Open Heart, Open Mind… Learning About Amio-Loading

I’m always learning something new. I called the cardiologist after an evaluation to report some severe orthostatic hypotension and the nurse and I got to talking. She was going back through the patient’s history and looking for why this may be happening. I had just finished assessing the patient in their home and they were about a week post-op from a CABGx4 with (B)SVG. They weren’t feeling well, very fatigued, and my typical post-CABG assessment (which involves a 5x Sit to Stand, a 6 minute walk test, a baseline neuro screening, and a functional home walkthrough) was NOT going to happen… I could hardly get them out of bed! So, I told the nurse on the other end of the phone all about these things and gave her my numbers.

She finally said, “Ah-Ha! He was amio-loaded.”

And I said, “Huh?”

I had absolutely no idea what she was referring to, but I took it from the context of the conversation that this had something to do with the patient being orthostatic. I had found a new realm of research for myself. I couldn’t believe that I had never heard of this because it was SO important and relevant to therapy practice. Apparently, it is also not that uncommon. Today, I want to tell you about amio-loading because it is relevant and important, but also because I’m betting no one else has ever told you about it.

Photo by Magdaline Nicole on
What is “Amio-Loading”?
  • The rapid, high-dose loading of amiodarone to treat a patient with ventricular or atrial fibrillations
  • Typically done after cardiac events (MI, AVR, TAVR, CABG, etc)
    • Can be IV, PO, or both

Amio-loading is typically performed in the hospital under cardiologist supervision while the patient stays in the hospital for a few days after and the effects tend to wear off. However, half-life of amio-loading is 40-55 days! This means that your patient may feel the effects for several weeks after being discharged from the hospital and even in to outpatient cardiac rehab. If amio-loading does not need to continue after the initial round, patients may wean down using a Class III Beta Blocker such as Sotalol (BetaPace). However, patients may continue with “chronic” dosing after the initial rapid dosing if their arrhythmias persist. Those patients on “chronic” dosing need to be monitored closely for side effects.

What kind of side effects are we talking here?

Lung Damage
Rapid Irregular Rhythms
Liver Failure
Heart Failure
Other CNS effects
Sudden Death

Not such a small deal… These side effects tend to be due to elongated Q-T Interval symptoms. And you thought hydroxychloroquine was bad… So what do you do if you have a patient who is on chronic amiodarone dosing that starts having these symptoms? Well considering they are pretty serious, especially that last one, you’ll need to immediately notify the physician if there are any signs of rhythm irregularities.

What Does this Mean for Us?

If you have a patient that was amioloaded or is doing long term amiodarone, you need to be aware of a few things. First off, we have to talk about the Frank-Starling mechanism. The Frank-Starling mechanism is when increased or decreased venous return changes stroke volume accordingly. When you exercise, venous return increases, so stroke volume has to also increase to get all that extra blood moving out of your heart and lungs which then carries more oxygen and nutrients to your muscles to support exercise. This mechanism relies on a feedback loop which means it takes more time. Because Amiodarone decreases SA and AV node conduction, your patient is more heavily reliant on the Frank-Starling mechanism for stroke volume and heart rate accommodations to exercise. Amiodarone makes the electrical system accommodations lag. This means that your patient will need an increased warmup time for exercise.

Another finding with patients who take amiodarone is prolonged bradycardia. We discussed in this post about assessing pulse using a pulse oximeter and conditions under which that probably won’t work. Long-term amiodarone dosing can be added to that list. Although it may still work, prolonged bradycardia needs to be measured in actual beats per minute, so you will need to always assess pulse manually. This is a great opportunity to teach your patient how to assess their own pulse, too.

Photo by Anna Shvets on

I once saw a man in his 40’s who recently had an MI. He had no orthostasis or symptoms of it, but his resting heart rate was 36 bpm. I thought I was just counting wrong. I spent close to 10 minutes just taking his pulse at different places for a full minute just to make sure I wasn’t crazy, even auscultating a heart rate right at the source. I thought, “well… he is asymptomatic so I should try to increase his heart rate,” with the full intention of calling his doctor afterward. Like I said, asymptomatic… I walked him around for a few minutes and he had no change in heart rate but his blood pressure dropped slowly and progressively as he walked. His cardiac output was dropping (or his river was drying up, if you remember my post about that). There was no electrical accommodation and his stroke volume wasn’t changing fast enough. His lack of symptoms was actually the problem. I contacted his doctor and we got him in for an ECG immediately. He needed cardioversion.

Some other things you will need to watch for include CNS and thyroid effects of amiodarone. Decreased cardiac output and irregular heart rhythms can also contribute to neurological symptoms (see seizures above!). For central nervous system effects, we are talking the big guys here: peripheral neuropathy, dyskinesia, loss of gross motor coordination, chorea, and vision changes. This means that performing that baseline neuro evaluation is essential. These patients may also fatigue quickly or more often, but may also have more intense thyroid symptoms like significant weight gain/loss, unusual sweating, or restless legs.

Is there anything else I need to know?

I know that it sounds like something that isn’t terribly relevant to physical therapy, but in the world of home health, PTs are fully responsible as case managers and that includes complete medical management. Therefore, the primary PT is fully responsible for finding, reporting, and resolving medication interactions for all medications, vitamins, and other inputs to the patient’s body. Guess what? Amiodarone has a TON of interacting drugs. Here’s an abbreviated list:

  • Antibiotics
  • Antifungals
  • Antidepressants
  • Antivirals
  • Statins
  • Blood Thinners
  • Methadone
  • Any CNS Depressants (including alcohol)

Can you think of many patients who aren’t on at least one of these things? Especially in the home health field or skilled nursing setting, you’d be hard-pressed to find anyone without something on that list. Lots of phone calls to the primary physician ensue when I’m admitting someone on amiodarone because they will, inevitably, have a medication interaction.

Photo by Pixabay on

As fully responsible case managers, or, as I like to call us, primary providers, it was also our job to ensure patients are aware of their medical appointments (we even created them a calendar!) and that they were able to get there, once their sternal precautions were lifted for driving (which included setting up transportation, training home exits, and car transfers). This comes into particular importance for patients who were Amio-loaded or who take long term amiodarone as they require frequent and ongoing monitoring to make sure they are still tolerating treatment. This includes:

Liver Function Tests (LFTs)
Pulmonary Function Tests (PFTs)
Chest X-Rays
Regular ECGs
TSH Levels

Keeping up on these appointments will hopefully help catch adverse reactions before they start and allow dosage adjustments or changes to other medications to treat side effects. Typically, if I was seeing a patient who was amio-loaded, they were also new to their beta blocker for weaning off the amiodarone and reducing pre-load to allow for cardiac tissue healing. If they were orthostatic, we would consult cardiology and were usually able to reduce or eliminate the beta blocker. But, you never know if you never ask.

Here is your short-list of take-aways:
  1. Be on the lookout for side effects, review medications
  2. Always take vitals before, during, and after activity
  3. Use a manual pulse
  4. Allow for increased warmup time
  5. Assess for orthostasis

Cardiac patients may be a small percentage of your case load, but when they do come around, you’ll want to make sure you know what to look out for. Amio-loading may be partially responsible for a lingering dizziness that doesn’t seem to show up on vertigo assessment. It may be a part of the chronic fatigue your patient keeps reporting that is preventing them from completing their home exercise program. It may be responsible for them passing out in your clinic. Maybe it’s why they feel cranky, have restless leg syndrome, difficulty sleeping, chronic fatigue syndrome, and have an upset stomach (I know these patients!). So, just keep it on your list of possibilities.

Do you screen for drug interactions when evaluating a new patient? Tell me in the comments!

More Reads…


Something went wrong. Please refresh the page and/or try again.

Follow my blog for more!


American Society of Health System Pharmacists. (2017). MedlinePlus: Amiodarone. Retrieved from

Kohli, P. (2016). Amiodarone: Top 3 Things to Know for Rate or Rhythm Control of AF. Practical Cardiology.

Mayo Clinic. (2019). Long Q-T Syndrome. Retrieved from

Follow @DoctorBthePT on Twitter for regular updates!

Blood Pressure Basics

Are you taking the blood pressure and heart rate of EVERY patient you see for a new evaluation? How about for every visit? A recent survey of over 1800 Outpatient PTs showed that although 51% of PTs reported that over half their caseload had risk factors for hypertension and cardiovascular disease, only 14% of them are taking blood pressure and heart rates at evaluation. One of the BIGGEST factors for not taking a blood pressure? It’s not having the equipment or knowledge of how to perform it. It’s “Lack of time” and “Lack of perceived importance.” Stab me in the heart RIGHT NOW. I’m going to bring out my Texas accent and say, “YA’LL gotta be kidding me!”

You should know by now that the “basics” are never basic for me. They are essential! Recently, Dr. Rich Severin (PT) and his team released the recommendations for measuring and monitoring blood pressure by physical therapists in the outpatient setting. These recommendations had me literally dancing up and down in my hallway! It has been a long-standing soapbox of mine and many others that taking a set of vitals (or several sets of vitals) for every patient at every visit is a crucial part of maintaining safe and responsible physical therapist practice in any and every setting and for all populations. Dr. Severin refers to this as the “ethical duty to screen” and I can’t think of a better way to explain it. It’s something I teach my students, it’s something I tell my colleagues, and it is a practice I live by regardless of the setting I work in (and I’ve worked in pretty much all of them…).

I have written in recent posts regarding monitoring for COVID-19 in the outpatient setting that taking temperature should reasonably and easily lead to taking heart rate, oxygen saturation, and blood pressure for all patients at rest. But why stop there? As physical therapists and other rehab clinicians, we have the responsibility of exposing our patients to activity and exercise, likely to an extent to which they have rarely, if ever, experienced. From maximal exercise testing to a simple set of bed mobility activities, we have the skill to expose our patients to these varying levels of activity, even in the throes of illness, even while on a ventilator, even while on ECMO, even after a heart attack, even after organ transplant, even after loss of a limb, even after a brain injury… and the list goes on.

But in order to do those things safely, we HAVE to be monitoring vitals. And, like I’ve mentioned before, not just once: resting, during activity, after activity, and after recovery. It’s these readings that truly tell us how a patient is responding to activity and wherein our skill as a PT lies: not in taking these measurements, but interpreting them and modifying activity based on them. So, with that call to action, let’s talk about blood pressure.

I gave a presentation back in January (before we could only meet in groups of 10 or less) to over 150 PTs and PTAs about how to prescribe high-intensity interval training for even the most medically fragile patients. Here’s the trick: it’s all about blood pressure (and other vitals, of course)! As part of that presentation, I demonstrated how to properly take a blood pressure. Here are the basics:

Resting Blood Pressure: the basis for all decision making


1. Patient position:

  • Supine is ideal to minimize muscle contractions that alter measurements but seated is probably more realistic in most settings.
  • Resting for 5 minutes prior to measurement. This may be achieved by having staff take blood pressure while in the waiting area.
  • Feet, arms, and legs uncrossed, and both feet on the floor.
  • Brachium at level of Right Atrium/Fourth intercostal space for measurement.

2. Cuff size and positioning:

  • Blood pressure cuffs come in several sizes for a reason! Find the right size for your patient based on arm length and circumference. The length of the air bladder within the cuff should be about 80% of the circumference of the brachium.
    • Undersized cuffs significantly falsely elevate measures
    • Oversized cuffs also give false measurements
  • Cuff should be placed on a bare arm (up to 40mmHg error for this violation!)
  • Cuff should be at the level of the heart, specifically the right atrium
    • Support the patients arm with a surface or with your own arm to achieve this positioning
    • This does NOT mean that the sleeve should be rolled up. Rolling the sleeve up creates a tourniquet effect.
  • Midline marker on the cuff should align with the brachial artery
    • Yes, this means you need to palpate it to find it
  • The arm should be straight for measurement
  • Place the stethoscope over the brachial artery where strongest palpation of the pulse was felt
The Steps of Proper Performance:

Step 1: Find the Systolic Max. If you pump up the cuff too high, you will cause error in your measurements. So, how do you know how high up to pump it? Well, you have to find the systolic max. To do this, once you have the above positioning figured out, palpate the ipsilateral radial pulse, inflate the cuff slowly until you feel the pulse disappear. The pressure number at which this happens is your systolic max. Deflate the cuff.

Step 2: Wait! You have to wait at least 1 minute between measures to prevent falsely elevated measures. So after you find the systolic max, you need to wait one minute before re-inflating the cuff.

Step 3: Re-Inflate. After you’ve waited your one minute, re-inflate the cuff to the systolic max pressure that you just found and then another 30mmHg. It used to be 20mmHg, but the newest guidelines, as mentioned above, by Severin et al, recommends 30 mmHg.

Step 4. SLOW DOWN! Deflate the cuff slowly. The rate that gives the most accuracy is between 2-3mmHg per second. Yes, I know, this feels like it takes forever. You’re right, it does. But this is the correct way to get the most accurate measure. The systolic pressure should be the pressure measurement at the sound of the first Korotkoff sound. The diastolic measure should be the pressure measure at the sound of the last Korotkoff sound.

Optional Step 5. When the Korotkoff sounds just keep going… Sometimes this happens. It is not necessarily a good or bad thing depending on the patient. However, it does change how you measure and record your blood pressure measurements. We need to take a closer look at Korotkoff sounds for this discussion. Take a look at the picture here:

If you find that your Korotkoff sounds continue all the way to zero, your diastolic measure will be the last muffled phase sound and then you will also record zero. You will end up with three blood pressure measures in stead of two in this case (136/64/0). I have definitely have this happen several times, typically in the geriatric population in patients who are small or frail as well as dehydrated or orthostatic. When that diastolic number is super low (as in with dehydration or orthostasis), sometimes the heart beats can just still be auscultated all the way to zero. Less tissue impedance to auscultation allows for better transmission of sound.

Are you more of a visual learner? Perfect! You can watch Dr. Severin himself demonstrate this here!

Performing Repeat Measures and Side-to-Side Comparisons

When you need to perform repeat measures, due to a sticky pressure valve, a malfunctioning cuff, a number that just can’t possibly be correct, or not properly identifying the systolic max, it is very important to wait at least 1 minute between measurements to avoid false elevation. Some research indicates that you actually SHOULD take more than one measurement one minute apart and use the average of the measurements to accurately determine a patient’s blood pressure.

Some things that may influence your measurement and may necessitate a repeated measure would include:

  • patient has a full bladder
  • patient talking during measurement
  • realizing half way through the measure that your BP cuff doesn’t fit
  • patient hasn’t taken their BP medication or just took it prior to measurement (may need 15-30 minutes prior to remeasuring)
  • patient had caffeine, alcohol, or cigarette just prior to measurement
  • you are wearing a white coat or are in a medical office (as opposed to the patient’s home) (aka white coat hypertension)
  • patient is taking a medication that can elevate BP (decongestant, oral contraceptives, NSAIDs, corticosteroids, some antidepressants, some antipsychotics, cyclosporine, some rheumatologics (end in -mab or -nib))
  • PPE items, especially masks, have been linked to transient hypertension

It is also normal for blood pressure to be somewhat different in the left arm from what it is in the right arm. If you think about the anatomical location of the vasculature and heart, blood moving toward the left upper extremity will be at a slightly higher pressure than blood moving toward the right upper extremity. Blood exiting the heart has a much shorter trip to reach the left arm.

Can’t I Just Use An Electronic Cuff?

Ugh… I hate this question. Yes, of course you can. BUT, electronic cuffs underestimate systolic and diastolic measurements. If the batteries are low, they won’t give you accurate measurements. Patients CANNOT position the cuff or themselves properly (see above list of positioning items required!). They need regular calibrating and that just doesn’t happen. They can also error and perform repeat measures too close together, resulting in falsely elevated measures. I need accuracy and precision. I need to know FOR SURE if my patient is safe to start, continue, and repeatedly perform exercise. An electronic cuff DOES NOT provide me with this information. Does your primary care provider use an electronic cuff? If so, you should probably switch providers. In our role as primary providers of healthcare services, we need to ensure proper measurement, screening, interpretation, and application of blood pressure for every patient we see.

“…almost two-thirds of hypertensive individuals would be denied morbidity preventing treatment if the diastolic blood pressure were underestimated by 5 mm Hg; the number of persons diagnosed with hypertension would more than double if systolic pressure were over estimated by 5 mm Hg.”

Freeze, et al. (2011)

Now that you have your numbers, what do you do with them?

Here is the information for the standard accepted classification of hypertension. Find where your patient falls and then determine your next steps. Is it safe to exercise?

  • Normal: systolic less than 120 mm Hg and diastolic less than 80 mm Hg
  • Elevated: systolic between 120-129 mm Hg and diastolic less than 80 mm Hg
  • Stage 1: systolic between 130-139 mm Hg or diastolic between 80-89 mm Hg
  • Stage 2: systolic at least 140 mm Hg or diastolic at least 90 mm Hg

You may find, as I have on many occasions, that your patient is in a hypertensive emergency. Hypertensive emergencies are defined as severe elevations in
BP (>180/120 mm Hg) associated with evidence of new or worsening target organ damage (AHA, 2017). This, of course, would warrant a big loud ride to the hospital for management. But, that is the skill of your intervention: assessing, interpreting, and managing appropriately. If your patient is demonstrating resting blood pressures above 180/120 but is asymptomatic, that is deemed a hypertensive urgency and the primary physician should be notified and consulted for instruction. Odds are, they are going in anyway.

Just because someone isn’t being seen for a cardiovascular diagnosis, doesn’t mean they cannot end up finishing their visit with you in the back of an ambulance. I can list several total joint replacement admission in home care that resulted in this. I can’t do your knee ROM if you’re in a hypertensive crisis, so you’ll need to get that taken care of first, and I’ll see you tomorrow! You shouldn’t be surprised if you find your patients in hypertensive crises from time to time. Compliance with pharmacological treatment for hypertension is about 48% so even if they have been to the doctor for treatment, they may not be taking it the way they are supposed to. But, if you never take that first measure, you’ll never know.

“Every 10% increase in effective HTN treatment could prevent an additional 14,000 deaths per year in the adult population.”

Severin, et al. (2020).

You may also find that your patient is hypotensive! We discuss that in great detail in the posts on orthostasis and beta blockers. This can result from several items other than medications and could indicate general hemodynamic instability which would definitely change your plan for the day.

You also may find that patients have interesting blood pressure responses to exercise, whether high or low. We will talk about how to interpret and address that in another post!

Finally, get going. Physical activity is one of the best evidence-based ways to provide long term treatment for high blood pressure. WE ARE THE EXPERTS OF MOVEMENT! We are the experts of prescribing proper intensities of physical activity. We should be gearing our practice toward this type of treatment provision and education. According to Dr. Severin, only 15% of providers utilize exercise as a primary intervention for hypertension. Maybe that’s because only 15% of therapists are taking blood pressures. Start upping the ante here! Start demonstrating your skill, knowledge, ability, and marketing to these other primary care providers! They have the evidence that what you are saying is true, they just need to know that you can provide it!

AHA, 2017

The “What Ifs” of Taking Blood Pressure

What if…

  • my patient doesn’t have one arm?
    • use the other arm
  • my patient has a PICC line?
    • use the other arm
  • my patient has a fistular or shunt?
    • use the other arm
  • my patient has a history of breast cancer with mastectomy on one side?
    • use the other arm
  • breast cancer with mastectomy on both sides?
  • my patient has lymphedema in an arm? or both arms?
  • my patient is always hypertensive?
    • call their primary care provider, discuss your findings, ask about treatment, discuss treatment compliance with the patient (pill counts, drug diaries, etc), or request altered parameters
  • I don’t have the right cuff size for my patient, it’s too small!
    • take the blood pressure at the forearm manually
  • I don’t have the right cuff size for my patient, it’s too big!
  • my patient had their radial artery removed for a CABG?
    • use the other arm or a lower leg until 2 weeks after surgery
  • my patient is pregnant?
    • take their blood pressure at every visit! You may catch early pre-eclampsia and save a life (or 2)!
    • women tend to experience hypotension due to vasodilation during pregnancy and may require supportive devices or activities
  • I can’t hear the Korotkoff sounds?
    • you can use a special amplified stethoscope provided by your employer under the ADA guidelines for those who are hard of hearing
    • you can use a doppler device to better target vasculature and increase volume of output
    • you can make sure your stethoscope is functioning properly
  • my patient’s upper arm is too short for my cuff or my cuff overhangs their elbow?
    • use a forearm measurement

Notes: When utilizing a blood pressure measure from a location other than the brachium, always note this in your charting as these measurement standards are not established and are not interchangeable. Distal blood pressures tend to be higher than brachial blood pressures.

Basically, you are going to have a really hard time convincing me that there is ever an incidence where you shouldn’t or can’t find a way to take a blood pressure. I discuss more of the details on taking blood pressure in the lower leg in the post on Ankle Brachial Indexes which you can view HERE!

This is all really just breaking the surface. This is only how to take a RESTING BLOOD PRESSURE properly. Let’s not forget that our job doesn’t stop there! We need to be assessing blood pressure response to exercise, especially in those who have a known cardiovascular pathology. We will be the ONLY ones who have the patient in a situation where an exercise blood pressure can and should be performed PRIOR to a major health event taking place. This means that we are the only ones who have the ability to detect, defer, and reduce the risk of the occurrence of this major event.

So now that you know the importance, I know you’ll take the time. I don’t have time to NOT take my patient’s vitals prior to treatment every single time and I don’t have time for a malpractice suit. Within our scope, within our ability, within our clinical judgement, therefore, our RESPONSIBILITY. Like Dr. Severin says, it is our “ethical duty to screen” and it is definitely our ethical and professional duty to continue to measure, interpret, and implement these measures and findings to guide our intervention intensity.

If you are from St. Scholastica and you’ve made it this far, drop a “Hi!” in the comments!

More Reads…

It’s Getting Hot in Here: Body Temperature

How many times have you had your temperature taken lately? I think I’ve had my temperature taken thousands of times in the last few months. We are seeing the increased use of forehead scanning thermometers and temporal scanners, all the non-contact forms of temperature assessment, to screen folks for COVID-19 symptoms upon entry to anyContinue reading “It’s Getting Hot in Here: Body Temperature”


Something went wrong. Please refresh the page and/or try again.

Follow my blog for more!


American Heart Association. (2017). Guideline for the Prevention,
Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hyppertension. 71(6). Retrieved from

APTA. (2019). Survey of PTs Reveals ‘Significantly Inadequate’ Rates of BP and HR Measurement. Retrieved from

APTA Cardiovascular and Pulmonary Section. (n.d.) Vitals Are Vital. Retrieved from

Frese, E. M., Fick, A., & Sadowsky, H. S. (2011). Blood pressure measurement guidelines for physical therapists. Cardiopulmonary physical therapy journal22(2), 5–12.

Pickering, T. G., Hall, J. E., Appel, L. J., Falkner, B. E., Graves, J., Hill, M. N., Jones, D. W., Kurtz, T., Sheps, S. G., Roccella, E. J., & Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research (2005). Recommendations for blood pressure measurement in humans and experimental animals: Part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research. Hypertension. 45(1), 142–161.

Severin, R., Sabbahi, R., Albarrati, A., Phillips, S. A., Arena, S. (2020). Blood Pressure Screening by Outpatient Physical Therapists: A Call to Action and Clinical Recommendations. Physical Therapy. 100(6):1008–1019. Retrieved from

Follow @DoctorBthePT on Twitter for regular updates!

header image source

ABGs (Part II)

So, now that you’ve read all the basics about ABGs in the first post, here is a little more about interpreting lab values and how to determine compensated conditions. This is where it gets fun!

First off, let’s take a look at what NORMAL lab values probably look like:

  • pH: 7.35-7.45
  • Partial pressure of oxygen (PaO2): 75 to 100 mmHg
  • Partial pressure of carbon dioxide (PaCO2): 35-45 mmHg
  • Bicarbonate (HCO3-): 22-26 mEq/L
  • Oxygen saturation (O2 Sat): 94-100%

There is some wiggle room (like, VERY little) on some of these and most EMR systems are going to flag them if they are out of normal range for the given population. We discuss some of these in greater detail in this post.

Partial pressure of carbon dioxide becomes particularly important when you are working with patients who have chronic obstructive lung conditions. If you recall from this post, a PaCO2 greater than 45mmHg indicates that someone is likely a CO2 Retainer.

Next, let’s talk about compensated conditions. The body is smart and will know when someone is having difficulty with acidosis or alkalosis conditions of either the metabolic or respiratory variety. If one system isn’t working properly, it will recruit the other system to compensate and attempt to normalize. However, remember that some conditions can only temporarily compensate and will continue to pose serious health risks unless they are medically treated. When the opposite system gets pulled in, the lab values that represent this system will be out of normal range. Because the body has compensated, pH will return to normal. These will be the key factors in identifying compensation on ABGs.

Photo by Karolina Grabowska on

In metabolic conditions, the lungs have to compensate so the lung values (PaCO2) will be out of normal range but the metabolic (kidney) values will be normal or only slightly elevated (HCO3-). pH is normal.

In respiratory conditions, the kidneys have to compensate so the kidney values (HCO3-) will be out of normal range but the pulmonary values (PaCO2) will be normal or only slightly elevated. pH is normal.

If pH and either the lung or kidney value are outside of normal range (depending on the dx), the condition is only partially compensated. Anion gap comes in to play here, but that is outside the scope of this post. You can also use the PaCO2 to guess. In metabolic conditions, PaCO2 and pH will move in the same direction (i.e. if pH goes up, so will PaCO2). In respiratory conditions, pH and PaCO2 move in opposite directions (i.e. if pH goes down, PaCO2 will go up).

Similar to how we read and interpret EKGs, there is a fixed process by which you should evaluate ABGs. If you follow the steps properly, you should arrive at the right answer. Here’s what to do:

  1. pH:
    • Out of normal range —> decompensated condition
    • Normal range —> compensated condition
      (or no condition but all other values need to also be normal for this to be the case)
  2. If the condition is decompensated:
    • What is out of range?
      1. PaCO2 —> Respiratory condition
      2. HCO3- —> Metabolic condition
  3. If the condition is compensated:
    • What is out of range?
      1. if PaCO2, respiratory compensation —> Metabolic condition
      2. if HCO3-, metabolic compensation —> Respiratory condition
  4. Acidosis or Alkalosis?
    1. pH > 7.45 —> alkalosis
    2. pH <7.35 —> acidosis

Let’s do some application here and practice your new skills. I’ll give you a few sets of ABGs and we will talk through them. Remember the process and follow the steps and you will get your answer. Big deep breath…… here we go!

Practice 1:

  • pH 7.49
  • HCO3- 34
  • PaCO2 46
  • PaO2 81
  • O2 saturation 95%

So let’s take this step by step. Obviously, if we were getting a full ABG, we would have more values to sort through, but I’m attempting to keep this easy.

Step 1: is pH out of range?
YES, so our condition is decompensated.

Step 2: what else is out of range?
HCO3-, so we have a metabolic condition

Step 3: is pH high or low?
HIGH so we have metabolic alkalosis.

This one was nice and straightforward. It will not typically be this simple. Let’s try something a bit harder…

Practice 2:

  • pH 7.35
  • HCO3- 32
  • PaCO2 64
  • PaO2 86
  • O2 saturation 93% on 3L cont via NC

Step 1: is pH out of range?
NO. So if there is a condition present, it is compensated.

Step 2: What is out of range?
HCO3-, but because this is compensated, a metabolic value indicates a respiratory condition.

Step 3: is pH high or low?
Neither, because the body has compensated. So let’s look at other indicators that might answer this question for us.

Look at the PaCO2 and correlate clinically. This patient has a VERY high PaCO2 indicating that they are a CO2 retainer. They are on 3L of supplemental O2 and their O2 saturation still isn’t great. This person is likely in respiratory acidosis because they are holding on to way too much CO2 (in the form of carbonic acid) and can’t get enough O2 in to hit that sweet spot on the curve. This is where the anion gap comes in. The anion gap is the factor that covers all the other missing acids (either digested or produced) in the body. You would need the anion gap measure to confirm acidosis, but from clinical correlation, the odds are good.

Ready for one more?

Practice 3:

  • pH 7.31
  • HCO3- 18
  • PaCO2 32
  • PaO2 73
  • O2 saturation 98%

Step 1: Is the pH abnormal?
Yes, the pH is abnormal so something is going on here that is decompensated.

Step 2: What is out of range?
Here is where we run in to a problem. Everything is out of range! HCO3- and PaO2 are both out of range. So, what the heck does that tell us? That means that this condition is in the process of compensating. When you have both factors presenting somewhat abnormal but nothing is crazy out of range, this signifies the process of compensation and is the most likely presentation you will see on ABGs. That’s why these people need to come to the hospital, right? To get help form medical staff to compensate and correct.

Step 3: Is the pH high or low?
The pH is slightly low so we can consider some type of acidosis. Determining the type would, again, require the anion gap. However, because both the pH AND PaCO2 are low, it is likely metabolic acidosis.

Characteristics of acid-base disturbances

DisorderpHPrimary problemCompensation
Metabolic acidosis↓ in HCO3↓ in PaCO2
Metabolic alkalosis↑ in HCO3↑ in PaCO2
Respiratory acidosis↑ in PaCO2↑ in [HCO3-]
Respiratory alkalosis↓ in PaCO2↓ in [HCO3-]
Kaufman, D. (2020)

Here is a nice table that lays it all out for you! Things can get really crazy when patients have more than one of these conditions present at the same time. It is actually possible to have both an alkalotic and acidotic presentation simultaneously. This can happen with COPD, sepsis, heart failure, or when someone has renal failure with pneumonia (like patients who have COVID-19). In that case, compensation becomes very tricky.

I hope you found these three steps for basic ABG interpretation an easy way to figure out what your patient is experiencing! And I hope you check out the first section of this post on basic ABG interpretation to learn more about what YOU as the PT can do to help someone in a critical condition so they can get the help they need!

How often do you utilize ABG outcomes in your treatment? Let me know in the comments!

More from the Pulmonary Rehab Toolbox…

Blow Out the Candles…

If there is any treatment that I feel like gets used in a cookie-cutter fashion, it’s pursed-lip breathing. As much as I hate seeing this technique used for every single patient that has shortness of breath, it does have clinical usefulness. So let’s talk about how to implement pursed-lip breathing properly based on patient presentationContinue reading “Blow Out the Candles…”

Sternal Precautions

“Patients exchanging habits of activity for complete rest are likely to become rapidly worse.” This quote fuels my everyday. These words have informed nonsurgical and surgical rehabilitation and its evolution from handing out bed rest like Oprah hands out cars to getting people moving early and keeping them moving often. Here’s the crazy thing: ThisContinue reading “Sternal Precautions”


Gosh, this is a fine line… Especially in the patients I regularly see. A colleague and I often say, “If you have any more water, you’ll die. If you don’t have any more water, you’ll die.” This is actually a frequent education topic that I cover with patients. Scary? Yes, but true. So, why isContinue reading “Dehydration”


Something went wrong. Please refresh the page and/or try again.

Follow my blog for more!


Kaufman, D. (2020). Clinical Education: Interpretation of Arterial Blood Gases (ABGs). American Thoracic Society. Retrieved from

Lewis, J. (2020). Acid-Base Disorders. Merck Manual Professional Version. Retrieved from

Follow @DoctorBthePT on Twitter for regular updates!


Research is piling in regarding the neurological effects of COVID-19 and the depth of the research is giving us some really concrete information to help guide treatment, screening, and monitoring strategies. The anecdotal evidence is continuing to build quickly so I’ve significantly updated this post to reflect some of the more recent changes and findings.

We are going to go through a few of these. Some you may not have heard of, and others may be more familiar. We previously thought that patients who have more severe cases of COVID-19 are more likely to end up with neurological deficits, but that is no longer true. Research is finding that even mild respiratory cases of COVID-19 can present acutely or delayed onset with significant neurological symptoms.

Photo by Gustavo Fring on

This is a respiratory virus! How does this happen? There is evidence that ACE2 receptors are also located in spinal neurons and several parts of the brain:

  • substantia nigra
  • ventricles
  • middle temporal gyrus
  • posterior cingulate cortex
  • olfactory bulb

There are also suggestions that SARS-CoV-2 enters the neurological system through the olfactory epithelium, as there are ACE2 receptors on the surface and within the cells, which can take about seven days after initial infection. So that would mean that neurological infection takes place up to seven days before respiratory symptoms can begin to present. Based on these and other findings indicating that the actual olfactory nerves do not express ACE2 receptors, anosmia – or lack of ability to smell – may be cause by damage to the olfactory epithelium, no the olfactory nerve itself. Infection may also occur due to the virus crossing the blood-brain barrier through damage to the endothelium – or capillary cells – within the barrier itself, allowing increased permeability, or by way of infected white blood cells.

So, it is definitely possible that some patients who will eventually end up positive for COVID-19 will initially present with neurological symptoms such as confusion, AMS, weakness, myalgias, headaches, dizziness, and a host of other symptoms that would indicate neurological involvement. What seems to be the difference is that the neurological symptoms have a fast onset and fast progression in severity, unlike the respiratory symptoms which tend to progress more slowly and take longer to present at all. A recent study found that up to 36% of COVID-19 patients demonstrated severe neurological symptoms, like a stroke or impaired consciousness. Let’s take a look at some of the documented neurological diagnoses that have been directly linked to COVID-19…

Hypoxic Brain Injury. This one is kind of obvious but maybe we didn’t think of it before. Patients with COVID-19 are well known to be significantly hypoxic for long periods of time, possible even before they seek assistance or before they show symptoms. This hypoxia results in several metabolic process going awry and the brain tissues swelling. If this goes on long enough, the damage can be permanent. Intracranial edema is one of the fastest growing concerns as it can be present for extended periods of time before a person begins to show symptoms and seek medical help.

Immune-Mediated Injury. This is what I’ve actually been hearing the most about. Those “cytokine storms” we keep hearing about don’t just have negative effects on the lungs. They are a total body inflammatory response so all the other organs are also affected. The brain can be on the end of this storm and receive that damage just like any other organ. (We briefly discussed this here.)

Encephalopathy/Encephalitis. Headaches were reported in 40% of patients as a COVID-19 symptom. Confusion/altered mental status is also a very prevalent symptom. This is believed to be due to the cytokine storm, which crosses the blood-brain barrier. Some patients also present with seizures or altered levels of consciousness. There has been at least one case of a child patient presenting in this manner with a COVID-19 infection. Growing bodies of evidence out of the UK are now showing larger populations with this issue and age is no longer a factor. Many people hospitalized with forms of encephalitis have been between 30 and 40 years old.

This particular category of conditions is of the largest concern in recent research. In a recent study in BRAIN, 31 of 43 patients who presented with neurological complications demonstrated these types of pathologies. Intracranial edema is a growing issue in hospitalized and nonhospitalized patients, with increased hemorrhage rates. Medical providers are even seeing clinical encephalopathy/encephalitis without any changes to imaging findings. Reports of delusions, hallucinations, altered consciousness, and decreased cognitive impairment have all been reported as a primary symptom for these patients with confirmed COVID-19, all with little to no respiratory symptoms.

Myelitis. Also attributed to the cytokine storm, myelitis can develop at any spinal level with presentation of flaccid paralysis below that level. Acute Disseminated Encephalomyelitis (ADEM), a rare form of myelitis that typically only effects children, is also becoming a more frequent concern, especially in young adults. Mechanisms for this may include direct anterior horn cell viral damage.

Cerebrovascular Accident (CVA). The providers in my social media groups are no longer asking questions about hypercoagulation. Now we just know it’s there. The questions are moreso circulating around best ways to treat it. We have definitely found that early use of anticoagulants is crucial for survival in many patients hospitalized with COVID-19. CVAs continue to vary in etiology. Both ischemic and hemorrhagic are being reported at increased frequency, but ischemic significantly moreso. They are also being seen in people who have no hypertensive history and with normal PT/INRs. However, those at highest risk are those 60 year old or more with a history of hypertension or other comorbid risk factor for stroke. Large vessel ischemic strokes in patients of all ages are becoming a hallmark sign of stroke related to COVID-19.

A high percentage of those with CVAs also present with pulmonary embolism and a disseminated prothrombotic state, and with no medical history of any condition that would lead to a CVA. Some studies are showing that about 6% of those infected with COVID-19 will have a CVA. However, of those who will require hospitalization for neurological symptoms, up to 77% will have a stroke. CVAs may also be copresent with encephalopathy which makes diagnosis more difficult.

Guillain Barre Syndrome (GBS). Ascending paralysis and/or parathesias caused by demyelinating polyneuropathy that presents without known cause or shortly after recovery from a respiratory viral infection would always be considered a HUGE red flag. But the chances of developing GBS after COVID-19 are higher than that of other viral infections such as influenza. This has been reported as “rapidly progressing” in many cases. Read more about this in the post dedicated to Guillain Barre Syndrome. Newer research is finding that some patients are developing GBS up to three weeks after their symptoms have resolved. Some cases of GBS after COVID-19 are deemed an axonal variant, meaning that only motor pathways of a given nerve distribution are affected while sensory function remains intact. This is called acute motor axonal neuropathy and you can read more about it here. Sympathetic nervous systems may also be affected by this variant and produce sympathetic symptoms.

Skeletal Muscle Damage. This is, so far, a lesser seen neurological effect of COVID-19 (estimated at about 5-6% of neurological cases, not all cases). These patients initially present with myalgias and elevated creatine kinase as a possible cause. Other mechanisms are believed to be involved including other aspects of the medical history. This is also thought to be due to the cytokine storm and is thought that it may be a different type of end-organ failure (similar to the renal and hepatic failure we have otherwise discussed). However, it could also be ischemic damage due to DIC. Rhabdo has also been implicated as a cause for this injury.

Seizures. Mostly present in children, especially those with pre-existing seizure disorders including febrile seizures, seizures have actually been one of the primary presentations of COVID-19 in infants.

Chemosensory dysfunction. (altered sense of taste or smell) was present in 82% and 86% of COVID-19 positive patients, respectively. If patients are reporting this as a new onset symptom, therapists need to strongly consider referring the patient for testing. Onset of these symptoms is sudden. See more details above on ACE2 receptor causes for this. These symptoms can occur in isolation and be the ONLY symptoms a person experiences. – Verified symptom now!

The Lancet Neurology has created the following depiction of symptom onset for several of the above neurological associated conditions for patients who have COVID-19. You can see that GBS, encephalitis, and CVA can actually present prior to the onset of any other symptoms.


So then, as a therapist, what do you need to know?

First off, you should note, especially when attempting to establish a neurological baseline on evaluation, that 67% of patients with “severe forms” of COVID-19 had positive upper motor neuron signs. So your Hoffman’s, Babinski, and Clonus may be positive. You may see increase muscle tone, hyper-reflexia, areflexia, or tongue deviation. These signs are never necessarily permanent because we know that lesions have some ability to heal, so you may notice them fading over time. You do need to know that, just because someone doesn’t have respiratory symptoms, doesn’t mean they don’t or won’t have a severe form of COVID-19. It’s really all about what end-organ system takes the brunt of the virus. If you suspect COVID-19, send the patient for testing.

Photo by Renzy Atibagos on

How does this apply to you and how should it inform your practice?

Many PTs treat patients for headaches. Many more PTs also treat patients for dizziness. Sometimes the headaches and dizziness are co-occuring. Rehab therapists need to be on alert when patients begin reporting these symptoms during this time. Their social distancing and safety behaviors need to be discussed and they may need to be tested for COVID-19. These symptoms are the most commonly reported in patients who experience neurological presentations of COVID-19. Few have offered reasoning behind this other than that these are typical symptoms of the body’s immune response to a virus and that we all feel these things sometimes when we are sick. But, like we mentioned above, brain edema can go undetected and present with these symptoms. Given that information, therapists evaluating patients (or continuing to treat patients for other things, but the patients begin reporting these symptoms) need to give strong consideration to the risk of the patient having COVID-19. The therapist needs to thoroughly examine the patient’s risk profile and refer for testing through the referring provider, PCP, or directly to a testing center if available. This is especially true if the patient is also reporting changes in sense of taste or smell.

One of the larger concerns coming forth is something I’ve talked about here before. When even mild cases of COVID-19 can present with moderate to severe neurologic impairments and damage in the acute phase, you have to wonder about long term effects. Many neuroscientists are concerned about the long term effects of COVID-19, and that delayed onset of medical issues resulting from infection could significantly impair someone’s ability to work and function. Post-COVID syndrome is still a very real concern. Only time will tell. But, early diagnosis can improve outcomes so be the front line. Be the primary care provider you should be.

There is a researcher at Cambridge who has opened a large-scale patient case study for those with COVID-19 who can take a series of tests related to their cognitive function. People can enroll in the study and take these tests to determine how their brain function may have changed as a result of COVID-19 infection. If you or your patients are interested in enrolling in the study, you can check out the link by clicking on the button below.

So, for all you therapists in the outpatient world out there treating those still in need, please keep your eyes peeled. Screening is key and early detecting and testing can save lives. Be on the lookout for symptoms of DVT and PE in addition to all the other COVID-19 symptoms we discussed here. As we see more patients transition to sub-acute, home, and outpatient settings, be sure to assess and document neurological baselines in your patients. These changes can literally be the difference between and ED visit and an ICU admission.

Be careful out there.

While treating your patients who have COVID-19, have you noticed any pattern of neurological findings? Let me know in the comments!

More Reads…

Diaphragmatic Breathing

Let’s talk about this super simple technique that can change everything. Diaphragmatic breathing is really just how we are all supposed to be breathing most of the time. The purpose of the diaphragm is to facilitate breathing. Diaphragmatic breathing improves gas exchange and increases lung volumes. These are all really good things if we need toContinue reading “Diaphragmatic Breathing”

I’ll Huff and I’ll Puff… But the Huff Will Be More Effective

What is a huff? Huffing is one of the more difficulty techniques to learn for airway clearance. I find that most of my patients have trouble mustering the strength to perform a good solid huff. It’s not just that it is unfamiliar, but also that it takes diaphragm strength that they just don’t have. ButContinue reading “I’ll Huff and I’ll Puff… But the Huff Will Be More Effective”

Vibration & Percussion

If you read my post on airway clearance techniques, you probably saw vibration and percussion down at the bottom of the force progression. Although I have covered several other pieces of the force progression (Active Cycle of Breathing, PEP Devices, etc) in subsequent posts, I haven’t touched on these topics yet because they haven’t beenContinue reading “Vibration & Percussion”


Something went wrong. Please refresh the page and/or try again.

Follow my blog for more!


Ahmad, I.; Rathore, F.A. Neurological Manifestations and Complications of COVID-19: A Literature Review. Preprints 2020, 2020040453 (doi: 10.20944/preprints202004.0453.v1).

Avula, A., Nalleballe, K., Narula, N., Sapozhnikov, S., Dandu, V., Toom, S., Glaser, A., Elsayegh, D. (2020). COVID-19 presenting as a stroke. Brain, Behavior, and Immunity. 87:115-119. Retrieved from

Chen,  R., Wang,  K., Yu,  J., Chen,  Z., Wen,  C., Xu,  Z. (2020). The spatial and cell-type distribution of SARS-CoV-2 receptor ACE2 in human and mouse brain.

Ellul, M. A., Benjamin, L., Singh, B., Lant, S., Michael, B. D., Easton, A., Kneen, R., Defres, S., Sejvae, J., Solomon, T. (2020). Neurological associations of COVID-19. The Lancet Neurology. [corrected proof in press] Retrieved from

Kelland, K. (2020). Scientists warn of potential wave of COVID-linked brain damage. Reuters. Retrieved from

Mao, L., Jin, H., Wang, M., et al. (2020). Neurologic manifestations of hospitalized patients with coronavirus disease 2019 in Wuhan, China. JAMA Neurol. Retrieved from

Mao, L., Wang, M., Chen, S., He, Q., Chang, J., Hong, C., Zhou, Y., Wang, D., Li, L., Jin, H., Hu, B. (2020). Neurological Manifestations of Hospitalized Patients with COVID-19
in Wuhan, China: a retrospective case series study. medRxiv.

Owen, A. (2020). Participate in the COVID-19 Brain Study—a global study of how the virus affects cognition. The Cambridge Brain Institute. Retrieve from

Paterson, R. W., Brown, R. L., Benjamin, L., Nortley, R., Wiethoff, S., Bharucha, T., Jayaseelan, D. L., Kumar, G., Raftopoulos, R. E., Zambreanu, L., Vivekanandam, V., Khoo, A., Geraldes, R., Chinthapalli, K., Boyd, E., Tuzlali, H., Price, G., Christofi, G., Morrow, J., McNamara, P., McLoughlin, B., Lim, S. T., Mehta, P. R., Levee, V., Keddie, S., Yong, W., Trip, S A., Foulkes, A. J. M., Hotton, G., Miller, T. D., Everitt, A. D., Carswell, C., Davies, N. W. S., Yoong, M., Attwell, D., Sreedharan, J., Silber, E., Schott, J. M., Chandratheva, A., Perry, R. J., Simister, R., Checkley, A., Longley, N., Farmer, S. F., Carletti, F., Houlihan, C., Thom, M., Lunn, M. P., Spillane, J., Howard, R., Vincent, A., Werring, D. J., Hoskote, C., Jäger, H. R., Manji, H., Zandi, M. S. (2020). The emerging spectrum of COVID-19 neurology: clinical, radiological and laboratory findings. Brain. [accepted manuscript] awaa240. Retrieved from

Steardo, L., Zorec, R., Verkhratsky, A. (2020). Neuroinfection may contribute to pathophysiology and clinical manifestations of COVID-19. Acta Physiol. (Oxf.) Article e13473

Woodward, A. (2020). The coronavirus may cause brain damage, even in patients with mild cases, a new study found. Retrieved from

Zubair, A. S., McAlpine, L. S., Gardin, T., Farhadian, S., Kuruvilla, D. E., Spudich, S. (2020). Neuropathogenesis and Neurologic Manifestations of the Coronaviruses in the Age of Coronavirus Disease 2019: A Review. JAMA Neurol. Published online. doi:10.1001/jamaneurol.2020.2065

Follow @DoctorBthePT on Twitter for regular updates!

According to the Scientific Community, It’s Time for Change

If you couldn’t tell, I’ve been hinting at this for a while. In several posts over the past few months, there has been discussion amongst the medical community that has created controversy regarding the mode of transmission of COVID-19. Many providers of all disciplines have been very concerned about their contraction rates and that of their coworkers, even when utilizing the proper droplet precautions prescribed by national guiding agencies. Many healthcare providers felt they were being mislead and that COVID-19 was actually being transmitted by another means, other than droplets.

I mentioned this controversy in the Webinar I gave for the Michigan Physical Therapy Association. I was also very clear that we were still under droplet precautions at that time and we currently are STILL under those precautions now. However, as of July 6, 2020, over 1000 healthcare providers around the world have died from COVID-19. You can read about all of them here.

Photo by Anna Shvets on

In addition to that, as of May 21, 2020, studies showed that only 1% of healthcare workers (outside of the US) contracted COVID-19. However, they found that a higher percentage of the healthcare workers that contracted it never worked in high risk areas or with positive patients than those who did not. They also found that as many as 93% of healthcare workers actually reported symptoms of COVID-19 but were never tested. This likely indicates that healthcare workers who worked in non-high risk places who did not utilize aerosol precautions in their PPE were more likely to contract COVID-19 from asymptomatic (and therefore untested) patients. The risk of nosocomial transmission was relatively low overall in high risk places because aerosol precautions were utilized.

And, let’s be very clear: TO DATE 94,097 healthcare workers have been confirmed positive with COVID-19 just in the US (per the CDC), with over 500 deaths. Here is a snapshot taken directly from their website today (July 8, 2020). As you can see, they only have data for a very small percentage of overall patient cases to determine employment status so this number is likely severely underestimated. You can also see they had just over half the data on deaths, so another likely underestimate.


I am not saying all of this to scare healthcare professionals, actually the opposite. I’m saying all of this because you all need to know your risk and you need to stand up for the proper safety equipment to protect yourselves. And you need the data to do it! Because some employers won’t put up for N95s or PAPRs or shields unless you have the data to back up your request. Thankfully, Ive been hearing from colleagues that many employers are now ordering the proper PPE for aerosol precautions. This also changes the definition of aerosol-generating procedures, as pretty much anything that produces breathing will now fall under this category for COVID-19. COVID-19 will join the ranks of airborne-transmission conditions along with tuberculosis and measles. And remember, these are things healthcare providers work with every single day.

Researchers all around the world have been working furiously to study the transmission of COVID-19 and their findings have been leaning a different direction. Many of them, including the MIT researchers I told you about in this post, are finding that live virus is easily aerosolized with activities as simple as talking, and especially when singing and exercising. But time and time again, this research has been ignored or shot down. To quote one of the researchers:

“…the importance of airborne transmission has not been considered in establishment of mitigation measures by government authorities.”

See original post

So, the big news is that, just yesterday, a national guiding association has acknowledged the importance of this research. Maria Van Kerkhove and Bendetta Allegranzi, technical leads on the COVID-19 pandemic for The World Health Organization (WHO), announced that they have begun to assess the research being performed, funding more of it, and considering the implications this may have for their guidelines. They are considering the changes that may need to be made given the new information, not just for healthcare but for the world. The evidence they are considering is that, to date, 239 scientists in 32 countries have outlined evidence of aerosol transmission. That’s a pretty big stack of articles to read.

If all (or even a good chunk) of those studies were performed with the proper scientific rigor, I think we will be seeing a big change in the required precautions for healthcare workers as well as the general public when it come to COVID-19. Given this information, I don’t think face masks will be going away anytime soon!

You can view the new briefing with the representatives from the WHO here (specific discussion regarding aerosol-based transmission is at about 10:00):


You can also read the open letter sent to the WHO from the 239 researchers (many of whom are engineers) which is in the accepted manuscript formate in Clinical Infectious Disease HERE, available free from Oxford Academic. Remember how important these folks are in the prevention of disease transmission? If you need more info on this, check out this post on engineering controls.

Do you feel you have the resources needed to ask for the proper equipment to protect yourself and your patients in your work setting? What else do you need? Let me know in the comments!

More Reads…

More Than Just A Respiratory Disease: The Tools You Need to Rehab COVID-19

Isn’t COVID-19 just a respiratory disease? If only that was true. We are good at treating respiratory infections. We have lots of drugs for viral, bacterial, parasitic, and fungal infections of the lungs. Most of them work really well! We also have several back-up treatments, inhaled medications, and adjuvant therapies (like rehab!) that make primaryContinue reading “More Than Just A Respiratory Disease: The Tools You Need to Rehab COVID-19”


Something went wrong. Please refresh the page and/or try again.

Follow my blog for more!


Centers for Disease Control and Prevention. (2020). Coronavirus Disease 2019: Cases in the US. Retrieved from on July 8, 2020.

Lidia Morawska & Donald K Milton. (2020). It is Time to Address Airborne Transmission of COVID-19, Clinical Infectious Diseases, ciaa939 [accepted manuscript], retrieved from

No Author. (July 8, 2020). WHO acknowledges ‘evidence emerging’ of airborne spread of COVID-19. The Economic Times: World News. Retrieved from

No Author. (April 1, 2020). In Memoriam: Healthcare Workers Who Have Died of COVID-19. Medscape. Retrieved from

World Health Organization. (2020). Media briefing on COVID-19 (July 7, 2020). Retrieved from

Van Beusekom, M. (2020). Studies: 1% of healthcare workers had COVID-19. Center for Infectious Disease Research and Policy: CIDRAP News. Retrieve from

Follow @DoctorBthePT on Twitter for regular updates!

ABGs (Part 1)

This is the first post in a two-part series about understanding and interpreting arterial blood gases! If you want the rest of the post, you’ll have to check back next week!

I’m getting real science-y again!

So, just a heads up: my undergraduate degree was in chemistry. Kind of by accident, I took a lot of chemistry courses. I know that sounds a bit weird, but I had an odd schedule and chemistry classes filled the gaps. I didn’t even necessarily like them, but I did gain a lot of understanding when it came down to organic chemistry and physiological concepts. When it came time to learn about acid-base buffers, I was ahead of the game. When it came time to apply that to the human body, I was all over it. That’s how I view arterial blood gases. It’s like a chemistry homework question from undergrad. You just have to apply the same conceptual framework every time and you will figure it out. So, I’m going to teach you that conceptual frame work, step by step. I promise, it won’t be that hard!

Arterial blood gases (ABGs) are performed when it is suspected that a patient may be in alkalosis or acidosis (depending on the circumstances). It is a relatively painful arterial puncture (…so I’m told. I’ve never had one, but all my patients say it hurts much more than venipuncture). The arterial blood is oxygenated (unlike venous blood), so it shows you a bunch of information about how the acid-base buffer system in the human body (the BiCarb Buffer System) is functioning. These tests are regularly performed on people who have chronic lung, heart, or kidney disease, because all three of these organ systems are intricately intertwined and have significant impact on the oxygenation of tissues. However, there are some other diagnoses that will result in a patient requiring ABGs to be checked and we will talk about some of those here, too!

H+ + HCO3- < — > H2CO3 < — > CO2 + H2O

The above equation basically runs our body chemistry. We want to hang out around the middle. Humans have a VERY small window in which we can properly function, but we’ll talk more about that later. For the basic purposes of this post, we will say that humans exhale CO2 and inhale oxygen. We know there are lots of other gases involved, but we are going to focus on those for now. So you can imagine, if we exhale too much, we lose too much CO2 and we fall too far toward the left. If we don’t exhale enough, we accumulate too much CO2 and we fall too far toward the right. CO2 has a higher affinity for hemoglobin than oxygen (that good old oxygen-hemoglobin dissociation curve from physiology soooo many years ago…) so we have to focus on CO2. I know, all of this sounds a bit overwhelming. There is a lot to know, but I promise, I will break it down and make it easy for you!

Oxygen-Hemoglobin Dissociation Curve - Respiratory - Medbullets Step 1

Basically, what this O2-HbG dissociation curves shows us is that the more oxygen we have, the easier it is to bind more oxygen. But as we lose oxygen and bind more CO2, it becomes easier to lose oxygen and bind more CO2. This is called the Bohr effect and, as you can see, it can hit a critical point. You can see that it is also effected by temperature and pressure. You can probably infer that profound anemia would also impact this curve. You can read more here about how the amount of hemoglobin affects your oxygen levels.

Chemistry is a really gray area in that it does its best to estimate amounts, but the reality is that, in a living system, they are estimates in time. Think about water. At any given time, you have liquid water, H2O, as well a gaseous hydrogen and oxygen molecules floating around binding and unbinding with each other in all different combinations (like H2O2 – hydrogen peroxide which is very volatile) in the same container. Water is a very stable molecule, but many bodily substances are not. Let’s talk about acidosis and alkalosis. We need to define a couple terms in case you aren’t as fresh on your chemistry:

pH. Typically thought of as “how acidic or basic something is”. A low pH indicates acidic, a high pH indicates basic. Normal human pH is 7.34 to 7.45.

Acidosis. When too many hydrogen ions [H+] build up in the body in some form (carbonic acid or lactic acid). Hydrogen ions are the basic unit of an acid. Body pH would be below 7.35.

Alkalosis. When too much bicarbonate [HCO3-] builds up in the body. Bicarbonate is a base. Body pH would be above 7.45.

Now that you’ve got the basics, let’s do some application.

Respiratory Acidosis. Results from hypoventilation leading to increased CO2 in blood and decreased pH. Things that cause this condition include pretty much anything that decreases your ability to remove CO2 (diffusion and ventilation). That would include respiratory suppression from drug usage, Giullian-Barre Syndrome, a brain injury to respiratory center, or airway obstruction (acute or chronic).

However, this condition can also be caused by an increased oxygen metabolism without compensating with a change in ventilation. What might cause that? A large amount of tissue damage requiring a large amount of healing such as in burns or sepsis (like COVID-19). When it presents acutely, respiratory acidosis is a medical emergency and requires immediate medical intervention. Acute-on-chronic respiratory acidosis would also require emergency medical intervention.

Photo by Pixabay on

Wait… Did Doctor B just say that a medically emergent condition can be chronic? Yep, I did. Respiratory acidosis can be chronic in patients with COPD and some other obstructive airway conditions. Their bodies get so used to being oxygen deprived that they no longer compensate with an increased respiratory rate. Respiratory acidosis just becomes their normal state. Arterial blood gases then really come in to play to establish when someone becomes a CO2 retainer. This is a HUGE safety factor and one of the most important reasons rehab professionals need to be able to interpret ABGs. Please read this post on CO2 retainers and this post on oxygen saturation for more information.

Respiratory Alkalosis. This happens when hyperventilation results in the removal of too much CO2 which results in increased pH. Respiratory alkalosis is rarely life threatening (unless the patient is also in acute respiratory distress) and can be easily treated. Panic attacks are sometimes characterized with these symptoms, and can result in people passing out, which effectively stabilizes their respiratory rate and they return to normal.

This is one of the complications for patients who have COVID-19. They are in respiratory distress due to low oxygen levels, but then can also push too far in to alkalosis by breathing too quickly trying to get more oxygen (which won’t be effective due to parenchymal damage). This can also be a complication in the process of recovering from COVID-19, as patients can demonstrate oxygen starvation resulting in similar behavior. Treatment is fairly simple if the patient isn’t in ARDS: reduce the respiratory rate or use a rebreather. These treatments can be achieved in a few different ways:

  • Reducing respiratory rate could be achieved by breathing control, diaphragmatic breathing, or increasing oxygen titration (as able). Sometimes distraction, prayer, meditation, biofeedback, or education can help with this also.
  • Using a rebreather is probably what you think of when you see someone breathing in to a paper bag. We, of course, would use medical equipment for this type of thing, with different rebreather masks available, but the concept is the same. The patient breathes in some of the CO2 they exhaled in to the bag/mask and the concentration of CO2 in their blood increases.

When treating respiratory alkalosis, you have to monitor to ensure your patient doesn’t swing the opposite direction in to respiratory acidosis by increasing their CO2 levels too much.

Metabolic acidosis. This results when the body produces too much acid and the kidneys cannot remove it quickly enough which results in a decreased pH. As with respiratory acidosis, this is a medical emergency, and can result in coma or death. Metabolic acidosis can be caused by several factors: rhabdomyolysis, starvation, exercise bulimia, aspirin (abbreviated ASA = acetyl-salicylic acid) overdose, etc… as these processes result in acid build up. Oddly, overuse of the laxative polypropylene glycol (MiraLax) that ALL of your patients are on can also cause metabolic acidosis due to the chemical breakdown of this substance. I know that sounds weird, because you’d think if they were getting rid of all that stomach acid, they would become alkaline, but that isn’t the case with this specific agent. MiraLax is metabolized in to an acid. Other causes may include kidney failure and acute/chronic ethanol intoxication, but many causes are possible and it is difficult to detect without ABGs.

Photo by Oleg Magni on

However, just like with respiratory acidosis, metabolic acidosis can also become chronic. This can happen in patients who have uncontrolled Type 2 Diabetes Mellitus. We just have a different name for it (ketoacidosis). Ketoacidosis can be acute as well, so you still need to be calling for medical help. Thankfully, there is something you can do for these patients:

  • If you happen upon someone who is in metabolic acidosis, you can help them temporarily (long enough to call 911 and get an ambulance to them) as this condition can be compensated using hyperventilation! This works by expelling the CO2 making up carbonic acid in their bodies to slightly offset the acid levels. Like I said, this is temporary and only buys time. It is NOT a cure! Metabolic acidosis will persist until treated.

Metabolic alkalosis. The removal of too much acid (or too many H+ ions) from the body which increases pH. Metabolic alkalosis can be caused by vomiting, diarrhea, severe diuresis, dehydration, or, in rare cases, loss of sodium in sweat glands solely associated with cystic fibrosis. Metabolic alkalosis cannot last long if the kidneys are well functioning, as the kidneys will compensate by retaining more H+ ions and Na+ ions. This condition typically presents with low blood pressure, low blood volume, elevated heart rate, and lethargy. Patients may be significantly orthostatic. However, it can also present with hypervolemia in the case of heart failure patients in fluid overload depending on the electrolyte factors involved and the kidney function impairments.

This condition can also be compensated in the same way respiratory alkalosis can be compensated: with use of a rebreather or by reducing the respiratory rate.

As it so happens, though, I see people with metabolic alkalosis ALL THE TIME who need medical intervention. My typical caseload involves people with mulitple complex chronic diseases. For many them, their kidneys are NOT functioning properly. For most, medical intervention takes the form of IV fluids with different levels of sodium (Na+), potassium (K+), or lactic acid (Ringer’s Lactate solution). For those with heart failure, they can actually be in fluid overload but not have any usable fluid so be exhibiting the symptoms of hypovolemia at the same time. This becomes a delicate dance of giving them enough usable fluid while simultaneously pulling off the unusable fluid, which has to be done under close observation in the inpatient setting.

OK, so now that you’ve got the basics, I’m going to let you marinate on that for a while. In Part II of this post, we will talk about compensated conditions, how to read ABGs, and how to tell what condition your patient is in. This will help you understand when it is safe to treat them based on these values. Keep checking back!

How often do you get the chance to read ABGs before the ordering provider? How do you use that information? Tell me about it in the comments!

More from the Pulmonary Rehab Toolbox…

Postural Drainage

We’ve all seen that dreaded picture in our textbooks… All the human figures laying in so many different positions with pillows and tables tilted all over… and I very clearly remember thinking, “How on earth am I supposed to remember all of those?” Well, good news. You really don’t have to. It’s great if youContinue reading “Postural Drainage”

Spilling the Box of Pearls: All the Tips on Supplemental Oxygen Management

In my recent post on COPD management, I mentioned that there are some really important parts of supplemental oxygen management that you need to be aware of and consider in your practice. If you are assisting patients who utilize supplemental oxygen regularly, you need to keep these things in mind. You also may be workingContinue reading “Spilling the Box of Pearls: All the Tips on Supplemental Oxygen Management”

Chronic Disease Part 2: Chronic Obstructive Pulmonary Disease (COPD)

This is part 2 in a multi-part series on the role of Rehab Providers in the management of chronic disease. Don’t forget to check out Part 1: Heart Failure! Chronic Obstructive Pulmonary Disease is a widely diagnosed disease of the lungs that includes the diagnoses of emphysema and chronic bronchitis. COPD can be caused byContinue reading “Chronic Disease Part 2: Chronic Obstructive Pulmonary Disease (COPD)”


Something went wrong. Please refresh the page and/or try again.

Kaufman, D. (2020). Clinical Education: Interpretation of Arterial Blood Gases (ABGs). American Thoracic Society. Retrieved from

Lewis, J. (2020). Acid-Base Disorders. Merck Manual Professional Version. Retrieved from

Follow @DoctorBthePT on Twitter for regular updates!

Aerosol Generating Procedures

The long awaited clarification on aerosol generating procedures for physical therapists and physical therapist assistants has finally dropped! The APTA just released its professional guidelines for what portions of physical therapist and physical therapist assistant care equates to an aerosol generating procedures, therefore requiring increased PPE for procedure performance to ensure clinician safety. On April 13, 2020, the Centers for Disease Control (CDC)  updated their guidance to indicate that aerosol generating procedures (AGPs) are medical procedures that are “more likely to generate higher concentrations of infectious respiratory aerosols than coughing, sneezing, talking, or breathing” and result in “uncontrolled respiratory secretions.” However, exactly what that meant when it came to Physical Therapist services was unclear. Most people, even in the medical world, forget that we do so much more than exercise.

In my Webinar on Combatting COVID, I was very clear that the WCPT guidelines listed exercise as an aerosol generating procedure. However, many healthcare organizations in the United States do not observe the WCPT guidelines, so were defaulting to the CDC guidelines which are silent on “exercise” as a specific term. The CDC guidelines did provide a nice table (which you can view here) that was supposed to guide which level of PPE all healthcare providers should be wearing. But, let’s be real. MOST healthcare providers are not performing the type of work-intensive and time-intensive interventions that we are in the rehab field. Respiratory therapists are definitely taking the brunt of the risk with the number of AGPs they regularly perform. However, many of these don’t take nearly as much time as what we need to perform. Time spent in exposure is one of the most important factors when deciding level of risk involved with a procedure (based on the CDC table mentioned above).

“Mobilization in and out of bed, ambulation, therapeutic exercise, and other similar physical therapist interventions are common procedures performed in intensive care units, hospital wards, inpatient rehabilitation units, other facilities, and patient’s homes. These sessions, which can last 30 minutes or more, result in extensive close body contact; for some procedures PTs and PTAs place their faces within inches of the patient’s face to ensure safety (Loeb, 2004).”

APTA (2020)

But we also need to talk about proximity. When we are transferring a patient, we are ALL UP IN THEIR BUSINESS. We are face to face, we are ear to ear, we are body to body. And for our SLP friends, you are very literally all up in their grill. So proximity increases the risk of allowing droplets to land in your muscosa (ew…). Many healthcare professionals get to stand back and observe, or take vitals using an automated machine and not have to touch. Even starting an IV, you can at least be at arms length. But not while working on perineal hygiene… NOPE. You are well within the danger zone.

Photo by cottonbro on

And finally, we are making the patient MOVE! We are working them harder than they may have worked in a several days, weeks, or months depending on the setting. We know from recent research that even talking can aerosolize viral particles in to droplet nuclei, so can you just imagine with the huffing and puffing of sit to stands will do? I know people are pretty upset about gyms being closed but, take it from a PT, there is darn good reason for gyms to be closed! You are in a small space with several people (even at 6 feet apart) all huffing and puffing increased lung volumes, forces, and depths, aerosolizing droplet nuclei in clouds, over and over and over again. There is no amount of environmental control that could save you. But, here comes therapy, down the hall in full PPE, ready to work the sickest folks and hang out them in that cloud for 30 minutes or more. So, the obvious answer was yes, therapy interventions OF COURSE are aerosol generating procedures. But you didn’t have to convince us of that…

“Assisting a patient in moving from supine to sitting increases the depth and rate of ventilation, and creates a shift in ventilation and perfusion patterns, in a manner that often elicits uncontrolled respiratory secretions and/or cough reflex. Rolling, proning, and supinating a patient in bed also are considered aerosol-generating procedures.”

APTA (2020)

We don’t really need to just focus on exercise and physical activity. Patients with COVID-19 are critically ill. Many of the patients I see regularly are critically ill because I work with many people who have complex chronic diseases. That means there is a significant likelihood that CPR may be needed at some point in time. I have had plenty of coworkers who have arrived at a home and had to start chest compressions. I’ve been a first responder to so many people just randomly out in public at train stations, sporting events, or even weddings. But then, to add strenuous physical activity on top of a critical illness, we are upping the ante (because that’s what we are trained to do). In the event we do have to perform CPR, if we are not already donned in appropriate PPE, the APTA has made it clear that it takes approximately 6 minutes to do so. That’s 6 minutes our patient goes without oxygen to their brain. That, my friends, is not a patient that will survive. Those 6 minutes are crucial so we need to be ready to go at the onset.

Photo by cottonbro on

Ultimately, rehab clinicians literally have to do all three things that create the most aerosol AND places the provider at highest risk. Yet there was no clear statement from any agency or authority, only “exercise” listed on the WCPT guidelines. Many saw that as not including physical activity like transfers or bed mobility. Thankfully, ASHA released a document clarifying the provision of Speech-Language Pathologist Services in regards to aerosol-generating procedures to set guidelines for their own profession. So, I (and many others, I’m sure) have just been waiting…

“Across respiratory conditions, mobility and exercise are known to be a form of airway clearance, often resulting in uncontrolled respiratory secretions and bouts of spasmodic coughing (Strickland, 2013).”

APTA (2020)

I hope everyone takes a read on this one, prints it out, takes it to work, posts it in the office, in the hallways, screams it from the mountaintops and whatever you need to do to make sure you get the proper equipment you need to keep yourself safe when treating patients. The highest number of new cases of COVID-19 are among those 20-40 years old. There are many people in the ICU within that age range including several without underlying conditions. I’ve said it before, and I’ll say it again, COVID doesn’t discriminate. Please take necessary precautions and stay safe out there.

Read the original publication here:

I know it’s been a long time coming, but are you getting the proper PPE yet? Let me know in the comments!

A Public Service Announcement: The Chain of Infection (and How YOU Can Break It!)

This post is written for one and all. If you are not a rehabilitation or medical professional, please read this post. Even if you are, please read this post. I’m going to address some things that need clarification. You can have all the opinions you would like, but there are some things that are justContinue reading “A Public Service Announcement: The Chain of Infection (and How YOU Can Break It!)”

Open Heart, Open Mind… Learning About Amio-Loading

I’m always learning something new. I called the cardiologist after an evaluation to report some severe orthostatic hypotension and the nurse and I got to talking. She was going back through the patient’s history and looking for why this may be happening. I had just finished assessing the patient in their home and they wereContinue reading “Open Heart, Open Mind… Learning About Amio-Loading”

Blood Pressure Basics

Are you taking the blood pressure and heart rate of EVERY patient you see for a new evaluation? How about for every visit? A recent survey of over 1800 Outpatient PTs showed that although 51% of PTs reported that over half their caseload had risk factors for hypertension and cardiovascular disease, only 14% of themContinue reading “Blood Pressure Basics”


Something went wrong. Please refresh the page and/or try again.

Follow my blog for more!


APTA. (2020). Taking Precautions for Mobility and Exercise as Potential Aerosol-Generating Procedures. Retrieved from

Follow @DoctorBthePT on Twitter for regular updates!

The Duet Device

Have you seen an Acapella Duet before? This is another one of those things I wish I could hand out to maybe half of my patients.

  • A Duet device is a special kind of Positive Expiratory Pressure (PEP) that provides resistive oscillatory pressure to exhalation which promotes increased lung volumes due to re-inflation of collapsed airways, but in addition to positive pressure reinflation, it also allows for the nebulization of medications simultaneously.
  • Typically given by RT while a person is hospitalized to increase efficacy and effectiveness of nebulizer treatments, however, patients are not typically instructed on how to use them independently. Or, if they are, they don’t remember by the time they get home or to their next facility.
Keylab Medical · Distribución de productos hospitalarios ...

Patients who benefit from Duet use:

Cystic Fibrosis
Chronic Bronchitis
Pre/Post Lung Transplant

Or anyone doing nebulizer treatments. However, nebulizer treatments are not being recommended for patients with COVID-19, unless they are in a closed environment (like a negative pressure room with only medical professionals in attendance) as nebulizers aerosolize viral particles into the air.

What does the evidence say about using PEP with nebulizers? Does it actually work?

  • In Cystic Fibrosis patients, nebulized medication deposition decreased but distribution increased when a duet device was used.
  • In Asthma patients, nebulized medication deposition increased and distribution increased, specifically to the middle and lower thirds of the lungs when a duet device was used.
  • Use of PEP in patients with COPD reduces post-exercise dyspnea and increases length of time the patient is able to participate in exercise. PEP also reduces dynamic hyperinflation, even at only 5cm of H2O of pressure.
  • In healthy subjects, tracers were used and researchers found that using PEP with nebulized medications improves membrane permeability (diffusion) of the medications. They also found that higher pressure were tolerable, from 10-20 cm of H2O.
  • As we discussed in this blog post, there is no evidence informed protocol for PEP use yet.

How to Set Up the Nebulizer with the Duet for treatments:

As more patients are coming home from acute care after COVID-19, and hopefully testing negative, some will continue to require ongoing treatment for the damage done to their lungs. This may be in the form of nebulized medications once they are no longer carrying the virus.

To improve your patients ability to participate in physical activity or exercise, they should be performing their nebulizer treatments at least 15-20 minutes before activity. This may mean that you need to instruct them how to do this and them as them to make sure it is done before you see them for the next visit. This gives the medications (typically bronchodilators) time to do their job: open up the airways to improve ventilation, and hopefully diffusion, and hopefully perfusion.

I always request duet devices for my patients who are running nebulizer treatments, if I feel they also need airway clearance or dynamic hyperinflation management. Have you ever used duet devices? Tell me about it in the comments!

More from the Pulmonary Hygiene Toolbox…

Aerosol Generating Procedures

The long awaited clarification on aerosol generating procedures for physical therapists and physical therapist assistants has finally dropped! The APTA just released its professional guidelines for what portions of physical therapist and physical therapist assistant care equates to an aerosol generating procedures, therefore requiring increased PPE for procedure performance to ensure clinician safety. On AprilContinue reading “Aerosol Generating Procedures”


I spent some really great times as an educator in a heart and lung transplant program at a large hospital system. Specifically, I was a therapy educator. I taught PTs, PTAs, OTs, COTAs, and SLPs what they needed to know to safely provide rehab to patient after heart and lung transplants. I saw so manyContinue reading “FEV1”


Something went wrong. Please refresh the page and/or try again.

Follow my blog for more!


Albuquerque, I. M., Cardoso, D. M., Masiero, P. R., Paiva, D. N., Resqueti, V. R., Fregonezi, G. A., & Menna-Barreto, S. S. (2016). Effects of positive expiratory pressure on pulmonary clearance of aerosolized technetium-99m-labeled diethylenetriaminepentaacetic acid in healthy individuals. Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia42(6), 404–408.

Alcoforado, L, et al. (2013). Evaluation of lung function and deposition of aerosolized bronchodilators carried by heliox associated with positive expiratory pressure in stable asthmatics: A randomized clinical trial. Volume 107, Issue 8, Pages 1178–1185;

Laube, B, et al. (2005). Positive Expiratory Pressure Changes Aerosol Distribution in Patients with Cystic Fibrosis. Respiratory Care, 50 (11) 1438-1444

Padkao, T., Boonsawat, W., & Jones, C. U. (2010). Conical-PEP is safe, reduces lung hyperinflation and contributes to improved exercise endurance in patients with COPD: a randomised cross-over trial. Journal of physiotherapy56(1), 33–39.

Ubolsakka-Jones C, Pongpanit K, Boonsawat W, Jones DA. Positive expiratory pressure breathing speeds recovery of postexercise dyspnea in chronic obstructive pulmonary disease. Physiother Res Int. 2019;24(1):e1750. doi:10.1002/pri.1750

Follow @DoctorBthePT on Twitter for regular updates!


I spent some really great times as an educator in a heart and lung transplant program at a large hospital system. Specifically, I was a therapy educator. I taught PTs, PTAs, OTs, COTAs, and SLPs what they needed to know to safely provide rehab to patient after heart and lung transplants. I saw so many of these patients both at our hospital and at their homes and helped transition them to cardiac and/or pulmonary rehab programs when they were ready. I loved working with this population! I mostly enjoyed the complexity of this type of case. Most of the time, they had a long course of illness prior to transplant. Some of them I even had the honor of pre-habbing prior to transplant and it was great to see them make that transition. After transplant, they felt like a new person!

But regularly seeing patients after transplant means knowing a specific set of symptoms to look out for because you have to be constantly monitoring for rejection. We will talk much more about transplants in another post but, some of those symptoms include:

  • Resting Heart Rate less than 60 bpm
  • Fatigue
  • Shortness of breath at rest
  • Malaise
  • A feeling of chest pressure
  • Dry cough
  • Decreased exercise or activity tolerance
  • A decrease in lung function of 10% or more

Let’s take a closer look at that last one. How can we know if someone’s lung function has decreased by 10%? Well, you have to look at a measure of lung function. The one we used was FEV1, or forced exploratory volume in 1 second. This is the percentage of air you are able to forcibly exhale from your lungs in 1 second, after taking a maximal inspiration, and in comparison to your predicted ability. This may seem like a strange measurement, especially since it’s different for everyone and based on several factors, like your gender, but let’s break it down and you’ll see why it’s so important.

If you remember how lung volume works as I described in my video in dynamic hyperinflation, after you take a deep breath in, you have to get all that air out. And if you have an obstructive disease, you have to get even more out than what you put in. So the strength of your diaphragm begins to become a significant factor in your lung function. Therefore, FEV1 is a significant diagnostic factor for obstructive and restrictive lung disease. This also continues to be true after transplant. These patients are typically working with a weakened diaphragm from whatever disease state they experienced prior to transplant. As they rehab and heal, we expect their diaphragm strength to increase and their forced exploratory volume to increase. They no longer have trapped air to fight against because their brand new lung doesn’t (hopefully) have disease.

GOLD stage of COPDPercentage of predicted FEV1 value
Mild80 percent or above (in the presence of known disease)
Moderate50 to 79 percent
Severe30 to 49 percent
Very severe29 percent or less
GOLD, 2016

Everyone has a residual volume that just hangs out in the lungs so that part is normal. If your patient has a lung disease and they were able to get all our air out of their lungs in 1 second, then they probably didn’t have that much air in their lungs to begin with which would signal poor inspiratory volume, so we are targeting greater than 80%. Some healthy people can even get as high as 120% of their predicted value! Remember, this isn’t a percentage of the volume you have its a percentage of the expected volume you can exhale.

That’s all fine and good, but how the heck do we measure something like that without PFTs (pulmonary function tests)? One of the cool things our hospital did was utilize a device that went home with the patient to regularly measure lung function. It actually did a whole bunch of other things, too, like record and remind them about their medications. If you’ve ever seen someone after transplant, you know they have a ton of medications that have to be taken a thousand times every day. It was called a Spiro PD.

As cool as this device was, it was incredibly difficult to use properly and patients tended to get measurements that were all over the map. I found that they needed to be properly trained in how to take a deep breath and perform an FEV1 test with their new lungs! So here are some tips to generally improve FEV1 and overall lung function. You probably already do some of these things and just don’t know it!

  • Stand up. This allows you to utilize your full lung volume better, all other factors being normal. If you are sitting, several postural factors can influence your ability to take a deep breath. This particular portion can become problematic if your patient has balance impairments, but they can always hold on to a hemi-bar, counter top, or their walker. Make sure they aren’t weight-bearing through their hands on whatever surface you are using because this facilitates accessory muscles. A maximal inspiration typically requires some trunk movement in to the posterior space, so be sure to guard them closely. Don’t make the gait belt too tight or you will impact their inspiratory volume.
  • Use a mirror. Patients sometimes have no idea what they are doing when they breathe. Honestly, who pays attention to that, anyway? We jus breathe and get on with things. But we all know that patients develop some pretty serious compensations when disease is present which results in them changing their breathing patterns to less efficient techniques. Putting them in front of a mirror and utilizing this visual feedback can be really helpful in remediating those inefficient patterns. If you are using a bathroom mirror, this also allow them to use the counter top for support as needed.
  • Pre-training in diaphragmatic breathing. Especially if your patient has experienced a pulmonary disease, they will have the need for diaphragm retraining. However, this is not limited to patients in a disease state. Diaphragm training can be helpful for athletes, too. If you can trigger that diaphragm to engage at the proper moment and increase the strength of contraction, you can help your patient improve their inspiratory volume. We will talk about this in greater detail in a different post. I find tactile cues to be really helpful, though! Find things that really help them focus on breathing OUT!
  • Be ready ahead of time. So many times, I would be using the SpiroPD to test my patient’s FEV1 and they would place it down on the table or counter or the seat of their walker and then have to go hunting for it when it was time to breathe out. This wasted so much of their energy and ability to forcefully exhale. If you are using a measurement device for FEV1 or other lung function measure testing, have it in the patient’s hand, ready to go during testing so they don’t waste any energy.
  • Coaching. Spirometry testing isn’t easy and patients are quick to give up if they don’t know how long this is actually going to take. When doing an FEV1 test on the Spiro device, the device needs to calculate ALL the air the comes out, not just what comes out in 1 second. That means the patient has to keep blowing as long as they can, or as long as the machine needs them to. THIS IS SO HARD! They will need you to coach them in continuing the test as long as needed. It will feel uncomfortably long!

Something I love to do with patients who have a SpiroPD device is have them do their normal testing with all their altered posters and inefficient techniques while I was with them. We would review their results which were typically pretty awful (30-40%), then train them, reposition them, and retest them. This almost always showed significant improvement in their measures. (I love using the test-retest method to show improvement and the value of our interventions! I talk about that here, too!) And, if it didn’t, I knew something was actually wrong and I could confidently report to the transplant team.

Another thing we do is some magical math to look at lung function. We take FEV1 and divide it by FVC (forced vital capacity). We want this ratio to be pretty close to 1 to indicate healthy lung function. If you would like to calculate your predicted FVC, FEV1, or many other lung function measures, you can do that here or here! My predicted FEV1 is 3.56 liters! So I would need to do a spirometry test to see what percent of that I actually get and that would be my clinical value.

Northwestern Medicine

What got me on the track of talking about lung transplants? Well, I recently read an article about the first patient to receive a lung transplant due to COVID-19. A woman in her 20’s was admitted to the hospital for acute respiratory distress due to COVID-19. She had been on a ventilator for two months and was still failing. They transitioned her to ECMO, but she continued to decline. Her kidneys and liver started to fail and there was no hope of returning to normal. The damage to her lungs became irreversible. Doctors found that not only did she have a viral COVID-19 infection, but also ended up with bacterial abscesses in her lungs. After the viral infection had cleared, they determined the only way to save her was a double lung transplant. That picture above is her lungs prior to transplant. You can see that the left lung is nothing but giant air pockets and the right one is completely full of consolidation of varying types. All in all, nothing here is viable.

The next picture is of a lung removed from this twenty year old female. This lung is one of the most damaged I have seen. It’s like the lung tissue liquified. It’s hard to even describe. If you don’t want to see it, keep scrolling, but in case you do, here you go.


Northwestern Medicine

After transplant, this woman began to make a significant recovery. Her major organ systems began to heal and was working on coming off of ECMO while rehabbing. She did begin to show some of those signs of rejection we talked about earlier, but the anti-rejection medications seemed to be working well. She has a long road ahead of her fo many reasons. She was intubated and ventilated in the ICU for more than two months so she was significantly deconditioned. So what’s the overall outlook?

Well, patients who undergo lung transplant have about a 50% chance of surviving five years afterward. That number is improving slowly as the medical community gets better at interventions aimed at rejection, but her odds are still better than what they were prior to transplant where she had, at best, days before dying of multisystem failure. Her transplant candidacy was due to her very young age and lack of comorbid conditions, as well as her severe decline. I realize that, for those that are familiar with the transplant world, this could be somewhat controversial. People wait years for lungs and many never get them.

For those who are not familiar with the transplant system, this is not a go-to intervention. You have to have transplantable lungs available which means people have to be dying. You have to have a donor match. You have to have lungs that haven’t been infected with COVID-19. And you have to have a patient who is healthy enough (other than COVID-19) to receive the lungs. They also have to be generally the right size (although lungs can be resized to a point). Similar to ECMO, this is a literal last resort. This type of intervention takes a large team, including an extra set of team members from the transplant team, like social workers, transplant surgeons, specialized nurses and rehab providers, in addition to all the other wonderful medical professionals and family involved. The transplant team from Northwestern that perform the transplant on this women spent two and a half days just repairing the donor lungs she received to ensure they were the best quality for her.

What are some techniques you use to improve lung function? Tell me about them in the comments!

More from the Pulmonary Hygiene Toolbox…

The Duet Device

Have you seen an Acapella Duet before? This is another one of those things I wish I could hand out to maybe half of my patients. A Duet device is a special kind of Positive Expiratory Pressure (PEP) that provides resistive oscillatory pressure to exhalation which promotes increased lung volumes due to re-inflation of collapsedContinue reading “The Duet Device”


Something went wrong. Please refresh the page and/or try again.

Follow my blog for more!


Herman, C. (2020). 1st-Known U.S. Lung Transplant For COVID-19 Patient Performed In Chicago. Shots: Health News from NPR. Retrieved from

LUNGFUNKTION — Practice compendium for semester 6. Department of Medical Sciences, Clinical Physiology, Academic Hospital, Uppsala, Sweden. Retrieved 2010.

MedlinePlus. (2020). Transplant rejection. Retrieved from

Thompson, E. G., & Russo, E. T. (2019) Forced Expiratory Volume and Forced Vital Capacity. University of Michigan Medicine.

Yeung, J. C., & Keshavjee, S. (2014). Overview of clinical lung transplantation. Cold Spring Harbor perspectives in medicine4(1), a015628.

Follow @DoctorBthePT on Twitter for regular updates!

header image credit

Remote Interventions for Pain Amid COVID-19

I am the first to admit that I find treating patients with chronic pain to be SO HARD. Thanks to a few helpful tips from friends and some continuing education, I can just barely touch my toe to the water. But, like many, I have been wondering how COVID-19 and lockdowns and masks and all of those things that have so drastically changed our way of life are changing the pain experience of my patients. Instead of making gross exclamations like so many new stories, I’m looking to the evidence.

Researchers in neuroscience, pain management, and psychology came together recently to write an article on this exact thing. How ARE patients who have chronic pain experiencing this pandemic lifestyle? How is it effecting their perceptions of pain? Is their life changing because of this? And what are the recommendations for what we do about it?

Over 500 people took part in the survey which asked them questions about their pain experience at different points during the pandemic (in the UK). Questions were asked pre- and post-lockdown and comparisons were made for pain behaviors, pain catastrophizing, and pain ratings. Psychological health conditions were also monitored.

The participants in the study were varied across ages and gender descriptions (including “other”), and the time period observed was about a month. It was amazing to me how much could change for the patients in only a months time with the onset of lockdown restrictions. Pain diagnoses were also varied with the highest number of participants demonstrating the diagnoses of “chronic widespread pain” and “chronic primary/secondary musculoskeletal pain”. However, some other more familiar categories were also present such as CRPS, chronic headache, and neuropathic pain.

Photo by Andrea Piacquadio on

Among other scales and tests, patients were asked to identify their pain on a 100 point VAS. The pre-COVID to post-COVID scores were significantly different, with a change of about 33 points in perceived pain on average across participants. That is a HUGE increase. Hoping all other factors were equal as much as they could have been, simply the presence of lockdown restrictions increased perceived pain by one third in patients who already had chronic pain. Now, I say perceived pain intentionally, as patients were also assessed in other ways to determine physical pain, which did not actually change throughout the time frame. The authors are clear that this demonstrates a psychological distress effect of lockdown restrictions on the perception of pain, not actual physical pain.

Patients with chronic pain were also eight times more likely to self-isolate and four times more likely to have a confounding illness during this time than their matched peers who did not have chronic pain.

Patients with chronic pain also experienced tiredness and loneliness twice as often, experienced pain catastrophizing twice as often, anxiety five and a half times as often, and depression nine times as often. They were also ten times more likely to reduce their physical activity.

“As pain catastrophizing was also the strongest predictor of self-perceived increases in pain in the full chronic pain cohort, this points to the need to make this a principle clinical outcome and
target for telemedicine pain management.”

Fallon, et al., 2020

The article has some recommendations for what we can provide remotely to help these patients. COVID-19 has opened the door to telerehab, telehealth, telemedicine, remote services, or whatever you have to call it to be able to bill for it. The reimbursement may not be awesome, but this method of providing care for rehab clinicians is here to stay. Do you know how I know that? Because Seema Verma said so. And if she is committing CMS to stick with it, most everyone else will follow suit. I have some information about telerehab on the resources page if you need more information about how to bring this in to your practice.


So, we know that opioids are NOT the answer to pain. But sometimes it feel like ONLY rehab clinicians actually know that because we still see them prescribed so often. However, this particular articles has some better options:

  • Now, like I said above, I’m no expert in chronic pain. But, I do know that education can be very effective in modulating and mitigating pain in certain populations and can be especially effective for patients who experience pain catastrophizing. This education can very easily be delivered through a remote platform.
  • Cognitive behavioral therapeutic techniques can also successfully be delivered remotely and are effective in the management of pain catastrophizing.
  • And the big one: physical exercise needs to be implemented. Not just to reorient fear-avoidance behaviors and provide neuromuscular re-education, but also to return patients with chronic pain to their prior level of function. Remember, we was above that they were significantly more likely to self-isolate and reduce their physical activity.

Now, obviously we don’t know if these interventions are AS effective when delivered remotely as they are in person, but that sounds like a really great research opportunity for some of my friends out there who primarily manage chronic pain! There is some preliminary evidence that telerehab interventions may be just as effective but we need more evidence.

We highlight the pivotal role of pain catastrophizing and reduced physical activity on the experience of people who live with chronic pain during lockdown conditions. This is significant because it points to potential clinical targets for therapeutic and behavioural interventions during the current, and future, crises.

Fallon, et al., 2020

If you aren’t treating patients remotely, yet, you need to start. Telerehab is the answer for chronic pain, now and in the future. Be ready to move with the rest of us.

What interventions are you providing remotely for your patients with chronic pain? Tell me about it in the comments!

More Reads…

ABGs (Part II)

So, now that you’ve read all the basics about ABGs in the first post, here is a little more about interpreting lab values and how to determine compensated conditions. This is where it gets fun! First off, let’s take a look at what NORMAL lab values probably look like: pH: 7.35-7.45 Partial pressure of oxygenContinue reading “ABGs (Part II)”


Research is piling in regarding the neurological effects of COVID-19 and the depth of the research is giving us some really concrete information to help guide treatment, screening, and monitoring strategies. The anecdotal evidence is continuing to build quickly so I’ve significantly updated this post to reflect some of the more recent changes and findings.Continue reading “COVID Brain”

According to the Scientific Community, It’s Time for Change

If you couldn’t tell, I’ve been hinting at this for a while. In several posts over the past few months, there has been discussion amongst the medical community that has created controversy regarding the mode of transmission of COVID-19. Many providers of all disciplines have been very concerned about their contraction rates and that ofContinue reading “According to the Scientific Community, It’s Time for Change”


Something went wrong. Please refresh the page and/or try again.

Follow my blog for more!


Ambrose KR, Golightly YM. Physical exercise as non-pharmacological treatment of chronic pain: Why and when. BEST PRACT RES CL RH 2015;29(1):120-130.

Fallon, N., Brown, C., Twiddy, H., Brian, E., Fank, B., Nurmikko, T., Stancak, A. (2020). Adverse effects of COVID-19 related lockdown on pain, physical activity, and psychological well-bring in people with chronic pain. medRxiv [made available pre-review]. Retrieved from

Geneen LJ, Moore RA, Clarke C, Martin D, Colvin LA, Smith BH. Physical activity and exercise for chronic pain in adults: an overview of Cochrane Reviews. Cochrane Database Syst Rev 2017(4).

Piga M, Cangemi I, Mathieu A, Cauli A. Telemedicine for patients with rheumatic diseases: Systematic review and proposal for research agenda. Seminars in Arthritis and Rheumatism 2017;47(1):121-128.

Schütze R, Rees C, Smith A, Slater H, Campbell JM, O’Sullivan P. How Can We Best Reduce Pain Catastrophizing in Adults With Chronic Noncancer Pain? A Systematic Review and MetaAnalysis. J Pain 2018;19(3):233-256.

Westman AE, Boersma K, Leppert J, Linton SJ. Fear-avoidance beliefs, catastrophizing, and distress: a longitudinal subgroup analysis on patients with musculoskeletal pain. Clin J Pain 2011;27(7):567-577.

Follow @DoctorBthePT on Twitter for regular updates!