802--1300 A.D..: The School of Salerno

Figure 1 - An early depiction of the School of Salerno

The Dark Ages of Medicine amid western civilization weren't completely dark.  There were various towns and cities in and around Europe where the old Greek and Roman traditions continued to be studied and worshiped.  One of the most significant of these towns as far as our medical history is concerned is that of Salerno in Naples.  It was here that medical schools were formed amid a flourishing medical community.

Salerno was a town in Southern Italy "that was beautifully situated in a district which as early as the times of the Roman Emperors was famous as a health resort and attracted a number of visitors to it's precincts."   (3, page 187)

Some authorities say the school was founded in 802 by Charlemagne, said historian Thomas Bradford, although no one knows for sure.  Others say if "dates from the destruction of the library of Alexandria by the Arabs." (6, page 103)

Ordericus Vitalis, a historian from the 12th century, said it was started in ancient times.  Another historian speculated it was formed by fugitives from Alexandria.  More realistically, there were probably towns like Salerno all over Europe where Greek tradition continued to flourish.  Physicians in Salerno, therefore, probably had no connection with the clergy that influenced the decline of the Roman Empire.  (3, page 187)

What is known is that a school, hospital, and university were established in in the town of Salerno, thus creating "bridge over which ancient culture took its way during the Middle Ages from East to West. They were the means of crystallizing the great thoughts of the early fathers so that we of the present times are enabled to understand them."  (6, page 106)

Salerno was on the route taken by pilgrims trying to escape the Christians who now ruled much of Europe and Asia, and therefore they took refuge in Salerno. There teachers at the School of Salerno (or Salernum) were a combination of Greek, Arabians and Jews, said Bradford. (6, page 103)

The School was referred to as The Schola Medica Solernitano.  It thrived between the 10th and 13th centuries. While exact dates of when it started and when it closed are unknown to historians, what is known is that the sick who wanted the best medical treatment went there, and medical students who wanted the best education went there.  It became known as the city of Hippocrates (Hippocratica Civitas or Hippocratica Urbs) (4)

By the mid 11th century Salerno it was a full, flourishing medical community that was significant to the evolution of the history of medicine. There were many physicians who worshiped under the traditions of Alexandrian medicine. They studied the works of Hippocrates, Galen, and the other ancient philosophers and physicians.

Here is a portrayal of a hospital at Salerno.  
"Patients eat and rest while workers share a meal and
 others engage in domestic tasks."  From the book:
De donservanda bona valetudine, opusculum
Scholae Salernitanae published 1545. It was written
 by Arnaldus de Villanova  who lived from 1240 to 1311. (5)

The school was a place where traditional Greek and Roman medicine commingled harmoniously with Jewish and Arabic medicine.  Many historians say that both men and women were involved in education there, with the main courses of education being, along with medicine, philosophy, theology and law. (4)

Students were taught by physicians from their own country, and in their own language the various subjects essential to medicine, which included "symptomatology, dietetics, treatment and materia medica," said Bradford.  "but little time was given to anatomy and physiology."  (6, page 104)

Of anatomy, however, Bradford said that:

In the twelfth century Frederick II (1194-1250) ordered a special provision with respect to the study of anatomy at this school, made in his medical code. It is said that by the emperor's direction a dissection was made every five years at Salernum. No one was allowed to practice medicine in the kingdom of Naples who had not been examined and created a master by the college of Salernum. In order to do this the student was obliged to study logic three years, and follow a course of medicine and surgery for five years. In order to become admitted to an examination at the end of the term, the student must present a certificate of his legitimate birth, and that he had attained his 25th year (according to Baas in his 21st year); after this he was examined publicly in the therapeutics of Galen, the first book of Avicenna, and the aphorisms of Hippocrates. He then took an oath to be faithful to good conduct, to submit to the rules of the profession, to give gratuitous attention to the poor and not to share in the profits of the apothecaries, to teach correctly according to the received doctrines, and to administer no poisons. All these things having been fulfilled, the candidate received a ring, a wreath of laurel, a kiss, and finally the benediction. The graduation was in public. Renouard says that after this the candidate must have his diploma confirmed by the proper officer of state, and was then obliged to continue with some experienced physician before entering into independent practice. Baas says that after the graduation he could teach and practice wherever he wished; the office of medical teacher was open also to him.
The degree conferred was that of magister, or doctor. (6, page 104-105)

During it's most prosperous times the "town of Salerno was famous for the skill of physicians." After the decree of Frederick II, it was perhaps the first school since the School of Alexandria in 300 B.C where dissections were performed and anatomy was studied.  (2, page 28)

It was also a town where successful surgeries were performed and where people traveled hundreds and thousands of miles in search of a treatment or cure for ailments.  (3, page 187)(6, page 105)

The schools, hospitals and universities of Salerno gradually declined, "until in the fourteenth century the poet Petrarch mentions the school as a memory." (6, page 103-104)

Two other schools of medicine that were significant to the transfer of medicine from the ancient world to the revival of medicine among western civilization were Monte Casino and Montpellier.  (6, page 102)

Bradford said the school of "Monte Casino was founded by the Benedictines on the site of an ancient temple of Apollo in Campania."  He said school of Monpellier "was first mentioned in 1137 when Bishop Adelbert II went there to listen to its medical teachers."  He said both the Jews and Christians lived among the city.  (6, page 102-106)

References:

1. Garrison, Fielding Hudson, "An introduction to the history of medicine," 1922, Philadelphia, W.B. Saunders Company
2. The John Hopkins Hospital bulleton," (volume XV 1904), "from the epoch of the Alexandria School (300 B.C.)"
3. Suppan, Leo, "The Medical School of Salerno and the Salernitan Writers," The National Druggist, May, 1918, 
4. "The Ancient Medical School of Salerno," associazioneermes.it, http://www.associazioneermes.it/MedicalSchoolSalerno.htm, accessed 12/5/12
5. "Arnoldus de Villanova (1240-1311) and the School of Salerno,"Vaulted Treasures, virginia.edu, http://exhibits.hsl.virginia.edu/treasures/arnaldus-de-villanova-ca-1240-1311-and-the-school-of-salerno/, accessed 12/5/12
6. Bradford, Thomas Lindsley, writer, Robert Ray Roth, editor, “Quiz questions on the history of medicine from the lectures of Thomas Lindley Bradford M.D.,” 1898, Philadelphia, Hohn Joseph McVey

1912-2001: Dr. Martin Wright x

If you were a respiratory therapist during the 1960s, 70, 80s and even the 1990s you probably heard of the name:  Wright.  You may not know a first name, or even the person, but you were familiar with his products:  the Wright Respirometer and the Wright Peak Flow Meter.

And even while his products have made their way to the dark side of shelves in the back of supply rooms, or simply faded into oblivion, his product line has been refined and re-introduced into the market by other names, or padded into other products, with their users having little knowledge of where they came from, nor who introduced them to the marketplace for us to use.  

His name is Basil Martin Wright.  He was a bio-engineer who had a flare for inventing things that measured inspiratory and expiratory flow.  The need for such devices developed during the 1950s when improved anesthetics and pain relievers allowed physicians to perform routine surgeries, particularly abdominal surgeries.  

Wright Respirometer

The need developed for a machine that would breathe for patients.  This was one of the main reasons for the invention of the positive pressure ventilators as you can see here.  On these old ventilators there needed to be some mechanism for measuring the volumes of inspiration and expiration, or tidal volumes, of patients.  This is where the Wright Spirometer comes into play.  

Although this is not how Wright came to invent his devices.  In 1949 he joined the Medical Research Council's for pneumoconiosis, a lung disease caused by inhaling mineral dust.  He realized the unit "lacked the mechanisms of monitoring and studying lung capacity of patients.  So it was for this council that, in 1959, he invented the Wright Peak Flow Meter, the first device for measuring peak expiratory flow (PEF).  This made studies of lung function possible and lead to a greater understanding of lung disease." (1, page 11)

Case for Wrights Spirometer

Such devices also allow the physician to assess the progress of the patient over time.  As the patient gets better, the PEF will get higher, and if the patient gets sicker the PEF may become lower.  The first peak flow meters were large and cumbersome, but in 1974 Wright invented a simpler, cheaper, portable device that could easily be used by the patient at home as a tool to monitor the progress of his disease.  I wrote about the history of the peak flow meter in this post  (1, page 11)

Today peak flow meters are made by a variety of manufacturers, are for single patient use, and are easy to use.  Most asthma experts recommend all asthmatics have one at home, and they blow into it every day at the same time, and to write down their highest number.  This number is referred to as the patient's personal best.  Then the patient makes some simple calculations, and as the PEF starts to drop to a certain point, a plan can be devises what to do and whether the doctor should be called, or whether to simply get to the emergency room, or call 911.  I wrote about the peak flow meter in this post.  

Basil Martin Wright 

In 1957 he started working for the National Institute for Medical Research in London, focusing on creating a similar device to allow anesthesiologists to monitor the tital volumes of patients under the power of anesthetics and pain relievers.  This was important because such medicine has the power to knock out the respiratory drive, and measuring tidal volumes is a great way to measure loss of drive to breath.  

The devices were used to help the anesthesiologist know if prolonged assistance with breathing was indicated, or if the patient required assistance with breathing by use of a mechanical ventilator.  The device was ultimately used by respiratory therapists to monitor the tidal volumes on patients with neuromuscular disorders, or to monitor the progress or regression of patients on mechanical ventilation.  We used to use the Wrights Respirometer daily as part of our weaning screen.  Today the measurements are made by the microprocessor on the ventilator.  

References:

1. World Almanac Library, "Cutting Edge Medicine:  Machines in Medicine," 2007, Arcturus Publishing Limited, page 11

1867: Is it the measles, or something else?

Dr. Abbots is pulled out of A Tale of Two Cities by a pounding on his front door.  Before he has a chance to rise from his chair, the door opens.  It's a boy of around twelve who looks ruffled.

The boy says, gasping, barely able to speak, ""Dr. Abbotts, sir!"

"Yes," the doctor said, as if to give the boy permission. He swiped sweat of his own brow.

The boy continued: "There are three boys at the school, and Mrs. Smith thinks they might have the measles and there might be an epidemic.  Please come quick!" 

Without hesitation Dr. Abbotts hurriedly opened a cabinet above his chair, and pulled from it a couple bottles.  He then knelt beside his chair and opened his brown leather medical bag, set the medicine inside, and zipped it shut.  He grabbed the handle, and said, "Let's go!"

The boy rushes from the house, followed closely by the doctor.  The screen door slams shut as the doctor lets go of it.  They both climb into the doctor's buggy, and as they did so an audible sound could be heard from the two stallions.  After a short, bumpy, and dusty ride the two arrive at the little red school house.

You rush into the school where there's complete silence; all the boys and girls, mouths agape, eagerly stare at the doctor as he enters the building.  In the front of the room he sees a teacher holding a rag over a boy's forhead.  The boy sitting on the teachers chair behind her dest.  Two other boys are sitting on the floor just under a chalk board covered with math problems. 

Mrs. Smith says, "Do you think it's the measles?  He says he's had runny eyes and nose for two days now. 

"The weather's been hot," he says on his way to the patient, "So I suppose it could be.  But let me see." He crouches before the boy, and feels his forhead."

"So, what's ailing you?" he says to the boy.

The boy sneezes, and wipes snot on his sleeve.  "That!" he says.  "I've been sneezing, my dose is sduffy, and my eyes..." He sneezed again, and rubbed his eyes.  Mrs. Smith removed the rag and stepped back.  "So what do you think?

"Does he attend to recess?"  Dr. Abbotts asks.

"Yes, he plays on the playground with the other kids," Mrs. Smith says.

"When was the grass cut?"

"Three days ago." 

The doctor looks at the boy.  "Have you ever felt this way before?"

"Yes, sir!" The boy answers.

"When?"

"Last year."

"Was it May, or June?"

"Yes, sir!"

There is a brief pause, then Dr. Abbotts smiles, and says, "I don't think it's the measles, Mrs. Smith, so at that you can ease your mind."

Mrs. Smith sighs. 

"I think what he has is hay fever."

"Hay fever?" Mrs. Smith says.  "I never heard of it.  He gets a fever from hay?"

"Well, sort of.  It may not be a fitting name, but that's what they call it."

Dr. Abbotts stands up, and continues: "As you can see there's haymaking in the immediate vicinity.  As I arrived I observed there was grass in the field next to the playground, and it looks recently cut.  Where the lad plays I can smell newly-made hay, and I can smell it in here too.  That's his problem, and I suppose the problem of these two boys as well."

"Whew, well that's a relief," says Mrs. Smith.  "So what can we do for these boys."

"I'll take them to my office.  I have a couple options for them."

Dr. Smith takes the boys to his office where he has a remedy, and returns the boys to their homes.  He treats the boys by correspondence, and all three recover in ten days. 

Coincidentally, it was only a few days earlier that Dr. Abbots read a book about the newly defined affection called summer cararrh or hay fever.

Reference:

1. Smith, William Abbotts, "On Hay-Fever, Hay-Asthma, or Summer Catarrh," 1867, London, Henry Renshaw, pages 30-31. This story is based on this here reference.

History of Pulse Oximetry and the 5th vital sign

Back in 1991 I visited the emergency room because my asthma was acting up.  It was my first visit to the ER since I was discharged from my six months stay at the asthma hospital (NJH/NAC) in 1985.  An RT came into my room to give me a breathing treatment and he slipped this thing over my finger.  That was my first exposure to pulse oximetry -- the fifth vital sign.

I had been to emergency rooms many, many times for asthma in my life, and never had I seen such an object.  A temperature, blood pressure, and heart rate check were common, but to slip something that glows red, and causes a red number to appear on this little box the RT held, or that sat on a bedside table, was something new.

"What is that?" I asked back then.  

Pulse Oximeter Finger Probe

The RT attempted an explanation that zoomed over my head.  "It's called a pulse oximeter.  It tells me how well you're oxygenating and gives me your heart rate."  

I wasn't satisfied with that answer.  I wanted to know more.  What was it?  How did it work?  What significance was it?  What did the number 98 mean anyway?  I asked these questions and, once again, the answer wafted over me like a cool breeze.

In the summer of 1993 I was a journalist for a small weekly newspaper.  The local fire department received funding to get a new piece of equipment that was supposed to help them help sick people.  The objects were quite bulky, pretty heavy, and covered by a large, black case.  

A cord loomed from both, and the EMT I was interviewing slipped the probe over my finger.  "This is what we call a pulse oximeter," he said.  He attempted an explanation, yet again the answer flew over my head.  I ended up taking a picture of the EMT holding the new pulse oximeters.  On the caption under I wrote:  "EMT Josh Paramedic is holding two new pulse oximeters purchased with money from a Grant by..."

My next exposure to the 5th vital sign came as an RT student.  Now for the first time I finally understood what it was, and the significance of it.

Modern Pulse Oximeter

What is pulse oximetry?

Simply put, pulse oximetry is basically the transmitting of two lights through your finger (or ear lobe or toe), through your artery, and then the light is collected by a sensor on the other side of your finger.  The red light you can see, and the infared light you cannot see.

By calculating the amount of infrared light returning to the sensor, the pulse oximeter will tell you what percentage of hemoglobin is carrying oxygen.  Since it's measurement is made by the pulse of arterial blood, it can also give you a heart rate.

A normal pulse oximeter reading is 98%, however, anything greater than 90% is deemed acceptable.  In this way, supplemental oxygen can be administered and adjusted accordingly to maintain an adequate hemoglobin saturation.  The reading is measured as SpO2 (S = saturation, p = pulse oximetry, O2 = oxygen).

The SpO2 is a noninvasive measurement, and is an estimate of oxygen saturated hemoglobin.  To get an actual saturation, a more invasive blood gas measurement is required.  The saturation obtained from a blood gas is measured as SaO2 (S = saturation, a = arterial, O2 = oxygen).

By using the oxyhemoglobin dissociation curve, we can use the SpO2 to estimate the actual amount of oxygen in the lungs by estimating the PO2 (P = Partial Pressure, O2 = oxygen).  To do this we use the 4-5-6-7-8-9 rule as follows:sdf:

4-5-6-7-8-9 Rule
40 PO2	70% SpO2
50 PO2	80% SpO2
60 PO2	90% Spo2

In this way you can save the patient from an invasive blood draw and estimate how well the patient is oxygenating.  According to this rule, you would want to maintain an SpO2 of 90% (or 92% to be on the safe side) or better. Therefore, the lowest amount of oxygen should be utilized to obtain the desired oxygenation saturation.  

How did the pulse oximeter come to be?  

When I was a kid and was having an asthma attack, the respiratory therapist would place a nasal cannula over my face, and I'd promptly proceed to peel it off.  He'd get mad at me saying, "You really need to keep this on.  We need you to get oxygen."

Yet was my oxygen level really low?  The only way to tell would be to either do an invasive arterial blood gas, something that was rarely done on a kid.  I don't recall an ABG being drawn on me until I was at least in my upper teens.

Other than an ABG, the only way to know if a patient was oxygenating well was to use objective measurements such as skin color.  Usually if a person isn't oxygenating well blood will be shunted from fingertips and lips, and these areas will appear grayish or blue.  This is referred to as acrocyanosis, and is not life threatening.  Usually a low dose of oxygen -- say 2lpm -- will be all that's needed to resolve the problem.

If the core of the the body is blue or gray in color, this is referred to as central cyanosis.  Central cyanosis is critical, meaning oxygen isn't getting into that person's body at all, and oxygenated blood -- what little there is -- is shunted directly to vital organs such as the heart, kidneys and lungs.  In these situations, usually large amounts of oxygen are needed to remedy the problem, and perhaps even some form of positive pressure breathing such as from an Ambu-Bag, BiPAP or ventilator.

Obviously if you see cyanosis you know supplemental oxygen is needed.  Still, how much oxygen do you give?  When do you taper it off?  And what if the patient isn't oxygenating well yet doesn't show any cyanosis?  What do you do then?  Chances are, in the days prior to pulse oximetry, you winged it.  Some patients got too much oxygen, and some didn't get enough.  Outside of doing an invasive ABG, you really didn't have any means of monitoring and adjusting oxygen.

This was pretty much how it was even up to the early 2000s at some institutions.  Yet then came along the 5th vital sign.  This vital sign -- pulse oximetry -- made the job of respiratory therapists, nurses, and doctors "much easier," notes Gennie Ridlen in her rtmagazine.com article Pulse Oximetry:  A Historical Perspective.

She notes the history of the pulse oximetry can be traced back to 1862: (1)

• In 1862 Hoppe-Seyler disovered that oxygen was transported by hemoglobin, and he referred to the oxygen-hemoglobin compound as oxyhemoglobin
• In 1864 Stokes proved that oxygen was transported in the blood by hemoglobin
• In 1862 von Vierodt invented the first pulse oximeter.  He measured oxygen consumption using transmitted light by wrapping a rubber band around his wrist to cut off circulation and shining a light on his hand, he saw the two bands of oxyhemoglobin disappeared and a band of deoxyhemoglobin appeared.  Using reflected light from a spectrometer, he measured the oxygen consumption of the living tissues by noting the time that elapsed as oxyhemoblogin changed into deoxyhemoglobin."

Reflection pulse ox (2)

John W. Severinghause, in his 2007 article in Anesthesia and Analgesia titled "Takuo Aoyagi: Discovery of Pulse Oximetry," (5) and the"Online Museum Catalog" (2) provide us with the following history:

• 1931:  Ludwig Nicolai repeated the study of  von Vierodt, and created a device that "measured red light transmission through a hand."  (5)  The device used spectrophotometers (instraments that measure different wavelengths and intensities of light). (2)
• 1934:  Reports of using pulse oximetry on animals (2)
• 1939:  WWII sparks interest in need to monitor oxygen levels of pilots at high altitudes.  (2)Germans invent an 'ear oxygen meter' that used red and infared light."  The man credited with inventing the ear oximeter that used an ear probe is Karl Matthes.  (5) 
• 1940-42:  A British researcher by the name of Glen Millikan (1906-1947) used "two wavelengths of light to produce a practical, lightweight aviation ear oxygen meter for which he coined the word 'oxymeter.'" (2)(5)
• 1949: While working for the Mayo Clinic, Earl Wood "modified the Milliken ear piece." (5)
• 1950s:  The system was refined and "manufactured by the Waters Company. This system was mainly used in physiology, aviation, and experimental studies" (2)
• In the 1970s Hewlet Packard marketed a 35 pound pulse oximeter that costs over $10,000 and had a "bulky, clumsy earpiece. However, it did allow for continuous noninvasive monitoring of arterial oxygenation." (2)

So between 1862 and 1977 technology that would ultimately become the pulse oximeter was improved upon to the point that the first pulse oximeter was marketed in the U.S. in 1977.  The oximeter used a finger probe with fibre optic cables that were very sensitive to motion. (1)

By the late 1970s new probes were invented to solve the problem with motion, and a heart rate tracker was added and the device was precalibrated to make it more accurate. (1)

Who invented the first effective pulse oximeter?

The first pulse oximeter was the OLV-5100 (left) that was invented by
Japanese bioengineer Takuo Aoyagi in 1975.  You can see here that the
ear probe used was large and bulky, and probably not very comfortable.

During the 1930s and 1940s physiologists invented the technology to construct ear oximeters with red and infared light to measure oxygen saturation in the blood.  The problem with these early devices is they required bulky fiber optic cables and they needed to be calibrated. (5)

This was probably the main reason such products were not marketable.  The task of solving this problem was given to a Japanese Physiological bioengineer by the name of Takuo Aoyagi.  He was ultimately the inventor of the marketable pulse oximeter.  According to Severinghaus, while studying the available knowledge he became impressed with the work of Wood, and he set out to improve upon it.

In another article, John W. Severinghaus and Yoshiyuki Honda, published in the April, 1987, issue of the Journal of Clinical Monitoring and titled "History of blood gas analysis. VII. Pulse Oximetry," explain that Aoyagi's work resulted in the first marketable pulse oximeter.  (3, page 135)

The article notes that Aoyagi was hired in 1971 to work for the Research Division of Nihon Kohden Corporation.  His work on a variety of equipment has impacted the medical profession in a variety of areas, including fetal heart monitoring during childbirth, pulmonary circulation, and cardiac output.  (3, page 135-136)

The article further explains that he worked with the idea of measuring "pulsatile changes in light transmission through living tissue to computer the arterial saturation.  He realized that these changes of light transmission at all wavelengths would solely be due to pulsatile variations of the intervening arterial blood volume.  Thus, the unpredictable absorption of light by tissue, bone, skin, and pigment would be eliminated from analysis  It was this key idea that permitted the development of instrumentation that required no calibration after its initial factory setting, as all human blood has essentially identical optical characteristics in the red and infared bands used in oximetry." (3, page 136)

Severinghaus and Honda said that Aoyagi filed for a patent in 1974, although so did another man by the name of Massaichiro Monishi who worked for Minolta Camera Company.  Our authors note that "How this competing application arose and whether Aoagi's idea was discovered and copied has never been established.  Konishi's patent application was rejected by the Japanese Patent Office on February 9, 1982.  However, Minolta applied for and obtained patent protection in the United States." (3, page 136-7)

They explain that the first pulse oximeter to be used clinically was a prototype made by Aoyagi.  It was a two wavelength ear oximeter that used the pulse to measure how much oxygen was absorbed by hemoglobin in the blood.  His product was referred to as the OLV-5100, and was commercially available in 1975. (3, page 137)  The patent was approved in 1979 (5, page 52) It was first used clinically in 1980 by Japanese anesthesiologist Yoshiya to monitor a patient's saturation during surgery.  (3, page 135, 137)(1)

Despite these facts, the invention of the first marketable pulse oximeter is often attributed to Konishi and Minolta.  Perhaps one reason for this, said Ridlen, is that "Nihon Kohden did not continue to develop or market this instrument and made no effort to patent it abroad," said Severinghaus and Honda.  (3, page 137)  Perhaps the reason for this product failure was that this "device used heavy, delicate, fiber-optic cables, which ultimately hampered its success." (1)

On the other hand (no pun intended), according to Severinghaus and Honda, Minolta did continue to seek patents and to market their product abroad.  Their initial product was released in 1977 as the Oximet MET-1471.  It had a "fingertip probe and fiberoptic cables... Nakajima and nine associates then tested and used this Minoruta fingertip pulse oximeter and described it in 1979." (3, page 137) Severinghaus explains that the Minolta company used the fingertip probe because it "took advantage of the greater pulse amplitude."

Regardless, while Konishi and Minoruta often get the credit, "All pulse oximeters today are based on Dr. Aoyagi's original principle of pulse oximetry," according to the Nihonkohden.com. (4)

What did initial studies show?

Minolta introduced the Oximet MET-1471, and it was used in clinical studies.  Severinghaus reports that the pulse oximeter "was reported to be linear and accurate to within 5% by Suzukawa et al. in 1978 and Yoshiya in 1980.

Yet other studies questioned the accuracy of pulse oximetry when the saturation was below 70%, as noted by Severinhaus:

When studied at Stanford in 1980 by Sarnquist et al. a Minolta model 101 [identical to Oximet MET-1471] seriously underestimated the severity of hypoxia: At 50% actual Sao2 it read about 70%. Yamanishi wrote me (personal communication, 2006): “The Sarnquist data was the very important trigger for us to improve the accuracy of our pulse oximeter.” In 1984, Y. Shimada (then anesthetist of Osaka University, nowprofessor of Nagoya University) with Minolta’s K. Hamaguri, I. Yoshiya, and N. Oka published data using a Minolta Oximet MET-1471 that agreed with Sarnquist’s evidence of under-reporting the degree of desaturation. (5, page 53)

This knowledge was used to refine the technology, yet it was also later acknowledged that pulse oximetry should not be considered as accurate when the reading is less than 70%.  Even to this day when I'm using a pulse oximeter, if the reading is less than 70% I'm skeptical of the results.

Yet it really doesn't matter, because if it's that low you know you either have a bad reading, or the oxygenation is low.  The best remedy when you question the results of the pulse oximeter is to assess your patient.  If the clinical picture shows the patient is not oxygenating, regardless of the reading on the pulse oximeter, you should treat the patient appropriately.

In 2010 Ben J. Wilson et al. studied the results of pulse oximetry on patients diagnosed with sepsis and septic shock.  The study concluded that pulse oximetry "overestimated measured SaO₂ by a mean of 2.75%."  These researchers recommend that "when SaO₂ needs to be determined with a high degree of accuracy in such patients arterial blood gases are recommended. (6)

Most studies that I've seen suggest that pulse oximetry is usually accurate withing +/- 2%.  However, when the reading is suspected to be inaccurate, or when the the spO2 does not match the clinical picture, an arterial blood gas should be drawn.  

When did pulse oximetry catch on?

As with any new discovery in medicine, it took a while for this new tool to catch on.  Severinghaus and Honda explain that "few foresaw its value in anesthesiology, intensive care, and other emergent situations, probably because conventional oximetry had never been convenient enough for these uses.  The Hewlett-Packard ear oximeter had been used almost entirely in pulmonary function laboratories and other physiologic environments.  Indeed, the initial work on pulse oximetry in the United States by several firms (Minolta, Corning, biox) considered these types of laboratories to be the probable market."

It took ten years for the pulse oximeter to make any real impact in the medical industry.  Interest finally started growing in the early 1980s as the device was determined useful when a patient was sedated to monitor oxygen saturation, and by 1986 pulse oximetry was recommended by the American Society of Anesthesiologists anytime a patient was sedated.  Pulse oximetry, therefore, became standard practice on sedated patient, operating rooms, critical care units and emergency rooms in 1986.  (1)

It was perhaps at this point that it became the 5th vital sign, alongside heart rate, respiratory rate, temperature, and blood pressure.  In 1994 the American Association for Respiratory Care released the first guidelines for the use of this 5th vital sign. (1)

The devices continued to be improved upon, and by 1995 small finger probes were introduced to the market.  (1) They were small enough to fit into your pocket, an d effective enough to produce an accurate oxygen saturation.  This made it easy to monitor saturation at any point in the clinical picture, including at home by patients when the prices dropped.  These products can now be purchased at Walmart for under a $100, and often times patients can be found with their own pulse oximeters.

By 1995 you had a choice between bulky bedside monitors and finger probes that could fit into your pocket. Some modern pulse oximeters are so advanced they provide accurate readings even on patients with poor circulation, and even on patients who are wriggly and squirmy, such as kids. In 2013 a new Oxitone oximetry device the utilizes no ear or finger probes, and can be wrapped around the wrist like a watch, was introduced to the market.  This new product was inspired by Steve Jobs.  This new oximeter even allows for the pulse rate and heart rate to be observed from an iPhone.

So depending on how much money you want to dole out, there are quite a few options available.  Even many patients are purchasing small pocket sized oximeters to use at home, so they know when to turn up or down their home oxygen flowmeters, and when to call their physician or 911.

Is pulse oximetry worth the investment?

It's very difficult to determine if a person is hypoxic simply by using the naked eye. Most studies indicate even the most well educated person has a difficult time recognizing hypoxemia until the saturation is below 80%., according to Amal Jibran in his 1999 article in Critical Care titled "Pulse Oximetry."(7)  For this reason, the pulse oximeter is a viable tool to not only determine that supplemental oxygen is necessary, but also how much oxygen to give. (7, page 11)

Of interest, another study showed that of those patients who desaturated to less than 90% for five minutes within their first 24 hours admitted to the hospital, had a threefold increased risk of mortality as compared to patients who did not desaturate.  So it is clearly evident that pulse oximetry is worth the investment. (7, page 11)

Studies have also confirmed that use of oximetry at the various points of patient care -- emergency room, operating room, critical care room -- greatly diminish mortality and morbidity caused by poor oxygenation. In fact, according to Jubran, with the proliferation of pulse oximeters in different locations of the hospital throughout the 1980s, several investigators demonstrated that episodic hypoxemia is much
more common than previously suspected with an incidence ranging from 20–82%. So, again, pulse oximetry is clearly worth the investment. (7, page 11)

Now it's obvious that even while pulse oximetry shows the risk of pulse oximetry, it does not show the cause.  However, pulse oximetry does provide medical caregivers, and sometimes the patients themselves, with the comfort of knowing the oxygenation of a patient, thus providing them with the ability to do something about it.  Or, at the very least, to investigate the possible cause.

Overall, pulse oximetry, and the use of the 5th vital sign, has been very useful in monitoring oxygenation in the patient population both in the hospital and the home setting.  Each time we're using one of these devices we ought to thank all the wonderful people who have invested time and money to the various projects that have brought us the 5th vital sign.


Further Reading and references:

1. Ridlen, Gennieer, "Pulse Oximetry:  A Historical Perspective," rtmagazine.com article, August/ September, 1998, issue of RT: For Decision Makers in Respiratory Therapy.
2. "Reflection Oximeter," Virtual Museum Catalog,  ttp://medicine.nus.edu.sg/anaesthesia/virtual_museum/reflection_oximeter.htm, accessed 5/11/13
3. Severinghaus, John W. Yoshiuki Honda, "History of blood gas analysis," Journal of Clilnical Monitoring, vol 3, no. 2, April, 1987, page 135-138
4. "History: 1970," nihonkohden.com, http://www.nihonkohden.com/company/history/1970s.html, accessed 5/11/13
5. Severinghaus, John W., "TakuoAoagi: Discovery of Pulse Oximetry," Anesthesia and Analgesia, vol. 105, issue 106, December 6, 2007, pages 51-54
6. Wilson, Ben J, et al., "The Accuracy of Pulse Oximetry in emergency department patients with severe sepsis and septic shock: a retroactive cohort study," BMC Emergency Medicine, 2010, biomedcentral.com, http://www.biomedcentral.com/content/pdf/1471-227X-10-9.pdf
7. Jubran, Amal, "Pulse Oximetry," Critical Care, 1999, vol. 3, no. 2, pages 11-17

1860-1870: Dr. Beard teaches about hay fever

George Miller Beard was president of the United States Hay Fever Association. He wrote a book about hay fever called "Observations on the Nature, Cause, and Treatment of Hay-Asthma" and he dedicated it to all the members of the association. He wanted the members to have an understanding of the condition they suffered from.

He said that in 1867 Dr. Pirrie postulated that there may be other symptoms of Hay Fever besides the usually runny nose, stuffy nose, itchy eyes and throat, and sneezing.  The other symptoms are (1, page 18):

• Languor (lack of energy)
• Malaise
• Insomnia
• Irritability

Pirrie, as with most of the other physicians who studied hay fever, believed the affection to be hereditary, and that it was caused by a nervous temperament.  He recommended the following as remedies (5, page 18):

• Quinine tonic
• Arsenic tonic
• Iron tonic
• Strychnine tonic
• Sedatives (as a palliative)
• Antispasmodics (belladonna, cannabis indica, camphor, stramonium, and the inhalation of chloroform)
• A resort to the seaside
• Carefulness in diet
• Avoidance of exhausting influences
• Keeping clear of hay, grass, flowering plants, and vegetation generally.

Beard said that Pirrie...

...admitted that the tonic treatment had often failed; but explained the failures in part by the fact that the patients had delayed until the beginning of an attack, and he distinctly advised preventive treatment in the intervals of the attacks."

Beard also said that in 1869, Dr. C. Binz of Bonn, Germany, published an essay on quinine, in Virchow's Archives, where he described a letter sent to him by Helmholz (who was not a physician)...:

...recommending the local application of sulphate of quinine in hay-fever.  Helmholtz stated that he had suffered since 1847 from what the English called "hay-fever;" that the disease came on about the 20th of May, and lasted till the end of June, and that the symptoms were aggravated by exposure to heat and sunshine. Helmholtz further stated that he had found in the nasal secretion at that time "certain vibrio-like bodies" (infusoria), very delicate and small, and which could only be seen with a very good Hartneck's microscope; and on becoming acquainted with the experiments of Binz, in which the poisonous action of quinine on infusoria was demonstrated, he resolved to test the treatment of his hay-fever by this method. Accordingly, in 1867, he injected a solution of quinine into his nostrils, lying on his back and moving his head to and fro, so that all parts might be affected. There was immediate relief; and this treatment repeated three times daily served to keep the disease at bay, and the vibrios disappeared from the secretion. After a few days of this treatment the symptoms entirely ceased, but if the applications were omitted the disease returned. (2, page 19)

In 1868 Helmholtz began this treatment early, with the very first appearance of the disease, and succeeded in keeping it off entirely. These vibrios were figured and described in this letter; and it was remarked that they did not come out of the nose with the drops of secretion, but only after sneezing, and from this Helmholtz argued that they were lodged in the deep recesses of the nasal passages. 
 (2, page 19-20)

This theory of Helmholtz has obtained in this country a wide popularity, in the profession and out of the profession. At the time I took up the investigation it was, so far as I could learn, the dominant theory among those medical men whose attention had been called to it. (2, page 20)

By the 1870s it the most sought after treatment for hay fever was to seek refuge in an area where people did not suffer from hay fever.  This started the era of the Hay Fever Resort or the Hay Fever Vacation.

References:

1. Beard, George, "Hay-Fever; or Summer Catarrh: It's Nature And Treatment," 1876, New York, Harper & Brothers
2. Beard, ibid, page 19.  The reference used by Beard was C. Binz, of Bonn, Germany, published in Virchow's Archives (Part I, February) an essay on quinine, under the title "Pharmakologische Studien iiber Chinin"

Further Reading:

1. Mittman, Gregg, "Breathing Space," 2007, New Haven and London, Yale University Press
2. Taylor, C.F., editor, "The Medical World," volume 16, 1898, Philadelphia, 
3. Fry, John, "The Natural History of Hay Fever," J. Coll. Gen. Practi1, 1963, 6, page 260
4. Ehrlich, Paul M., Elizabeth Shimer Bowers, "Living with Allergies," 2008
5. Beard, George, "Hay-Fever; or Summer Catarrh: It's Nature And Treatment," 1876, New York, Harper & Brothers
6. Beard, ibid, pages 12 and 13, referenced by Beard from Dr. Mr. W. Gordon's paper "Observations on the Nature, Cause, and Treatment of Hay-Asthma," London Medical Gazette, 1829, vol. iv, page p. 266
7. Beard, ibid, pages 13 and 14, referenced from "On the use of Nux Vomica as a Remedy in Hay Fever, Lancet, 1850, vol. 1, page 692

1862: Phoebus writes symptoms of 'summer catarrh'

Since Dr. John Bostock defined hay-fever for the medical community in 1819 and 1828, there was little mention of the ailment until Dr. Philipp Phoebus published a book titled "On the Typical Catarrh of Early Summer, or the so called Hay-fever or Hay-asthma" in 1862.  (1)

Dr. Phoebus was professor of medicine at the University Giessen in Germany. He describes six groups of symptoms, of which may vary from one case to another.

1.  Nostrils.  Severe catarrh (inflammation).  This results in "severe sneezing, which is very and frequent and recurs in paroxysms of ten, twenty, or more sneezing in rapid succession, coming on at short intervals; so that the sufferer may sneeze as often as several hundred times in the course of a day."

2.  Eyes.  Catarrh and increased secretions. The eye feels full, itchy and irritating.  The eye looks red and swollen.  Eyesight is weakened, and there is an intolerance to light. Both eyes are usually affected simultaneously.

3.  Throat. Pharynx is red, and swollen; there is intense itching of the fauces (back of the mouth behind the tongue) and posterior part of the soft palate; and this unpleasant sensation is aggravated by the ineffectual efforts which the patient makes to relieve it by moving the tongue about the mouth.  Sometimes there is difficulty swallowing. 

4.  Head.  Headache.  "Some more slight, but more frequently severe, and situated either at the forehead, which is hot and burning, at he occiput (back part), or over the whole of the head. The pain is often brought on and increased by the paroxysms of sneezing, and, assuming a neuralgic character, may extend along the course of the facial nerve, or into the external auditory passage. The patient complains of a constant feeling of irritation and itching about the forehead, the nose, the chin, and the ears."

5.  Lungs.  Mucus membrane of larynx to bronchi. Bronchial catarrh. Asthma. Dyspnea (shortness of breath). Cough may be insignificant or severe and loud. Expectoration may occur with this cough.  Irritation of larynx and trachea, and "feeling of weight and pressure within the chest; the patient's voice becomes muffled and coarse... The difficulty of breathing is occasionally very distressing, and wheezing, sibilant sounds may then be heard throughout the greater parts of the lungs. The attacks of dyspnea are more strongly marked towards evening, and continue through the whole of the night. It is in this class of cases that the patient's sufferings are the most severe.Generally, after having been asleep for one or two hours, or a longer period, the patient wakes up suddenly, gasping and struggling for breath, as if every moment would be his last; his eyes are protruded, his lips and face become livid, and ho eagerly throws open the doors and windows of his room in his ineffectual efforts to get more air, until at last he sinks down completely exhausted. When he falls asleep, his slumber is short and restless, and he is again aroused, after a brief interval of repose, by the same painful constriction across the chest, and difficulty of breathing. When the asthmatic symptoms are well-marked the dyspnoeal paroxysms come on earlier at night, or in the evening, and continue until the next morning."  These are thus called asthma attacks, or hay asthma, or periodic asthma.

6.  Nervous disturbance.  This is coupled with catarrhal fever. Shivering and cold perspirations with sneezing and coughing. "The patient is uncomfortable, restless, , and unfit to attend to his ordinary avocation, and complains of weariness, defective memory, inability to fix his attention upon what he is doing, and heightened susceptibility to external impressions. There is a sense of general irritability, and the least noise, draughts of cold air, and various trifling inconveniences, which at other times would pass unheeded, disturb and distress the patient very much; and his sufferings are too frequently increased by the want of sympathy and apparent disbelief of the severity of his ailment, shown by persons about him, who, enjoying perfect immunity themselves, cannot form any adequate idea of the extent of the patient's sufferings."

These symptoms generally "make their appearance suddenly, and remain for some weeks, or even, in severe cases, months." 

What brings on the attack?

• Flowering of the grass
• In the fields where a late crop of hay is grown
• Emanations given out by decomposing leaves and other vegetable matter
• Operation in low-lying localities, near stagnant water

Just think for a moment of suffering from the above mentioned symptoms in 1862 when there was absolutely nothing you could do for it.  I mean, there were remedies, but nothing even remotely as effective as what we have at our disposal today.  In the worse cases, modern medicines only take the edge off.

I can honestly say there have been many times I have suffered from the above.  I have experienced the burning, itchy eyes that I can't help but to rub, and this rubbing merely exacerbates the problem.  I remember the itchy throat, and scratching it by rubbing my upper palate to the lower, and sometimes by making a grunting noise that my family and friends teased me about. And this just made the itching worse. 

When I was a kid in the 1970s there was a warning on the package of antihistamines that said don't use if you have asthma.  My parents and doctors took this seriously, and so I often had to suffer much as a hay-fever sufferer would have in 1862.  There were many agonizing days and nights. 

As a sufferer myself, I can't help but to have empathy for these sufferers.  I can't help but to see them, and feel their agony.

 "Unless the length of the attack is abridged by medical means, the patient often remains for many weeks, at least, in deplorable condition, and is incapacitated from following his ordinary occupation."

References:

1. Smith, William Abbotts, "On Hay-Fever, Hay-Asthma, or Summer Catarrh," 1867, London, Henry Renshaw, pages 17-24.  The quotations are from Smith's descriptions of Phoebus's ideas. 

1873: Blackley studies hay fever

Dr. John Bostock defined hay-fever for the medical industry in 1819, and by 1840 physicians in England and the United States were diagnosing patients with the disease.  The quest was on to better understand the condition, and the person up to the task was Dr. Charles Harrison Blackley, a surgeon from Manchester, England. 

He was born in 1820, and worked as a printer and engraver until he was 35.  He studied at Royal Manchester School of Medicine, and he qualified as a doctor in 1838.  Yet he did not receive his M.D. until 1854 in Brussels.

References:

1. "Charles Harrison Blackley, 1820-1900," The University of Manchester: The John Ryland University Library: Manchester Medical Collection, http://archives.li.man.ac.uk/ead/search?operation=full&rsid=dc.title%20any%2Frelevant%2Fproxinfo%20%22William%20Charles%20Henry%22&firstrec=1621&numreq=20&highlight=1&hitposition=1638, accessed 9/13/14
2. Blackley, Charles Harrison, "

and by the time he was 28, in 1848, he was diagnosed with the newly defined disease called hay-fever.  He wanted to learn as much as he could about his disease, and he "carefully read over most of the scanty bits of literature of the disease then existing," Blackley explained in his 1873 book "Hay-fever: its causes, treatment, and effective prevention." (2, page 8)

His quest frustrated him, as he wasn't able to generate any knowledge about the "nature of the cause," he writes.  "I was inclined to regard heat as the principle exciting cause, but my experiences did not quite coincide with the opinions of those who had written on the disorder, and this experience had, unfortunately, compelled me to come to the conclusion that until something more was known than I had learned from the writings of others, or from my own previous observations, there was no chance of escape from the annual torment. I had thus a personal interest in getting a more thorough knowledge than I then possessed of all the phenomena of hay-fever." (2, page 8)

So he decided to do experiments.  At first he tried to find subjects to experiment on, yet only a few volunteered.  So this basically forced him to resort to experimenting on himself, which he started doing in the year 1859.  Surely there were some who criticised him for this, although his experiments were so well founded that they were readily accepted by the medical community.  (2, page x)

John Fry, in his 1963 article "The Natural History of Hay Fever," which appeared in the Journal of the College of General practice, wrote that hay fever was usually diagnosed "in patients who presented with characteristic bouts of sneezing with dry nose and running eyes during the 'hay fever season' between the end of May and the end of July." (1, page 260)

Fry explains that by the mid 19th century many studies were performed on the reproduction of plants, and it was determined that plants reproduce sexually, and pollen was discovered.  It was learned that some plants were pollinated by bees and others by wind. (1)

Also at this time there were many new ideas to explain diseases.  One of the greatest scientists of the 19th century was Louis Pasteur (1822-1895).  He performed many studies and became among the first physicians to believe -- and prove -- that diseases were caused by tiny microbes. (1)

Pasteur proved that by injecting small amounts of proteins from harmful microbes into a person you could protect people from certain diseases, and even cure some diseases (such as rabies).  This type of therapy was referred to as prophylaxis, which means protection from. (1)

So other doctors soon picked up on Pasteur's ideas. Fry explains that Dr. Blackley believed his own hay-fever was the result of exposure to grass pollen not hay.  So he decided to perform tests on himself to prove his theory.  In 1873 he published his work in a book called "Experimental Researches on the Cause and Nature on Catarrhus Aesivus (Hay-Fever, or Hay-Asthma)." (1)(2)

Blackley made two significant observations about hay fever:

1. It was caused by grass pollen, not hay
2. It was a disease of the educated, upper class and wealthy, including physicians and clergy

Terry Allen Hicks, in his book "Allergies," (2006, China, page 40) describes how Blackely saved some grass pollen in a jar until winter.  When all the grass was dead he opened the jar, inhaled, and almost immediately started sneezing.  He thus proved that allergy symptoms were not caused by hay but pollen.  Yet despite this evidence, the term 'hay fever' stuck. (3)

Blackley performed another test on himself where he "inserted pollen into a small cut on his skin and a rash developed within 20 minutes.  He later determined that this test proved he was allergic to pollen, and his experiment became the first ever allergy skin test.  Today's allergy testing is similar to what Blackely used," wrote Paul Ehrlich and Shimer Bowers in their 2008 book "Living with Allergies."  (5)

Bostock believed hay fever was a condition of the upper and middle classes.  Philipp Phoebus came to the same conclusion.  William Abbotts Smith considered this theory, although he writes that he witnessed "many well-marked cases of Hay-fever amongst the poorest classes."  (7, page 36)

Blackley tended to agree more with Bostock and Phoebus.  He said he experienced only two cases of working class people with hay fever, and therefore concluded the disease to be an "aristrocratic disease." (2, page 6)

Gregg Mitman, in his 2007 book "Breathing Space," explains Blackley's thinking on this subject.  He writes that...

 "before the industrial revolution... a large portion of the population in England was exposed to the atmospheric conditions of country life, either through the cultivation of the soil or the production of woolen, linen, and cotton goods, largely in rural villages and towns.  As England's population increased, large numbers of people moved from the 'country to the workshops and mills of towns.'  In doing so, they removed themselves from pollen and other exacerbating factors to which agricultural laborers were continually exposed.  At the same time, the influx of population into cities, where greater educational opportunities, wealth, and luxury prevailed, created circumstances 'favorable to the development of the pre-disposition to hay fever.'  The frenzied pace of urban life, the mental demands of modern business, and the removal from nature, which could fortify the body and calm the hurried mind, had strained the nervous system of the city's educated and well-to-do classes.  'As population increases and as civilization and education advance,' Blackey warned, hay fever 'will become more common'" (2, page 14)

So Charles Blackley was a significant contributor to the knowledge of hay fever.  Of interest is that his theory about hay fever being a disorder of the upper class is an idea that still emulates in the medical community.  A new theory is that it's a disease that develops because the immune system isn't exposed to enough germs, and therefore the immune system doesn't develop properly, and hay fever (allergies) and asthma develop. A theory now is that it's a disease associated with modern civilization. He passed away in the year 1900.
References:

1. Fry, John, "The Natural History of Hay Fever," Journal of the College of General Practice, 1963, 6, page 260
2. Blackely, Charles Harrison, "Hay-fever: its causes, treatment, and effective prevention," 1873, 1880 2nd edition, London, Bailliere
3. Hicks, Terry Allen, "Allergies," 2006, China, page 40
4. Mittman, Gregg, "Breathing Space," 2007, New Haven and London, Yale University Press
5. Ehrlich, Paul M., Elizabeth Shimer Bowers, "Living with Allergies," 2008
6. Beard, ibid, pages 12 and 13, referenced by Beard from Dr. Mr. W. Gordon's paper "Observations on the Nature, Cause, and Treatment of Hay-Asthma," London Medical Gazette, 1829, vol. iv, page p. 266, reference from "Experimental Researches on the Cause and Nature on Catarrhus Aesivus (Hay-Fever, or Hay-Asthma), by Dr. Charles Blackly, London, 1873
7. Smith, William Abbotts, "On Hay-Fever, Hay-Asthma, or Summer Catarrh," 1867, London, Henry Renshaw, pages 17-24.  The quotations are from Smith's descriptions of Phoebus's ideas.