Pathophysiology of the respiratory system

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Pathophysiology of the respiratory system
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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.

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• 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.

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Neurochemical respiratory control system
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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.

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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

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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).

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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).

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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.

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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) .

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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).

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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).

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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.

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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.

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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.

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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.

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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.

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• 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 .)

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Causes of bronchial asthma
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Mechanism that limits maximal expiratory ?ow rate
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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.

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The alveoli filled with residual air because of
emphysema
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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.

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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.

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Atelectasis

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

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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.

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Obstruction of larynx leads to hypoxia

• ? normal larynx ? Obstruction of larynx from
  edema caused by croup.

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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.

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Acute respiratory distress syndrome (ARDS)