Pathology of respiration. (Subject 15)
1. Pathology of Respiration24 March 2015
2. Respiratory failureLungs are unable to provide:
an adequate supply of O2
and/or to remove CO2 efficiently
In arterial blood: pO2 - 95 - 100 mm Hg
pCO2 - 43 - 46 mm Hg
Acute failure – minutes to hours (bronchial asthma
attack, acute pneumonia).
Subacute –days to weeks (pneumonia, bronchitis).
Chronic – months to years (emphysema of lungs,
disseminated lung fibrosis).
3. Respiratory failure classificationType 1 – hypoxia without hypercapnia
low oxygen in the air
pnemonia, lung edema
gases diffusion disturbances
Type 2 – hypoxia with hypercapnia
reduced breathing effort;
increased resistance to breathing (asthma);
in the area of the lung that is not available
for gas exchange (COPD,emphysema).
4. Reasons of respiratory failureDisturbances of lungs function
alveolar ventilation-perfusion ratio,
gases diffusion through alveolarcapillary membrane.
5. Reasons of respiratory failureExtra-lungs disturbances of:
nervous regulation of respiration (brain
stroke or trauma, tumour, drugs overdose),
respiratory muscles function (myasthenia,
chest respiratory movements (fracture of
ribs or spinal column, chest wall deformities),
blood circulation in the lungs (cardiac
failure, severe anemia).
6. Disturbances of alveolar ventilationMIXED
VIOLATIONS OF RESPIRATION
of respiratory center
7. Obstructive lung disordersObstruction of the upper respiratory ways:
embolism (foreign substance),
spasm of larynx (neurogenous, inflammatory).
Decreased permeability of the lower respiratory
increased bronchial muscles tonus (bronchospasm),
embolism of bronchi:
edema of bronchial mucous membranes
hypersecretion of mucus by bronchial glands
Violation of bronchi flexibility
8. Restrictive lung diseasesDisturbances of lung’s expansion
area of lung (resection, tuberculosis)
elasticity of lung tissue
(pneumosclerosis, lung fibrosis,
Alveolar or interstitial lung edema
Acute respiratory distress syndrome
Deficiency of surfactant (premature
9. Restrictive lung diseasesExtrapulmonary reasons:
Changes in pleura and mediastinum
(exudative pleurisy, pneumothorax,
Changes of thorax and respiratory
muscles (deformation of thorax,
paralysis of diaphragm).
Changes of abdominal cavity organs
10. Disorders of perfusionHyperperfusion
Local - pneumonia.
Total - stress reaction or asphyxia.
Erythrocytes have less time for normal
gas exchange hypoxemia.
The diffusion of CO2– not altered.
Type 1 respiratory failure
11. Disorders of perfusionHypoperfusion
heart pathology (heart failure, valvular
vessels pathology (atherosclerosis,
low cardiac output
opening of shunts between arteries and
veins of pulmonary circulation
obstruction of lung vessels
Type 1 respiratory failure
12. Mismatching of ventilation and perfusionVentilation/perfusion ratio differs in lungs
Reason of pathological mismatch:
Problems with ventilation
Collapsed airways (emphysema)
Bronchoconstriction (COPD, asthma)
Inflammation (bronchitis, pneumonia)
Lung diseases (fibrosis, pulmonary vascular
Low oxygen in alveoli perfusion
Carbon dioxide is increased
Type 2 respiratory failure
13. Diffusion impairmentdistance for diffusion (lung edema,
inflammation, fibrous changes).
permeability of the alveolar
capillary membrane ( ARDS,
pulmonary edema, emphysema).
Type 1 respiratory failure
14. Manifestations of respiratory failureHypoxemia - pO2 < 50 mm Hg
Hypercapnia - pCO2 >50 mm Hg.
resulting from impaired function of
resulting from activation of
15. Hypoxemia Manifestationsimpairment of mental performance
central or peripheral cyanosis
heart rate, hyperventilation
16. Hypercapnia ManifestationspH and respiratory acidosis
compensated by renal bicarbonate
vasodilating effect of CO2 :
increase in cerebral blood flow and cerebral
spinal fluid pressure (headache);
warm and flushed skin.
Nervous system effects of CO2 progressive somnolence, disorientation,
17. Acute respiratory distress syndrome (ARDS)Causes
aspiration of gastric contents, toxic
trauma (with or without fat emboli),
pneumonia, alveolar bleedings
reactions to drugs and toxins.
18. ARDS pathogenesis and clinicsand
permeability of the
•Neutrophils - inactivate
surfactant and damage
of the alveolar cells.
• lung becomes harder
19. ARDS clinical manifestationrapid onset, 12 to 18 hours after
in respiratory rate
signs of respiratory failure
diffuse bilateral consolidation of the
multiple organ failure (kidneys, GIT,
CNS, and cardiovascular system)
20. Pulmonary edemacardiogenic (left-sided heart failure)
21. Non-cardiogenic pulmonary edemaalveolar walls damage by toxic compounds
(Phosporus), proteolytic enzymes (a.
microbe affection of lungs (local – bacterial
pneumonia, systemic – sepsis)
quick intravenous infusion of big amount of
fluid (physiological solution, blood substitutes)
– due to ”blood dilution”
anaphylactic allergic reaction – due to BAS
catecholamines – generalized
vasoconstriction lung hypertension and
22. Pulmonary edema symptomsAcute
coughing up blood
coma and death
urination at night)
to lie down flat due to
dyspnea (episodes of
23. Pulmonary edema symptomsChronic pulmonary
(inability to lie
down flat due to
24. Short breath (dyspnea)violation of frequency, depth, rhythm
changes of respiratory movements
25. Dyspnea classificationAccording to pathogenesis
Cerebral dyspnoea (central) - violation of
respiratory center or cortex function.
Lung dyspnoea– diseases of lungs,
Cardiac dyspnoea - heart diseases with
Hematic dyspnoea - in blood oxygen
capacity (anaemia), acidosis.
26. Dyspnea classificationDue to dyspnea character:
Due to altered phase of respiration:
27. Dyspnoe mechanismsHumoral – increase of pCO2 and
decrease of pO2, shift of pH to the
Neuroregulatory – violated
impulsion from chemoreceptors
Central – dysfunction of respiratory
center, or cortex neurons.
28. Cerebral dyspneaExcitation of respiratory centre - frequent
Inhibition of respiratory center - frequent
Periodic breathing appears at brain
endogenous and exogenous intoxications
29. Cheyne-Stokes respirationfailure of the respiratory center
bigger concentrations of CO2 are needed
for the excitation of respiratory centre.
causes: strokes, head injuries or brain
tumors, congestive heart failure, morphine
30. Bioth's respirationscluster respiration.
damage to the medulla oblongata
(stroke, trauma, compression).
31. Kussmaul breathingThe cause of Kussmaul breathing is
respiratory compensation for a
metabolic acidosis (ketoacidosis,
low pCO2 due to deep breathing.
32. Agonal respirationshallow, irregular inspirations
followed by irregular pauses.
gasping, labored breathing,
accompanied by strange
vocalizations and myoclonus.
extreme hypoxia or anoxia
33. Other dyspnea typesLungs dyspnea
Embolism or narrowing of upper respiratory
ways (stenotic breath)
bronchial asthma (expiratory dyspnoea)
cardiac failure, heart valves pathology
metHb formation (CO poisoning).
34. Asphyxiaa condition of severe deficiency of oxygen
supply with severe disorders of nervous
system, respiration and circulation of the
Insufficient environmental oxygen:
Inhalation of non-oxygen gases (helium,
Loss of aircraft cabin pressure;
Exposure to a vacuum.
35. Asphyxia causesPhysical obstruction of air flow
Drowning (water or other liquids).
Choking due to object in the airways or inhalation
Narrowing of the airways (anaphylaxis, asthma).
Disturbances of respiration
Pulmonary agents (phosgene),blood agents
36. Asphyxia stages1st stage - frequency of breathing, BP
and heart rate - phase of inspiratory
dyspnea – compensation of acute hypoxia.
2nd stage- more rare respiration with
enforced expiration, slowing-down of heart
rate and BP - phase of expiratory
3rd stage - temporary (from several
seconds to several minutes) stopping of
breathing (preterminal pause); low BP,
reflexes, loss of consciousness.
4th stage - terminal or agonal breathing
(rare deep convulsive «sighs» during
several minutes); respiratory centre
paralysis and death.
37. Lung volumes measurementForced expiratory volume in one second
(FEV1) is the 1-s-volume exhaled with forceful
pressure from maximal inspiration.
Forced vital capacity (FVC) is the maximum
amount of air forcibly expired after maximum
Total lung capacity (TLC) is the total volume of
air in the lungs, when they are maximally
Residual volume (RV) the volume of air left in
the lungs after a maximal expiration.
38. Difference between obstructive, restrictive and mixed disordersMeasure