The Work of Breathing

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The Work of Breathing
Chapters 38, 39, and 42

• Do we generally think of breathing as work?
• Remember, for the normal person,
• during normal, unforced breathing,
• inhale (active), exhale (passive)?

• Respiratory disease is generally classified as
  obstructive or restrictive.
• Obstructive disease relates to blockage of
  airways
• Restrictive disease relates to expansion issues
  in the lung/chest wall.

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How can we change Lung volume?
Transpulmonary pressure (palv-pip)?
Lung compliance
Intrapleural pressure
Contractile activity of breathing muscles
Surface tension of fluid lining alveoli
Elastic tissue in lung wall
Elastic recoil of lungs
Elastic recoil of chest wall
surfactant
Motor neurons to diaphragm and intercostals
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The Work of Breathing

• The two major difficulties in breathing involve
• 1. Overcoming resistance of airways
• ?P airflow x resistance
• 2. Overcoming elasticity of lung
• Normal elastic recoil? When the two are
  dissociated at the pleural space
• Lung tissue recoils inward (atelectasis)?
• Chest wall recoils outward

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Question

• Total ventilation Rate x Depth
• Can you guess which, rate or depth, a person with
  obstructive disease will depend on most?
• .what about a person with restrictive disease?
• (Hint consider the work of breathing for each
  patient. Which is the most effort, stretching
  the lung, or moving air? We breathe in the
  manner that causes us the least work possible.)?

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The Work of Breathing Airways Resistance

• Overcoming resistance of airways
• Poiseuilles law resistance vs. radius
• How open is the airway? Airway resistance limits
  airflow, R is inversely related to radius to
  fourth power.
• Then apply this to Ohms Law
• ?P airflow x resistance

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Obstructive Disease

• Difficulty moving air in/out of the lungs
• This is especially noticeable during expiration
• actively exhaling creates an elevated
  intrathoracic pressure that narrows the small
  airways, even shutting them down, while trying to
  to force air out of alveoli.
• The narrowed bronchioles (high resistance!!(Poise
  uilles Law!) results in trapped air in alveoli.
  
• (Note the high FRC in obstructive lung disease!)?
• Examples
• emphysema
• chronic bronchitis
• asthma

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Obstructive Respiratory Disease
Lumen of trachea and bronchus

• Increased resistance to airflow
• Lumen
• excessive secretions (e.g. mucus in asthma and
  bronchitis)?
• Increased capillary permeability during asthma
  attack (histamine release)?
• obstruction due to aspiration
• Airway
• contraction of smooth muscle (asthma)?
• hypertrophy of bronchial wall
• Outside of airway
• destruction of lung parenchyma (alveolar walls,
  tissue)
• Bigger alveoli loss of surface area fewer
  numbers!

alveolus
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P atm 760 torr

• Think about Poiseuilles Law and increasing
  resistance
• Resistance 8 ?l
• r 4
• Ex. If airway narrows to half its original
  diameter (radius) then what happens to
  resistance?
• ?P flow x resistance, so if resistance
  increases by 16 times, then to maintain the same
  airflow of the normal airway, the patient must
  increase the pressure gradient by 16 times.
• Normal pressure gradient of 2 torr, must be
  increased to 32 torr.
• How? Well see how we control alveolar
  pressures by changing the volume of the lung
  (alveoli)?

p alveolar 758 torr
Air moves from high to low pressure
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Obstructive disorders

• Expiration or exchange disorders
• Bronchitis excessive mucus production less
  surface area for exchange of oxygen
• Asthma- inflammation response, fluid from blood
  vessels leaks into alveoli less surface area for
  gas exchange
• Emphysema- collapsed alveoli-less surface area
  for exchange and over compliance

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Asthma Up close

• IgE is associated with allergies and asthma.
  Stem of IgE anchors to mast Cell, a specialized
  WBC. When an antigen (allergen) comes along,
  binds to IgE in bridging formation. This causes
  Mast cell to release histamine.
• Histamine makes blood vessels dilate and leaky.
  This causes edema locally or systemically.
• Inflammation alone can narrow airways.
• Mucus production also narrows airway.
• Signal molecules trigger bronchial constriction
  (bronchospasm) which further narrows the airways.
  
• Treatment anti-inflammatory drugs, B2 agonist,
  or block mACh receptors such as albuterol and
  ipratropium

• Breathing coughing to help with expiration,
  wheezing, and distant breath sounds due to air
  trapping.

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Chronic Bronchitis

• Inflammation of airways lasting 3 months to one
  year for 2 consecutive years
• Thickening of airway lining
• Increased mucus production
• Need anti-inflammatory drug
• Blue bloaters- can not compensate due to mismatch
  of perfusion and ventilation (hypoxemia,
  hypercapnia)?
• Polycythemia
• Right ventricular failure, systemic edema (club
  fingers)?
• Coughing, shortness of breath

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Emphysema

• This is a restrictive and obstructive lung
  disease!!!!
• Elastic components lost
• Lung easily inflated, but difficult to deflate
  (recoil compromised).
• Barrel chest (chest wins!)?
• Pursed lips breathing longer airway, means more
  resistance, can build up back pressure sufficient
  to prevent their collapse (pink puffers- can
  compensate by over-ventilating).

www.pathguy.com/lectures/emphysema_blues.jpg
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The Work of Breathing Overcoming Elasticity

• Overcoming elasticity of lung and chest wall
• Elastic recoil vs. compliance
• Elasticity (elastic recoil) tendency to snap
  back
• Compliance tendency or ease of stretching
• too much or too little recoil vs. compliance
  disease states
• Setpoint

emphysema
Surfactant lack
Elastic recoil
Compliance
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Anatomy of alveolar sacs

• Most alveoli occur in clusters called alveolar
  sacs
• Adjacent alveoli are NOT completely independent
  structuresconnected by alveolar pores (allows
  equilibrium of pressure)?
• They share adjacent walls, so they are
  interdependent, that is, they depend on the
  expansion (inflation) of neighboring alveoli to
  help them inflate

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• Loss of alveolar walls results in
• Loss of surface area for diffusion (Ficks Law!)?
• Loss of interdependence (greater tendency to
  collapse local regions of atelectasis)?

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The Work of Breathing

• There are two things responsible for lung
  compliance
• Elastic fibers in the lung tissue. Only account
  for 1/3 of total elasticity of lung. (When dry)
• Surface tension of water. When lung is moist,
  find that water moisture in alveolus contributes
  other 2/3 of elasticity of lung.
• Surface tension- attraction of water molecules
  for each other. Cohesive force. Acts as way to
  pull alveolus inward or shrink it in size
  (collapse).

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Surface tension of Water inside Alveoli

• Cohesiveness, or attraction of water molecules,
  at air-water interface (hydrogen bonds)?
• Resultant vector force translates to force
  favoring collapse of alveoli
• Surface tension is lowered by surfactant

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How can we change lung compliance?

• Use of detergent molecule, surfactant from type
  II cells
• Thickness of lung tissues affects compliance,
  reduce thickness
• If compliance decreases (harder to stretch),
  respiratory muscles must do more work to expand
  the lungs to a given volume.

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Surfactant

• Is composed of Dipalmitoyl lecithin
• (dipalmitoyl phosphatidyl choline) plus 4
  proteins and salts
• It is a detergent
• (part polar, hydrophilic part nonpolar,
  hydrophobic amphipathic molecule)?
• It becomes interspersed in the water monolayer
  lining alveolar walls, allows water molecules to
  separate (lowers their cohesion) so surface
  tension is reduced.
• Easier to inflate alveoli and less tendency to
  collapse

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LaPlaces Law

• Lets pretend that the alveolus is a perfect,
  independent, sphere (its not, but lets pretend
  anyway.....)?
• P 2T R
• if there is 1 liquid surface(such as lining an
  alveolus)?
• PPressure in sphere
• RRadius of sphere
• TSurface tension of liquid
• How much pressure would it take for you to spread
  out a drop of water?
• If no surfactant, small alveoli would have higher
  surface tension (pressure inward) and collapse,
  making an area of high pressure. How would the
  air flow in the picture here?

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• An additional action of surfactant
• Helps lung to inflate uniformly
• As alveoli go through cycle of inflation/deflation
  , surface area inside increases/decreases.
• Surfactant becomes less/more concentrated
• Provides more help to the smaller alveoli which
  have a greater tendency to collapse

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Surfactant Pathology

• Respiratory distress syndrome
• Failure to make surfactant
• ARDS damage to type II cells
• Smoke inhalation
• Long-term positive pressure breathing
• IRDS
• Premature babies, before approx 26 weeks
• Testing amniocentesis ratio L/S
• Treatment artificial surfactant prostaglandin
  stimulus

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Infant respiratory distress syndrome

• Surfactant is produced at about 26-28 weeks of
  gestation and throughout life.
• Work effort to inflate against surface tension of
  lung would cause Respiratory Failure.
  Amnio/sonogram--The test is called LS RATIO. It
  is Ratio of Lecithin to Sphingomyelin.
• Sphingomyelin is constant component of amniotic
  fluid. Lecithin, component of surfactant. When
  Lecithin rises (to level of 2 or higher),
  relative to sphingomyelin, then indicates
  production of surfactant.
• Read surfactant paper! (Babies and Bubbles)?

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Restrictive Disease

• Defined as changes in the compliance of chest
  wall or lung (difficult to inflate!)?
• Lung volumes
• reduced VC, FRC, normal airway resistance
• Examples
• Diffuse Interstitial Pulmonary Fibrosis
• thick collagen deposits
• Pneumothorax
• Broken ribs /muscular diseases/ Chest wall
  deformities/ kyphosis /scoliosis
• Emphysema (destruction of surfactant cells)?
• Surfactant lack
• Cystic fibrosis

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Evaluating the Work of Breathing Spirometry

• Determined by the amount of effort required to
  move air through the conducting pathways and ease
  of lung expansion (i.e., compliance).
• Persons with stiff and noncompliant lungs will
  breathe at faster rates and keep TV low.
• Persons with Obstructive disorders- can inflate
  easily, but expend more energy to move air in
  passageways- they will take deeper breaths and
  breathe at slower rate.

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Forced Vital CapacityFEV1.0 / FVC Ratio
80
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Restrictive Disorders- fight between compliance
and elasticity

• Generally inspiratory problem (compliance) To
  overcome lung elasticity is the problem.
• Work of breathing comes from stretching the lung.
  
• pts more likely to take more shallow breaths,
  more rapidly.
• Pulmonary fibrosis- lung tissue replaced with
  fibrous material (collagen), little compliance
• Pneumothorax- air on your lungs breaks the
  pleural seal and allows more elastic recoil
  resulting in a collapsed lung (atelectasis-imperfe
  ct expansion)-elasticity of lung wins.
• Anything preventing opening of rib cage. (even
  broken rib!)?
• Decreased Surfactant

myhome.naver.com/.../s-lecture/general(m3).html
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When do we see hypoxia?

• Hypoxia (def.) tissues, cells low in oxygen
• inadequate oxygenation of lungs
• atmosphere
• decrease muscle activity (neuromuscular
  disorders)?
• pulmonary disease
• inadequate transport
• anemia, abnormal hemoglobin
• blood flow
• inadequate usage
• Cyanide- poison to cellular oxidation enzymes

www.pbs.org/wnet/secrets/case_killerflu