Mechanics of Respiration

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Mechanics of Respiration

• Chapter 16

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• Chapter 16 Outline
• Respiratory Structures
• Physical Aspects of Ventilation
• Mechanics of Breathing
• Pulmonary Disorders

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Respiration

• 3 related functions ventilation, gas exchange,
  02 utilization (cellular respiration)
• Ventilation moves air in out of lungs (external
  respiration)
• Gas exchange between blood tissues, O2 use by
  tissues internal respiration
• Gas exchange passive via diffusion

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Structure of Respiratory System

• Air ? mouth ? trachea ? right left bronchi ?
  bronchioles ? terminal bronchioles ? respiratory
  bronchioles ? alveoli

Fig 16.4
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Structure of Respiratory System

• Gas exchange occurs in respiratory bronchioles
  alveoli ( respiratory zone)
• All other structures conducting zone
• Alveoli clustered at ends of respiratory
  bronchioles

Fig 16.4
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Structure of Respiratory System continued

• Gas exchange occurs across the 300 million
  alveoli (60-80 m2 total surface area)
• 1 alveolar 1 endothelial cell between air and
  blood

Insert 16.1
Fig 16.1
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Conducting Zone

• Warms humidifies inspired air
• Mucus lining filters cleans inspired air
• Mucus moved by cilia to be expectorated

Insert fig. 16.5
Fig 16.5
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Thoracic Cavity

• Bordered by the diaphragm
• Heart, large blood vessels, trachea, esophagus,
  thymus, lungs
• Below diaphragm is abdominopelvic cavity
• Intrapleural space thin fluid layer between
• visceral pleura covers lungs
• parietal pleura lines thoracic cavity walls

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Physical Aspects of Ventilation

• Pressure differences induced by changes in lung
  volumes
• Air moves from higher to lower pressure
• Ease of ventilation influenced by
• Compliance
• Elasticity
• surface tension

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Intrapulmonary Intrapleural Pressures

• Visceral parietal pleurae adhere to each other
  so lungs remain in contact with chest walls
• expand contract with thoracic cavity

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• Inspiration/expiration Intrapulmonary is always
  higher than intrapleural pressure
• Positive transmural pressure (intrapulmonary -
  intrapleural pressure) keeps lungs inflated

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Boyles Law (P 1/V)

• Changes in intrapulmonary pressure occur as a
  result of changes in lung volume
• Pressure of gas is inversely proportional to
  volume
• Increase in lung volume decreases intrapulmonary
  pressure inspiration
• Decrease in lung volume raises intrapulmonary
  pressure expiration

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Compliance

• How easily lung expands with pressure
• Change in lung volume per change in transmural
  pressure (DV/DP)
• Reduced by factors that cause resistance to
  distension

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Elasticity

• Tendency to return to initial size after
  distension
• Due to high content of elastin proteins
• Elastic tension increases during inspiration is
  reduced by recoil during expiration

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Surface Tension (ST)

• ST elasticity forces that promote alveolar
  collapse resist distension
• Lungs secrete absorb fluid, normally leaving a
  thin film of fluid on alveolar surface
• Fluid absorption occurs by osmosis driven by Na
  active transport
• Fluid secretion driven by active transport of Cl-
  out of alveolar epithelial cells

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Surface Tension continued

• Law of Laplace pressure in alveolus is directly
  proportional to ST inversely to radius of
  alveoli
• pressure in smaller alveoli would be greater than
  in larger alveoli, if ST were same in both

Insert fig. 16.11
Fig 16.11
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Surfactant

• Phospholipids secreted by type II alveolar cells
• Lowers ST by getting between H20 molecules, cant
  hydrogen bond

Fig 16.12
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Surfactant continued

• Prevents ST from collapsing alveoli
• Surfactant secretion begins in late fetal life
• Premies are often born with Respiratory Distress
  Syndrome or RDS)
• In adults, septic shock may cause acute
  respiratory distress syndrome (ARDS) which
  decreases compliance surfactant secretion

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Mechanics of Breathing

• Pulmonary ventilation consists of inspiration
  (inhalation) expiration (exhalation)
• Alternately increasing decreasing volumes of
  thorax lungs

inspiration
expiration
Fig 16.13
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Quiet Breathing

• Inspiration diaphragm contracts, increasing
  thoracic volume vertically
• Parasternal external intercostal contraction
  contributes by raising ribs, increasing volume
  laterally
• Expiration is due to passive recoil

Fig 16.14
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Deep Breathing

• Inspiration contraction of extra muscles to
  elevate ribs scalenes, pectoralis minor,
  sternocleidomastoid muscles
• Expiration contraction of internal intercostals
  abdominal muscles

Fig 16.14
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Mechanics of Pulmonary Ventilation
Insert fig. 16.15
Fig 16.15
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Pulmonary Function Tests

• Assessed clinically by spirometry measures
  volumes of air moved during inspiration
  expiration
• Anatomical dead space air in conducting zone
  where no gas exchange occurs

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Pulmonary Function Tests continued

• Tidal volume amount of air expired/breath in
  quiet breathing
• Vital capacity amount of air that can be
  forcefully exhaled after a maximum inhalation
• sum of inspiratory reserve, tidal volume,
  expiratory reserve

Fig 16.16
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Restrictive Disorders

• Characterized by reduced vital capacity but with
  normal forced vital capacity
• E.g. pulmonary fibrosis

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Obstructive Disorders

• Normal vital capacity but expiration is retarded
• E.g. asthma
• Diagnosed by tests, such as forced expiratory
  volume, that measure rate of expiration

Insert fig. 16.17
Fig 16.17
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Pulmonary Disorders

• Frequently accompanied by dyspnea, a feeling of
  shortness of breath
• Asthma results from episodes of obstruction of
  air flow thru bronchioles
• Caused by inflammation, mucus secretion,
  broncho constriction
• Inflammation contributes to increased airway
  responsiveness to agents that promote bronchial
  constriction
• Provoked by allergic reactions that release IgE,
  by exercise, by breathing cold, dry air, or by
  aspirin

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Pulmonary Disorders continued

• Emphysema a chronic, progressive condition that
  destroys alveolar tissue, resulting in fewer,
  larger alveoli
• Reduces surface area ability of bronchioles to
  remain open during expiration
• Collapse of bronchiole during expiration causes
  air trapping, decreasing gas exchange
• Commonly occurs in long-term smokers
• Cigarette smoking stimulates macrophages
  leukocytes to secrete protein-digesting enzymes
  that destroy tissue

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emphysema
normal lung
Fig 16.18
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Pulmonary Disorders continued

• Sometimes lung damage leads to pulmonary fibrosis
  instead of emphysema
• Characterized by accumulation of fibrous
  connective tissue
• Occurs from inhalation of particles lt6?m in size,
  such as in black lung disease (anthracosis) from
  coal dust

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