The Nervous Theory Of Asthma: A Review

Earlier, I wrote that “Occupational Asthma” was “one of the oldest asthma subgroups.” I would like to make the case here that the oldest of oldest of oldest asthma subgroups is none other than “Nervous Asthma.” To help me make my case I thought a little history of nervous asthma would prove helpful. 

400 B.C. Hippocrates (400 B.C.) referred to asthma as epilepsy of the lungs. This is because he believed it was caused by phlegm draining down from the brain. He, therefore, believed asthma was caused by airway spasms similar to the body spasms of epilepsy. He also alluded to asthma as a nervous disorder when he said, "the asthmatic should guard himself against his own anger." 

1st Century. Galen (120-200 A.D.) is a physician who created theories about medicine that were well respected by physicians all the way up to the 19th century, and even into the 20th century. He performed one experiment (and probably on a stolen body) where he severed the spinal cord to produce asthma symptoms artificially. (1)

 
2nd Century.  Maimonides (1138-1204) said nervousness makes one prone to illness and may have been the first to describe how illness can contribute to diseases. He did describe asthma, but he did not link the two.

1550. Felix Platerus (1536-1614) observed asthma symptoms when nothing wrong could be seen with the lungs. He believed asthma was caused by an obstructed pulmonary artery, although he also believed it was caused fluid flowing down from the larger nerves from the brain.

17th century. Jean Baptiste van Helmont (1579-1644) was the first physician to focus on the idea that asthma was caused by airway spasms. However, he believed this was the result of nerve irritation due to stress. He thought this was the case because no scars were observed in the lungs of asthmatic patients. He gave examples of how stress could induce asthma. In one case he described how a woman developed it just by being exposed to flowers, and in a second case, he described how a man developed it and died just after being exposed to stress.

17th century.  Thomas Willis (1621-1675) also described asthma as having occurred despite any observable changes in the person. Paul Ammann (1634-1691) described in a book of law cases how asthmatics should be absolved from crimes because the fear that resulted could result in an asthmatic attack. This meant that all asthmatics must be kept out of stressful situations.

1850’s. Dr. Henry Hyde Salter published a series of articles that were eventually published in 1960 as “On Asthma: Its Pathology and Treatment.” In these articles, later published as chapters, he proved for the medical community that asthma was due to spasms of the air passages caused by irritation of nerves. Salter’s asthma theories are frequently cited in medical texts regarding asthma for the next 50 years. Those physicians who accepted Salter’s theories -- and this consisted of most physicians -- referred to Salter’s nervous theory as the “Nervous Theory of Asthma.”

1899. Dr. Henry Osler, the Father of Modern Medicine, referred to asthma as a "neurotic affection" in his medical texts, "The Principles And Practice Of Medicine." This book would be the main textbook used by medical students much of the next century, and so would have a significant impact on shaping the views of the medical profession.

1900. The discovery of epinephrine created a lot of buzz among the medical community, and it was trialed for a variety of diseases, including asthma. This worked to confirm an old theory, that asthma was due to airway spasms, and a new theory, that asthma was due to dilated blood vessels resulting in pulmonary congestion. These theories spawned from the fact that epinephrine both dilates airways and constricts blood vessels. So, for the first time in many years, the nervous theory becomes less significant among asthma physicians.

1910. This was the year that allergies were linked with asthma. This revelation would have no immediate impact on our history, but it will within the next 20 years. 

1920’s. German physicians became infatuated with psychosomatic medicine, and out of this infatuation grew an increasing interest in the idea that asthma was a psychosomatic disorder. Among these physicians was Dr. Franz Alexander, who will make a significant contribution to our history about 30 years later.

1930’s and 1940’s. Most American physicians continued to believe that asthma was triggered by emotions. However, their main emphasis now was attempting to control allergies. Also, as researchers started learning more about allergies, they realized that asthma symptoms were the result of an abnormal immune response to allergens. Spearheading the idea that allergies caused asthma was the germ theory of asthma. At this time it was believed that most diseases were caused by bacteria or some similar substance, so this theory sort of spearheaded the idea of allergies as a contributing cause of asthma. So, the nervous theory of asthma takes a back seat to this new thinking about asthma.

At the same time that was going on, German physicians, lead by Dr. Franz Alexander, were beginning to study the relationship between asthma and psychosomatic disorders like stress, anxiety, and depression. This sort of was a rebirth of the old theory of asthma as a nervous disorder. The main theme here was that strong emotions caused by an asthmatics separation, or threat of separation, from his mother were one of the main contributing causes of asthma. One treatment for this was psychological therapy. 

1951.  By now, Dr. Franz Alexander had migrated to the United States, and here he wrote a paper listing asthma as one of the seven psychosomatic disorders. This, in turn, re-established credibility of the nervous theory of asthma for physicians in the developed world. This was also the decade that corticosteroids were first used to reduce airway inflammation that was present during acute asthma attacks.

1957. The first metered dose inhalers enter the market. They were the Medihaler Epi and the Medihaler Iso. This was a great revelation for asthmatics as it gave them a lightweight, portable, and easy to use means for obtaining quick asthma relief.

1960s.   It was also discovered that corticosteroids come with side effects. So, by the end of the 1950's, steroids were soon reserved for only the severest asthma attacks that responded poorly to other treatments. However, researchers began a quest to see if they could develop an inhaled corticosteroid steroid to reduce the risks for systemic side effects. So, this was the decade where researchers started studying the benefits of inhaled corticosteroids on asthma.

1980’s.  By 1982 two inhaled corticosteroids were on the market. Studies showed they seemed to work very well for asthmatics. Research to learn how they worked lead to the discovery that asthma was an inflammatory disorder, where all asthmatics have some degree of underlying airway inflammation. It was now well accepted that asthma symptoms occurred due to exposure to asthma triggers, which may include strong emotions and stress, but also allergens, respiratory viruses, certain foods, exercise, etc. Researchers now understood that asthma was a respiratory disease consisting of chronic underlying airway inflammation and that this inflammation worsened when exposed to asthma triggers resulting in bronchospasm, increased mucus production, and asthma symptoms. This spearheaded the quest to understanding the exact genes, cells, and biological processes responsible for asthma. Rather than focusing on asthma as a nervous disorder, asthma was considered a disease associated with an overactive immune response to innocuous substances in the air inhaled. So, this new theory set aside any notions of asthma as a nervous disorder caused by stress, anxiety, and depression. That said, nervous disorders were still thought contribute to asthma by triggering it, maybe even making it worse, but it was no longer suspected to be the causative agent. 

1990’s. You might hear things like: “While stress and anxiety are no longer thought to cause asthma, both may act as asthma triggers.” I'm not sure who came up with this line, but I have heard it over and over by various asthma experts, often without citation. This may have acted as a relief, of sorts, for asthmatics, who were tired of hearing about asthma being all in their heads. However, it offered no advantage to the many asthmatics who continued to deal with both anxiety and asthma. 

2017. Modern evidence has brought upon a resurgence, of sorts, of the nervous theory of asthma. Studies seem to show that asthma might contribute to anxiety and depressive disorders, and that anxiety and depressive disorders might contribute to asthma. This new evidence comes with a modern twist, which includes the idea that not all asthma is nervous in origin. However, knowledge of a possible link should make physicians better armed to both diagnose and treat anxiety and depressive disorders in asthmatics in an effort to help them obtain ideal asthma control.http://asthmahistory.blogspot.com/2017/03/1950-alexander-defines-asthma-as-one-of.html

1899: Is asthma simply a "Nerve Storm?"

Nerve Storm: Seizure, as in seizure of the entire body (epilepsy), seizure of the muscles of a certain joint (gout) or seizure of the respiratory bronchi (asthma). The seizure is caused by some imbalance either internal (emotion) or external that triggers the abnormal response of the brain.

I've read about asthma being described this way in many older journals, yet Dr. Joe Shoemaker, in his 1899 book, "The Monthly Encyclopedia of Practical Medicine" (Philadelphia, Vol. XIII), uses this term with force.

He further describes asthma as:

• A disease essentially due to some nervous change (this was the accepted dogma of the time)
• Partial hereditary (so we still think this)
• It's occurrence is largely in "neurotic" subjects
• It's occurrence in families subject to migraine (hmmm, where does this come from?)
• Attacks are characteristic of asthma (dyspnea due to bronchospasm)
• Pt inclined to hold to a chair or bed railing firmly to help expiratory muscles of expiration
• And all this is caused by a "nervous storm"
• Triggered by some unknown cause
• The cause of who has such a "nervous change" also remains a mystery
• It's seen in children and some adults
• It's rare
• Sudden in onset
• Occurs between 2-4 a.m. (remember, this is based on his observations)
• Accessory and natural muscles of respiration are contracting vigorously
• Dusky face shows embarrassment to circulation and deficient oxygen in the blood
• Sweating skin shows muscular exertion
• Lungs enlarged during paroxysm
• Yet auscultation shows little to no air entering them
• No normal respiratory murmur, instead expiratory whistle is heard upon austultation
• Sonorous rhonchi often heard (which is what we now call a wheeze)
• Duration of attack is variable, yet is often over by morning
• Duration may last 24 hours or longer
• Attack ends with expulsion of mucus
• No continued cough or expectoration

This is all part of the nervous storm we call asthma. What do you think?

1950s: The first peak flow meter

Wrights original peak flow meters (circa 1950s)

If you're an asthmatic you may not be familiar with Dr. Martin Wright, but you probably are familiar with an instrument he invented:  the peak flow meter.  It was a convenient, inexpensive, hand held tool that could be used by patients at home or in the hospital setting to assess the effects of bronchitis and asthma.  

It was first introduced in the 1950s by London physician, Dr. Martin Wright, of the Clinical Research Center at Northwick Park Hospital.  It was an instrument specifically designed to measure 'peak flow,' or the amount of air that can be forced out of a patient's lungs after a maximum inhalation.  

The original Wright Peak Flow Meter was a large, heavy, clock shaped device that was too expensive for the common person to have at home. It was generally used in hospitals to assess patients. It worked by the patient blowing air into the meter, and this air rotated a pointer on a dial against the resistance of a spring. The device gave the first accurate readings of a peak flow.

Mini Wrights Peak Flow Meters (circa 1970s)

In the 1970s, Dr. Wright invented a new device that was inexpensive and portable.  It's basically just a "tube with a spring inside and a calibrated scale along the outside.  The puff from the patient under test pushes the spring back.  A pointer registers the furthest point reached.  The meter comes complete with a set of cardboard mouthpieces.  Doctors recon that the instrument could be useful in home treatment. Patient's could monitor their own lung power in a simple and cheap way of determining recovery from lung ailments." (1, page 675)

This instrument was called a "Mini Wright," although ultimately it became known as the peak flow meter. The devices were ultimately manufactured by various companies, and now you can get an array of different types. The first ones were not disposable, although they were soon thereafter manufactured for single patient use only, and the separate cardboard mouthpieces are no longer needed  

Many peak flow meters available today

I remember the "Mini Wright" from when I was an asthma patient back in the late 1970s and throughout the 1980s. Gone are the days of the Mini Wright, replaced by the even cheaper plastic models.

Can you guess how many peak flow meter brands are on the market today?  I couldn't even fathom a guess, although I've had over 20 in my grasp at one point or another.

Reference:

1. "Hot Air Invention," New Scientist, March 1, 1979, page 675

Further reading and another picture:

1. Check out: Wrights Peak Flow Meter, The Virtual Museum Library,  http://medicine.nus.edu.sg/anaesthesia/virtual_museum/airmed_spirometer.htm

1980-2000: Evolution of Artificial Respiration

So we must continue on our journey through the evolution of artificial resuscitation or respiration. This journey made it's way from simple mouth to mouth breathing all the way to volume ventilators. That pretty much takes us to the 1980's.

Figure 1 -- Drawing of Down's Flow Generator
Face Mask CPAP

1980s: Down's Flow Generator:
Continuous Positive Airway Pressure (CPAP) was something that was researched in the 1930's and 40's and then dropped. This research was picked up again as it was believed a continuous flow of pressure during inspiration and expiration might be helpful to patients with sleep apnea and chronic lung diseases.

The most common mode of delivery was by using a Down's Flow Generator. The generator was connected to a 50 PSI source and corrugated tubing. The opposite end of the tubing was connected to a mask with a Positive End Expiratory Pressure (PEEP) valve. (Keep in m;ind here that PEEP and CPAP are basically the same thing.)  The mask was securely strapped to the patient's face.

A pressure manometer was sometimes attached to the mask and an oxygen analyzer was sometimes added to the circuit using a T-piece to monitor how much oxygen the patient was receiving. A venturi-system allowed the caregiver to determine the percentage of oxygen allowed to the patient.

Ideally, a CPAP of 7.5 was supposed to increase the partial pressure of oxygen of alveolar air (PaO2) by one percent, just enough to force more oxygen into the blood to make a clinical difference. It is in this way that CPAP or PEEP were determined to improve oxygenation. (1)

A nice thing about these generators is they were completely pneumatic, meaning no electricity was needed. A downside to these generators is that they did not have alarms, meaning there was no way of knowing for sure that the patient was getting in the dialed in CPAP.

This system was used until the mid 1990s when electronic noninvasive positive pressure breathing machines entered the scene. We had one of these units at Memorial Medical Center when I started working, although I never had the good fortune of using one.

While rarely used in hospitals today, they are still used by Paramedics in the field.

1980s: Pressure Support Ventilation:

1980s: Pressure Controlled Ventilation:

1980s:  Airway Pressure Release Ventilation:  here is a good article.

1980s: Inverse Ratio Ventilation:

Puritan Bennete 7200

1983:  Puritan Bennett 7200 Micro-processor Ventilator:  This was the first microprocessor volume ventilator to hit the market. The machine was very durable and simple to use.  The settings were set by scrolling through an LED screen, and alarms were set in the same way.

It was easily used, portable, and worked well for the patient.  It quickly became the "most widely used ventilator around the world, capturing a 60 percent share of the international market by the end of the decade. (2)

This was the most common ventilator when I entered the respiratory therapy scene in 1995. It was in a majority of hospitals I worked as a student.

Bird 6400 ST

1986:   The Bird 6400 ST:   This ventilator was the first of the new generation of volume ventilators to hit the market. It was a rectangular shaped ventilator with all your basic knobs on the front, including volume control, assist control, SIMV, PS and CPAP modes. It also had a PEEP valve that was easily adjusted by a dial, and a full set of alarms.

The only knock on this simple device was the expiratory valves needed to be cleaned between each use and were a pain in the butt to put back together and keep in functioning order. It was a very compact ventilator for its time. We had two of these ventilators at Memorial Medical Center (MMC) when I started in November of 1997.

After purchasing a Servo 300 Ventilator around 2000, we kept one Bird in circulation until 2008.

1988: Respironics BiPAP:  It was introduced to provide noninvasive positive pressure ventilation to spontaneously breathing patients in the hospital setting using a mask. It could be set in ST mode to deliver IPAP and EPAP, or it could be set in CPAP mode to deliver CPAP.

Servo 300

1991: Seimen's Servo 300 Ventilator. This was a replacement ventilator for the Servo 900 and was generally created to complete with the the Puritan Bennett 7200.  It was much simpler to use than the old 900 version, and therefore was less intimidating. It included some very nice features, and some new modes, as noted below.

1991:  Pressure Regulated Volume Control: It had a new mode called Pressure Regulated Volume Control (PRVC) which made it so the patient could get a guaranteed volume, yet a sensor in the machine sensed changes in patient lung compliance to make sure the lowest pressure possible was given.

1991:  Volume Support:  Similar to pressure support, although it guaranteed the patient achieved a certain tidal volume with each breath. It was basically a pressure support breath that guaranteed tidal volumes. When weaning a patient.

1991: Automode: The Servo 300 had an option called automode. The caregiver would set the patient up in a control mode. As the patient began spontaneously breathing, the machine would sense this and switch over to a support mode. For instance, if PRVC was the set mode, the machine would switch to volume support (VS). If Pressure Control was the set mode, the machine would switch to pressure support (PS).

Servo 300 A Control Panel

This was nice because it allowed patients to control the ventilator rather than the other way around. This was another mode that made mechanical ventilation more comfortable for patients.

It could also be useful as a tool to see if patients were ready to be weaned. For instance, a post operative patient would be started in PRVC mode with automode. When the patient began to wake up and spontaneously breathe, the machine would sense this and switch over to volume support.

Of course, if the patient stopped spontaneously breathing, the machine would sense this and switch back to PRVC.

1991:  Flowby:  Another neat feature of this machine was that it allowed caregivers to choose between pressure sensitivity or flow sensitivity. Prior to the Servo 300, most ventilators used pressure sensitivity, meaning the patient had to make an effort to draw in a set pressure, usually 2-3cwp.

Flowby actually made machines more sensitive to the needs of the patient. A constant flow was maintained throughout the circuit. As the patient drew some of this flow, a breath was given.

Therapists had a choice between setting the sensitivity between 2-14 cwp, or in the green flowby range. As therapists became educated on the benefits of flowby it became the preferred choice. I believe most newer ventilator models do not even offer pressure sensitivity as a choice, and simply go with flowby.

1991:  Ventilator Graphics:  Another neat feature of this ventilator is that it also allowed for a graphics screen to be added. I think our machine did not have the graphics screen initially, but it was eventually added. This was nice because you could use graphics to adjust settings to improve patient comfort. Graphics also helped determine if suctioning was needed, or if there was a leak in the system. This was all part of improving patient comfort.

And that's not all.  It was also the first ventilator that could be adjusted for use by adults, pediatrics, and neonates. This made it a more universal device. Safety valves were in place, whereby neonates could not receive a tidal volume higher than 40, and pediatrics could not receive a tidal volume higher than 400.

Alarms were all red knobs. The LED showing dialed in settings were green. The LED showing what the patient was doing were all red. This made it easy to know what the machine was doing and what the patient was doing. We would often tell nurses, "Red bed, Green machine."   (d)

 This ventilator was used at MMC until the purchase of a Servo i made it no longer relevant. It continued to be a back-up ventilator until taken out of service in 2015.


1992:  V.I.P. Bird Infant Pediatric System

It was referred to as the T-Bird ventilator. At the time it was also the first and only ventilator that was mobile.

1988:  Noninvasive Positive Pressure Ventilation (NIPPV): Providing positive pressure breaths using a ventilator hooked up to an endotracheal tube was nice, although it was associated with a host of complications, and this was mainly due to the fact that it was invasive. Invasive ventilation essentially entails providing mechanical breaths through an endotracheal tube.

It was linked with an increased risk for nosocomial pneumonia. It was also difficult to get patients with end stage lung diseases weaned from ventilators. This created an ideal market for NIPPV.

NIPPV is essentially mechanical ventilation without the use of an endotracheal tube. It generally entails using applying a mask to the patient's face. In the hospital setting a full face mask is used, or a mask that covers the mouth and nose. However, a nasal mask or full

Now, technically speaking, IPPB was a form of NIPPV before NIPPV became a common acronym for CPAP and BiPAP machines. Electronic CPAP machines became common for the treatment of sleep apnea. A constant flow of pressure during inspiration and expiration helped to keep airways open. This assured the upper airway did not collapse while sleeping, and made sure that apnea episodes did not happen. It also kept alveoli open to assure adequate oxygenation.

Electronic CPAP machines were produced by a variety of manufacturers for use at home. These machines have become smaller, quieter, and more convenient over the years.

BiPAP is an acronym for Bilevel Positive Airway Pressure. It was first used in 1988 by professor Benzer of Innsbruck. It refers to a machine that delivers PEEP/ CPAP during expiration, and Pressure Support during inspiration.

When BiPAP is used, different acronyms are used as follows

• Inspiratory Positive Airway Pressure (IPAP): This refers to pressure support, or a flow of positive pressure during inspiration to assist with inspiration. This basically helps to control ventilation, or to assure adequate tidal volumes. This is adjusted to blow off carbon dioxide. However, increases in tidal volume may also improve oxygenation. 
• Expiratory Positive Airway Pressure (EPAP): This refers to a constant flow of pressure on expiration, also known as CPAP or PEEP. This keeps airways open. It increases the partial pressure of oxygen in the alveoli to force more oxygen into the blood stream. This is adjusted to improve oxygenation. 

Machines used in the hospital setting tended to be larger than home machines. This was due to the need for alarms in the hospital setting to monitor tidal volume, pressure, and oxygen levels. 

BiPAP machines became increasingly popular during the 1990s. Most were capable of providing patients with either CPAP or BiPAP, and this made it so that Downs Flow Generators were no longer needed and were phased out. This was about the phase I entered into. As a matter of fact, when I was in RT school BiPAP was covered vaguely. When I started as an RT it was only occasionally used. 

Early machines were were electric although not connected to oxygen. This meant that oxygen had to be bleed into the circuit from an external source. This sometimes made it difficult to meet oxygen demands of patients, and resulted in some patients being intubated. This problem was solved by later BiPAP models, such as the Vision. 

Regardless, early BiPAP macines gave physicians another option for helping patients. They were increasingly used for who were in respiratory failure or impending respiratory failure. This basically offered physicians a noninvasive method of treating hypoxia and ventilatory failure in patients who had a spontaneous drive to breathe, and who were capable of ripping the mask off if necessary. These machines prevented many patients from needing a ventilator, and they are still used to this day. 

1996: Respironics Vision:  

 Some of the initial models were crude and called for supplemental oxygen to be connected into the system, but new systems, such as the Vision, are touch screen, have flow and pressure waveforms, and allow the machines to be used pretty much like a ventilator.  The advantage is you can ventilate a patient and improve oxygenation without having to intubate the patient.  Masks can be removed for eating and drinking and taking medicine, and also oral care.  Studies show these machines work great for COPD, CHF and even some asthma patients.  They also work well for home use for patients with obstructive sleep apnea. Modern BiPAP machines are also more effective than the aforementioned down's flow generator in delivering CPAP, and the machines also allow for alarms and patient monitoring. 

2000:  Servo i, 840, Avea Ventilators

It has all the same features as the Sero 300 except that the flaws of the 300 have been corrected.  Instead of having all the dials on the front the settings are set by an easy to use touch screen.  The basic settings of rate, tital volume, and FiO2 could be set either this way or by quick access dials on the bottom of the screen.  The ventilator was also connected to a graphics screen for easy to see ventilator graphics.  (d)  Other similar ventilators include the Puritan-Bennett 840 and the Avea Ventilator.  These newer vents are microprocessor vents that include a variety of modes to improve patient comfort.  They also include waveforms to monitor the patient, and a variety of alarms.  Modern vents are also upgradeable. 

The future:  What will the future bring?  


References:

1. n l Need Reference
2. "Puritan Bennett Corporation History," fundinguniverse.com, http://www.fundinguniverse.com/company-histories/puritan-bennett-corporation-history/, accessed 4/8/16

References

1. (d)"About us:  History of Ventilation," maquet.com,  http://www.maquet.com/sectionPage.aspx?m1=112599762812&m2=112599885558&m3=112600545105&m4=112806653448&wsectionID=112806653448&languageID=4, accessed February 27, 2012
2. "Face Mask CPAP," 

1950: Life for polio victims inside an iron lung

This is Richard Daggett in an iron lung. The photo was
added by Dagett at Poliotoday.org. 

There were various versions of the Emerson Lung, and the Drinker and Shaw Respirator, that were available in hospitals around the United States and Europe by the 1950s. Richard Daggett, in his 2010 book "Not just polio: my life," explains that the machines made a whooshing sound as air entered and exited the patient's lungs. He explained that he was placed in a Drinker Collins Iron Lung in the early 1950s, and he described waking up in the machine: (4, page 30, 31)

There was a mirror over my head and, in the mirror, I could see a row of large black bellows across the room.  They were going up and down.  I didn't know much about respirators, but I figured one of them must be making me breathe.  I tried to figure which one it was by timing my breathing with the motion of each bellows.  None of them seemed to match my breathing pattern. It wasn't until later in the day, when my mirror was adjusted upward, that I realized that those bellows were all attached to the underside of other respirators.  I couldn't see mine because it was beneath me.... I was in a Drinker Collins Iron Lung."  (4, page 29)

Daggett and his parents during his first trip home from the hospital
in December of 1953.  Photos added by Daggett at Poliotoday.org. 

Daggett said that as a child it was difficult to grasp the seriousness of having bulbospinal polio and, ultimately, pneumonia.  He wrote: "I was very naive. I had no understanding of how serious my condition was.  Oh, I knew I was completely paralyzed, but the long-term impact did not sink in.  My greatest concern was that I might miss the first day of school." (4, page 33)

It must have been common for these patients to develop pneumonia, as their would have been constant secretions forming in the upper air passages that needed to be cleared, or they would be inhaled, thus causing respiratory infections such as pneumonia.  Daggett mentions the constant urge to blow his nose, which he often did "without even using a tissue." (4, page 31, 33)

Daggett during a trip home in 1954.  He is wearing
metal hand sprints, and sitting in his first wheel chair.
Photo added by Daggett at Poliotoday.org.

The desire to clear secretions would be a constant concern for caregivers because due to paralyzed muscles they did not have the ability to swallow, and therefore these patients lost the ability to control their airway.  This would have posed a greater serious problem back when the Drinker Respiratory was first used on polio victims, as a patient may survive because of the respirator only to later drown in his own secretions a few days later.

To treat this problem the patient's bed had to be slid out from iron lung, and the patient had to be turned by one attendant, while another used rags to wipe away secretions.  This probably would have been necessary often for some patients, further compounding the workload of the staff and the stress of the patient.

However, this problem was remedied somewhat with the invention of a suction device in 1937. By the 1950s caregivers could simply apply suction to the nose and mouth and suck out secretions.  Many such patients had a tracheostomy in place for just this reason.  And this brings me back to Daggett.

Daggett describes being awake when the tracheostomy was inserted into his neck.  He was later put inside an iron lung, which proceeded to breathe or him.  He notes that it was by means of his tracheostomy that his caregivers, all of whom wore cloth gowns (some wore masks), would clear his air passages, probably with one of these original suction devices.  (4, page 30, 33)  Of the tracheostomy, he wrote:

Those of us with significant paralysis of our breathing muscles also had additional air forced into our lungs through a tracheostomy.  The tracheostomy can also be used to suction mucous from our lungs.  I'm sure the tracheostomy saved my life." (4, page 30)

While iron lungs gave medical professionals an opportunity to save lives, they were also viewed as a terrible way to spend the end of ones life, although, thankfully, they allowed many children, such as Daggett, an opportunity to live to tell about it.

Iron lungs were ultimately replaced by other more complicated machines, such as intermittent positive pressure breathing (IPPB) machines, the Monaghan Ventalung Respirator, and the Bird Mark 7 Respirator. All of these newer ventilators were among a new breed of respirators that applied positive pressure to the lungs, as opposed to negative pressure.

So the iron lung has a significant place in the history of respiratory therapy.  It was an idea created to save the lives of millions of children who would have otherwise met an early demise due to a disease called infantile poliomyelitis.  To all the children saved from a dreaded diseases they were simply a Godsend.

Daggett was ultimately transferred to Rancho Los Amigos Hospital (now Rancho Los Amigos National Rehabilitation Center) where he could be rehabilitated.  He went on to become an "active journalist" who lives in Southern California who has "written extensively on disability and the human condition."  (1, last page)

References:

1. Daggett, Richard Lloyd, "Not just polio: my life story," 2010, Bloomington, IN, iUniverse

1940-1970: The decline and return of tuberculosis

By the 1940s there were a variety of antibiotics that allowed physicians to control most cases of tuberculosis. For patients that seek medical attention and follow the prescription of their physician, tuberculosis can be controlled and even cured. By 1969 it seemed that the disease had been conquered, and attention was diverted from it.

It seems to be normal for human beings to forget that of which they do not see. When we don't have a war for a while, we tend to assume one will never occur again and we cut our military spending. When a war occurs, we usually aren't prepared. The same can be said of disease. When we go years without a plague, we assume the disease is cured. When the plague strikes, we aren't prepared. A perfect example of this is the Spanish Flu of 1918.  

There was a friend of mine who often said that we ought to have a war every ten years so we don't forget that freedom comes with a price. We should have a plague every so often so that we don't take these diseases for granted. Surely we don't want wars or plagues, but my friend had a valid point.

By the 1930s and 40s sulfa drugs and antibiotics were discovered as a means of treating infection. These and other medicines allowed physicians to effectively treat and even cure tuberculosis. This decade saw a rapid decline in the number of tuberculosis patients.  

According to Elaine Landau, in her 1995 book "Tuberculosis:"

As late as 1969, the federal government was still channeling annually more than $20 million in TB project grants to local clinics and hospitals throughout the nation. But the declining TB rate made people feel that the crisis was over. So when the government began giving blocks of aid to states and municipalities to be used at the areas' discretion, the funding generally was not expended for TB controll. 

As time passed,countless successful TB programs were dismantled. In New York City alone, more than one thousand beds formerly reserved for TB patients were eliminated from municipal hospitals. Although outpatient services were supposed to be established to ensure the disease's continued decline, these were never made available. Instead, funding was diverted to meet more immediate needs. As one physician who's treated numerous TB victims described the situation, "We knew how to cure it. We had it in our hands. But we dropped the ball. (1, page 3, 4)

Once the "ball was dropped" it was difficult to pick it up again. Organizations with the ability to provide methods of preventing the spread of such diseases, such as the Centers for Disease Control and Prevention (CDC), were not provided with enough funds to effectively perform this task. (1, page 34)

In 1989 a plan was made to provide the CDC with $30 to $34 million dollars to create a TB control plan. Yet the plan was never made "because each year that it was proposed, the White House eliminated its funding from the budget." A similar plan was proposed in 1993 to offer $484 million for TB prevention, but the budget was cut by the Clinton administration to $124 million before it was sent to Congress. So the return of a disease that once ravaged a nation was greatly ignored by Reagan, Bush and Clinton. (1, page 35)

What may have opened the eyes of the government was the AIDS epidemic that struck during the 1980s. Studies showed that with weakened immune systems, up to 50 percent of AIDS victims were developing tuberculosis, and were unable to fight it off. This is one reason tuberculosis spread through prisons and homeless shelters rather fast, particularly in cities like New York "where nearly one-fifth of prison inmates have TB, but none of the jails have separately ventilated cells for contagious cases." (1, page 35-37)

To make matters worse the TB bacteria has the ability to mutate to create drug resistant strains. This occurs when people who are given antibiotics, which are proven to cure TB if used properly, were not taking the antibiotics once they started feeling better. Effective treatment usually takes 6-9 months, but many would stop taking it within weeks.

Landau also said that "this is actually worse than not taking any medication at all, because over a period of time the illness no longer responds to any form of medication, and they have, in fact, dissipated the drug's effectiveness... Unfortunately, significant numbers of people have misused their medication this way. The tendency to do so appears to cut across racial, class, and economic lines." (1, page 39)

Studies show that up to 50 percent of TB patients do not take their medicine as prescribed, and that 14.1 percent of TB cases responded poorly to TB medicines. Studies also showed that TB resistant strains have a 50 percent mortality rate. (1, page 39-40)

References:

1. Landau, Elaine, "Tuberculosis," 1995, New York, Chicago, London, Toronto and Sydney, Franklin Watts 

1956: The A-B-Cs of CPR are born

In 1949,  Dr. James Elam, an anesthesiologist, investigated old records of how mouth to mouth breathing was used on newborn infants.  While trying to save the life of a boy, he used this method and it worked.  This was the beginning of the re-birth of mouth to mouth resuscitation.  (1)

I say re-birth because when the Royal Humane Society was established in 1773, mouth to mouth resuscitation was recommended as one of many options for reanimating victims of near drownings. It as later removed from the list due to complaints that it was gross and unhygienic. The Sylvester and Shaefer methods of reanimation were added in its place.

Dr. Elam and Dr. Peter Safar would prove that neither the Sylvester nor Shaefer method provided enough tidal volume, although mouth to mouth breathing did. So this brought back the method once thought to be gross and unhygienic.

Also recommended by the Humane Society back in 1773 were chest compressions and abdominal thrusts, and these were ultimately phased out.

By the 1890s chloroform was a common anaesthetic during operations. Occasionally a patient would go into what was then referred to as "chloroform syncopy." This was a term used to describe patient's who stopped breathing and ceased to have a heartbeat, or who were in cardiac arrest. Physicians had no treatment for this, and so it was almost always fatal. (3, page 6)

However, in his 1891 book, "General Surgery," Dr. Franz Koenig of Germany described using "external cardiac massage" to treat such a patient at the University of Goettingen. He recommended compression of the chest over the heart at a rate the person would spontaneously breathe. He later settled on a rate of 30-40 per minute, and recommended chest compressions during "chloroform sycopy" instead of one of the other methods of resuscitation.  (3, page 6) (4, page 2968)

A search was ongoing to determine the optimal rate to perform chest compressions. The first official recommendation was to perform 60 compressions per minute. (3, page 6) (4, page 2968)

A year later, a resident at the University of Goettingen, Dr. Fredrick Maass, and a student to Dr. Koenig, published a paper in the Berlin Clinical Weekly called "Resuscitation technique following cardiac death after inhalation of chloroform." Here he described the first successful use of external cardiac massage. He observed a clinical response from the patient at a compression rate of 120 per minute.  (3, page 6) (4, page 2968)

Ever since then the rate of chest compressions has been the subject of much debate and many studies. The recommendation as of March 28, 2010, by the American Heart Association is 100 per minute. The main reason for choosing this number is seems to be effective and easy to remember.

Studies during the 1940s showed that chest compressions stimulated blood to circulate through the body, and this was essential during artificial resuscitation.  This revolutionary idea transformed artificial respiration to cardiopulmonary resuscitation, otherwise known as CPR.

In 1956, while having a conversation with Dr. Elam, Dr. Peter Safar came up with the following anagram for artificial resuscitation: (1)

• A (Airway)
• B (Breathing)

Although the anagram was later changed to:

• A (Airway)
• B (Breathing)
• C (Circulation)

Thus was the beginning of the modern A-B-C's of artificial resuscitation, now more commonly referred to as cardiopulmonary resuscitation, or CPR). It was taught to all the citizens of the world who aspired, or were required by their employers, to save lives.

The American Heart Association officially endorsed CPR in 1963, and in 1966 adapted their first guidelines for performing CPR. These guidelines are reviewed every five years and updated.

A most significant change came on October 8, 2010. Here the decision was made to change A-B-C to C-A-B. The reason for the change was noted in the "2010 Guidelines for CPR and ECC: "

There are many reasons for this change. First, this change allows rescuers to begin chest compressions right away. As we know, most victims of sudden cardiac arrest (SCA) receive no bystander CPR. One of the reasons for this may be that the A-B-C CPR sequence began with opening the airway, the most difficult and daunting task for the rescuer. This change attempts to decrease the barriers to performing CPR by allowing the rescuer to start with chest compressions. Also, the vast majority of SCAs occur in adults who suffer a witnessed arrest and ventricular fibrillation or pulseless ventricular tachycardia. In these victims, critical elements of resuscitation are chest compressions and early defibrillation, which can begin earlier if there is no delay to open the airway and provide breaths. The process of opening the airway (which may involve getting a barrier device or setting up ventilation equipment) takes time and delays the start of CPR. Using the C-A-B sequence lessens this delay. 

For those not familiar with the terms "ventricular fibrillation" or "pulseless ventricular tachycardia," these are names for life threatening cardiac arrhythmias, or ineffective heart rhythms. This change included adults, children and infants, but not newborn infants. The ABC algorithm should be used for newborns, because "newborn cardiac arrest is most often respiratory."

The American Heart Association made one other change to increase the chances that CPR would be performed by bystanders: it removed the recommendation to perform mouth to mouth breathing. Once coming upon a witnessed or non-witnessed cardiac arrest, and once confirming that the person is non-responsive, the recommendation is now to perform effective chest compressions until emergency responders are on the scene. 

Modern studies also proved the following: 

• Mouth to mouth breathing provided enough positive pressure, coupled with the natural recoil of the chest after a compression, to allow for enough ventilation to occur. 
• That circulation was far more important than breathing (It may also be underestood that chest compressions causes pressure changes within the chest to allow for ventilation to occur, thus eliminating the need for mouth to mouth breathing.) 
• That bystanders were more likely to do CPR when all they had to do was chest compressions

That's all I'm going to write about CPR. 

References: 

1. Donahue, Mary, "History of Lifesaving," DeAnza Collegge, http://faculty.deanza.edu/donahuemary/Historyoflifesaving, accessed 8/10/13
2. "2010 AHA Guidelines for CPR & ECC," American Heart Association, 2010, http://cpr.heart.org/idc/groups/heart-public/@wcm/@ecc/documents/downloadable/ucm_317319.pdf, accessed March 28, 2010
3. Figl, Marcus,  et al., "Resuscitation Great: Franz Koenig and Friedrich Maass," Resuscitation, July, 2006, 70, pages 6-9
4. Nolan, Jerry P., et al, "Editorials: Chest Compression Rate: Where Is The Sweet Spot?" Circulation, 2012, 125, pages 2968-2970)