Does Room Air Oxygen Cause Lung Cancer?

Your Question: You mentioned in your post "What is oxidative stress?" that inside the body oxygen breaks down into single molecules with unpaired electrons. They in turn become free radicals. Surely these free radicals can be neutralized with antioxidants. But you wrote that oxidative stress may cause lung cancer. So, does oxygen itself cause lung cancer?

My answer. To answer your question, under normal circumstances, oxygen by itself does not cause cancer. As it turns into free radicals, there are plenty of antioxidants available to neutralize it. So, under normal circumstances, the 21% oxygen in room air will not increase your risk for developing oxidative stress nor increase your risk for lung cancer.

However, inhaling supplemental oxygen can increase your risk of overwhelming antioxidants. In these situations, the risk of oxidative stress is increased along with the cancer risk. Things that might cause oxidative stress like this are abnormal circumstances, such as inhaling supplemental oxygen long-term or inhaling high doses of oxygen short-term. Certain disease processes (such as COPD) can cause it. Aging may change your internal environment in such a way as to cause oxidative stress.

So, to answer your question, inhaling room air oxygen should not increase your risk for developing cancer. And, I would surmise, as more is learned on this, only people with certain genetic predispositions at risk for developing cancers even in the presence of oxidative stress. So, there is so little known about this at the present time. It will be neat to see what researchers learn in the coming years.

References.

1. Reuter, et al., "Oxidative stress, inflammation, cancer: How are they linked?" Free Radical Biology & Medicine, 2011, December 1, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990475/, accessed 8/19/19

Oxidative Stress: How Asthma, COPD, Oxygen May Increase Lung Cancer Risk

There is some evidence linking supplemental oxygen with certain cancers. So, is it true that supplemental oxygen may cause cancer? Why might this happen? Let's investigate the evidence.

In 2002, we wrote how high concentrations of oxygen were linked with cancer. That article noted that inhalation of an FiO2 of 100% for three hours increased the risk for developing cancer later in life. The reason was due to oxidative stress.

In a future post I want to investigate oxidative stress. What exactly does this do to the body? What causes it? What does it actually involve? How might it lead to cancer? So, that's a future investigation we will undertake.

For now, all you need to know is that oxygen, once it gets inside your body, splits into unpaired electrons. When a molecule has an unpaired electrons it is said to be unstable. It is referred to as a free radical. Free radicals will steal an electron from other molecules.

Under ideal circumstances, it steals an electron from an antioxidant. These are substances inside our body's meant to neutralize free radicals by donating an electron. Antioxidants can be ingested by eating certain foods, such as those containing vitamin C and E.

Sometimes, however, your body becomes overwhelmed with free radicals. There are certain disease processes that can cause this. Certain drugs can cause this, and one example is supplemental oxygen. In this case, your body becomes so overwhelmed with free radicals that they overwhelm antioxidants.

In excess, free radicals steal electrons from cells. So the cell now becomes unstable. It then it in turn steals an electron from a nearby cell. This creates a chain reaction of sorts. And this is what is referred to as oxidative stress. Cells become stressed. When this happens they release a substance called Reactive Oxygen Species (ROS). This triggers an immune response.

And, when this happens, they release chemicals such as cytokines and chemokines. These are your proinflammatory chemicals. They warn your immune system that something is wrong. And your immune cells release more cytokines and chemokines. These chemicals are helpful when you are exposed to bacteria and viruses. But, in excess, they can also be damaging to cells.

Other things that can cauuse oxidative stress like this are exposure to allergens and exposure to toxic chemicals in cigarette and wood smoke. This may explain how airways of asthmatics and COPD patients become chronically inflamed. So, it can explain many disease processes. And this includes cancers.

Oxidative stress may cause chronic inflammation. This may be what causes inflammatory diseases, such as asthma, COPD, diabetes, cardiovascular disease, and neurological diseases. And, as noted, it may also explain the links between some of these diseases and various cancers.

Under prolonged stress like this, oxidative stress is prolonged. So you end up with lots of ROS and similar substances roaming around. They can also cause gene mutations. Some of these mutations may cause the gene to produce harmful substances that may begin the cancer process.

This may explain the link between COPD and lung cancer. It actually might explain links between asthma and lung cancer. Studies show asthmatics are 2-6 times more likely to develop lung cancer than non-asthmatics. So, this may explain this link.

This is all very complex. There are very long and almost inexplicable articles on this stuff. But, my goal is to make it easy to understand. So, just keep in mind there is a lot more involved here than what I explain.

So, this may explain how long-term oxygen therapy, while relatively safe, is not without potential long-term side effects. It may also explain how those high doses of oxygen, even for short terms, may cause cancers later in life.
References.

1. Van Eaden, Stephan F., “Oxidative stress in chronic obstructive pulmonary disease: A lung and systemic process,” Canadian Respiratory Journal, Jan-Feb, 2013, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628643/, accessed 5/28/17
2. Mandal, Anaya, “What is oxidative stress?”, News Medical Life Sciences, http://www.news-medical.net/health/What-is-Oxidative-Stress.aspx, accessed 5/28/17
3. CHSS Emory University, “What is oxidative stress,” Youtube.com. https://www.youtube.com/watch?v=9r07MhA_S9E, accessed 5/28/17
4. Kacmarek, Robert M., James K. Stoller, Albert J. Heuer, editors, “Egan’s Fundamentals of Respiratory Care,” 10th edition, 2013, Elsevier, pages 913
5. Domej, et al., “Oxidative stress and free radicals in COPD – implications and relevance for treatment,” International Journal of Chronic Obstructive Pulmonary Disease, 2014, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207545/, accessed 5/29/17
6. "What happens in your body during oxidative stress?" HealthOlution. Youtube.com, https://www.youtube.com/watch?v=p1PEWZRHylo&t=15s, accessed 5/28/17
7. Parichha, Arpan, "Reactive oxygen species and oxidative stress," Youtube.com, https://www.youtube.com/watch?v=IhvyFBecgAY, accessed 5/2917
8. Nele, Cielen, Karen Maes, Ghislaine Gayen-Ramirez, "Musculoskeletal Disorders in Chronic Obstructive Pulmonary Disease," Biomed Research International, 2014, https://www.hindawi.com/journals/bmri/2014/965764/, 5/31/17
9. Eldridge, Lynne, "Does Asthma Increase The Risk Of Lung Cancer?" verywell health, 2017, June 19, https://www.verywellhealth.com/does-asthma-raise-the-risk-of-lung-cancer-2248983, accessed 8/19/19
10. Reuter, et al., "Oxidative stress, inflammation, cancer: How are they linked?" Free Radical Biology & Medicine, 2011, December 1, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990475/, accessed 8/19/19

Investigating High Flow Oxygen For Pneumothorax

Depiction of high flow nasal cannula.
Image taken from Google Images. 

We respiratory therapists are often skeptical. Recently, many doctors are prescribing high flow nasal cannula's (HFNC) for pneumothoraces. A common question is: Does this treatment do any good? Let's investigate.

What is a pneumothorax?

As we all know (or should know), a pneumothorax is a collapsed lung. It's when air seeps into the the space between the lungs and chest wall. It is air that seeps into the pleural space. This air pushes on the lungs to make them collapse. An entire lobe may collapse or just a small portion of it.^1-2

A small pneumothorax may cause no symptoms. It may resolve on it's own. A larger pneumothorax may cause symptoms. These include low oxygen levels and shortness of breath. They may also include sharp chest pains, rapid breathing, and rapid heart rate. 

They are either spontaneous or iatrogenic. 

• Spontaneous (Primary). This means they occur in otherwise healthy individuals.  The cause usually remains inexplicable. Those most likely to develop them are of the tall and lean type. Others at risk may include smoking tobacco or marijuana. 
• Iatrogenic (Secondary). This means they are secondary to treatment for a disease process. A good example here is secondary to a thorocentesis. The doctor inserts the needle too far and it pierces the lungs. Severe asthma, sarcoidosis, cystic fibrosis, pulmonary fibrosis, and emphysema are also potential secondary causes. Another cause may be barotrauma due to using high pressures during mechanical ventilation  ^2-4

How do they resolve?

They resolve as air is reabsorbed into nearby tissues. A small pneumothorax may cause no symptoms. These may also resolve on their own. Treatment here is observation. 

A larger pneumothorax may cause some symptoms. In these cases some treatment is probably needed. What to do is dependent on what guidelines you are referring to. Some recommend a needle aspiration to relieve the pneumo. Others recommend insertion of a chest tube. I think here in the U.S. a chest tube is recommended. ³

Oxygen also seems to help. A study in 1983 showed that higher oxygen levels increased the speed of pneumothorax resolution. Previous studies had patients inhaling room air. So, those study results were already known to the researchers. So, their goal was to see if higher oxygen concentrations (i.e. greater than 28%) improved the speed of pneumothorax resolution. ¹

Here's what the researchers reported: 

"6 patients with pneumothoraces of less than 30% showed a mean resolution rate of 4.2% per day with reduction to one-third original size in the first 72 h. This was more than three times the rate of resolution (1.25% per day) previously reported with breathing room air alone. In 2 patients who initially received a lower concentration of inspired oxygen via nasal cannula, the rate of absorption increased after placing them on a partial rebreathing mask." ¹

They concluded that high flow oxygen speeds up the pneumothorax resolution process. The theory is that oxygen washes out alveolar nitrogen. This in turn lowers the partial pressure of nitrogen. This is good because nitrogen slows absorption of air. So, it's not so much the oxygen that speeds up re absorption, it's the lowered partial pressure of nitrogen that speeds it up. 

At least that's the theory.

Is this theory credible?

This theory seems credible. It was during the 1960s that it was suspected. This was when it was learned that the partial pressure in the capillaries and venous system was the same as atmospheric pressure. However, this changed when 100% oxygen was administered.

With 100% oxygen nitrogen is washed out of alveoli. In the 1960s, it was observed that this effect causes a drop in the partial pressure of alveolar nitrogen from 573 to zero. This is a result of the partial pressure of arterial oxygen increasing from 100 to 640 mmHg. This in effect causes a change in the partial pressure of alveolar oxygen. This in turn changes the partial pressure of oxygen in capillaries.⁵

While inhaling room air, the partial pressure of capillary oxygen is It's 706 mmHg. While inhaling 100% oxygen, this decreases to 146 mmHg. This is important, as the flow of air travels to areas of higher pressure to lower pressures. So, this change in pressure causes an increased rate of reabsorption of air from the pleural space.⁵

What are the risks?

The potential risks always have to be weighed against potential benefits. Potential benefits in the case of pneumothorax is recovery. Although, one might speculate this would happen with or without high flow oxygen. Still, high flow oxygen speeds up the process. So, this is definitely a benefit. 

One study showed that wearing a nonrebreather for as little as three hours increased the risk for developing certain cancers. More recent studies link long-term low flow supplemental oxygen use with lung cancer. A common theory explaining this phenomenon is oxidative stress.^6-8 

Another risk is hypercarbia. John Haldane (1860-1936) described how oxygen has a higher affinity for hemoglobin than carbon dioxide. So, inhaling 100% FiO2 causes lots of oxygen molecules to enter arterial blood. These oxygen molecules push carbon dioxide off hemoglobin. These carbon dioxide molecules increase the partial pressure of arterial blood. This effect can be toxic to some people with COPD. This theory makes more sense than the hypoxic drive hoax.

So, these are two risks worthy of consideration.

What to make of this?

There is ample evidence supporting oxygen use for treating pneumothorax patients. The goal is to exceed 28% FiO2, although higher FiO2s seem to prove beneficial for these patients. I have yet to see any studies of HFNCs for these patients. So, at the present time, it's my conclusion that HFNCs are recommended mainly due to patient comfort. They allow delivery of high oxygen levels without having to wear an uncomfortable mask. If you are aware of any such studies please let me know in the comments below. As we learn more we will be sure to keep you posted. 

References.

1. Chadha T.S., Chon M.A., "Noninvasive Treatment of Pneumothorax with Oxygen Inhalation," Respiration, 1983, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600088/, accessed 8/18/19
2. Currie, et al, "Pneumothorax: An Update," Postgraduate medical Journal, 2007, July, https://www.mayoclinic.org/diseases-conditions/pneumothorax/symptoms-causes/syc-20350367, accessed 8/18/19
3.  Choi, Won-II, "Pneumothorax," Tuberculosis And Respiratory Disease (Seoul), 2014, March, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982243/, accessed 8/18/19
4. Johnson, Jon, "Pneumothorax: Causes, Symptoms, And Treatment," 2017, June, https://www.medicalnewstoday.com/articles/318110.php, accessed 8/18/19
5. Northfield, T.C., "Oxygen Therapy for Spontaneous Pneumothorax," British Medical Journal, 1971, https://pdfs.semanticscholar.org/48ec/cf2353788a28b02355a31a23844a298cf618.pdf, accessed 8/18/19
6. Garcia, et al., "Lung Cancer in COPD patients on Home Oxygen Therapy, European Respiratory Journal, 2016, https://erj.ersjournals.com/content/48/suppl_60/PA2794, accessed 8/18/19
7. Valavanidis, et al., "Pulmonary oxidative stress, inflammation and cancer: respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms," International Journal of Environmental Research and Public Health, 2013, August 27, https://www.ncbi.nlm.nih.gov/pubmed/23985773, accessed 8/18/19
8. "Can Inhaled Oxygen Cause Cancer," Science Daily, 2015, January 13, https://www.sciencedaily.com/releases/2015/01/150113090550.htm, accessed 8/18/19

Does your patient need and qualify for oxygen therapy

The following was originally published on April 15, 2015 at healthcentral.com/copd.

Do you need oxygen therapy? 

Sometimes people with COPD need to inhale more oxygen than what is provided in the air. The way this is accomplished is by using oxygen therapy. So what is oxygen therapy, and do you need it?

Oxygen in room air contains 21 percent oxygen. Usually this is plenty of oxygen. However, certain disease conditions, such as what may occur as COPD progresses, or during COPD flare-ups, may create areas inside your lungs where oxygen is inhaled, but cannot get to your bloodstream. When enough of these areas exist, your blood oxygen levels may decline.

To learn more about oxygen and oxygen levels, please read my post “Understanding Oxygen and Oxygen Levels with COPD.”

What is oxygen therapy? It involves inhaling supplemental oxygen, or oxygen percentages that are greater than 21 percent. It allows you to inhale 22-100 percent oxygen, depending on the device used.

Nasal Cannula. This involves inserting prongs into your nose. A low flow allows you to inhale anywhere from 22-44 percent oxygen. This is all that is needed for most people with COPD. It is very comfortable and tolerable.

Masks. A variety of masks can used to provide up to 100 percent oxygen. These are not used very often, but are available if needed.

To learn more about oxygen devices read my post “Oxygen Therapy Made Easy.”

There are three ways of getting oxygen therapy into your home.

1. Compressed Oxygen Gas Cylinders. These are tanks with regulators and flowmeters. Some are larger and stay at your home, and some are smaller for travel. 
2. Liquid Oxygen. They hold more oxygen and are smaller and more lightweight, making them ideal for people who are constantly on the move.
3. Oxygen Concentrators. They are electronic devices about the size of end tables that make oxygen by concentrating oxygen from room air. These are nice because, so long as you have electricity, you always have a source of supplemental oxygen. 

These are described in more detail in the post “The Three Types of Oxygen Therapy for COPD.”

Most people who require oxygen therapy will use oxygen concentrators at home, and have a variety of tanks as a backup in case of a power outage, and also for travel.

Do you need oxygen therapy? If your oxygen levels are chronically low, this puts strain on your body that can shorten your lifespan. That said, supplemental oxygen is the only drug proven to prolong life.

Common signs and symptoms of low blood oxygen levels (hypoxemia) are.

• Bluish tinge to your fingertips, toes and lips
• Rapid heartbeat
• Sweating
• Confusion
• Feeling winded, especially with exertion

If you, or a loved one, observes these signs, you should seek medical attention immediately. Your doctor may at first treat your COPD flare-up. Once you are deemed to be in a “chronic stable state,” your doctor may qualify you for oxygen therapy.

Do you qualify for home oxygen therapy? The qualifications for home oxygen are set by the Centers for Medicare and Medicaid Services (CMS), and they prefer numbers over subjective signs and symptoms. So qualifying is determined by the following test results:

• Arterial Blood Gas: Your PO2 is at or below 55
• Pulse Oximetry: Your SpO2 is at or below 88 percent

The basic premise goes like this: you qualify for oxygen therapy if your:

• PO2 is 55 or less or your SpO2 is 88 percent or less at rest while breathing room air.
• PO2 is 55 or less or your SpO2 is 88 percent or less while you are sleeping; or, if your PO2 drops 10 percent or more, or your SpO2 drops 5 percent or more, while you are sleeping, and you are also displaying symptoms of hypoxemia. 
• PO2 is 55 or less or your SpO2 is 88 percent or less while you are exercising.

How much oxygen do you need? The goal of oxygen therhapy is to provide you with the least amount of supplemental oxygen to maintain an SpO2 at 90 percent or greater. Usually, a low flow of 2-3 LPM using a nasal cannula works great. And, considering the benefits, most people tolerate it very well.

Further Reading:

• Understanding Oxygen and Oxygen Levels with COPD
• The Natural Progression of COPD
• The Three Types of Oxygen Therapy for COPD
• Oxygen Therapy Made Easy
• How to qualify for home oxygen therapy
• What are blood gases
• Pulse Oximetry Monitoring -- Do You Need It?: 

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

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

Myth Buster: A high FiO2 is protective

So you have a patient come into the emergency room in severe respiratory distress, possibly heart failure, but the SpO2 is normal. In the past it was acceptable to place these patients on a nonrebreather to prevent the patients condition from deteriorating, thus allowing you time to react. This, however, may no longer be acceptable.

I think doctors have gotten much better at not panicking in this regard, as even patients with heart failure, while the used to always get a nonrebreather, that seems to no longer be the case. As with chest pain and any other condition, no oxygen is given unless the SpO2 drops below 94%.

The reasoning for the change was described in an October, 2013, article in Respiratory Care, by Thomas Blakeman.  He said:

According to Downs, the only true indication for prophylactic hyperoxyxgenation is prior to tracheal intubation. Downs furher states that, hypothetically, a patient on FiO2 of 100% and having a PaO2 of 650 m Hg, could drop to 90 mm Hg due to lung function deterioration over a period of 15-20 minutes, but the SpO2 would not drop below 98%. This drop would not be enough to indicate a problem. But over the next 5 minutes the SpO2 wold drop to 92%, alerting the caregiver to investigate. In this scenario the elapsed time until a problem is detected would be 20-25 minutes. If that same patient was on an FiO2 of 30% with a PaO2 of 90 mm Hg and an SpO2 of 99% and experienced the same problem, the SpO2 would decrease to 94% within 10 minutes, alerting caregivers to a problem much earlier. Additionally, if a patient is already receiving FiO2 of 100%, there is no room to increase once a problem is detected."

So, over-oxygenating, a common occurrence in hospitals, may mask an underlying problem, delaying treatment.

References:

1. Blakeman, Thomas C., "Evidence for Oxygen in the Hospitalized Patient: Is more Really the Enemy of Good," Respiratory Care, October, 2013, volume 58, number 10, pages 1679-1693

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Myth Buster: FiO2 less than 60% is safe

One of the myths of respiratory therapy is if we get the FiO2 down to 60% we are safe.  In fact, most of us were taught in school that an FiO2 greater than 60% produced more side effects than an FiO2 less than 60%.

This apparently is a myth, and the following is the evidence:

1. Register et al conducted a study with subjects under going open heart surgery, all of whom were breathing room air preoperatively  It was found that in subjects administered FiO2s of 0.50 postoperatively had a greater degree of hypoxemia on room air on postoperative day 2 than those given sufficient oygen to maintain SpO2 (greater than) 90%.  After repeating the study using only room air intra- and post-operatively, and finding that most subjects did not have a decrease in blood oxygen levels, as compared to preoperative values, it was postulated that the hypoxemia experienced in the first study was due to the use of oxygen during and after surgery.

1. Garner et al exposed rats with peritonitis to FiO2 of 0.80, 0.4, or 0.21. Mortality was lowest in the FiO2 O.21 group, and highest in the Fio2 0.80 group.  Upon postmortem examination it was found that lung pathology did not differ between the groups but there was substantial liver damage with FiO2 (greater than) 0.21.  It was postulated that free radical formation caused the liver damage. 

This is yet another example that oxygen should not be administered unless necessary, and that every effort should be made to reduce oxygen as soon as possible.  Thankfully, most hospital oxygen protocols call for maintaining an SpO2 of somewhere in the range of 88-94%.  

References:

1. Blakeman, Thomas C., "Evidence for Oxygen in the Hospitalized Patient: Is more Really the Enemy of Good," Respiratory Care, October, 2013, volume 58, number 10, pages 1679-1693

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Myth Buster: Routine use of oxygen is safe

There is now ample evidence that oxygen is a drug with side effects.  No longer should health care providers administer oxygen under the philosophy "it may not help, but it won't hurt."

Oxygen used to be considered useful, or at least harmless, for any of the following situations, despite lack of evidence it does any good:

• Emergency departments
• Post-anasthesia care units
• Conscious sedation
• Chest pain
• Shortness of breath
• Critical Care Units

ACLS used to recommend 2-4lpm by nasal cannula for chest pain. The idea here is that if a low flow of oxygen to the heart is causing the chest pain, the oxygen "might" help.  

However, there was never any science to show this.  Plus, it makes no sense, because if you are getting an SpO2 reading of 98%, then you know the heart has an ample amount of oxygen.  If it's not getting enough oxygen it's because of a blockage in the coronary arteries, not the supply of oxygen to the heart. 

ACLS currently recommends oxygen only if the SpO2 is less than 94%.  This makes much more sense to me.  

Plus, most hospital-wide oxygenation protocols call for an SpO2 of 90-94%, and even 88% is often acceptable.  This makes sense particularly if you look at the deoxyhemoglobin curve.  

One of the main reasons why it's important not to oxygenate until the SpO2 decreases is that the use of supplemental may mask that an underlying problem may be occurring.  

A patient may have decreased ventilations, but this will not be recognized because the SpO2 is already artificially maintained with supplemental oxygen.  When such a patient is not on oxygen, a dip in SpO2 would be noticed at a routine check, and oxygen could be administered at this time, with appropriate measures being taken to recognize and resolve the underlying cause. 

The new policies make sense, especially when you consider that oxygen is a drug with side effects and an expense. To oxygenate based on a myth that it will help but won't hurt is not good medicine. 

References:

1. Blakeman, Thomas C., "Evidence for Oxygen in the Hospitalized Patient: Is more Really the Enemy of Good," Respiratory Care, October, 2013, volume 58, number 10, pages 1679-1693

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What is a normal oxygen percentage in the blood?

Pocket size pulse oximeter

Your question:  What is the normal percentage of oxygen in the blood?

My humble answer:  I believe you are referring to pulse oximetry, or spo2.  Your blood has many red blood cells (RBC), and each RBC has a hemoglobin molecule.  After passing through the lungs, an oxygen molecule binds with a hemoglobin molecule.  So, an spo2 gives a percentage of hemoglobin molecules (in arterial blood) that are carrying an oxygen molecule.  A normal percentage is 98%.  However, anything over 90% is acceptable.  As we age, sleep, and with various disease conditions it's normal for this percentage to decrease.  Pulse oximetry is now considered the 5th vital sign after blood pressure, heart rate, respiratory rate and temperature.

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Adult Oxygen Therapy Made Easy

If a patient is unable to oxygenate appropriately on room air, supplemental oxygen may be indicated. This Course should provide you with the wisdom you need to determine what oxygen device to use (if any) and how much oxygen to give to your patient.

First we need some basic definitions:

Supplemental oxygen: Any device that provides more oxygen than what one would get breathing room air.

PaO2: This is the level of oxygen in the blood.  It’s obtained by invasive Arterial Blood Gas (ABG).

• Normal:  80-100
• Mild Hypoxemia:  60-79
• Moderate Hypoxemia: 40-59
• Severe Hypoxemia: 39 or less

SpO2: It's a measure of how saturated hemoglobin are with oxygen.

• Normal: 95-98%
• Accepetable: 90% or better, and sometimes 88% or better with some disease conditions
• CMS will not pay for oxygen unless the SpO2 is 88% or lower on room air at rest

Be aware that a person’s normal SpO2 decreases with age, while sleeping, and with some disease processes. The only way it can get to 100% is with supplemental oxygen.

4-5-6-7-8-9-Rule.  Allows you to use SpO2 to estimate PaO2.

• SpO2 70% = PO2 of 40 (supplemental oxygen is essential on any patient)
• SpO2 80% = PO2 of 50 (some chronic lungers live here)
• SpO2 90% = PO2 of 60 (This is what you want to maintain for most patients)

Therefore, ideally, for most patients, you will want the SpO2 to be 90% or greater, or as specified by hospital protocol, or specific physician order.

Fraction of Inspired Oxygen (FiO2): This is the percent of oxygen a patient is inhaling. Room air FiO2 is 21%. By applying supplemental oxygen, the FiO2 can go as high as 100%.
Indications for Oxygen Therapy:

• To correct hypoxemia
• To reduce oxygen demand on the heart
• Suspected or acute marcardial infarction (MI)
• Severe trauma
• Post anesthesia recovery

Low flow oxygen devices: These are oxygen devices where some room air will be entrained, and therefore the exact FiO2 cannot be calculated, however it can be estimated.
How much FiO2 is delivered to the patient is dependent on:

• Liter flow set at the flowmeter
• Respiratory rate and pattern of the patient
• Equipment reservoir (stores oxygen)

The following are low flow oxygen devices:

1. Nasal Cannula: The nasal cannula is the most common oxygen device used and the most convenient for the patient. A nasal cannula at 2lpm is usually a good place to start.

You may at times need to estimate the FiO2. How to estimate FiO2 on a nasal cannula? For every liter per minute, the FiO2 increases by 4% as per the chart below:

• 1 lpm = 24%
• 2 lpm = 28%
• 3 lpm = 32%
• 4 lpm = 36%
• 5 lpm = 40%
• 6 lpm = 44%

The liter flow on a nasal cannula should never exceed 6lpm, as studies show doing so is of no added benefit to the patient. Also note that the prongs of a nasal cannula should face down.

A bubbler can be added to humidify the nose to prevent nasal drying and bleeds. This is automatically set up at flows greater than 4lpm, or as ordered by physician.

3. Non-Rebreather Mask (NRB): This is a mask that ideally will bring in 100% Fio2 so long as the liter flow is 15 and there is a good seal between the mask and the patient's face. And all three one-way valves are on the mask to prevent air entrainment.

For legal purposes, however, one flap is always removed just in case the oxygen gets shut off. And therefore the highest FiO2 you can get from an NRB is 75%. The bag acts as a reservoir for oxygen, and therefore allows device to provide higher FiO2s to the patient.

4. Partial Rebreather Mask (PRB): This is basically an NRB with both one-way valves removed from the mask. The estimated FiO2 is 60-65%. Flow should be set at 6-15 lpm.

High Flow Oxygen Devices: These devices meet the inspiratory flow of the patient, and generate accurate FiO2s so long as there is a good seal between the mask and the patient's face. The flows are such that the patient will not be entraining room air that will lower the FiO2. Respiratory rate and tidal volume of the patient have no effect on FiO2 delivered.

Ideally, the larger the entrainment port on the device the lower the FiO2, and the smaller the entrainment port the higher the FiO2. A major disadvantage is a mask is required, and this may be a bit more uncomfortable than a nasal cannula.

1. Venturi Mask: This mask is ideal for patients who are in respiratory distress with high tidal volumes or high respiratory rate to guarantee a certain amount of oxygen.
If a nasal cannula does not provide adequate oxygenation, Venturi Masks set from 28% to 40% are ideal for COPD patients.

Modern Venturi masks come with one or more color coded caps, and whichever one you use the desired liter flow for that particular cap is written right on the cap.
The Venturi Masks used at MMC are set up as follows:

A. White cap:

• 35% FiO2 set lpm at 9
• 40% FiO2 set lpm at 12
• 50% FiO2 set lpm at 15

B. Green cap:

• 24% FiO2 set lpm at 3lpm
• 26% FiO2 set lpm at 3lpm
• 28% FiO2 set lpm at 6lpm
• 30% FiO2 set lpm at 6 lpm

The liter flow must be at least set at the recommended liter flow for any particular FiO2 that is dialed in. It's okay if it is set too high, yet if it's too low the patient may retain CO2 and the FiO2 may not be lower than what you dialed in.

2. Aerosol set-up: This device will deliver anywhere from 21 to 100% FiO2 depending on how it is set up. The desired flow to set the flow meter at is written write on the cap
Usually a humidity device is connected to the flowmeter, and wide bore tubing connects this to the patient's mask Wide bore tubing acts as a reservoir to obtain higher FiO2s.

These are ideal for patients with tracheotomies because it allows for inspired air to be oxygenated, humidified and even heated if necessary. They can be hooked up to a simple mask, tracheotomy mask, and even a t-piece.

The flow may exceed the required flow, although if it is less the patient may retain CO2, and the FiO2 be lower than desired. On inhalation a mist should be seen coming from mask or reservoir.

3.  High flow nasal cannula:  An Fio2 of 21% to 100% may be maintained because the flow meets the patient's spontaneous inspiratory demand.  This is made possible due to thicker tubing and humidified oxygen. 

Other oxygen devices you might see:

1. BiPAP: This is a discussion for another day. Still, pressure can be given by a non-invasive mask over the patient’s face to improve ventilation, and to supply any FiO2 from 21% to 100%. These also have other means of improving oxygenation.

4. Ventilator: This is also a discussion for another day. Yet for patients whose oxygen demands exceed any of the above devices, intubation and ventilation with a ventilator may be required. These can supply any FiO2 from 21% to 100%, and also have other means of improving oxygenation.

Hazards of oxygen therapy:

• Oxygen may suppress the respiratory drive for some COPD patients, and should be used with caution.
• FIO2s greater than 60% for greater than three hours have been linked to increased risk for lung injury and other future consequences.

What device do you use? Where to start?

• For most patients, you will start low and work your way up if needed
• We usually start at 2lpm for most patients and adjust accordingly.
• If you have a patient in respiratory distress, you may want to start at 40%.
• However, if the patient is in severe respiratory distress, or is the victim of a trauma, you may want to simply start at 100% and decrease as appropriate
• All patients suspected of chronic heart failure should be placed on 100% FiO2 and adjusted down from there.
• All patients who are suspected to be CO2 retainers should be started on 2lpm or, if in respiratory distress, on a venturi mask set no higher than 40%.
• Still, a majority of patients do quite well on 2lpm.

How much oxygen does a patient need?

Ideally, whatever oxygen device is needed to maintain a SpO2 of 90% or greater or as otherwise specified by a specific oxygen protocol or physician order is indicated.

Oxygen supplementation for uncomplicated acute coronary syndrome is no longer routinely indicated and should only be applied only if the oxyhemoglobin saturation is less than or equal to 94 percent.  The old recommendation was to place all patients complaining of chest pain on 4lpm with the belief that it would increase oxygen to the heart and decrease work of breathing.  I'm simply noting this here because some physicians prefer to stick with the old recommendations, and that's fine.

Sedatives, analgesics (like Morphine) and anesthesia may also depress respiratory drive, and these patients are often placed on oxygen. The amount used is usually 2-3 lpm via nasal cannula, however this depends on the patient, physician, or protocol.

How to determine if oxygen therapy is working:

You know oxygen therapy is working when:

• SpO2 improved to patient normal (or as determined by physician)
• Respiratory rate improves
• Patient tidal volume is not erratic
• Patient notes improved work of breathing
• Pulse is normal or improved or improving
• Blood pressure is improved or improving
• Underlying condition is improving, or whatever occurred to cause the hypoxemia

How long with an e-cylinder last?

So you want to use an e-cylinder to take a patient to x-ray and you want to know if you have enough oxygen in the tank to make it there. You can use the following formula:
e-cylinder time remaining = .30 (PSI) / LPM

Physician's order:  Ideally, the order should be for protocol, and this allows the therapist and nurse to use the least amount of oxygen to maintain a desired SpO2.  However, if a physician wants a specific device, here is how the order should be written:

• Nasal cannula:  flow should be indicated: 1-6 lpm (this is because FiO2 fluctuates based on minute ventilation)
• High flow nasal cannula:  FiO2 should be indicated, not flow
• Venturi Mask:  FiO2 should be indicated, not flow
• Non Rebreather: FiO2 should be indicated, not flow
• Partial Rebreather: FiO2 should be indicated, not flow

Related Links:

• Oxyhemoglobin Dissociation Curve
• ABG Interpretation Made Easy
• How to know if a patient is a CO2 retainer
• Why do people breathe?

This RT not a fan of the labcoat

The Anonymous RT over at Respiratory Therapy 101 posed a great question recently regarding lab coats. Do you wear one?

Okay, so it's a boring question, but I'm sure there's one or two RTs out there that care what RTs at other hospitals do or don't do.

Most students are required to wear one. And, actually, our hospital policy says that we have to wear one. But I never do. I hate wearing a lab coat. All it is is a big bulky thing that makes you hotter in an already hot place. You know, old people like it H-O-T.

So usually I walk around in scrubs only. I have to add something else to this. I hate wearing my stethescope around my neck, so I carry it in one of my pockets -- 99% of the time the left pocket.

My meds go in the right pocket. That's my system. Now, some of my scrubs don't have pockets. If I have a lot of patients, I try to avoid wearing these scrubs. But, when I'm on a lazy streak and have not done my laundry, then I have no choice but to wear these pocketless crubs.

So on these days I have no choice but to wear the stethescope on my neck, or carry it over my clipboard, and store my drugs at randoms spots around the hospital. You know, I just stash a stack at a few random spots. Unless, that is, I have a chest pocket, then I plop some amps in there -- one of each (obviously I can't do this when it's busy. On those days I might be forced to wear the lab coat.)

The anonymous RT says he quit wearing a lab coat because he kept getting confused for a dr. While that has happened to me on occasion, at this small hospital there aren't enough random doctors for people to get THAT confused.

But, on those nights when I have few patients and the workload is low, and my metabolism slows way down, it can get quite cold. So, I tend to keep in nearby.

Still, when I do wear it I travel light. I keep as few drugs on me as possible. Usually I stock up on Duonebs because that seems to be the drug of choice by Dr. Q1, of whom I usually get stuck working with, and then a few of the other bronchodilators (depending on what the floor patients require).

I also might stock of few other RT essentials, like nipple adaptors and o2 connector tubing.

I honestly HATE wearing my stethescope over my shoulders. I got out of this habit the first time
the tubing on my Littman got hard and snapped in half. The company explained to me the oil in my skin dries out the tubing. I had to pay to get it fixed, and from then on it stays on my pocket.

Of course I could pay for a stethescope cover (one of my coworkers makes them), but I hate wearing on my neck anyway. (So, how did I get from lab coats to stethescopes. What a lame post this turned out to be.)

It's funny how each RT has his or her own system. One of my coworkers carries her meds around in a ziplock bag. Another wears a shirt and tie and dress clothes under his lab coat.

My answers to your RT queries

Every week I check my statcounter to see who's typing things into Google or Yahoo and being linked to my RT Cave blog. Assuming the queries were not answered, I provide in this spot each week my humble responses.

And, hey, if the query is comical, it deserves a comical response. If it's serious, I treat it as serious. That in mind, here are this weeks queries:

1. an ideal rsbi prior to weaning from a ventilator: RSBI is VT/RR. A result of anything less than 110 means that the patient has a 75% chance of not being re-intubated according to studies. At our hospital, we use 100. Each hospital is different.

2. soul therapy, stripping class: Soul therapy is good, but stripping in a hospital would be frowned upon, unless you are an old patient with a saggy butt.

3. cheer copd patients up: The company of an RT sometimes does this. There's this neat drug called PalButerol we RTs comically use to Cheer up our patients. If you don't believe me, see my ad on the right. There's a picture of santa.

4. best cigarettes for asthmatics: If you are an asthmatic and smoke you are a knucklehead. However,asthma cigarettes used to be a front line therapy for asthma. Check out this link and read more.

5. side effects of bipap: It's not a drug, so there really are no side effects. The pressures used are usually low, so it's not common to cause barotrauma, but it's still something to watch out for. Basically, the biggest side effect (if that's what you want to call it) is patient driven discomfort or non-compliance.

6. does copd mean your a co2 retainer: No. Most experts predict that fewer than 10% of COPDers are retainers. But don't tell doctors that, because many of them treat all COPDers as retainers, which is unfortunate for the patient because they are unnecessarily kept hypoxic (note: hypoxic means they aren't getting sufficient oxygen to their tissues).

7. what diagnosis use ventimask: A ventimask should be used when a patient has an irregular respiratory rate, or if the patient is labored. The reason for this is a ventimask is a high flow oxygen device that guarantees the dialed in FiO2 regardless of respiratory rate. Ideally, your goal as an RT is to use the lowest FiO2 to maintain an SpO2 of 92% or greater. Now, if you have a CO2 retainer who is laboring, and you want to guarantee an FiO2 to get his sats high as possible, a ventimask can work well. Usually we use 40% FiO2 or less for this to maintain an SpO2 that is appropriate for the patient (I prefer 92% or greater, but some patients live around the mid to upper 80s). For more information on CO2 retainers, check out this link.

8. miracle asthma drug: When I was a kid it was Susprin (I will write about this soon enough on my asthm blog), which is no longer even mentioned in the PDR. I would say that it is Ventolin, but most asthmatics shouldn't even need to use Ventolin if they take Advair. Singulair might be the new miracle allergy drug.

9. prolonged use of rescue inhalers instead of preventative medicines: Is foolish. This is what a Goofus Asthmatic would do.

10. diarrhea and cpap machine: There is nothing in common between the two. And if you have diarrhea, you do not have to take the mask off unless you want. Unless you are talking about diarrhea of the mouth.

Now, if you guys and gals have any further questions for me, serious or not, let me know and I well try to answer them for you. If I don't know the answer, I will seek out a sagacious RT who does, or maybe even a doctor.

You can email me at freadom1776@yahoo.com, or write a comment below.

The case of the missing christmas trees

Do you ever wonder what happens to all the nipple adaptors (christmas trees) and tubing connectors? They seem to disapear faster than the money I hold in my hands on payday.

You go to do a treatment, the patient has a bubbler hooked up to the flowmeter, and you easily find the nebulizer, but the christmas tree is nowhere to be found. How the heck did so and so do a treatment all day with no christmas tree? Grrrrr!!

By habit, RTs seem to pick up those things up, stuff them into their pockets, take them home, and that's where they stay. Your wife (or you or your mommy) does your laundry, empties your pockets, and tosses those things into the trash thinking they are just junk -- of which they are to anyone who doesn't work with oxygen.

Of course if you leave them sitting on a shelf in the room they get knocked on the floor and swept away by the cleaning service.

Along with those christmas trees, o2 connector tubing seems to find a way to disappeare too. Or, connected to the o2 tubing is a suction connector. One thing I've learned is if you go into a room because the nurse told you the patients sat is low, I check the flowmeter first. If it's on, I check the connector sites. Often times, the connector is a suction connector, and is disconnected.

So you have to go out of your way to find a new nipple adaptor or connector. Unless, that is, you happen to have it handy in your pocket or something.

The ER calls me all the time for more oxygen connector tubings. Well, at least they do if the RN working isn't lazy and decides to simply use the suction connector that's readily available.

Here at shoreline our ER beds are a little too far from the flowmeter, so we keep an o2 tubing connected to each flowmeter with a connector on the end. We hook up o2 or a treatment to the connector.

But I'm telling you, if a suction connector is in the place of the o2 connector,
all this does is cause trouble for all of us.

So what happens to these things? It's not like patients are taking them home.

Or is it?

There's a theory.

I know some COPD patients who have asked for oxygen connector tubing so they can connect their 1000 feet of oxygen tubing through their homes. Maybe they lose their own as fast as we lose them here in the hospital.

So when they see all that tubing above their hospital bed, their eyes light up. As soon as they have their discharge papers in hand, and the nurse leaves them alone to get dressed, they snatch up the extra equipment they need for home.

Most people are honorable and won't do this, but I suppose this theory goes along with the Bible in the Hotel theory, "What's in the room is mine, so I'm taking it."

Connectors probably just get thrown away in ER for whatever reason.

To be nice, about once a week I take a handful of 02 tubing connectors to ER and put them in a cup for the nurses to use, and the connectors STILL keep disappearing.

Where do these things go?

Here's another theory regarding the christmas trees: people are taking them home and using them to decorate their gardens or something? They are neat looking little things.

I wouldn't be surprised to see them in those little Christmas towns people use to decorate their homes at Christmas time. Some day I'm going to see one of my christmas trees decorated with little dots of white snow amid a miniature snowy park.

Oxygen therapy: Stripping the threads

I always tell my patients that the hardest part of the job is screwing stuff into the oxygen flowmeters. It's something I never really think of except for when I'm in the process of doing it, so it's my patients I usually mention it to.

And I've had patients, or nurses, laugh at me as I struggle to screw on that nipple adaptor (often referred to as Christmas Trees), or that bubbler, onto the flowmeter. And I grumble and gripe as I try again and again to get it to screw on just right without stripping the plastic threads.

That has got to be the hardest part of this job. It's not so bad when a patient doesn't require a bubbler, but when a patient has a bubbler, and a treatment is indicated, you have to unscrew the bubbler and screw on the nipple adaptor. Those cheap nipple adaptors never seem to go on just right.

Yet, if you aren't patient, and you strip the threads, you have to walk all the way to the supply room to get a new one, that is unless you just so happen to have a spare in your pocket, of which I usually do except for when I need one.

And then, once the treatment is done, you have to thread the bubbler back into place.

Sometimes, as I struggle to do this, I find myself thinking maybe I should just say "screw it," and leave the nipple adaptor in place so I don't have to go through this process again in four hours. But, being the good RTs we are, we have to do the right thing and hook the bubbler back up.

Today, though, as I was doing my last treatment, I thought that when you have a code, you never seem to have a problem hooking up the AMBU bag to the flowmeter. That's because these things are designed to be fool proof, so you can just plug it onto the flowmeter.

My thought was, why can't nipple adaptors and bubblers be that easy? Why do we have to screw the darn things on? Why can't some entrepreneur invent an easy way to hook stuff up to flowmeters.

Thankfully, I never have a problem screwing in the ventilator tubing, but those things aren't made out of plastic either. I think it's the cheap plastic that causes this frustration. I suppose that's the cost we pay for cheaper, disposable equipment.

I searched the Internet to see if maybe some company had made a screwless nipple adaptor, but I have yet to find one. However, I suppose it really doesn't matter, because hospitals usually sign contracts, and get whatever supplies are provided by the one company.

So, I suppose we'll continue to be stuck with these cheap plastic nipple adaptors, and cheap plastic bubblers that never seem to want to thread on easy, or at least not when we are in a hurry.

That, my friends, is the thought of the day.

The basics of oxygen therapy: part 2

(This is part 2 of an ongoing series, to view the rest click here)

There are a few exceptions to this rule I'm about to state, but for the most part, no patient admitted to the hospital should ever be ordered on a specific oxygen device at a specific FiO2 or a specific liter flow.

Personally, with the exception of the exceptions I will list in a moment, the amount of oxygen a patient receives should be based on the patients sat, otherwise known as the SpO2.

This is why I love it when doctors order oxygen per protocol, because both our oxygen and ventilator protocols call to maintain an SpO2 of 92% unless otherwise specified.

We must realize that as a patient ages, or a chronic illness progresses, his or her normal resting SpO2 drops. This is especially true as an aging person sleeps. If I had a dollar for every time I was called to an elderly person's bedside because his or her sat was 88-89% while the patient was sleeping, I'd be rich.

To me, that's an exception to my rule. I see no reason to provide supplemental oxygen to these patients, unless they show complications. The same thing is true with a chronic CO2 retainer. If he or she is maintaining an SpO2 of 88-90% and shows no complications, then leave that patient alone.

Three more exceptions: the anemic patient, carbon monoxide toxicity, and the cardiac patient. For these patients, you probably want to maintain an SpO2 of 98%. Otherwise, 92% should be the target SpO2.

That should be plenty of oxygen to maintain a PO2 of greater than 60, and thus prevent hypoxemia, or too low oxygen level to the blood supply which causes the heart to be overworked in normal patients.

So, basically, if a doctor orders a 40% ventimask because the patient's sat was 88% on 3LPM, you should question the order. What if the sat is 100% on 40%. Then why can't you decrease the oxygen to 30%, or even 28%, or even lower if that maintains the required SpO2?

Why keep someone on a nonrebreather for two days with a sat of 100%, when you could just as easily get by with a 50% ventimask to maintain the sat.

See what I mean. The RT should always have the opportunity to lower the oxygen to maintain that sat.

He should also have the opportunity to increase the oxygen should that be required. Now, if I had to increase oxygen from 2LPM to 4LPM no big deal. But if the oxygen now required is 50% instead of the 2LPM the patient was on, then I'd sure be calling the doctor so he knows that something is changing with this patient.

However, as it stands where I work, we can go down on oxygen without an order, but we cannot go up over the original order. But, if I had my way, I'd add the above paragraph into our protocol.

A ventimask should be ordered in only two situations: 1) if the nasal cannula just isn't quite cutting it, but a partial rebreather isn't needed 2) the patient has a normal SpO2, but has an irregular respiratory rate. A ventimask will guarantee that FiO2 of 24-50% regardless of the patients minute ventilation.

One rule of thumb for a ventimask: to maintain the desired FiO2, you have to dial in the recommended liter flow. It usually goes something like this: 24% and 26% = 3LPM, 28% and 30% = 6LPM, 35% = 9LPM, 40% = 12LPM, and 50% = 15LPM.

If you set the mask to 50% and you do not at least set the flow at 15, the patient will not be getting 50% FiO2, and he may be retaining CO2. We don't want that. However, it is okay to go over the recommended liter flow.

If a patient is so bad off that a ventimask isn't working, then order a non-rebreather (NRB). However, don't assume a NRB delivers 100% Fio2, because it doesn't. It only provides about 75% FiO2. So don't call it a 100% NRB. With both flaps on it would deliver 100%, but since by law one of the flaps has to be removed, it only delivers 75%.

If a patient still needs more oxygen on an NRB, then turn that flowmeter to flush. If that still don't work (and perhaps even if it does work) you may want to consider CPAP, BiPAP or the more invasive ventilator.

If that sat on 75%FiO2 is 96%, then take off the other flap and turn the NRB into a partial rebreather (PRB). Now you are giving the patient about 60% FiO2. But certainly don't keep it there if a 50% ventimask would suffice to maintain that 92% sat.

Why all this complicity about oxygen? Because oxygen is a drug, and it can cause complications. Not only that, but it costs money to have patients on oxygen when they don't need it.

And this includes post-operative patients. Let's not be putting patients on 2LPM just because they had surgery. If the sat is 92%, lets cut them off.

So, technically speaking, and with the exception of the exceptions stated above, liter flow and FiO2 really don't matter so long as you are maintaining the recommended SpO2.

Regardless, doctors often have exceptions of their own, and we RTs do what we are ordered to do. But that doesn't mean we can't question an order, or push for changes that might benefit the patient.

The basics of oxygen therapy: Part 1

To view rest of series, click here.

As I've written before, I think I've spent more time debunking oxygen myths and educating about oxygen than anything else I have to teach regarding respiratory therapy stuff. And I'm not talking patients.

Don't get me wrong, I don't have a problem with this, nor am I implying that nurses are stupid. I think one of the big differences in RN school and RT school is that RN school covers a little about a lot, and RT school teaches a lot about a little.

Sure, oxygen therapy is covered in RN school, but only briefly. Which explains why we RTs have to explain the basics from time to time.

Respiratory Therapy Driven has good post today about some RT basics. A non-rebreather, for instance, is ideally supposed to deliver 100% FiO2, but because of the slim chance the oxygen gets shut off, the masks come with one one-way valve instead of two. Thus, the FiO2 obtained is only 75%. But try explaining that 100 times.

"Yep, chart 100% if you want," is what I usually tell them now. This gets to be a tricky thing to explain at three o-clock in the morning.

We have one old school doctor who orders a bubbler with every nasal cannula order, but our protocol states that one is not needed unless the flow is 4LPM or greater.

And like Djanvk wrote, all our post op patients are ordered up on 2-3LPM times 24 hours. What's the deal with that?

We estimate adult nasal cannula FiO2s based on the following formula:

1. 2LPM = 28%


2. 3LPM = 32%


3. 4LPM = 36%


4. 5LPM = 40%


5. 6LPM = 44%

However, don't dare put a nasal cannula on a three week old baby at 6LPM. That would be the equivalent of an adult sticking his head out the window while traveling 60MPH down the highway

We have a special flowmeter now that maxes out at 3LPM to prevent someone from accidentally (or purposefully) turning up the flow too high. Then we start at low as 1/4 LPM. Obviously, increasing to maintain a specified SpO2 (in my opinion 92%, but most of your docs like 94%.)

The reason I bring this up, and actually the reason for this blog post, is I'm curious to know what the estimated FiO2s would be for neonates and smaller children. It can't possibly be the same as for adults.

I have never found the answer on the Internet nor in any RT literature. I asked the question on Ventworld.com once, and no one there knew the answer either.

Maybe nobody cares but me

My guess is it would be something like this:

• 0.5LPM = 28%


• 1 LPM = 32%


• 1.5LPM = 36%


• 2 LPM = 40%


• 2.5LPM = 44%

Of course I'm just making these neo numbers up. Technically speaking it really doesn't matter what the FiO2 is, so long as you're maintaining a sat, but I'm still curious.