Critical Thinking: When It's Okay To Tell Doctors What They Want To Hear And Then Disobey Them To Do What You Think Is Right

So, we RTs are responsible for setting up ventilators. We assist with intubation, secure the airway, and then have someone bag while we set up the ventilator. At my hospital our hospitalists trust us to determine the best settings. And then, sometimes, when we have a very difficult patient, a specialist from Big City Hospital calls us to talk about fine tuning the ventilator. 

And this is fine. You talk back and forth. And this can allay our stress and the stress of the hospitalist. However, sometimes it doesn't help at all. A recent such episode involved the fact that a patient kept high pressuring despite being on a low tidal volume. The peak pressure was hitting 40 and the PEEP was set at 5. So this meant that the driving pressure was 35. And so the concern here was how to get the driving pressure down to 30, or as low as possible. 

And so my phone pings. It was the Video ICU calling from Big City Hospital. A nurse there said that the vICU doctor wanted to talk to me about the ventilator. And this kind of stressed me out because I was spending time trying to figure out how to get the pressures down and to get the high pressure alarm from stop going off without in effect lowering the high pressure alarm, which I had set at 50. 

I had informed the hospitalist and attending nurses that the problem, I was sure, was not the ventilator but the fact that the patient was not sedated enough. Plus it also might have something to do with the fact the patient had bad lungs to begin with. I don't think I need to get into the details of the patient's condition to make the point I want to make by this post. 

So, the hospitalist and the nurses respected what I was saying. And efforts were being made to better sedate the patient. And, of course, I'm continuing to reach into the information stored in the gray matter of my mind all the while staring at this machine to see if there were some adjustment I could make on my end to remedy this situation -- and I pretty much came to the conclusion that there were not -- the problem was on the patient end. The patient needed to be better sedated -- and efforts were being done by the team to do this. So, we were fine. Once the patient was sedated, we would be fine -- the patient would be fine. So, no stress. 

And then the hospitalist hands me his phone. He said, "The vICU doc wants to talk to you." 

And so I take the doctor's phone and place it up to my ear. And this is where I remember that there is a video camera on the wall behind me. And so the vICU nurse and doctor could see everything we were doing. They could see us, they could see the ventilator, they could see the patient. So, I realized they must have been watching as we struggled to get the patient under control. 

A male voice came through on the phone, belonging to a vICU doctor whose identity I wasn't aware of at the time. The doctor was eager to propose various solutions to address the problem at hand. Despite having already attempted the adjustments he suggested and knowing they were unlikely to work, I went ahead and made the tweaks. This approach allowed him to see firsthand the ineffectiveness of those particular adjustments.

In the end, he insisted, "You need to switch vents; the current one must not be working."

As if my stress level wasn't already at its peak, my face likely turned red with anger. I vehemently asserted, "There is nothing wrong with this ventilator. The problem lies in the lack of synchronization with the patient due to issues on the patient's end. My ventilator is functioning perfectly."

Yet he insisted I change the ventilator. 

"Sure, I said. 

Once he was satisfied, he asked for me to hand the phone back to the hospitalist, which I did. But I made absolutely zero efforts to change the ventilator, as I knew that was not the problem. And, as I expected, within the next 20 minutes efforts to properly sedate the patient succeeded. And the pressures came down to the acceptable range. 

Here's another scenario I often share with young Respiratory Therapists. Imagine you receive a patient transferred from surgery, and the surgeon instructs you to set the patient up on a tidal volume of 1000. You respond with a respectful 'Yes, Sir!' but, per your protocol and assessment, you decide that a tidal volume of 500 is safer for the patient. In these situations, it's crucial to balance following orders with making decisions in the best interest of the patient, using your expertise and protocols to guide your actions.

I've found myself in this situation numerous times, and my colleagues share similar experiences. It's a practice we humorously call 'pleasing the doctor'—nodding along, and then doing what we know is safest for the patient. As respiratory therapists, we are the experts in airway management, a responsibility that goes beyond the scope of surgeons or other doctors less familiar with ventilator care. This isn't about singling out surgeons; it's about emphasizing the importance of our expertise in ensuring patient safety when it comes to managing ventilators.

The key takeaway here is the importance of trusting your instincts and expertise. In critical situations, there's a delicate balance between following your gut instincts and managing the expectations of the medical team. It's crucial to recognize when to adhere to established protocols and when to assert your professional judgment.

In this instance, while doctors can prescribe treatment plans, the choice of a ventilator ultimately falls within the respiratory therapist's domain. Trusting your knowledge of the equipment, critical thinking skills, and experience is paramount.

Addressing alarms doesn't always mean the equipment is faulty; it requires a thoughtful analysis of the entire clinical picture. Sometimes, managing the situation involves not only technical adjustments but also effective communication to assure the medical team.

Moreover, in the complex landscape of healthcare, there are moments when telling doctors what they want to hear becomes a strategy to maintain harmony, allowing you the space to execute what you believe is right for the patient. It's a delicate dance of managing expectations, ensuring patient safety, and upholding the integrity of your role as a respiratory therapist.

Should You Become A Respiratory Therapist?

I get a lot of emails from people who are considering going to college to become a Respiratory Therapist. But because of something a respiratory therapist said, you are now having second thoughts. My humble advice to you is:

Don't fail to do something you think you'd enjoy because of something someone else said. 

Okay? Don't do it. Don't let someone else's negativity towards their own job sway you from doing something.

Let me just give you some of my own examples. I'm 47 years old now. Often I wonder what my life would be like today if I had become a teacher. I had thought long and hard about choosing the career of teaching long before I ever became a respiratory therapist.

So, here I was a Senior in High School. I had two teachers I really respected. I asked both these guys if teaching was a good profession. To my dismay, they were both very negative about the job, "There's a lot of burnout! The pay isn't good!" Are some of the negative comments they made about their job.

I did not go into teaching simply based on what these two teachers said. And, to be honest, I have regretted it ever since. I have always thought I would have been a great teacher. I think I would have loved that profession.

The same with counseling. I had actually thought of becoming a counselor at one time. However, I had a friend who was a counselor, and she said, "There's a lot of burnout! The pay isn't good!"

I sort of became a respiratory therapist by default. It was never at the top of any of my lists. However, since I didn't have a friend trash that profession, that's what I chose.

And, don't get me wrong, I love being a respiratory therapist. It's one of the better things to happen to me in my life. It has taught me a lot about my own asthma, allowed me to meet a lot of great people, and has to lead me to this profession as a health blogger.

That said: I'm burned out, and the pay isn't that good. See my point! All jobs lead to, or most, lead to a time when you're going to realize your pay is poor and you are burned out. It's a fact of life. It's why many people switch jobs or go back to school at certain times in their lives.

Some high school students tell me that they were told by a respiratory therapist that there is no respect for the profession. Sure, there are some things that need to be improved.

But, respect isn't one of them.

Our profession is a new one, and so there is still some room for the profession to grow. And you can be a part of making it better. So, if you are thinking about becoming a respiratory therapist: Go for it!

And if you decide later on that you want to do more and make more money, then the profession of respiratory therapy is a great stepping stone for other healthcare jobs, including a Physician's Assistant. I can surely tell you that any PA with an RRT background is going to be one hell of a PA.

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.)

References:

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

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Debunking The Hypoxic Drive Theoery: The Truth About The Affects Of Oxygen On COPD

Originally published January 6, 2016.

I was recently interviewed by Rebecca Knutsen, a staff writer working for Advance for Respiratory Therapists.  She said she was working on a brief article that explores when to administer oxygen to hypoxemic patients with chronic obstructive pulmonary disorder.

The following are her questions followed by my answers.  

1.  Please describe hypoxic and hypercapnic drive:

Hypercapnic Drive: The central chemoreceptors on the medulla monitors the partial pressure of arterial CO2 (PaCO2). A normal PaCO2 level is 35-45 mmHG. When PaCO2 is high (>45 mmHg) a signal is sent to the medulla oblongata at the base of the brain to speed up breathing in order to blow off excess PaCO2. When PaCO2 levels are low (<35 mmHg) a signal is sent to the medulla oblongata at the base of the brain to decrease breathing in order to allow PaCO2 to accumulate. This is the main drive to breathe.

Hypoxic Drive: The peripheral chemoreceptors located at the bifurcations of the aortic arteries and the aortic arch monitor partial pressure of arterial oxygen (PaO2). This drive only becomes active when the PaO2 is less than 60 mmHg. This hypoxic response is far slower than signals sent by central chemoreceptors, and therefore the hypoxic drive has only a minor role in breathing.

2.  What tests does your organization use and what do they measure?

ABG: This is a blood draw from the radial, brachial or femoral artery that measures PaO2, PaCO2 and arterial pH.

Pulse oximeter: It’s a noninvasive device that slips over a finger, toe, or ear lobe. It determines the SpO2, which is an estimation of hemoglobin in the blood that are saturated with oxygen. This percentage can be used to estimate PO2. Generally, an SpO2 of 90 indicates the PO2 is about 60.

End Tidal CO2 Monitor: It’s a noninvasive device that can be connected to special nasal cannulas or endotracheal tubes. It determines the ETCO2, which is an estimation of the amount of CO2 exhaled. This percentage can be used to estimate PaCO2. In a person with healthy lungs, the EtCO2 is about 2-5 mmHg less than PaCO2.

3.  When is it recommended to administer oxygen to hypoxemic patients with COPD? 

Most medical experts now recommend administering the lowest amount of oxygen needed to maintain an SpO2 of 88-92%, or as directed by a physician.

4.  Why is hypoxic drive so controversial? 

The hypoxic drive is not controversial, it’s the hypoxic drive theory that’s controversial. To understand why it is so controversial it’s important to understand a little of the history of it. 

Back in the late 1940s and 50s, when oxygen first started to be used for patients with chronic obstructive pulmonary disease, it was observed that some of them became lethargic or lapsed into a coma after receiving high levels of oxygen.

Initial studies showed a decrease in ventilation in 26 of 35 patients with COPD given oxygen therapy, with a rise in CO2 and a fall in pH. A further study showed that stopping and starting oxygen therapy led to a fall and rise in CO2 respectively.

The concern became so great that in the 1950s a study was performed that ultimately lead Dr. EJM Campbell to give a lecture to pulmonologists in 1960 about the dangers of giving too much oxygen to COPD patients. It was this lecture that forever linked hypoxic drive with COPD, and gave birth to the hypoxic drive theory.

What is the hypoxic drive theory? The hypoxic drive theory states that some patients with COPD develop chronically elevated arterial CO2 levels, and so their hypercapnic drive becomes blunted, so they use their hypoxic drive to breathe instead. 

Therefore, giving high amounts of oxygen to these patients may blunt the hypoxic drive as well, thus completely blunting their drive to breathe. This may cause PaCO2 levels to rise to critical levels, resulting in narcosis and possible death. For this reason, COPD patients with suspected CO2 retention are limited to 2-3 lpm by nasal cannula, or 40% by venturi mask.

What’s wrong with this theory? The problem with this theory is that it’s a myth concocted on incomplete evidence. The study cited by Campbell included only four patients with COPD, and later studies failed to validate this theory. Yet it has continued to be a gold standard theory when dealing with COPD patients.

Under the guise of this theory, many patients who desperately need higher levels of supplemental oxygen to survive are deprived of it. Plus, as many respiratory therapists, nurses, and physicians have observed, when these patients are given the oxygen they need, rarely does this lead to complications.

When these patients go into respiratory failure, it’s going to happen regardless of how much oxygen they receive. And while higher levels of oxygen may cause CO2 to rise, it’s not due to oxygen blunting their hypoxic drive, which the hypoxic drive theory postulates, it’s due to either the Haldane effect or V/Q mismatching.

The Haldane effect: This was postulated by John Haldane, a pioneer in oxygen therapy. He proved that the Deoxygenation of arterial blood increases its ability to carry carbon dioxide. In other words, as fewer oxygen molecules are attaching to hemoglobin, more CO2 are attaching to hemoglobin.

Oxygen is more soluble in water and therefore has a higher affinity for hemoglobin, so if you increase oxygen in the blood, CO2 molecules are forced off hemoglobin and oxygen takes its place. This causes an increase PaCO2.

Add into this the fact that patients with COPD have limited reserves to increase their respiratory rate to blow off excessive CO2. Also add into this that many COPD patients already have an elevated hemoglobin levels, and so these patients are going to have lots of extra arterial CO2 molecules.

Out of respect for this theory, COPD patients should be maintained on the lowest level of oxygen required to maintain an oxygen saturation between 88-92%.

The Haldane effect was proven by a study described in 1996 in Critical Care Medicine, "Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease."

V/Q Mismatching: The air passages of COPD lungs become narrow due to remodeling, increased mucus production, and bronchospasm. Where this occurs the lungs are perfused but poorly ventilated. CO2 returning to these areas remain in arterial bloodstream, thus causing PaCO2 to rise.

Add into this that when alveoli are poorly ventilated the vasculature around them will constrict so oxygen goes to alveoli that are ventilated well. This is how these patients make efficient use of their diseased lungs.

Now add 100% oxygen and you screw up this naturally occurring phenomenon. Now the vasculature around that non-ventilating alveoli dilates, and this causes blood to be sent to the non functioning alveoli. Now you have even greater V/Q mismatching and more CO2 that doesn't get out of arterial blood. The end result is an increase in PaCO2.

If a patient with COPD is going to fail this is going to be the reason. If they need oxygen you give it to them, because doing otherwise will further compromise them. If they go into respiratory failure, you treat it with either noninvasive ventilation or mechanical ventilation.

V/Q Mismatching was proven via a study completed in 1980 and reported in American Review of Respiratory Disorders, "Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure,"

Conclusion: Modern evidence suggests that the hypercapnic drive is never completely blunted, and therefore even COPD patients with chronically elevated PaCO2 will not stop breathing in the presence of higher oxygen levels. There is such a thing as the hypoxic drive, but the hypoxic drive theory is a myth.

To read the final published version of my interview read "Oxygen and COPD: Debunking the hypoxic drive theory."

Further References:

• Campbell, E.J.M, "The J. Burns Amberson Lecture - Management of Acute Respiratory Failure in Chronic Bronchitis and Emphysema," American Review of Respiratory Diseases, October 1967, Volume 96, Issue 4 (no link available)
• Campbell, E.J.M, "Respiratory Failure," The British Medical Journal, June 1965, 1451-1460 (article provided by link)
• Schmidt, Greggory A., Jesse B. Hall M.D "Oxygen Therapy and Hypoxic Drive to Breath: Is There Danger in the patient with COPD?" Critical Care Digest, 1989, 8, pages 52-53

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CPR works, but not as well as most think

Doctors die with grace and dignity.  Actually, anyone who works with sick people for any length of time develops the skills necessary to die with grace and dignity. This is not always true of the general population, especially in a world where people are not exposed to death, and are exposed to the fantasy world of Hollywood where CPR works an amazing 64% of the time.

There are many examples of CPR being performed in a movie or TV show and the person living.  One such incidence that is fresh on my mind occurred in an episode of "Walker, Texas Ranger," which starred Chuck Norris from 1993-2001.  I described it n my post "No Vent, DNR, or Full Code: What's Your Choice?"

What might confuse people is what you see in the movies. There was one episode of "Walker, Texas Ranger," where Chuck Norris's character was having chest compressions performed on him, and his friend who broke his arm was watching on. Then Chuck woke up, the ambulance arrived, and the person who was taken away on the ambulance was not Chuck, but Chuck's friend with the broken arm.

A recent study performed at the University of Southern California Davis School of Gerontology showed that the survival rate for CPR was actually as high as 37%, although the survival rate of CPR performed on TV was a whopping 70%.  No wonder people get a warmed view of what modern medicine can do.

The study also revealed that:

The depictions show CPR mostly being performed on adults age 18 to 65, when in reality more than 60 percent of CPR recipients are older adults over 65... Also, trauma was behind nearly 40 percent of the CPR instances in the shows, even though traumatic injury cases only account for 2 percent of all CPR usage in real life.

When comparing these results to a similar study conducted in 1996, accuracy rates of television CPR depictions appear to not be improving. And though they seem like harmless entertainment, widespread inaccuracies in medical dramas could have real-life consequences.

Harmless indeed! Some experts speculate that the false perception of what medicine can do has lead many to falsely believe doctors can fix any problem, prolong life by "doing everything" including CPR, and that after "doing everything" quality of life will not be impeded.

This is not harmless.  It causes people to delay dealing with end of life care.  It causes people to avoid discussing with their loved ones, with their doctors, how they want to die.  And considering the difficulty of the discussion, doctors tend to avoid the subject altogether.

Just to provide an example, a 67 year old lady with end stage COPD was rushed to the emergency room by ambulance. The first question the doctor asked her was, "What do you want us to do if your heart stops."  She said, "I want everything done."

An hour later she was intubated and put on a ventilator.  Then her blood pressure dropped so low we couldn't feel a pulse.  Now we are forced to begin full blown CPR with chest compressions.  Yes, this did result in ribs cracking.

The chances of her surviving this are not good.  If she does survive, she's going to still have end stage COPD, meaning she is going to feel dyspneic. Only now she is also going to have some pretty bad chest pain due to the chest compressions.

Did we do the right thing.  Well, the emergency room doctor had no choice.  We had no choice but to follow the wishes of the patient, even though we all knew full well that this patient had set a path to a death that was not going to be very pretty.  She was not going to die with grace and dignity.

What can be learned from this.  Doctors must talk to their patients about end of life care.  They must be honest with their patients.  "Hey, you have end stage COPD.  If you should end up in an emergency room in respiratory failure, what do you want done? How far do you want us to take you with our medicine? Do you want CPR?"

Of course this discussion must progress to a definition of what CPR is.  It may progress to a discussion of what intubation is, and of what a ventilator is? It may progress to a discussion about the difficulty of getting a patient with end stage COPD off a ventilator? It may progress to a discussion of recent studies that show that ventilatory support has yet to be shown as useful in patients with chronic respiratory failure?

Options must be discussed. Hospice must be discussed. It must be explained to the patient that choosing to be a DNR, or choosing hospice, does not mean giving up: it means dying with grace and dignity.

Further reading:

• Wall Street Journal: Why Doctors Die Differently (or find full article at zocalopublicsquare.org)
• RT Magazine: CPR: It's Not Always A Lifesaver, But It Plays One On TV
• RT Cave: No Vent, DNR, or Full Code: What's Your Choice?
• RT Cave: How do people die?

Study links rescue inhaler overuse to depression

A new research study reveals that "overuse of rescue inhaler in chronic asthmatics linked to depression." While the researchers were not conclusive on how to interpret these results, they seem to be leaning towards blame the asthmatic.

The study was conducted by the University of Arizona and involved 416 patients.  The results were as follows:

• About half of all participants used albuterol as expected, while 27 percent of participants overused albuterol and 22 percent underused albuterol.
• 45 percent of over-users used albuterol on a daily basis.
• Participants across the board used albuterol on symptom-free days about 20 percent of the time.
• Eighty-eight percent of daily users were over-users of albuterol.
• Over-users had more days in which they had symptoms and scored worse on the asthma control questionnaire, the shortness of breath questionnaire and the asthma symptom utility index.
• Over-users of albuterol had worse mental functioning when compared to expected users of albuterol.

So that was the first part of the study.  The participants were also studied to see how they scored on a depression test, with the following results. 

• 19% of those who underused albuterol had a depression score of 16 or more
• 17% of those who used albuterol as expected had a depression score of 16 or more
• 32% of those who used albuterol too much had a depression score of 16 or more

Researchers who interpret studies concluded the following: 

What isn’t clear is whether depression leads to worsened asthma symptoms and an increase in albuterol use or whether albuterol use contributes to the development of depression. Asthma has a significant relationship with one’s mental status, and emotional states like anxiety can contribute to asthma exacerbations, leading to the need for a rescue inhaler.

It also isn’t clear whether or not albuterol over-users were more or less compliant with the chronic medications asthmatics take on a regular basis in order to avoid exacerbations of their disease process. If this is the case, doctors need to educate patients — depressed or not — on the use of chronic asthma medications so rescue inhalers like albuterol are less necessary.

My problem with these results is this: Why do they always blame the asthmatic?  If I don't have good asthma control, it's because I don't take my asthma controller medicines.  Plus, how do you define albuterol overuse? I mean, I know they define it as using it more frequently than a doctor prescribes for, but how do they know the doctor is right.

Let me put it this way, many recent studies have confirmed that corticosteroids, a top line medicine used to reduce inflammation in asthmatic lungs to make them less sensitive to asthma triggers, does not work on those with severe asthma. Inhaled corticosteroids do not help those with severe asthma gain good asthma control.  So these patients, by default, will need to use their rescue medicine more frequently.

Likewise, most asthmatics do not have pure asthma, or asthma by itself.  Like myself, most asthmatics have something else with it, like allergies.  Actually, studies show that 75% of asthmatics also have allergies, and this is a double whammy.  My point here is that, even if you have good control, you can still have trouble breathing on a regular basis.  You may still need to use your rescue inhaler daily.

Yes, if you have pure asthma you shouldn't need your rescue inhaler more than 2-3 times in a 2 week period. There are many asthmatics who would fall into this category.  Still, there are likewise many asthmatics who do not qualify for this method of defining control because they do not have pure asthma.

I describe what real asthma control is in my post"What is good asthma control?"  I wrote:

The National Heart Lung and Blood Institutes (NHLBI) Asthma Guidelines define control pretty much the same as the GINA guidelines: Control is the degree the above guidelines are met plus the degree YOUR goals of therapy are met.

Your goals may be:

• I just want to be able to walk
• I want to be able to exercise
• I don't want to miss any more school or work due to my asthma

Another means to monitor control is your own personal satisfaction. Are you satisfied with your life given your asthma severity?

Plus this notion of monitoring control by how often you use your rescue inhaler doesn't work if you don't have pure asthma.  For instance, my current doctor ordered my rescue inhaler to be used four times a day. Well, how does he know when I'm going to be short of breath?  Sometimes I go weeks without using it. Other times, such as right now when I have a cold, I use it several times a day.

My point here is that you need to be careful when reading the results of research like this.  You have to take what you read, even in peer reviewed journals, with a grain of salt. While the studies themselves come to accurate conclusions, the people who interpret the results sometimes get it wrong.  They get it wrong because they do not have asthma so they don't know what it's like.

Further reading:

• Eureka Alert: Study: Severe asthma fails to respond to mainstay treatment
• Hardluck Asthma: What's it like to have asthma?
• NHLBI: Asthma Guidelines
• RT Magazine: overuse of rescue inhaler in chronic asthmatics linked to depression
• Lung Disease News: Overuse of rescue inhalers in asthmatics linked to depression
• Healthcentral: What is good asthma control?
• Healthcentral: How to obtain good control of your asthma?

Medicine based on consensus, not science

Medicine is an art based on science.  Much of medicine is based on flawed science. Or, as Richard Feynman once said, science is the belief in the ignorance of experts. 

Much of science is not even science: it's consensus.  It's basically the world's leading experts voting on what they think is fact, rather than waiting for the evidence to reveal the truth.  It's creating theories and voting on which ones should be in the forefront of our minds.  So when deciding on what to believe, we must never forget that "science is about evidence, not consensus."  

It is so hard in the medical profession to separate consensus from science.  In fact, one of the things that fascinated me most about the medical profession is it's loose relationship with science.  In fact, early on in my studies I learned that medicine is loosely based on science, and more so based on consensus, which is not science at all. 

Look at the hypoxic drive theory.  It was based on a study of four COPD patients, and became a gold standard based on a presentation by EJM Campbell to pulmonologists in 1960 about the results of a study based on only four COPD patients.  So basically the hypoxic drive theory, or hoax as I like to call it, was based on a consensus of experts, and had nothing to do with science. 

So basically physician's under oxygenated their patients for over 70 years, and many still do, based on a consensus.

Look at all the breathing treatments we give based on a consensus that albuterol cures every lung ailment you can think of. Our new healthcare law insists that a lung patient must be sick enough to need 3 breathing treatments for reimbursement criteria to be met. This includes COPD, CHF, Asthma, Pneumonia, etc. So 3 breathing treatments are ordered on all these patients, and it's assumed they are needed. What's wrong with this picture? It certainly has nothing to do with science. 

Other examples of consensus over science include:

• BiPAP pushes fluid out of lungs
• The earth is flat
• Man made global warming
• The continents cannot drift
• Stress causes ulcers
• Asthma is one of the seven pychosomatic disorders
• Phlogiston was necessary for combustion to take place

All of these theories are, or were, so widespread, and so well accepted, that they caused people to focus on treatments and therapies that probably did more harm than good (like under oxygenating COPD patients). As in the case with asthma, consensus caused experts to focus so much on a dead end path that it prevented the advancement of knowledge to the detriment of those who suffered from it (i.e., experts focused on treating asthma with psychosomatic medicines when they should have been looking treatments for inflammation and bronchospasm). 

So when you're thinking about whether or not you want to believe something is true, consider the evidence and not the consensus.  The fact that a majority of people believe something to be true does not make it so. In other words, it's okay to oppose the majority opinion, so long as the evidence is on your side. 

When a doctor orders something, it's your job as a therapist, or a nurse, to do as you are instructed.  For instance, if a doctor orders you to give a breathing treatment, then you must give it regardless that you know it is a waste of time.  As the old saying goes, "It can't hurt." 

Still, it really does hurt, because you're putting medicine into someone that doesn't need to be there, and, even though we can't always see them, all medicines come with side effects.  And then there's also the side effect of second hand ventolin on those who are doling it out all day long.

However, when a doctor orders for you to maintain an SpO2 in the low 80s because of the hypoxic drive myth, it's time to rise up and challenge the consensus for the benefit of the patient, because, Lord knows, oxygen is beneficial to the living heart. Thankfully the hypoxic drive consensus/hoax is slowly fading, and COPD patients are actually being oxygenated these days. 

Further reading.

• Rush Limbaugh: Peer Reviewed Science Exposed as Fraud
• NY TIMES:  Many Psychology Findings Not As Strong As Claimed, Study Says
• Wall Street Journal: Science is About Evidence, Not Consensus
• RT Cave: Second Hand Albuterol

Clinical Trials Made Easy

In the ancient world, and throughout most of history, whether or not a medicine worked was determined by speculation.  In the modern world, it is determined by a clinical trial.  Let us assume that albuterol is the medicine being tested, and we will walk you through the process.

In order to find out if albuterol actually makes asthmatics feel better, we have to have something to compare albuterol with. For this reason, we are going to create two groups:

• Experimental Group.  When a medicine is tested, these are the individuals who actually get to take the medicine.  If albuterol were being tested, these folks would actually get the medicine. 
• Control Group.  When a medicine is tested, these are the individuals who do not get to take the actual medicine.  They take a placebo instead.  This is needed so the examiners have something to compare the results with. If albuterol were being tested, these folks would just inhale normal saline.
• Tested Drug. Albuterol with 3 cc normal saline
• Comparator.  Normal Saline
• Placebo.  The comparator. A harmless or fake medicine. 
• Null Hypothesis.  To begin, experimenters will assume that both the tested drug and the comparator are equal, that there is no difference between the two.  The study will then prove whether this is true, or whether the tested drug generates a benefit. 

So now let us assume that all the people in the experimental group and all the patients in the control group have been diagnosed with moderate to severe asthma and have uncontrolled asthma.  None of the patients have taken any asthma medicine within the previous 12 hours.  Pulmonary function testing is done on all the patients, followed by a period of 20 minutes of rest.  The experimental group is then given the tested drug (albuterol with 3cc of normal saline) and the control group is given the placebo (3cc normal saline). Both the tested drug and the placebo are inhaled over 10 minutes using a nebulizer. 

All the patients now take another pulmonary function test.  Obviously, many such studies were performed in the past showing that albuterol improves lung function while the placebo did not improve lung function.  The null hypothesis is now proven wrong as albuterol is shown to improve lung function while normal saline alone does not. 

Let us take another example here.  Many respiratory therapists have said that a majority of patients who receive an albuterol breathing treatment say they feel better after the treatment.  The hypothesis here is that a placebo will work just as well as albuterol in generating a perceived benefit.  This hypothesis was tested recently on 39 mild to moderate asthmatics. 

This calls for some more definitions. 

• Perceived Response. This is when people who participate in the control group and received a placebo document that they feel better.  Of course we know it's not possible because they did not even receive the medicine. 
• Placebo Response (Placebo Effect).  This is where a patient reports a perceived response from the placebo.  They think they received albuterol so they think they feel better.  The study showed that 50% of those in the placebo group reported a perceived response to the medicine. 

As I wrote regarding this study before: "This is interesting to say the least.  We know that albuterol really does make breathing easier in patients who are having actual bronchospasm.  However, evidence also suggests that giving albuterol to anyone who is short of breath may produce the placebo response.  So now you know why doctors treat all pulmonary diseases as asthma."

You also now know how clinical trials work. You also now understand how we must take the interpretations of clinical trials with a grain of salt, because they are not always accurate.  

Further reading:

• Placebo Effect: Misinterpreted Study Proves It
• PubMed: Clinical trials: active control vs placebo--what is ethical?

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Wisdom of a Random Respiratory Therapist

I received an email from a respiratory therapist friend of mine who works for a hospital I will not name to protect my friend.

He said the patient had a shadow on the x-ray, and so the physician proudly said this was the reason for the breathing treatment.

He said another patient was diagnosed with end stage COPD, and the physician won't realize it's heart failure for a couple days.

He said an albuterol breathing treatment opened up one patient's airways so  much it made the patient's airways wet.

He said that the reason Duoneb is usually ordered rather than just albuterol is not because a study showed ipatropium bromide given in tandem benefits patients, it's because someone with a bright idea decided that if one medicine works great another given with it must work better.

Seriously, this is how medical research works, folks.

He reminded us of the study done once on 100 post op patients.  They were all given a bronchodilator QiD and were all eventually discharged.  So for the next 30 years all post op patients were given a bronchodilator

Of course he also reminded us of the interns who were ordered to do all the ABGs they ordered: the number of ABG orders diminished by 50 percent.

He said he told the nurse's aid the patient was wet, and she proceeded to change the patient's diaper. To her defense, she was new. He said the aid was a good sport and even she had a good laugh about it.

He said that most of what we do as respiratory therapists we do just so the hospital can get reimbursed. How else do you explain orders for three albuterol breathing treatments when all that was needed was one or none.

This doesn't make sense unless you understand that CMS Regulation says patients with any lung disease are only sick enough to be admitted if they fail three albuterol breathing treatments.

He said it's not the fault of the hospital, nor the physician, that so many frivolous therapies are ordered, it's the result of politicians sitting in leather chairs in Washington D.C. who have too much time on their hands and think that doing something is better than doing nothing.

Just to give you an idea of the idiocy of the medical profession, consider that Hippocrates defined asthma as all dyspnea.  Even while scientists have since extricated hundreds of diseases out from under the rubric term asthma, physicians still treat all dypsnea as asthma, and usually under the ruse: "Well, at least it can't hurt."

And yes, he said, a pulmonary diseases are also still treated as asthma.  I even had a very credible doctor once go into a 10 minute long discussion with me on how she believed albuterol helped people in CHF.  He said, "That ten minutes was a long time, because I had to somehow prevent myself from laughing."

He said that when posed with a problem, people who are making hospital regulations ask the question: "Does it make me feel good."  Sure, it feels good to come up with A solution.  Still, their solutions usually result in chaos.  What they ought to ask themselves is: "Will it do any good?"

He said these same people who, when they see a minor problem, say things like: "We have to do something." A better saying would be: "It's better to do nothing than something stupid," or "It's better to do nothing than just something that makes us feel good."

Bottom line, he said, is, rather than create regulations because they make sense, they make regulations because it sounds like a good idea and makes them feel good about themselves.  Yet the end result is usually chaos.  Chaos for an RT is RT Apathy and Burnout.

He said we RTs do not complain because we don't want to work.  We complain because too much of what we do is a waste of time or delays time.

Funny thing is, he said, I talk to many doctors who feel the same way.  They get tired of ordering therapies just to make the family think we are doing something, or just to make sure the hospital gets reimbursed. Regulations create doctor apathy too.  "Regulations cause chaos."

Oh, and one more thing.  I had a doctor the other day say to me, "Why are you always insulting my patients.  I said, "What do you mean?"  He said, "Well, you are always saying they are 'dim and clear.'"

Aerosols no longer indicated for airway clearance

We respiratory therapists seem to grumble and gripe a lot about useless breathing treatments, and usually to no avail.  However, it seems the good people working for American Association For Respiratory Care (AARC) have heeded some of the criticism and performed some of their own research into the matter.

RT Magazine reports the following:

A new evidence-based Clinical Practice Guideline (CPG) published in Respiratory Care found that evidence is lacking that proves pharmacologic agents routinely administered for airway clearance are effective in improving oxygenation and respiratory mechanics, reducing ventilator time and ICU stay, or resolving atelectasis.

The CPG is based on the work of an American Association for Respiratory Care (AARC) task force and Vanderbilt University researchers.

The following are the new recommendations regarding use of aerosols for

• The routine use of aerosolized acetylcysteine (Mucomyst) to improve airway clearance is not recommended in hospitalized adult and pediatric patients. 
• Aerosolized agents to change mucus biophysical properties or promote airway clearance are not recommended for adult or pediatric patients with neuromuscular disease, respiratory muscle weakness, or impaired cough.
• Mucolytics are not recommended to treat atelectasis in postoperative adult or pediatric patients, and the routine administration of bronchodilators to postoperative patients is not recommended. 
• There is no high-level evidence related to the use of bronchodilators, mucolytics, mucokinetics, and novel therapy to promote airway clearance in the studied populations. 

This is vindication, of sorts, to all of us RTs who have complained for years that this type of therapy rarely results in the desired benefits.  We'll have to wait and see if the medical profession eventually catches on to this new wisdom.  Using history as our guide, this will probably occur in the year 2035.

Further reading:

• RT Magazine: New CPG Questions Value of Aerosols for Airway Clearance
• RT Cave: Hypoxic Drive Theory: Reality or Hoax

Researchers discover cause of pulmonary fibrosis

Good news for five million people world wide diagnosed with idiopathic pulmonary fibrosis.  Researchers now believe they have discovered the cause of the condition, and this may lead to potential treatments and possibly even a cure.

What has been known is that repeated exposure to various substances -- such as an infection, drugs, or inhaled chemicals -- may irritate the interstitium, or tissue that lines and supports the alveolar air sacs, causing it to become inflamed, and then increasingly scarred and thickened.  This makes it so oxygen is unable to diffuse across alveoilar-capillary membranes.  This results in progressively worsening and irreversible dyspnea.

Pink = Chromosome
Green = Telomeres

So, while normal air sacs are very elastic like balloons, expanding and contracting with each breath, a thickened interstitium makes it so they become stiffer and less elastic, therefore less able to expand and contract with each breath.

At the present time treatment is generally supportive, such as oxygen therapy and anxiolytics.

Researchers now believe that the causative agents may cause damage to telomeres that are present in every cell in the human body. Telomeres are the caps of DNA that protect our chromosome, like the plastic tips on the ends of shoelaces.  They prevent the strands of DNA, and therefore the cell, from breaking apart.  When they do break apart this in essence speeds up the aging process.

The researchers discovered that some mice lacked a protein necessary to build telomeres in a specific cell population.  By studying these mice, they learned that they develop progressively worsening pulmonary fibrosis similar as to what occurs in the human population.

They also learned that lack of telomeres is lethal to type II alveolar cells, making it so epithelial cells cannot regenerate and cannot repair damage.  This results in the natural breakdown (aging) of the cells causing them to become inflamed, resulting in increased scarring and thickening (fibrosis).

While this was only one research project, it should give something to focus on with the hopes of coming up with some form of treatment for this condition that is more than just supportive.

Further reading:

• What is pulmonary fibrosis?

Things all respiratory therapists have in common

Things common among most respiratory therapists.

1.  Usually listen to lung sounds from bottom up, side to side, and without telling the patient to take a deep breath. Because...

2.  We know that when they take a deep breath you hear adventitious lung sounds that are not bronchospasm noises (such as rhonchi and crackles)

3.  We understand that bronchospasm wheezes are only heard upon auscultation.

4.  We understand that if a wheeze is audible it's not bronchospasm but secretions or fluid sitting over the vocal cords (or upper airway wheeze, or rhonchi)

5.  After we listen for bronchospasm wheezes (which are not present for 80% of the treatments we do) we have the patient take deep breaths so we can hear those hidden crackles that are so often missed by others.

6.  We generally develop an apathetic approach to our work

7.  We develop dry senses of humor.

8.  We think we know more than doctors about anything respiratory

9.  We think we know more than nurses about respiratory stuff

10.  We can tell the difference between pneumonia and heart failure from bronchospasm without even looking at the patient.

11.  We can solve all the problems in the hospital because we have been exposed to so much ventolin to obtain the increased wisdom that results from it; in essence, we know more than administrators, but most of us still don't want to be them (why not?)

Myth Buster: Exercise causes weight loss

I think I wrote about this before on this blog, that you can't lose weight just by exercising alone. I tried it last winter, and I actually ended up gaining weight.

You see ads galore trying to get you to buy one gadget or another to lose weight. They show you a picture of the gadget, and a picture of some guy with six pack abs and say, "This could be you if you buy this product."

The truth is, that person never lost weight using that product. If fact, he probably had that six pack long before the product was ever even invented.

Truth is, it doesn't matter what product you buy, you will not lose weight by exercising alone. You have to diet. Losing weight is a matter of ins and outs. If you take in less than what goes out of your body, you will naturally lose weight.

Yes, there are advantages to exercising. I've written about them too on this blog and my asthma blog. The benefits of exercise is overwhelming, and I highly recommend you do it.  Exercising strengthens your heart and lungs, improves your immune system and makes you feel better overall.

Yet exercise alone will not result in weight loss.  It may help you burn fat faster, but it will not cause you to lose weight if you do not also eat a healthy diet.

I've always believed this, yet trying to find proof in a world dominated by marketers, and a media, that is content to have you believe that exercise is the key to weight loss so they can brainwash you to buy their products is never easy.

However, I found an article at time.com called, " Why Exercise Won't Make You Thin," by John Cloud (Thursday, Aug. 06, 2009) that explains quite simply why exercise alone won't make you thin.

Cloud said that if exercise alone made people thin, the fact that the percentage of people exercising increased from 47% to 57% from 1980 to 2000 would result in a thinner society. Yet, the opposite is true, as America is fatter than ever before.

He said:

"The basic problem is that while it's true that exercise burns calories and that you must burn calories to lose weight, exercise has another effect: it can stimulate hunger. That causes us to eat more, which in turn can negate the weight-loss benefits we just accrued. Exercise, in other words, isn't necessarily helping us lose weight. It may even be making it harder."

He also mentions a study where 464 women were asked to maintain their normal diet. Most were told to exercise, while one group was told not to exercise.

The results:

"The findings were surprising. On average, the women in all the groups, even the control group, lost weight, but the women who exercised — sweating it out with a trainer several days a week for six months — did not lose significantly more weight than the control subjects did....Some of the women in each of the four groups actually gained weight, some more than 10 lb. each."

He said that a paper written by a group of psychologists explains why this happens:

"Many people assume that weight is mostly a matter of willpower — that we can learn both to exercise and to avoid muffins and Gatorade. A few of us can, but evolution did not build us to do this for very long. In 2000 the journal Psychological Bulletin published a paper by psychologists Mark Muraven and Roy Baumeister in which they observed that self-control is like a muscle: it weakens each day after you use it. If you force yourself to jog for an hour, your self-regulatory capacity is proportionately enfeebled. Rather than lunching on a salad, you'll be more likely to opt for pizza."

It is possible, Cloud concludes, that the recent trend to get people to exercise more has caused America to get fatter?

Originally published on 8/17/2009; edited

Further reading:

• Why exercise won't make you thin -- by John Cloud in Time
• Jogging may not be bad for joints
• Myth Buster: You must eat a breakfast to feel good 
• Exercise: The News You Don't Want to Hear -- Huffington Post

Ventilator Pressures: Static -vs- Plateau

With every ventilator check it is important to measure how much pressure is needed to deliver a tidal volume. There are two different pressures that we typically check: Peak Inspiratory Pressure (PIP), and Static Pressure, also known as plateau pressure (p-plat).

Now to define these two pressures:

• PIP:  This is the pressure at peak inspiration with flow.  
• p-plat:  This is the pressure at peak inspiration after holding your breath.  This is the measure of pressure without flow. 

The best way I can explain these two pressures is by having you take in a deep breath.  Take in a breath as deep as you can.  PIP is the pressure right at the end of inspiration.  Now, hold your breath and relax your chest while still holding your breath.  This is the pressure minus flow.  It is called static or plateau. 

These two pressures are important.  They should both be recorded with each ventilator check.  Now, here is how they can be used.

1.  To monitor resistance and compliance.  

• Both PIP and p-plat go up, or are trending up together, this is probably due to the fact that the patient's lungs are becoming stiff, or less compliant.  In this case, the static compliance may be decreasing.   Efforts should be made to keep the static compliance under 30, such as decreasing tital volume.  This is one reason why low tidal volume strategies are used on patients with ARDS. 
• PIP goes up and p-plat stays the same.  This indicates increased resistance.  It can be measured by taking PIP and subtracting p-plat = resistance.  It may indicate increased resistance, meaning the patient work of breathing (WOB) will be increased, or the patient has to work hard to obtain a desired tital volume.  There are three causes of this:
• Water in the circuit.  Solution is to empty this water (empty water traps)
• Secretions in airway.  Solution is to suction
• Bronchospasm.  Treatment is bronchodilator

Squiggly lines may indicate water in tubing or secretions in airway.

There is another simple method of observing if secretions or water in the circuit are the cause of increased resistance.  When this happens the you will probably observe squiggly lines on the graphics.  When the water is removed from the circuit, or after suctioning, the lines will be normal again.  

A rule of thumb is, if you see squiggly lines, check the circuit for water.  If that doesn't solve the problem, suction should be the next thing to try.  

A recheck of PIP and p-plat after resolving these problems SHOULD result in PIP decreasing, and thus lowering the resistance.  The patient should now be able to breathe easier, or work of breathing should be reduced.

2.  To determine readiness to wean.  Such as, if the patient is requireing more than resistance to obtain adequate ventilation, then the patient is not ready to wean.  Determine resistance by the formula PIP minus p-plat. This is one of the nice things about the servo ventilators, because they have volume support.  In this mode the patient determines his own PS and flow, and therefore you can see how much PS is needed to obtain a tidal volume.  When we want to see if a patient is ready to wean, we turn the patient into volume support.  If the support drawn in by the patient is greater than resistance, the patient is not ready to wean.

Example.  The patient is in assist control or pressure regulated volume support.  Check the PIP and p-plat. Use the formula: PIP minus p-plat = resistance.  PIP =15, P-plat = 10, resistance = 5.  Switch the patient to volume support.  If the pressure is using a PIP of 10, then you know this patient is requiring too much assistance to maintain an adequate tidal volume, and is not ready to wean.  If the patient is requiring only a PS or 5, then he is probably ready to wean.

However, determining readiness to wean involves more than just looking at numbers.

3.   To determine adequate pressure support (PS).  Frequently it occurs that a physician, or a therapist, just makes up a number for PS.  Yet the purpose of PS is to make up for resistance caused by the circuit and endotracheal tube, to make it so it doesn't feel to the patient that he is breathing through a straw.

• PIP minus p-plat = resistance of tubing, endotracheal tube, and airway.  
• Example.  PIP 20 and p-plat 15 = resistance of 5
• 5 should be more than what is needed to make up for the resistance of tubing and ETT, and should make ventilator breaths feel more like normal breathing.  
• Usually this number is somewhere around 5.  However, in patients with lung disease, it may be higher.
• If PS is set at lower than resistance, in this case 5, this results in increased WOB, and this can cause anxiety.  It may result in unnecessary sedation, and failure to wean. 

So, hopefully this information will help you better manage your ventilator patients.  If you find this useful, please let me know.  If you have more tips to add, please feel free to leave a comment below. 

This post was originally published on August 22, 2008 on respiratory therapy cave.  It was updated and edited for accuracy and simplicity by Rick Frea. 

Further reading:

• Medscape, Benjamin D. Singer, Basic Invasive Mechanical Ventilation
• Considerations for readiness to wean
• Acute Respiratory Distress Syndrome
• Respiratory Therapy Formulas and Normal Values

Healthcare: Quality -vs- Quantity

As an advertising student at Ferris State University, we learned about quality versus quantity.  We learned that you could reach a lot of customers a few times with your ads, or you can reach a few customers many times with your ads.  You cannot do both.  You can either have quantity or quality.

Justin Williams, in describing the dilemma of quality versus quantity in marketing, said that "In a perfect world, a brand sends the perfect number of perfectly composed emails to elicit the maximum response possible. In the real world, email marketers must balance between quantity and quality."

I think about this often as I'm doing my work as a respiratory therapist.  On some days I have only a few patients, and they get 100% of my attention all the time.  Sometimes I'm able to sit and talk to them, and this type of social interaction brings joy to both me and my patients.  Other times I can spend more time assessing my patients, resulting in them getting better care.  

On these days, when the emergency room calls, they have my undivided attention right away.  When a nurse or hospitalist needs my services, they have my undivided attention right away. This results in better patient care, better coworker satisfaction, and better satisfaction for myself too.  

On other days, however, I have many patients, and doctors are writing many orders.  On these days I'm hard pressed to get my work done in a timely manner.  I usually get it done, yet at the end of the day I'm often left wondering if I could have given better care.  I never feel satisfied at the end of these days.

On the other hand, some say that we as RTs accomplish more on the busy days, and therefore should feel good about ourselves.  It's being busy like this that results in us keeping our jobs and the hospital making money.  Yet what those people fail to see is that such busy days result in quantity at the expense of quality. You see, you can't have it both ways.  

I think of this when my coworkers complain when it's too busy.  I think of this when my RT friends online tell me how overwhelmed they feel at work.  I think of this when nurses complain that they have too many patients due to poor staffing.  

Keep in mind here that sacrificing quality for quantity is not all the hospitals fault, nor the physician's fault. For instance, it's not their fault, on certain days, weeks and months, every person with a chronic disease gets sick and requires the services of a hospital.  Technically speaking, there's no way to plan for these busy days.

An ongoing conundrum of the healthcare industry, as well as any other industry, is finding the perfect balance between quality and quantity.

Yet in healthcare, this is a time tested challenge that may never be overcome.  For instance, store managers can look at sales from April to May last year and plan for this year based on last year's sales.  It's not so easy to do in healthcare, mainly because it's impossible to know when people will get sick.  

To twist Justin William's words for our own purposes:  "In a perfect world, a hospital staffs the perfect number of perfectly performing physicians, nurses, and respiratory therapists to elicit the maximum care possible. In the real world, staffing is a balance between quantity and quality."

Here's what you need to know about the respiratory membrane

Once in the lungs, various elements effects oxygen's ability to cross the alveolar-capillary membrane, which is also known as the respiratory membrane. In my post "Diffusion of oxygen from air to tissues" I described how oxygen travels from the lungs to the tissues.

The ability of oxygen to cross the alveolar-capillary (respiratory) membrane depends on.

1. Rate of diffusion of oxygen across the respiratory membrane.  
2. Pulmonary Capillary Blood Volume or Flow 
3. Transit time
4. The ability of O2 to bind with Hemoglobin (Hgb)

1.  The rate of diffusion across the respiratory membrane is determined by.

• Thickness of the respiratory membrane (disease processes may damage it).  
• Normal thickness: 0.4-0.6 micrograms (sometimes as low as 0-.2 micrograms)
• Pulmonary edema, fibrosis, deposition of substances, may increase thickness
• Surface area of the respiratory membrane 
• Total capillary-alveolar surface area in normal, healthy person is 70 square meters.  
• There are over 300 million alveoli
• There is usually about 60-140 ml of blood in pulmonary capillaries
• This allows for plenty of surface area for oxygen to diffuse from alveoli to capillaries.
• Diseases like emphysema greatly reduce surface area for gas exchange to occur.
• The diffusion coefficient of gases (oxygen)
• This is essentially how soluble is the gas in water, as it has to go from alveolar air to capillary blood, a solution. 
• Solubility coefficient = concentration of dissolved gas + partial pressure (no need to memorize this)
• CO2 is 20 times more soluble than Oxygen, so CO2 diffuses 20 times more rapidly across the respiratory membrane as oxygen does.  
• The difference between alveoli (PAO2) and capillary (PcO2).  PAO2 is 104, and venous blood is 40.  This results in a pressure gradient of 64 mm Hg. 

2.  Pulmonary Capillary Blood Volume or Flow is determined by.

• Capacity of blood, especially red blood cells
• Polycythemia: Oxygen diffuses at a higher rate
• Anemia: Oxygen diffuses at a lower rate

3.  Transit Time is determined by. 

• Determined by dividing pulmonary capillary blood volume by cardiac output.  
• Normal Transit Time: 70 ml divided by 5,000 = 0.8 seconds
• This is the time available for diffusion to occur. 
• Most diffusion occurs in first 0.3 seconds of Transit Time
• This leaves 0.5 seconds, providing a large safety margin.  This explains why adequate oxygenation can still occur when a person is exercising, even thought the transit time is reduced to 2/3 of normal, or 0.1 seconds. 

4.  Capacity of binding of Oxygen with Hemoglobin is determined by.

• This is a discussion for another day, and we will not go there.

Normal Arterial Oxygen Tension can be calculated. 

• A-a Gradient:  PAO2 - PaO2
• 104-97 = 7 mm Hg
• Normal is below 15 mm Hg
• Normal range is 5-25
• Upper range may increase with age to 20 or even 30
• The following formula allows you to determine A-a Gradient adjusted for age.
• PaO2 = 102 - Age/3
• Depends on.
• Ventilation (V) 
• Perfusion (Q) 
• Shunt (Mixed venous blood)
• Is the main cause of hypoxemia (drop in PaO2) and hypercapnea (increase in PaCO2)
• V/Q Mismatching:  Oxygen is inhaled but cannot get to the blood in certain areas of the lungs.  
• Shunt: Blood doesn't come into contact with alveoli, blood is shunted away from alveoli.  No gas exchange occurs.  
• True Shunt (anatomical). Natural shunts that purposefully bypass the lungs, such as the shunt noted above whereby unoxygenated blood from bronchial veins is shunted to the pulmonary artery. 
• False Shunt (physiological).  This is where blood is supposed to come into contact with an alveoli, but this cannot happen due to a disease process.
• The best indicator of a shunt is PaO2.  This is because a small reduction in O2 results in a large reduction in PaO2 (about 7 mm Hg).  A small increase in CO2 results in a small increase in PaCO2 (less than 1 mm Hg)
• Up to the presence of a 50% shunt, Increases in FiO2 will have no effect on PaO2

Why is a normal SpO2 98%?

Question:  Why is a normal oxygen saturation 98% and not 100%?

Answer:  After the diffusion of oxygen from the alveoli to the capillary occurs, this oxygenated blood moves to the pulmonary vein to the left atrium.  This blood contains a PaO2 of 104, on average.  This blood constitutes 98% of cardiac output.  Another 2% of the cardiac output comes from the bronchial veins, and this blood has a PaO2 of 40.  This unoxygenated blood is shunted into the pulmonary vein, and mixes with arterial blood.  It is because of this natural shunt that a normal saturation is 98% and not 100%.

Diffusion of oxygen from air to tissues

Today we're going to take a molecule of oxygen, and show how it travels from the air inhaled, through the lungs, the blood and then to the tissues.  Then we'll do the same for carbon dioxide, showing how it travels from the tissues to the lungs to be exhaled.

Basically, it must be understood that a gas travels from areas of high pressure gradient to areas of lower pressure gradient.  There are a couple laws of physics to help explain how this is possible.

Please note that all the numbers and percentages in this post are either estimates or averages.

Fick's First Law of Diffusion.  The rate of oxygen diffusion is proportionate to the concentration difference of oxygen and the surface area.  In other words, it travels from areas of high pressure to areas of lower pressure.  This explains how oxygen travels through tissues.

Henry's Law.  Gases dissolve in liquids in proportion to their partial pressures, depending also on how soluble they are in specific fluids and on the temperature.  This is important because most oxygen inside the body is stored in fluid, such as blood.  Inside the nose it is hunidified, and the alveoli are saturated with water vapor which has its own partial pressure.  

Total Pressure.  This is the tension given off by a molecule of a gas if it were to be confined inside a container.  The pressure is caused by movement of the molecules, and the pressure or tension they cause by constantly impacting the surface of the container.  The total pressure of a gas is summed up by the total pressure of all the molecules contained in it.

Partial Pressure.  This is the pressure exerted by a single gas component in a mixture.  It is the pressure of an individual gas of a mixture.

Dalton's Law.  The total pressure of a mixture of gases equals the sum of the partial pressures of the individual gases in that mixture. 

Room Air.  Contains about 79% nitrogen and 21% oxygen (There are other gases in the air, although they will be omitted here for to make this easier to understand).  Usually, 21% is generally designated as the Fraction of Inspired Oxygen in Room Air.  

Total Pressure of Atmospheric Air as sea level:  760 mmHg

• Partial Pressure of Nitrogen (PN2) in room air:   600 mmHg
• Partial Pressure of Oxygen (PO2) in room air:  160 mmHg

These pressures may vary depending on the temperature, humidity, and atmospheric pressure. 

Diffusion:  Pressure moves, diffuses, from areas of higher pressure to lower pressure.  So, by the natural process of respiration, air is inhaled.  It is humidified and warmed to body temperature by the nasal passages.  

• PNO2 after humidified and heated to normal body temperature (37°C): 564 mmHg
• PO2 after humidified and heated to normal body temperature (37°C):  149 mmHg

It then makes it's way though air passages to the alveoli.  

Partial Pressure of Alveolar Oxygen.  Designated as PAO2 = 104 mm Hg.  

This may be estimated by FiO2 * 5 (21% * 5 = 105).  There are other more accurate formulas, although this one is the simplest to perform in the clinical setting.  Remember that it is just an estimate using numbers that are rounded off for simplicity purposes. 

PAO2 may also be lowered due to disease processes.  As the formula suggests, the PAO2 may be higher when higher concentrations of oxygen are inhaled (or FiO2 from 22% to100%).  Likewise, less oxygen may be inhaled when breathing is relaxed while sleeping.  Less oxygen may also be inhaled due to lung disease, causing the PAO2 to become lowered.  (This may be reflected by a measure of PaO2 -- see below -- as obtained from an arterial blood gas)

Again, oxygen, unlike CO2, requires a high pressure gradient to diffuse.  

Partial pressure of capillary venous blood (PvO2) is 40

So oxygen moves from the alveoli, across the respiratory membrane, to the capillary blood because of the pressure difference:

• 104-40 = 64 mmHg pressure difference. 

This pressure difference, or pressure gradient, is perfect for oxygen diffusion to occur from the alveoli to the capillary system.  So, oxygen molecules are released from the alveoli (PAO2 104) into the venous capillary system (PvO2 O2 40).

Inside the venous side of the capillary system is reduced hemoglobin.  This is hemoglobin that does not carry an oxygen molecule.  Since it carries no oxygen molecule, it is said to have a high affinity for oxygen. Because of this, almost as soon as oxygen enters the capillary plasma, it joins with a hemoglobin molecule. This immediately turns the capillary blood into arterial blood.

Partial pressure of arterial blood (PaO2) is 104

In the capillary system the PO2 quickly rises as more and more oxygen molecules enter the plasma.  The blood now moves pulmonary vein and then to the left atrium.  By this time, the accumulation of oxygen in the arterial system has caused a build-up of tension that causes the partial pressure of oxygen to rise to 104, the same as it was in the Alveoli.

Keep in mind that hemoglobin molecules have no impact on the partial pressure of oxygen.  This means that the PaO2, as measured by an arterial blood gas (ABG), should be about 104 (estimated to be a normal of 80-100).

Freshly oxygenated hemoglobin constitutes about 98% of cardiac output.  Another 2% of the cardiac output comes from the bronchial veins, and this blood has a PvO2 of 40.  This unoxygenated blood is shunted into the pulmonary vein, and mixes with arterial blood.  It is because of this natural shunt that a normal hemoglobin saturation is 98% and not 100%.  This in turn brings the PO2 of left ventricle down to 97 mmHg.

The saturation of arterial hemoglobin (SaO2), as measured by ABG, is normally about 98%.  The saturation of arterial hemoglocin, as measured by pulse oximeter (SpO2) is also about.

The PO2 of the left atrium:  97 mmHg

The heart contracts, and sends oxygenated blood through the arterial system.

Partial Pressure of Arterial Oxygen.  Designated as PaO2.

Because of normal variations in PAO2 (as explained above), the PaO2 may likewise vary.  So, that said, the following is generally considered as true of PaO2. 

• Normal: 80-100
• Hypoxemia:  60-80
• Severe Hypoxemia:  40-60

So now, the oxygen molecule is attached to a hemoglobin molecule.  Hemoglobin now has a low affinity for oxygen.  It rides the bloodstream until it finds a cell that has a low enough PO2 for it to diffuse into that cell.  The cell then has a higher affinity for oxygen than the hemoglobin molecule, and so oxygen is released into the cell tissue. Here the oxygen molecule is used to create energy.

Partial Pressure of Tissue Oxygen.  

• Varies from tissue to tissue
• Some tissues have a PO2  of 22-35
• The PO2 varies in different areas of a cell

Once oxygen leaves the arterial system, this leaves the hemoglobin in venous blood without oxygen. This blood then returns to the lungs via the venous system to get some more oxygen. 

Partial Pressure of Venous Oxygen. Designated as PvO2, is 40.

Now the system starts all over again.  However, if we determine that the patient has a disease process that causes hypoxemia (defined as PaO2 less than 60), and the patient is given a higher FiO2 than what is in room air (22% to 100%), the rate of diffusion of oxygen from the lungs to the tissues will increase.

Once in the cell, the oxygen is quickly absorbed into the mitochondria and is used as part of cellular respiration.  Energy is the byproduct, and this allows the cell do perform its work.  A wasteproduct is Carbon Dioxide (CO2)

About 200 ml of CO2 is produced by each cell per minute. This CO2 has to be quickly eliminated from to prevent acidosis.  CO2 is 20 times more soluble than oxygen, and therefore diffuses quickly. Likewise, while oxygen requires a high pressure gradient to diffuse, CO2 requires only a small pressure gradient.

Partial Pressure of  Venous Carbon Dioxide (PvCO2):  46 mm Hg

Partial Pressure of Alveolar Carbon Dioxide (PACO2): 40 mmHg

Partial Pressure of Arterial Carbon Dioxide (PaCO2):  40 mmHg

Partial Pressure of Room Air Carbon Dioxide:  0.2

So even while the pressure gradient between the venous system and alveoli is only 6, this is enough for CO2 to diffuse through the system.

Therefore, under normal conditions, CO2 is easily diffused through the body, and exhaled.  Oxygen is inhaled and easily diffuses through the body to the cells.  Of course, effecting these are atmospheric variations like humidity and temperature, disease processes like COPD, and aging.

References and further reading.

• Oxyhemoglobin Dissociation Curve Made Easy
• Textbook of Anesthesia for Postgraduates, edited by T.K. Agasti, pages 43-48
• Cardiovascular Physiology Concepts, By Richard Klabunde, pages 182-183
• Respiratory Therapy Formulas