to appropriate bronchodilator
therapy, initiated in the emergency room
and which
 - requires hospitalization in an intensive
care clinic.
B. Asthmatic status (acute
asthma)
 The trigger factors of asthma are:
 - viral respiratory infections;
 - Exposure to a high concentration allergen /
irritant;
 - intense physical stress at low temperatures;
 - using aspirin / non-steroidal anti-inflammatory
drugs (NSAIDs);
 - Sudden discontinuation of corticosteroid
therapy / excessive use of beta-
sympathomimetics
B. Asthmatic status (acute
asthma)
 Clinical
 Subjective
 The patient describes:
 - expiratory dyspnea that persists despite
bronchodilator treatment;
 - wheezing, initially during exhale, then in both
respiratory phases, and finally disappears, indicating a
severe degree of bronchial obstruction;
 - the absence of cough because the patient can not
expire, the chest being fixed to the maximum
inspiration.
B. Asthmatic status (acute
asthma)
 Objective
 - The patient is polyphenic (30 breaths / min),
orthopneic, cyanotic, anxious (causes the
feeling of imminent asphyxia);
 - hyperinflated thorax, blocked in the
inspiration, intercostal draft and action of
accessory respiratory muscles
(sternocleidomastoid and intercostal);
 - decreased amplitude of respiratory
movements;
B. Asthmatic status (acute
asthma)
 - pulmonary hypersonority, with lowered
lung bases
 - diminished vesicular murmur, with few
sibilant rales.
 - tachycardia;
 - paradoxal pulse present.
C. Chronic bronchial
asthma
 It occurs in a patient with intermittent
asthma, where obstructive episodes
appear more and more frequently due to
recurrent respiratory infections, ultimately
resulting in infectious bronchial asthma.
C. Chronic bronchial
asthma
 • Clinical presentation
 Subjectively the patient accuses:
 - chronic coughing, mucous or mucopurulent
expectoration, and persistent or effort expiratory
dyspnea;
 - On this background, intense dyspnea and cough with
abundant mucopurulent expectoration appear.
 Objective
 - emphysematous thorax, hypersonority, with
diminished vesicular murmur, prolonged expiration,
permanent sibilant and subcrepitants rales.
C. Chronic bronchial
asthma
 Differential diagnosis is primarily done
with COPD: in chronic BA, FEVS1
values ​after administration of an inhaler
bronchodilator show an improvement of
more than 12% (200 ml) from baseline.
C. Chronic bronchial
asthma
 Paraclinic
 1. Spirometry records an obstructive ventilator
dysfunction with low FEVS1 reversible after
inhalation of bronchodilators (> 12% or 200
ml).
 2. Peakflowmetry measures PEF variability
(PEF - peak expiratory flow or maximum
expiratory flow) over a day and compares
these values ​to each other. The high variability
(over 20%) of PEF values ​indicates the
presence of bronchial asthma.
 3. Inducing test (to determine bronchial
reactivity) using bronchoconstrictors.
C. Chronic bronchial
asthma
 4. Gasometry:
 - slight / moderate BA: PaO2 and PaCO2 -
normal, but with respiratory alkalosis;
 - severe BA: very low PaO2; Normal PaCO2.
 The combination of increased PaCO2 (
hypercapnia) with respiratory acidosis and
symptoms of respiratory failure (polypnea and
cyanosis) indicate the need for mechanical
ventilation
C. Chronic bronchial
asthma
 5. Skin allergy tests are required to identify the
allergen involved;
 6. Immunological tests indicate IgE titres elevated in
allergic BA;
 7. Pulmonary radiography highlights:
 a. hyperinflation of the lungs
 b. decrease of vascular drawing in the periphery of
lung fields;
 c. exclusion of other diseases that mimic asthma;
 d. Complications of bronchial asthma (pneumothorax),
which do not allow the recovery of lung function.
C. Chronic bronchial
asthma
 8. Hemogram shows the nominal
leukocyte count, with increased
percentage of eosinophils (allergic BA) or
neutrophils (infectious BA).
 9. The sputum examination may reveal
the presence of Curshmann spirals and
Leyden crystals in allergic asthma
3. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
(COPD)
 • Definition
 COPD is a complex pathological concept
that defines the clinical forms commonly
encountered in medical practice and is
characterized by the association of:
 - bronchial and obstructive phenomena
(COB) with
 - Pulmonary hyperinflation (PE)
phenomena.
3. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
(COPD)
 Essential features
 - current (or past) smoker;
 - chronic productive cough, persistent, 2
months / year, 2 consecutive years (CB)
and dyspnea (PE);
 - bronchial rallies, decreased vesicular
murmur and prolonged expiration;
 - Limiting respiratory flows to FVT.
3. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
(COPD)
 Classification
 Depending on the dominant clinical
manifestations, two clinical forms of
COPD have been described
 - predominantly emphysematous and
 - predominantly bronchial type.
A. Predominantly emphysematous or pink
puffers (PP); COPD type A

 Clinical
 Subjective:
 long history of:
 • dyspnea at ​effort;
 • dry cough;
 • minimal mucous expectoration;
 • rare respiratory infectious episodes.
Predominantly emphysematous or
pink puffers (PP); COPD type A

 Objective
 General Inspection
 • Asthenic patients, underweight, with
discrete cyanosis, orthopneic, intensely
polypneic, using accessory expiratory
muscles (stay in a sitting position, lean
forward, leaning on there hands at the
edge of the bed).
Predominantly emphysematous or
pink puffers (PP); COPD type A

 Respiratory system
 • inspection: emphysematous thorax;
 • palpation: low amplitude of respiratory
movements, low pectoral murmur;
 • percussion: pulmonary hypersonority, lowered
lung bases, immobile with breathing;
 • Auscultation: diminished vesicular murmur,
prolonged expiration and fine sibilant rallies,
expiration problems;
Predominantly emphysematous or
pink puffers (PP); COPD type A

 • Paraclinical
 • Low PaO2 (<70 mmHg); PaCO2 normal
/ low (polypneic);
 • FVT: Increased TPC and RV; VC and
low FEVS1;
 • The elastic properties of the lungs are
diminished;
 • Low DLCO.
Predominantly emphysematous or
pink puffers (PP); COPD type A

 • Lungs radiograph:
 - hypertransparency of lung fields;
 - flattening of the diaphragm;
 -alveolar drawing in the periphery;
 - Expansion of clear retrosternal space;
 - small, verticalized cord.
 • Hemoglobin and hematocrit: normal /
low (without poliglobulia);
Predominantly bronchial or
blue bloaters (BB); COPD
type B
 Clinical
 Subjective:
 - Appears in a big smoker;
 - with a long history of: chronic cough and
mucous / mucopurulent expectoration, which in
time become more frequent and prolonged;
 - dyspnea appears late, initially as an effort
dyspnea, which progressively becomes
permanent dyspnea and whose severity is
appropriate to the degree of obstruction.
Predominantly bronchial or
blue bloaters (BB); COPD
type B
 Objective:
 General Inspection
 • Overweight, cyanotic, polypneic patients who
do not use accessory respiratory muscles.
 Respiratory system
 • normally conformed thorax;
 • normosonority / hipersonority;
 • subcrepitant rales ± sibilant and ronflant rales
+- diminished vesicular whispering.
Predominantly bronchial or
blue bloaters (BB); COPD
type B
 Cardiovascular:
 • enlargement of the right ventricle
(Harzer sign present);
 • Systolic bouts of tricuspid insufficiency
(TI);
 • turgescent jugular ;
 • peripheral edema and cyanosis
Predominantly bronchial or
blue bloaters (BB); COPD
type B
 • Paraclinical
 • Gasometry: PaCO2 increased (> 50
mmHg), low PaO2, low SaO2;
 • FVT: Low FEVS1; TPC normal; RV
normally increased slightly;
 • Alveolo-capillary membrane diffusion
capability: Normal DLCO.
Predominantly bronchial or
blue bloaters (BB); COPD
type B
 • Pulmonary Radiography:
 - emphasizing the peribronhovascular
drawing in the lower areas;
 - cranial distribution of pulmonary
circulation;
 - increase of the cardiac figure on the
right side;
Predominantly bronchial or
blue bloaters (BB); COPD
type B
 • Differential diagnosis is done with:
 1. Persistent bronchial asthma.
 2. Congestive heart failure (CHF)
associated with stasis of chronic
bronchitis 3. bronchiectasis
 4. Tuberculosis (TB)
 5. Sarcoidosis