62
1. O2 2. CO2
3. O2/CO2 exchange
4. perfusion
RESPIRATORY DISORDERS
restrictive obstructive
RESPIRATORY FAILURE
o a condition with impaired exchange of gases between thealveolar space and pulmonary cappilaries
o a state, developing during various disorders.
• manifested by changes of the PO2 a PCO2 in arterial blood:
PCO2 >PO2 < physiological value
blood gases normal value RF
PO2 10 – 13.3 kPa (75 – 100 mmHg) < 8 kPa (60 mmHg)
PCO2 4.8 – 6.1 kPa (36 – 46 mmHg) > 7 kPa (55 mmHg)
RESPIRATORY FAILURE
ACUTE CHRONIC
• chronic obstructive pulmonary
disease
• chronic diffuse infiltration ofthe pulmonary parenchyma
• pulmonary edema
• sleep apnea
• neuromuscular disorder
• acute infiltration of the pulmonary parenchyma (pneumonia)
• inhalation of toxins
• pulmonary edema
• embolism in pulmonary circulation
• ARDS
• injury of thorax
• disorders or injury of CNS
• administration of substances depressing the respiration center (anesthetics, sedatives, opiates, barbiturates, alcohol)
RESPIRATORY FAILURE
type I type II
PARTIAL RF GLOBAL RF
o oxygenation failure
o hypoxemia
↓ PO2 & normal PCO2
e.g.: ↓ ambient O2 – high altitude,
pulmonary embolism, diffusion
problems - pneumonia
o ventilation failure
o hypoxemia &
hypercapnia
↓ PO2 & ↓ PCO2
e.g.: suffocation, COPD, substances
depressing the respiration center
RESPIRATORY FAILURE
HYPOXIA
changes in CNS functions & cardiovascular system
first signs: motor instability, irritability, confusionlater: depressive effect on the respiratory center
tachycardia ↑ blood pressure
HYPERCAPNIA
acute – changes in CNS functions : drowsiness, confusion, coma, deathslow – headache, somnolence vasodilation of the cerebral vessels
administration of O2 in ↑ concentrations – a depression of respiration leadingto increased hypercapnia.
Chronic obstructive pulmonary disease (COPD )
o group of respiratory diseases whose common feature isdifficulty exhaling (greater exhalation force is neededand exhaling is slowed)
o from pathophysiological point of view – usually result of
• chronic bronchitis
• emphysema
• asthma
Chronic obstructive pulmonary disease (COPD)
Chronic obstructive pulmonary disease (COPD)
Blanco, Ignacio, et al. "Geographic distribution of COPD prevalence in the World displayed by Geographic Information System maps." European Respiratory Journal(2019): 1900610.Blanco, Ignacio, et al. "Geographical distribution of COPD prevalence in Europe, estimated by an inverse distance weighting interpolation technique." International journal of chronic obstructive pulmonary disease 13 (2018): 57.
Chronic obstructive pulmonary disease (COPD)
Blanco, Ignacio, et al. "Geographic distribution of COPD prevalence in the World displayed by Geographic Information System maps." European Respiratory Journal(2019): 1900610.Blanco, Ignacio, et al. "Geographical distribution of COPD prevalence in Europe, estimated by an inverse distance weighting interpolation technique." International journal of chronic obstructive pulmonary disease 13 (2018): 57.
Chronic obstructive pulmonary disease (COPD)
risk factors:
• exposure to cigarettesmoke (active, passive)
• exposure to chemicals• air pollution
• genetic predisposition• ♀ sex and age• lower social and economic
status• hyperresponsiveness of
respiratory tract• recurrent broncho-
pulmonal infections
Chronic obstructive pulmonary disease (COPD)
o limitation of airflow in bronchi (bronchial obstruction),progressive in nature and associated with an inflammatoryresponse of the lungs to harmful particles or gases in thesurrounding air
chronic bronchitis emphysema
asthma
COPD
airw
ay o
bst
ruct
ion
CHRONIC BRONCHITIS
inflammatory airways disease:
+ excessive production of mucus
+ cough lasting for three monthsin course of two or more following years
+ the absence of bronchiectasis,tuberculosis or any other cause of mentioned symptoms
CHRONIC BRONCHITIS
chronic inflammation
bronchoconstriction
mucus accumulation
obstruction
hyperplasia of submucosal glands
loss of elasticity
damaged mucociliaryapparatus
FACTORS:
CHRONIC BRONCHITIS
o mucus hyperproductiono ↓ ability to clean airways
o ↓ resistance towards infections
o chronic inflammationo bronchoconstrictiono loss of airway elasticity
CHRONIC BRONCHITIS
• mucus hypersecretion• inflammation• loss of elasticity• bronchoconstriction
obstruction
alveolar hypoxia
abnormal ventilation & perfusion
V/Q mismatch
vasoconstriction
↓ ↓
CHRONIC BRONCHITIS
alveolar hypoxia
↓O2 – hypoxemia
↑CO2 – hypercapnia
polyglobulia (polycythemia)
respiratory acidosis
↑ HGB
CHRONIC BRONCHITIS
alveolar hypoxia hypoxic pulmonary vasoconstriction
↓O2
↑ pulmonary resistance↑ blood pressure
CHRONIC BRONCHITIS
PULMONARY HYPERTENSION(Pulmonary hypertension due to lung diseases with/without hypoxia)
↑ afterload of the right ventricle
stagnation of blood
RV decompensation
RV failure
↑ pressure &
resistance
↓CO of the left ventricle
RAAS activation
↑ EC volume
CHRONIC BRONCHITIS
SIGNS AND SYMPTOMS
mucous
sputum
productive
cough
wheezing
↑ jugular
venous
pressure
reduced
resistance
towards
infections
dyspnea/
orthopnea
fatigue,
weakness
edema
cyanosis
PULMONARY EMPHYSEMA
o an abnormal and permanent distention of airways peripheral to terminal bronchioles - alveoli, associated with lung tissue damage without fibrosis
PULMONARY EMPHYSEMA
alveolar macrophage
neutrophils
cytokinesproteases
elastases
alveolar damage
capillary damage
the dominance of proteolytic cleavage over the action of the antiprotease system
PULMONARY EMPHYSEMA
alpha-1-antitrypsin
alpha-1-antitrypsindeficiency
PULMONARY EMPHYSEMA
the dominance of proteolytic cleavage over the action of the antiprotease system
PULMONARY EMPHYSEMA
lung hyperinflation (air trapping)
PULMONARY EMPHYSEMA
lung hyperinflation
(air trapping)
PULMONARY EMPHYSEMA
centroacinar paraacinar
PULMONARY EMPHYSEMA
o loss of airway elasticity ↑ resistance↓ ventilation
o destruction of intraalveolar septa↓ surface area for gas exchange
o airway collapse during exhalation hyperinflation - ↓O2 ↑CO2
o destruction of pulmonary capillaries↓ perfusionhypoxemia – respiratory acidosispulmonary hypertension
SIGNS AND SYMPTOMS
PULMONARY EMPHYSEMA
barrel chest
SIGNS AND SYMPTOMS
dyspnea
(exertional-
at rest )
fatigue,
weakness
cachexia
PULMONARY EMPHYSEMA
cough
wheezing
barrel chest
failure of right
ventricle
pursed-lip breathingengagement
of accessory muscles of respiration
Chronic obstructive pulmonary disease (COPD
CHRONIC BRONCHITIS and PULMONARY EMPHYSEMA - develop as two distinct processes usually simultaneously
- temporarily or permanently dominated by one of these processes
„Blue bloaters“ „Pink puffers“
BRONCHIAL ASTHMA
inflammatory disease of airways, characterized by
o increased responsiveness of airways to various stimulio attacks with escalated reversible bronchoconstrictiono expiratory dyspnea o cougho wheezing
turbulent airflow through the narrowed airways
+↑ viscous secretion
5-6 x ↑ resistance
50 % ↓ VC
progressive – moderate yet permanent airway obstruction
BRONCHIAL ASTHMA
1. inflammation• ↑ numb. of
inflammatory cells
2. airways hyperactivity 3. obstruction • edema• cell infiltration• epithelial cells peeling
BRONCHIAL ASTHMA
ANAPHYLACTIC REACTION
1. exposure re-exposure
BRONCHIAL ASTHMA
atopic non - atopic
inflammation due to systemic IgEproduction
inflammation due to local IgEproduction
BRONCHIAL ASTHMA
ANAPHYLACTIC REACTION
bronchoconstriction
1. early asthmatic response 2. late asthmatic response
participation of inflammatory cells
adhesion & migration of leukocytes
BRONCHIAL ASTHMA
tachypnoe
cough wheezing
dyspnea
tachycardia
↑ systolic
blood
pressure
cyanosis
during asthma attack :
HYPOXIAHYPOCAPNIA→ respiratory alkalosis
during asthma attack: !respiratory acidosis → severe airway
obstruction
restlessness
Restrictive lung disease
o a group of respiratory diseases, in which the expansion of lungs isreduced, leading to reduced lung compliance, inadequateventilation and oxygen saturation of tissues
• parenchymal
• extra-parenchymal
• acute
• chronic
Restrictive lung disease
parenchymal
• interstitial lung diseases
• idiopathic pulmonary fibrosis
• sarcoidosis
• induced by inhalation of dust particles
• induced by drugs
extra-parenchymal
• pleural effusion
• pneumothorax
• tumors
• lung resection
• kyphoscoliosis
• ribs fracture
• obesity
• neuromuscular disorders
• myasthenia gravis
• muscular dystrophy
• cervical spinal cord injury
• acute damage oflung parenchyma
• ARDS
INTERSTITIAL LUNG DISEASES
o a group of diseases with common feature –
diffuse inflammatory alterations in terminal parts of the
lungs and airways
thickening of interstitial alveolar walls due to fibroticchanges
INTERSTITIAL LUNG DISEASES
• damage of epithelial cells of alveoli in terminal bronchioles• damage of endothelial cells in lung capillaries
destruction of alveolar-capillary units
INTERSTITIAL LUNG DISEASES
5 – 10 μm
↑ alveolar-capillary membrane
↓ alveolar volume
INTERSTITIAL LUNG DISEASES
alveolar-capillary unit
INTERSTITIAL LUNG DISEASESIDIOPHATIC PULMONARY FIBROSIS
neutrophil-macrophage alveolitis leading progressively to destruction of the alveolar-capillary units
• inflammatory cells in the walls and epithelium of alveoli • macrophages
INTERSTITIAL LUNG DISEASESIDIOPHATIC PULMONARY FIBROSIS
• alveolar macrophages – production of growth factors:PDGF –platelet derived growth factor fibronectinTGF – transforming growth factor
neutrophil-macrophage alveolitis leading progressively to destruction of the alveolar-capillary units
• inflammatory cells in the walls and epithelium of alveoli • macrophages• eosinophils• neutrophils – ROS and
proteases
• destruction of pneumocytes I• proliferation of pneumocytes II• proliferation of mesenchymal
cells – collagen production
• rapture of basement membrane-intraalveolar fibrosis
• damage of endothelial capillary cells
INTERSTITIAL LUNG DISEASESIDIOPHATIC PULMONARY FIBROSIS
INTERSTITIAL LUNG DISEASESIDIOPHATIC PULMONARY FIBROSIS
INTERSTITIAL LUNG DISEASESIDIOPHATIC PULMONARY FIBROSIS
INTERSTITIAL LUNG DISEASES
SARCOIDOSIS
chronic multisystem disorder, where the organs are damaged by inflammatory process with the formation of necrotizing granulomas
• ↑ number of T- lyphocytes and mononuclear phagocytes
formation of necrotizing granulomas
INTERSTITIAL LUNG DISEASES
FIBROSIS OF THE LUNGS IN SYSTEMIC DISEASES
• rheumatoid arthritis• lupus erythematosus• idiopathic lung hemosiderosis
• HIV • chronic eosinophil pneumonia
INTERSTITIAL DISEASES DUE TO DUSTS INHALATION
• anorganic particles – PNEUMOKONIOSIS• asbestosis, silicosis, beryliosis
• organic particles – HYPERSENSITIVE PNEUMONITIS• byssinosis, farmer‘s lungs
INTERSTITIAL LUNG DISEASES INDUCES BY DRUGS
• antineoplastic drugs• antibiotics• radiotherapy• O2 inhalation in high concentrations
SIGNS AND SYMPTOMS
dyspnea
(exertional -
at rest)
fatigue,
weakness
INTERSTITIAL LUNG DISEASES
tissue hypoxia
failure of right
ventricle
cyanosis
PNEUMONIA
o an inflammatory process affecting the pulmonaryparenchyma, primarily terminal bronchioles and alveoli
• in majority of cases it is caused by infection• spreads to the interstitium surrounding the alveoli
2
1
34
microorganisms entering the lungs:
1. by direct inhalation of microbes from the air
2. from the mouth and nasopharynx
3. by penetration from the surroundings
4. by the haematogenous spread fromanother part of organism
PNEUMONIA
RISK FACTORS
PNEUMONIA
anatomical barrier of mechanical type
surmounted during sleep
aspiration of 0,0001 ml of secretion
PNEUMONIA
1. cytokines production• vasodilation• ↑ vascular permeability
2. neutrophil transfer to the alveoli• proteolytic enzymes• tissue damage
fluid transfer to interstitiumand alveoli
PNEUMONIA
• affects the lung lobe• develops distally and
spreads proximally
1. congestionexudate formation - ↑ protein content hyperemiamicrobes multiplication
2. red hepatizationspreading of exsudate into the alveoliaccumulation of polymorphonuclear neutrophilesextravagation of red blood cells into alveolar spaces
PNEUMONIA
2. red hepatization
PNEUMONIA
• affects the lung lobe• develops distally and
spreads proximally
1. congestionexudate formation - ↑ protein content hyperemiamicrobes multiplication
2. red hepatizationspreading of exsudate into the alveoliaccumulation of polymorphonuclear neutrophilesextravagation of red blood cells into alveolar spaces
3. grey hepatization↑ fibrin productiondisintegration of red blood cells
PNEUMONIA
3. grey hepatization
PNEUMONIA
• affects the lung lobe• develops distally and
spreads proximally
1. congestionexudate formation - ↑ protein content hyperemiamicrobes multiplication
2. red hepatizationspreading of exsudate into the alveoliaccumulation of polymorphonuclear neutrophilesextravagation of red blood cells into alveolar spaces
3. grey hepatization↑ fibrin productiondisintegration of red blood cells
4. resolutionexsudate reabsorption
PNEUMONIA
• affects different parts of the lung tissue in both lungs
• it spreads along the bronchioles until it reaches the alveolus
PNEUMONIA
• interleukin-1• catecholamines
dyspnea
cough
fever
> 38.5 °Cchest pain
(pleuritís)
tachycardia100 -140
bpm
sputum
production
chills
dry→productive
