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Tuesday, April 11, 2017

What is PEEP? How to do a PEEP study?

PEEP is an abbreviation for Positive End Expiratory Pressure. It's a small amount of pressure above what is in room air that remains at the end of expiration.

The benefits of PEEP are.
  1. Increased Residual Capacity. This essentially means that it increases the amount of air that stays in the lungs. This works to...
  2. Recruit collapsed (atelectic) alveoli. This makes it so they participate in gas exchange. It also works to...
  3. Keep alveoli from collapsing. It keeps alveoli open so the effects of fluid or atelectasis do not cause shunting. This also helps to reduce V/Q mismatching. This also makes it so you have an...
  4. Increased PaO2 for a given FiO2. It's a good way of improving oxygenation. 
  5. Decreases Cardiac preload and afterload. It reduces the amount of blood returning to the heart, and thereby reduces the amount of blood leaving the heart. In this way, it can help patients who are in heart failure (pulmonary edema) by reducing the amount of work their heart has to do to pump blood through your body. This also means that too much PEEP can be observed by drops in cardiac output, which can be measured by bloodpressure and oxygen saturation (SpO2). 
  6. Reduction in tissue injury and inflammation. It prevents the alveoli from constantly opening and closing and thereby inuring them and causing inflammation, which may be associated with the development of ARDS. Studies have shown that it is protective against "ventilator induced lung injury." This is often called volutrauma. Volutrauma was more prevalent back in the days when it was thought that people on ventilators should be on higher tidal volumes, hence the old formula of setting tidal volumes based on 10-15cc/kg ideal body weight. This has now been lowered to 6-8cc/kg ideal body weight in order to prevent volutrauma. 
There are disadvantages of this.
  1. Over-distention of alveoli. It causes too much air to stay in the lungs resulting in decreased cardiac output, as would be shown by blood pressure and SpPO2. There are certain instances where you would benefit from higher PEEP, although too much PEEP can lead to over-distention and volutrauma, which may mimic respiratory disease states. So, in such instances, you would want the highest PEEP that doesn't cause over-distention. (Described below is how to accomplish this with a PEEP study). Over-distention results in increased dead space, increased work of breathing, and medical disorders such as ARDS. 
  2. Diminished Cardiac Function. As noted, PEEP that is set too high can decrease venous return and cardiac output. This can be measured by complex formulas, although the simplest way is by taking a blood pressure and monitoring pulse oximetry. 
  3. Diminished Renal Function. May decrease renal blood flow resulting in diminished urinary output. So, this is another reason to keep PEEP as low as clinically possible, especially when you have a patient in heart or kidney failure. 
  4. Increased Intracraneal Pressure. When venous return decreases, intracraneal pressure may increase. This is usually not clinically significant. However, if you have a patient who already has an elevated intracraneal pressure (ICP), such as due to a head trauma, this is something you'll need to watch out for. This is another reason to raise the head of the bed, as this may offset any increase in ICP (the other reason for raising the head is to prevent GERD, which can increase the risk for ventilator associated pneumonia). 
Now that you know about PEEP, along with its benefits and disadvantages, we can now get into how to perform a PEEP study. The purpose here is to determine the perfect PEEP for an individual patient at any given moment in time. Keep in mind here that the ideal PEEP may increase or decrease over time, especially as a patient's medical condition worsens or improves.

Here is the basics of any PEEP study.
  1. Increase PEEP by 2-3 cwp every 20 minutes and continue to monitor the patient. You should write down the patients blood pressure and SpO2. If desired, you can also jot down the patients P/F Ratio and static compliance.
  2. If static compliance, P/F Ratio &/or SpO2 increase, you know it's working. 
  3. Stop when the patient's blood pressure and SpO2 start to drop. Also stop when the P/F Ration is equal or greater than 200. Also stop when the static compliance decreases. 
  4. The required PEEP should be set at the PEEP setting used just prior to where the hazards of PEEP were observed. 
  5. Do not increase PEEP if systolic BP is less than 90
  6. Also, keep mean airway pressure (MAP) less than 15. This is one of the newer markers of too much PEEP. When it starts to drop, this is an early indicator that cardiac output is about to decrease. 
  7. Ideally, static complliance should be between 60-100.
I also have a shortcut. Maybe I shouldn't teach you this, but here goes: essentially, based on the wisdom we learned above, all you really need to do is monitor pulse oximetry and blood pressure. If either starts to drop, then you know it's time to lower your PEEP by 2 cwp, which would be your ideal PEEP. This makes it simple. 

The optimal goal of any PEEP study is to find the optimal PEEP to maintain a desired SpO2 and PO2.

If any of my fellow respiratory therapists has anything further to add (any tips), please feel free to share.

(Post originally published on 8/9/08. It has been edited and updated by RT Cave Staff). 

  1. Vincent, Jean Louis, editor, "Intensive Care Medicine: Annual Update 2002," 2002, Springer, pages 302-303
  2. Criner, Gerard J., Rodger E. Barnette, Gilbert E. D’Alonzo, editors, “Critical Care Study Guide: Text and Review,” 2nd edition, 2010, Springer
  3. Kacmarek, Robert M., James K. Stoller, Albert J. Heuer, “Egan’s Fundamentals of Respiratory Care,” 10th edition, 2013, Elsevier Mosby
  4. Saura, Pilar, Lluis Blanch, "Conference Proceedings: How to set Positive End Expiratory Pressure," Respiratory Care,, accessed 4/11/17
  5. Respiratory Update: "Benefits, Contraindications, Adverse Effects for PEEP/CPAP,", accessed 4/17/17
  6. Valenza, et al., "Positive end-expiratory pressure delays the progression of lung injury during ventilator strategies involving high airway pressure and lung overdistention," Critical Care Medicine, 2003, July, 31 (7), pages 1993-08,, accessed 4/11/17
  7. Respiratory Therapy Cave: Respiratory Failure Lexicon
  8. Respiratory Therapy Cave: ABG Lexicon

Monday, April 10, 2017

When it's busy, this kind of stuff happens

So, I enter the patient's room and leave my cow by her bed. I left because her inhaler was in another cow. I walked to the other cow. I opened the other cow. I took the inhaler out of it, and returned to my patient's room. The curtain was pulled around the bed. A nurse was behind the curtain.

I said to the nurse, "Is my cow back behind there with you?"

She said, "No!"

I said, "I just left it there. Where could it have gone?" I said this in a facetious manner, knowing she must have moved it.

She said, poking her head out from behind the curtain, smiling. "I don't know where it is?"

I walked out of the room. I looked at the room number. I realized I was in room 9. The room I left my cow in was room 11. I said, "Well, it seems I'm in the wrong room."

She laughed. She said, "It seems you need to drink some more coffee."

"Agreed!" I said.

Wednesday, April 5, 2017

We do not do conventional wisdom here at the cave

I love it. In response to my post, "Here is what albuterol does and does not do," just one of the 125,000 plus people who viewed the article as of this writing complained about it. This person wrote the following:
"I'm not impressed. He does make a couple good points but, in looking further at his website, the author is rather smug and also has out-dated ideologies. I would not promote him as a reference.
I love it. I am a respiratory therapist. I have a job. I have to tackle these complicated issues from sort of a humorous angle, otherwise I would not be able to write about them. Keep in mind I have a wife and kids and don't want to lose my job. But at the same time, it's good that we educate each other.

I had one email about the subject. The person wrote:
I am getting some questions after sharing a post of yours. Do you have a citation or explanation why audible (without a stethoscope) wheezes are not brocho-spastic in nature?
My response was simple:
Ask your friends this question: Where is the evidence that a wheeze produced by airways that are 0.5-1 mm in diameter and buried deep inside your chest can be heard without the aid of a stethoscope?
It would be easy if I just went the conventional route and agreed with everything we are taught in respiratory therapy school. I could easily just say, "If it's ordered, it's needed."

Now, I know most people reading this now have been reading my blog long enough to know that I summarily reject conventional wisdom. Whatever it is, I go a different way. Because conventional wisdom does not result from thinking. Whatever it is, I go a different way.

This is because conventional wisdom does not result from critical thinking or analysis. Conventional wisdom is group think and a desire for sameness. Conventional wisdom is something where people who practice it seek comfort, trying to tell themselves things that they really don't know that make themselves feel better about things.

Conventional wisdom has also become a marker or a measurement for intelligence and perceptiveness inside the media, Washington, and even the medical profession. It's been that way for years. In fact, it's been that way since the beginning of civilization.

Here, I will give you one example, although you can just read any of my previous posts and find many more. Since the 1960s doctors have been under oxygenating people with COPD under the guise of the hypoxic drive theory. There has been no science showing that this is true. It was just one man, based on a study of 4 COPD patients, who postulated this theory in a presentation before a group of doctors. The hypoxic drive myth was born.

Save to say that not one study was ever done proving it. In fact, every time a respiratory therapist gives a breathing treatment with oxygen, he is essentially disproving the hypoxic drive theory. Yes, the hypoxic drive exists, but it is not blunted by too much oxygen. If your oxygen goes low enough, it will cause you to breathe. However, it is not blunted if you are a CO2 retainer. That is the myth.

So, then they come back at me. I mean, I know all the arguments. I have heard them all. People feel good about defending conventional wisdom. One argument, a famous one is: "Well, I have seen it. I have seen people with COPD stop breathing because of too much oxygen."

No, you have not. You have seen them stop breathing, or become lethargic, because of V/Q mismatching. They go into respiratory failure because they poop out. It doesn't matter if they are getting 21% or 100% oxygen. Chances it was just a coincidence that a person on oxygen became lethargic, as the logical response to hypoxia is to put a person on oxygen. So it only makes sense they fail after being put on oxygen.

However, the reason they fail has been the subject of perhaps one of the worse myths in respiratory therapy. I often wonder how many people with COPD died because of this myth -- because of intentional hypoxia due to a myth perceived as fact.

Another argument I get is: "Well, a consensus of doctors believe in it." So what. What does a consensus prove anyway? It proves nothing. A consensus is not science. Science means it either is or is not. You can have a consensus believe in global warming, for example, and you do have one. You have 99% of scientists (according to one poll anyway) believe in it. But that does not make it true.

A good way of defining "conventional wisdom" is by watching the crowds. Or, in the case of the medical profession, simply polling the people who take care of the patients. In our case, that's us -- respiratory therapists.  If you poll respiratory therapists, I bet a majority have observed that oxygenating COPD patients doesn't kill them. Sure it may drive up their CO2 somewhat, but it's not due to they hypoxic drive, it's due to the Haldane effect and V/Q mismatching. And I've been over all this before.

If you poll respiratory therapists, you'd learn what the wisdom is. You'd learn that most breathing treatments aren't needed. I'm convinced of this. And if you polled them, you'd find where the wisdom is. It's because most respiratory therapists think the same way. It's because most people are smart. They know what works and what doesn't. 

So, if most respiratory therapists think all of these are myths, then it has to be right. If so many people think the same, it has to be brilliant. 

Further reading:

Monday, April 3, 2017

Sigh! The hypoxic drive hoax lives on

It's a flat out fallacy, folks.
This is not true. 
Editors Note:  The following is a guest post from an anonymous therapist. He said it was okay to publish his name. I decided to hold it to make sure he doesn't get into trouble and lose his job for being honest.

I am soooooo tired of nurses taking patients off their oxygen because "they are retainers." The patient was wide awake and alert, and showed no signs of being lethargic, but based on a myth we are going to keep his sat at 85%. In the past I've tried to educate, but now I just roll my eyes and leave the room before I say something I might regret. This myth does not bode well, and never has, for patients.

Two days ago the patient had sats in the mid 80s, and the doctor (my favorite doctor) said to increase the oxygen. So, with his permission, I placed the patient on a high flow nasal cannula ad 15 lpm. The patient was happy that he didn't have to wear a mask, and we were happy that he felt better due to being oxygenated. He was happy on this for two days, and he showed no signs of any side effects to the high flow. But, then a night shift crew came on that believed in the hypoxic drive hoax, and the patient was taken off oxygen. 

So, I come on. I want to take the patient off his nighttime BiPAP. I go to hook up the patient to the high flow oxygen, and it is gone. "Where is it?" I chime to the patient's nurse.  The nurse says, ""Uh, the patient is a CO2 retainer. It was making the CO2 go up."  

Here is where I roll my eyes and...


I have explained about the hypoxic drive theory to nurses ad nauseum. I have written articles. My friends have written articles. I have even been interviewed for peer reviewed journals. And here I am ten years later and I still have to deal with it. And, to make matters worse, the nurses I'm dealing with is a nurse I've explained it to 100 times. It's as though I have wasted my time. And so, I just... 


I am going to start smoking. I have severe asthma. If I smoke, I will get COPD within a few days. If you have severe asthma, and you smoke, you can get a diagnosis of COPD real fast. I want to get COPD, and I want to need oxygen. And I want to be admitted. I want to be admitted for COPD. I want my oxygen.

And when a nurse puts me on a 2lpm nasal cannula, and my saturation is 85%, I'm going to demand more. and when they don't give it to me, I'm going to sue. I'm going to sue because I didn't get the oxygen I needed. This put me at risk of dying of a heart attack. Then maybe I will be heard.

And when they site their evidence, they will only have one study that was done way back in the late 1960s based on four COPD patients. I will have as my evidence over a hundred studies

I think this would give me a more credible voice, because no one listens to RTs -- obviously. If I were a doctor and championed for the abandonment of the hypoxic drive myth, then I'd be laughed at and mocked, like Rene Lenaec was when he invented the stethoscope. So, I think a COPD patient is a must. I think the only course of action here is through the law. We need to end the hypoxic drive hoax once and for all. 

And for you folks in Rio Linde, I'm joking about smoking. But, my point is still valid: the hypoxic drive theory is nothing more than a hoax that causes needless suffering and even kills. 

Thursday, March 30, 2017

How do respiratory and cardiac medicines work?

I thought it would be neat to do a pithy review of how respiratory and cardiac medicines work. We will begin here with a basic anatomy lesson, beginning with the nervous system. As we proceed through our discussion I will introduce some of the medicine we commonly use. So, let us begin.

There are two nervous systems.
  1. Autonomic Nervous System:  It controls the many body functions that you do not have control over, such as your heart, vessels, stomach, and intestines.  
  2. Somatic Nervous System:  It allows you to control various parts of your body, such as your arms, legs, and breathing.  
For the case of this post, we are only concerned with the sympathetic nervous system. I will delve into the somatic nervous system in a future post.

Sympathetic Nervous System:  It has two divisions that both effect heart, smooth muscles, iris of the eye, salivary glands, and urinary bladder.
  1. Sympathetic Nervous System (SNS): Also called flight or fright.  It prepares the body to handle stress, either real or perceived. The stress could be trauma, or it could be someone holding a gun to your head.  It could be that you just heard about a family member dying, or your boss is screaming at you.  When any sort of stress occurs, your sympathetic response causes vasoconstriction to increase your blood pressure and heart rate. At the same time, this response relaxes your involuntary smooth muscles to dilate air passages to make breathing clear and easy. It also relaxes the involuntary smooth muscles of your bladder and gastrointestinal tract (might make you have an accident). The purpose of all this is to prepare you to do battle, or to run from it. Various medicines can mimic all or any of the sympathetic responses, and are called sympathomimetic medicine, or adrenergic agonist medicines.  
  2. Parasympathetic Nervous System (PNS): It generally does the opposite of the sympathetic. It causes vasodilation to lower blood pressure and lower heart rate. It also causes involuntary smooth muscles to constriction to normalize the flow of air through air passages, and to help you gain control of your bladder and gastrointestinal tract. Medicines that mimic this response are called parasympathomimetic or cholineric agonists. Medicines that block this are called anticholinergic medicines. 
Receptors:  Along all the muscles and vessels inside your body are receptor sites.  Many of these are attached along nerves, and are at the receiving end of an impulse.  When certain hormones are sent along the nerve and received by that receptor, a series of chemical reactions occur that causes a response by the muscle or vessel (either dilation or contraction). 

The main organ that makes the hormone that we are concerned with is the adrenal gland, which sits on either side of the kidney.  When you become excited or stressed, this gland secretes adrenaline that is sent down neurons to the various receptor sites.  Adrenalin extracts were discovered and named just prior to the turn of the 20th century, and isolated in 1901. It was learned that these extracts (later learned to be the hormone adrenaline) mimic the sympathetic response, and worked great for asthma and hay fever.  It is for this reason that receptor sites for this system are called adrenergic receptors.  In Britain the term adrenaline continues to be used, although in the United States the name epinephrine is used.  So this should explain some of the wording used here.  

Alpha Receptor sites:  Hormones released by the SNS system become attached to the following receptors to cause the following responses:
  1. Beta 1 (B1):  Located on heart muscle. When stimulated, it causes vasoconstriction. This makes blood vessels narrow, so the heart will have to generate a stronger force to pump blood through them. Your heart rate will also increase. Cardiac output is directly correlated with blood pressure, so a rising cardiac output can be measured by taking a blood pressure. It can also be felt when you palpate a full and bounding pulse. It is for this effect that epinephrine is used during cardiac arrest. It is a strong vasopressor (increases blood pressure). It's easy to remember because you have 1 heart. 
  2. Beta 2 (B2):  Located in lungs.  Causes smooth muscles that wrap around the airways to relax and this causes bronchodilation.  This is easy to remember because you have 2 lungs (right and left).
  3. Alpha 1 (A1):  Located in peripheral blood vessels.  Causes vasoconstriction to increase heart rate and force of contraction (increased blood pressure). It's easy to remember because you have 1 heart. 
  4. Alpha 2 (A2): Located by the nerve synapse.  Causes vasodilation to lower blood pressure. These act like a thermostat, and once the heart rate and force are too high, it shuts turns them down.  
Adrenaline (epinephrine):  This hormone regulates the SNS response and readies the body for flight or fight.  Adrenaline is released and attaches to B2, A1, or A2 receptors. It's a strong bronchodilator and vasopressor. 
Noradrenaline (norepinephrine):  Attach to B2 and A1 to act as vasopressors. 

Dopamine:  It is also created by the adrenal gland, and drugs that mimic it attach to A1 and A2 receptors to cause vasoconstriction and increased rate and force of heart and increased blood pressure. When attached to receptor sites, it stimulates the release of norepinephrine to generate a better blood pressure (vasopressor)

Dobutamine:  Effects B1 receptor sites and causes increased heart rate and strength of cardiac contraction (increased blood pressure).  It is generally used for heart failure (CHF) to make the heart a stronger muscle.  It increases cardiac output and blood pressure without much increase in heart rate. 

Beta blockers:  These are drugs that block the beta receptors.  The effect is mainly to try to control blood pressure, although a major side effect may be to cause narrowed air passages.  It is for this reason Beta blockers should be used with caution on patients with asthma or similar lung diseases. 

Albuterol:  It is a refined version of epinephrine without the side effects.  It has a strong affinity to B2 receptors and only slight affinity to B1 and A1.  Studies in the early 1990's showed that epinephrine was no better than albuterol for treating asthma. Side effects are also considered to be generally negligible. It has gone on to become the best selling asthma medicine of all time.

Levalbuterol:  It is a refined version of Albuterol, having the same strong B2 effect with minimal B1 and A1 affect. Some early studies showed that it was stronger and with fewer side effects than albuterol, although this has not been confirmed in the clinical setting. It is still under patent, and so most clinicians prefer to use the lesser expensive albuterol. 

Adrenal Gland:  It makes the hormones that effect upon the adrenergic receptor sites.  It makes the neurotransmitter dopamine, which goes through a series of chemical changes to become the neurotransmitter norepinephrine and then the neurotransmitter epinephrine. It also makes the neurotransmitter acetylcholinen which acts upon the PNS receptor sites, which are referred to as Cholinergic Receptor Sites. 

Cholinergic Receptor Sites:  Receptor sites used for the PNS are called cholinergic receptors.  The main neurotransmitter here is acetylcholine, hence the name cholinergic. It is used to cause bronchoconstriction and vasodilation, or to return things back to normal.  It basically has the opposite effect as the SNS.  The two types of receptors are:
  1. Nicotonic:   Found in central nervous system, autonomic ganglia, and striated muscle. 
  2. Muscarine:  Found in cardiac and smooth muscle, exocrine glands and brain
Atropine:  It competes with aceylcholine for muscarine receptors, and therefore blocks the effects of the PNS.  This results in an increase heart rate and bronchodilation.  It is used for bradycardia and asystole (flatline, non beating heart).   Herbs that contained this chemical were used for asthma-like symptoms going all the way back to ancient Egypt.  So when you read the history of asthma, you will probably hear about asthma cigarettes, incense, and other inhaled methods.  The active ingredient was always atropine, and the herbs it was contained in were strammonium and belladonna. 

Atrovent:  This is a refined version of atropine without the side effects.  It is recommended as a preventative medicine for COPD and severe asthma.  It needs to be taken four times a day to obtain the full effect, as it only lasts 4-6 hours. 

Spiriva:  This is a refined version of Atrovent that lasts 12 hours and only needs to be taken twice a day.

(Originally published in 3/9/13; edited and updated for accuracy.)

  1. Guy, Jeffrey, "Pharmacology for the prehospital setting," 2007, U.S., Jones and Bartlett Learning, 

Sunday, March 26, 2017

Myth: Epinephrine is stronger than albuterol, and better at ending asthma attacks

Sus-Prhine was once a top-line
treatment for asthma
in emergency rooms.
I am a victim of a myth. I am guilty. I believed, and have for a long time, that epinephrine is better at opening airways and ending asthma attacks than albuterol. I am guilty of thinking, at times, "Why don't we just give epinephrine?" However, truth be told, according to studies, epinephrine is not any better than albuterol.

This is one of the few times where the medical profession dispelled a myth and realized the truth before me. Various studies in the late 1980's and early 1990's showed that albuterol was equally effective as epinephrine at opening airways. It was also shown to be far safer.

The most convincing study was published in 1991, and I wrote about it in my post, "1991: Study finds albuterol works just as well as albuterol."

The study gave albuterol and epinephrine to various children of an average age around 8-years-old, and the various testing done showed that both medicines were equally effective at ending asthma attacks.

So, it is basically for this reason why doctors give albuterol to asthmatics rather than epinephrine. Epinephrine is sometimes offered as a last resort prior to intubating asthmatics, but it's either never given because albuterol eventually works (or, more likely, the systemic corticosteroids start working), or it is given and fails to work. It fails to work because albuterol was already probably given ad nauseum, and epinephrine is not better than albuterol.

Even recently I have wondered why we don't just give epinephrine to some asthmatic patients who come in with asthma exacerbations. Here we have access to this shot that could just open them up in a matter of minutes, as opposed to giving albuterl ad nauseum.

The reason I am such a victim of this myth is because epinephrine benefited me so many times when I was a kid. I'd go to the doctor's office or emergency room and the shot would start opening my airways within five minutes. It created a feeling of euphoria. I mean, if you can't breathe and all of a sudden you can, you'd feel euphoria too. Although, some of this effect was probably the product of the medicine.

The last time I was given it was in 1991. When I asked for Sus-phrine, which was basically a long-acting form of epinephrine, the doctor had no idea what I was talking about. At this point, it had been six years since I had needed it or asked for it.

However, the pharmacist found a vial, and I was given it. And it opened my airways up. A few months later I went to the emergency room again. This time the doctor convinced me to try this new medicine called albuterol. I had actually had an albuterol inhaler, but never tried the solution before.

To my surprise, it worked just as well as the epinephrine at opening my airways up. I remember being excited about this new medicine. When I asked about it the therapist said it was a safer version of Alupent (the solution I had at home at the time).

A week later I had my own prescription for albuterol. I have been using it ever since.  Still, it never dawned on me that this new albuterol thing was equally as effective as epinephrine for another 16 years. I mean, it's kind of a "Duh!"  But, you know, it was hard for me to give up on the idea that a medicine that saved my life so many times could be replaced.

If you want to learn more about epinephrine, Sus-phrine, or gain access to the study referenced here, check out the following links.

Further reading:

Monday, March 20, 2017

E-cigarettes linked to loss of lung function

It's a free country. If my niece wants to use e-cigarettes, all the power to her. However, she should also be properly educated as to the risks of using them. And, apparently, they start reducing lung function as soon as you start using them, according to studies.

They are marketed as a safe alternative to smoking. However, many experts have warned for years of the potential dangers of using them. They had no studies, however, as to which to site until now.

The study of 54 young e-cigarette smokers, 27 of whom had asthma, had increased airway inflammation and reduced lung function, even after short term use of e-cigarettes.

It only makes sense. You're inhaling a foreign substance directly into your lungs. There is a good chance that it might cause mutations on genes that are responsible for COPD or some other lung disease.

Obviously, further studies will be needed. But it appears that e-cigarettes being marketed as safe may be false advertising.

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