1955-1985: The IPPB Revolution

"This 1960s Monaghan Ventalung ad is a part 

of our IPPB Virtual Museum.http://museum.aarc.org/gallery/ippb/,"

said an AARC Facebook post on 3/25/16

Respiratory therapists who worked between 1955 and 1985, and many of their patients, became well acquainted with Intermittent Positive Pressure Breathing (IPPB).

IPPB therapy was first described in 1947, although wouldn't become popular until the Bird Mark 7 was introduced in 1955.

According to the 2012 edition of "Respiratory Care: Principles And Practice of Medicine," IPPB is "short-term or episodic mechanical ventilation for the primary purpose of assisting ventilation and providing short duration hyperinflation therapy." (2, page 370)

The lungs were inflated with a flow of pressure during inspiration, and expiration occurs when the flow is stopped by natural recoil of the lungs. (3, page 1158)

The machines were pneumatic, meaning they were operated by gas under pressure and not electricity. Tubing from the machine was connected to a 50 PSI source, and this was all that was needed to operate them.

Bird Mark 7

Any positive pressure breathing machine could be used, although the Bird Mark 7 is often cited as the machine that made IPPB therapy famous. This is because it was the first lightweight, portable, and durable, pneumatic pressure breathing machine.  It was also very easy to operate. However, other common IPPB machines were the Mark 1, Bennet TV-2P, and Monaghan Ventalung Respirator.

IPPB therapy for the treatment of post operative complications was first described in 1947, although the introduction of the Bird Mark 7 in 1955 would give birth to the IPPB Revolution that would last until 1985. At some hospitals, this type of therapy would not be phased out until the 2000s.

What were IPPB Treatments?

 Many hospitals set up IPPB Rooms, where several IPPB machines were lined up in a row. Patients would come in for their 15-20 minutes of IPPB therapy 3-4 times every day. Inpatients would be wheeled to this room, although bedside therapy could also be performed.  Eventually IPPB rooms would be phased out in favor of bedside therapy.

Therapists would set up the machines by dialing the appropriate sensitivity, flow and pressure levels. The flow level determined how much pressure was given to the patient. Sensitivity determined how hard the patient had to work to trigger a breath. The pressure was usually set between 10 and 20 cwp. A circuit from the machine was then connected to either a mouthpiece or mask.

As an adjunct, nebulized medicine could be added to the circuit via a nebulier cup that was connected to a flowmeter via oxygen tubing. The most common medicines used during the 1950s were the bronchodilator Isuprel, mucus thinners called Alevaire and Mucomyst, surface tension reducer ethyl alcohol (to control foaming pulmonary edema, antibiotics, and other medicines.

Patients were encouraged to create a tight seal around the mouthpiece. A mask and nose clips could be used as necessary. Patients were then encouraged to start a breath and let the machine do the work. The medicine, if included, was inhaled during inspiration. The treatments would generally last around 15 minutes, depending on how coordinated and cooperative the patient was.

For patients, it felt as though a rush of air was filling their airways. For therapists, constant monitoring was necessary to make sure patients were getting effective breaths. They could adjust settings as necessary. The most common setting to adjust was flow, which determined how fast a breath filled airways. Flow was essential to coordinating machine breaths with patient breaths.  Pressure may also be increased or decreased depending on the comfort level of the patient.

What were IPPB Theoeries?

Over time, three theories regarding IPPB therapy were developed.

1. Hyperinflation therapy. It was believed hyper-inflating airways acted as a means of preventing and treating atelectasis and pneumonia, particularly in post-operative or bedridden patients, or anyone receiving large doses or sedatives or narcotics to control pain or anxiety. 
2. Inflation therapy.  It was believed that positive pressure breaths would open up airways, particularly terminal airways and alveoli, that had collapsed. This, or so it was thought, would treat atelectasis, particularly post operative atelectasis caused by shallow breathing due to anaesthetics or narcotics. 
3. Nebulizer therapy.  It was believed that inhaling respiratory medicine with positive pressure would result in better distribution of the medicine.

During the 1960s IPPB therapy became famous for treating and preventing post operative atelectasis and pneumonia.  During the 1970s IPPB therapy was increasingly used to treat respiratory ailments. So, while initially used mainly to treat and prevent and treat post operative complications, it was ultimately used for just about any patient in the hospital settings.

When was IPPB ordered?

According to a 1957 article in the The American Journal of Nursing, "Nebulization Under Intermittent Positive Pressure," the following were marked as conditions treatable with this IPPB therapy: (8)

1. Pulnonary edema
2. Atelectasis
3. Bronchial asthma
4. Bronchiectatsis
5. Emphysema
6. Pulmonary fibrosis
7. Silicosis
8. Impairment of respiratory function resulting from barbituate poisoning
9. Impairment of respiratory function resulting from Poliomyelitis." (3, page 1158)

The article cited the following indications for this therapy: 

1. Overcome breathing resistance
2. Provide more uniform alveolar aeration
3. Distribute aerosols to terminal bronchioles where absorption takes place
4. Relieve bronchospasm
5. Improve bronchial drainage
6. Provide exercise for respiratory muscles
7. Improve pulmonary functon (3, page 1158)

What medicines were used with IPPB therapy?

Most circuits were fitted with nebulizers so medicine could be inhaled during therapy. In 1957, the most common solutions for nebulization with IPPB were:

• Ethyl alcohol: To calm the foaming bubbles in pulmonary edema
• Isuprel: a bronchodilator used to relax smooth muscles in asthma, COPD
• Vaponephrine (Racemic epinephrine): which acts as a fast acting bronchodilator
• Mucomyst: A mucus thinner used to help COPD, CF patients expectorate sputum
• Alevaire (tyloxapol solution): A mucus thinner also used to help patients with thick sputum expectorate it.  (3, page 1158)

Other solutions used at one time or another included:

1. Tergemist. Another mucus thinner
2. Alupent (metraproterenol). A short acting bronchodilator
3. Ventolin (Albuterol). A short acting bronchodilator

Over time ethyl alcohol and alevaire were phased out, and Isuprel was replaced by alupent and later albuterol. Occasionally, other medicines would be thrown into the mix. A treatment session generally lasted until the medicine was gone, or about 15-30 minutes, depending on how cooperative an individual patient was with the therapy. 

What caused the decline of the IPPB Revolution?

Doctors were basically writing way too many IPPB orders, and respiratory therapists were required to do them. It probably didn't take long for therapists to question the effectiveness of this type of therapy.

You see, back then respirator therapy procedures were fully reimbursable. IPPB therapy was far more expensive than nebulizer therapy, so this would have resulted in huge profits. So, despite concerns by therapists, administrators had no incentive to buck the system and question the relevance of orders.

The party ended during the 1970s when insurance agents looking to cut costs gained wind of the skepticism and began to scrutinize IPPB therapy. They pressured researchers to find evidence it did what it was believed to do. And the returns did not paint a rosy picture. (2)

For instance:

• Studies showed a 25 percent increase in tidal volume was needed for this therapy to be effective, yet there was no means of measuring tidal volumes.
• Studies showed that IPPB therapy deposit 32% less aerosolized medicine to the lungs than a simple aerosol treatment. (2,, page 370)
• Any benefits provided from the therapy were also proven to be short lived, lasting less than an hour. (2, page 370)
• IPPB therapy has been shown to have no greater benefit than other lung expansion techniques, such as having patients use insentive spirometers and chest physiotherapy. (2, page 370)
• In fact, a 1978 study showed that atelectasis occurred in 35% of patients using IPPB, 15% using incentive spirometry, and 8% using blow bottles. (6)
• A study published in Chest in 1961 showed that IPPB did not prevent post-operative complications. A theory postulated was that inhalations were not deep enough to be therapeutic, and "these findings occurred despite constant urgings by competently trained inhalation therapists to the patients to make maximum respiratory efforts In both depth and length." (7, page 130-131)
• It was shown to only overinflate good alveoli while having no effect on collapsed alveoli.

The 1961 study also noted the following:

"Each treatment was personally supervised by an inhalation therapist, a condition that would exist in few hospitals today. This emphasizes even more forcibly the danger of leaving the work of stimulating the post-operative patient to breathe to a "machine" even when supervised. Elevating the pressure might help force the issue making It more difficult for the patient to voluntarily stop inspiration. The recognition of these facts compromise the real value of this study. The I.P.P.B. machine, as used in this study, cannot replace the bedside work of the post-operative surgical team." (7, page 132)

Furthermore, the researchers noted:

Early circuites were non-disposable,
and most contained a nebulizer cup.

I.P.P.B. did not seem to reduce post-operative discomfort, did not hasten ambulation time, and did not reduce total hospital stay. These are expected observations when it was shown the post-operative pulmonary complications were not prevented. (7, page 132) 

So studies as far back as 1961 failed to confirm the efficacy of this type of therapy, and they were pretty much ignored. However, during the 1970s, this form of therapy would come under scrutiny by insurance agents, who started accusing doctors and hospitals of abusing the system.  The RT textbook, "Foundations of Respiratory Care," sums it up nicely:  (3)

"The Overuse of IPPB was eventually to become an embarrassment to the profession, but in the 1950s and 1960s, IPPB devices could be seen throughout most hospitals in the United States." 

When did the IPPB Revolution end? It did not die quickly. Despite the evidence, physicians were still convinced that it did some good. They were convinced that giving certain patients intermittent mechanical breaths would prevent respiratory failure and the need for intubation and continuous mechanical ventilation.

When I first started as a therapist in 1996 it seemed there were quite a few IPPB orders. Although as time went by, there were fewer and fewer. I remember one of my coworkers grumbling with each new order, saying, "Studies show that all they do is over-inflate good alveoli." He showed me the study he was referencing proving that he was right.

My last IPPB order came in 2012. Like my coworkers, I grumbled and griped about the order, but did the best with the knowledge I had to coach the patient toward correct technique. The patient was not cooperative, and refused to finish the treatment. And that was the end of any dust that remained of the IPPB Revolution.

Many larger hospitals had relegated their Mark 7 Respirators to the render regions of their storage rooms where they collected dust for several years just in case an order came. Our two Mark 7's made for nice coat hangers before they were finally taken away in during the summer of 2015.

For nearly 50 years IPPB therapy was a fixture in hospitals, and this was despite any evidence that it ever did any good. This is a theme that plays out so many times in our history, where theories are treated as facts until proven false.

References:

1. Glover, Dennis, "History of Respiratory Therapy," 
2. Hess, Dean R., et al, "Respiratory Care:  Principles and Practice," 2012, "Intermittent Positive Pressure Breathing," chapter 18, page 370 
3. Stephen, Phyllis Jean, "Nebulization Under Intermittent Positive Pressure," The American Journal of Nursing," 1957, Sept., vol. 57, No. 9, pages 1158-1160
4. Hess, Dean R., et al, "Respiratory Care:  Principles and Practice," 2012, "Intermittent Positive Pressure Breathing," chapter 18, page 370
5. Wyka, Kenneth A., Paul J. Mathews, William F. Clark, ed., "Fundamentals of Respiratory Care," 2002, . page 630, Section IV, Essential Therapeutics
6. Iverson, Li, et al., "A comparative study of IPPB, the incentive spirometer, blow bottles: the prevention of atelectasis following cardiac surgery," Annals of Thoracic Surgery, 1978, March 25, (3), pages 197-200, http://www.ncbi.nlm.nih.gov/pubmed/345985, accessed March 4, 2016
7. Sands, James H., et al., A Controlled Study Using Intermittent Positive Pressure Breathing in the Post-Surgical Patient," Chest, 1961, August, 40, pages 128-133, http://publications.chestnet.org/pdfAccess.ashx?url=%2Fdata%2FJournals%2FCHEST%2F21358%2F128.pdf,, accessed March 3, 2016