RESPIRATORY PHYSIOLOGY

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RESPIRATORY PHYSIOLOGY

• By
• Dr. RASHA ABULMAGD

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Respiratory System

• Primary function is to obtain oxygen for use by
  body's cells eliminate carbon dioxide that
  cells produce
• Includes respiratory airways leading into ( out
  of) lungs plus the lungs themselves
• Pathway of air nasal cavities (or oral cavity) gt
  pharynx gt trachea gt primary bronchi (right
  left) gt secondary bronchi gt tertiary bronchi gt
  bronchioles gt alveoli (site of gas exchange)

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Breathing is an active process

• The external intercostals plus the diaphragm
  contract to bring about inspiration
• Diaphragm a sheet separating the thorax from the
  abdomen. Innervation is from the phrenic nerves
  (C3-5)
• Contraction of external intercostal
  musclesinnervated by their intercostal nerves
  T1-12)
• Accessory muscles of respiration only become
  important during exercise or respiratory distress

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To exhale

• During quiet breathing expiration is a passive
  process, relying on the elastic recoil of the
  lung and chest wall.
• When ventilation is increased, such as during
  exercise, expiration becomes active with
  contraction of the muscles of the abdominal wall
  and the internal intercostals.

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• Rhythmicity center of the
• medulla controls automatic breathing
• consists of interacting neurons that fire either
  during inspiration (I neurons) or expiration (E
  neurons)
• I neurons - stimulate neurons that innervate
  respiratory muscles (to bring about inspiration)
• E neurons - inhibit I neurons (to 'shut down' the
  I neurons bring about expiration)
• Apneustic center (located in the pons) -
  stimulate I neurons (to promote inspiration)
• Pneumotaxic center (also located in the pons) -
  inhibits apneustic center inhibits inspiration
  

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Factors Involved in Increasing Respiratory Rate

• Chemoreceptors
• Peripheral in aorta carotid arteries
• Central medulla
• -They are stimulated more by increased CO2
  levels than by decreased O2 levels
• -They stimulate Rhythmicity Areas
  ?increased rate of respiration
• Heavy exercise ? greatly increases respiratory
  rate
• Possible factors
• reflexes originating from body movements
  (proprioceptors)
• increase in body temperature
• epinephrine release (during exercise)
• Voluntary Control through impulses from the
  cerebral cortex

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• Tidal Volume each normal quiet breath (
  7-10ml/kg)
• Inspiratory Reserve Volume
• maximal additional volume that can be
  inspired above TV
• Expiratory Reserve Volume
• maximal additional volume that can be
  expired above TV
• Residual Volume volume remaining after maximal
  expiration
• Functional Residual Capacity is the volume of
  air in the lungs at the end of a normal
  expiration
• Vital Capacity max volume of gas that can be
  exhaled after max inspiration

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Dead SpacePart not participating in gas exchange

• Anatomical dead-space tracheobronchial tree
  down to respiratory bronchioles. Normally 2ml/kg
  or 150ml in an adult, roughly a third of the
  tidal volume.
• Alveolar Dead Space Non perfused alveoli
• Physiologic Dead Space Anatomical Alveolar

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Factors Affecting Dead Space

• Factors Increasing Dead Space
• Upright position
• Neck extension
• Age
• ve pressure ventilation
• Decreased pulmonary perfusion
• Lung disease
• Factors Decreasing Dead Space
• Supine position
• Neck flexion
• Endotracheal Intubation

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• The tidal volume (500ml) multiplied by the
  respiratory rate (14 breaths/min) is the minute
  volume (7,000ml/min)
• The part of the tidal volume which does take part
  in respiratory exchange multiplied by the
  respiratory rate is known as the alveolar
  ventilation (approximately 5,000ml/min)

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Resistance/Compliance

• Two aspects oppose lung expansion and airflow and
  therefore need to be overcome by respiratory
  muscle activity. These are
• the airway resistance
• the compliance of the lung and chest wall.
• Resistance of the airways describes the
  obstruction to airflow provided by the conducting
  airways, resulting largely from the larger
  airways , plus a contribution from tissue
  resistance resulting produced by friction as
  tissues of the lung slide over each other during
  respiration.

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• Compliance denotes distensibility (stretchiness),
  and in a clinical setting refers to the lung and
  chest wall combined, being defined as the volume
  change per unit pressure change.
• Low Compliance the lungs are stiffer and more
  effort is required to inflate the alveoli.
• Conditions that worsen compliance, such as
  pulmonary fibrosis, produce restrictive lung
  disease.

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Compliance varies within the lung according to
the degree of inflation

• Poor compliance is seen at low volumes (because
  of difficulty with initial lung inflation) and at
  high volumes (because of the limit of chest wall
  expansion)
• Best compliance is in the mid-expansion range.

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ALVEOLI

• The walls of alveoli are coated with a thin film
  of water this creates a potential problem.
  Water molecules, are more attracted to each other
  than to air, and this attraction creates a force
  called surface tension.
• During exhalation surface tension increases as
  water molecules come closer together.
  Potentially, surface tension could cause alveoli
  to collapse and, in addition, would make it more
  difficult to 're-expand' the alveoli.
• Serious problems if alveoli collapsed they'd
  contain no air no oxygen to diffuse into the
  blood , if 're-expansion' was more difficult,
  inhalation would be very, very difficult if not
  impossible.

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Role of Pulmonary Surfactant

• Surfactant decreases surface tension which
• increases pulmonary compliance (reducing the
  effort needed to expand the lungs)
• reduces tendency for alveoli to collapse

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What is Partial Pressure?

• The individual pressure exerted independently by
  a particular gas within a mixture of gasses.
• The air we breath is a mixture of gasses
  primarily nitrogen, oxygen, carbon dioxide.
• The total pressure generated by the air is due in
  part to nitrogen, in part to oxygen, in part to
  carbon dioxide.
• That part of the total pressure generated by
  oxygen is the 'partial pressure' of oxygen, while
  that generated by carbon dioxide is the 'partial
  pressure' of carbon dioxide. A gas's partial
  pressure, therefore, is a measure of how much of
  that gas is present (e.g., in the blood or
  alveoli).  

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• The partial pressure exerted by each gas in a
  mixture equals the total pressure times the
  fractional composition of the gas in the mixture.
• So, given that total atmospheric pressure (at sea
  level) is about 760 mm Hg and, further, that air
  is about 21 oxygen, then the partial pressure of
  oxygen in the air is 0.21 times 760 mm Hg or 160
  mm Hg.

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Partial Pressures of O2 and CO2 in the body

• Alveoli
• PO2 100 mm Hg
• PCO2 40 mm Hg
• Alveolar capillaries
• Entering the alveolar capillaries
• PO2 40 mm Hg (relatively low because this blood
  has just returned from the systemic circulation
  has lost much of its oxygen)
• PCO2 45 mm Hg (relatively high because the
  blood returning from the systemic circulation has
  picked up carbon dioxide)

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• Blood leaving the alveolar capillaries returns to
  the left atrium is pumped by the left ventricle
  into the systemic circulation. Entering the
  systemic capillaries
• PO2 100 mm Hg
• PCO2 40 mm Hg
• Body cells (resting conditions)
• PO2 40 mm Hg
• PCO2 45 mm Hg
• Because of the differences in partial pressures
  of oxygen carbon dioxide in the systemic
  capillaries the body cells, oxygen diffuses
  from the blood into the cells, while carbon
  dioxide diffuses from the cells into the blood.
• Leaving the systemic capillaries
• PO2 40 mm Hg
• PCO2 45 mm Hg
• Blood leaving the systemic capillaries returns to
  the heart (right atrium) via venules veins This
  blood is then pumped to the lungs (and the
  alveolar capillaries) by the right ventricle.

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Gas Diffusion

• The alveoli provide an enormous surface area for
  gas exchange with pulmonary blood (between
  50-100m2)
• Under resting conditions pulmonary capillary
  blood is in contact with the alveolus for about
  0.75 second in total and is fully equilibrated
  with alveolar oxygen after only about a third of
  the way along this course.
• Lung disease impairs diffusion
• At rest there is usually still sufficient time
  for full equilibration of oxygen
• During exercise, pulmonary blood flow is quicker,
  shortening the time available for gas exchange,
  and so those with lung disease are unable to
  oxygenate the pulmonary blood fully and thus have
  a limited ability to exercise.
• Carbon dioxide diffuses across the
  alveolar-capillary membrane 20 times faster than
  oxygen so the above factors are less liable to
  compromise transfer from blood to alveoli.

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How are Oxygen Carbon Dioxide Transported in
Blood

• Oxygen is carried in blood
• 1 - bound to hemoglobin (98.5 of all oxygen in
  the blood)
• 2 - dissolved in the plasma (1.5)
• Because almost all oxygen in the blood is
  transported by hemoglobin, the relationship
  between the concentration (partial pressure) of
  oxygen and hemoglobin saturation (the of
  hemoglobin molecules carrying oxygen) is an
  important one.
• Hemoglobin saturation
• extent to which the hemoglobin in blood is
  combined with O2
• depends on PO2 of the blood

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• At high partial pressures of O2 (above 40 mm Hg),
  hemoglobin saturation remains rather high
  (typically about 75 - 80). This rather flat
  section of the oxygen-hemoglobin dissociation
  curve is called the 'plateau.'
• Under resting conditions, only about 20 - 25 of
  hemoglobin molecules give up oxygen in the
  systemic capillaries. This is significant (in
  other words, the 'plateau' is significant)
  because it means that you have a substantial
  reserve of oxygen.

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• When you do become more active, partial pressures
  of oxygen in your (active) cells may drop well
  below 40 mm Hg. A look at the oxygen-hemoglobin
  dissociation curve reveals that as oxygen levels
  decline, hemoglobin saturation also declines -
  and declines precipitously. This means that the
  blood (hemoglobin) 'unloads' lots of oxygen to
  active cells - cells that, of course, need more
  oxygen.

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Factors Affecting Oxygen Haemoglobin Dissociation
Curve

• The oxygen-hemoglobin dissociation curve 'shifts'
  under certain conditions
• pH changes
• temperature changes
• 2,3-diphosphoglycerate levels
• CO2 levels

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Carbon Dioxide-transported from the body cells
back to the lungs as

• 1 - Bicarbonate (HCO3) - 60
• formed when CO2 (released by cells making ATP)
  combines with H2O (due to the enzyme in red blood
  cells called carbonic anhydrase)
• 2 Carbaminohemoglobin-30
• formed when CO2 combines with hemoglobin
  (hemoglobin molecules that have given up their
  oxygen)
• 3 - Dissolved in plasma-10

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Perfusion/Ventilation/ShuntPerfusion

• Distribution throughout the lung is largely due
  to the effects of gravity.
• Therefore in the upright position this means that
  the perfusion pressure at the base of the lung is
  equal to the mean pulmonary artery pressure
  (15mmHg or 20cmH2O) plus the hydrostatic pressure
  between the main pulmonary artery and lung base
  (approximately 15cmH2O).
• At the apices the perfusion pressure is very low,
  and may at times even fall below the pressure in
  the alveoli leading to vessel compression and
  intermittent cessation of blood flow

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Ventilation

• The distribution of ventilation across the lung
  is related to the position of each area on the
  compliance curve at the start of a normal tidal
  inspiration (the point of the FRC)
• Because the bases are on a more favourable part
  of the compliance curve than the apices, they
  gain more volume change from the pressure change
  applied and thus receive a greater degree of
  ventilation.
• Although the inequality between bases and apices
  is less marked for ventilation than for
  perfusion, overall there is still good V/Q
  matching and efficient oxygenation of blood
  passing through the lungs.

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V/Q Mismatching

• Diseased lungs may have marked mismatch between
  ventilation and perfusion. Some alveoli are
  relatively overventilated while others are
  relatively overperfused
• Even normal lungs have some degree of
  ventilation/perfusion mismatchthe upper zones
  are relatively overventilated while the lower
  zones are relatively overperfused
  underventilated

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Shunt

• Shunt occurs when deoxygenated venous blood from
  the body passes unventilated alveoli to enter the
  pulmonary veins and the systemic arterial system
  with an unchanged PO2 (40 mmHg).
• Atelectasis (collapsed alveoli), consolidation of
  the lung, pulmonary oedema or small airway
  closure (see later) will cause shunt

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Oxygen Cascade

• Oxygen moves down the pressure or concentration
  gradient from a relatively high level in air, to
  the levels in the respiratory tract and then
  alveolar gas, the arterial blood, capillaries and
  finally the cell. The PO2 reaches the lowest
  level (4-20 mmHg) in the mitochondria.
• This decrease in PO2 from air to the
  mitochondrion is known as the oxygen cascade and
  the size of any one step in the cascade may be
  increased under pathological circumstances and
  may result in hypoxia.  

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Non-Respiratory Lung Functions

• Reservoir of blood available for circulatory
  compensation
• Filter for circulation
• thrombi, microaggregates etc
• Metabolic activity
• activation
• angiotensin III
• inactivation
• noradrenaline
• bradykinin
• 5 H-T
• some prostaglandins
• Immunological
• IgA secretion into bronchial mucus

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