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Monday, May 8, 2017

How can we make the RT profession better?

The following is a guest post.

By Wanda Bunch
I'd like to voice my frustrations as a Respiratory Therapist today. I'd like some ideas or suggestions on how we can make changes on a state level for Respiratory Therapist. I want my ideas/opinions/ and my voice to be heard.

I LOVE being a therapist (5 years) in Oklahoma. The respect and understanding of what we truly are capable of doing needs to be recognized. Our career (notice I didn't put job) is in jeopardy due to health care changes and we need to grow with the changes; so our career path we choose can continue to exist.

It sadness me to hear therapist of under 10 years talk about being burnt out due to being disappointed (due to department leadership and policies ). I feel the field has become stagnant with old policies/ goals/ and career ladder.

YES we have them available to us. I feel strongly about my career choice and want to continue to Excel at it and make improvements. So all therapist around the US should be asking themselves if we want to better this career and it to continue to exist 

What do we need to do to better the system?

So my questions to all of you.

  1. How do we get changes made on a state level? 
  2. Why are some states so behind in our field (Oklahoma)?
  3. How do we get rid of this stagnant ideas/policies and leadership?
  4. How can we bring up the morale among us and others?
  5. How can we encourage health care professionals that they need us and worth so much more?

Monday, May 1, 2017

BiPAP and CPAP: Answering all your questions

Your question: How high can you set CPAP? What are the disadvantages of CPAP that is too high?

My answer. This is a good question. According to Egans, CPAP is a continuous flow of pressure on inspiration and expiration.If there are alveoli that are collapsed due to atelectasis, CPAP acts to recruit them, and open them up. It thereby acts as a splint to keep them open to improve oxygenation. If CPAP levels are set too high, alveoli will be over-distended, and this may result in air trapping. (1, page 1066)

Another thing to keep in mind here is that CPAP acts to reduce venous return to the heart so the heart doesn't have to work so hard to pump blood through the body. This is the advantage of using CPAP to treat heart failure. If CPAP is set too high, this pressure may ultimately reduce venous return enough as to cause a reduction in cardiac output, which can be measured by a drop in blood pressure.

Over-distended alveoli and air trapping can also result in a drop in oxygen levels, and this can be measured by oxygen saturation monitor.

Your Question. How high can you set IPAP on a BiPAP machine?

My answer. The best answer I can give to this question is a theory, as is much of the medical profession. From what I have read (and you can help me find a source here) is that a pressure support or IPAP higher than 20 in a non-intubated patient may act to obstruct, or block, the esophagus. This can prevent the patient from swallowing. You can exceed a pressure of 20 if you absolutely must to improve oxygenation or ventilation. However, if you must do this, talk to the doctor about ordering a nasal gastric tube (NG)

While it's generally not a good idea to exceed the recommended settings, I have from time to time had doctors insist I do this. I just make sure to remind the physician that there is a down side to too much pressure.

Your question.  Is it true that you need an IPAP greater than 10 to be therapeutic?

My answer. The goal of IPAP is to assist with inhalation to reduce work of breathing and improve ventilation. If an IPAP of 10 results in an ideal tidal volume for that patient, then an IPAP of 10 will be fine. Some patients have small frames, in which case an IPAP of 10 (or less) may provide adequate support. Keep in mind here that some people with COPD do not have enough lung function, especially during flare-ups, to adequately blow off CO2. For these patients, just assisting them get to their normal, ideal tidal volumes will be all that is needed. So, you do not necessarily have to blast patients with the highest pressure support. If you are getting adequate tidal volumes (using your usual formula of 6- ml/kg ideal body weight), then you are probably fine.

Your question. Is it true you can't set a rate on BiPAP?

My answer. Part of the advantage of BiPAP, is if the machines senses that a patient hasn't taken a breath, it can force the patient to take a breath. This is ideal for preventing sleep apnea. So, ideally, you should set the BiPAP rate at around 6-8. Usually patients will breathe over this set rate. However, if they don't, then the machine will assure at least a minimum respiratory rate.

Your question. How are CPAP and BiPAP set? What are the ideal settings to use?

My answer. The ideal settings should be determined by doing a sleep study. A sleep study technician will titrate settings until the best settings are determined. You will want the lowest setting necessary to keep airways open and maintain adequate oxygenation. Of course, you don't want too high to prevent drops in blood pressure and oxygenation as noted above. There are also newer machines that are auto-titrating.

Your question. When you are setting up a patient on BiPAP in the clinical setting, what are good start settings?

My answer. This is open to debate. It is also open to varying opinions. The general consensus where I work is ideal start-up settings are IPAP 10 and EPAP 4. Settings can be adjusted until an ideal tital volume and oxygenation status is determined.

Your question. How big of a gap between IPAP and EPAP do you need.

My answer. The answer here is another one that is open to personal opinion. The general consensus where I work is that you would like to keep the gap at a minimum of 5. For example, you will want to set the IPAP at least 5 over EPAP. Keep in mind, however, the ventilator that you are using.

Your question. How is Pressure Support (PS) measured on BiPAP. It depends on the machine you are using. On the V60, it is measured over PEEP. So, if you are using a V60 ventilator, and you have the IPAP set at 10 and the EPAP set at 5, you are essentially using a Pressure Support of 10 and a CPAP of 5. On the other hand, if you are using a machine that does not measure PS over PEEP, and you use settings of 10/4, then the measured PS is 5. So, this is why it's important to know your machine.

Your question. Is it true that if a patient requires BiPAP post extubation that the patient never should have been extubated and should be re-intubated?

My answer. Actually, this subject has been extensively studied, and the results are relatively inconclusive. However, some studies show that BiPAP post extubation may prove useful in some patients, especially those with end stage COPD where airway protection and pulmonary toilet is not a concern. This may occur when patients are incorrectly assessed for readiness to wean, or when patients self extubate. It may also occur in some patients, such as those with end stage COPD who are anticipated to still need some support although you don't want to risk further complications of intubation, and a trial of post-extubation BiPAP is done on purpose. Some studies do show this may prove beneficial. However, it should also be noted that the patients described here have a 40% mortality rate.  (5)

Your Question. Does BiPAP really help with heart failure? Doctors say it pushes fluid out of the lungs.

My answer. Both CPAP and BiPAP, by providing increased intrathoracic pressure, have been shown to reduce both cardiac preload and afterload, which reduces the amount of work the heart has to do. Some physicians think it works by pushing fluid out of interstitial spaces, and this is why it works. However, while this does occur to a small extent, it's not enough to have a therapeutic benefit. (5)

Your Question. Does BiPAP truly benefit people with COPD.

My answer. Yes. Studies seem to show that IPAP reduces airway resistance due to bronchospasm and secretions to make it easier to take in a breath and reduce dyspnea The machines can also sense when a patient has not taken a breath to force them to take a breath, thereby preventing apnea. EPAP also acts to splint the upper and lower airways to keep them open at end expiration. This prevents soft tissues in the upper airway from collapsing and causing apnea, and it also recruits collapsed alveoli and keeps them open to improve oxygenation. Various studies have shown that BiPAP used to treat episodes of severe COPD, whether caused by COPD or heart failure, in the hospital setting greatly improves outcomes and hospital length of stays, and reduced hospital costs. Part of this is because BiPAP often prevents the need for invasive intubation and mechanical ventilation. Nocturnal BiPAP used every day at home for a minimum of four hours per day significantly reduces COPD flare-ups and makes them less-severe when they do occur. This has made it so that people living with COPD can live long lives with quality. (1, 4, 6)

  1. Kacmarek, Robert M., James K. Stoller, Albert J. Heuer, “Egan’s Fundamentals of Respiratory Care,” 10th edition, 2013, Elsevier Mosby, pages 1066, 1134-5
  2. “Non-Invasive Ventilation in COPD Exacerbations,” Nursing Times, September 3, 2013,
  3. Criner, Gerard J., Rodger E. Barnette, Gilbert E. D’Alonzo, editors, “Critical Care Study Guide: Text and Review,” 2nd edition, 2010, Springer
  4. Respiratory Therapy Magazine: Noninvasive BiPAP Systems May Help COPD Patients, January 28, 2015,, accessed 3/31/17
  5. Maclntyre, Neil R., “Mechanical Ventilation: Noninvasive Strategies in the Acute Care Setting,” Medscape,, accessed 3/31/17
  6. Ankjærgaard, Kasper Linde , et al., "Home Non Invasive Ventilation (NIV) treatment for COPD patients with a history of NIV-treated exacerbation a randomized, controlled, multi-center study," BMC Pulmonary Medicine, 2016,, accessed 4/1/17
  7. Respiratory Therapy Magazine: Nocturnal BiLevel Ventilation for the COPD patient," February 7, 2007, accessed 4/1/17
  8. Lainscak, Mitja, Stefan D. Anker, "Heart failure, chronic obstructive pulmonary disease, and asthma: numbers, facts, and challenges," ESC Heart Failure, volume 2, issue 3, 2015, pages 103-107,, accessed 4/2/17

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,