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Pathophysiology of the respiratory system

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Pathophysiology of the respiratory system * Reasons for respiratory dysfunction Dysfunction of the respiratory neurons; Chest pathology Respiratory muscles and ... – PowerPoint PPT presentation

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Title: Pathophysiology of the respiratory system


1
Pathophysiology of the respiratory system
2
Reasons for respiratory dysfunction
  • Dysfunction of the respiratory neurons
  • Chest pathology
  • Respiratory muscles and diaphragm pathology
  • Injure of pleura
  • Obstructive lung disease
  • Restrictive lung disease.

3
  • The pathological factors impair metabolism,
    structure and function of nerve cells.
  • They are hypoxia, hypoglycemia, toxic agents,
    inflammatory processes in the brain tissue,
    compression of the medulla, traumas, circulatory
    disorders in the brain.

4
Neurochemical respiratory control system
5
Investigation of terminal breathing in experiment
  • 1 normal breathing
  • 2 apneustic breathing after cutting both vagal
    nerves and brain between pneumotaxic and
    apneustic centers
  • 3 gasping after cutting under dorsal
    respiratory group
  • 4 an arrest of breathing after cutting medulla
    under respiratory neurons.

6
Pathological Patterns of Breathing
  • Eupnea - normal breathing movements
  • Bradypnea - decreased rate of breathing
  • Hyperpnea - increased breathing movement
  • Polypnea increased rate and decreased depth of
    breathing
  • Apnea - arrested breathing
  • Periodic breathing
  • Terminal breathing
  • Asphyxia - inability to breathe

7
Bradypnea
  • Bradypnea decreased rate of breathing, cased by
    lack of impulsation from respiratory neurons,
    that leads to hypoventilation.
  • Bradypnea is observed in hypertension (reflexes
    from carotid sinus baroreceptors), in increased
    ventilatory resistance, inhibition of respiratory
    neurons by hypoxia, effect of narcotic drugs to
    brain that decrease the sensitivity of the
    respiratory neurons to pH or CO2 in CSF,
    functional impaction of nervous system (neurosis,
    hysteria).

8
Hyperpnea
  • Hyperpnea - increased breathing movement.
  • Hyperpnea is a result of intensive nerve or
    humoral stimulation of respiratory neuronal area
    (lack of pO2 in ihaled air, extra pCO2 in ihaled
    air, anemia, acidosis).

9
Polypnoe
  • Polypnea increased rate and decreased depth of
    breathing because of changed activity of
    respiratory neurons by reflex regulation.
  • Polypnea revealed in fever, functional impaction
    of nervous system (hysteria), injure of lungs
    (atelectasis, pneumonia, impaired perfusion),
    pain syndrome in body organs engaged in
    ventilatory function.
  • Polypnea affects breathing in such a manner
    that ultimately sufficient O2 uptake and CO2
    release can no longer be guaranteed.

10
Apnea
  • Apnea - an arrest of breathing lasting a few
    seconds. It is more likely in the presence of a
    metabolic alkalosis because decrease pCO2 in
    blood (after artificial lung ventilation),
    giving adrenalin in blood, inhibition of
    respiratory neurons (as a result of hypoxia,
    toxic effects, organic pathology of the brain) .

11
Periodic breathing
  • CheyneStokes breathing is irregular. The depth
    of breathing periodically becomes gradually
    deeper and then gradually more shallow. It is
    caused by a delayed response of respiratory
    neurons to changes in blood gases resulting in an
    overshooting reaction. It occurs when there is
    hypoperfusion of the brain, or when breathing is
    regulated by a lack of oxygen (hypoxia?, uremia,
    immature infants).
  • Biot breathing consists of a series of normal
    breaths interrupted by long pauses. It is an
    expression of damage to respiratory neurons.
    Gasping also signifies a marked disorder in the
    regulation of breathing (meningitis,
    encephalitis).

12
Terminal breathing
  • In terminal conditions the apneustic breathing
    and severe gasping are revealed.
  • Apneustic breathing consist of prolonged spastic
    inhales, interrupted by brief exhalations
    (impaired connections of apneustic, pneuvmotaxic
    centers and vagal nerve).
  • Severe gasping characterized by gradually
    decreased rate and depth of inhales because of
    arrest of resperatory neurons activity above
    dorsal and ventral respiratory group in medulla
    (in agony of death, terminal period of asphyxia).

13
Short wind
  • Short wind increased breathing because of
    subjective feeling lack of air, when excitatory
    influences to respiratory neurons are more
    intensive, then pathological effects.
  • (in loss of diffusion area, lack of perfusion,
    inflammation and activation of reflexes from
    irritant receptors in pneumonia, decreased
    impulsation from baroreceptors in aorta and
    carotids in blood loss, shock increased
    impulses from chemoreceptors in hypoxia,
    hypercapnia, acidosis, overstratching respiratory
    muscles because of decreased lung elastic recoil,
    obstruction of upper respiratory pathways.

14
Acute deficiency of breathing
  • Acute deficiency of breathing develops in some
    minutes to hours and progressing rapidly.
  • The main pathological mechanisms are hypoxemia,
    hypercapnia, acidosis, central nerve control
    disturbances. Acute deficiency of breathing can
    result in coma.

15
Chronicle deficiency of breathing
  • Chronicle deficiency of breathing is
    characterized by gradual enhance of hypoxemia and
    hypercapnia.
  • Pathological disturbances in chronicle
    deficiency of breathing are less intensive, than
    in acute deficiency of breathing due to
    activation of compensatory mechanisms.

16
Damage to the chest
  • The contamination of air in the pleural cavity is
    called pneumothorax (opened, closed, valvular).
  • If air can enter the pleural cavity and go out
    by place of trauma, this is opened pneumothorax.
  • In case of shift the damaged tissues the air
    cannot go out the pleural cavity and closed
    pneumothorax develops.
  • When mild tissues in the place of trauma permit
    entering of air and prevent outflow of air from
    the pleural cavity, the valvular pneumothorax
    develops.

17
Damage of the respiratory muscles
  • Damage of motoneurons of spinal cord that control
    respiratory muscles may occur due to inflammatory
    and degenerative processes (with amyotrophic
    lateral sclerosis, poliomyelitis, syringomyelia),
    due to intoxication (strychnine, tetanus toxin).
  • Violation of the conduction impulses in the
    peripheral nerves that supply respiratory muscles
    can occur because of inflammation, vitamin
    deficiency, trauma. Diaphragmatic nerve lesion
    leads to paralysis of the diaphragm, which
    manifests its paradoxical movements according to
    changes in pressure in the chest cavity - at the
    inhalation diaphragm rises, at the exhale gets
    plant. Violation of neuromuscular transmission of
    impulses occurs in myasthenia, botulism,
    introduction of muscle relaxants. In all these
    cases, the ventilation function get disturbed.

18
  • When obstructive respiratory insufficiency,
    airway can be broken due to their narrow, leading
    to increased resistance to air movement (when
    inhaled forensic particles, thickening of the
    walls of airways due to inflammation, muscle
    spasm of the larynx, bronchial compression due to
    swelling, inflammation, enlarged thyroid gland .)

19
Causes of bronchial asthma
20
Mechanism that limits maximal expiratory ?ow rate
21
Emphysema
  • In emphysema the lungs lose their elasticity and
    stretch considerably with less transpulmonary
    pressure, so there is lack of pressure from
    within bronchioles - their clearance decreases,
    increases resistance to air movement, difficult
    breath.
  • Exhalation becomes active due to decreased
    elasticity of the lungs, the pressure increases
    and bronchioles collapse, so alveoli are filled
    with residual air.

22
The alveoli filled with residual air because of
emphysema
23
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24
Pathology of the lung in end-stage cystic fibrosis
  • Key features are
  • the widespread mucus impaction of airways and
    bronchiectasis (U)
  • small cysts (C)
  • hemorrhagic pneumonia in lower lobe.

25
Atelectasis
  • Atelectasis caused by airway obstruction and
    absorption of air from the involved lung area on
    the left and by compression of lung tissue on the
    right.

26
Atelectasis
  • The right lung of an infant (left side of photo)
    is pale and expanded by air, whereas the left
    lung is collapsed.

27
Asphyxia
  • The first stage is characterized by deep and
    rapid breathing with a predominance of
    inspiratory phase (inspiratory dyspnea). In the
    second stage begins a gradual decline in
    respiration rate against the background of deep
    respiratory movements. Phase exhalation prevails
    over the inspiratory phase (expiratory
    dyspnea). In the third stage of the frequency
    and depth of respiratory movements decreased
    steadily up to a complete stop breathing. After a
    short term of absent respiration (preterminal
    pause) several rare deep respiratory movements
    are observed (terminal or agonic, breathing).
    Stimulation of breathing at the beginning of
    asphyxia associated with direct and reflex
    excitation of carbon dioxide and respiratory
    center hipoksemichnoyu blood. With the growth
    inhibition of hypoxic brain come the respiratory
    center and complete paralysis of its functions.
    The appearance of terminal respiration explained
    by the excitation of neurons of the caudal
    medulla oblongata.

28
Obstruction of larynx leads to hypoxia
  • ? normal larynx ? Obstruction of larynx from
    edema caused by croup.

29
Violation of ventilation-perfusion ratio
  • To maintain the gas composition of blood it is
    important to not only the absolute value of
    alveolar ventilation, but the proper balance
    between ventilation and perfusion lung. The
    amount of blood flowing through the lungs for 1
    min, equal to 4.5-5 liters, approximately
    corresponds to the value cardiac output. The
    optimal ratio of alveolar ventilation and
    perfusion lung is 0.8 (4 l/ 5 l). It may vary
    upward or downward. In both cases, normal blood
    gas composition can not provide. The
    predominance of ventilation pressure of oxygen in
    the alveoli in blood is sufficient, but blood
    carry out too much carbon dioxide (hipokapniya).
    If, however, ventilation is slower than
    perfusion, hypoxemia and hypercapnia occur.

30
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31
Acute respiratory distress syndrome (ARDS)
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