1870-1900: The Pneumatometer (Part II)

By 1903 there were various pressure devices used to provide positive pressure breaths for therapeutic reasons and for artificial respiration.  The devices were mainly operated by some form of physical labor, such as through pumps and bellows.  

Stoerk's Apparatus (Figure 30)
(1, page 211)

Please note that all of these apparatus's are described in a book called, "Pneumotherapy: Including Aerotherapy and inhalation methods," by Paul Lewis Alexandre Tissier, and edited by Solomon Solis Cohen.

Stoerk's Apparatus:  It allows for inspiration by positive pressure and exhalation through rarified (less oxygen that what's in the air) air.  Rarified air caused a sort of suction or negative pressure that caused a negative intrathoracic pressure that induced expiration.  (1, pages 211-212)

Unlike the other pressure devices, this one didn't require direct or physical depression of bellows or pumps, instead "compression is obtained by a change of level in the water in a system of communicating vessels, brought about by setting up an oscillatory movement which changes their relative positions (Fig. 30). (pages 211-212)

An oscillating motion was created by swinging it back and forth with your hand. So the oscillations cause positive pressure (condensation) to cause inspiration, and negative pressure (rarified air or suction) that caused expiration.  (pages 211-212)

Dorell's Residual Air Pump (1, page 213)

Dobell's Residual Air Pump:  The device was small and compact, and could be carried in your pocket.  (See figure 31) (1, page 213)

It's described as "kind of mask which isfitted to the front of the mouth and held in place with a ribbon which passes around behind the ears; the apparatus is provided with valves to embarrass inspiration while expiration remains free. As a result the intrathoracic air is rarefied, and at the end of three to six respirations the residual air is reduced to a minimum and the diaphragm attains its maximum elevation. The patient then inspires in ordinary air, and this inspiration being freer than he is accustomed to, he experiences a sense of increased comfort. The same manoeuver is repeated several times at each sitting. The apparatus is certainly ingenious, but there is no means of determining with accuracy the degree of success attained."

Water Engine Bellows (Figure 32)
(1, page 214)

Water Engine Bellows:  It's also referred to as The Water-blower or Double Ventilator of Geigel and Mayer. The container is made of sheet iron and is filled to two thirds of it's capacity with water.  The container is completely enclosed except for four openings at the top.  To of these openings communicate with room air.  One holds a meter to measure volumes.  The fourth opening is where the pressure escapes.  A tube is connected to this opening, and a rubber mask is connected to the opposite end.  (1, pages 213-215)

Bellows inside are operated by a crank. The principle is similar to the way water engine or gasometer is operated. The patient holds the mask over his face, and turns the crank  As the crank is turned pressure escapes through the fourth opening, and this caused inspiration.  (see figure 32)  (1, pages 213-215)

Dupont's Apparatus (Figure 35)
(1, page 216)

Dupont's Apparatus:  It's based on the principle of the Bunson water pump or aspirator, is inexpensive, allows for inspiration as deep as you desire, and can be used wherever there is a flow of water.  The pressure is regulated by a mercury pressure manometer. (1, pages 216-217)

Tissier said it was the best apparatus for the reasons indicated in the previous paragraph.  Rarification and compression of air is done simply by pumping a pump alongside the apparatus.  Pressure is determined by flow of water or by working a stopcock on the patient tubing.  (1, pages 216-217)

S. Solis Cohen's Double Apparatus:  This is combination gasometer (a container that stores gas)  and water pump and was created by the author of one of our other 19th century respiratory therapy books and the editor of of Tissier's book.  There were various advantages to this device: (1, pages 217-221)

1. It corrects the flaws of the other pressure devices
2. It is continuous in action and relatively compact
3. The price is moderate
4. It can be used by the patient at his or her home

Cohen's Apparatus (1))

The device was described as follows:   (1, pages 217-221)

"It is true that the degree of compression of the air is regulated by means of weights placed on the upper portion of the condensed-air cylinder, and that the degree of rarefaction is regulated by means of weights attached to a system of cords and pulleys by which the cylinder containing the rarefied air is raised; but the apparatus is operated and the pressure modification obtained by means of a double-acting bellows—so that air is drawn out from the cylinder which is to contain rarefied air and discharged into the outer atmosphere, while fresh air is forced into the cylinder intended for condensed air. Although one stroke of the footlever accomplishes both condensation and rarefaction, the two systems are independent, and there is no communication between the cylinders except through the air-passages of the patient. This is an extremely ingenious idea, which, in addition to the other good qualities of the apparatus, should insure its success."  (1, pages 217-221)

The Cohen's Apparatus was invented in 1883, and introduced to the medical community via the New York Medical Journal in the October 18 issue

I think these were all "ingenious" inventions meant to help people with breathing difficulty.  It would be another century before such devices were mastered and redesigned for patient comfort and convenience.

References:

1. Tissier,Paul Lewis Alexandre, edited by Solomon Solis Cohen, "Pneumotherapy: Including Aerotherapy and inhalation methods," volume X, 1903, Philadelphia, P. Blakiston's Sons and Co., pages 296-224.  If the profession of respiratory therapy existed in their era, we would be reading their books.  However, as it was, their books were written for the medical profession.

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1870-1900: The Pneumatometer

Due to the perceived therapeutic benefits of pressure therapy, between 1800 and 1870 various apparatus's were invented to provide "pneumotherapy" for such conditions as asthma, throat edema, emphysema, bronchitis, or dyspnea caused by diphtheria(2, page 45)

If you were a physician at this time you saw before your own eyes the evolution of pressure therapy.  By 1903 pneumotherapy was mentioned in various medical books, although it was still "under-utilized." Paul Louis Alexandre Tissier's, in his 1903 text, "Pneumotherapy: Including Aerotherapy and Inhalation Methods and Therapy," provides a detailed description of pneumotherapy. (1)

He expains that the machines available provided pressure changes upon the respiratory passages (1): 

• By inspiration of condensed air (we now call it positive pressure)
• By expiration into condensed air (what we now call PEEP)

And the following methods decrease pressure in the lungs (1):

• By expiration into rarified air (what we now call negative pressure)
• By inspiration of rarified air 

Tissier described the following devices.  Most of them were used in the patient's home mainly by the patient placing a rubber mask over his face, although some may also be used by physicians as spirometers or to provide artificial respiration.  (1)

Hawke's Apparatus

1.  Hauke's Apparatus:  After a series of tests by Hawke from Vienna, it was introduced around 1870. (3, page 577)

It's basically a tank filled with water to supply pressure or rarified air upon expiration and inspiration as provided by a pump or bellows.  Rubber tubing connects from the tank to a rubber mask that fits over the mouth and nose, held in place by the patient. (1, pages 196-197)

Hauke recommended using this to offset the "dyspnea caused by diphtheretic laryngitis in which it was not always successful."  It was also used successfully for pulmonary tuberculosis and emphysema.  The problem with this device is there was no way of measuring breaths given  (1, pages 196-197)

Waldenburg's
Appartus

2.  Waldenburg's Apparatus:  The flaws with the Hauke design were corrected by Waldenburg of Berlin.  The 1873 model consists of two reservoirs of sheet iron, and an inner and outer cylinder, with the inner cylinder gliding on the outer one.  (1, pages 197-199)

A cap on the outer cylinder is 10 cm in height and wider than the outer cylinder.  The inner cylinder is moved up and down by means of weights and pulleys.  "Water is poured into the apparatus so that, when the inner cylinder is forced down into the outer cylinder, the apparatus is filled to the brim, the cylindrical cap at the top of the outer cylinder being destined to receive the water that overflows when the inner cylinder descends."  (1, pages 197-199)

Graduated scales allow for measuring volume.  A rubber hose is connected to a spun metal mask cushioned with rubber.  Both positive and pressure breaths can be given with the device, and the breaths can be measured "regularly and accurately."  In fact, the device could also be used as a spirometer to measure lung volumes.  (1, pages 197-199)

Figures 21 and 22

Air could be moistened and warmed by adding a wolffe bottle.  Tissier also notes that the "apparatus has been deemed worthy of detailed description, as it has probably been used more frequently than any other."  (1, pages 197-199)

The apparatus was later modified by Cube, Weil, Schnitzler, and other folks you'd be familiar with if you were a respiratory therapist in this era. (1, page 200)

As you can see by figures 21 and 22, some of these wouldn't be applicable for home use, and may even be too bulky and expensive even for hospital use.  

Apparatus of Finkler and Kochs:  "With this apparatus (Fig. 25) condensed air is forced into the lungs during inspiration, expiration being assisted by withdrawal of air from the lung." (1, pages 204-206)

Inspiration is basically caused by positive pressure, and expiration occurs by negative pressure or suction.  (1, pages 204-206)

Figure 25 --Apparatus of Finkler and Kochs

The device can also be used as a spirometer to measure forced expiratory capacity, or "the quantity of air that can be expired after the fullest possible inspiration."(1, pages 204-206)

Beidert's Instrument:  This is an interesting device that's designed similar to a musical instrument called the harmonica, "to one extremity weights are affixed...  it's walls are made of leather, air tight, and have a necessary strength to maintain their original form against overpressure of air." (1, pages 206-209)

The machine is operated this way:  "The machine is placed upright on the margin of a table, so that the tube will be in a groove cut into the wooden base, and the desired quantity of (iron) weights is fastened to the upper cover of the bellows. If the upper end is turned down, the weights will sink and the bellows will fill itself with air. The bellows is then turned back, while the patient compresses the rubber tube with his fingers until he is ready to inhale through the mouthpiece attached; he then gradually inhales the air as the weights compress the bellows. While the patient expires into the free air the bellows is filled again by turning, and the operation continued in this manner indefinitely." (1, pages 204-206)

Pressure can also be applied in the following manner:   "For expiration into rarefied air, the tube is compressed and the bellows turned weights downward; applying the tube to the mouth, the air passes from the lungs into the partial vacuum produced by the expansion of the bellows. The bellows filled with the expiratory air is emptied by turning, while the patient inspires air at the atmospheric pressure, and the operation is repeated." (1, pages 204-206)

It appears like it would be a lot of work, but if it made a person feel better, then it must have been worth the effort.  

Frenkel's Apparatus:  If you think the figure to the right looks like an accordion, you would be... wrong.  You sat with the apparatus on your lab, and between your palms.  You place the mask over your mouth and nose. 

The air is rarified when you pull the accordion out, and when the device is compressed the air is condensed.  So pulling the "accordion" out will cause expiration, and pushing it in will cause inspiration.  (1, pages 209-210)

Frenkel's Apparatus

In compliance with all pressure devices since the Hauke Apparatus, "on the margin of the apparatus is a centimetric measure to measure how many centimeters the wooden disks are separated or brought together." It is by this means that volumes can be measured.  (1, pages 209-210)

So it appears to have been a very interesting device, and perhaps the simplest and easiest to use.  It could easily be used at home by the patient whenever needed.  The device coule also be used at a doctor's office or hospital for artificial respiration in the case of asphyxia or poisoning.  It could also be used as a spirometer.  

So these were some of the first pressure breathing machines. While many people think such machines are a modern innovation, the concept has been around for over 100 years.  The main difference between now and then is we have the ability to tame electricity.

References:

1. Tissier,Paul Lewis Alexandre, edited by Solomon Solis Cohen, "Pneumotherapy: Including Aerotherapy and inhalation methods," volume X, 1903, Philadelphia, P. Blakiston's Sons and Co., pages 296-224.  If the profession of respiratory therapy existed in their era, we would be reading their books.  However, as it was, their books were written for the medical profession. All of the material from this post is from Tissier's book unless otherwise noted in the above paragraphs. 
2. Minnesota State Medical Society, "Transaction of the Minnesota State Medical Society," 1886, St. Paul, H. M. Smyth Printing Co. 
3. Rose, A., "Treatment of Disease of Respiration and Circulation by the Pneumatic Method," New York, The Medical Record: A Weekly Journal of Medicine and Surgery, Edited by George F. Shrady, M.D., Volume 10, Jan. 2, 1875 to Dec. 25, 1875, New York, William Good and Co., page 577
4. Foster, Frank, editor, "Practical Therapeutics," Volume I, 1897, New York, Appleton and Co., page 19

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1870: Bert's experiments advance respiratory wisdom

Paul Bert (1833-1886)

"It can be said of Paul Bert as it has been of Vesalius, Harvey and Boyle, that the full significance of his work could not be fully appreciated until long after his death." (8, page v)

This was a quote from John F. Fulton, who wrote the forward to the 1843 edition of Bert's book "Barometric Pressure."

Bert's experiments would have a broad and lasting impact on surgery, aviation, mountain climbing, deep sea excursions, mining, pressure breathing machines, and even the definition of asthma.

He was born in Auxerre, France, on October 17, 1833, attended school in Paris, and received his medical degree in 1863. (2)(8, page V)

Fulton said that while in Paris he was assistant to Dr. Claude Bernard in his laboratory.  Fulton said "Bernard recognized his ingenious mind and predicted a brilliant future." (8, page VI)

Denis Jourdanet (1815-1892)

His thesis on grafting of animal tissue gained him public acclaim, and this helped him to quickly earn fame in the medical community. (2)(8, page VI)

Animal grafting, and later skin grafting, was "an operation consisting of the removal of a living part and transplanting it so that it shall continue to live on another part of the same individual or on another individual," said the authors of an 1888 biography of Dr. Bert in Popular Science Monthly.(2)(8, page V)

In 1865, the Academy of Sciences awarded him a prize in experimental physiology for his work on animal grafting and skin grafting.  This work was significant because it allowed physicians to perform plastic surgery on soldiers injured during the war of 1870.  (2)(5, page ?)(8, page V-VI)

In 1867 he was appointed to a chair in the Faculty of Sciences at Bordeaux where he taught zoology.  Then he became Bernard's successor in December of 1869 when he was named Professor of Physiology at the Faculty of Sciences in Paris. (2)(8, page VI)(13, page 599)

In 1870 Bert became interested in respiratory disorders, such as asthma, chronic bronchitis, and emphysema.  He performed experiments to learn more about these diseases, and to find methods of helping people with these diseases.   (1, page 194)(8, page VII)

In 1854 Alton Wintrich performed experiments that seemed to disprove the spasmotic theory of asthma in favor of the diaphragmatic theory of asthma.  For 16 years Wintrich gained many followers.  But Bert aimed to prove him wrong.

In 1870 he attempted, with improved methods of scientific research compared to that used by Williams and Longet, to stimulate the vagi of dogs.  As he expected, this indeed produced dyspnea.  His experiment reaffirmed for the medical community the spasmotic theory of asthma.   (10, page 10)(11, page 37)(12, pages 5-6)(13, page 16)(14, page 599)

According to W.H. Geddings in 1885, along with demonstrating that respiration could be "arrested by irritation of the pneumogastri (vagi)," it could also be arrested by irritation of the "laryngeal nerves or the Schneiderian membrane of the nose (membrane lining the maxillary sinus cavity)." (1, page 194)

In 1855, Ludwig Traube came to a similar conclusion.

Bert's experiment was important because it prevented physicians from spending what minimal time and money was dedicated to asthma form being wasted on areas that were already disproved.

Around this time, said Fulton, a friend of his, Dr. Denis Jourdanet, had just returned from an excursion to Mexico where he had spent time in the mountains at great heights and suffered mountain sickness.  The two decided that Bert should dedicate his time performing experiments on the effects of pressure on plants, animals and humans. Jourdanet was a wealthy man, and he offered to provide any funds that Bert needed. (8, page VII)

Bert's first experiment was performed on April 15, 1874.  He sent three balloon enthusiasts and equipment in a hot air balloon called Zenith.  The mission was to collect data from the the upper atmosphere.  Another goal, however, was to exceed 24,000 feet, which was the height accomplished by an English balloonist named Glaisher in 1862.

At 26,000 feet all of the men were unconscious.  Upon the Zenith's return to the earth, two of the men had perished, and the third was insensible.  Bert hypothesized the reason was due to lack of oxygen to the brain (2)(5, page 112)(8, page VII)

This was a set back for Bert in which none of the equipment, and obviously none of the men, were able to function at that height due to cold and rarified (negative pressure, suction) air.  Most of the equipment was also damaged in the efforts made to get the balloon back down to earth, so no data could have been obtained anyway.  (2)(5, page 112)(8, page VII)

While this was a set back, it did not keep him from marching forward.  Instead of using humans to perform his studies from here on out, he did them in his laboratory using small animals.  Only when perfected his experiments did he resort to using humans.  (2)(5, page 112)(8, page VII)

The first order of business for Bert was to invent a device for measuring pressure and put together compression chambers.  He used a smaller compression chamber for small animals, and a larger one for himself and his friends.  (see figures)(2)(8, page VI)

In a laboratory experiment Bert placed a sparrow in the compression chamber made of pneumatic glass bells and exposed it to low pressures.  When it started to suffer he administered oxygen, at which point the bird "at once became himself again."  Upon this success, he performed the same experiment on himself, and he observed at higher pressures that his heart would beat faster and he'd have palpitations.  At one point he wanted to write in his tablet, but could not.  When he inhaled oxygen these symptoms went away. (7)

By these experiments he concluded that the lower the atmospheric pressure (as what would occur with high altitudes) results in oxygen tensions in the air and blood too low to support life. Instead of inhaling 21% oxygen which is present in normal room air, he was inhaling a lower percentage of oxygen.  (7)

High altitudes, or high atmospheric pressures, subject humans to the risk of suffocation or asphyxia. Early symptoms are increased heart rate,weakness, malaise, nausea, and vomiting. The colder the air the earlier these symptoms appear. For instance, the symptoms appear earlier in the Alps than in the Himalaya, Bert said. (7)

The remedy here would be "the respiration of an air sufficiently rich in oxygen to maintain the tension of that gas at its normal value." (2)

In another laboratory experiment Bert placed a sparrow in the compression chamber made of pneumatic glass bells and exposed it to high pressures (compression).  He then decompressed the bird rapidly to atmospheric pressure, at which time the bird suddenly died.  Upon inspection of the body he found air bubbles in the arteries and heart.  The same effect resulted during similar experiments performed with rats and small dogs. (5, page 115)

Robert Boyl had observed bubbles in the eyes of a snake he placed in a compression tank he invented, although no further investigations were made at that time into the nature or cause of the bubbles.  Bert, however, benefited from improved laboratory equipment.  (5, page 116)

Bert concluded that higher atmospheric pressures (as what would occur as one travels deeper under water) result in increased oxygen tensions in the air and blood.  The remedy here would be avoidance of too high a pressure (such as greater than 5-6 atmospheres), and gradual decompression back to atmospheric pressure (1 atmosphere). (2)

He observed that the effects of high pressures may kill not only humans and animals, but plants too.  (2)

While the significance of this work may not have been immediately known, the value of it was immediately recognized by the scientific community.  For this work the Academy of Sciences awarded him a prize of twenty thousand francs. (2)

His experiments would have an impact in many areas of science and medicine.

His conclusions about the effects of diminished pressure resulted in equipment, such as oxygen tanks and masks that made aviation possible.  For this reason, he is often referred to as the father of aviation medicine.

Improved methods of storing and delivering oxygen was also thought to benefit people with respiratory disorders, and so research was eventually done in this regard, some of it by Bert himself.

His conclusions about the effects of increased pressure resulted in better knowledge of decompression sickness or bends.

Bends occurs when a person moves from deep water (where the pressure is higher) to the surface (where the pressure is lower) too fast.  This causes bubbles to escape into the blood and tissues, and can cause symptoms such as headache, joint pain, nose bleeding, vertigo, shortness of breath, nausea, vomiting, and sometimes death.

This is a small compression chamber made of a pneumatic glass jar.
Bert was able to use it to expose a sparrow to low pressures.
He reduced the pressure using a manometric tube,
observing at what point the bird started to suffer.
He used the India rubber bag to administer oxygen to the bird,
and "at once the bird becomes himself again," he wrote.
He concluded that at high altitudes, where the pressure was low,
: "it appears it is not the lowering of mechanical pressure
that produces the symptoms, but the low tension of oxygen
of the dilated air, which low tension prevents the oxygen from
entering the blood in sufficient quantity." (7)

So Bert became interested in helping people with breathing difficulties during the early 1870s.  He said it was already known (such as by the works of Tavarie) that compressed air (higher pressure) helped people with anemia, chronic bronchitis, and emphysematous asthma. The result was easier breathing, and a lower heart rate. (7)(8 page VII)

Improved knowledge of the effects of high pressure on the human body resulted in Bert, and various other physicians, trying to invent machines that would adjust the pressure of inspired air to relieve the feeling of air hunger. Such machines would be experimented on patients of various lung disorders, including asthma.

In fact, in his 1877 article "Atmospheric pressure and life," Bert said:

The great influence that may be exerted upon living beings by atmospheric pressure is now questioned by none, and there is even a disposition to exaggerate its importance. If the barometric column rises or falls a few millimetres, nervous people affected with the asthma perceive phenomena, whether of a beneficial or of a noxious kind, which they do not hesitate to attribute to the weight or to the lightness of the atmosphere. But if this were the only cause of their sensations, then they should experience the same symptoms whenever they subject themselves to equal variations of pressure, as in passing from the level of the sea to a point only a few feet above it, or vice versa. (7)

In his 1878 book "Barometric Pressure," he published the results of his experiments on barometric pressure. He dedicated the book to his friend, and the man who funded the project, Dr. Jourdanet.

This is a compression chamber that allowed Bert to measure
the effects of barometric pressure on himself and others.
Inside was an Indian rubber bag so he could inhale oxygen.
Access points allowed him to take blood samples
to determine changes in blood oxygen tensions.
He exposed himself to decreased pressures.  Once he
started to feel symptoms he inhaled oxygen.  He wrote:
"But all these symptoms disappeared as by enchantment
so soon as I respired some of the oxygen in the bag;
returning, however, when I again breathed the air in
the cylinder."  (7) 

There would be many devices invented, and many failed experiments, over the next hundred years, before a truly effective, and mass producible, device would be invented to truly help patient's with respiratory disorders.  Yet it was Bert's work that got it all started.

He also performed work using anesthetics such as chloroform, and to administer it he devised an apparatus that allowed the patient to inhale an ideal percentage of the compound.   (2)(3, page 427)

Along with being a successful physician and scientist, he was also a successful politician.

As Bert was performing his experiments on pressure,
he started to wonder how the world was created.
In regards to animals dying due to compression, he wrote:
"Thus it is the oxygen that is to blame.  Oxygen at too high
a tension destroys animal life.  Long I hesitated to characterize
as a poison the 'nursing father' of everything that lives, but there
was no help for it.  Oxygen, which gives us life, slays also,
when administered in too strong a dose.  I have had to study
thoroughly this paradoxal poison to determine the different
effects of varying doses, and its action upon our tissues. (7)

So after Williams, Longet and Bert all performed experiments to prove the spasmotic theory of asthma, you probably thought the subject was settled.  Well, not quite. There still remained skeptics with credible arguments against it.

J.B. Berkart, in his 1878 book "On Asthma," explained that, during his work on asthma, Bert had a difficult time getting the air passages to contract until he realized that he had been over inflating the lungs.

Berkart said it was only when he provided less inflation that he was finally able to induce the air passages to...

"contract... upon electrical irritation, applied either directly to it or to the pneumogastric nerve.  But the contractions were so feeble and slow as to induce Bert to think that they had no active share in the mechanism of respiration.  Moreover, the paralysis of the bronchial muscles, following the section of the vagus, did not appear to influence in that least the function of nutrition of the lungs.  Thus the integrity of those muscles, not being indispensable to an efficient ventilation of the lungs, it seemed not unreasonable to conclude that their spasmodic contractions could hardly have the effect generally assigned to them."  (4, page 42-43)(9,page 5)

Berkart said that Bert's experiments did not initially demonstrate contraction of the lungs because he over inflated them.

Berkart believed that Bert's experiments demonstrated proof that the air passages may constrict as Williams proved, but this did not occur in asthma because most asthmatics also present with emphysema, which is essentially over inflation of the lungs.  (4, page 103)

Berkart's theory was respected among the medical community, although it did not have a long lasting influence.

In 1886 Bert was appointed governor-general of Tonquin, and soon thereafter his health started to fail.  On a return to France during the year he gave a farewell speech at a meeting of the Academy of sciences, supposedly because he knew he was ill. He died of dysentry on November, 11, 1886. (2)

References:

1. Geddings, W.H., author of the chapter on "Bronchial Asthma," in the book  "A System of Practical Medicine," edited by William Pepper and Louis Star,Volume 3, 1885, Philadelphia, Lea Brothers and Co.
2. "Sketch of Paul Bert," Popular Science Monthly," July, 1888, Volume 33, compliments of wikisource.org, http://en.wikisource.org/wiki/Popular_Science_Monthly/Volume_33/July_1888/Sketch_of_Paul_Bert, accessed 2/6/14
3. Waller, A., "Meeting of the society of Anaesthetists: Dosage in Anaesthetics," The Clinical Journal, April 6, 1898, pages 426-430, volume XI, October 27- April 20, 1898, Sixth Year, Edited by L. Eliot Creasy, 1898, London, The Medical Publishing Company
4. Berkart, J.B., "On Asthma: It's pathology and treatment," 1878, London, J. & A. Churchill
5. Phillips, John L., "The Bends," 1998, Yale University
6. Tissier,Paul Lewis Alexandre, edited by Solomon Solis Cohen, "Pneumotherapy: Including Aerotherapy and inhalation methods," volume X, 1903, Philadelphia, P. Blakiston's Sons and Co., pages 296-224.  If the profession of respiratory therapy existed in their era, we would be reading their books.  However, as it was, their books were written for the medical profession. All of the material from this post is from Tissier's book unless otherwise noted in the above paragraphs. Tissier page 72
7. Bert, Paul,  "Atmospheric pressure and life," Translated from the French by J. Fitzgerald, Popular Science Monthy, July, 1877, volume 11, http://en.wikisource.org/wiki/Popular_Science_Monthly/Volume_11/July_1877/Atmospheric_Pressure_and_Life, accessed 2/8/14
8. Fulton, John F., author of the Forward to Paul Bert's book "Barometric Pressure," 1843, Columbus, Ohio, The F. J. Heer Printing Company
9. Bert, Paul,  "Barometric Pressure," 1843, Columbus, Ohio, The F. J. Heer Printing Company
10. Dobell, Horace, "On Asthma: It's nature and treatment," 1886, London, Smith, Elder and Co
11. Brown, Orville Harry, "Asthma, presenting an exposition of nonpassive expiration theory," 1917, St. Louis, C.V. Mosby Company
12. Thorowgood, John Charles, "Notes on Asthma," 1878, 3rd edition, London, J and A Churchill
13. Thowowgood, John Charles, "The Lettsomian Lectures: delivered at the Medical Society of London, 1879, on bronchial asthma: it's causes, pathology and treatment," 1879, London, Bailliere, Tindall, and Cox
14. West, Samuel Hatch, "Diseases of the organs of respiration," volume II, 1902, London, Charles Griffin & Company, Limited 

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1973: Alupent inhaler my story

In 1973 I was 3-years old. This was the year that a little white inhaler called Alupent was approved by the FDA. there was other rescue medicine on the market too, including Alupent solution. So, while I may have been too young for an inhaler in 1973, I certainly was old enough for my mom to give me breathing treatments when I was feeling short of breath.


This did not happen. I do not fault my doctors for this. I am sure they remember quite well the fact that the asthma death rate spiked in the late 1950s following the introduction of the Medihaler Epi to the market. They were well aware that, while asthma rescue medicine opened airways, it also had a strong cardiac effect.


After the Medihaler Epi and Medihaler Iso were introduced to the market in 1956, doctors were eager to prescribe these medicines for their asthma patients. And asthmatic patients love the convenient, and quick relief provided by these inhalers. They became an overnight sensation among the asthma community.


Asthmatics stuffed them in their pockets. They stuffed them in their purses. They took them with them wherever they went. And when they felt asthma symptoms, they pulled out their handy inhalers and they puffed. If their breath did not come back, the kept puffing until it did.


So, one theory is they became over-reliant on their inhalers. After puffing too many times, the cardiac affect caused their hearts to stop. They went into cardiac arrest and died.


There was also a second theory that postulated that the inhalers gave asthmatics a false sense of hope. that, rather than seeking help when they needed it, they kept puffing on their inhaler. By the time the decided they needed to seek help, it was too late. I personally prefer this theory.


However, that is neither here nor there. I am simply relaying this bit of information so you know that the medical community was fearful of rescue medicine. Doctors surely wanted to help asthmatics, but they didn't want the medicine they prescribed to harm their patients either. So, they did not prescribe me this kind of medicine. I had asthma attacks, and if I needed help my parents had to recognize it and take me to the doctor or hospital.


The fact I was a child asthmatic probably made Dr. Gunderson even more fearful of prescribing rescue medicine. So, regardless of how bad my asthma became over the course of the next seven years, my parents had no rescue medicine to help me breathe better.

1870: Biermer proves spasmotic theory once and for all

Michael Anton Biermer (1827-1892)

By experiments he published in 1854, Dr. M. Alton Wintrich convinced many physicians that asthma was caused by spasms of the diaphragm and not spasms of the bronchial tubes in the lungs.  Yet in 1870, experiments published by Michael Alton Biermer proved the spasmotic theory once and for all.

After Bert performed his experiments, Biermer ardently supported the spasmotic theory of asthma in a series of lectures in 1870. (1, page 194) (2, page 43)(3, pages 13-14) (5, page 11)

He believed the objections to the spasmotic theory of asthma based on the experiments of Bert "irrelevant," said Berkart, "for contraction of the thorax and the deficient resonance on percussion... could take place only if asthma were a spasm of the alveoli.

Along with the theories put forth by Bert, he proved that irritation of the vagus nerve caused contraction of bronchial muscles.(6, page 4)

According to Orville Brown he also "says that asthma is the result of swelling of the bronchial mucosa and a consequent obstruction of the smaller bronchi; the residual air in the alveoli then develop a greater tension and causes thereby a reflex spasm of the bronchial musculature. He reports a patient whose asthmatic seizures ended after the expectoration of a small feather." (16, page 34)

Thorowgood said:

Biermer observes that the bronchial muscles antagonise the muscles of inspiration, and so prevent over distension of lung. When, by frequent attacks of spasm, the nutrition of the bronchial muscles begins to fail, they no longer are able to antagonise the force of inspiration; or, by their contraction, to assist expiration, and thus that permanent condition of lung distension known as emphysema is brought about. (4, page 7)

Biermer published his wisdom on asthma in his 1870 book "Ueber Bronchioalasthma," and with Joseph Coats in the 1876 book "On bronchial Asthma."

References:

1. Geddings, W.H., author of the chapter on "Bronchial Asthma," in the book "A System of Practical Medicine," edited by William Pepper and Louis Star,Volume 3, 1885, Philadelphia, Lea Brothers and Co.
2. Berkart, J.B., "On Asthma: It's pathology and treatment," 1878, London, J. & A. Churchill
3. Thorowgood, John C., "Asthma and Chronic Bronchitis: A New Edition of Notes on Asthma and Bronchial Asthma," 1894, London, Bailliere, Tyndall, & Cox
4. Thorowgood, John Charles, "Notes on Asthma," 1878, 3rd edition, London, J and A Churchill
5. Dobell, Horace, "On Asthma; Its Nature and Treatment," 1886, London, Smith, Elder & Co.
6. Shmiegelow, Ernst, "Asthma, considered specially in relation to nasal disease," 1890, London, H.K. Lewis

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1970: The Beginning: Born with asthma genes

I was born on January 4, 1970. I was born with asthma genes. None of this was known at the time. In fact, not even scientists knew about asthma genes.

It wouldn't be until about 30 years later that the concept of asthma genes was even conceived.

I cannot guarantee this, but based on what I have read to this date, I can state with some degree of confidence that I was not born with asthma.

Does that make sense? I was born with asthma genes. In fact, i was born with a random assortment of the over 100 asthma genes. This meant that I had genes that were ready to tell my immune system to do something abnormal. However, this wasn't about to happen until these genes were exposed to some "environmental factor."

Environmental factors are substances around me, either in the air or inside me, that act as "keys" to turn genes on. Examples of environmental factors may include particles or chemicals in the air, such as those produced from wood or cigarette smoke. They may also include allergens, such as dust mites, pollen, mold spores, animal dander, cockroach urine, non-steroidal anti-inflammatory medicine (like Aspirin), an certain foods (like eggs, nuts, peanuts, etc.). Another example are respiratory infections, such as those caused by respiratory syncytial virus

So, I do not think people are born with it. Now, this is just my theory, but it's based on pretty good research. In fact, I think most asthma researchers would agree with me.

I know I was exposed to cigarette smoke from an early age. Mom didn't smoke, and dad didn't smoke in the house. In fact, I really don't have any memory of dad smoking in front of us kids. Whether or not he did when i was very little I would have no idea, and mom denies allowing him to smoke in the house. When we were at grandma ans grandpa Bottrell's house, though, I was exposed to smoke. I have some good memories of grandpa smoking. And, when we were over at their house, other people smoked too.

I was probably also exposed to viruses. But what I think caused my asthma, or turned on (activated) my asthma genes, were allergens. Mom says I was always sneezing, wheezing, and breathing heavy, and so I think I was exposed to allergens. I was exposed to dust mites particularly, and seasonal mold and pollen. Day after day exposure to these, perhaps coupled with smoke and viruses, caused me to develop allergies and asthma prior to the age of two.

My mom might have taken me to see the doctor. It was at the corner of U.S. 31 and 8th street. I can picture myself as a baby with a snotty nose and retractions. The doctor (was it Dr. Gunderson back then?) probably prescribed some over the counter medicine and sent me home with my mom. Considering both my memories and peer reviewed medical articles from the time, I highly doubt I was prescribed antihistamines, which I'm convinced would have helped.

There is some evidence that viruses (such as RSV, influenza and para influenza) may damage lower airway cells in such a way as to make a person susceptible to developing allergies. This would have caused me to develop a hyperactive immune response to allergens. And this response to allergens would have caused upper airway inflammation, which in turn caused the sniffles, wheezes and runny nose. it probably also caused rhinitis, which made my nose stuffy and caused me to breathe heavy.

Can you imagine how miserable this would have made me feel. And add into this the fact my older brother was annoyed with all the noises I made, particularly my heavy breathing. No matter he and I had issues getting along when we were growing up.

And I think the allergies, coupled probably with the virus induced asthma, probably ultimately lead to me developing lower airway inflammation, which made my lower airways hyperactive (twitchy) to asthma triggers, which included most of the allergens listed above and some.

There is evidence that allergies make colds more severe. So, every time I got a cold, every time i was exposed to allergens, I suffered from the gamut of symptoms: stuffy nose, runny nose, sneezes, wheezes, chest tightness. nasal irritation, scratchy throat, etc. I remember all these symptoms. I remember my eyes itching. I remember it all. No wonder I was a nerd as a kid. No wonder I had a low self esteem. No wonder why I became depressed in November of each year. No wonder I sat on the bench during school rather than participate in recess.

Of course, most of that would be later on. But, it all began with asthma genes. My genotype included asthma genes. My phenotype was allergic asthma. My endotype was a combination of cytokines, chemokines, histamine, and leukotrienes that were abnormally produced at increased levels by asthma genes and secreted by immune cells. Over time this got worse and worse, especially as I was increasingly exposed to my asthma triggers. And this lead to me developing severe allergic asthma at an early age.

Anyway, something turned on my asthma genes. Another theory is that it was allergies. Still, something had to turn on my allergy gene. So, perhaps a virus or chemicals turned on my asthma genes, and allergies turned on my asthma genes. Who knows. What is known is that I did develop asthma.

I talked to mom about this many times in my life. Her story has been consistent. She said I had a constant cold the first two years of my life (a virus, perhaps? Or was it allergies already?). She said I would stand up in the car and breathe heavy. My older brother Bobby hated the sound of my breathing, so I would have to stand in the front seat.

Okay, I know you are asking: "Why was he standing in the car?" That's just what we did. I have memories of standing in the car. I remember standing in the back seat. This was nice because then you could see. Back then, back in the 1970s and 1980s, kids were safe in cars; kids did not die in accidents. Nothing killed us. The idea of car seats was not even an idea.

So, mom says I got dibs on the front seat. I stood in the front seat, she said. I would often fall asleep, and breathe heavy. I breathed heavy even when I wasn't asleep.

As a side note hear. Seatbelts weren't worn then either. The only seatbelt for me was, when mom slammed on the brakes, her hand automatically went up, as though it would be strong enough to prevent me from shooting out the front window.

Okay, so mom was my seatbelt. Those things on the seat were just annoying knobs that you had to sit on. They were not used. Seatbelts were never used.

I'm sure there was medicine that would have helped a snotty kid who probably had retractions. his chest was being sucked in, but nothing was done. I'm speculating here. But, based on my experience as a respiratory therapist, I bet if I had a head cold all the time, I probably also showed some signs of asthma, and maybe even some severe signs of asthma. And it was all brushed off as a cold, even by my doctor. And so any medicine that would have helped me was no better than the seatbelts.

Not my parents fault here. Not my doctor's fault here either. It was just the way it was back then. They did not know I had asthma genes. The probably didn't know I had asthma. It was not uncommon for it to be brushed off as a cold.

So, I breathed heavy. I had a stuffy nose all the time. I was always coughing. I had snot on my nose. I was diagnosed with asthma when I was two-years-old.

1851-1913: The history of asthma sputum

Ernst Victor von Leyden (1832-1910 discovered
crystals in asthmatic sputum and suspected these
to be the cause of asthma. During his era, he was
the closest supporter of Dr. Robert Bree's
bronchitic theory of asthma. (9, pages 14-15)
He believed these crystals somehow irritated the
"vagus in the mucous membrane of the bronchials,
and hereby caused by reflex action a spasm
of the muscles of the small bronchial tubes."
(10, page 8)

Most people find sputum disgusting, and so will have nothing to do with it. But as far back as 400 B.C., the medical significance of it was observed by ancient Greek physicians, and probably even earlier than that.
If you mention it at the dinner table your mother might smack your hand. But for the sake of gaining a complete grasp on the history of asthma and respiratory disease, we must delve into the topic of sputum.  Sorry, but we must.

It must have been observed at an early date in history that people with breathing issues produce sputum, sometimes consisting of a putrid smell, often consisting of many varied colors such as red, yellow, brown and white.

Yet rather than being petrified by the grossness of the substance, Greek philosophers became fascinated by it. They even gave it its own classification as one of the four humors that, along with determining one's personality, also determined whether was healthy or sick.

Prior to the philosophical medicine of the ancient Greeks, other ancient societies, and the primitive clans and families that roamed the lands before them, believed sputum was the production of some evil spirit, demon or god. When a person expectorated the substance, they were, in essence, expectorating an evil substance that caused the symptoms they were suffering from.

From the ancient world to the scientific revolution there were few changes in the way physicians viewed diseases and treated their patients.  In 1799 Dr. Robert Bree speculated that sputum contained a poison that it was trying to get out of the body, and asthma was the result.  This theory wasn't much different than any idea Hippocrates might have postulated.

Since the sputum preceded the asthmatic fit, Bree essentially speculated that asthma was essentially bronchitis, and thus created the bronchitic theory of asthma.  Others, without much more evidence, speculated sputum was the effect of asthma rather than the cause.

Such speculation gradually tapered off, but never really came to an end, during the scientific revolution, and mainly due to the inventions of the microscope, which allowed physicians to see that the human body was made up of substances too small to be seen by the unassisted eye, and the stethoscope, which allowed physicians to hear changes that occurred inside the chest and to diagnose diseases with accuracy prior to autopsy.

The microscope allowed physicians to learn that air passages were surrounded by smooth muscle and that it was capable of spasming when stimulated.  The stethoscope allowed them to hear when sputum accumulated in the chest, and learn that it was the effect and not the cause of asthma.

So, pretty much, prior to the 1850s asthma was basically considered to be a disease of excess sputum, mainly because this was all physicians could observe with the unaided eye and ear.

Yet by the 1850s, it was looking pretty clear that asthma was also a disease associated with spasms of the air passages, particularly by the wheezes heard by air flowing through narrowed air passages, and rhonchi heard as air flowed through sputum lined air passages.  (1, pages 592-595)

In 1851, Dr. Beau, along with his assistant Cozart, observed that fits of asthma usually ended with a wad of sputum being coughed up. Beau used this observation as evidence to support his theory that asthma was a disease of chronic catarrh, and that asthma was caused by increased sputum in the air passages.  (3, page 31)

When this sputum dried out mucus plugs formed that were capable of blocking the air passages, thus resulting in dyspnea and other symptoms of asthma, including the "sonorous and sibilant rhonchi -- their 'rales vibrants' heard upon auscultation with a stethoscope."  (3, page 31)

The fit, therefore, was resolved when mucus plugs were broken up with a fit of coughing.  (3, page 31)

Then, in 1878, at a time when most physicians had accepted the nervous and spasmotic theories,  J.B. Berkart used Beau's research as evidence of the bronchitic theory of asthma.

Berkart said:

With the displacement of the mucous plug into the larger bronchus, or on its expulsion by means of a fit of coughing, the dyspnea ceases, and with it also the rales disappear.  This form of bronchitis is, in their (Beau and Crozant's) opinion, due partly to an idiosyncrasy of the patient, partly to exciting causes, which greatly vary in different individuals."

Tiny crystals were first observed in sputum in 1851 by Jean-Martin Charcot, but it wasn't until 1872 that these crystals were linked to asthma by Ernst Victor von Leyden. So history has given credit for this discovery to both men by calling the crystals Charcot-Leyden crystals.

Leyden, whose asthma theories were similar to Dr. Bree's bronchitic theory, believed Charcot-Leyden crystals caused asthma by irritating...

...the peripheral extremities of the vagus nerve, and produce reflex spasm of the bronchial muscle."  

The asthma attack, as Bree and Beau observed, ended when a wad of sputum was coughed up during a fit of coughing. (4, page 14-15

However, it was the discovery of these Charcot-Leyden crystals that would ultimately put an end to the bronchitis theory of asthma.  This was noted by Dr. John Charles Thorowgood in 1878.  He said that these crystals were found in sputum obtained from patients with "ordinary catarrh and croupus bronchitis."  (4, page 15)

Thorowgood said:

The asthmatic patient while in a fit presents abundance of symptoms distressing enough to endure or to witness; and yet, when things seem to be at their worse, and the patient well-nigh at his last gasp, a remission comes on, the spasm yields, air enters the lungs, and the attack subsides, coincidentally often with access of cough and mucous expectoration." (4, page 16)(9, page 1,2)

In 1879, bacteriologist Paul Erlich discovered the eosinophil, and it was soon discovered that elevated levels of eosinophils (eosinophilia) was commonly found in asthmatics. (5)

In 1882 Heinrich Crushmann observed other spirals in asthma sputum and believed they were associated with causing asthma. He believed since Leyden's crystals didn't cause asthma, perhaps his crystals did. (5)

Later Curshmann's crystals were determined to be fragments of mucus plugs associated with asthma, and Leyden crystals were determined to be fragments of eosinophils. Eosinophils were later learned to be a type of white blood cell that, along with mast cells, are involved in the allergic reaction.

In 1911 Hermann Sahli described eosinophils in asthmatic sputum. Yet Sahli noted another author from 1891 who described eosinophils in the asthmatic blood, and he concluded that these must be pathological with asthma. Yet he also noted that neither the cause of the eosinophils nor their origin was known. (7)

Sahli could isolate the area where the sputum came from based on epithelial cells in it, yet he did not understand the mechanisms of its production as we do today. (7)

Dr. James Adams describes asthma sputum in 1913: (8)

"Asthmatic sputum varies. Often there is none till the end of the attack; then it is in the typical form of small, tough pellets expelled by laborious coughing. The attack may then cease, or it may go on till a more free and profuse expectoration occurs."

He also wrote:  (8)

"The sputum does not readily decompose, and is said to be wonderfully free from microbes; but this is not always so, as I have occasionally found it teeming with them."

The true purpose of sputum is to ball up microbes inside the lungs and haul them out, and in this way, the lungs stay sterile.  Surely asthma can be caused by inhaling a microbe, such as a bacteria, but it's also caused by asthma triggers (dust mites, smoke, fumes, chemicals, pollution, animal dander) that are non-infecting agents.

So this might explain why Adams most often found asthmatic sputum without an infecting agent, and sometimes "teeming with them."

Backing up a moment to 1906, Australian pediatrician Clemons van Pirquet coined the term allergy when he observed that some of his patients were hypersensitive to substances that did not bother other people (what we now refer to as allergens, or asthma triggers).  This was the first time asthma was linked with allergies.

By 1910 Histamine was discovered and found to be a major component in the allergic response.  So some went on to speculate that finding a way to block histamine would cure both allergies and asthma.
In 1937, the first antihistamine was synthesized in a lab, and in 1946 antihistamines hit the market. Within a decade they were among the most commonly prescribed medicines.

Yet as time went by, it was learned that there was more to asthma and allergies than just histamine.  It was learned that asthmatic and allergic immune systems respond irrationally to allergens and asthma triggers by increasing production of eosinophils and this spearheads inflammation of the bronchial muscles.

Another weapon of the immune system is mast cells that line the respiratory tract and eyes, and these were discovered in 1953.  .

In 1967 Immunoglobulin E antibodies (IgE) were discovered.  It was later learned IgE has a significant role in the asthmatic and the allergic response.  The first time asthmatics are exposed to asthma triggers (allergens), say dust mites, their immune systems develop dust mite IgE antibodies that attach to mast cells that line the epithelial layer of the skin or respiratory tract.

The second time that person is exposed to that allergen (dust mites in this case), a mast cell that has a dust mite IgE antibody attached to it explodes and releases its contents:  the mediators of inflammation.  A mediator of inflammation called histamine was discovered in 1910, and others called cytokines and leukotrienes were discovered in the 1970s.

These mediators, when released into the blood stream, cause inflammation of the respiratory tract, thus causing the allergic and asthmatic responses.

In the allergic person, they can also cause inflammation of the upper respiratory tract, which includes the back of the throat and nose.  The offending substance (dust in our case) is recognized by the immune system, trapped in the mucus layer, absorbed by the mucus, balled up by the mucus, and sent on it's way up the respiratory track to be coughed up.

So this would explain what Dr. Bree, Beau, and Berkart observed. While hacking up a wad of sputum may have been related to the fit of asthma, it was not the cause, and had nothing to do with the cure.

Later it was learned that asthmatic lungs tended to produce an abnormal number of goblet cells, this results in an abnormal increase in mucus production during an asthma attack.  While some of this sputum may be coughed up, some becomes trapped in obstructed air passages, dries out to form mucus plugs, and this further blocks the air passages, thus compounding the asthma response.

When the fit ends, when the air passages relax and dilate, which may be a result of time or medications, the asthmatic will probably expectorate this sputum, which will usually be, if no bacteria or virus is balled up within it, white and sterile.  It will also have IgE and eosinophils in it, hence your Charcot-Leyden and Curshmann crystals.

So it's easy to understand how this production of sputum at the end of an attack could easily be misinterpreted as the cause, rather than the effect, of asthma.

References:

1. Lotval, J., "Contractility of Lungs and air tubes: experiments performed in 1840 by Charles J.B. Williams, European Respiratory Journal, 1994, (7) pages 592-595
2. Bree, Robert, "A Practical Inquiry into Disordered Respiration Distinguishing the Species of Convulsive Asthma, their Causes and Indication for a Cure," 4th ed, 1810, London, page pages 117-118
3. Berkart, J.B., "On Asthma: Its Pathology and Treatment," 1878
4. Thorowgood, John C., "Asthma and Chronic Bronchitis: A New Edition of Notes on Asthma and Bronchial Asthma," 1894, London, Bailliere, Tyndall, & Cox
5. Lipkowitz, Myron, Tova Navarra, "Encyclopedia of Allergies," 2001
6. Brenner, Barry E, "Emergency Medicine, 1998, page 10
7. Sahli, Hermann, "A treatise on diagnostic methods of examination," 1911
8. Adams, James, Asthma and it's Radical Treatment, 1913
9. Thorowgood, John C., "Notes on Asthma," 1878, 3rd edition, London, J & A Churchill
10. Shmiegelow, Ernst, "Asthma, considered specially in relation to nasal disease," 1890, London, H.K. Lewis

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