Take a breath!

Anatomical illustration of alveolar clusters by LifeArt Collection Images by TechPool Studios, Cleveland, Ohio, used under license registered to DeKalb College.
Title, other anatomical illustrations, and characters from "Art Explosion 40,000," copyright Nova Development Corporation, Calabasas, CA.; used under terms of license granted to Dr. J.V. Aliff.
 

Chapter 22, Respiratory System Study Guide. p. 804, 8th ed.

PATH OF AIR IN BREATHING - LABEL THE DIAGRAM BELOW AS WE
PROCEED

1. Nasal Cavities: filters, moistens and warms inhaled air. Dime-sized patches of
   olfactory epithelium sample the air for molecules that lock and key with the ciliary
   processes. Sensory Neuron processes relay smell messages to the frontal lobes of
   the brain through holes in the cribriform plate of the ethmoid bone of the skull
   (olfactory foramina). Ciliated columnar epithelium with mucus cells pushes trapped
   dust toward the back of the throat to be swallowed and sent to the acidic stomach
   contents. Nasal conchae increase the surface areas for the mucus epithelium.
2. Nasopharynx: two passages carry material to the back of the throat. Its distal
   borders are guarded by tonsils. See p. 832, 7th ed.; p . 805-806, 8th ed.

   -

   

1. Pharynx: (pronounced fair-inks): the tonsils are lymphatic nodes in the roof and
   floor of the pharynx. Their normal function is to fight infection. If they become too
   swollen during an infection, they can restrict breathing and are then removed.
2. Larynx: (pronounced lair-inks) - the voice box is constructed of a frame of hyaline
   cartilage (clear and brittle). When viewed anteriorly the most superior is the thyroid
   cartilage and the epiglottis (elastic cartilage); inferior is the cricoid cartilage.
   Viewed posteriorly, the paired corniculate and arytenoid cartilages can be
   viewed. Muscles that control the tension of the vocal cords attach to the corniculate
   catriliages. The arytenoid cartilages suspend the true vocal cords that have a mixture
   of collagen and elastic fibers.  See p. 832-835, 7the ed.; p. 808-811, 8th ed.

   
   Label the thyroid, arytenoid, coriculate and cricoid cartilages,
   and the hyoid bone and epiglottis. Is this an anterior or posterior view?

   Laryngitis occurs more frequently in smokers or ex-smokers. The vocal cords
   become inflamed and cannot vibrate normally. It contains the vocal cords which,
   according to the speed of vibrations controlled by laryngeal muscles, determines the
   pitch (high or low) of the voice (tighter vocal cords - greater rate of vibration - higher pitch).
   Laryngitis occurs more frequently in smokers or ex-smokers. The vocal cords
   become inflamed and cannot vibrate normally.
   

   
   Label the epiglottis and vocal cords.

    

3. Epiglottis: the epiglottis is a flexible elastic cartilage-supported flap that covers
   the opening of the trachea (glottis). It automatically closes the glottis when the
   pharyngeal muscles contract and pressurize the air above the epiglottis and when it
   is pulled up toward the hyoid bone during swallowing. If you eat too fast and start to
   burp as food is swallowed, you can get food lodged in the trachea. The Heimlich
   maneuver is used to pop the food out and back into the pharynx.
4. Trachea: the trachea is lined with ciliated columnar epithelium and mucus cells,
   which is also found in the smaller bronchi and the still smaller bronchioles. The
   trachea is supported by "C" shaped rings of hyaline cartilage. The mucus is pushed
   up toward the larynx where trapped dust and mucus are sent down to the stomach.
   Remember the heavy morning cough of heavy smokers? It is caused by a lack of
   cilia.  See p. 839, 7th ed.; p. 812-813, 8th ed.

Label the thryoid, cricoid and carina cartilages, trachea and  bronchi.

1. Bronchi: the trachea divides into the primary bronchi. The carina is a
   cartilage that is quite sensitive to noxious substances; which when detected,
   causes bronchial constriction and a cough reflex.
2. Bronchioles: have a mucus/ciliated membrane with smooth muscle underneath.
   See p. 841, 7th ed.; p. 814, 8th ed.
3. Respiratory bronchioles are lined by non-ciliated cuboidal cells and have
   individual squamous-lined air sacs or alveoli. The respiratory bronchiole leads
   to the blind ends of the respiratory system, a cluster of alveolar sacs.
    
   Label terminal bronchiole, respiratory bronchiole, alveoli,
   and smooth muscle cells. See pg. 846//839//841.

    

4. Alveoli: The alveoli have a very thin wall constructed of the cell membranes
   and thin cytoplasm of flat squamous cells. Oxygen and carbon dioxide readily
   diffuse between the capillary blood and the alveolar air spaces. High acidity a
   and high temperature favor the breakdown of HbO₂ and low temperature and
   lower acidity of blood favor its formation. The arterioles leading to the lung
   capillary beds auto-constrict when pH is low (acidity is high) and oxygen is low.
   These arterioles auto-dilate if pH is high and oxygen is high. This insures that
   more blood will flow where it is needed. Alveoli have a few Type II  
   (septal) squamous cells that produce a chemical called surfactant. Surfactant
   causes a thin layer of water to spread out and against the wall of the air sac,
   helping it to resist collapse. Some premature babies lack these secretions and
   develop a lung disease called infant respiratory distress  (IRDS) resulting in suffocation.
   See pg. 854//848//851.

If alveolar walls are destroyed and their elastic fibers destroyed (usually accompanied
by collagenous thickening of the remaining and enlarged air sac wall) the disease of
emphysema is seen. Loss of ciliated mucous epithelium in the
bronchioles leads to mucus plugs, which leads to infection of the alveoli, which leads to
macrophages eating up the alveolar walls, the destruction of elastic fibers in the
walls, and the increase of scar tissue collagen in the wall. Emphysema is one chronic
obstructive pulmonary disease (COPD) that limits breathing by obstructing air passages.
Chronic bronchitis is also a COPD.  See also below and pg. 875//869//871.

What does alveolar surface area have to do with breathing efficiency?

What process discussed in the previous chapter will lead to the decrease of acidity of
the lung capillary blood? (Hint: breakdown of H₂CO₃ into gases!)

Black Lung Disease is a killer of heavy smokers and coal miners. Brown Lung
Disease was a similar occupational disease of cotton mill workers, before the 1970's.
Free macrophages, also called dust cells, would migrate into the alveolus and eat
the indigestible carbon and cellulose fibers. Then the dust cells would carry the fibers
or particles.

Cystic fibrosis is caused by defective Chloride channels in the plasma membranes of the
epithelial cells of the bronchioles, sweat glands and the pancreatic duct
(and many tubular organs). The chloride deprived mucus becomes thick, clogging
airways. Pneumonia is frequent pancreatic duct enzymes cannot reach the small intestine,
resulting in foul-smelling stools. CF babies are frequently first recognized by their salty
tasting skin.

CYSTIC FIBROSIS AND CHLORIDE CHANNELS

      "A seventeenth century English saying is, “A child that is salty to taste will die shortly after birth,” described the consequence of abnormal chloride channels in the inherited illness cystic fibrosis (CF). The disorder affects 1 in 2,500 Caucasians, 1 in 14,000 blacks, and 1 in 90,000 Asians, and is inherited from two unaffected parents who are carriers. The major symptoms of impaired breathing, respiratory infections, and a clogged pancreas result from extremely thick mucus secretions. Affected individuals undergo twice daily exercise sessions to shake free the sticky mucus, and take supplemental digestive enzymes to aid pancreatic function. Strong antibiotics are used to combat their frequent lung infections.
      In 1989, researchers identified the microscopic defect that causes CF as abnormal chloride channels in cells lining the lung passageways and ducts in the pancreas. The primary defect in the chloride channels also causes sodium channels to malfunction. The result is salt trapped inside affected cells, which draws moisture in, thickening the surrounding mucus. Several experimental gene therapies attempt to correct affected cells’ instructions for building chloride channel proteins."

Anita Lisokowski, Northland College.
 

Allergic Responses of the Lung

Asthma may have an allergen (antigen) as a cause. If so, a series of events takes
place that resemble an inflammation response (See Circulation, Blood and Immunity
study guide and text.) Macrophages ingest the allergen (pollen) and migrate into the
bronchiole walls. B-cells change into plasma cells that make an antibody (IgE):
the antibody bonds to mast cells. The binding of pieces of the allergen to the
antibodies on the mast cells causes release of histamines, leukotrienes and
neurotransmitters by the mast cells. The result is bronchial constriction and edema
in the bronchial wall that almost closes the air passages leading to the alveoli.
See p, 872, 7th ed.; p. 841, 8th ed..

There are several approaches to treatiung asthma. One is to control the inflaammation,
one is to control excessive mucous secretion, another is to prevent mast cells from releasing
histamines and leucotrienes. Drugs used to treat asthma include sympathetic (attach to Beta₂ receptors)
neurotransmitter mimics (B₂ agonists) that dilate  bronchioles, antihistamines that reduce
mucus secretion, steroids that reduce the edema in the bronchial wall and chromolyn to prevent
mast cell release of histamines and leucotrienes.

Why do these drugs occasionally cause heart fibrillation?

Mechanics of Breathing - See p. 846, 7th ed.; p. 819, 8th ed.

There are four groups of muscles which expand the thoracic (chest) cavity to produce
or assist inhalation, or contract the cavity to produce exhalation. The lungs are filled
when air pressure is reduced in the thoracic cavity around the lungs. The principle of
gas pressure is this: when you reduce thoracic air pressure (negative pressure)
relative to the outside air pressure, air will move from higher pressure to lower
pressure areas. This principle also governs the weather. "Nature abhors a vacuum,"
is an old cliche'. It is also the same effect as expanding a bellows used to fan a fire.
Squeezing the bellows to make its cavity smaller makes the air whoosh out.

Negative pressure in the pleural cavities helps (along with surfactant) keep the
lungs from collapsing. If the pleural cavity is punctured, air may leak into it and
pneumothorax results - the patient can't inflate the affected lung well or it may
collapse.

Muscle Groups

1. Diaphragm: used for relaxed or quiet breathing. The diaphragm is a sheet-like muscle
   which is normally dome-shaped, the dome pressing against the lungs. When the
   diaphragm contracts, it flattens and increases the volume of the thoracic cavity,
   drawing in air (inhalation).

As the air enters the lungs and is warmed by the proximity to blood, it expands,
thereby assisting inhalation. When the diaphragm relaxes, it returns to its up (dome)
position and makes the thoracic cavity smaller and increases thoracic air pressure -
exhalation results.

1. Rib Cage Muscles, specifically the external intercostal muscles: between the ribs,
   move the sternum up and forward, thus also, increasing the volume of the thoracic
   cavity. They are used for vigorous breathing. Internal intercostal muscles return
   the ribs to resting position, the sternum lowers and cavity volume is reduced.
   Another related principle of gas pressure, Boyle's Law, states that an increase in
   volume lowers gas pressure and a decrease of volume increases gas pressure
   How does this relate to breathing?

1. Sternocleidomastoid Muscles: can literally lift the sternum during gasping
   breathing, producing the chest heaving motion. They run from the mastoid process
   on the skull, to the clavicle and sternum. The pectoralis minor and scalene muscles
   assist.
2. "Stomach" Muscles of the Abdominal Wall: the external and internal oblique,
   transverse abdominus and the rectus abdominus assist exhalation. Singers learn
   how to use abdominal muscles to assist breathing, contracting them during
   exhalation, and expanding them (sticking the "stomach" out) during inhalation.

SPIROMETRY - See p. 852, 7th ed.; p. 825, 8th ed.

Pulmonary Volumes

1. Tidal Volume - and average of 500 ml is moved into and out of the respiratory
   tree in relaxed breathing. Of the 500 ml, 150 ml do not reach the alveoli, coming to lie
   in anatomic dead space.
2. Inspiratory Reserve Volume - a deep breath. An additional 3.1 liters (average)
   can be inspired above the tidal volume.
3. Expiratory Reserve Volume - exhaling vigorously forces out 1200 ml of air in
   addition to the tidal volume. After expiration 1200 ml of air remains in the lung as a
   residual volume.
4. Vital Capacity - the sum of inspiratory reserve, tidal and expiratory reserve
   volumes.

   In emphysema, tidal volume may be normal even as the rate of respiration
   increases in the "pink puffer." Their pink skin indicated that breathing rate is
   keeping up with oxygen need. However, expiratory reserve and vital
   capacity fall over time. Then, the "blue bloater" is cyanotic and barrel-chested
   because breathing can't keep up with the demands for oxygen. Supplemental oxygen
   must be given. Blood acidosis inhibits the breathing rhythmicity center and worsens
   the cyanosis.

Dalton's Law describes a mixture of gases as each having a partial pressure.
Standard air pressure = 760 mm Hg, the partial pressure of oxygen = 21% (approx.)
of 760 = 159. Partial pressure of pO₂ is 80 at 18,000 ft. Mountain climbers become
disoriented at these altitudes without supplemental oxygen. O₂ levels are sensed in
the heart and carotid arteries and breathing depth and rate are increased as one
ascends in altitude.
 

The Bends

Nitrogen gas dissolves in the blood when compressed air is breathed at depths (30 ft+)
by divers. Henry's Law says gas solubility increases with pressure and vice versa
at low pressures. If a diver ascends from high pressure/great depths too quickly,
bubbles of nitrogen gas come out of solution and block blood vessels. It is very
painful. Why are the divers then placed in pressure chambers?

Nitrogen narcosis may also affect divers because nitrogen oxides which increase
when dissolved nitrogen increases can alter neural activity, resulting in euphoria and hallucinations.

Gas Exchange with the Blood in Tissues and Lungs (review) See p. 862, 7th ed.; p. 827, 8th ed.

Hemoglobin Functions:

       In the lung capillaries
Fe+²-Hb + O₂   ----->   Fe+³ HbO₂ (oxyhemoglobin)
       In the tissue capillaries
                       <-----

Colder temperatures and higher pH favors the formation of oxyhemoglobin.
See pg. 801.

        In the tissue capillaries
  Hb + CO₂   ---->   HbCO₂ (carbaminohemoglobin, small amount)
        In lung capillaries
                           <------
 

Higher temperatures and lower pH favors the breakdown of oxyhemoglobin.
The increase of acidity and the increased delivery of oxygen to tissues is called
the Bohr Effect. Is this Bohring? See pg. 864//858//860.

Most CO₂ is carried as bicarbonate.
 

in tissue capillary beds (forward Rx)

CO₂ + H₂O   -->     H₂CO₃ --> H⁺ (+)   HCO₃ (bicarbonate)
 

in the lungs (reverse Rx)    <---                   <---

What happens to blood acidity (pH) if you hold your breath? (HINT: You are holding
CO₂ in the blood.) An abnormal increase in blood acidity is called respiratory blood acidosis.
The blood pH would be below 7.35. A small increase in blood acidity stimulates the breathing
rhythmicity center. When the interstitial fluids in the medulla increase in acidity slightly
(e.g., 7.35) breathing rate increases. This is the primary mechanism of stimulation.
 

What happens to blood acidity if you breathe too fast? (You release too much CO₂.)
An abnormal decrease in blood acidity is called respiratory blood alkalosis.
The blood ph will be above 7.45. A decrease in acidity tends to stimulate the nervous system.

Blood pH must be maintained between 7.35 and 7.45. If it rises to 8, you will have life
threatening convulsions. If it falls below 7, the brain shuts off and shock results.
 

OXYHEMOGLOBIN

1. Oxy Hb forms when temperature is slightly lower, pH is higher, and pCO₂ is lower.
   As CO₂ binds to Hb, oxygen binding decreases and vice versa. .
2. The release of oxygen from Hb is enhanced by higher temperature, lower pH and
   higher pCO₂.
3. Fetal Hb has a higher affinity for oxygen than adult normal Hb.

HYPOXIA can be caused by:

1. High altitude.
2. Asthma, emphysema, bronchitis, etc.
3. Pneumonia or fluid in the lungs caused by pulmonary edema.
4. Anemia.
5. Heart failure or pulmonary embolisms.
6. HCN (cyanide) poisoning blocks O₂ utilization in cells.
7. CO (carbon monoxide) poisoning. Carbon monoxide has 200x the affinity for
   hemoglobin than does O₂; i.e., Hb + CO   ----->   HbCO (carboxyhemoglobin).

   Respiratory or Breathing Rhythmicity Centers - control relaxed breathing by
   alternately stimulating and inhibiting inspiration for 2 seconds and 3 seconds, respectively.
   The breathing inspiratory and expiratory centers are located in the brain stem, specifically,
   the medulla oblongata. In strenuous breathing, as stretch receptors in the alveolar
   walls expand to a point of near-burst, a signal is sent to the pneumotaxic center in
   the pons and the medullary breathing rhythmicity center resulting in exhalation.
   After three seconds when the alveoli shrink to near collapse point, a signal goes back
   to the inspiratory center which results in inhalation. Gasping is caused by
   prolongation of inhalation provoked by cold water, holding your breath, or heavy
   exercise. The apneustic center does this by prolonging inspiration. See p. 868, 7th ed.; p. 636, 8th ed.

   Other regulatory mechanisms that stimulate an increase of  breathing rate

   The respiratory center is stimulated, increasing the rate and depth of breathing by
   the following:

   1. The cerebral cortex - voluntary. Works for a short time.

   2. Chemical - the aortic and carotid bodies have chemoceptors that detect
   (via the glossopharyngeal IX and vagus X cranial nerves) increased CO₂,
   decreased O₂ and decreased pH (increased H⁺). Increased CO₂ is called
   hypercapnia.

   3. Hering-Breuer inflation reflex (see pneumotaxic reflex, above) inhibits inspiration.

   4. Blood pressure increases and decreases are indirectly proportional to breathing rates
   as a short-term homeostatic mechanism.

   5. Limbic system stimulation because of increased emotions or anxiety.

   6. Temperature (directly proportional).

   7. Pain.

   8. Stretching the anal sphincter.

   9. Airway irritation by noxious substances.

A common lung cancer first develops in a precancerous stage from multiplying basal
cells which create a stratified squamous layer which replaces the normal ciliated
pseudostratified columnar epithelium. This is called metaplasia (change in normal
cell types). If the cells become more numerous (hyperplasia) a tumor is formed.
They become cancerous when they break through the basement membrane using
protease enzymes. Then the cells move into blood vessels or lymphatics and create
satellite tumors (metastasis). Known mutagens in cigarette smoke include alpha
particle emitters and benzopyrenes (in the tar or vaporized liquid). Also CO and HCN
are thought to cause lesions which begin atherosclerotic plaque formation.
Substances in smoke inhibit a protein, alpha antitrypsin, that normally inhibits an enzyme,
elastase, which breaks down elastic connective tissue fibers. This process also
enhances the decrease in expiratory reserve seen in emphysema. Why?
 

Study Questions

1. Describe the pressure changes in the lungs during inhalation and exhalation as
   compared with the outside air and pleural cavity pressures. Use diaphragmatic
   breathing in the example.
2. Describe the actions of the major breathing muscles.
3. Compare relaxed and  vigorous breathing.
4. Describe respiratory acidosis and alkalosis.
5. How does the medullary breathing rhythmicity center work?
6. Describe the risk factors and development of emphysema and lung cancer
    

REMINDER! THINK TO YOURSELF . . .

I AM RESPONSIBLE FOR WHAT      I  MAKE!